{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: 0-dimensional biomaterials lack inductive properties.\n\nDocument title: New opportunities: the use of nanotechnologies to manipulate and track stem cells.\n\nAbstract sentences:\n[0] Nanotechnologies are emerging platforms that could be useful in measuring, understanding, and manipulating stem cells.\n[1] Examples include magnetic nanoparticles and quantum dots for stem cell labeling and in vivo tracking; nanoparticles, carbon nanotubes, and polyplexes for the intracellular delivery of genes/oligonucleotides and protein/peptides; and engineered nanometer-scale scaffolds for stem cell differentiation and transplantation.\n[2] This review examines the use of nanotechnologies for stem cell tracking, differentiation, and transplantation.\n[3] We further discuss their utility and the potential concerns regarding their cytotoxicity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 0, "doc_id": 31715818, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [31715818], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: 1 in 5 million in UK have abnormal PrP positivity.\n\nDocument title: Prevalent abnormal prion protein in human appendixes after bovine spongiform encephalopathy epizootic: large scale survey\n\nAbstract sentences:\n[0] OBJECTIVES To carry out a further survey of archived appendix samples to understand better the differences between existing estimates of the prevalence of subclinical infection with prions after the bovine spongiform encephalopathy epizootic and to see whether a broader birth cohort was affected, and to understand better the implications for the management of blood and blood products and for the handling of surgical instruments.\n[1] DESIGN Irreversibly unlinked and anonymised large scale survey of archived appendix samples.\n[2] SETTING Archived appendix samples from the pathology departments of 41 UK hospitals participating in the earlier survey, and additional hospitals in regions with lower levels of participation in that survey.\n[3] SAMPLE 32,441 archived appendix samples fixed in formalin and embedded in paraffin and tested for the presence of abnormal prion protein (PrP).\n[4] RESULTS Of the 32,441 appendix samples 16 were positive for abnormal PrP, indicating an overall prevalence of 493 per million population (95% confidence interval 282 to 801 per million).\n[5] The prevalence in those born in 1941-60 (733 per million, 269 to 1596 per million) did not differ significantly from those born between 1961 and 1985 (412 per million, 198 to 758 per million) and was similar in both sexes and across the three broad geographical areas sampled.\n[6] Genetic testing of the positive specimens for the genotype at PRNP codon 129 revealed a high proportion that were valine homozygous compared with the frequency in the normal population, and in stark contrast with confirmed clinical cases of vCJD, all of which were methionine homozygous at PRNP codon 129.\n[7] CONCLUSIONS This study corroborates previous studies and suggests a high prevalence of infection with abnormal PrP, indicating vCJD carrier status in the population compared with the 177 vCJD cases to date.\n[8] These findings have important implications for the management of blood and blood products and for the handling of surgical instruments."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"RESULTS Of the 32,441 appendix samples 16 were positive for abnormal PrP, indicating an overall prevalence of 493 per million population (95% confidence interval 282 to 801 per million).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 2, "doc_id": 13734012, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [13734012], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: 1-1% of colorectal cancer patients are diagnosed with regional or distant metastases.\n\nDocument title: Relation between Medicare screening reimbursement and stage at diagnosis for older patients with colon cancer.\n\nAbstract sentences:\n[0] CONTEXT Medicare's reimbursement policy was changed in 1998 to provide coverage for screening colonoscopies for patients with increased colon cancer risk, and expanded further in 2001 to cover screening colonoscopies for all individuals.\n[1] OBJECTIVE To determine whether the Medicare reimbursement policy changes were associated with an increase in either colonoscopy use or early stage colon cancer diagnosis.\n[2] DESIGN, SETTING, AND PARTICIPANTS Patients in the Surveillance, Epidemiology, and End Results Medicare linked database who were 67 years of age and older and had a primary diagnosis of colon cancer during 1992-2002, as well as a group of Medicare beneficiaries who resided in Surveillance, Epidemiology, and End Results areas but who were not diagnosed with cancer.\n[3] MAIN OUTCOME MEASURES Trends in colonoscopy and sigmoidoscopy use among Medicare beneficiaries without cancer were assessed using multivariate Poisson regression.\n[4] Among the patients with cancer, stage was classified as early (stage I) vs all other (stages II-IV).\n[5] Time was categorized as period 1 (no screening coverage, 1992-1997), period 2 (limited coverage, January 1998-June 2001), and period 3 (universal coverage, July 2001-December 2002).\n[6] A multivariate logistic regression (outcome = early stage) was used to assess temporal trends in stage at diagnosis; an interaction term between tumor site and time was included.\n[7] RESULTS Colonoscopy use increased from an average rate of 285/100,000 per quarter in period 1 to 889 and 1919/100,000 per quarter in periods 2 (P<.001) and 3 (P vs 2<.001), respectively.\n[8] During the study period, 44,924 eligible patients were diagnosed with colorectal cancer.\n[9] The proportion of patients diagnosed at an early stage increased from 22.5% in period 1 to 25.5% in period 2 and 26.3% in period 3 (P<.001 for each pairwise comparison).\n[10] The changes in Medicare coverage were strongly associated with early stage at diagnosis for patients with proximal colon lesions (adjusted relative risk period 2 vs 1, 1.19; 95% confidence interval, 1.13-1.26; adjusted relative risk period 3 vs 2, 1.10; 95% confidence interval, 1.02-1.17) but weakly associated, if at all, for patients with distal colon lesions (adjusted relative risk period 2 vs 1, 1.07; 95% confidence interval, 1.01-1.13; adjusted relative risk period 3 vs 2, 0.97; 95% confidence interval, 0.90-1.05).\n[11] CONCLUSIONS Expansion of Medicare reimbursement to cover colon cancer screening was associated with an increased use of colonoscopy for Medicare beneficiaries, and for those who were diagnosed with colon cancer, an increased probability of being diagnosed at an early stage.\n[12] The selective effect of the coverage change on proximal colon lesions suggests that increased use of whole-colon screening modalities such as colonoscopy may have played a pivotal role."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 4, "doc_id": 22942787, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [22942787], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: 10% of sudden infant death syndrome (SIDS) deaths happen in newborns aged less than 6 months.\n\nDocument title: Sudden infant death syndrome.\n\nAbstract sentences:\n[0] Despite declines in prevalence during the past two decades, sudden infant death syndrome (SIDS) continues to be the leading cause of death for infants aged between 1 month and 1 year in developed countries.\n[1] Behavioural risk factors identified in epidemiological studies include prone and side positions for infant sleep, smoke exposure, soft bedding and sleep surfaces, and overheating.\n[2] Evidence also suggests that pacifier use at sleep time and room sharing without bed sharing are associated with decreased risk of SIDS.\n[3] Although the cause of SIDS is unknown, immature cardiorespiratory autonomic control and failure of arousal responsiveness from sleep are important factors.\n[4] Gene polymorphisms relating to serotonin transport and autonomic nervous system development might make affected infants more vulnerable to SIDS.\n[5] Campaigns for risk reduction have helped to reduce SIDS incidence by 50-90%.\n[6] However, to reduce the incidence even further, greater strides must be made in reducing prenatal smoke exposure and implementing other recommended infant care practices.\n[7] Continued research is needed to identify the pathophysiological basis of SIDS."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 6, "doc_id": 2613775, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [2613775], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: 32% of liver transplantation programs required patients to discontinue methadone treatment in 2001.\n\nDocument title: Liver transplantation and opioid dependence.\n\nAbstract sentences:\n[0] ContextChronic hepatitis C is the leading cause for liver transplantation in the United States.\n[1] Intravenous drug use, the major risk factor, accounts for approximately 60% of hepatitis C virus transmission.\n[2] Information from the United Network of Organ Sharing (UNOS) does not address substance use among liver transplantation patients.\n[3] ObjectiveTo identify addiction-related criteria for admission to the UNOS liver transplantation waiting list and posttransplantation problems experienced by patients who are prescribed maintenance methadone.\n[4] Design, Setting, and ParticipantsMail survey of all 97 adult US liver transplantation programs (belonging to UNOS) in March 2000 with telephone follow-up conducted in May and June 2000.Main Outcome MeasuresPrograms' acceptance and management of patients with past or present substance use disorder.\n[5] ResultsOf the 97 programs surveyed, 87 (90%) responded.\n[6] All accept applicants with a history of alcoholism or other addictions, including heroin dependence.\n[7] Eighty-eight percent of the responding programs require at least 6 months of abstinence from alcohol; 83% from illicit drugs.\n[8] Ninety-four percent have addiction treatment requirements.\n[9] Consultations from substance abuse specialists are obtained by 86%.\n[10] Patients receiving methadone maintenance are accepted by 56% of the responding programs.\n[11] Approximately 180 patients receiving methadone maintenance are reported to have undergone liver transplantation.\n[12] ConclusionsMost liver transplantation programs have established policies for patients with substance use disorders.\n[13] Opiate-dependent patients receiving opiate replacement therapy seem underrepresented in transplantation programs.\n[14] Little anecdotal evidence for negative impact of opiate replacement therapy on liver transplantation outcome was found.\n[15] Policies requiring discontinuation of methadone in 32% of all programs contradict the evidence base for efficacy of long-term replacement therapies and potentially result in relapse of previously stable patients."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [15]\nExplanation: Evidence states: \"Policies requiring discontinuation of methadone in 32% of all programs contradict the evidence base for efficacy of long-term replacement therapies and potentially result in relapse of previously stable patients.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 9, "doc_id": 44265107, "label": "SUPPORTS", "evidence_sentence_ids": [15], "cited_doc_ids": [44265107], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: 4-PBA treatment decreases endoplasmic reticulum stress in response to general endoplasmic reticulum stress markers.\n\nDocument title: Wolfram syndrome 1 and adenylyl cyclase 8 interact at the plasma membrane to regulate insulin production and secretion\n\nAbstract sentences:\n[0] Endoplasmic reticulum (ER) stress causes pancreatic β-cell dysfunction and contributes to β-cell loss and the progression of type 2 diabetes.\n[1] Wolfram syndrome 1 (WFS1) has been shown to be an important regulator of the ER stress signalling pathway; however, its role in β-cell function remains unclear.\n[2] Here we provide evidence that WFS1 is essential for glucose- and glucagon-like peptide 1 (GLP-1)-stimulated cyclic AMP production and regulation of insulin biosynthesis and secretion.\n[3] Stimulation with glucose causes WFS1 translocation from the ER to the plasma membrane, where it forms a complex with adenylyl cyclase 8 (AC8), an essential cAMP-generating enzyme in the β-cell that integrates glucose and GLP-1 signalling.\n[4] ER stress and mutant WFS1 inhibit complex formation and activation of AC8, reducing cAMP synthesis and insulin secretion.\n[5] These findings reveal that an ER-stress-related protein has a distinct role outside the ER regulating both insulin biosynthesis and secretion.\n[6] The reduction of WFS1 protein on the plasma membrane during ER stress is a contributing factor for β-cell dysfunction and progression of type 2 diabetes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 10, "doc_id": 32587939, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [32587939], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: 4-PBA treatment raises endoplasmic reticulum stress in response to general endoplasmic reticulum stress markers.\n\nDocument title: Wolfram syndrome 1 and adenylyl cyclase 8 interact at the plasma membrane to regulate insulin production and secretion\n\nAbstract sentences:\n[0] Endoplasmic reticulum (ER) stress causes pancreatic β-cell dysfunction and contributes to β-cell loss and the progression of type 2 diabetes.\n[1] Wolfram syndrome 1 (WFS1) has been shown to be an important regulator of the ER stress signalling pathway; however, its role in β-cell function remains unclear.\n[2] Here we provide evidence that WFS1 is essential for glucose- and glucagon-like peptide 1 (GLP-1)-stimulated cyclic AMP production and regulation of insulin biosynthesis and secretion.\n[3] Stimulation with glucose causes WFS1 translocation from the ER to the plasma membrane, where it forms a complex with adenylyl cyclase 8 (AC8), an essential cAMP-generating enzyme in the β-cell that integrates glucose and GLP-1 signalling.\n[4] ER stress and mutant WFS1 inhibit complex formation and activation of AC8, reducing cAMP synthesis and insulin secretion.\n[5] These findings reveal that an ER-stress-related protein has a distinct role outside the ER regulating both insulin biosynthesis and secretion.\n[6] The reduction of WFS1 protein on the plasma membrane during ER stress is a contributing factor for β-cell dysfunction and progression of type 2 diabetes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 11, "doc_id": 32587939, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [32587939], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: 40mg/day dosage of folic acid and 2mg/day dosage of vitamin B12 does not affect chronic kidney disease (CKD) progression.\n\nDocument title: Effect of homocysteine lowering on mortality and vascular disease in advanced chronic kidney disease and end-stage renal disease: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT High plasma homocysteine levels are a risk factor for mortality and vascular disease in observational studies of patients with chronic kidney disease.\n[1] Folic acid and B vitamins decrease homocysteine levels in this population but whether they lower mortality is unknown.\n[2] OBJECTIVE To determine whether high doses of folic acid and B vitamins administered daily reduce mortality in patients with chronic kidney disease.\n[3] DESIGN, SETTING, AND PARTICIPANTS Double-blind randomized controlled trial (2001-2006) in 36 US Department of Veterans Affairs medical centers.\n[4] Median follow-up was 3.2 years for 2056 participants aged 21 years or older with advanced chronic kidney disease (estimated creatinine clearance < or =30 mL/min) (n = 1305) or end-stage renal disease (n = 751) and high homocysteine levels (> or = 15 micromol/L).\n[5] INTERVENTION Participants received a daily capsule containing 40 mg of folic acid, 100 mg of pyridoxine hydrochloride (vitamin B6), and 2 mg of cyanocobalamin (vitamin B12) or a placebo.\n[6] MAIN OUTCOME MEASURES The primary outcome was all-cause mortality.\n[7] Secondary outcomes included myocardial infarction (MI), stroke, amputation of all or part of a lower extremity, a composite of these 3 plus all-cause mortality, time to initiation of dialysis, and time to thrombosis of arteriovenous access in hemodialysis patients.\n[8] RESULTS Mean baseline homocysteine level was 24.0 micromol/L in the vitamin group and 24.2 micromol/L in the placebo group.\n[9] It was lowered 6.3 micromol/L (25.8%; P < .001) in the vitamin group and 0.4 micromol/L (1.7%; P = .14) in the placebo group at 3 months, but there was no significant effect on mortality (448 vitamin group deaths vs 436 placebo group deaths) (hazard ratio [HR], 1.04; 95% CI, 0.91-1.18).\n[10] No significant effects were demonstrated for secondary outcomes or adverse events: there were 129 MIs in the vitamin group vs 150 for placebo (HR, 0.86; 95% CI, 0.67-1.08), 37 strokes in the vitamin group vs 41 for placebo (HR, 0.90; 95% CI, 0.58-1.40), and 60 amputations in the vitamin group vs 53 for placebo (HR, 1.14; 95% CI, 0.79-1.64).\n[11] In addition, the composite of MI, stroke, and amputations plus mortality (P = .85), time to dialysis (P = .38), and time to thrombosis in hemodialysis patients (P = .97) did not differ between the vitamin and placebo groups.\n[12] CONCLUSION Treatment with high doses of folic acid and B vitamins did not improve survival or reduce the incidence of vascular disease in patients with advanced chronic kidney disease or end-stage renal disease.\n[13] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00032435."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"RESULTS Mean baseline homocysteine level was 24.0 micromol/L in the vitamin group and 24.2 micromol/L in the placebo group.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 12, "doc_id": 33409100, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [33409100], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: 40mg/day dosage of folic acid and 2mg/day dosage of vitamin B12 does not affect chronic kidney disease (CKD) progression.\n\nDocument title: Effect of homocysteine lowering on mortality and vascular disease in advanced chronic kidney disease and end-stage renal disease: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT High plasma homocysteine levels are a risk factor for mortality and vascular disease in observational studies of patients with chronic kidney disease.\n[1] Folic acid and B vitamins decrease homocysteine levels in this population but whether they lower mortality is unknown.\n[2] OBJECTIVE To determine whether high doses of folic acid and B vitamins administered daily reduce mortality in patients with chronic kidney disease.\n[3] DESIGN, SETTING, AND PARTICIPANTS Double-blind randomized controlled trial (2001-2006) in 36 US Department of Veterans Affairs medical centers.\n[4] Median follow-up was 3.2 years for 2056 participants aged 21 years or older with advanced chronic kidney disease (estimated creatinine clearance < or =30 mL/min) (n = 1305) or end-stage renal disease (n = 751) and high homocysteine levels (> or = 15 micromol/L).\n[5] INTERVENTION Participants received a daily capsule containing 40 mg of folic acid, 100 mg of pyridoxine hydrochloride (vitamin B6), and 2 mg of cyanocobalamin (vitamin B12) or a placebo.\n[6] MAIN OUTCOME MEASURES The primary outcome was all-cause mortality.\n[7] Secondary outcomes included myocardial infarction (MI), stroke, amputation of all or part of a lower extremity, a composite of these 3 plus all-cause mortality, time to initiation of dialysis, and time to thrombosis of arteriovenous access in hemodialysis patients.\n[8] RESULTS Mean baseline homocysteine level was 24.0 micromol/L in the vitamin group and 24.2 micromol/L in the placebo group.\n[9] It was lowered 6.3 micromol/L (25.8%; P < .001) in the vitamin group and 0.4 micromol/L (1.7%; P = .14) in the placebo group at 3 months, but there was no significant effect on mortality (448 vitamin group deaths vs 436 placebo group deaths) (hazard ratio [HR], 1.04; 95% CI, 0.91-1.18).\n[10] No significant effects were demonstrated for secondary outcomes or adverse events: there were 129 MIs in the vitamin group vs 150 for placebo (HR, 0.86; 95% CI, 0.67-1.08), 37 strokes in the vitamin group vs 41 for placebo (HR, 0.90; 95% CI, 0.58-1.40), and 60 amputations in the vitamin group vs 53 for placebo (HR, 1.14; 95% CI, 0.79-1.64).\n[11] In addition, the composite of MI, stroke, and amputations plus mortality (P = .85), time to dialysis (P = .38), and time to thrombosis in hemodialysis patients (P = .97) did not differ between the vitamin and placebo groups.\n[12] CONCLUSION Treatment with high doses of folic acid and B vitamins did not improve survival or reduce the incidence of vascular disease in patients with advanced chronic kidney disease or end-stage renal disease.\n[13] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00032435."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"CONCLUSION Treatment with high doses of folic acid and B vitamins did not improve survival or reduce the incidence of vascular disease in patients with advanced chronic kidney disease or end-stage renal disease.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 12, "doc_id": 33409100, "label": "SUPPORTS", "evidence_sentence_ids": [12], "cited_doc_ids": [33409100], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: 5'-nucleotidase metabolizes 6MP.\n\nDocument title: Relapse specific mutations in NT5C2 in childhood acute lymphoblastic leukemia\n\nAbstract sentences:\n[0] Relapsed childhood acute lymphoblastic leukemia (ALL) carries a poor prognosis, despite intensive retreatment, owing to intrinsic drug resistance.\n[1] The biological pathways that mediate resistance are unknown.\n[2] Here, we report the transcriptome profiles of matched diagnosis and relapse bone marrow specimens from ten individuals with pediatric B-lymphoblastic leukemia using RNA sequencing.\n[3] Transcriptome sequencing identified 20 newly acquired, novel nonsynonymous mutations not present at initial diagnosis, with 2 individuals harboring relapse-specific mutations in the same gene, NT5C2, encoding a 5'-nucleotidase.\n[4] Full-exon sequencing of NT5C2 was completed in 61 further relapse specimens, identifying additional mutations in 5 cases.\n[5] Enzymatic analysis of mutant proteins showed that base substitutions conferred increased enzymatic activity and resistance to treatment with nucleoside analog therapies.\n[6] Clinically, all individuals who harbored NT5C2 mutations relapsed early, within 36 months of initial diagnosis (P = 0.03).\n[7] These results suggest that mutations in NT5C2 are associated with the outgrowth of drug-resistant clones in ALL."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 14, "doc_id": 641786, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [641786], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: 50% of patients exposed to radiation have activated markers of mesenchymal stem cells.\n\nDocument title: KLF4-dependent phenotypic modulation of smooth muscle cells has a key role in atherosclerotic plaque pathogenesis\n\nAbstract sentences:\n[0] Previous studies investigating the role of smooth muscle cells (SMCs) and macrophages in the pathogenesis of atherosclerosis have provided controversial results owing to the use of unreliable methods for clearly identifying each of these cell types.\n[1] Here, using Myh11-CreERT2 ROSA floxed STOP eYFP Apoe−/− mice to perform SMC lineage tracing, we find that traditional methods for detecting SMCs based on immunostaining for SMC markers fail to detect >80% of SMC-derived cells within advanced atherosclerotic lesions.\n[2] These unidentified SMC-derived cells exhibit phenotypes of other cell lineages, including macrophages and mesenchymal stem cells (MSCs).\n[3] SMC-specific conditional knockout of Krüppel-like factor 4 (Klf4) resulted in reduced numbers of SMC-derived MSC- and macrophage-like cells, a marked reduction in lesion size, and increases in multiple indices of plaque stability, including an increase in fibrous cap thickness as compared to wild-type controls.\n[4] On the basis of in vivo KLF4 chromatin immunoprecipitation–sequencing (ChIP-seq) analyses and studies of cholesterol-treated cultured SMCs, we identified >800 KLF4 target genes, including many that regulate pro-inflammatory responses of SMCs.\n[5] Our findings indicate that the contribution of SMCs to atherosclerotic plaques has been greatly underestimated, and that KLF4-dependent transitions in SMC phenotype are critical in lesion pathogenesis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 15, "doc_id": 22080671, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [22080671], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: 53% of perinatal mortality is due to low birth weight.\n\nDocument title: Estimates of global prevalence of childhood underweight in 1990 and 2015.\n\nAbstract sentences:\n[0] CONTEXT One key target of the United Nations Millennium Development goals is to reduce the prevalence of underweight among children younger than 5 years by half between 1990 and 2015.\n[1] OBJECTIVE To estimate trends in childhood underweight by geographic regions of the world.\n[2] DESIGN, SETTING, AND PARTICIPANTS Time series study of prevalence of underweight, defined as weight 2 SDs below the mean weight for age of the National Center for Health Statistics and World Health Organization (WHO) reference population.\n[3] National prevalence rates derived from the WHO Global Database on Child Growth and Malnutrition, which includes data on approximately 31 million children younger than 5 years who participated in 419 national nutritional surveys in 139 countries from 1965 through 2002.\n[4] MAIN OUTCOME MEASURES Linear mixed-effects modeling was used to estimate prevalence rates and numbers of underweight children by region in 1990 and 2015 and to calculate the changes (ie, increase or decrease) to these values between 1990 and 2015.\n[5] RESULTS Worldwide, underweight prevalence was projected to decline from 26.5% in 1990 to 17.6% in 2015, a change of -34% (95% confidence interval [CI], -43% to -23%).\n[6] In developed countries, the prevalence was estimated to decrease from 1.6% to 0.9%, a change of -41% (95% CI, -92% to 343%).\n[7] In developing regions, the prevalence was forecasted to decline from 30.2% to 19.3%, a change of -36% (95% CI, -45% to -26%).\n[8] In Africa, the prevalence of underweight was forecasted to increase from 24.0% to 26.8%, a change of 12% (95% CI, 8%-16%).\n[9] In Asia, the prevalence was estimated to decrease from 35.1% to 18.5%, a change of -47% (95% CI, -58% to -34%).\n[10] Worldwide, the number of underweight children was projected to decline from 163.8 million in 1990 to 113.4 million in 2015, a change of -31% (95% CI, -40% to -20%).\n[11] Numbers are projected to decrease in all subregions except the subregions of sub-Saharan, Eastern, Middle, and Western Africa, which are expected to experience substantial increases in the number of underweight children.\n[12] CONCLUSIONS An overall improvement in the global situation is anticipated; however, neither the world as a whole, nor the developing regions, are expected to achieve the Millennium Development goals.\n[13] This is largely due to the deteriorating situation in Africa where all subregions, except Northern Africa, are expected to fail to meet the goal."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 17, "doc_id": 1606628, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [1606628], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: 61% of colorectal cancer patients are diagnosed with regional or distant metastases.\n\nDocument title: Relation between Medicare screening reimbursement and stage at diagnosis for older patients with colon cancer.\n\nAbstract sentences:\n[0] CONTEXT Medicare's reimbursement policy was changed in 1998 to provide coverage for screening colonoscopies for patients with increased colon cancer risk, and expanded further in 2001 to cover screening colonoscopies for all individuals.\n[1] OBJECTIVE To determine whether the Medicare reimbursement policy changes were associated with an increase in either colonoscopy use or early stage colon cancer diagnosis.\n[2] DESIGN, SETTING, AND PARTICIPANTS Patients in the Surveillance, Epidemiology, and End Results Medicare linked database who were 67 years of age and older and had a primary diagnosis of colon cancer during 1992-2002, as well as a group of Medicare beneficiaries who resided in Surveillance, Epidemiology, and End Results areas but who were not diagnosed with cancer.\n[3] MAIN OUTCOME MEASURES Trends in colonoscopy and sigmoidoscopy use among Medicare beneficiaries without cancer were assessed using multivariate Poisson regression.\n[4] Among the patients with cancer, stage was classified as early (stage I) vs all other (stages II-IV).\n[5] Time was categorized as period 1 (no screening coverage, 1992-1997), period 2 (limited coverage, January 1998-June 2001), and period 3 (universal coverage, July 2001-December 2002).\n[6] A multivariate logistic regression (outcome = early stage) was used to assess temporal trends in stage at diagnosis; an interaction term between tumor site and time was included.\n[7] RESULTS Colonoscopy use increased from an average rate of 285/100,000 per quarter in period 1 to 889 and 1919/100,000 per quarter in periods 2 (P<.001) and 3 (P vs 2<.001), respectively.\n[8] During the study period, 44,924 eligible patients were diagnosed with colorectal cancer.\n[9] The proportion of patients diagnosed at an early stage increased from 22.5% in period 1 to 25.5% in period 2 and 26.3% in period 3 (P<.001 for each pairwise comparison).\n[10] The changes in Medicare coverage were strongly associated with early stage at diagnosis for patients with proximal colon lesions (adjusted relative risk period 2 vs 1, 1.19; 95% confidence interval, 1.13-1.26; adjusted relative risk period 3 vs 2, 1.10; 95% confidence interval, 1.02-1.17) but weakly associated, if at all, for patients with distal colon lesions (adjusted relative risk period 2 vs 1, 1.07; 95% confidence interval, 1.01-1.13; adjusted relative risk period 3 vs 2, 0.97; 95% confidence interval, 0.90-1.05).\n[11] CONCLUSIONS Expansion of Medicare reimbursement to cover colon cancer screening was associated with an increased use of colonoscopy for Medicare beneficiaries, and for those who were diagnosed with colon cancer, an increased probability of being diagnosed at an early stage.\n[12] The selective effect of the coverage change on proximal colon lesions suggests that increased use of whole-colon screening modalities such as colonoscopy may have played a pivotal role."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 18, "doc_id": 22942787, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [22942787], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: 7-day-old adult Caenorhabditis elegans exhibit approximately 5% of the learning capacity seen in 1-day old adults.\n\nDocument title: Insulin Signaling and Dietary Restriction Differentially Influence the Decline of Learning and Memory with Age\n\nAbstract sentences:\n[0] Of all the age-related declines, memory loss is one of the most devastating.\n[1] While conditions that increase longevity have been identified, the effects of these longevity-promoting factors on learning and memory are unknown.\n[2] Here we show that the C. elegans Insulin/IGF-1 receptor mutant daf-2 improves memory performance early in adulthood and maintains learning ability better with age but, surprisingly, demonstrates no extension in long-term memory with age.\n[3] By contrast, eat-2 mutants, a model of Dietary Restriction (DR), exhibit impaired long-term memory in young adulthood but maintain this level of memory longer with age.\n[4] We find that crh-1, the C. elegans homolog of the CREB transcription factor, is required for long-term associative memory, but not for learning or short-term memory.\n[5] The expression of crh-1 declines with age and differs in the longevity mutants, and CREB expression and activity correlate with memory performance.\n[6] Our results suggest that specific longevity treatments have acute and long-term effects on cognitive functions that decline with age through their regulation of rate-limiting genes required for learning and memory."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 19, "doc_id": 3202143, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [3202143], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: 7-day-old adult Caenorhabditis elegans exhibit approximately 75% of the learning capacity seen in 1-day old adults.\n\nDocument title: Insulin Signaling and Dietary Restriction Differentially Influence the Decline of Learning and Memory with Age\n\nAbstract sentences:\n[0] Of all the age-related declines, memory loss is one of the most devastating.\n[1] While conditions that increase longevity have been identified, the effects of these longevity-promoting factors on learning and memory are unknown.\n[2] Here we show that the C. elegans Insulin/IGF-1 receptor mutant daf-2 improves memory performance early in adulthood and maintains learning ability better with age but, surprisingly, demonstrates no extension in long-term memory with age.\n[3] By contrast, eat-2 mutants, a model of Dietary Restriction (DR), exhibit impaired long-term memory in young adulthood but maintain this level of memory longer with age.\n[4] We find that crh-1, the C. elegans homolog of the CREB transcription factor, is required for long-term associative memory, but not for learning or short-term memory.\n[5] The expression of crh-1 declines with age and differs in the longevity mutants, and CREB expression and activity correlate with memory performance.\n[6] Our results suggest that specific longevity treatments have acute and long-term effects on cognitive functions that decline with age through their regulation of rate-limiting genes required for learning and memory."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 20, "doc_id": 3202143, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [3202143], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: 70% of burn patients are admitted for hospitalization and further treatment after appearing at hospital emergency wards or outpatient clinics.\n\nDocument title: ABC of burns. Introduction.\n\nAbstract sentences:\n[0] Burns are one of the most devastating conditions encountered in medicine.\n[1] The injury represents an assault on all aspects of the patient, from the physical to the psychological.\n[2] It affects all ages, from babies to elderly people, and is a problem in both the developed and developing world.\n[3] All of us have experienced the severe pain that even a small burn can bring.\n[4] However the pain and distress caused by a large burn are not limited to the immediate event.\n[5] The visible physical and the invisible psychological scars are long lasting and often lead to chronic disability.\n[6] Burn injuries represent a diverse and varied challenge to medical and paramedical staff.\n[7] Correct management requires a skilled multidisciplinary approach that addresses all the problems facing a burn patient.\n[8] This series provides an overview of the most important aspects of burn injuries for hospital and non-hospital healthcare workers.​workers.\n[9] Figure 1    Top: Child with 70% full thickness burns, which required resuscitation, intensive care support, and extensive debridement and skin grafting.\n[10] Left: The same child one year later at a burns camp, having made a good recovery.\n[11] A reasonable outcome is possible ..."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 21, "doc_id": 41493639, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [41493639], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: 76-85% of people with severe mental disorder receive no treatment in low and middle income countries.\n\nDocument title: Prevalence, severity, and unmet need for treatment of mental disorders in the World Health Organization World Mental Health Surveys.\n\nAbstract sentences:\n[0] CONTEXT Little is known about the extent or severity of untreated mental disorders, especially in less-developed countries.\n[1] OBJECTIVE To estimate prevalence, severity, and treatment of Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) mental disorders in 14 countries (6 less developed, 8 developed) in the World Health Organization (WHO) World Mental Health (WMH) Survey Initiative.\n[2] DESIGN, SETTING, AND PARTICIPANTS Face-to-face household surveys of 60 463 community adults conducted from 2001-2003 in 14 countries in the Americas, Europe, the Middle East, Africa, and Asia.\n[3] MAIN OUTCOME MEASURES The DSM-IV disorders, severity, and treatment were assessed with the WMH version of the WHO Composite International Diagnostic Interview (WMH-CIDI), a fully structured, lay-administered psychiatric diagnostic interview.\n[4] RESULTS The prevalence of having any WMH-CIDI/DSM-IV disorder in the prior year varied widely, from 4.3% in Shanghai to 26.4% in the United States, with an interquartile range (IQR) of 9.1%-16.9%.\n[5] Between 33.1% (Colombia) and 80.9% (Nigeria) of 12-month cases were mild (IQR, 40.2%-53.3%).\n[6] Serious disorders were associated with substantial role disability.\n[7] Although disorder severity was correlated with probability of treatment in almost all countries, 35.5% to 50.3% of serious cases in developed countries and 76.3% to 85.4% in less-developed countries received no treatment in the 12 months before the interview.\n[8] Due to the high prevalence of mild and subthreshold cases, the number of those who received treatment far exceeds the number of untreated serious cases in every country.\n[9] CONCLUSIONS Reallocation of treatment resources could substantially decrease the problem of unmet need for treatment of mental disorders among serious cases.\n[10] Structural barriers exist to this reallocation.\n[11] Careful consideration needs to be given to the value of treating some mild cases, especially those at risk for progressing to more serious disorders."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Although disorder severity was correlated with probability of treatment in almost all countries, 35.5% to 50.3% of serious cases in developed countries and 76.3% to 85.4% in less-developed countries received no treatment in the 12 months before the interview.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 22, "doc_id": 6490571, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [6490571], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: 90% of patients with melanoma and an objective response to PD-1 blockade will experience a progression in their melanoma.\n\nDocument title: Association of Pembrolizumab With Tumor Response and Survival Among Patients With Advanced Melanoma.\n\nAbstract sentences:\n[0] IMPORTANCE The programmed death 1 (PD-1) pathway limits immune responses to melanoma and can be blocked with the humanized anti-PD-1 monoclonal antibody pembrolizumab.\n[1] OBJECTIVE To characterize the association of pembrolizumab with tumor response and overall survival among patients with advanced melanoma.\n[2] DESIGN, SETTINGS, AND PARTICIPANTS Open-label, multicohort, phase 1b clinical trials (enrollment, December 2011-September 2013).\n[3] Median duration of follow-up was 21 months.\n[4] The study was performed in academic medical centers in Australia, Canada, France, and the United States.\n[5] Eligible patients were aged 18 years and older and had advanced or metastatic melanoma.\n[6] Data were pooled from 655 enrolled patients (135 from a nonrandomized cohort [n = 87 ipilimumab naive; n = 48 ipilimumab treated] and 520 from randomized cohorts [n = 226 ipilimumab naive; n = 294 ipilimumab treated]).\n[7] Cutoff dates were April 18, 2014, for safety analyses and October 18, 2014, for efficacy analyses.\n[8] EXPOSURES Pembrolizumab 10 mg/kg every 2 weeks, 10 mg/kg every 3 weeks, or 2 mg/kg every 3 weeks continued until disease progression, intolerable toxicity, or investigator decision.\n[9] MAIN OUTCOMES AND MEASURES The primary end point was confirmed objective response rate (best overall response of complete response or partial response) in patients with measurable disease at baseline per independent central review.\n[10] Secondary end points included toxicity, duration of response, progression-free survival, and overall survival.\n[11] RESULTS Among the 655 patients (median [range] age, 61 [18-94] years; 405 [62%] men), 581 had measurable disease at baseline.\n[12] An objective response was reported in 194 of 581 patients (33% [95% CI, 30%-37%]) and in 60 of 133 treatment-naive patients (45% [95% CI, 36% to 54%]).\n[13] Overall, 74% (152/205) of responses were ongoing at the time of data cutoff; 44% (90/205) of patients had response duration for at least 1 year and 79% (162/205) had response duration for at least 6 months.\n[14] Twelve-month progression-free survival rates were 35% (95% CI, 31%-39%) in the total population and 52% (95% CI, 43%-60%) among treatment-naive patients.\n[15] Median overall survival in the total population was 23 months (95% CI, 20-29) with a 12-month survival rate of 66% (95% CI, 62%-69%) and a 24-month survival rate of 49% (95% CI, 44%-53%).\n[16] In treatment-naive patients, median overall survival was 31 months (95% CI, 24 to not reached) with a 12-month survival rate of 73% (95% CI, 65%-79%) and a 24-month survival rate of 60% (95% CI, 51%-68%).\n[17] Ninety-two of 655 patients (14%) experienced at least 1 treatment-related grade 3 or 4 adverse event (AE) and 27 of 655 (4%) patients discontinued treatment because of a treatment-related AE.\n[18] Treatment-related serious AEs were reported in 59 patients (9%).\n[19] There were no drug-related deaths.\n[20] CONCLUSIONS AND RELEVANCE Among patients with advanced melanoma, pembrolizumab administration was associated with an overall objective response rate of 33%, 12-month progression-free survival rate of 35%, and median overall survival of 23 months; grade 3 or 4 treatment-related AEs occurred in 14%.\n[21] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT01295827."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 24, "doc_id": 3471191, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [3471191], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: 90% of sudden infant death syndrome (SIDS) deaths happen in newborns aged less than 6 months.\n\nDocument title: Sudden infant death syndrome.\n\nAbstract sentences:\n[0] Despite declines in prevalence during the past two decades, sudden infant death syndrome (SIDS) continues to be the leading cause of death for infants aged between 1 month and 1 year in developed countries.\n[1] Behavioural risk factors identified in epidemiological studies include prone and side positions for infant sleep, smoke exposure, soft bedding and sleep surfaces, and overheating.\n[2] Evidence also suggests that pacifier use at sleep time and room sharing without bed sharing are associated with decreased risk of SIDS.\n[3] Although the cause of SIDS is unknown, immature cardiorespiratory autonomic control and failure of arousal responsiveness from sleep are important factors.\n[4] Gene polymorphisms relating to serotonin transport and autonomic nervous system development might make affected infants more vulnerable to SIDS.\n[5] Campaigns for risk reduction have helped to reduce SIDS incidence by 50-90%.\n[6] However, to reduce the incidence even further, greater strides must be made in reducing prenatal smoke exposure and implementing other recommended infant care practices.\n[7] Continued research is needed to identify the pathophysiological basis of SIDS."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 25, "doc_id": 2613775, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [2613775], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A 100g dose of chloroquine chemoprophylactic regimen results in retinal toxicity after 1 year of weekly intake.\n\nDocument title: Prevention of malaria in long-term travelers.\n\nAbstract sentences:\n[0] CONTEXT Long-term travelers, defined here as those traveling for periods of 6 months or longer, face particular challenges regarding malaria prevention.\n[1] Current guidelines for malaria prevention primarily address prevention of Plasmodium falciparum infections in short-term travelers.\n[2] OBJECTIVES To examine the risk of malaria in long-term travelers, recent developments in personal protective measures, and the safety and tolerability of malaria chemoprophylaxis during long-term use and to consider prevention strategies including continuous chemoprophylaxis, stand-by emergency self-treatment, seasonal prophylaxis, and strategies to prevent primary infection and relapses from P vivax malaria.\n[3] EVIDENCE ACQUISITION Comprehensive search of scientific publications including MEDLINE via both OVID and PubMED for relevant studies and articles with a cutoff date of July 2006, using the search terms long-term travel and malaria prevention, long-term malaria chemoprophylaxis, and insect repellent and malaria.\n[4] Additional references were obtained from searching the bibliographies of the selected articles, from dissertations, and from the proceedings of relevant conferences on travel medicine.\n[5] There were no language restrictions.\n[6] EVIDENCE SYNTHESIS Long-term travelers have a higher risk of malaria than short-term travelers.\n[7] Long-term travelers underuse personal protective measures and adhere poorly to continuous chemoprophylaxis regimens.\n[8] A number of strategies are used during long-term stays: discontinuation of chemoprophylaxis after the initial period, sequential regimens with different medications for chemoprophylaxis, stand-by emergency self-treatment, and seasonal chemoprophylaxis targeting high-incidence periods or locations.\n[9] All strategies have advantages and drawbacks.\n[10] Counterfeit drugs sold in countries endemic for malaria pose serious concern for long-term travelers who purchase their medications overseas.\n[11] Vivax malaria causes significant illness in travelers, but relapses of vivax malaria are not prevented with the current first-line chemoprophylaxis regimens.\n[12] Consensus guidelines are needed for prevention of malaria in long-term travelers.\n[13] CONCLUSIONS Prevention of malaria in long-term travelers is a complex issue and requires expert advice from travel medicine specialists.\n[14] Recommendations for prevention of malaria in long-term travelers must be individualized."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 26, "doc_id": 32390525, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [32390525], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A 100g dose of chloroquine chemoprophylactic regimen results in retinal toxicity after 5-6 years of weekly intake.\n\nDocument title: Prevention of malaria in long-term travelers.\n\nAbstract sentences:\n[0] CONTEXT Long-term travelers, defined here as those traveling for periods of 6 months or longer, face particular challenges regarding malaria prevention.\n[1] Current guidelines for malaria prevention primarily address prevention of Plasmodium falciparum infections in short-term travelers.\n[2] OBJECTIVES To examine the risk of malaria in long-term travelers, recent developments in personal protective measures, and the safety and tolerability of malaria chemoprophylaxis during long-term use and to consider prevention strategies including continuous chemoprophylaxis, stand-by emergency self-treatment, seasonal prophylaxis, and strategies to prevent primary infection and relapses from P vivax malaria.\n[3] EVIDENCE ACQUISITION Comprehensive search of scientific publications including MEDLINE via both OVID and PubMED for relevant studies and articles with a cutoff date of July 2006, using the search terms long-term travel and malaria prevention, long-term malaria chemoprophylaxis, and insect repellent and malaria.\n[4] Additional references were obtained from searching the bibliographies of the selected articles, from dissertations, and from the proceedings of relevant conferences on travel medicine.\n[5] There were no language restrictions.\n[6] EVIDENCE SYNTHESIS Long-term travelers have a higher risk of malaria than short-term travelers.\n[7] Long-term travelers underuse personal protective measures and adhere poorly to continuous chemoprophylaxis regimens.\n[8] A number of strategies are used during long-term stays: discontinuation of chemoprophylaxis after the initial period, sequential regimens with different medications for chemoprophylaxis, stand-by emergency self-treatment, and seasonal chemoprophylaxis targeting high-incidence periods or locations.\n[9] All strategies have advantages and drawbacks.\n[10] Counterfeit drugs sold in countries endemic for malaria pose serious concern for long-term travelers who purchase their medications overseas.\n[11] Vivax malaria causes significant illness in travelers, but relapses of vivax malaria are not prevented with the current first-line chemoprophylaxis regimens.\n[12] Consensus guidelines are needed for prevention of malaria in long-term travelers.\n[13] CONCLUSIONS Prevention of malaria in long-term travelers is a complex issue and requires expert advice from travel medicine specialists.\n[14] Recommendations for prevention of malaria in long-term travelers must be individualized."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 27, "doc_id": 32390525, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [32390525], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A T helper 2 cell (Th2) environment impedes disease development in patients with systemic lupus erythematosus (SLE).\n\nDocument title: BASOPHILS AND THE T HELPER 2 ENVIRONMENT CAN PROMOTE THE DEVELOPMENT OF LUPUS NEPHRITIS\n\nAbstract sentences:\n[0] In systemic lupus erythematosus (SLE), self-reactive antibodies can target the kidney (lupus nephritis), leading to functional failure and possible mortality.\n[1] We report that activation of basophils by autoreactive IgE causes their homing to lymph nodes, promoting T helper type 2 (T(H)2) cell differentiation and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in mice lacking the Src family protein tyrosine kinase Lyn (Lyn(-/-) mice).\n[2] Individuals with SLE also have elevated serum IgE, self-reactive IgEs and activated basophils that express CD62 ligand (CD62L) and the major histocompatibility complex (MHC) class II molecule human leukocyte antigen-DR (HLA-DR), parameters that are associated with increased disease activity and active lupus nephritis.\n[3] Basophils were also present in the lymph nodes and spleen of subjects with SLE.\n[4] Thus, in Lyn(-/-) mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in individuals with SLE IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"We report that activation of basophils by autoreactive IgE causes their homing to lymph nodes, promoting T helper type 2 (T(H)2) cell differentiation and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in mice lacking the Src family protein tyrosine kinase Lyn (Lyn(-/-) mice).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 28, "doc_id": 12670680, "label": "CONTRADICTS", "evidence_sentence_ids": [1], "cited_doc_ids": [12670680], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A T helper 2 cell (Th2) environment impedes disease development in patients with systemic lupus erythematosus (SLE).\n\nDocument title: BASOPHILS AND THE T HELPER 2 ENVIRONMENT CAN PROMOTE THE DEVELOPMENT OF LUPUS NEPHRITIS\n\nAbstract sentences:\n[0] In systemic lupus erythematosus (SLE), self-reactive antibodies can target the kidney (lupus nephritis), leading to functional failure and possible mortality.\n[1] We report that activation of basophils by autoreactive IgE causes their homing to lymph nodes, promoting T helper type 2 (T(H)2) cell differentiation and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in mice lacking the Src family protein tyrosine kinase Lyn (Lyn(-/-) mice).\n[2] Individuals with SLE also have elevated serum IgE, self-reactive IgEs and activated basophils that express CD62 ligand (CD62L) and the major histocompatibility complex (MHC) class II molecule human leukocyte antigen-DR (HLA-DR), parameters that are associated with increased disease activity and active lupus nephritis.\n[3] Basophils were also present in the lymph nodes and spleen of subjects with SLE.\n[4] Thus, in Lyn(-/-) mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in individuals with SLE IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Individuals with SLE also have elevated serum IgE, self-reactive IgEs and activated basophils that express CD62 ligand (CD62L) and the major histocompatibility complex (MHC) class II molecule human leukocyte antigen-DR (HLA-DR), parameters that are associated with increased disease activity and active lupus nephritis.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 28, "doc_id": 12670680, "label": "CONTRADICTS", "evidence_sentence_ids": [2], "cited_doc_ids": [12670680], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A T helper 2 cell (Th2) environment impedes disease development in patients with systemic lupus erythematosus (SLE).\n\nDocument title: BASOPHILS AND THE T HELPER 2 ENVIRONMENT CAN PROMOTE THE DEVELOPMENT OF LUPUS NEPHRITIS\n\nAbstract sentences:\n[0] In systemic lupus erythematosus (SLE), self-reactive antibodies can target the kidney (lupus nephritis), leading to functional failure and possible mortality.\n[1] We report that activation of basophils by autoreactive IgE causes their homing to lymph nodes, promoting T helper type 2 (T(H)2) cell differentiation and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in mice lacking the Src family protein tyrosine kinase Lyn (Lyn(-/-) mice).\n[2] Individuals with SLE also have elevated serum IgE, self-reactive IgEs and activated basophils that express CD62 ligand (CD62L) and the major histocompatibility complex (MHC) class II molecule human leukocyte antigen-DR (HLA-DR), parameters that are associated with increased disease activity and active lupus nephritis.\n[3] Basophils were also present in the lymph nodes and spleen of subjects with SLE.\n[4] Thus, in Lyn(-/-) mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in individuals with SLE IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Thus, in Lyn(-/-) mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in individuals with SLE IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 28, "doc_id": 12670680, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [12670680], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A breast cancer patient's capacity to metabolize tamoxifen influences treatment outcome.\n\nDocument title: Association between CYP2D6 polymorphisms and outcomes among women with early stage breast cancer treated with tamoxifen.\n\nAbstract sentences:\n[0] CONTEXT The growth inhibitory effect of tamoxifen, which is used for the treatment of hormone receptor-positive breast cancer, is mediated by its metabolites, 4-hydroxytamoxifen and endoxifen.\n[1] The formation of active metabolites is catalyzed by the polymorphic cytochrome P450 2D6 (CYP2D6) enzyme.\n[2] OBJECTIVE To determine whether CYP2D6 variation is associated with clinical outcomes in women receiving adjuvant tamoxifen.\n[3] DESIGN, SETTING, AND PATIENTS Retrospective analysis of German and US cohorts of patients treated with adjuvant tamoxifen for early stage breast cancer.\n[4] The 1325 patients had diagnoses between 1986 and 2005 of stage I through III breast cancer and were mainly postmenopausal (95.4%).\n[5] Last follow-up was in December 2008; inclusion criteria were hormone receptor positivity, no metastatic disease at diagnosis, adjuvant tamoxifen therapy, and no chemotherapy.\n[6] DNA from tumor tissue or blood was genotyped for CYP2D6 variants associated with reduced (*10, *41) or absent (*3, *4, *5) enzyme activity.\n[7] Women were classified as having an extensive (n=609), heterozygous extensive/intermediate (n=637), or poor (n=79) CYP2D6 metabolism.\n[8] MAIN OUTCOME MEASURES Time to recurrence, event-free survival, disease-free survival, and overall survival.\n[9] RESULTS Median follow-up was 6.3 years.\n[10] At 9 years of follow-up, the recurrence rates were 14.9% for extensive metabolizers, 20.9% for heterozygous extensive/intermediate metabolizers, and 29.0% for poor metabolizers, and all-cause mortality rates were 16.7%, 18.0%, and 22.8%, respectively.\n[11] Compared with extensive metabolizers, there was a significantly increased risk of recurrence for heterozygous extensive/intermediate metabolizers (time to recurrence adjusted hazard ratio [HR], 1.40; 95% confidence interval [CI], 1.04-1.90) and for poor metabolizers (time to recurrence HR, 1.90; 95% CI, 1.10-3.28).\n[12] Compared with extensive metabolizers, those with decreased CYP2D6 activity (heterozygous extensive/intermediate and poor metabolism) had worse event-free survival (HR, 1.33; 95% CI, 1.06-1.68) and disease-free survival (HR, 1.29; 95% CI, 1.03-1.61), but there was no significant difference in overall survival (HR, 1.15; 95% CI, 0.88-1.51).\n[13] CONCLUSION Among women with breast cancer treated with tamoxifen, there was an association between CYP2D6 variation and clinical outcomes, such that the presence of 2 functional CYP2D6 alleles was associated with better clinical outcomes and the presence of nonfunctional or reduced-function alleles with worse outcomes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"At 9 years of follow-up, the recurrence rates were 14.9% for extensive metabolizers, 20.9% for heterozygous extensive/intermediate metabolizers, and 29.0% for poor metabolizers, and all-cause mortality rates were 16.7%, 18.0%, and 22.8%, respectively.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 30, "doc_id": 24341590, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [24341590], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A breast cancer patient's capacity to metabolize tamoxifen influences treatment outcome.\n\nDocument title: Association between CYP2D6 polymorphisms and outcomes among women with early stage breast cancer treated with tamoxifen.\n\nAbstract sentences:\n[0] CONTEXT The growth inhibitory effect of tamoxifen, which is used for the treatment of hormone receptor-positive breast cancer, is mediated by its metabolites, 4-hydroxytamoxifen and endoxifen.\n[1] The formation of active metabolites is catalyzed by the polymorphic cytochrome P450 2D6 (CYP2D6) enzyme.\n[2] OBJECTIVE To determine whether CYP2D6 variation is associated with clinical outcomes in women receiving adjuvant tamoxifen.\n[3] DESIGN, SETTING, AND PATIENTS Retrospective analysis of German and US cohorts of patients treated with adjuvant tamoxifen for early stage breast cancer.\n[4] The 1325 patients had diagnoses between 1986 and 2005 of stage I through III breast cancer and were mainly postmenopausal (95.4%).\n[5] Last follow-up was in December 2008; inclusion criteria were hormone receptor positivity, no metastatic disease at diagnosis, adjuvant tamoxifen therapy, and no chemotherapy.\n[6] DNA from tumor tissue or blood was genotyped for CYP2D6 variants associated with reduced (*10, *41) or absent (*3, *4, *5) enzyme activity.\n[7] Women were classified as having an extensive (n=609), heterozygous extensive/intermediate (n=637), or poor (n=79) CYP2D6 metabolism.\n[8] MAIN OUTCOME MEASURES Time to recurrence, event-free survival, disease-free survival, and overall survival.\n[9] RESULTS Median follow-up was 6.3 years.\n[10] At 9 years of follow-up, the recurrence rates were 14.9% for extensive metabolizers, 20.9% for heterozygous extensive/intermediate metabolizers, and 29.0% for poor metabolizers, and all-cause mortality rates were 16.7%, 18.0%, and 22.8%, respectively.\n[11] Compared with extensive metabolizers, there was a significantly increased risk of recurrence for heterozygous extensive/intermediate metabolizers (time to recurrence adjusted hazard ratio [HR], 1.40; 95% confidence interval [CI], 1.04-1.90) and for poor metabolizers (time to recurrence HR, 1.90; 95% CI, 1.10-3.28).\n[12] Compared with extensive metabolizers, those with decreased CYP2D6 activity (heterozygous extensive/intermediate and poor metabolism) had worse event-free survival (HR, 1.33; 95% CI, 1.06-1.68) and disease-free survival (HR, 1.29; 95% CI, 1.03-1.61), but there was no significant difference in overall survival (HR, 1.15; 95% CI, 0.88-1.51).\n[13] CONCLUSION Among women with breast cancer treated with tamoxifen, there was an association between CYP2D6 variation and clinical outcomes, such that the presence of 2 functional CYP2D6 alleles was associated with better clinical outcomes and the presence of nonfunctional or reduced-function alleles with worse outcomes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"Compared with extensive metabolizers, there was a significantly increased risk of recurrence for heterozygous extensive/intermediate metabolizers (time to recurrence adjusted hazard ratio [HR], 1.40; 95% confidence interval [CI], 1.04-1.90) and for poor metabolizers (time to recurrence HR, 1.90; 95% CI, 1.10-3.28).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 30, "doc_id": 24341590, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [24341590], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A breast cancer patient's capacity to metabolize tamoxifen influences treatment outcome.\n\nDocument title: Association between CYP2D6 polymorphisms and outcomes among women with early stage breast cancer treated with tamoxifen.\n\nAbstract sentences:\n[0] CONTEXT The growth inhibitory effect of tamoxifen, which is used for the treatment of hormone receptor-positive breast cancer, is mediated by its metabolites, 4-hydroxytamoxifen and endoxifen.\n[1] The formation of active metabolites is catalyzed by the polymorphic cytochrome P450 2D6 (CYP2D6) enzyme.\n[2] OBJECTIVE To determine whether CYP2D6 variation is associated with clinical outcomes in women receiving adjuvant tamoxifen.\n[3] DESIGN, SETTING, AND PATIENTS Retrospective analysis of German and US cohorts of patients treated with adjuvant tamoxifen for early stage breast cancer.\n[4] The 1325 patients had diagnoses between 1986 and 2005 of stage I through III breast cancer and were mainly postmenopausal (95.4%).\n[5] Last follow-up was in December 2008; inclusion criteria were hormone receptor positivity, no metastatic disease at diagnosis, adjuvant tamoxifen therapy, and no chemotherapy.\n[6] DNA from tumor tissue or blood was genotyped for CYP2D6 variants associated with reduced (*10, *41) or absent (*3, *4, *5) enzyme activity.\n[7] Women were classified as having an extensive (n=609), heterozygous extensive/intermediate (n=637), or poor (n=79) CYP2D6 metabolism.\n[8] MAIN OUTCOME MEASURES Time to recurrence, event-free survival, disease-free survival, and overall survival.\n[9] RESULTS Median follow-up was 6.3 years.\n[10] At 9 years of follow-up, the recurrence rates were 14.9% for extensive metabolizers, 20.9% for heterozygous extensive/intermediate metabolizers, and 29.0% for poor metabolizers, and all-cause mortality rates were 16.7%, 18.0%, and 22.8%, respectively.\n[11] Compared with extensive metabolizers, there was a significantly increased risk of recurrence for heterozygous extensive/intermediate metabolizers (time to recurrence adjusted hazard ratio [HR], 1.40; 95% confidence interval [CI], 1.04-1.90) and for poor metabolizers (time to recurrence HR, 1.90; 95% CI, 1.10-3.28).\n[12] Compared with extensive metabolizers, those with decreased CYP2D6 activity (heterozygous extensive/intermediate and poor metabolism) had worse event-free survival (HR, 1.33; 95% CI, 1.06-1.68) and disease-free survival (HR, 1.29; 95% CI, 1.03-1.61), but there was no significant difference in overall survival (HR, 1.15; 95% CI, 0.88-1.51).\n[13] CONCLUSION Among women with breast cancer treated with tamoxifen, there was an association between CYP2D6 variation and clinical outcomes, such that the presence of 2 functional CYP2D6 alleles was associated with better clinical outcomes and the presence of nonfunctional or reduced-function alleles with worse outcomes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"Compared with extensive metabolizers, those with decreased CYP2D6 activity (heterozygous extensive/intermediate and poor metabolism) had worse event-free survival (HR, 1.33; 95% CI, 1.06-1.68) and disease-free survival (HR, 1.29; 95% CI, 1.03-1.61), but there was no significant difference in overall survival (HR, 1.15; 95% CI, 0.88-1.51).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 30, "doc_id": 24341590, "label": "SUPPORTS", "evidence_sentence_ids": [12], "cited_doc_ids": [24341590], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A breast cancer patient's capacity to metabolize tamoxifen influences treatment outcome.\n\nDocument title: Association between CYP2D6 polymorphisms and outcomes among women with early stage breast cancer treated with tamoxifen.\n\nAbstract sentences:\n[0] CONTEXT The growth inhibitory effect of tamoxifen, which is used for the treatment of hormone receptor-positive breast cancer, is mediated by its metabolites, 4-hydroxytamoxifen and endoxifen.\n[1] The formation of active metabolites is catalyzed by the polymorphic cytochrome P450 2D6 (CYP2D6) enzyme.\n[2] OBJECTIVE To determine whether CYP2D6 variation is associated with clinical outcomes in women receiving adjuvant tamoxifen.\n[3] DESIGN, SETTING, AND PATIENTS Retrospective analysis of German and US cohorts of patients treated with adjuvant tamoxifen for early stage breast cancer.\n[4] The 1325 patients had diagnoses between 1986 and 2005 of stage I through III breast cancer and were mainly postmenopausal (95.4%).\n[5] Last follow-up was in December 2008; inclusion criteria were hormone receptor positivity, no metastatic disease at diagnosis, adjuvant tamoxifen therapy, and no chemotherapy.\n[6] DNA from tumor tissue or blood was genotyped for CYP2D6 variants associated with reduced (*10, *41) or absent (*3, *4, *5) enzyme activity.\n[7] Women were classified as having an extensive (n=609), heterozygous extensive/intermediate (n=637), or poor (n=79) CYP2D6 metabolism.\n[8] MAIN OUTCOME MEASURES Time to recurrence, event-free survival, disease-free survival, and overall survival.\n[9] RESULTS Median follow-up was 6.3 years.\n[10] At 9 years of follow-up, the recurrence rates were 14.9% for extensive metabolizers, 20.9% for heterozygous extensive/intermediate metabolizers, and 29.0% for poor metabolizers, and all-cause mortality rates were 16.7%, 18.0%, and 22.8%, respectively.\n[11] Compared with extensive metabolizers, there was a significantly increased risk of recurrence for heterozygous extensive/intermediate metabolizers (time to recurrence adjusted hazard ratio [HR], 1.40; 95% confidence interval [CI], 1.04-1.90) and for poor metabolizers (time to recurrence HR, 1.90; 95% CI, 1.10-3.28).\n[12] Compared with extensive metabolizers, those with decreased CYP2D6 activity (heterozygous extensive/intermediate and poor metabolism) had worse event-free survival (HR, 1.33; 95% CI, 1.06-1.68) and disease-free survival (HR, 1.29; 95% CI, 1.03-1.61), but there was no significant difference in overall survival (HR, 1.15; 95% CI, 0.88-1.51).\n[13] CONCLUSION Among women with breast cancer treated with tamoxifen, there was an association between CYP2D6 variation and clinical outcomes, such that the presence of 2 functional CYP2D6 alleles was associated with better clinical outcomes and the presence of nonfunctional or reduced-function alleles with worse outcomes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"CONCLUSION Among women with breast cancer treated with tamoxifen, there was an association between CYP2D6 variation and clinical outcomes, such that the presence of 2 functional CYP2D6 alleles was associated with better clinical outcomes and the presence of nonfunctional or reduced-function alleles with worse outcomes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 30, "doc_id": 24341590, "label": "SUPPORTS", "evidence_sentence_ids": [13], "cited_doc_ids": [24341590], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A country's Vaccine Alliance (GAVI) eligibility is not indictivate of accelerated adoption of the Hub vaccine.\n\nDocument title: Accelerating Policy Decisions to Adopt Haemophilus influenzae Type b Vaccine: A Global, Multivariable Analysis\n\nAbstract sentences:\n[0] BACKGROUND Adoption of new and underutilized vaccines by national immunization programs is an essential step towards reducing child mortality.\n[1] Policy decisions to adopt new vaccines in high mortality countries often lag behind decisions in high-income countries.\n[2] Using the case of Haemophilus influenzae type b (Hib) vaccine, this paper endeavors to explain these delays through the analysis of country-level economic, epidemiological, programmatic and policy-related factors, as well as the role of the Global Alliance for Vaccines and Immunisation (GAVI Alliance).\n[3] METHODS AND FINDINGS Data for 147 countries from 1990 to 2007 were analyzed in accelerated failure time models to identify factors that are associated with the time to decision to adopt Hib vaccine.\n[4] In multivariable models that control for Gross National Income, region, and burden of Hib disease, the receipt of GAVI support speeded the time to decision by a factor of 0.37 (95% CI 0.18-0.76), or 63%.\n[5] The presence of two or more neighboring country adopters accelerated decisions to adopt by a factor of 0.50 (95% CI 0.33-0.75).\n[6] For each 1% increase in vaccine price, decisions to adopt are delayed by a factor of 1.02 (95% CI 1.00-1.04).\n[7] Global recommendations and local studies were not associated with time to decision.\n[8] CONCLUSIONS This study substantiates previous findings related to vaccine price and presents new evidence to suggest that GAVI eligibility is associated with accelerated decisions to adopt Hib vaccine.\n[9] The influence of neighboring country decisions was also highly significant, suggesting that approaches to support the adoption of new vaccines should consider supply- and demand-side factors."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"CONCLUSIONS This study substantiates previous findings related to vaccine price and presents new evidence to suggest that GAVI eligibility is associated with accelerated decisions to adopt Hib vaccine.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 32, "doc_id": 12428497, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [12428497], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A deficiency of folate increases blood levels of homocysteine.\n\nDocument title: Randomized trial of folic acid supplementation and serum homocysteine levels.\n\nAbstract sentences:\n[0] BACKGROUND Lowering serum homocysteine levels with folic acid is expected to reduce mortality from ischemic heart disease.\n[1] Homocysteine reduction is known to be maximal at a folic acid dosage of 1 mg/d, but the effect of lower doses (relevant to food fortification) is unclear.\n[2] METHODS We randomized 151 patients with ischemic heart disease to 1 of 5 dosages of folic acid (0.2, 0.4, 0.6, 0.8, and 1.0 mg/d) or placebo.\n[3] Fasting blood samples for serum homocysteine and serum folate analysis were taken initially, after 3 months of supplementation, and 3 months after folic acid use was discontinued.\n[4] RESULTS Median serum homocysteine level decreased with increasing folic acid dosage, to a maximum at 0.8 mg of folic acid per day, when the homocysteine reduction (placebo adjusted) was 2.7 micromol/L (23%), similar to the known effect of folic acid dosages of 1 mg/d and above.\n[5] The higher a person's initial serum homocysteine level, the greater was the response to folic acid, but there were statistically significant reductions regardless of the initial level.\n[6] Serum folate level increased approximately linearly (5.5 nmol/L for every 0.1 mg of folic acid).\n[7] Within-person fluctuations over time in serum homocysteine levels, measured in the placebo group, were large compared with the effect of folic acid, indicating that monitoring of the reduction in an individual is impractical.\n[8] CONCLUSIONS A dosage of folic acid of 0.8 mg/d appears necessary to achieve the maximum reduction in serum homocysteine level across the range of homocysteine levels in the population.\n[9] Current US food fortification levels will achieve only a small proportion of the achievable homocysteine reduction."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"RESULTS Median serum homocysteine level decreased with increasing folic acid dosage, to a maximum at 0.8 mg of folic acid per day, when the homocysteine reduction (placebo adjusted) was 2.7 micromol/L (23%), similar to the known effect of folic acid dosages of 1 mg/d and above.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 34, "doc_id": 11705328, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [11705328], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A deficiency of vitamin B12 decreases blood levels of homocysteine.\n\nDocument title: Folic acid improves endothelial function in coronary artery disease via mechanisms largely independent of homocysteine lowering.\n\nAbstract sentences:\n[0] BACKGROUND Homocysteine is a risk factor for coronary artery disease (CAD), although a causal relation remains to be proven.\n[1] The importance of determining direct causality rests in the fact that plasma homocysteine can be safely and inexpensively reduced by 25% with folic acid.\n[2] This reduction is maximally achieved by doses of 0.4 mg/d.\n[3] High-dose folic acid (5 mg/d) improves endothelial function in CAD, although the mechanism is controversial.\n[4] It has been proposed that improvement occurs through reduction in total (tHcy) or free (non-protein bound) homocysteine (fHcy).\n[5] We investigated the effects of folic acid on endothelial function before a change in homocysteine in patients with CAD.\n[6] METHODS AND RESULTS A randomized, placebo-controlled study of folic acid (5 mg/d) for 6 weeks was undertaken in 33 patients.\n[7] Endothelial function, assessed by flow-mediated dilatation (FMD), was measured before, at 2 and 4 hours after the first dose of folic acid, and after 6 weeks of treatment.\n[8] Plasma folate increased markedly by 1 hour (200 compared with 25.8 nmol/L; P<0.001).\n[9] FMD improved at 2 hours (83 compared with 47 microm; P<0.001) and was largely complete by 4 hours (101 compared with 51 microm; P<0.001).\n[10] tHcy did not significantly differ acutely (4-hour tHcy, 9.56 compared with 9.79 micromol/L; P=NS).\n[11] fHcy did not differ at 3 hours but was slightly reduced at 4 hours (1.55 compared with 1.78 micromol/L; P=0.02).\n[12] FMD improvement did not correlate with reductions in either fHcy or tHcy at any time.\n[13] CONCLUSIONS These data suggest that folic acid improves endothelial function in CAD acutely by a mechanism largely independent of homocysteine."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 35, "doc_id": 5152028, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [5152028, 11705328], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A deficiency of vitamin B6 decreases blood levels of homocysteine.\n\nDocument title: Folic acid improves endothelial function in coronary artery disease via mechanisms largely independent of homocysteine lowering.\n\nAbstract sentences:\n[0] BACKGROUND Homocysteine is a risk factor for coronary artery disease (CAD), although a causal relation remains to be proven.\n[1] The importance of determining direct causality rests in the fact that plasma homocysteine can be safely and inexpensively reduced by 25% with folic acid.\n[2] This reduction is maximally achieved by doses of 0.4 mg/d.\n[3] High-dose folic acid (5 mg/d) improves endothelial function in CAD, although the mechanism is controversial.\n[4] It has been proposed that improvement occurs through reduction in total (tHcy) or free (non-protein bound) homocysteine (fHcy).\n[5] We investigated the effects of folic acid on endothelial function before a change in homocysteine in patients with CAD.\n[6] METHODS AND RESULTS A randomized, placebo-controlled study of folic acid (5 mg/d) for 6 weeks was undertaken in 33 patients.\n[7] Endothelial function, assessed by flow-mediated dilatation (FMD), was measured before, at 2 and 4 hours after the first dose of folic acid, and after 6 weeks of treatment.\n[8] Plasma folate increased markedly by 1 hour (200 compared with 25.8 nmol/L; P<0.001).\n[9] FMD improved at 2 hours (83 compared with 47 microm; P<0.001) and was largely complete by 4 hours (101 compared with 51 microm; P<0.001).\n[10] tHcy did not significantly differ acutely (4-hour tHcy, 9.56 compared with 9.79 micromol/L; P=NS).\n[11] fHcy did not differ at 3 hours but was slightly reduced at 4 hours (1.55 compared with 1.78 micromol/L; P=0.02).\n[12] FMD improvement did not correlate with reductions in either fHcy or tHcy at any time.\n[13] CONCLUSIONS These data suggest that folic acid improves endothelial function in CAD acutely by a mechanism largely independent of homocysteine."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 37, "doc_id": 5152028, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [5152028, 11705328], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A diminished ovarian reserve does not solely indicate infertility in an a priori non-infertile population.\n\nDocument title: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\n\nAbstract sentences:\n[0] Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential.\n[1] Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age.\n[2] Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area.\n[3] Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH.\n[4] Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle).\n[5] Conception was defined as a positive pregnancy test result.\n[6] Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis.\n[7] After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively).\n[8] Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (63%; 95% CI, 50%-73%) compared with women (n = 654) with normal values (62%; 95% CI, 57%-66%) or after 12 cycles of attempt (82% [95% CI, 70%-89%] vs 75% [95% CI, 70%-78%], respectively).\n[9] Women with high urinary FSH values (>11.5 mIU/mg creatinine [n = 69]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (61%; 95% CI, 46%-74%) compared with women (n = 660) with normal values (62%; 95% CI, 58%-66%) or after 12 cycles of attempt (70% [95% CI, 54%-80%] vs 76% [95% CI, 72%-80%], respectively).\n[10] Inhibin B levels (n = 737) were not associated with the probability of conceiving in a given cycle (hazard ratio per 1-pg/mL increase, 0.999; 95% CI, 0.997-1.001).\n[11] Conclusions and Relevance Among women aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, biomarkers indicating diminished ovarian reserve compared with normal ovarian reserve were not associated with reduced fertility.\n[12] These findings do not support the use of urinary or blood follicle-stimulating hormone tests or antimüllerian hormone levels to assess natural fertility for women with these characteristics."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 39, "doc_id": 13497630, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [13497630], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A diminished ovarian reserve does not solely indicate infertility in an a priori non-infertile population.\n\nDocument title: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\n\nAbstract sentences:\n[0] Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential.\n[1] Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age.\n[2] Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area.\n[3] Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH.\n[4] Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle).\n[5] Conception was defined as a positive pregnancy test result.\n[6] Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis.\n[7] After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively).\n[8] Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (63%; 95% CI, 50%-73%) compared with women (n = 654) with normal values (62%; 95% CI, 57%-66%) or after 12 cycles of attempt (82% [95% CI, 70%-89%] vs 75% [95% CI, 70%-78%], respectively).\n[9] Women with high urinary FSH values (>11.5 mIU/mg creatinine [n = 69]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (61%; 95% CI, 46%-74%) compared with women (n = 660) with normal values (62%; 95% CI, 58%-66%) or after 12 cycles of attempt (70% [95% CI, 54%-80%] vs 76% [95% CI, 72%-80%], respectively).\n[10] Inhibin B levels (n = 737) were not associated with the probability of conceiving in a given cycle (hazard ratio per 1-pg/mL increase, 0.999; 95% CI, 0.997-1.001).\n[11] Conclusions and Relevance Among women aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, biomarkers indicating diminished ovarian reserve compared with normal ovarian reserve were not associated with reduced fertility.\n[12] These findings do not support the use of urinary or blood follicle-stimulating hormone tests or antimüllerian hormone levels to assess natural fertility for women with these characteristics."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (63%; 95% CI, 50%-73%) compared with women (n = 654) with normal values (62%; 95% CI, 57%-66%) or after 12 cycles of attempt (82% [95% CI, 70%-89%] vs 75% [95% CI, 70%-78%], respectively).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 39, "doc_id": 13497630, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [13497630], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A diminished ovarian reserve does not solely indicate infertility in an a priori non-infertile population.\n\nDocument title: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\n\nAbstract sentences:\n[0] Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential.\n[1] Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age.\n[2] Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area.\n[3] Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH.\n[4] Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle).\n[5] Conception was defined as a positive pregnancy test result.\n[6] Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis.\n[7] After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively).\n[8] Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (63%; 95% CI, 50%-73%) compared with women (n = 654) with normal values (62%; 95% CI, 57%-66%) or after 12 cycles of attempt (82% [95% CI, 70%-89%] vs 75% [95% CI, 70%-78%], respectively).\n[9] Women with high urinary FSH values (>11.5 mIU/mg creatinine [n = 69]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (61%; 95% CI, 46%-74%) compared with women (n = 660) with normal values (62%; 95% CI, 58%-66%) or after 12 cycles of attempt (70% [95% CI, 54%-80%] vs 76% [95% CI, 72%-80%], respectively).\n[10] Inhibin B levels (n = 737) were not associated with the probability of conceiving in a given cycle (hazard ratio per 1-pg/mL increase, 0.999; 95% CI, 0.997-1.001).\n[11] Conclusions and Relevance Among women aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, biomarkers indicating diminished ovarian reserve compared with normal ovarian reserve were not associated with reduced fertility.\n[12] These findings do not support the use of urinary or blood follicle-stimulating hormone tests or antimüllerian hormone levels to assess natural fertility for women with these characteristics."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Women with high urinary FSH values (>11.5 mIU/mg creatinine [n = 69]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (61%; 95% CI, 46%-74%) compared with women (n = 660) with normal values (62%; 95% CI, 58%-66%) or after 12 cycles of attempt (70% [95% CI, 54%-80%] vs 76% [95% CI, 72%-80%], respectively).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 39, "doc_id": 13497630, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [13497630], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A diminished ovarian reserve does not solely indicate infertility in an a priori non-infertile population.\n\nDocument title: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\n\nAbstract sentences:\n[0] Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential.\n[1] Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age.\n[2] Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area.\n[3] Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH.\n[4] Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle).\n[5] Conception was defined as a positive pregnancy test result.\n[6] Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis.\n[7] After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively).\n[8] Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (63%; 95% CI, 50%-73%) compared with women (n = 654) with normal values (62%; 95% CI, 57%-66%) or after 12 cycles of attempt (82% [95% CI, 70%-89%] vs 75% [95% CI, 70%-78%], respectively).\n[9] Women with high urinary FSH values (>11.5 mIU/mg creatinine [n = 69]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (61%; 95% CI, 46%-74%) compared with women (n = 660) with normal values (62%; 95% CI, 58%-66%) or after 12 cycles of attempt (70% [95% CI, 54%-80%] vs 76% [95% CI, 72%-80%], respectively).\n[10] Inhibin B levels (n = 737) were not associated with the probability of conceiving in a given cycle (hazard ratio per 1-pg/mL increase, 0.999; 95% CI, 0.997-1.001).\n[11] Conclusions and Relevance Among women aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, biomarkers indicating diminished ovarian reserve compared with normal ovarian reserve were not associated with reduced fertility.\n[12] These findings do not support the use of urinary or blood follicle-stimulating hormone tests or antimüllerian hormone levels to assess natural fertility for women with these characteristics."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Inhibin B levels (n = 737) were not associated with the probability of conceiving in a given cycle (hazard ratio per 1-pg/mL increase, 0.999; 95% CI, 0.997-1.001).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 39, "doc_id": 13497630, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [13497630], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A diminished ovarian reserve does not solely indicate infertility in an a priori non-infertile population.\n\nDocument title: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\n\nAbstract sentences:\n[0] Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential.\n[1] Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age.\n[2] Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area.\n[3] Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH.\n[4] Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle).\n[5] Conception was defined as a positive pregnancy test result.\n[6] Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis.\n[7] After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively).\n[8] Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (63%; 95% CI, 50%-73%) compared with women (n = 654) with normal values (62%; 95% CI, 57%-66%) or after 12 cycles of attempt (82% [95% CI, 70%-89%] vs 75% [95% CI, 70%-78%], respectively).\n[9] Women with high urinary FSH values (>11.5 mIU/mg creatinine [n = 69]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (61%; 95% CI, 46%-74%) compared with women (n = 660) with normal values (62%; 95% CI, 58%-66%) or after 12 cycles of attempt (70% [95% CI, 54%-80%] vs 76% [95% CI, 72%-80%], respectively).\n[10] Inhibin B levels (n = 737) were not associated with the probability of conceiving in a given cycle (hazard ratio per 1-pg/mL increase, 0.999; 95% CI, 0.997-1.001).\n[11] Conclusions and Relevance Among women aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, biomarkers indicating diminished ovarian reserve compared with normal ovarian reserve were not associated with reduced fertility.\n[12] These findings do not support the use of urinary or blood follicle-stimulating hormone tests or antimüllerian hormone levels to assess natural fertility for women with these characteristics."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"Conclusions and Relevance Among women aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, biomarkers indicating diminished ovarian reserve compared with normal ovarian reserve were not associated with reduced fertility.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 39, "doc_id": 13497630, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [13497630], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A diminished ovarian reserve is a very strong indicator of infertility, even in an a priori non-infertile population.\n\nDocument title: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\n\nAbstract sentences:\n[0] Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential.\n[1] Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age.\n[2] Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area.\n[3] Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH.\n[4] Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle).\n[5] Conception was defined as a positive pregnancy test result.\n[6] Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis.\n[7] After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively).\n[8] Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (63%; 95% CI, 50%-73%) compared with women (n = 654) with normal values (62%; 95% CI, 57%-66%) or after 12 cycles of attempt (82% [95% CI, 70%-89%] vs 75% [95% CI, 70%-78%], respectively).\n[9] Women with high urinary FSH values (>11.5 mIU/mg creatinine [n = 69]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (61%; 95% CI, 46%-74%) compared with women (n = 660) with normal values (62%; 95% CI, 58%-66%) or after 12 cycles of attempt (70% [95% CI, 54%-80%] vs 76% [95% CI, 72%-80%], respectively).\n[10] Inhibin B levels (n = 737) were not associated with the probability of conceiving in a given cycle (hazard ratio per 1-pg/mL increase, 0.999; 95% CI, 0.997-1.001).\n[11] Conclusions and Relevance Among women aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, biomarkers indicating diminished ovarian reserve compared with normal ovarian reserve were not associated with reduced fertility.\n[12] These findings do not support the use of urinary or blood follicle-stimulating hormone tests or antimüllerian hormone levels to assess natural fertility for women with these characteristics."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 40, "doc_id": 13497630, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [13497630], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A diminished ovarian reserve is a very strong indicator of infertility, even in an a priori non-infertile population.\n\nDocument title: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\n\nAbstract sentences:\n[0] Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential.\n[1] Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age.\n[2] Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area.\n[3] Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH.\n[4] Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle).\n[5] Conception was defined as a positive pregnancy test result.\n[6] Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis.\n[7] After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively).\n[8] Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (63%; 95% CI, 50%-73%) compared with women (n = 654) with normal values (62%; 95% CI, 57%-66%) or after 12 cycles of attempt (82% [95% CI, 70%-89%] vs 75% [95% CI, 70%-78%], respectively).\n[9] Women with high urinary FSH values (>11.5 mIU/mg creatinine [n = 69]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (61%; 95% CI, 46%-74%) compared with women (n = 660) with normal values (62%; 95% CI, 58%-66%) or after 12 cycles of attempt (70% [95% CI, 54%-80%] vs 76% [95% CI, 72%-80%], respectively).\n[10] Inhibin B levels (n = 737) were not associated with the probability of conceiving in a given cycle (hazard ratio per 1-pg/mL increase, 0.999; 95% CI, 0.997-1.001).\n[11] Conclusions and Relevance Among women aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, biomarkers indicating diminished ovarian reserve compared with normal ovarian reserve were not associated with reduced fertility.\n[12] These findings do not support the use of urinary or blood follicle-stimulating hormone tests or antimüllerian hormone levels to assess natural fertility for women with these characteristics."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (63%; 95% CI, 50%-73%) compared with women (n = 654) with normal values (62%; 95% CI, 57%-66%) or after 12 cycles of attempt (82% [95% CI, 70%-89%] vs 75% [95% CI, 70%-78%], respectively).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 40, "doc_id": 13497630, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [13497630], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A diminished ovarian reserve is a very strong indicator of infertility, even in an a priori non-infertile population.\n\nDocument title: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\n\nAbstract sentences:\n[0] Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential.\n[1] Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age.\n[2] Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area.\n[3] Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH.\n[4] Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle).\n[5] Conception was defined as a positive pregnancy test result.\n[6] Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis.\n[7] After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively).\n[8] Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (63%; 95% CI, 50%-73%) compared with women (n = 654) with normal values (62%; 95% CI, 57%-66%) or after 12 cycles of attempt (82% [95% CI, 70%-89%] vs 75% [95% CI, 70%-78%], respectively).\n[9] Women with high urinary FSH values (>11.5 mIU/mg creatinine [n = 69]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (61%; 95% CI, 46%-74%) compared with women (n = 660) with normal values (62%; 95% CI, 58%-66%) or after 12 cycles of attempt (70% [95% CI, 54%-80%] vs 76% [95% CI, 72%-80%], respectively).\n[10] Inhibin B levels (n = 737) were not associated with the probability of conceiving in a given cycle (hazard ratio per 1-pg/mL increase, 0.999; 95% CI, 0.997-1.001).\n[11] Conclusions and Relevance Among women aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, biomarkers indicating diminished ovarian reserve compared with normal ovarian reserve were not associated with reduced fertility.\n[12] These findings do not support the use of urinary or blood follicle-stimulating hormone tests or antimüllerian hormone levels to assess natural fertility for women with these characteristics."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Women with high urinary FSH values (>11.5 mIU/mg creatinine [n = 69]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (61%; 95% CI, 46%-74%) compared with women (n = 660) with normal values (62%; 95% CI, 58%-66%) or after 12 cycles of attempt (70% [95% CI, 54%-80%] vs 76% [95% CI, 72%-80%], respectively).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 40, "doc_id": 13497630, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [13497630], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A diminished ovarian reserve is a very strong indicator of infertility, even in an a priori non-infertile population.\n\nDocument title: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\n\nAbstract sentences:\n[0] Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential.\n[1] Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age.\n[2] Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area.\n[3] Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH.\n[4] Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle).\n[5] Conception was defined as a positive pregnancy test result.\n[6] Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis.\n[7] After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively).\n[8] Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (63%; 95% CI, 50%-73%) compared with women (n = 654) with normal values (62%; 95% CI, 57%-66%) or after 12 cycles of attempt (82% [95% CI, 70%-89%] vs 75% [95% CI, 70%-78%], respectively).\n[9] Women with high urinary FSH values (>11.5 mIU/mg creatinine [n = 69]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (61%; 95% CI, 46%-74%) compared with women (n = 660) with normal values (62%; 95% CI, 58%-66%) or after 12 cycles of attempt (70% [95% CI, 54%-80%] vs 76% [95% CI, 72%-80%], respectively).\n[10] Inhibin B levels (n = 737) were not associated with the probability of conceiving in a given cycle (hazard ratio per 1-pg/mL increase, 0.999; 95% CI, 0.997-1.001).\n[11] Conclusions and Relevance Among women aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, biomarkers indicating diminished ovarian reserve compared with normal ovarian reserve were not associated with reduced fertility.\n[12] These findings do not support the use of urinary or blood follicle-stimulating hormone tests or antimüllerian hormone levels to assess natural fertility for women with these characteristics."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Inhibin B levels (n = 737) were not associated with the probability of conceiving in a given cycle (hazard ratio per 1-pg/mL increase, 0.999; 95% CI, 0.997-1.001).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 40, "doc_id": 13497630, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [13497630], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A diminished ovarian reserve is a very strong indicator of infertility, even in an a priori non-infertile population.\n\nDocument title: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\n\nAbstract sentences:\n[0] Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential.\n[1] Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age.\n[2] Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area.\n[3] Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH.\n[4] Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle).\n[5] Conception was defined as a positive pregnancy test result.\n[6] Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis.\n[7] After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively).\n[8] Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (63%; 95% CI, 50%-73%) compared with women (n = 654) with normal values (62%; 95% CI, 57%-66%) or after 12 cycles of attempt (82% [95% CI, 70%-89%] vs 75% [95% CI, 70%-78%], respectively).\n[9] Women with high urinary FSH values (>11.5 mIU/mg creatinine [n = 69]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (61%; 95% CI, 46%-74%) compared with women (n = 660) with normal values (62%; 95% CI, 58%-66%) or after 12 cycles of attempt (70% [95% CI, 54%-80%] vs 76% [95% CI, 72%-80%], respectively).\n[10] Inhibin B levels (n = 737) were not associated with the probability of conceiving in a given cycle (hazard ratio per 1-pg/mL increase, 0.999; 95% CI, 0.997-1.001).\n[11] Conclusions and Relevance Among women aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, biomarkers indicating diminished ovarian reserve compared with normal ovarian reserve were not associated with reduced fertility.\n[12] These findings do not support the use of urinary or blood follicle-stimulating hormone tests or antimüllerian hormone levels to assess natural fertility for women with these characteristics."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"Conclusions and Relevance Among women aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, biomarkers indicating diminished ovarian reserve compared with normal ovarian reserve were not associated with reduced fertility.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 40, "doc_id": 13497630, "label": "CONTRADICTS", "evidence_sentence_ids": [11], "cited_doc_ids": [13497630], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A high microerythrocyte count protects against severe anemia in homozygous alpha (+)- thalassemia trait subjects.\n\nDocument title: Increased Microerythrocyte Count in Homozygous α+-Thalassaemia Contributes to Protection against Severe Malarial Anaemia\n\nAbstract sentences:\n[0] BACKGROUND The heritable haemoglobinopathy alpha(+)-thalassaemia is caused by the reduced synthesis of alpha-globin chains that form part of normal adult haemoglobin (Hb).\n[1] Individuals homozygous for alpha(+)-thalassaemia have microcytosis and an increased erythrocyte count.\n[2] Alpha(+)-thalassaemia homozygosity confers considerable protection against severe malaria, including severe malarial anaemia (SMA) (Hb concentration < 50 g/l), but does not influence parasite count.\n[3] We tested the hypothesis that the erythrocyte indices associated with alpha(+)-thalassaemia homozygosity provide a haematological benefit during acute malaria.\n[4] METHODS AND FINDINGS Data from children living on the north coast of Papua New Guinea who had participated in a case-control study of the protection afforded by alpha(+)-thalassaemia against severe malaria were reanalysed to assess the genotype-specific reduction in erythrocyte count and Hb levels associated with acute malarial disease.\n[5] We observed a reduction in median erythrocyte count of approximately 1.5 x 10(12)/l in all children with acute falciparum malaria relative to values in community children (p < 0.001).\n[6] We developed a simple mathematical model of the linear relationship between Hb concentration and erythrocyte count.\n[7] This model predicted that children homozygous for alpha(+)-thalassaemia lose less Hb than children of normal genotype for a reduction in erythrocyte count of >1.1 x 10(12)/l as a result of the reduced mean cell Hb in homozygous alpha(+)-thalassaemia.\n[8] In addition, children homozygous for alpha(+)-thalassaemia require a 10% greater reduction in erythrocyte count than children of normal genotype (p = 0.02) for Hb concentration to fall to 50 g/l, the cutoff for SMA.\n[9] We estimated that the haematological profile in children homozygous for alpha(+)-thalassaemia reduces the risk of SMA during acute malaria compared to children of normal genotype (relative risk 0.52; 95% confidence interval [CI] 0.24-1.12, p = 0.09).\n[10] CONCLUSIONS The increased erythrocyte count and microcytosis in children homozygous for alpha(+)-thalassaemia may contribute substantially to their protection against SMA.\n[11] A lower concentration of Hb per erythrocyte and a larger population of erythrocytes may be a biologically advantageous strategy against the significant reduction in erythrocyte count that occurs during acute infection with the malaria parasite Plasmodium falciparum.\n[12] This haematological profile may reduce the risk of anaemia by other Plasmodium species, as well as other causes of anaemia.\n[13] Other host polymorphisms that induce an increased erythrocyte count and microcytosis may confer a similar advantage."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1, 9]\nExplanation: Evidence states: \"Individuals homozygous for alpha(+)-thalassaemia have microcytosis and an increased erythrocyte count. We estimated that the haematological profile in children homozygous for alpha(+)-thalassaemia reduces the risk of SMA during acute malaria compared to children of normal genotype (relative risk 0.52; 95% confidence interval [CI] 0.24-1.12, p = 0.09).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 41, "doc_id": 18174210, "label": "SUPPORTS", "evidence_sentence_ids": [1, 9], "cited_doc_ids": [18174210], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A high microerythrocyte count protects against severe anemia in homozygous alpha (+)- thalassemia trait subjects.\n\nDocument title: Increased Microerythrocyte Count in Homozygous α+-Thalassaemia Contributes to Protection against Severe Malarial Anaemia\n\nAbstract sentences:\n[0] BACKGROUND The heritable haemoglobinopathy alpha(+)-thalassaemia is caused by the reduced synthesis of alpha-globin chains that form part of normal adult haemoglobin (Hb).\n[1] Individuals homozygous for alpha(+)-thalassaemia have microcytosis and an increased erythrocyte count.\n[2] Alpha(+)-thalassaemia homozygosity confers considerable protection against severe malaria, including severe malarial anaemia (SMA) (Hb concentration < 50 g/l), but does not influence parasite count.\n[3] We tested the hypothesis that the erythrocyte indices associated with alpha(+)-thalassaemia homozygosity provide a haematological benefit during acute malaria.\n[4] METHODS AND FINDINGS Data from children living on the north coast of Papua New Guinea who had participated in a case-control study of the protection afforded by alpha(+)-thalassaemia against severe malaria were reanalysed to assess the genotype-specific reduction in erythrocyte count and Hb levels associated with acute malarial disease.\n[5] We observed a reduction in median erythrocyte count of approximately 1.5 x 10(12)/l in all children with acute falciparum malaria relative to values in community children (p < 0.001).\n[6] We developed a simple mathematical model of the linear relationship between Hb concentration and erythrocyte count.\n[7] This model predicted that children homozygous for alpha(+)-thalassaemia lose less Hb than children of normal genotype for a reduction in erythrocyte count of >1.1 x 10(12)/l as a result of the reduced mean cell Hb in homozygous alpha(+)-thalassaemia.\n[8] In addition, children homozygous for alpha(+)-thalassaemia require a 10% greater reduction in erythrocyte count than children of normal genotype (p = 0.02) for Hb concentration to fall to 50 g/l, the cutoff for SMA.\n[9] We estimated that the haematological profile in children homozygous for alpha(+)-thalassaemia reduces the risk of SMA during acute malaria compared to children of normal genotype (relative risk 0.52; 95% confidence interval [CI] 0.24-1.12, p = 0.09).\n[10] CONCLUSIONS The increased erythrocyte count and microcytosis in children homozygous for alpha(+)-thalassaemia may contribute substantially to their protection against SMA.\n[11] A lower concentration of Hb per erythrocyte and a larger population of erythrocytes may be a biologically advantageous strategy against the significant reduction in erythrocyte count that occurs during acute infection with the malaria parasite Plasmodium falciparum.\n[12] This haematological profile may reduce the risk of anaemia by other Plasmodium species, as well as other causes of anaemia.\n[13] Other host polymorphisms that induce an increased erythrocyte count and microcytosis may confer a similar advantage."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"CONCLUSIONS The increased erythrocyte count and microcytosis in children homozygous for alpha(+)-thalassaemia may contribute substantially to their protection against SMA.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 41, "doc_id": 18174210, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [18174210], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A low percentage of hematopoietic progenitor cells are susceptible to HIV-1 infection ex vivo.\n\nDocument title: HIV–1 Infects Multipotent Progenitor Cells Causing Cell Death and Establishing Latent Cellular Reservoirs\n\nAbstract sentences:\n[0] HIV causes a chronic infection characterized by depletion of CD4(+) T lymphocytes and the development of opportunistic infections.\n[1] Despite drugs that inhibit viral spread, HIV infection has been difficult to cure because of uncharacterized reservoirs of infected cells that are resistant to highly active antiretroviral therapy (HAART) and the immune response.\n[2] Here we used CD34(+) cells from infected people as well as in vitro studies of wild-type HIV to show infection and killing of CD34(+) multipotent hematopoietic progenitor cells (HPCs).\n[3] In some HPCs, we detected latent infection that stably persisted in cell culture until viral gene expression was activated by differentiation factors.\n[4] A unique reporter HIV that directly detects latently infected cells in vitro confirmed the presence of distinct populations of active and latently infected HPCs.\n[5] These findings have major implications for understanding HIV bone marrow pathology and the mechanisms by which HIV causes persistent infection."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 43, "doc_id": 7224723, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [7224723], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A mutation in HNF4A leads to an increased risk of developing diabetes by the age of 14 years.\n\nDocument title: Macrosomia and Hyperinsulinaemic Hypoglycaemia in Patients with Heterozygous Mutations in the HNF4A Gene\n\nAbstract sentences:\n[0] Background  Macrosomia is associated with considerable neonatal and maternal morbidity.\n[1] Factors that predict macrosomia are poorly understood.\n[2] The increased rate of macrosomia in the offspring of pregnant women with diabetes and in congenital hyperinsulinaemia is mediated by increased foetal insulin secretion.\n[3] We assessed the in utero and neonatal role of two key regulators of pancreatic insulin secretion by studying birthweight and the incidence of neonatal hypoglycaemia in patients with heterozygous mutations in the maturity-onset diabetes of the young (MODY) genes HNF4A (encoding HNF-4α) and HNF1A/TCF1 (encoding HNF-1α), and the effect of pancreatic deletion of Hnf4a on foetal and neonatal insulin secretion in mice."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"We assessed the in utero and neonatal role of two key regulators of pancreatic insulin secretion by studying birthweight and the incidence of neonatal hypoglycaemia in patients with heterozygous mutations in the maturity-onset diabetes of the young (MODY) genes HNF4A (encoding HNF-4α) and HNF1A/TCF1 (encoding HNF-1α), and the effect of pancreatic deletion of Hnf4a on foetal and neonatal insulin secretion in mice.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 44, "doc_id": 56893404, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [56893404], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A mutation in HNF4A leads to an increased risk of diabetes by the age of 14 years.\n\nDocument title: Macrosomia and Hyperinsulinaemic Hypoglycaemia in Patients with Heterozygous Mutations in the HNF4A Gene\n\nAbstract sentences:\n[0] Background  Macrosomia is associated with considerable neonatal and maternal morbidity.\n[1] Factors that predict macrosomia are poorly understood.\n[2] The increased rate of macrosomia in the offspring of pregnant women with diabetes and in congenital hyperinsulinaemia is mediated by increased foetal insulin secretion.\n[3] We assessed the in utero and neonatal role of two key regulators of pancreatic insulin secretion by studying birthweight and the incidence of neonatal hypoglycaemia in patients with heterozygous mutations in the maturity-onset diabetes of the young (MODY) genes HNF4A (encoding HNF-4α) and HNF1A/TCF1 (encoding HNF-1α), and the effect of pancreatic deletion of Hnf4a on foetal and neonatal insulin secretion in mice."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 45, "doc_id": 56893404, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [56893404], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A single nucleotide variant the gene DGKK is strongly associated with increased risk of hypospadias.\n\nDocument title: Common variants in DGKK are strongly associated with risk of hypospadias\n\nAbstract sentences:\n[0] Hypospadias is a common congenital malformation of the male external genitalia.\n[1] We performed a genome-wide association study using pooled DNA from 436 individuals with hypospadias (cases) and 494 controls of European descent and selected the highest ranked SNPs for individual genotyping in the discovery sample, an additional Dutch sample of 133 cases and their parents, and a Swedish series of 266 cases and 402 controls.\n[2] Individual genotyping of two SNPs (rs1934179 and rs7063116) in DGKK, encoding diacylglycerol kinase κ, produced compelling evidence for association with hypospadias in the discovery sample (allele-specific odds ratio (OR) = 2.5, P = 2.5 × 10−11 and OR = 2.3, P = 2.9 × 10−9, respectively) and in the Dutch (OR = 3.9, P = 2.4 × 10−5 and OR = 3.8, P = 3.4 × 10−5) and Swedish (OR = 2.5, P = 2.6 × 10−8 and OR = 2.2, P = 2.7 × 10−6) replication samples.\n[3] Expression studies showed expression of DGKK in preputial tissue of cases and controls, which was lower in carriers of the risk allele of rs1934179 (P = 0.047).\n[4] We propose DGKK as a major risk gene for hypospadias."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Individual genotyping of two SNPs (rs1934179 and rs7063116) in DGKK, encoding diacylglycerol kinase κ, produced compelling evidence for association with hypospadias in the discovery sample (allele-specific odds ratio (OR) = 2.5, P = 2.5 × 10−11 and OR = 2.3, P = 2.9 × 10−9, respectively) and in the Dutch (OR = 3.9, P = 2.4 × 10−5 and OR = 3.8, P = 3.4 × 10−5) and Swedish (OR = 2.5, P = 2.6 × 10−8 and OR = 2.2, P = 2.7 × 10−6) replication samples.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 46, "doc_id": 380526, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [380526], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: A strong bias in the phage genome locations where the spacers were derived has been observed in many CRISPR subtypes that confer the immunity to phage.\n\nDocument title: Strong bias in the bacterial CRISPR elements that confer immunity to phage.\n\nAbstract sentences:\n[0] Clustered regularly interspaced short palindromic repeats (CRISPR)-Cas systems provide adaptive immunity against phage via spacer-encoded CRISPR RNAs that are complementary to invasive nucleic acids.\n[1] Here, we challenge Streptococcus thermophilus with a bacteriophage, and used PCR-based metagenomics to monitor phage-derived spacers daily for 15 days in two experiments.\n[2] Spacers that target the host chromosome are infrequent and strongly selected against, suggesting autoimmunity is lethal.\n[3] In experiments that recover over half a million spacers, we observe early dominance by a few spacer sub-populations and rapid oscillations in sub-population abundances.\n[4] In two CRISPR systems and in replicate experiments, a few spacers account for the majority of spacer sequences.\n[5] Nearly all phage locations targeted by the acquired spacers have a proto-spacer adjacent motif (PAM), indicating PAMs are involved in spacer acquisition.\n[6] We detect a strong and reproducible bias in the phage genome locations from which spacers derive.\n[7] This may reflect selection for specific spacers based on location and effectiveness."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"We detect a strong and reproducible bias in the phage genome locations from which spacers derive.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 47, "doc_id": 26996935, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [3512154, 26996935], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: ALDH1 expression is associated with poorer prognosis for breast cancer primary tumors.\n\nDocument title: ALDH1 is a marker of normal and malignant human mammary stem cells and a predictor of poor clinical outcome.\n\nAbstract sentences:\n[0] Application of stem cell biology to breast cancer research has been limited by the lack of simple methods for identification and isolation of normal and malignant stem cells.\n[1] Utilizing in vitro and in vivo experimental systems, we show that normal and cancer human mammary epithelial cells with increased aldehyde dehydrogenase activity (ALDH) have stem/progenitor properties.\n[2] These cells contain the subpopulation of normal breast epithelium with the broadest lineage differentiation potential and greatest growth capacity in a xenotransplant model.\n[3] In breast carcinomas, high ALDH activity identifies the tumorigenic cell fraction, capable of self-renewal and of generating tumors that recapitulate the heterogeneity of the parental tumor.\n[4] In a series of 577 breast carcinomas, expression of ALDH1 detected by immunostaining correlated with poor prognosis.\n[5] These findings offer an important new tool for the study of normal and malignant breast stem cells and facilitate the clinical application of stem cell concepts."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"In a series of 577 breast carcinomas, expression of ALDH1 detected by immunostaining correlated with poor prognosis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 52, "doc_id": 45638119, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [45638119], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: AMP-activated protein kinase (AMPK) activation reduces inflammation-related fibrosis in the lungs.\n\nDocument title: Metformin reverses established lung fibrosis in a bleomycin model\n\nAbstract sentences:\n[0] Fibrosis is a pathological result of a dysfunctional repair response to tissue injury and occurs in a number of organs, including the lungs1.\n[1] Cellular metabolism regulates tissue repair and remodelling responses to injury2-4.\n[2] AMPK is a critical sensor of cellular bioenergetics and controls the switch from anabolic to catabolic metabolism5.\n[3] However, the role of AMPK in fibrosis is not well understood.\n[4] Here, we demonstrate that in humans with idiopathic pulmonary fibrosis (IPF) and in an experimental mouse model of lung fibrosis, AMPK activity is lower in fibrotic regions associated with metabolically active and apoptosis-resistant myofibroblasts.\n[5] Pharmacological activation of AMPK in myofibroblasts from lungs of humans with IPF display lower fibrotic activity, along with enhanced mitochondrial biogenesis and normalization of sensitivity to apoptosis.\n[6] In a bleomycin model of lung fibrosis in mice, metformin therapeutically accelerates the resolution of well-established fibrosis in an AMPK-dependent manner.\n[7] These studies implicate deficient AMPK activation in non-resolving, pathologic fibrotic processes, and support a role for metformin (or other AMPK activators) to reverse established fibrosis by facilitating deactivation and apoptosis of myofibroblasts."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Pharmacological activation of AMPK in myofibroblasts from lungs of humans with IPF display lower fibrotic activity, along with enhanced mitochondrial biogenesis and normalization of sensitivity to apoptosis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 55, "doc_id": 49556906, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [49556906], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: AMP-activated protein kinase (AMPK) activation reduces inflammation-related fibrosis in the lungs.\n\nDocument title: Metformin reverses established lung fibrosis in a bleomycin model\n\nAbstract sentences:\n[0] Fibrosis is a pathological result of a dysfunctional repair response to tissue injury and occurs in a number of organs, including the lungs1.\n[1] Cellular metabolism regulates tissue repair and remodelling responses to injury2-4.\n[2] AMPK is a critical sensor of cellular bioenergetics and controls the switch from anabolic to catabolic metabolism5.\n[3] However, the role of AMPK in fibrosis is not well understood.\n[4] Here, we demonstrate that in humans with idiopathic pulmonary fibrosis (IPF) and in an experimental mouse model of lung fibrosis, AMPK activity is lower in fibrotic regions associated with metabolically active and apoptosis-resistant myofibroblasts.\n[5] Pharmacological activation of AMPK in myofibroblasts from lungs of humans with IPF display lower fibrotic activity, along with enhanced mitochondrial biogenesis and normalization of sensitivity to apoptosis.\n[6] In a bleomycin model of lung fibrosis in mice, metformin therapeutically accelerates the resolution of well-established fibrosis in an AMPK-dependent manner.\n[7] These studies implicate deficient AMPK activation in non-resolving, pathologic fibrotic processes, and support a role for metformin (or other AMPK activators) to reverse established fibrosis by facilitating deactivation and apoptosis of myofibroblasts."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"In a bleomycin model of lung fibrosis in mice, metformin therapeutically accelerates the resolution of well-established fibrosis in an AMPK-dependent manner.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 55, "doc_id": 49556906, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [49556906], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: AMP-activated protein kinase (AMPK) activation reduces inflammation-related fibrosis in the lungs.\n\nDocument title: Metformin reverses established lung fibrosis in a bleomycin model\n\nAbstract sentences:\n[0] Fibrosis is a pathological result of a dysfunctional repair response to tissue injury and occurs in a number of organs, including the lungs1.\n[1] Cellular metabolism regulates tissue repair and remodelling responses to injury2-4.\n[2] AMPK is a critical sensor of cellular bioenergetics and controls the switch from anabolic to catabolic metabolism5.\n[3] However, the role of AMPK in fibrosis is not well understood.\n[4] Here, we demonstrate that in humans with idiopathic pulmonary fibrosis (IPF) and in an experimental mouse model of lung fibrosis, AMPK activity is lower in fibrotic regions associated with metabolically active and apoptosis-resistant myofibroblasts.\n[5] Pharmacological activation of AMPK in myofibroblasts from lungs of humans with IPF display lower fibrotic activity, along with enhanced mitochondrial biogenesis and normalization of sensitivity to apoptosis.\n[6] In a bleomycin model of lung fibrosis in mice, metformin therapeutically accelerates the resolution of well-established fibrosis in an AMPK-dependent manner.\n[7] These studies implicate deficient AMPK activation in non-resolving, pathologic fibrotic processes, and support a role for metformin (or other AMPK activators) to reverse established fibrosis by facilitating deactivation and apoptosis of myofibroblasts."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"These studies implicate deficient AMPK activation in non-resolving, pathologic fibrotic processes, and support a role for metformin (or other AMPK activators) to reverse established fibrosis by facilitating deactivation and apoptosis of myofibroblasts.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 55, "doc_id": 49556906, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [49556906], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: APOE4 expression in iPSC-derived neurons results in decreased tau phosphorylation.\n\nDocument title: Gain of toxic Apolipoprotein E4 effects in Human iPSC-Derived Neurons Is Ameliorated by a Small-Molecule Structure Corrector\n\nAbstract sentences:\n[0] Efforts to develop drugs for Alzheimer's disease (AD) have shown promise in animal studies, only to fail in human trials, suggesting a pressing need to study AD in human model systems.\n[1] Using human neurons derived from induced pluripotent stem cells that expressed apolipoprotein E4 (ApoE4), a variant of the APOE gene product and the major genetic risk factor for AD, we demonstrated that ApoE4-expressing neurons had higher levels of tau phosphorylation, unrelated to their increased production of amyloid-β (Aβ) peptides, and that they displayed GABAergic neuron degeneration.\n[2] ApoE4 increased Aβ production in human, but not in mouse, neurons.\n[3] Converting ApoE4 to ApoE3 by gene editing rescued these phenotypes, indicating the specific effects of ApoE4.\n[4] Neurons that lacked APOE behaved similarly to those expressing ApoE3, and the introduction of ApoE4 expression recapitulated the pathological phenotypes, suggesting a gain of toxic effects from ApoE4.\n[5] Treatment of ApoE4-expressing neurons with a small-molecule structure corrector ameliorated the detrimental effects, thus showing that correcting the pathogenic conformation of ApoE4 is a viable therapeutic approach for ApoE4-related AD."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Using human neurons derived from induced pluripotent stem cells that expressed apolipoprotein E4 (ApoE4), a variant of the APOE gene product and the major genetic risk factor for AD, we demonstrated that ApoE4-expressing neurons had higher levels of tau phosphorylation, unrelated to their increased production of amyloid-β (Aβ) peptides, and that they displayed GABAergic neuron degeneration.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 58, "doc_id": 4709641, "label": "CONTRADICTS", "evidence_sentence_ids": [1], "cited_doc_ids": [4709641], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: ART has no effect on the infectiveness of HIV-positive people.\n\nDocument title: HIV Treatment as Prevention: Systematic Comparison of Mathematical Models of the Potential Impact of Antiretroviral Therapy on HIV Incidence in South Africa\n\nAbstract sentences:\n[0] BACKGROUND Many mathematical models have investigated the impact of expanding access to antiretroviral therapy (ART) on new HIV infections.\n[1] Comparing results and conclusions across models is challenging because models have addressed slightly different questions and have reported different outcome metrics.\n[2] This study compares the predictions of several mathematical models simulating the same ART intervention programmes to determine the extent to which models agree about the epidemiological impact of expanded ART.\n[3] METHODS AND FINDINGS Twelve independent mathematical models evaluated a set of standardised ART intervention scenarios in South Africa and reported a common set of outputs.\n[4] Intervention scenarios systematically varied the CD4 count threshold for treatment eligibility, access to treatment, and programme retention.\n[5] For a scenario in which 80% of HIV-infected individuals start treatment on average 1 y after their CD4 count drops below 350 cells/µl and 85% remain on treatment after 3 y, the models projected that HIV incidence would be 35% to 54% lower 8 y after the introduction of ART, compared to a counterfactual scenario in which there is no ART.\n[6] More variation existed in the estimated long-term (38 y) reductions in incidence.\n[7] The impact of optimistic interventions including immediate ART initiation varied widely across models, maintaining substantial uncertainty about the theoretical prospect for elimination of HIV from the population using ART alone over the next four decades.\n[8] The number of person-years of ART per infection averted over 8 y ranged between 5.8 and 18.7.\n[9] Considering the actual scale-up of ART in South Africa, seven models estimated that current HIV incidence is 17% to 32% lower than it would have been in the absence of ART.\n[10] Differences between model assumptions about CD4 decline and HIV transmissibility over the course of infection explained only a modest amount of the variation in model results.\n[11] CONCLUSIONS Mathematical models evaluating the impact of ART vary substantially in structure, complexity, and parameter choices, but all suggest that ART, at high levels of access and with high adherence, has the potential to substantially reduce new HIV infections.\n[12] There was broad agreement regarding the short-term epidemiologic impact of ambitious treatment scale-up, but more variation in longer term projections and in the efficiency with which treatment can reduce new infections.\n[13] Differences between model predictions could not be explained by differences in model structure or parameterization that were hypothesized to affect intervention impact."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"For a scenario in which 80% of HIV-infected individuals start treatment on average 1 y after their CD4 count drops below 350 cells/µl and 85% remain on treatment after 3 y, the models projected that HIV incidence would be 35% to 54% lower 8 y after the introduction of ART, compared to a counterfactual scenario in which there is no ART.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 60, "doc_id": 13899137, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [13899137, 13901073], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: ART has no effect on the infectiveness of HIV-positive people.\n\nDocument title: HIV Treatment as Prevention: Systematic Comparison of Mathematical Models of the Potential Impact of Antiretroviral Therapy on HIV Incidence in South Africa\n\nAbstract sentences:\n[0] BACKGROUND Many mathematical models have investigated the impact of expanding access to antiretroviral therapy (ART) on new HIV infections.\n[1] Comparing results and conclusions across models is challenging because models have addressed slightly different questions and have reported different outcome metrics.\n[2] This study compares the predictions of several mathematical models simulating the same ART intervention programmes to determine the extent to which models agree about the epidemiological impact of expanded ART.\n[3] METHODS AND FINDINGS Twelve independent mathematical models evaluated a set of standardised ART intervention scenarios in South Africa and reported a common set of outputs.\n[4] Intervention scenarios systematically varied the CD4 count threshold for treatment eligibility, access to treatment, and programme retention.\n[5] For a scenario in which 80% of HIV-infected individuals start treatment on average 1 y after their CD4 count drops below 350 cells/µl and 85% remain on treatment after 3 y, the models projected that HIV incidence would be 35% to 54% lower 8 y after the introduction of ART, compared to a counterfactual scenario in which there is no ART.\n[6] More variation existed in the estimated long-term (38 y) reductions in incidence.\n[7] The impact of optimistic interventions including immediate ART initiation varied widely across models, maintaining substantial uncertainty about the theoretical prospect for elimination of HIV from the population using ART alone over the next four decades.\n[8] The number of person-years of ART per infection averted over 8 y ranged between 5.8 and 18.7.\n[9] Considering the actual scale-up of ART in South Africa, seven models estimated that current HIV incidence is 17% to 32% lower than it would have been in the absence of ART.\n[10] Differences between model assumptions about CD4 decline and HIV transmissibility over the course of infection explained only a modest amount of the variation in model results.\n[11] CONCLUSIONS Mathematical models evaluating the impact of ART vary substantially in structure, complexity, and parameter choices, but all suggest that ART, at high levels of access and with high adherence, has the potential to substantially reduce new HIV infections.\n[12] There was broad agreement regarding the short-term epidemiologic impact of ambitious treatment scale-up, but more variation in longer term projections and in the efficiency with which treatment can reduce new infections.\n[13] Differences between model predictions could not be explained by differences in model structure or parameterization that were hypothesized to affect intervention impact."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Considering the actual scale-up of ART in South Africa, seven models estimated that current HIV incidence is 17% to 32% lower than it would have been in the absence of ART.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 60, "doc_id": 13899137, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [13899137, 13901073], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: ART has no effect on the infectiveness of HIV-positive people.\n\nDocument title: HIV Treatment as Prevention: Systematic Comparison of Mathematical Models of the Potential Impact of Antiretroviral Therapy on HIV Incidence in South Africa\n\nAbstract sentences:\n[0] BACKGROUND Many mathematical models have investigated the impact of expanding access to antiretroviral therapy (ART) on new HIV infections.\n[1] Comparing results and conclusions across models is challenging because models have addressed slightly different questions and have reported different outcome metrics.\n[2] This study compares the predictions of several mathematical models simulating the same ART intervention programmes to determine the extent to which models agree about the epidemiological impact of expanded ART.\n[3] METHODS AND FINDINGS Twelve independent mathematical models evaluated a set of standardised ART intervention scenarios in South Africa and reported a common set of outputs.\n[4] Intervention scenarios systematically varied the CD4 count threshold for treatment eligibility, access to treatment, and programme retention.\n[5] For a scenario in which 80% of HIV-infected individuals start treatment on average 1 y after their CD4 count drops below 350 cells/µl and 85% remain on treatment after 3 y, the models projected that HIV incidence would be 35% to 54% lower 8 y after the introduction of ART, compared to a counterfactual scenario in which there is no ART.\n[6] More variation existed in the estimated long-term (38 y) reductions in incidence.\n[7] The impact of optimistic interventions including immediate ART initiation varied widely across models, maintaining substantial uncertainty about the theoretical prospect for elimination of HIV from the population using ART alone over the next four decades.\n[8] The number of person-years of ART per infection averted over 8 y ranged between 5.8 and 18.7.\n[9] Considering the actual scale-up of ART in South Africa, seven models estimated that current HIV incidence is 17% to 32% lower than it would have been in the absence of ART.\n[10] Differences between model assumptions about CD4 decline and HIV transmissibility over the course of infection explained only a modest amount of the variation in model results.\n[11] CONCLUSIONS Mathematical models evaluating the impact of ART vary substantially in structure, complexity, and parameter choices, but all suggest that ART, at high levels of access and with high adherence, has the potential to substantially reduce new HIV infections.\n[12] There was broad agreement regarding the short-term epidemiologic impact of ambitious treatment scale-up, but more variation in longer term projections and in the efficiency with which treatment can reduce new infections.\n[13] Differences between model predictions could not be explained by differences in model structure or parameterization that were hypothesized to affect intervention impact."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"CONCLUSIONS Mathematical models evaluating the impact of ART vary substantially in structure, complexity, and parameter choices, but all suggest that ART, at high levels of access and with high adherence, has the potential to substantially reduce new HIV infections.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 60, "doc_id": 13899137, "label": "CONTRADICTS", "evidence_sentence_ids": [11], "cited_doc_ids": [13899137, 13901073], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: ART substantially reduces infectiveness of HIV-positive people.\n\nDocument title: HIV Treatment as Prevention: Systematic Comparison of Mathematical Models of the Potential Impact of Antiretroviral Therapy on HIV Incidence in South Africa\n\nAbstract sentences:\n[0] BACKGROUND Many mathematical models have investigated the impact of expanding access to antiretroviral therapy (ART) on new HIV infections.\n[1] Comparing results and conclusions across models is challenging because models have addressed slightly different questions and have reported different outcome metrics.\n[2] This study compares the predictions of several mathematical models simulating the same ART intervention programmes to determine the extent to which models agree about the epidemiological impact of expanded ART.\n[3] METHODS AND FINDINGS Twelve independent mathematical models evaluated a set of standardised ART intervention scenarios in South Africa and reported a common set of outputs.\n[4] Intervention scenarios systematically varied the CD4 count threshold for treatment eligibility, access to treatment, and programme retention.\n[5] For a scenario in which 80% of HIV-infected individuals start treatment on average 1 y after their CD4 count drops below 350 cells/µl and 85% remain on treatment after 3 y, the models projected that HIV incidence would be 35% to 54% lower 8 y after the introduction of ART, compared to a counterfactual scenario in which there is no ART.\n[6] More variation existed in the estimated long-term (38 y) reductions in incidence.\n[7] The impact of optimistic interventions including immediate ART initiation varied widely across models, maintaining substantial uncertainty about the theoretical prospect for elimination of HIV from the population using ART alone over the next four decades.\n[8] The number of person-years of ART per infection averted over 8 y ranged between 5.8 and 18.7.\n[9] Considering the actual scale-up of ART in South Africa, seven models estimated that current HIV incidence is 17% to 32% lower than it would have been in the absence of ART.\n[10] Differences between model assumptions about CD4 decline and HIV transmissibility over the course of infection explained only a modest amount of the variation in model results.\n[11] CONCLUSIONS Mathematical models evaluating the impact of ART vary substantially in structure, complexity, and parameter choices, but all suggest that ART, at high levels of access and with high adherence, has the potential to substantially reduce new HIV infections.\n[12] There was broad agreement regarding the short-term epidemiologic impact of ambitious treatment scale-up, but more variation in longer term projections and in the efficiency with which treatment can reduce new infections.\n[13] Differences between model predictions could not be explained by differences in model structure or parameterization that were hypothesized to affect intervention impact."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"For a scenario in which 80% of HIV-infected individuals start treatment on average 1 y after their CD4 count drops below 350 cells/µl and 85% remain on treatment after 3 y, the models projected that HIV incidence would be 35% to 54% lower 8 y after the introduction of ART, compared to a counterfactual scenario in which there is no ART.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 61, "doc_id": 13899137, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [13899137, 13901073], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: ART substantially reduces infectiveness of HIV-positive people.\n\nDocument title: HIV Treatment as Prevention: Systematic Comparison of Mathematical Models of the Potential Impact of Antiretroviral Therapy on HIV Incidence in South Africa\n\nAbstract sentences:\n[0] BACKGROUND Many mathematical models have investigated the impact of expanding access to antiretroviral therapy (ART) on new HIV infections.\n[1] Comparing results and conclusions across models is challenging because models have addressed slightly different questions and have reported different outcome metrics.\n[2] This study compares the predictions of several mathematical models simulating the same ART intervention programmes to determine the extent to which models agree about the epidemiological impact of expanded ART.\n[3] METHODS AND FINDINGS Twelve independent mathematical models evaluated a set of standardised ART intervention scenarios in South Africa and reported a common set of outputs.\n[4] Intervention scenarios systematically varied the CD4 count threshold for treatment eligibility, access to treatment, and programme retention.\n[5] For a scenario in which 80% of HIV-infected individuals start treatment on average 1 y after their CD4 count drops below 350 cells/µl and 85% remain on treatment after 3 y, the models projected that HIV incidence would be 35% to 54% lower 8 y after the introduction of ART, compared to a counterfactual scenario in which there is no ART.\n[6] More variation existed in the estimated long-term (38 y) reductions in incidence.\n[7] The impact of optimistic interventions including immediate ART initiation varied widely across models, maintaining substantial uncertainty about the theoretical prospect for elimination of HIV from the population using ART alone over the next four decades.\n[8] The number of person-years of ART per infection averted over 8 y ranged between 5.8 and 18.7.\n[9] Considering the actual scale-up of ART in South Africa, seven models estimated that current HIV incidence is 17% to 32% lower than it would have been in the absence of ART.\n[10] Differences between model assumptions about CD4 decline and HIV transmissibility over the course of infection explained only a modest amount of the variation in model results.\n[11] CONCLUSIONS Mathematical models evaluating the impact of ART vary substantially in structure, complexity, and parameter choices, but all suggest that ART, at high levels of access and with high adherence, has the potential to substantially reduce new HIV infections.\n[12] There was broad agreement regarding the short-term epidemiologic impact of ambitious treatment scale-up, but more variation in longer term projections and in the efficiency with which treatment can reduce new infections.\n[13] Differences between model predictions could not be explained by differences in model structure or parameterization that were hypothesized to affect intervention impact."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Considering the actual scale-up of ART in South Africa, seven models estimated that current HIV incidence is 17% to 32% lower than it would have been in the absence of ART.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 61, "doc_id": 13899137, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [13899137, 13901073], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: ART substantially reduces infectiveness of HIV-positive people.\n\nDocument title: HIV Treatment as Prevention: Systematic Comparison of Mathematical Models of the Potential Impact of Antiretroviral Therapy on HIV Incidence in South Africa\n\nAbstract sentences:\n[0] BACKGROUND Many mathematical models have investigated the impact of expanding access to antiretroviral therapy (ART) on new HIV infections.\n[1] Comparing results and conclusions across models is challenging because models have addressed slightly different questions and have reported different outcome metrics.\n[2] This study compares the predictions of several mathematical models simulating the same ART intervention programmes to determine the extent to which models agree about the epidemiological impact of expanded ART.\n[3] METHODS AND FINDINGS Twelve independent mathematical models evaluated a set of standardised ART intervention scenarios in South Africa and reported a common set of outputs.\n[4] Intervention scenarios systematically varied the CD4 count threshold for treatment eligibility, access to treatment, and programme retention.\n[5] For a scenario in which 80% of HIV-infected individuals start treatment on average 1 y after their CD4 count drops below 350 cells/µl and 85% remain on treatment after 3 y, the models projected that HIV incidence would be 35% to 54% lower 8 y after the introduction of ART, compared to a counterfactual scenario in which there is no ART.\n[6] More variation existed in the estimated long-term (38 y) reductions in incidence.\n[7] The impact of optimistic interventions including immediate ART initiation varied widely across models, maintaining substantial uncertainty about the theoretical prospect for elimination of HIV from the population using ART alone over the next four decades.\n[8] The number of person-years of ART per infection averted over 8 y ranged between 5.8 and 18.7.\n[9] Considering the actual scale-up of ART in South Africa, seven models estimated that current HIV incidence is 17% to 32% lower than it would have been in the absence of ART.\n[10] Differences between model assumptions about CD4 decline and HIV transmissibility over the course of infection explained only a modest amount of the variation in model results.\n[11] CONCLUSIONS Mathematical models evaluating the impact of ART vary substantially in structure, complexity, and parameter choices, but all suggest that ART, at high levels of access and with high adherence, has the potential to substantially reduce new HIV infections.\n[12] There was broad agreement regarding the short-term epidemiologic impact of ambitious treatment scale-up, but more variation in longer term projections and in the efficiency with which treatment can reduce new infections.\n[13] Differences between model predictions could not be explained by differences in model structure or parameterization that were hypothesized to affect intervention impact."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"CONCLUSIONS Mathematical models evaluating the impact of ART vary substantially in structure, complexity, and parameter choices, but all suggest that ART, at high levels of access and with high adherence, has the potential to substantially reduce new HIV infections.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 61, "doc_id": 13899137, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [13899137, 13901073], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: ATF4 is a general endoplasmic reticulum stress marker.\n\nDocument title: Wolfram syndrome 1 and adenylyl cyclase 8 interact at the plasma membrane to regulate insulin production and secretion\n\nAbstract sentences:\n[0] Endoplasmic reticulum (ER) stress causes pancreatic β-cell dysfunction and contributes to β-cell loss and the progression of type 2 diabetes.\n[1] Wolfram syndrome 1 (WFS1) has been shown to be an important regulator of the ER stress signalling pathway; however, its role in β-cell function remains unclear.\n[2] Here we provide evidence that WFS1 is essential for glucose- and glucagon-like peptide 1 (GLP-1)-stimulated cyclic AMP production and regulation of insulin biosynthesis and secretion.\n[3] Stimulation with glucose causes WFS1 translocation from the ER to the plasma membrane, where it forms a complex with adenylyl cyclase 8 (AC8), an essential cAMP-generating enzyme in the β-cell that integrates glucose and GLP-1 signalling.\n[4] ER stress and mutant WFS1 inhibit complex formation and activation of AC8, reducing cAMP synthesis and insulin secretion.\n[5] These findings reveal that an ER-stress-related protein has a distinct role outside the ER regulating both insulin biosynthesis and secretion.\n[6] The reduction of WFS1 protein on the plasma membrane during ER stress is a contributing factor for β-cell dysfunction and progression of type 2 diabetes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 62, "doc_id": 32587939, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [32587939], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: ATM and Rad3 related protein are critical for sensing DNA damage.\n\nDocument title: Deletion of the developmentally essential gene ATR in adult mice leads to age-related phenotypes and stem cell loss.\n\nAbstract sentences:\n[0] Developmental abnormalities, cancer, and premature aging each have been linked to defects in the DNA damage response (DDR).\n[1] Mutations in the ATR checkpoint regulator cause developmental defects in mice (pregastrulation lethality) and humans (Seckel syndrome).\n[2] Here we show that eliminating ATR in adult mice leads to defects in tissue homeostasis and the rapid appearance of age-related phenotypes, such as hair graying, alopecia, kyphosis, osteoporosis, thymic involution, fibrosis, and other abnormalities.\n[3] Histological and genetic analyses indicate that ATR deletion causes acute cellular loss in tissues in which continuous cell proliferation is required for maintenance.\n[4] Importantly, thymic involution, alopecia, and hair graying in ATR knockout mice were associated with dramatic reductions in tissue-specific stem and progenitor cells and exhaustion of tissue renewal and homeostatic capacity.\n[5] In aggregate, these studies suggest that reduced regenerative capacity in adults via deletion of a developmentally essential DDR gene is sufficient to cause the premature appearance of age-related phenotypes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 63, "doc_id": 40349336, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [40349336], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: ATM and Rad3 related protein have no role in sensing DNA damage.\n\nDocument title: Deletion of the developmentally essential gene ATR in adult mice leads to age-related phenotypes and stem cell loss.\n\nAbstract sentences:\n[0] Developmental abnormalities, cancer, and premature aging each have been linked to defects in the DNA damage response (DDR).\n[1] Mutations in the ATR checkpoint regulator cause developmental defects in mice (pregastrulation lethality) and humans (Seckel syndrome).\n[2] Here we show that eliminating ATR in adult mice leads to defects in tissue homeostasis and the rapid appearance of age-related phenotypes, such as hair graying, alopecia, kyphosis, osteoporosis, thymic involution, fibrosis, and other abnormalities.\n[3] Histological and genetic analyses indicate that ATR deletion causes acute cellular loss in tissues in which continuous cell proliferation is required for maintenance.\n[4] Importantly, thymic involution, alopecia, and hair graying in ATR knockout mice were associated with dramatic reductions in tissue-specific stem and progenitor cells and exhaustion of tissue renewal and homeostatic capacity.\n[5] In aggregate, these studies suggest that reduced regenerative capacity in adults via deletion of a developmentally essential DDR gene is sufficient to cause the premature appearance of age-related phenotypes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 64, "doc_id": 40349336, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [40349336], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: AZT given with ribavirin increases anemia.\n\nDocument title: Hepatotoxicity associated with antiretroviral therapy in adults infected with human immunodeficiency virus and the role of hepatitis C or B virus infection.\n\nAbstract sentences:\n[0] CONTEXT Use of antiretroviral drugs, including protease inhibitors, for treatment of human immunodeficiency virus (HIV) infection has been anecdotally associated with hepatotoxicity, particularly in persons coinfected with hepatitis C or B virus.\n[1] OBJECTIVES To ascertain if incidence of severe hepatotoxicity during antiretroviral therapy is similar for all antiretroviral drug combinations, and to define the role of chronic viral hepatitis in its development.\n[2] DESIGN Prospective cohort study.\n[3] SETTING University-based urban HIV clinic.\n[4] PATIENTS A total of 298 patients who were prescribed new antiretroviral therapies between January 1996 and January 1998, 211 (71%) of whom received protease inhibitors as part of combination therapy (median follow-up, 182 days) and 87 (29%) of whom received dual nucleoside analog regimens (median follow-up, 167 days).\n[5] Chronic hepatitis C and B virus infection was present in 154 (52%) and 8 (2.7%) patients, respectively.\n[6] MAIN OUTCOME MEASURE Severe hepatotoxicity, defined as a grade 3 or 4 change in levels of serum alanine aminotransferase and aspartate aminotransferase, evaluated before and during therapy.\n[7] RESULTS Severe hepatotoxicity was observed in 31 (10.4%) of 298 patients (95% confidence interval [CI], 7.2%-14.4%).\n[8] Ritonavir use was associated with a higher incidence of toxicity (30%; 95% CI, 17.9% -44.6%).\n[9] However, no significant difference was detected in hepatotoxicity incidence in other treatment groups, ie, nucleoside analogs (5.7%; 95% CI, 1.2%-12.9%), nelfinavir (5.9%; 95% CI, 1.2%-16.2%), saquinavir (5.9%; 95% CI, 0.15%-28.7%), and indinavir(6.8%; 95% CI, 3.0%-13.1 %).\n[10] Although chronicviral hepatitis was associated with an increased risk of severe hepatotoxicity among patients prescribed nonritonavir regimens (relative risk, 3.7; 95% CI, 1.0-11.8), most patients with chronic hepatitis C or B virus infection (88%) did not experience significant toxic effects.\n[11] Rate of severe toxicity with use of any protease inhibitor in patients with hepatitis C infection was 12.2% (13/107; 95% CI, 6.6%-19.9%).\n[12] In multivariate logistic regression, only ritonavir (adjusted odds ratio [AOR], 8.6; 95% CI, 3.0-24.6) and a CD4 cell count increase of more than 0.05 x 10(9)/L (AOR, 3.6; 95% CI, 1.0-12.9) were associated with severe hepatotoxicity.\n[13] No irreversible outcomes were seen in patients with severe hepatotoxicity.\n[14] CONCLUSIONS Our data indicate that use of ritonavir may increase risk of severe hepatotoxicity.\n[15] Although hepatotoxicity may be more common in persons with chronic viral hepatitis, these data do not support withholding protease inhibitor therapy from persons coinfected with hepatitis B or C virus."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 66, "doc_id": 14806256, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14806256], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Activated Cdk5 phosphorylates the ATM protein in response to DNA damage.\n\nDocument title: Phosphorylation of ATM by Cdk5 mediates DNA damage signaling and regulates neuronal death\n\nAbstract sentences:\n[0] The phosphatidylinositol-3-kinase-like kinase ATM (ataxia-telangiectasia mutated) has a central role in coordinating DNA damage responses, including cell-cycle checkpoint control, DNA repair and apoptosis.\n[1] Mutations of ATM cause a spectrum of defects ranging from neurodegeneration to cancer predisposition.\n[2] However, the mechanism by which DNA damage activates ATM is poorly understood.\n[3] Here we show that Cdk5 (cyclin-dependent kinase 5), activated by DNA damage, directly phosphorylates ATM at Ser 794 in post-mitotic neurons.\n[4] Phosphorylation at Ser 794 precedes, and is required for, ATM autophosphorylation at Ser 1981, and activates ATM kinase activity.\n[5] The Cdk5-ATM signal regulates phosphorylation and function of the ATM targets p53 and H2AX.\n[6] Interruption of the Cdk5-ATM pathway attenuates DNA-damage-induced neuronal cell cycle re-entry and expression of the p53 targets PUMA and Bax, protecting neurons from death.\n[7] Thus, activation of Cdk5 by DNA damage serves as a critical signal to initiate the ATM response and regulate ATM-dependent cellular processes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Here we show that Cdk5 (cyclin-dependent kinase 5), activated by DNA damage, directly phosphorylates ATM at Ser 794 in post-mitotic neurons.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 67, "doc_id": 21295300, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [21295300], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Activated Cdk5 phosphorylates the ATM protein in response to DNA damage.\n\nDocument title: Phosphorylation of ATM by Cdk5 mediates DNA damage signaling and regulates neuronal death\n\nAbstract sentences:\n[0] The phosphatidylinositol-3-kinase-like kinase ATM (ataxia-telangiectasia mutated) has a central role in coordinating DNA damage responses, including cell-cycle checkpoint control, DNA repair and apoptosis.\n[1] Mutations of ATM cause a spectrum of defects ranging from neurodegeneration to cancer predisposition.\n[2] However, the mechanism by which DNA damage activates ATM is poorly understood.\n[3] Here we show that Cdk5 (cyclin-dependent kinase 5), activated by DNA damage, directly phosphorylates ATM at Ser 794 in post-mitotic neurons.\n[4] Phosphorylation at Ser 794 precedes, and is required for, ATM autophosphorylation at Ser 1981, and activates ATM kinase activity.\n[5] The Cdk5-ATM signal regulates phosphorylation and function of the ATM targets p53 and H2AX.\n[6] Interruption of the Cdk5-ATM pathway attenuates DNA-damage-induced neuronal cell cycle re-entry and expression of the p53 targets PUMA and Bax, protecting neurons from death.\n[7] Thus, activation of Cdk5 by DNA damage serves as a critical signal to initiate the ATM response and regulate ATM-dependent cellular processes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Thus, activation of Cdk5 by DNA damage serves as a critical signal to initiate the ATM response and regulate ATM-dependent cellular processes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 67, "doc_id": 21295300, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [21295300], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Activated Cdk5 regulates DNA damage-induced neuronal death.\n\nDocument title: Phosphorylation of ATM by Cdk5 mediates DNA damage signaling and regulates neuronal death\n\nAbstract sentences:\n[0] The phosphatidylinositol-3-kinase-like kinase ATM (ataxia-telangiectasia mutated) has a central role in coordinating DNA damage responses, including cell-cycle checkpoint control, DNA repair and apoptosis.\n[1] Mutations of ATM cause a spectrum of defects ranging from neurodegeneration to cancer predisposition.\n[2] However, the mechanism by which DNA damage activates ATM is poorly understood.\n[3] Here we show that Cdk5 (cyclin-dependent kinase 5), activated by DNA damage, directly phosphorylates ATM at Ser 794 in post-mitotic neurons.\n[4] Phosphorylation at Ser 794 precedes, and is required for, ATM autophosphorylation at Ser 1981, and activates ATM kinase activity.\n[5] The Cdk5-ATM signal regulates phosphorylation and function of the ATM targets p53 and H2AX.\n[6] Interruption of the Cdk5-ATM pathway attenuates DNA-damage-induced neuronal cell cycle re-entry and expression of the p53 targets PUMA and Bax, protecting neurons from death.\n[7] Thus, activation of Cdk5 by DNA damage serves as a critical signal to initiate the ATM response and regulate ATM-dependent cellular processes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Interruption of the Cdk5-ATM pathway attenuates DNA-damage-induced neuronal cell cycle re-entry and expression of the p53 targets PUMA and Bax, protecting neurons from death.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 68, "doc_id": 21295300, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [21295300], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Activation of PPM1D enhances p53 function.\n\nDocument title: Exome sequencing identifies somatic gain-of-function PPM1D mutations in brainstem gliomas\n\nAbstract sentences:\n[0] Gliomas arising in the brainstem and thalamus are devastating tumors that are difficult to surgically resect.\n[1] To determine the genetic and epigenetic landscape of these tumors, we performed exomic sequencing of 14 brainstem gliomas (BSGs) and 12 thalamic gliomas.\n[2] We also performed targeted mutational analysis of an additional 24 such tumors and genome-wide methylation profiling of 45 gliomas.\n[3] This study led to the discovery of tumor-specific mutations in PPM1D, encoding wild-type p53-induced protein phosphatase 1D (WIP1), in 37.5% of the BSGs that harbored hallmark H3F3A mutations encoding p.\n[4] Lys27Met substitutions.\n[5] PPM1D mutations were mutually exclusive with TP53 mutations in BSG and attenuated p53 activation in vitro.\n[6] PPM1D mutations were truncating alterations in exon 6 that enhanced the ability of PPM1D to suppress the activation of the DNA damage response checkpoint protein CHK2.\n[7] These results define PPM1D as a frequent target of somatic mutation and as a potential therapeutic target in brainstem gliomas."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5, 6]\nExplanation: Evidence states: \"PPM1D mutations were mutually exclusive with TP53 mutations in BSG and attenuated p53 activation in vitro. PPM1D mutations were truncating alterations in exon 6 that enhanced the ability of PPM1D to suppress the activation of the DNA damage response checkpoint protein CHK2.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 69, "doc_id": 5956380, "label": "CONTRADICTS", "evidence_sentence_ids": [5, 6], "cited_doc_ids": [5956380, 4414547], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Activation of PPM1D enhances p53 function.\n\nDocument title: Mosaic PPM1D mutations are associated with predisposition to breast and ovarian cancer\n\nAbstract sentences:\n[0] Improved sequencing technologies offer unprecedented opportunities for investigating the role of rare genetic variation in common disease.\n[1] However, there are considerable challenges with respect to study design, data analysis and replication.\n[2] Using pooled next-generation sequencing of 507 genes implicated in the repair of DNA in 1,150 samples, an analytical strategy focused on protein-truncating variants (PTVs) and a large-scale sequencing case–control replication experiment in 13,642 individuals, here we show that rare PTVs in the p53-inducible protein phosphatase PPM1D are associated with predisposition to breast cancer and ovarian cancer.\n[3] PPM1D PTV mutations were present in 25 out of 7,781 cases versus 1 out of 5,861 controls (P = 1.12 × 10−5), including 18 mutations in 6,912 individuals with breast cancer (P = 2.42 × 10−4) and 12 mutations in 1,121 individuals with ovarian cancer (P = 3.10 × 10−9).\n[4] Notably, all of the identified PPM1D PTVs were mosaic in lymphocyte DNA and clustered within a 370-base-pair region in the final exon of the gene, carboxy-terminal to the phosphatase catalytic domain.\n[5] Functional studies demonstrate that the mutations result in enhanced suppression of p53 in response to ionizing radiation exposure, suggesting that the mutant alleles encode hyperactive PPM1D isoforms.\n[6] Thus, although the mutations cause premature protein truncation, they do not result in the simple loss-of-function effect typically associated with this class of variant, but instead probably have a gain-of-function effect.\n[7] Our results have implications for the detection and management of breast and ovarian cancer risk.\n[8] More generally, these data provide new insights into the role of rare and of mosaic genetic variants in common conditions, and the use of sequencing in their identification."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Functional studies demonstrate that the mutations result in enhanced suppression of p53 in response to ionizing radiation exposure, suggesting that the mutant alleles encode hyperactive PPM1D isoforms.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 69, "doc_id": 4414547, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [5956380, 4414547], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Activation of the Rac1 homolog CED-10 kills viable cells in SRGP-1 mutant Caenorhabditis elegans.\n\nDocument title: Loss of the RhoGAP SRGP-1 promotes the clearance of dead and injured cells in Caenorhabditis elegans\n\nAbstract sentences:\n[0] Multicellular animals rapidly clear dying cells from their bodies.\n[1] Many of the pathways that mediate this cell removal are conserved through evolution.\n[2] Here, we identify srgp-1 as a negative regulator of cell clearance in both Caenorhabditis elegans and mammalian cells.\n[3] Loss of srgp-1 function results in improved engulfment of apoptotic cells, whereas srgp-1 overexpression inhibits apoptotic cell corpse removal.\n[4] We show that SRGP-1 functions in engulfing cells and functions as a GTPase activating protein (GAP) for CED-10 (Rac1).\n[5] Interestingly, loss of srgp-1 function promotes not only the clearance of already dead cells, but also the removal of cells that have been brought to the verge of death through sublethal apoptotic, necrotic or cytotoxic insults.\n[6] In contrast, impaired engulfment allows damaged cells to escape clearance, which results in increased long-term survival.\n[7] We propose that C. elegans uses the engulfment machinery as part of a primitive, but evolutionarily conserved, survey mechanism that identifies and removes unfit cells within a tissue."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4, 5]\nExplanation: Evidence states: \"We show that SRGP-1 functions in engulfing cells and functions as a GTPase activating protein (GAP) for CED-10 (Rac1). Interestingly, loss of srgp-1 function promotes not only the clearance of already dead cells, but also the removal of cells that have been brought to the verge of death through sublethal apoptotic, necrotic or cytotoxic insults.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 71, "doc_id": 1127562, "label": "SUPPORTS", "evidence_sentence_ids": [4, 5], "cited_doc_ids": [1127562], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Activator-inhibitor pairs are provided ventrally by Xrl-sizzled.\n\nDocument title: Regulation of ADMP and BMP2/4/7 at Opposite Embryonic Poles Generates a Self-Regulating Morphogenetic Field\n\nAbstract sentences:\n[0] Embryos have the ability to self-regulate and regenerate normal structures after being sectioned in half.\n[1] How is such a morphogenetic field established?\n[2] We discovered that quadruple knockdown of ADMP and BMP2/4/7 in Xenopus embryos eliminates self-regulation, causing ubiquitous neural induction throughout the ectoderm.\n[3] ADMP transcription in the Spemann organizer is activated at low BMP levels.\n[4] When ventral BMP2/4/7 signals are depleted, Admp expression increases, allowing for self-regulation.\n[5] ADMP has BMP-like activity and signals via the ALK-2 receptor.\n[6] It is unable to signal dorsally because of inhibition by Chordin.\n[7] The ventral BMP antagonists Sizzled and Bambi further refine the pattern.\n[8] By transplanting dorsal or ventral wild-type grafts into ADMP/BMP2/4/7-depleted hosts, we demonstrate that both poles serve as signaling centers that can induce histotypic differentiation over considerable distances.\n[9] We conclude that dorsal and ventral BMP signals and their extracellular antagonists expressed under opposing transcriptional regulation provide a molecular mechanism for embryonic self-regulation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 73, "doc_id": 6076903, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [6076903], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Active H. pylori urease has a polymeric structure consisting of five distinct subunits.\n\nDocument title: Structure of the proton-gated urea channel from the gastric pathogen Helicobacter pylori\n\nAbstract sentences:\n[0] Half the world's population is chronically infected with Helicobacter pylori, causing gastritis, gastric ulcers and an increased incidence of gastric adenocarcinoma.\n[1] Its proton-gated inner-membrane urea channel, HpUreI, is essential for survival in the acidic environment of the stomach.\n[2] The channel is closed at neutral pH and opens at acidic pH to allow the rapid access of urea to cytoplasmic urease.\n[3] Urease produces NH(3) and CO(2), neutralizing entering protons and thus buffering the periplasm to a pH of roughly 6.1 even in gastric juice at a pH below 2.0.\n[4] Here we report the structure of HpUreI, revealing six protomers assembled in a hexameric ring surrounding a central bilayer plug of ordered lipids.\n[5] Each protomer encloses a channel formed by a twisted bundle of six transmembrane helices.\n[6] The bundle defines a previously unobserved fold comprising a two-helix hairpin motif repeated three times around the central axis of the channel, without the inverted repeat of mammalian-type urea transporters.\n[7] Both the channel and the protomer interface contain residues conserved in the AmiS/UreI superfamily, suggesting the preservation of channel architecture and oligomeric state in this superfamily.\n[8] Predominantly aromatic or aliphatic side chains line the entire channel and define two consecutive constriction sites in the middle of the channel.\n[9] Mutation of Trp 153 in the cytoplasmic constriction site to Ala or Phe decreases the selectivity for urea in comparison with thiourea, suggesting that solute interaction with Trp 153 contributes specificity.\n[10] The previously unobserved hexameric channel structure described here provides a new model for the permeation of urea and other small amide solutes in prokaryotes and archaea."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 74, "doc_id": 4387784, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4387784], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Active Ly49Q induces neutrophil polarization.\n\nDocument title: The Ly49Q receptor plays a crucial role in neutrophil polarization and migration by regulating raft trafficking.\n\nAbstract sentences:\n[0] Neutrophils rapidly undergo polarization and directional movement to infiltrate the sites of infection and inflammation.\n[1] Here, we show that an inhibitory MHC I receptor, Ly49Q, was crucial for the swift polarization of and tissue infiltration by neutrophils.\n[2] During the steady state, Ly49Q inhibited neutrophil adhesion by preventing focal-complex formation, likely by inhibiting Src and PI3 kinases.\n[3] However, in the presence of inflammatory stimuli, Ly49Q mediated rapid neutrophil polarization and tissue infiltration in an ITIM-domain-dependent manner.\n[4] These opposite functions appeared to be mediated by distinct use of effector phosphatase SHP-1 and SHP-2.\n[5] Ly49Q-dependent polarization and migration were affected by Ly49Q regulation of membrane raft functions.\n[6] We propose that Ly49Q is pivotal in switching neutrophils to their polarized morphology and rapid migration upon inflammation, through its spatiotemporal regulation of membrane rafts and raft-associated signaling molecules."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Here, we show that an inhibitory MHC I receptor, Ly49Q, was crucial for the swift polarization of and tissue infiltration by neutrophils.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 76, "doc_id": 5531479, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [5531479], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Active Ly49Q induces neutrophil polarization.\n\nDocument title: The Ly49Q receptor plays a crucial role in neutrophil polarization and migration by regulating raft trafficking.\n\nAbstract sentences:\n[0] Neutrophils rapidly undergo polarization and directional movement to infiltrate the sites of infection and inflammation.\n[1] Here, we show that an inhibitory MHC I receptor, Ly49Q, was crucial for the swift polarization of and tissue infiltration by neutrophils.\n[2] During the steady state, Ly49Q inhibited neutrophil adhesion by preventing focal-complex formation, likely by inhibiting Src and PI3 kinases.\n[3] However, in the presence of inflammatory stimuli, Ly49Q mediated rapid neutrophil polarization and tissue infiltration in an ITIM-domain-dependent manner.\n[4] These opposite functions appeared to be mediated by distinct use of effector phosphatase SHP-1 and SHP-2.\n[5] Ly49Q-dependent polarization and migration were affected by Ly49Q regulation of membrane raft functions.\n[6] We propose that Ly49Q is pivotal in switching neutrophils to their polarized morphology and rapid migration upon inflammation, through its spatiotemporal regulation of membrane rafts and raft-associated signaling molecules."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"We propose that Ly49Q is pivotal in switching neutrophils to their polarized morphology and rapid migration upon inflammation, through its spatiotemporal regulation of membrane rafts and raft-associated signaling molecules.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 76, "doc_id": 5531479, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [5531479], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Active Ly49Q prevents neutrophil polarization.\n\nDocument title: The Ly49Q receptor plays a crucial role in neutrophil polarization and migration by regulating raft trafficking.\n\nAbstract sentences:\n[0] Neutrophils rapidly undergo polarization and directional movement to infiltrate the sites of infection and inflammation.\n[1] Here, we show that an inhibitory MHC I receptor, Ly49Q, was crucial for the swift polarization of and tissue infiltration by neutrophils.\n[2] During the steady state, Ly49Q inhibited neutrophil adhesion by preventing focal-complex formation, likely by inhibiting Src and PI3 kinases.\n[3] However, in the presence of inflammatory stimuli, Ly49Q mediated rapid neutrophil polarization and tissue infiltration in an ITIM-domain-dependent manner.\n[4] These opposite functions appeared to be mediated by distinct use of effector phosphatase SHP-1 and SHP-2.\n[5] Ly49Q-dependent polarization and migration were affected by Ly49Q regulation of membrane raft functions.\n[6] We propose that Ly49Q is pivotal in switching neutrophils to their polarized morphology and rapid migration upon inflammation, through its spatiotemporal regulation of membrane rafts and raft-associated signaling molecules."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Here, we show that an inhibitory MHC I receptor, Ly49Q, was crucial for the swift polarization of and tissue infiltration by neutrophils.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 77, "doc_id": 5531479, "label": "CONTRADICTS", "evidence_sentence_ids": [1], "cited_doc_ids": [5531479], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Active Ly49Q prevents neutrophil polarization.\n\nDocument title: The Ly49Q receptor plays a crucial role in neutrophil polarization and migration by regulating raft trafficking.\n\nAbstract sentences:\n[0] Neutrophils rapidly undergo polarization and directional movement to infiltrate the sites of infection and inflammation.\n[1] Here, we show that an inhibitory MHC I receptor, Ly49Q, was crucial for the swift polarization of and tissue infiltration by neutrophils.\n[2] During the steady state, Ly49Q inhibited neutrophil adhesion by preventing focal-complex formation, likely by inhibiting Src and PI3 kinases.\n[3] However, in the presence of inflammatory stimuli, Ly49Q mediated rapid neutrophil polarization and tissue infiltration in an ITIM-domain-dependent manner.\n[4] These opposite functions appeared to be mediated by distinct use of effector phosphatase SHP-1 and SHP-2.\n[5] Ly49Q-dependent polarization and migration were affected by Ly49Q regulation of membrane raft functions.\n[6] We propose that Ly49Q is pivotal in switching neutrophils to their polarized morphology and rapid migration upon inflammation, through its spatiotemporal regulation of membrane rafts and raft-associated signaling molecules."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"We propose that Ly49Q is pivotal in switching neutrophils to their polarized morphology and rapid migration upon inflammation, through its spatiotemporal regulation of membrane rafts and raft-associated signaling molecules.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 77, "doc_id": 5531479, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [5531479], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Active caspase-11 participate in regulating phagosome-lysosome fusion.\n\nDocument title: Caspase-11 promotes the fusion of phagosomes harboring pathogenic bacteria with lysosomes by modulating actin polymerization.\n\nAbstract sentences:\n[0] Inflammasomes are multiprotein complexes that include members of the NLR (nucleotide-binding domain leucine-rich repeat containing) family and caspase-1.\n[1] Once bacterial molecules are sensed within the macrophage, the inflammasome is assembled, mediating the activation of caspase-1.\n[2] Caspase-11 mediates caspase-1 activation in response to lipopolysaccharide and bacterial toxins, and yet its role during bacterial infection is unknown.\n[3] Here, we demonstrated that caspase-11 was dispensable for caspase-1 activation in response to Legionella, Salmonella, Francisella, and Listeria.\n[4] We also determined that active mouse caspase-11 was required for restriction of L. pneumophila infection.\n[5] Similarly, human caspase-4 and caspase-5, homologs of mouse caspase-11, cooperated to restrict L. pneumophila infection in human macrophages.\n[6] Caspase-11 promoted the fusion of the L. pneumophila vacuole with lysosomes by modulating actin polymerization through cofilin.\n[7] However, caspase-11 was dispensable for the fusion of lysosomes with phagosomes containing nonpathogenic bacteria, uncovering a fundamental difference in the trafficking of phagosomes according to their cargo."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"However, caspase-11 was dispensable for the fusion of lysosomes with phagosomes containing nonpathogenic bacteria, uncovering a fundamental difference in the trafficking of phagosomes according to their cargo.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 78, "doc_id": 5099266, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [5099266], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Active caspase-11 protein promotes pyroptosis.\n\nDocument title: Caspase-11 promotes the fusion of phagosomes harboring pathogenic bacteria with lysosomes by modulating actin polymerization.\n\nAbstract sentences:\n[0] Inflammasomes are multiprotein complexes that include members of the NLR (nucleotide-binding domain leucine-rich repeat containing) family and caspase-1.\n[1] Once bacterial molecules are sensed within the macrophage, the inflammasome is assembled, mediating the activation of caspase-1.\n[2] Caspase-11 mediates caspase-1 activation in response to lipopolysaccharide and bacterial toxins, and yet its role during bacterial infection is unknown.\n[3] Here, we demonstrated that caspase-11 was dispensable for caspase-1 activation in response to Legionella, Salmonella, Francisella, and Listeria.\n[4] We also determined that active mouse caspase-11 was required for restriction of L. pneumophila infection.\n[5] Similarly, human caspase-4 and caspase-5, homologs of mouse caspase-11, cooperated to restrict L. pneumophila infection in human macrophages.\n[6] Caspase-11 promoted the fusion of the L. pneumophila vacuole with lysosomes by modulating actin polymerization through cofilin.\n[7] However, caspase-11 was dispensable for the fusion of lysosomes with phagosomes containing nonpathogenic bacteria, uncovering a fundamental difference in the trafficking of phagosomes according to their cargo."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Here, we demonstrated that caspase-11 was dispensable for caspase-1 activation in response to Legionella, Salmonella, Francisella, and Listeria.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 79, "doc_id": 5099266, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [5099266], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Active caspase-11 protein promotes pyroptosis.\n\nDocument title: Caspase-11 promotes the fusion of phagosomes harboring pathogenic bacteria with lysosomes by modulating actin polymerization.\n\nAbstract sentences:\n[0] Inflammasomes are multiprotein complexes that include members of the NLR (nucleotide-binding domain leucine-rich repeat containing) family and caspase-1.\n[1] Once bacterial molecules are sensed within the macrophage, the inflammasome is assembled, mediating the activation of caspase-1.\n[2] Caspase-11 mediates caspase-1 activation in response to lipopolysaccharide and bacterial toxins, and yet its role during bacterial infection is unknown.\n[3] Here, we demonstrated that caspase-11 was dispensable for caspase-1 activation in response to Legionella, Salmonella, Francisella, and Listeria.\n[4] We also determined that active mouse caspase-11 was required for restriction of L. pneumophila infection.\n[5] Similarly, human caspase-4 and caspase-5, homologs of mouse caspase-11, cooperated to restrict L. pneumophila infection in human macrophages.\n[6] Caspase-11 promoted the fusion of the L. pneumophila vacuole with lysosomes by modulating actin polymerization through cofilin.\n[7] However, caspase-11 was dispensable for the fusion of lysosomes with phagosomes containing nonpathogenic bacteria, uncovering a fundamental difference in the trafficking of phagosomes according to their cargo."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"We also determined that active mouse caspase-11 was required for restriction of L. pneumophila infection.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 79, "doc_id": 5099266, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [5099266], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Acute ablation of KRAS causes severe growth impairment.\n\nDocument title: Long-Term ERK Inhibition in KRAS-Mutant Pancreatic Cancer Is Associated with MYC Degradation and Senescence-like Growth Suppression.\n\nAbstract sentences:\n[0] Induction of compensatory mechanisms and ERK reactivation has limited the effectiveness of Raf and MEK inhibitors in RAS-mutant cancers.\n[1] We determined that direct pharmacologic inhibition of ERK suppressed the growth of a subset of KRAS-mutant pancreatic cancer cell lines and that concurrent phosphatidylinositol 3-kinase (PI3K) inhibition caused synergistic cell death.\n[2] Additional combinations that enhanced ERK inhibitor action were also identified.\n[3] Unexpectedly, long-term treatment of sensitive cell lines caused senescence, mediated in part by MYC degradation and p16 reactivation.\n[4] Enhanced basal PI3K-AKT-mTOR signaling was associated with de novo resistance to ERK inhibitor, as were other protein kinases identified by kinome-wide siRNA screening and a genetic gain-of-function screen.\n[5] Our findings reveal distinct consequences of inhibiting this kinase cascade at the level of ERK."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 80, "doc_id": 4920376, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4920376], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Acute ablation of Snail in the embryonic cortex affects the proliferation and number of embryonic cortical precursors.\n\nDocument title: Control of Apoptosis by Asymmetric Cell Division\n\nAbstract sentences:\n[0] Asymmetric cell division and apoptosis (programmed cell death) are two fundamental processes that are important for the development and function of multicellular organisms.\n[1] We have found that the processes of asymmetric cell division and apoptosis can be functionally linked.\n[2] Specifically, we show that asymmetric cell division in the nematode Caenorhabditis elegans is mediated by a pathway involving three genes, dnj-11 MIDA1, ces-2 HLF, and ces-1 Snail, that directly control the enzymatic machinery responsible for apoptosis.\n[3] Interestingly, the MIDA1-like protein GlsA of the alga Volvox carteri, as well as the Snail-related proteins Snail, Escargot, and Worniu of Drosophila melanogaster, have previously been implicated in asymmetric cell division.\n[4] Therefore, C. elegans dnj-11 MIDA1, ces-2 HLF, and ces-1 Snail may be components of a pathway involved in asymmetric cell division that is conserved throughout the plant and animal kingdoms.\n[5] Furthermore, based on our results, we propose that this pathway directly controls the apoptotic fate in C. elegans, and possibly other animals as well."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 81, "doc_id": 1797622, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [1797622], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Addition of BMP4, activin A, CHIR99021, and SU504 to reprogramming fibroblasts generates, expands and maintains cardiovascular progenitor cells (CPCs)\n\nDocument title: Expandable Cardiovascular Progenitor Cells Reprogrammed from Fibroblasts.\n\nAbstract sentences:\n[0] Stem cell-based approaches to cardiac regeneration are increasingly viable strategies for treating heart failure.\n[1] Generating abundant and functional autologous cells for transplantation in such a setting, however, remains a significant challenge.\n[2] Here, we isolated a cell population with extensive proliferation capacity and restricted cardiovascular differentiation potentials during cardiac transdifferentiation of mouse fibroblasts.\n[3] These induced expandable cardiovascular progenitor cells (ieCPCs) proliferated extensively for more than 18 passages in chemically defined conditions, with 10(5) starting fibroblasts robustly producing 10(16) ieCPCs.\n[4] ieCPCs expressed cardiac signature genes and readily differentiated into functional cardiomyocytes (CMs), endothelial cells (ECs), and smooth muscle cells (SMCs) in vitro, even after long-term expansion.\n[5] When transplanted into mouse hearts following myocardial infarction, ieCPCs spontaneously differentiated into CMs, ECs, and SMCs and improved cardiac function for up to 12 weeks after transplantation.\n[6] Thus, ieCPCs are a powerful system to study cardiovascular specification and provide strategies for regenerative medicine in the heart."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 82, "doc_id": 3619372, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [3619372], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Adult tissue-resident macrophages are seeded before birth.\n\nDocument title: Fate mapping reveals origins and dynamics of monocytes and tissue macrophages under homeostasis.\n\nAbstract sentences:\n[0] Mononuclear phagocytes, including monocytes, macrophages, and dendritic cells, contribute to tissue integrity as well as to innate and adaptive immune defense.\n[1] Emerging evidence for labor division indicates that manipulation of these cells could bear therapeutic potential.\n[2] However, specific ontogenies of individual populations and the overall functional organization of this cellular network are not well defined.\n[3] Here we report a fate-mapping study of the murine monocyte and macrophage compartment taking advantage of constitutive and conditional CX(3)CR1 promoter-driven Cre recombinase expression.\n[4] We have demonstrated that major tissue-resident macrophage populations, including liver Kupffer cells and lung alveolar, splenic, and peritoneal macrophages, are established prior to birth and maintain themselves subsequently during adulthood independent of replenishment by blood monocytes.\n[5] Furthermore, we have established that short-lived Ly6C(+) monocytes constitute obligatory steady-state precursors of blood-resident Ly6C(-) cells and that the abundance of Ly6C(+) blood monocytes dynamically controls the circulation lifespan of their progeny."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"We have demonstrated that major tissue-resident macrophage populations, including liver Kupffer cells and lung alveolar, splenic, and peritoneal macrophages, are established prior to birth and maintain themselves subsequently during adulthood independent of replenishment by blood monocytes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 85, "doc_id": 7521113, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [7521113, 22406695], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Adult tissue-resident macrophages are seeded before birth.\n\nDocument title: Origin and functions of tissue macrophages.\n\nAbstract sentences:\n[0] Macrophages are distributed in tissues throughout the body and contribute to both homeostasis and disease.\n[1] Recently, it has become evident that most adult tissue macrophages originate during embryonic development and not from circulating monocytes.\n[2] Each tissue has its own composition of embryonically derived and adult-derived macrophages, but it is unclear whether macrophages of distinct origins are functionally interchangeable or have unique roles at steady state.\n[3] This new understanding also prompts reconsideration of the function of circulating monocytes.\n[4] Classical Ly6c(hi) monocytes patrol the extravascular space in resting organs, and Ly6c(lo) nonclassical monocytes patrol the vasculature.\n[5] Inflammation triggers monocytes to differentiate into macrophages, but whether resident and newly recruited macrophages possess similar functions during inflammation is unclear.\n[6] Here, we define the tools used for identifying the complex origin of tissue macrophages and discuss the relative contributions of tissue niche versus ontological origin to the regulation of macrophage functions during steady state and inflammation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Recently, it has become evident that most adult tissue macrophages originate during embryonic development and not from circulating monocytes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 85, "doc_id": 22406695, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [7521113, 22406695], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Adult tissue-resident macrophages are seeded before birth.\n\nDocument title: Fate mapping reveals origins and dynamics of monocytes and tissue macrophages under homeostasis.\n\nAbstract sentences:\n[0] Mononuclear phagocytes, including monocytes, macrophages, and dendritic cells, contribute to tissue integrity as well as to innate and adaptive immune defense.\n[1] Emerging evidence for labor division indicates that manipulation of these cells could bear therapeutic potential.\n[2] However, specific ontogenies of individual populations and the overall functional organization of this cellular network are not well defined.\n[3] Here we report a fate-mapping study of the murine monocyte and macrophage compartment taking advantage of constitutive and conditional CX(3)CR1 promoter-driven Cre recombinase expression.\n[4] We have demonstrated that major tissue-resident macrophage populations, including liver Kupffer cells and lung alveolar, splenic, and peritoneal macrophages, are established prior to birth and maintain themselves subsequently during adulthood independent of replenishment by blood monocytes.\n[5] Furthermore, we have established that short-lived Ly6C(+) monocytes constitute obligatory steady-state precursors of blood-resident Ly6C(-) cells and that the abundance of Ly6C(+) blood monocytes dynamically controls the circulation lifespan of their progeny."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"We have demonstrated that major tissue-resident macrophage populations, including liver Kupffer cells and lung alveolar, splenic, and peritoneal macrophages, are established prior to birth and maintain themselves subsequently during adulthood independent of replenishment by blood monocytes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 86, "doc_id": 7521113, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [7521113, 22406695], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Adult tissue-resident macrophages are seeded before birth.\n\nDocument title: Origin and functions of tissue macrophages.\n\nAbstract sentences:\n[0] Macrophages are distributed in tissues throughout the body and contribute to both homeostasis and disease.\n[1] Recently, it has become evident that most adult tissue macrophages originate during embryonic development and not from circulating monocytes.\n[2] Each tissue has its own composition of embryonically derived and adult-derived macrophages, but it is unclear whether macrophages of distinct origins are functionally interchangeable or have unique roles at steady state.\n[3] This new understanding also prompts reconsideration of the function of circulating monocytes.\n[4] Classical Ly6c(hi) monocytes patrol the extravascular space in resting organs, and Ly6c(lo) nonclassical monocytes patrol the vasculature.\n[5] Inflammation triggers monocytes to differentiate into macrophages, but whether resident and newly recruited macrophages possess similar functions during inflammation is unclear.\n[6] Here, we define the tools used for identifying the complex origin of tissue macrophages and discuss the relative contributions of tissue niche versus ontological origin to the regulation of macrophage functions during steady state and inflammation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Recently, it has become evident that most adult tissue macrophages originate during embryonic development and not from circulating monocytes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 86, "doc_id": 22406695, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [7521113, 22406695], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Adult tissue-resident macrophages possess a self-renewing capacity.\n\nDocument title: Fate mapping reveals origins and dynamics of monocytes and tissue macrophages under homeostasis.\n\nAbstract sentences:\n[0] Mononuclear phagocytes, including monocytes, macrophages, and dendritic cells, contribute to tissue integrity as well as to innate and adaptive immune defense.\n[1] Emerging evidence for labor division indicates that manipulation of these cells could bear therapeutic potential.\n[2] However, specific ontogenies of individual populations and the overall functional organization of this cellular network are not well defined.\n[3] Here we report a fate-mapping study of the murine monocyte and macrophage compartment taking advantage of constitutive and conditional CX(3)CR1 promoter-driven Cre recombinase expression.\n[4] We have demonstrated that major tissue-resident macrophage populations, including liver Kupffer cells and lung alveolar, splenic, and peritoneal macrophages, are established prior to birth and maintain themselves subsequently during adulthood independent of replenishment by blood monocytes.\n[5] Furthermore, we have established that short-lived Ly6C(+) monocytes constitute obligatory steady-state precursors of blood-resident Ly6C(-) cells and that the abundance of Ly6C(+) blood monocytes dynamically controls the circulation lifespan of their progeny."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"We have demonstrated that major tissue-resident macrophage populations, including liver Kupffer cells and lung alveolar, splenic, and peritoneal macrophages, are established prior to birth and maintain themselves subsequently during adulthood independent of replenishment by blood monocytes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 88, "doc_id": 7521113, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [7521113, 22406695], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Adult tissue-resident macrophages stem from the embryonal yolk sac and fetal liver.\n\nDocument title: Fate mapping reveals origins and dynamics of monocytes and tissue macrophages under homeostasis.\n\nAbstract sentences:\n[0] Mononuclear phagocytes, including monocytes, macrophages, and dendritic cells, contribute to tissue integrity as well as to innate and adaptive immune defense.\n[1] Emerging evidence for labor division indicates that manipulation of these cells could bear therapeutic potential.\n[2] However, specific ontogenies of individual populations and the overall functional organization of this cellular network are not well defined.\n[3] Here we report a fate-mapping study of the murine monocyte and macrophage compartment taking advantage of constitutive and conditional CX(3)CR1 promoter-driven Cre recombinase expression.\n[4] We have demonstrated that major tissue-resident macrophage populations, including liver Kupffer cells and lung alveolar, splenic, and peritoneal macrophages, are established prior to birth and maintain themselves subsequently during adulthood independent of replenishment by blood monocytes.\n[5] Furthermore, we have established that short-lived Ly6C(+) monocytes constitute obligatory steady-state precursors of blood-resident Ly6C(-) cells and that the abundance of Ly6C(+) blood monocytes dynamically controls the circulation lifespan of their progeny."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 89, "doc_id": 7521113, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [7521113, 22406695], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Adult tissue-resident macrophages stem from the embryonal yolk sac and fetal liver.\n\nDocument title: Origin and functions of tissue macrophages.\n\nAbstract sentences:\n[0] Macrophages are distributed in tissues throughout the body and contribute to both homeostasis and disease.\n[1] Recently, it has become evident that most adult tissue macrophages originate during embryonic development and not from circulating monocytes.\n[2] Each tissue has its own composition of embryonically derived and adult-derived macrophages, but it is unclear whether macrophages of distinct origins are functionally interchangeable or have unique roles at steady state.\n[3] This new understanding also prompts reconsideration of the function of circulating monocytes.\n[4] Classical Ly6c(hi) monocytes patrol the extravascular space in resting organs, and Ly6c(lo) nonclassical monocytes patrol the vasculature.\n[5] Inflammation triggers monocytes to differentiate into macrophages, but whether resident and newly recruited macrophages possess similar functions during inflammation is unclear.\n[6] Here, we define the tools used for identifying the complex origin of tissue macrophages and discuss the relative contributions of tissue niche versus ontological origin to the regulation of macrophage functions during steady state and inflammation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 90, "doc_id": 22406695, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [22406695], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Aged patients are less susceptible to ischaemia/reperfusion injury.\n\nDocument title: Restoration of chaperone-mediated autophagy in aging liver improves cellular maintenance and hepatic function\n\nAbstract sentences:\n[0] Chaperone-mediated autophagy (CMA), a selective mechanism for degradation of cytosolic proteins in lysosomes, contributes to the removal of altered proteins as part of the cellular quality-control systems.\n[1] We have previously found that CMA activity declines in aged organisms and have proposed that this failure in cellular clearance could contribute to the accumulation of altered proteins, the abnormal cellular homeostasis and, eventually, the functional loss characteristic of aged organisms.\n[2] To determine whether these negative features of aging can be prevented by maintaining efficient autophagic activity until late in life, in this work we have corrected the CMA defect in aged rodents.\n[3] We have generated a double transgenic mouse model in which the amount of the lysosomal receptor for CMA, previously shown to decrease in abundance with age, can be modulated.\n[4] We have analyzed in this model the consequences of preventing the age-dependent decrease in receptor abundance in aged rodents at the cellular and organ levels.\n[5] We show here that CMA activity is maintained until advanced ages if the decrease in the receptor abundance is prevented and that preservation of autophagic activity is associated with lower intracellular accumulation of damaged proteins, better ability to handle protein damage and improved organ function."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 91, "doc_id": 1084345, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [1084345], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Aged patients are more susceptible to ischaemia/reperfusion injury.\n\nDocument title: Restoration of chaperone-mediated autophagy in aging liver improves cellular maintenance and hepatic function\n\nAbstract sentences:\n[0] Chaperone-mediated autophagy (CMA), a selective mechanism for degradation of cytosolic proteins in lysosomes, contributes to the removal of altered proteins as part of the cellular quality-control systems.\n[1] We have previously found that CMA activity declines in aged organisms and have proposed that this failure in cellular clearance could contribute to the accumulation of altered proteins, the abnormal cellular homeostasis and, eventually, the functional loss characteristic of aged organisms.\n[2] To determine whether these negative features of aging can be prevented by maintaining efficient autophagic activity until late in life, in this work we have corrected the CMA defect in aged rodents.\n[3] We have generated a double transgenic mouse model in which the amount of the lysosomal receptor for CMA, previously shown to decrease in abundance with age, can be modulated.\n[4] We have analyzed in this model the consequences of preventing the age-dependent decrease in receptor abundance in aged rodents at the cellular and organ levels.\n[5] We show here that CMA activity is maintained until advanced ages if the decrease in the receptor abundance is prevented and that preservation of autophagic activity is associated with lower intracellular accumulation of damaged proteins, better ability to handle protein damage and improved organ function."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 92, "doc_id": 1084345, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [1084345], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Aggravated inflammation is dependent on NLRP3 inflammasome activation.\n\nDocument title: Gout-associated uric acid crystals activate the NALP3 inflammasome\n\nAbstract sentences:\n[0] Development of the acute and chronic inflammatory responses known as gout and pseudogout are associated with the deposition of monosodium urate (MSU) or calcium pyrophosphate dihydrate (CPPD) crystals, respectively, in joints and periarticular tissues.\n[1] Although MSU crystals were first identified as the aetiological agent of gout in the eighteenth century and more recently as a ‘danger signal’ released from dying cells, little is known about the molecular mechanisms underlying MSU- or CPPD-induced inflammation.\n[2] Here we show that MSU and CPPD engage the caspase-1-activating NALP3 (also called cryopyrin) inflammasome, resulting in the production of active interleukin (IL)-1β and IL-18.\n[3] Macrophages from mice deficient in various components of the inflammasome such as caspase-1, ASC and NALP3 are defective in crystal-induced IL-1β activation.\n[4] Moreover, an impaired neutrophil influx is found in an in vivo model of crystal-induced peritonitis in inflammasome-deficient mice or mice deficient in the IL-1β receptor (IL-1R).\n[5] These findings provide insight into the molecular processes underlying the inflammatory conditions of gout and pseudogout, and further support a pivotal role of the inflammasome in several autoinflammatory diseases."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here we show that MSU and CPPD engage the caspase-1-activating NALP3 (also called cryopyrin) inflammasome, resulting in the production of active interleukin (IL)-1β and IL-18.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 93, "doc_id": 2692522, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [2692522], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Aggravated inflammation is dependent on NLRP3 inflammasome activation.\n\nDocument title: Gout-associated uric acid crystals activate the NALP3 inflammasome\n\nAbstract sentences:\n[0] Development of the acute and chronic inflammatory responses known as gout and pseudogout are associated with the deposition of monosodium urate (MSU) or calcium pyrophosphate dihydrate (CPPD) crystals, respectively, in joints and periarticular tissues.\n[1] Although MSU crystals were first identified as the aetiological agent of gout in the eighteenth century and more recently as a ‘danger signal’ released from dying cells, little is known about the molecular mechanisms underlying MSU- or CPPD-induced inflammation.\n[2] Here we show that MSU and CPPD engage the caspase-1-activating NALP3 (also called cryopyrin) inflammasome, resulting in the production of active interleukin (IL)-1β and IL-18.\n[3] Macrophages from mice deficient in various components of the inflammasome such as caspase-1, ASC and NALP3 are defective in crystal-induced IL-1β activation.\n[4] Moreover, an impaired neutrophil influx is found in an in vivo model of crystal-induced peritonitis in inflammasome-deficient mice or mice deficient in the IL-1β receptor (IL-1R).\n[5] These findings provide insight into the molecular processes underlying the inflammatory conditions of gout and pseudogout, and further support a pivotal role of the inflammasome in several autoinflammatory diseases."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Macrophages from mice deficient in various components of the inflammasome such as caspase-1, ASC and NALP3 are defective in crystal-induced IL-1β activation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 93, "doc_id": 2692522, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [2692522], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Albendazole is used to treat soil-transmitted helminths.\n\nDocument title: “Rapid-Impact Interventions”: How a Policy of Integrated Control for Africa's Neglected Tropical Diseases Could Benefit the Poor\n\nAbstract sentences:\n[0] Over the past two decades there have been significant achievements in the control of a handful of important human tropical infections [1].\n[1] These achievements include the substantive reductions in the prevalence and incidence of the so-called neglected diseases such as lymphatic filariasis, onchocerciasis, guinea worm, leprosy, and trachoma (Box 1) [2].\n[2] Each of these neglected diseases is a poverty-promoting and often stigmatizing condition occurring primarily in rural areas of low-income countries (Box 2) [3].\n[3] They are ancient afflictions, described in the Bible and other ancient texts, which have burdened humanity for millennia [3].\n[4] But now, as a result of aggressive regional vertical interventions, there is a possibility that some neglected tropical infections could be eventually controlled to the point of elimination in some areas of endemicity [2–8].\n[5] In the case of guinea worm infection, disease eradication might also soon be possible [9].\n[6] Box 2.\n[7] Common Features of the Neglected Tropical Diseases          Ancient afflictions that have burdened humanity for centuries      Poverty-promoting conditions      Associated with stigma      Rural areas of low-income countries and fragile states      No commercial markets for products that target these diseases      Interventions, when applied, have a history of success"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 95, "doc_id": 1215116, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [1215116], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Algerian physicians constitue the largest component of sub-Saharan Africa-trained physicians in the United States.\n\nDocument title: Physician Emigration from Sub-Saharan Africa to the United States: Analysis of the 2011 AMA Physician Masterfile\n\nAbstract sentences:\n[0] BACKGROUND The large-scale emigration of physicians from sub-Saharan Africa (SSA) to high-income nations is a serious development concern.\n[1] Our objective was to determine current emigration trends of SSA physicians found in the physician workforce of the United States.\n[2] METHODS AND FINDINGS We analyzed physician data from the World Health Organization (WHO) Global Health Workforce Statistics along with graduation and residency data from the 2011 American Medical Association Physician Masterfile (AMA-PM) on physicians trained or born in SSA countries who currently practice in the US.\n[3] We estimated emigration proportions, year of US entry, years of practice before emigration, and length of time in the US.\n[4] According to the 2011 AMA-PM, 10,819 physicians were born or trained in 28 SSA countries.\n[5] Sixty-eight percent (n = 7,370) were SSA-trained, 20% (n = 2,126) were US-trained, and 12% (n = 1,323) were trained outside both SSA and the US.\n[6] We estimated active physicians (age ≤ 70 years) to represent 96% (n = 10,377) of the total.\n[7] Migration trends among SSA-trained physicians increased from 2002 to 2011 for all but one principal source country; the exception was South Africa whose physician migration to the US decreased by 8% (-156).\n[8] The increase in last-decade migration was >50% in Nigeria (+1,113) and Ghana (+243), >100% in Ethiopia (+274), and >200% (+244) in Sudan.\n[9] Liberia was the most affected by migration to the US with 77% (n = 175) of its estimated physicians in the 2011 AMA-PM.\n[10] On average, SSA-trained physicians have been in the US for 18 years.\n[11] They practiced for 6.5 years before US entry, and nearly half emigrated during the implementation years (1984-1999) of the structural adjustment programs.\n[12] CONCLUSION Physician emigration from SSA to the US is increasing for most SSA source countries.\n[13] Unless far-reaching policies are implemented by the US and SSA countries, the current emigration trends will persist, and the US will remain a leading destination for SSA physicians emigrating from the continent of greatest need.\n[14] Please see later in the article for the Editors' Summary."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 96, "doc_id": 14500725, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14500725], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Alirocumab treatment reduces apo(a) fractional clearance rate.\n\nDocument title: Effects of PCSK9 Inhibition With Alirocumab on Lipoprotein Metabolism in Healthy Humans\n\nAbstract sentences:\n[0] BACKGROUND Alirocumab, a monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9), lowers plasma low-density lipoprotein (LDL) cholesterol and apolipoprotein B100 (apoB).\n[1] Although studies in mice and cells have identified increased hepatic LDL receptors as the basis for LDL lowering by PCSK9 inhibitors, there have been no human studies characterizing the effects of PCSK9 inhibitors on lipoprotein metabolism.\n[2] In particular, it is not known whether inhibition of PCSK9 has any effects on very low-density lipoprotein or intermediate-density lipoprotein (IDL) metabolism.\n[3] Inhibition of PCSK9 also results in reductions of plasma lipoprotein (a) levels.\n[4] The regulation of plasma Lp(a) levels, including the role of LDL receptors in the clearance of Lp(a), is poorly defined, and no mechanistic studies of the Lp(a) lowering by alirocumab in humans have been published to date.\n[5] METHODS Eighteen (10 F, 8 mol/L) participants completed a placebo-controlled, 2-period study.\n[6] They received 2 doses of placebo, 2 weeks apart, followed by 5 doses of 150 mg of alirocumab, 2 weeks apart.\n[7] At the end of each period, fractional clearance rates (FCRs) and production rates (PRs) of apoB and apo(a) were determined.\n[8] In 10 participants, postprandial triglycerides and apoB48 levels were measured.\n[9] RESULTS Alirocumab reduced ultracentrifugally isolated LDL-C by 55.1%, LDL-apoB by 56.3%, and plasma Lp(a) by 18.7%.\n[10] The fall in LDL-apoB was caused by an 80.4% increase in LDL-apoB FCR and a 23.9% reduction in LDL-apoB PR.\n[11] The latter was due to a 46.1% increase in IDL-apoB FCR coupled with a 27.2% decrease in conversion of IDL to LDL.\n[12] The FCR of apo(a) tended to increase (24.6%) without any change in apo(a) PR.\n[13] Alirocumab had no effects on FCRs or PRs of very low-density lipoproteins-apoB and very low-density lipoproteins triglycerides or on postprandial plasma triglycerides or apoB48 concentrations.\n[14] CONCLUSIONS Alirocumab decreased LDL-C and LDL-apoB by increasing IDL- and LDL-apoB FCRs and decreasing LDL-apoB PR.\n[15] These results are consistent with increases in LDL receptors available to clear IDL and LDL from blood during PCSK9 inhibition.\n[16] The increase in apo(a) FCR during alirocumab treatment suggests that increased LDL receptors may also play a role in the reduction of plasma Lp(a).\n[17] CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov.\n[18] Unique identifier: NCT01959971."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9, 10]\nExplanation: Evidence states: \"RESULTS Alirocumab reduced ultracentrifugally isolated LDL-C by 55.1%, LDL-apoB by 56.3%, and plasma Lp(a) by 18.7%. The fall in LDL-apoB was caused by an 80.4% increase in LDL-apoB FCR and a 23.9% reduction in LDL-apoB PR.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 98, "doc_id": 6540064, "label": "CONTRADICTS", "evidence_sentence_ids": [9, 10], "cited_doc_ids": [6540064], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Alirocumab treatment reduces apo(a) fractional clearance rate.\n\nDocument title: Effects of PCSK9 Inhibition With Alirocumab on Lipoprotein Metabolism in Healthy Humans\n\nAbstract sentences:\n[0] BACKGROUND Alirocumab, a monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9), lowers plasma low-density lipoprotein (LDL) cholesterol and apolipoprotein B100 (apoB).\n[1] Although studies in mice and cells have identified increased hepatic LDL receptors as the basis for LDL lowering by PCSK9 inhibitors, there have been no human studies characterizing the effects of PCSK9 inhibitors on lipoprotein metabolism.\n[2] In particular, it is not known whether inhibition of PCSK9 has any effects on very low-density lipoprotein or intermediate-density lipoprotein (IDL) metabolism.\n[3] Inhibition of PCSK9 also results in reductions of plasma lipoprotein (a) levels.\n[4] The regulation of plasma Lp(a) levels, including the role of LDL receptors in the clearance of Lp(a), is poorly defined, and no mechanistic studies of the Lp(a) lowering by alirocumab in humans have been published to date.\n[5] METHODS Eighteen (10 F, 8 mol/L) participants completed a placebo-controlled, 2-period study.\n[6] They received 2 doses of placebo, 2 weeks apart, followed by 5 doses of 150 mg of alirocumab, 2 weeks apart.\n[7] At the end of each period, fractional clearance rates (FCRs) and production rates (PRs) of apoB and apo(a) were determined.\n[8] In 10 participants, postprandial triglycerides and apoB48 levels were measured.\n[9] RESULTS Alirocumab reduced ultracentrifugally isolated LDL-C by 55.1%, LDL-apoB by 56.3%, and plasma Lp(a) by 18.7%.\n[10] The fall in LDL-apoB was caused by an 80.4% increase in LDL-apoB FCR and a 23.9% reduction in LDL-apoB PR.\n[11] The latter was due to a 46.1% increase in IDL-apoB FCR coupled with a 27.2% decrease in conversion of IDL to LDL.\n[12] The FCR of apo(a) tended to increase (24.6%) without any change in apo(a) PR.\n[13] Alirocumab had no effects on FCRs or PRs of very low-density lipoproteins-apoB and very low-density lipoproteins triglycerides or on postprandial plasma triglycerides or apoB48 concentrations.\n[14] CONCLUSIONS Alirocumab decreased LDL-C and LDL-apoB by increasing IDL- and LDL-apoB FCRs and decreasing LDL-apoB PR.\n[15] These results are consistent with increases in LDL receptors available to clear IDL and LDL from blood during PCSK9 inhibition.\n[16] The increase in apo(a) FCR during alirocumab treatment suggests that increased LDL receptors may also play a role in the reduction of plasma Lp(a).\n[17] CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov.\n[18] Unique identifier: NCT01959971."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"The FCR of apo(a) tended to increase (24.6%) without any change in apo(a) PR.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 98, "doc_id": 6540064, "label": "CONTRADICTS", "evidence_sentence_ids": [12], "cited_doc_ids": [6540064], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Alirocumab treatment reduces apo(a) fractional clearance rate.\n\nDocument title: Effects of PCSK9 Inhibition With Alirocumab on Lipoprotein Metabolism in Healthy Humans\n\nAbstract sentences:\n[0] BACKGROUND Alirocumab, a monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9), lowers plasma low-density lipoprotein (LDL) cholesterol and apolipoprotein B100 (apoB).\n[1] Although studies in mice and cells have identified increased hepatic LDL receptors as the basis for LDL lowering by PCSK9 inhibitors, there have been no human studies characterizing the effects of PCSK9 inhibitors on lipoprotein metabolism.\n[2] In particular, it is not known whether inhibition of PCSK9 has any effects on very low-density lipoprotein or intermediate-density lipoprotein (IDL) metabolism.\n[3] Inhibition of PCSK9 also results in reductions of plasma lipoprotein (a) levels.\n[4] The regulation of plasma Lp(a) levels, including the role of LDL receptors in the clearance of Lp(a), is poorly defined, and no mechanistic studies of the Lp(a) lowering by alirocumab in humans have been published to date.\n[5] METHODS Eighteen (10 F, 8 mol/L) participants completed a placebo-controlled, 2-period study.\n[6] They received 2 doses of placebo, 2 weeks apart, followed by 5 doses of 150 mg of alirocumab, 2 weeks apart.\n[7] At the end of each period, fractional clearance rates (FCRs) and production rates (PRs) of apoB and apo(a) were determined.\n[8] In 10 participants, postprandial triglycerides and apoB48 levels were measured.\n[9] RESULTS Alirocumab reduced ultracentrifugally isolated LDL-C by 55.1%, LDL-apoB by 56.3%, and plasma Lp(a) by 18.7%.\n[10] The fall in LDL-apoB was caused by an 80.4% increase in LDL-apoB FCR and a 23.9% reduction in LDL-apoB PR.\n[11] The latter was due to a 46.1% increase in IDL-apoB FCR coupled with a 27.2% decrease in conversion of IDL to LDL.\n[12] The FCR of apo(a) tended to increase (24.6%) without any change in apo(a) PR.\n[13] Alirocumab had no effects on FCRs or PRs of very low-density lipoproteins-apoB and very low-density lipoproteins triglycerides or on postprandial plasma triglycerides or apoB48 concentrations.\n[14] CONCLUSIONS Alirocumab decreased LDL-C and LDL-apoB by increasing IDL- and LDL-apoB FCRs and decreasing LDL-apoB PR.\n[15] These results are consistent with increases in LDL receptors available to clear IDL and LDL from blood during PCSK9 inhibition.\n[16] The increase in apo(a) FCR during alirocumab treatment suggests that increased LDL receptors may also play a role in the reduction of plasma Lp(a).\n[17] CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov.\n[18] Unique identifier: NCT01959971."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [14]\nExplanation: Evidence states: \"CONCLUSIONS Alirocumab decreased LDL-C and LDL-apoB by increasing IDL- and LDL-apoB FCRs and decreasing LDL-apoB PR.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 98, "doc_id": 6540064, "label": "CONTRADICTS", "evidence_sentence_ids": [14], "cited_doc_ids": [6540064], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Alirocumab treatment reduces apo(a) fractional clearance rate.\n\nDocument title: Effects of PCSK9 Inhibition With Alirocumab on Lipoprotein Metabolism in Healthy Humans\n\nAbstract sentences:\n[0] BACKGROUND Alirocumab, a monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9), lowers plasma low-density lipoprotein (LDL) cholesterol and apolipoprotein B100 (apoB).\n[1] Although studies in mice and cells have identified increased hepatic LDL receptors as the basis for LDL lowering by PCSK9 inhibitors, there have been no human studies characterizing the effects of PCSK9 inhibitors on lipoprotein metabolism.\n[2] In particular, it is not known whether inhibition of PCSK9 has any effects on very low-density lipoprotein or intermediate-density lipoprotein (IDL) metabolism.\n[3] Inhibition of PCSK9 also results in reductions of plasma lipoprotein (a) levels.\n[4] The regulation of plasma Lp(a) levels, including the role of LDL receptors in the clearance of Lp(a), is poorly defined, and no mechanistic studies of the Lp(a) lowering by alirocumab in humans have been published to date.\n[5] METHODS Eighteen (10 F, 8 mol/L) participants completed a placebo-controlled, 2-period study.\n[6] They received 2 doses of placebo, 2 weeks apart, followed by 5 doses of 150 mg of alirocumab, 2 weeks apart.\n[7] At the end of each period, fractional clearance rates (FCRs) and production rates (PRs) of apoB and apo(a) were determined.\n[8] In 10 participants, postprandial triglycerides and apoB48 levels were measured.\n[9] RESULTS Alirocumab reduced ultracentrifugally isolated LDL-C by 55.1%, LDL-apoB by 56.3%, and plasma Lp(a) by 18.7%.\n[10] The fall in LDL-apoB was caused by an 80.4% increase in LDL-apoB FCR and a 23.9% reduction in LDL-apoB PR.\n[11] The latter was due to a 46.1% increase in IDL-apoB FCR coupled with a 27.2% decrease in conversion of IDL to LDL.\n[12] The FCR of apo(a) tended to increase (24.6%) without any change in apo(a) PR.\n[13] Alirocumab had no effects on FCRs or PRs of very low-density lipoproteins-apoB and very low-density lipoproteins triglycerides or on postprandial plasma triglycerides or apoB48 concentrations.\n[14] CONCLUSIONS Alirocumab decreased LDL-C and LDL-apoB by increasing IDL- and LDL-apoB FCRs and decreasing LDL-apoB PR.\n[15] These results are consistent with increases in LDL receptors available to clear IDL and LDL from blood during PCSK9 inhibition.\n[16] The increase in apo(a) FCR during alirocumab treatment suggests that increased LDL receptors may also play a role in the reduction of plasma Lp(a).\n[17] CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov.\n[18] Unique identifier: NCT01959971."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [16]\nExplanation: Evidence states: \"The increase in apo(a) FCR during alirocumab treatment suggests that increased LDL receptors may also play a role in the reduction of plasma Lp(a).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 98, "doc_id": 6540064, "label": "CONTRADICTS", "evidence_sentence_ids": [16], "cited_doc_ids": [6540064], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Allogeneic mechanical circulatory support is not as effective as autologous mechanical circulatory support for treating acute myocardial infarction.\n\nDocument title: Comparison of allogeneic vs autologous bone marrow–derived mesenchymal stem cells delivered by transendocardial injection in patients with ischemic cardiomyopathy: the POSEIDON randomized trial.\n\nAbstract sentences:\n[0] CONTEXT Mesenchymal stem cells (MSCs) are under evaluation as a therapy for ischemic cardiomyopathy (ICM).\n[1] Both autologous and allogeneic MSC therapies are possible; however, their safety and efficacy have not been compared.\n[2] OBJECTIVE To test whether allogeneic MSCs are as safe and effective as autologous MSCs in patients with left ventricular (LV) dysfunction due to ICM.\n[3] DESIGN, SETTING, AND PATIENTS A phase 1/2 randomized comparison (POSEIDON study) in a US tertiary-care referral hospital of allogeneic and autologous MSCs in 30 patients with LV dysfunction due to ICM between April 2, 2010, and September 14, 2011, with 13-month follow-up.\n[4] INTERVENTION Twenty million, 100 million, or 200 million cells (5 patients in each cell type per dose level) were delivered by transendocardial stem cell injection into 10 LV sites.\n[5] MAIN OUTCOME MEASURES Thirty-day postcatheterization incidence of predefined treatment-emergent serious adverse events (SAEs).\n[6] Efficacy assessments included 6-minute walk test, exercise peak VO2, Minnesota Living with Heart Failure Questionnaire (MLHFQ), New York Heart Association class, LV volumes, ejection fraction (EF), early enhancement defect (EED; infarct size), and sphericity index.\n[7] RESULTS Within 30 days, 1 patient in each group (treatment-emergent SAE rate, 6.7%) was hospitalized for heart failure, less than the prespecified stopping event rate of 25%.\n[8] The 1-year incidence of SAEs was 33.3% (n = 5) in the allogeneic group and 53.3% (n = 8) in the autologous group (P = .46).\n[9] At 1 year, there were no ventricular arrhythmia SAEs observed among allogeneic recipients compared with 4 patients (26.7%) in the autologous group (P = .10).\n[10] Relative to baseline, autologous but not allogeneic MSC therapy was associated with an improvement in the 6-minute walk test and the MLHFQ score, but neither improved exercise VO2 max.\n[11] Allogeneic and autologous MSCs reduced mean EED by −33.21% (95% CI, −43.61% to −22.81%; P < .001) and sphericity index but did not increase EF.\n[12] Allogeneic MSCs reduced LV end-diastolic volumes.\n[13] Low-dose concentration MSCs (20 million cells) produced greatest reductions in LV volumes and increased EF.\n[14] Allogeneic MSCs did not stimulate significant donor-specific alloimmune reactions.\n[15] CONCLUSIONS In this early-stage study of patients with ICM, transendocardial injection of allogeneic and autologous MSCs without a placebo control were both associated with low rates of treatment-emergent SAEs, including immunologic reactions.\n[16] In aggregate, MSC injection favorably affected patient functional capacity, quality of life, and ventricular remodeling.\n[17] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT01087996."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"The 1-year incidence of SAEs was 33.3% (n = 5) in the allogeneic group and 53.3% (n = 8) in the autologous group (P = .46).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 104, "doc_id": 40164383, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [40164383], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Allogeneic mechanical circulatory support is not as effective as autologous mechanical circulatory support for treating acute myocardial infarction.\n\nDocument title: Comparison of allogeneic vs autologous bone marrow–derived mesenchymal stem cells delivered by transendocardial injection in patients with ischemic cardiomyopathy: the POSEIDON randomized trial.\n\nAbstract sentences:\n[0] CONTEXT Mesenchymal stem cells (MSCs) are under evaluation as a therapy for ischemic cardiomyopathy (ICM).\n[1] Both autologous and allogeneic MSC therapies are possible; however, their safety and efficacy have not been compared.\n[2] OBJECTIVE To test whether allogeneic MSCs are as safe and effective as autologous MSCs in patients with left ventricular (LV) dysfunction due to ICM.\n[3] DESIGN, SETTING, AND PATIENTS A phase 1/2 randomized comparison (POSEIDON study) in a US tertiary-care referral hospital of allogeneic and autologous MSCs in 30 patients with LV dysfunction due to ICM between April 2, 2010, and September 14, 2011, with 13-month follow-up.\n[4] INTERVENTION Twenty million, 100 million, or 200 million cells (5 patients in each cell type per dose level) were delivered by transendocardial stem cell injection into 10 LV sites.\n[5] MAIN OUTCOME MEASURES Thirty-day postcatheterization incidence of predefined treatment-emergent serious adverse events (SAEs).\n[6] Efficacy assessments included 6-minute walk test, exercise peak VO2, Minnesota Living with Heart Failure Questionnaire (MLHFQ), New York Heart Association class, LV volumes, ejection fraction (EF), early enhancement defect (EED; infarct size), and sphericity index.\n[7] RESULTS Within 30 days, 1 patient in each group (treatment-emergent SAE rate, 6.7%) was hospitalized for heart failure, less than the prespecified stopping event rate of 25%.\n[8] The 1-year incidence of SAEs was 33.3% (n = 5) in the allogeneic group and 53.3% (n = 8) in the autologous group (P = .46).\n[9] At 1 year, there were no ventricular arrhythmia SAEs observed among allogeneic recipients compared with 4 patients (26.7%) in the autologous group (P = .10).\n[10] Relative to baseline, autologous but not allogeneic MSC therapy was associated with an improvement in the 6-minute walk test and the MLHFQ score, but neither improved exercise VO2 max.\n[11] Allogeneic and autologous MSCs reduced mean EED by −33.21% (95% CI, −43.61% to −22.81%; P < .001) and sphericity index but did not increase EF.\n[12] Allogeneic MSCs reduced LV end-diastolic volumes.\n[13] Low-dose concentration MSCs (20 million cells) produced greatest reductions in LV volumes and increased EF.\n[14] Allogeneic MSCs did not stimulate significant donor-specific alloimmune reactions.\n[15] CONCLUSIONS In this early-stage study of patients with ICM, transendocardial injection of allogeneic and autologous MSCs without a placebo control were both associated with low rates of treatment-emergent SAEs, including immunologic reactions.\n[16] In aggregate, MSC injection favorably affected patient functional capacity, quality of life, and ventricular remodeling.\n[17] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT01087996."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"At 1 year, there were no ventricular arrhythmia SAEs observed among allogeneic recipients compared with 4 patients (26.7%) in the autologous group (P = .10).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 104, "doc_id": 40164383, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [40164383], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Allogeneic mechanical circulatory support is not as effective as autologous mechanical circulatory support for treating acute myocardial infarction.\n\nDocument title: Comparison of allogeneic vs autologous bone marrow–derived mesenchymal stem cells delivered by transendocardial injection in patients with ischemic cardiomyopathy: the POSEIDON randomized trial.\n\nAbstract sentences:\n[0] CONTEXT Mesenchymal stem cells (MSCs) are under evaluation as a therapy for ischemic cardiomyopathy (ICM).\n[1] Both autologous and allogeneic MSC therapies are possible; however, their safety and efficacy have not been compared.\n[2] OBJECTIVE To test whether allogeneic MSCs are as safe and effective as autologous MSCs in patients with left ventricular (LV) dysfunction due to ICM.\n[3] DESIGN, SETTING, AND PATIENTS A phase 1/2 randomized comparison (POSEIDON study) in a US tertiary-care referral hospital of allogeneic and autologous MSCs in 30 patients with LV dysfunction due to ICM between April 2, 2010, and September 14, 2011, with 13-month follow-up.\n[4] INTERVENTION Twenty million, 100 million, or 200 million cells (5 patients in each cell type per dose level) were delivered by transendocardial stem cell injection into 10 LV sites.\n[5] MAIN OUTCOME MEASURES Thirty-day postcatheterization incidence of predefined treatment-emergent serious adverse events (SAEs).\n[6] Efficacy assessments included 6-minute walk test, exercise peak VO2, Minnesota Living with Heart Failure Questionnaire (MLHFQ), New York Heart Association class, LV volumes, ejection fraction (EF), early enhancement defect (EED; infarct size), and sphericity index.\n[7] RESULTS Within 30 days, 1 patient in each group (treatment-emergent SAE rate, 6.7%) was hospitalized for heart failure, less than the prespecified stopping event rate of 25%.\n[8] The 1-year incidence of SAEs was 33.3% (n = 5) in the allogeneic group and 53.3% (n = 8) in the autologous group (P = .46).\n[9] At 1 year, there were no ventricular arrhythmia SAEs observed among allogeneic recipients compared with 4 patients (26.7%) in the autologous group (P = .10).\n[10] Relative to baseline, autologous but not allogeneic MSC therapy was associated with an improvement in the 6-minute walk test and the MLHFQ score, but neither improved exercise VO2 max.\n[11] Allogeneic and autologous MSCs reduced mean EED by −33.21% (95% CI, −43.61% to −22.81%; P < .001) and sphericity index but did not increase EF.\n[12] Allogeneic MSCs reduced LV end-diastolic volumes.\n[13] Low-dose concentration MSCs (20 million cells) produced greatest reductions in LV volumes and increased EF.\n[14] Allogeneic MSCs did not stimulate significant donor-specific alloimmune reactions.\n[15] CONCLUSIONS In this early-stage study of patients with ICM, transendocardial injection of allogeneic and autologous MSCs without a placebo control were both associated with low rates of treatment-emergent SAEs, including immunologic reactions.\n[16] In aggregate, MSC injection favorably affected patient functional capacity, quality of life, and ventricular remodeling.\n[17] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT01087996."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"Allogeneic and autologous MSCs reduced mean EED by −33.21% (95% CI, −43.61% to −22.81%; P < .001) and sphericity index but did not increase EF.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 104, "doc_id": 40164383, "label": "CONTRADICTS", "evidence_sentence_ids": [11], "cited_doc_ids": [40164383], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Allogeneic mechanical circulatory support is not as effective as autologous mechanical circulatory support for treating acute myocardial infarction.\n\nDocument title: Comparison of allogeneic vs autologous bone marrow–derived mesenchymal stem cells delivered by transendocardial injection in patients with ischemic cardiomyopathy: the POSEIDON randomized trial.\n\nAbstract sentences:\n[0] CONTEXT Mesenchymal stem cells (MSCs) are under evaluation as a therapy for ischemic cardiomyopathy (ICM).\n[1] Both autologous and allogeneic MSC therapies are possible; however, their safety and efficacy have not been compared.\n[2] OBJECTIVE To test whether allogeneic MSCs are as safe and effective as autologous MSCs in patients with left ventricular (LV) dysfunction due to ICM.\n[3] DESIGN, SETTING, AND PATIENTS A phase 1/2 randomized comparison (POSEIDON study) in a US tertiary-care referral hospital of allogeneic and autologous MSCs in 30 patients with LV dysfunction due to ICM between April 2, 2010, and September 14, 2011, with 13-month follow-up.\n[4] INTERVENTION Twenty million, 100 million, or 200 million cells (5 patients in each cell type per dose level) were delivered by transendocardial stem cell injection into 10 LV sites.\n[5] MAIN OUTCOME MEASURES Thirty-day postcatheterization incidence of predefined treatment-emergent serious adverse events (SAEs).\n[6] Efficacy assessments included 6-minute walk test, exercise peak VO2, Minnesota Living with Heart Failure Questionnaire (MLHFQ), New York Heart Association class, LV volumes, ejection fraction (EF), early enhancement defect (EED; infarct size), and sphericity index.\n[7] RESULTS Within 30 days, 1 patient in each group (treatment-emergent SAE rate, 6.7%) was hospitalized for heart failure, less than the prespecified stopping event rate of 25%.\n[8] The 1-year incidence of SAEs was 33.3% (n = 5) in the allogeneic group and 53.3% (n = 8) in the autologous group (P = .46).\n[9] At 1 year, there were no ventricular arrhythmia SAEs observed among allogeneic recipients compared with 4 patients (26.7%) in the autologous group (P = .10).\n[10] Relative to baseline, autologous but not allogeneic MSC therapy was associated with an improvement in the 6-minute walk test and the MLHFQ score, but neither improved exercise VO2 max.\n[11] Allogeneic and autologous MSCs reduced mean EED by −33.21% (95% CI, −43.61% to −22.81%; P < .001) and sphericity index but did not increase EF.\n[12] Allogeneic MSCs reduced LV end-diastolic volumes.\n[13] Low-dose concentration MSCs (20 million cells) produced greatest reductions in LV volumes and increased EF.\n[14] Allogeneic MSCs did not stimulate significant donor-specific alloimmune reactions.\n[15] CONCLUSIONS In this early-stage study of patients with ICM, transendocardial injection of allogeneic and autologous MSCs without a placebo control were both associated with low rates of treatment-emergent SAEs, including immunologic reactions.\n[16] In aggregate, MSC injection favorably affected patient functional capacity, quality of life, and ventricular remodeling.\n[17] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT01087996."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [15]\nExplanation: Evidence states: \"CONCLUSIONS In this early-stage study of patients with ICM, transendocardial injection of allogeneic and autologous MSCs without a placebo control were both associated with low rates of treatment-emergent SAEs, including immunologic reactions.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 104, "doc_id": 40164383, "label": "CONTRADICTS", "evidence_sentence_ids": [15], "cited_doc_ids": [40164383], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Alteration of origin firing causes changes in termination zones of Okazaki fragments.\n\nDocument title: Quantitative, genome-wide analysis of eukaryotic replication initiation and termination.\n\nAbstract sentences:\n[0] Many fundamental aspects of DNA replication, such as the exact locations where DNA synthesis is initiated and terminated, how frequently origins are used, and how fork progression is influenced by transcription, are poorly understood.\n[1] Via the deep sequencing of Okazaki fragments, we comprehensively document replication fork directionality throughout the S. cerevisiae genome, which permits the systematic analysis of initiation, origin efficiency, fork progression, and termination.\n[2] We show that leading-strand initiation preferentially occurs within a nucleosome-free region at replication origins.\n[3] Using a strain in which late origins can be induced to fire early, we show that replication termination is a largely passive phenomenon that does not rely on cis-acting sequences or replication fork pausing.\n[4] The replication profile is predominantly determined by the kinetics of origin firing, allowing us to reconstruct chromosome-wide timing profiles from an asynchronous culture."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Using a strain in which late origins can be induced to fire early, we show that replication termination is a largely passive phenomenon that does not rely on cis-acting sequences or replication fork pausing.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 105, "doc_id": 36606083, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [36606083], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ambulatory blood pressure monitoring is inaccurate at diagnosing hypertension.\n\nDocument title: Relative effectiveness of clinic and home blood pressure monitoring compared with ambulatory blood pressure monitoring in diagnosis of hypertension: systematic review\n\nAbstract sentences:\n[0] OBJECTIVE To determine the relative accuracy of clinic measurements and home blood pressure monitoring compared with ambulatory blood pressure monitoring as a reference standard for the diagnosis of hypertension.\n[1] DESIGN Systematic review with meta-analysis with hierarchical summary receiver operating characteristic models.\n[2] Methodological quality was appraised, including evidence of validation of blood pressure measurement equipment.\n[3] DATA SOURCES Medline (from 1966), Embase (from 1980), Cochrane Database of Systematic Reviews, DARE, Medion, ARIF, and TRIP up to May 2010.\n[4] Eligibility criteria for selecting studies Eligible studies examined diagnosis of hypertension in adults of all ages using home and/or clinic blood pressure measurement compared with those made using ambulatory monitoring that clearly defined thresholds to diagnose hypertension.\n[5] RESULTS The 20 eligible studies used various thresholds for the diagnosis of hypertension, and only seven studies (clinic) and three studies (home) could be directly compared with ambulatory monitoring.\n[6] Compared with ambulatory monitoring thresholds of 135/85 mm Hg, clinic measurements over 140/90 mm Hg had mean sensitivity and specificity of 74.6% (95% confidence interval 60.7% to 84.8%) and 74.6% (47.9% to 90.4%), respectively, whereas home measurements over 135/85 mm Hg had mean sensitivity and specificity of 85.7% (78.0% to 91.0%) and 62.4% (48.0% to 75.0%).\n[7] CONCLUSIONS Neither clinic nor home measurement had sufficient sensitivity or specificity to be recommended as a single diagnostic test.\n[8] If ambulatory monitoring is taken as the reference standard, then treatment decisions based on clinic or home blood pressure alone might result in substantial overdiagnosis.\n[9] Ambulatory monitoring before the start of lifelong drug treatment might lead to more appropriate targeting of treatment, particularly around the diagnostic threshold."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Compared with ambulatory monitoring thresholds of 135/85 mm Hg, clinic measurements over 140/90 mm Hg had mean sensitivity and specificity of 74.6% (95% confidence interval 60.7% to 84.8%) and 74.6% (47.9% to 90.4%), respectively, whereas home measurements over 135/85 mm Hg had mean sensitivity and specificity of 85.7% (78.0% to 91.0%) and 62.4% (48.0% to 75.0%).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 106, "doc_id": 25515907, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [25515907, 5151024], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ambulatory blood pressure monitoring is inaccurate at diagnosing hypertension.\n\nDocument title: Relative effectiveness of clinic and home blood pressure monitoring compared with ambulatory blood pressure monitoring in diagnosis of hypertension: systematic review\n\nAbstract sentences:\n[0] OBJECTIVE To determine the relative accuracy of clinic measurements and home blood pressure monitoring compared with ambulatory blood pressure monitoring as a reference standard for the diagnosis of hypertension.\n[1] DESIGN Systematic review with meta-analysis with hierarchical summary receiver operating characteristic models.\n[2] Methodological quality was appraised, including evidence of validation of blood pressure measurement equipment.\n[3] DATA SOURCES Medline (from 1966), Embase (from 1980), Cochrane Database of Systematic Reviews, DARE, Medion, ARIF, and TRIP up to May 2010.\n[4] Eligibility criteria for selecting studies Eligible studies examined diagnosis of hypertension in adults of all ages using home and/or clinic blood pressure measurement compared with those made using ambulatory monitoring that clearly defined thresholds to diagnose hypertension.\n[5] RESULTS The 20 eligible studies used various thresholds for the diagnosis of hypertension, and only seven studies (clinic) and three studies (home) could be directly compared with ambulatory monitoring.\n[6] Compared with ambulatory monitoring thresholds of 135/85 mm Hg, clinic measurements over 140/90 mm Hg had mean sensitivity and specificity of 74.6% (95% confidence interval 60.7% to 84.8%) and 74.6% (47.9% to 90.4%), respectively, whereas home measurements over 135/85 mm Hg had mean sensitivity and specificity of 85.7% (78.0% to 91.0%) and 62.4% (48.0% to 75.0%).\n[7] CONCLUSIONS Neither clinic nor home measurement had sufficient sensitivity or specificity to be recommended as a single diagnostic test.\n[8] If ambulatory monitoring is taken as the reference standard, then treatment decisions based on clinic or home blood pressure alone might result in substantial overdiagnosis.\n[9] Ambulatory monitoring before the start of lifelong drug treatment might lead to more appropriate targeting of treatment, particularly around the diagnostic threshold."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"If ambulatory monitoring is taken as the reference standard, then treatment decisions based on clinic or home blood pressure alone might result in substantial overdiagnosis.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 106, "doc_id": 25515907, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [25515907, 5151024], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ambulatory blood pressure monitoring is inaccurate at diagnosing hypertension.\n\nDocument title: Relative effectiveness of clinic and home blood pressure monitoring compared with ambulatory blood pressure monitoring in diagnosis of hypertension: systematic review\n\nAbstract sentences:\n[0] OBJECTIVE To determine the relative accuracy of clinic measurements and home blood pressure monitoring compared with ambulatory blood pressure monitoring as a reference standard for the diagnosis of hypertension.\n[1] DESIGN Systematic review with meta-analysis with hierarchical summary receiver operating characteristic models.\n[2] Methodological quality was appraised, including evidence of validation of blood pressure measurement equipment.\n[3] DATA SOURCES Medline (from 1966), Embase (from 1980), Cochrane Database of Systematic Reviews, DARE, Medion, ARIF, and TRIP up to May 2010.\n[4] Eligibility criteria for selecting studies Eligible studies examined diagnosis of hypertension in adults of all ages using home and/or clinic blood pressure measurement compared with those made using ambulatory monitoring that clearly defined thresholds to diagnose hypertension.\n[5] RESULTS The 20 eligible studies used various thresholds for the diagnosis of hypertension, and only seven studies (clinic) and three studies (home) could be directly compared with ambulatory monitoring.\n[6] Compared with ambulatory monitoring thresholds of 135/85 mm Hg, clinic measurements over 140/90 mm Hg had mean sensitivity and specificity of 74.6% (95% confidence interval 60.7% to 84.8%) and 74.6% (47.9% to 90.4%), respectively, whereas home measurements over 135/85 mm Hg had mean sensitivity and specificity of 85.7% (78.0% to 91.0%) and 62.4% (48.0% to 75.0%).\n[7] CONCLUSIONS Neither clinic nor home measurement had sufficient sensitivity or specificity to be recommended as a single diagnostic test.\n[8] If ambulatory monitoring is taken as the reference standard, then treatment decisions based on clinic or home blood pressure alone might result in substantial overdiagnosis.\n[9] Ambulatory monitoring before the start of lifelong drug treatment might lead to more appropriate targeting of treatment, particularly around the diagnostic threshold."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Ambulatory monitoring before the start of lifelong drug treatment might lead to more appropriate targeting of treatment, particularly around the diagnostic threshold.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 106, "doc_id": 25515907, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [25515907, 5151024], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ambulatory blood pressure monitoring is inaccurate at diagnosing hypertension.\n\nDocument title: Cost-effectiveness of options for the diagnosis of high blood pressure in primary care: a modelling study.\n\nAbstract sentences:\n[0] BACKGROUND The diagnosis of hypertension has traditionally been based on blood-pressure measurements in the clinic, but home and ambulatory measurements better correlate with cardiovascular outcome, and ambulatory monitoring is more accurate than both clinic and home monitoring in diagnosing hypertension.\n[1] We aimed to compare the cost-effectiveness of different diagnostic strategies for hypertension.\n[2] METHODS We did a Markov model-based probabilistic cost-effectiveness analysis.\n[3] We used a hypothetical primary-care population aged 40 years or older with a screening blood-pressure measurement greater than 140/90 mm Hg and risk-factor prevalence equivalent to the general population.\n[4] We compared three diagnostic strategies-further blood pressure measurement in the clinic, at home, and with an ambulatory monitor-in terms of lifetime costs, quality-adjusted life years, and cost-effectiveness.\n[5] FINDINGS Ambulatory monitoring was the most cost-effective strategy for the diagnosis of hypertension for men and women of all ages.\n[6] It was cost-saving for all groups (from -£56 [95% CI -105 to -10] in men aged 75 years to -£323 [-389 to -222] in women aged 40 years) and resulted in more quality-adjusted life years for men and women older than 50 years (from 0·006 [0·000 to 0·015] for women aged 60 years to 0·022 [0·012 to 0·035] for men aged 70 years).\n[7] This finding was robust when assessed with a wide range of deterministic sensitivity analyses around the base case, but was sensitive if home monitoring was judged to have equal test performance to ambulatory monitoring or if treatment was judged effective irrespective of whether an individual was hypertensive.\n[8] INTERPRETATION Ambulatory monitoring as a diagnostic strategy for hypertension after an initial raised reading in the clinic would reduce misdiagnosis and save costs.\n[9] Additional costs from ambulatory monitoring are counterbalanced by cost savings from better targeted treatment.\n[10] Ambulatory monitoring is recommended for most patients before the start of antihypertensive drugs.\n[11] FUNDING National Institute for Health Research and the National Institute for Health and Clinical Excellence."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"BACKGROUND The diagnosis of hypertension has traditionally been based on blood-pressure measurements in the clinic, but home and ambulatory measurements better correlate with cardiovascular outcome, and ambulatory monitoring is more accurate than both clinic and home monitoring in diagnosing hypertension.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 106, "doc_id": 5151024, "label": "CONTRADICTS", "evidence_sentence_ids": [0], "cited_doc_ids": [25515907, 5151024], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ambulatory blood pressure monitoring is inaccurate at diagnosing hypertension.\n\nDocument title: Cost-effectiveness of options for the diagnosis of high blood pressure in primary care: a modelling study.\n\nAbstract sentences:\n[0] BACKGROUND The diagnosis of hypertension has traditionally been based on blood-pressure measurements in the clinic, but home and ambulatory measurements better correlate with cardiovascular outcome, and ambulatory monitoring is more accurate than both clinic and home monitoring in diagnosing hypertension.\n[1] We aimed to compare the cost-effectiveness of different diagnostic strategies for hypertension.\n[2] METHODS We did a Markov model-based probabilistic cost-effectiveness analysis.\n[3] We used a hypothetical primary-care population aged 40 years or older with a screening blood-pressure measurement greater than 140/90 mm Hg and risk-factor prevalence equivalent to the general population.\n[4] We compared three diagnostic strategies-further blood pressure measurement in the clinic, at home, and with an ambulatory monitor-in terms of lifetime costs, quality-adjusted life years, and cost-effectiveness.\n[5] FINDINGS Ambulatory monitoring was the most cost-effective strategy for the diagnosis of hypertension for men and women of all ages.\n[6] It was cost-saving for all groups (from -£56 [95% CI -105 to -10] in men aged 75 years to -£323 [-389 to -222] in women aged 40 years) and resulted in more quality-adjusted life years for men and women older than 50 years (from 0·006 [0·000 to 0·015] for women aged 60 years to 0·022 [0·012 to 0·035] for men aged 70 years).\n[7] This finding was robust when assessed with a wide range of deterministic sensitivity analyses around the base case, but was sensitive if home monitoring was judged to have equal test performance to ambulatory monitoring or if treatment was judged effective irrespective of whether an individual was hypertensive.\n[8] INTERPRETATION Ambulatory monitoring as a diagnostic strategy for hypertension after an initial raised reading in the clinic would reduce misdiagnosis and save costs.\n[9] Additional costs from ambulatory monitoring are counterbalanced by cost savings from better targeted treatment.\n[10] Ambulatory monitoring is recommended for most patients before the start of antihypertensive drugs.\n[11] FUNDING National Institute for Health Research and the National Institute for Health and Clinical Excellence."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"INTERPRETATION Ambulatory monitoring as a diagnostic strategy for hypertension after an initial raised reading in the clinic would reduce misdiagnosis and save costs.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 106, "doc_id": 5151024, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [25515907, 5151024], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Amitriptyline is an effective treatment for chronic tension-type headaches.\n\nDocument title: Management of chronic tension-type headache with tricyclic antidepressant medication, stress management therapy, and their combination: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Chronic tension-type headaches are characterized by near-daily headaches and often are difficult to manage in primary practice.\n[1] Behavioral and pharmacological therapies each appear modestly effective, but data are lacking on their separate and combined effects.\n[2] OBJECTIVE To evaluate the clinical efficacy of behavioral and pharmacological therapies, singly and combined, for chronic tension-type headaches.\n[3] DESIGN AND SETTING Randomized placebo-controlled trial conducted from August 1995 to January 1998 at 2 outpatient sites in Ohio.\n[4] PARTICIPANTS Two hundred three adults (mean age, 37 years; 76% women) with diagnosis of chronic tension-type headaches (mean, 26 headache d/mo).\n[5] INTERVENTIONS Participants were randomly assigned to receive tricyclic antidepressant (amitriptyline hydrochloride, up to 100 mg/d, or nortriptyline hydrochloride, up to 75 mg/d) medication (n = 53), placebo (n = 48), stress management (eg, relaxation, cognitive coping) therapy (3 sessions and 2 telephone contacts) plus placebo (n = 49), or stress management therapy plus antidepressant medication (n = 53).\n[6] MAIN OUTCOME MEASURES Monthly headache index scores calculated as the mean of pain ratings (0-10 scale) recorded by participants in a daily diary 4 times per day; number of days per month with at least moderate pain (pain rating >/=5), analgesic medication use, and Headache Disability Inventory scores, compared by intervention group.\n[7] RESULTS Tricyclic antidepressant medication and stress management therapy each produced larger reductions in headache activity, analgesic medication use, and headache-related disability than placebo, but antidepressant medication yielded more rapid improvements in headache activity.\n[8] Combined therapy was more likely to produce clinically significant (>/=50%) reductions in headache index scores (64% of participants) than antidepressant medication (38% of participants; P =.006), stress management therapy (35%; P =.003), or placebo (29%; P =.001).\n[9] On other measures the combined therapy and its 2 component therapies produced similar outcomes.\n[10] CONCLUSIONS Our results indicate that antidepressant medication and stress management therapy are each modestly effective in treating chronic tension-type headaches.\n[11] Combined therapy may improve outcome relative to monotherapy."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"RESULTS Tricyclic antidepressant medication and stress management therapy each produced larger reductions in headache activity, analgesic medication use, and headache-related disability than placebo, but antidepressant medication yielded more rapid improvements in headache activity.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 108, "doc_id": 6191684, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [6191684, 22995579, 23865182], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Amitriptyline is an effective treatment for chronic tension-type headaches.\n\nDocument title: Management of chronic tension-type headache with tricyclic antidepressant medication, stress management therapy, and their combination: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Chronic tension-type headaches are characterized by near-daily headaches and often are difficult to manage in primary practice.\n[1] Behavioral and pharmacological therapies each appear modestly effective, but data are lacking on their separate and combined effects.\n[2] OBJECTIVE To evaluate the clinical efficacy of behavioral and pharmacological therapies, singly and combined, for chronic tension-type headaches.\n[3] DESIGN AND SETTING Randomized placebo-controlled trial conducted from August 1995 to January 1998 at 2 outpatient sites in Ohio.\n[4] PARTICIPANTS Two hundred three adults (mean age, 37 years; 76% women) with diagnosis of chronic tension-type headaches (mean, 26 headache d/mo).\n[5] INTERVENTIONS Participants were randomly assigned to receive tricyclic antidepressant (amitriptyline hydrochloride, up to 100 mg/d, or nortriptyline hydrochloride, up to 75 mg/d) medication (n = 53), placebo (n = 48), stress management (eg, relaxation, cognitive coping) therapy (3 sessions and 2 telephone contacts) plus placebo (n = 49), or stress management therapy plus antidepressant medication (n = 53).\n[6] MAIN OUTCOME MEASURES Monthly headache index scores calculated as the mean of pain ratings (0-10 scale) recorded by participants in a daily diary 4 times per day; number of days per month with at least moderate pain (pain rating >/=5), analgesic medication use, and Headache Disability Inventory scores, compared by intervention group.\n[7] RESULTS Tricyclic antidepressant medication and stress management therapy each produced larger reductions in headache activity, analgesic medication use, and headache-related disability than placebo, but antidepressant medication yielded more rapid improvements in headache activity.\n[8] Combined therapy was more likely to produce clinically significant (>/=50%) reductions in headache index scores (64% of participants) than antidepressant medication (38% of participants; P =.006), stress management therapy (35%; P =.003), or placebo (29%; P =.001).\n[9] On other measures the combined therapy and its 2 component therapies produced similar outcomes.\n[10] CONCLUSIONS Our results indicate that antidepressant medication and stress management therapy are each modestly effective in treating chronic tension-type headaches.\n[11] Combined therapy may improve outcome relative to monotherapy."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Combined therapy was more likely to produce clinically significant (>/=50%) reductions in headache index scores (64% of participants) than antidepressant medication (38% of participants; P =.006), stress management therapy (35%; P =.003), or placebo (29%; P =.001).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 108, "doc_id": 6191684, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [6191684, 22995579, 23865182], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Amitriptyline is an effective treatment for chronic tension-type headaches.\n\nDocument title: Management of chronic tension-type headache with tricyclic antidepressant medication, stress management therapy, and their combination: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Chronic tension-type headaches are characterized by near-daily headaches and often are difficult to manage in primary practice.\n[1] Behavioral and pharmacological therapies each appear modestly effective, but data are lacking on their separate and combined effects.\n[2] OBJECTIVE To evaluate the clinical efficacy of behavioral and pharmacological therapies, singly and combined, for chronic tension-type headaches.\n[3] DESIGN AND SETTING Randomized placebo-controlled trial conducted from August 1995 to January 1998 at 2 outpatient sites in Ohio.\n[4] PARTICIPANTS Two hundred three adults (mean age, 37 years; 76% women) with diagnosis of chronic tension-type headaches (mean, 26 headache d/mo).\n[5] INTERVENTIONS Participants were randomly assigned to receive tricyclic antidepressant (amitriptyline hydrochloride, up to 100 mg/d, or nortriptyline hydrochloride, up to 75 mg/d) medication (n = 53), placebo (n = 48), stress management (eg, relaxation, cognitive coping) therapy (3 sessions and 2 telephone contacts) plus placebo (n = 49), or stress management therapy plus antidepressant medication (n = 53).\n[6] MAIN OUTCOME MEASURES Monthly headache index scores calculated as the mean of pain ratings (0-10 scale) recorded by participants in a daily diary 4 times per day; number of days per month with at least moderate pain (pain rating >/=5), analgesic medication use, and Headache Disability Inventory scores, compared by intervention group.\n[7] RESULTS Tricyclic antidepressant medication and stress management therapy each produced larger reductions in headache activity, analgesic medication use, and headache-related disability than placebo, but antidepressant medication yielded more rapid improvements in headache activity.\n[8] Combined therapy was more likely to produce clinically significant (>/=50%) reductions in headache index scores (64% of participants) than antidepressant medication (38% of participants; P =.006), stress management therapy (35%; P =.003), or placebo (29%; P =.001).\n[9] On other measures the combined therapy and its 2 component therapies produced similar outcomes.\n[10] CONCLUSIONS Our results indicate that antidepressant medication and stress management therapy are each modestly effective in treating chronic tension-type headaches.\n[11] Combined therapy may improve outcome relative to monotherapy."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"CONCLUSIONS Our results indicate that antidepressant medication and stress management therapy are each modestly effective in treating chronic tension-type headaches.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 108, "doc_id": 6191684, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [6191684, 22995579, 23865182], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Amitriptyline is an effective treatment for chronic tension-type headaches.\n\nDocument title: Amitriptyline is effective in chronic but not in episodic tension-type headache: pathogenetic implications.\n\nAbstract sentences:\n[0] The tricyclic antidepressant, amitriptyline, is an effective drug for the treatment of chronic tension-type headache and for other chronic pain syndromes, but it is also effective in the prophylaxis of an episodic type of headache such as migraine.\n[1] However, its efficacy in episodic tension-type headache has not yet been clarified.\n[2] We compared the efficacy of amitriptyline (25 mg/day) in 82 nondepressed patients with either chronic or episodic tension-type headache in an open-label study.\n[3] Amitriptyline significantly reduced (P < 0.05) frequency and duration of headache as well as analgesic consumption in chronic, but not in episodic, tension-type headache.\n[4] Further placebo-controlled trials, possibly with higher doses of amitriptyline, might confirm if the different pattern of response to amitriptyline can be explained in terms of different involvement of central nociception and of peripheral myofascial factors in the chronic and in the episodic forms of tension-type headache."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"The tricyclic antidepressant, amitriptyline, is an effective drug for the treatment of chronic tension-type headache and for other chronic pain syndromes, but it is also effective in the prophylaxis of an episodic type of headache such as migraine.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 108, "doc_id": 22995579, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [6191684, 22995579, 23865182], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Amitriptyline is an effective treatment for chronic tension-type headaches.\n\nDocument title: Amitriptyline is effective in chronic but not in episodic tension-type headache: pathogenetic implications.\n\nAbstract sentences:\n[0] The tricyclic antidepressant, amitriptyline, is an effective drug for the treatment of chronic tension-type headache and for other chronic pain syndromes, but it is also effective in the prophylaxis of an episodic type of headache such as migraine.\n[1] However, its efficacy in episodic tension-type headache has not yet been clarified.\n[2] We compared the efficacy of amitriptyline (25 mg/day) in 82 nondepressed patients with either chronic or episodic tension-type headache in an open-label study.\n[3] Amitriptyline significantly reduced (P < 0.05) frequency and duration of headache as well as analgesic consumption in chronic, but not in episodic, tension-type headache.\n[4] Further placebo-controlled trials, possibly with higher doses of amitriptyline, might confirm if the different pattern of response to amitriptyline can be explained in terms of different involvement of central nociception and of peripheral myofascial factors in the chronic and in the episodic forms of tension-type headache."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Amitriptyline significantly reduced (P < 0.05) frequency and duration of headache as well as analgesic consumption in chronic, but not in episodic, tension-type headache.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 108, "doc_id": 22995579, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [6191684, 22995579, 23865182], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Amitriptyline is an effective treatment for chronic tension-type headaches.\n\nDocument title: Efficacy and tolerability of amitriptylinoxide in the treatment of chronic tension-type headache: a multi-centre controlled study.\n\nAbstract sentences:\n[0] Amitriptyline is the medication of first choice in the treatment of chronic tension-type headache.\n[1] In 197 patients with chronic tension-type headache (87M and 110F with a mean age of 38 +/-\n[2] 13 (18-68)) efficacy and tolerability of 60-90 mg amitriptylinoxide (AO) were compared with 50-75 mg amitriptyline (AM) and placebo (PL) in a double-blind, parallel-group trial consisting of a four weeks' baseline phase and 12 weeks of treatment.\n[3] The primary study endpoint was a reduction of at least 50% of the product of headache duration and frequency and a reduction of at least 50% in headache intensity.\n[4] Statistics used were Fisher's exact test and analysis of variance.\n[5] No significant difference emerged between AO, AM and PL with respect to the primary study endpoint.\n[6] Treatment response occurred in 30.3% of the AO, 22.4% of the AM and 21.9% of the PL group.\n[7] A reduction in headache duration and frequency of at least 50% was found in 39.4% on AO, in 25.4% on AM and in 26.6% on PL (PAO-PL = .1384, PAM-PL = 1.000, PAO-AM = .0973).\n[8] A reduction in headache intensity of at least 50% was found in 31.8% on AO, in 26.9% on AM and in 26.6% on PL (PAO-PL = .5657, PAM-PL = 1.000, PAO-AM = .5715).\n[9] Trend analysis with respect to a significant reduction of headache intensity (p < 0.05) and the product of headache duration and frequency revealed a superior effect of AO.(ABSTRACT TRUNCATED AT 250 WORDS)"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Amitriptyline is the medication of first choice in the treatment of chronic tension-type headache.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 108, "doc_id": 23865182, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [6191684, 22995579, 23865182], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Amitriptyline is an effective treatment for chronic tension-type headaches.\n\nDocument title: Efficacy and tolerability of amitriptylinoxide in the treatment of chronic tension-type headache: a multi-centre controlled study.\n\nAbstract sentences:\n[0] Amitriptyline is the medication of first choice in the treatment of chronic tension-type headache.\n[1] In 197 patients with chronic tension-type headache (87M and 110F with a mean age of 38 +/-\n[2] 13 (18-68)) efficacy and tolerability of 60-90 mg amitriptylinoxide (AO) were compared with 50-75 mg amitriptyline (AM) and placebo (PL) in a double-blind, parallel-group trial consisting of a four weeks' baseline phase and 12 weeks of treatment.\n[3] The primary study endpoint was a reduction of at least 50% of the product of headache duration and frequency and a reduction of at least 50% in headache intensity.\n[4] Statistics used were Fisher's exact test and analysis of variance.\n[5] No significant difference emerged between AO, AM and PL with respect to the primary study endpoint.\n[6] Treatment response occurred in 30.3% of the AO, 22.4% of the AM and 21.9% of the PL group.\n[7] A reduction in headache duration and frequency of at least 50% was found in 39.4% on AO, in 25.4% on AM and in 26.6% on PL (PAO-PL = .1384, PAM-PL = 1.000, PAO-AM = .0973).\n[8] A reduction in headache intensity of at least 50% was found in 31.8% on AO, in 26.9% on AM and in 26.6% on PL (PAO-PL = .5657, PAM-PL = 1.000, PAO-AM = .5715).\n[9] Trend analysis with respect to a significant reduction of headache intensity (p < 0.05) and the product of headache duration and frequency revealed a superior effect of AO.(ABSTRACT TRUNCATED AT 250 WORDS)"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"The primary study endpoint was a reduction of at least 50% of the product of headache duration and frequency and a reduction of at least 50% in headache intensity.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 108, "doc_id": 23865182, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [6191684, 22995579, 23865182], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Amitriptyline is an effective treatment for chronic tension-type headaches.\n\nDocument title: Efficacy and tolerability of amitriptylinoxide in the treatment of chronic tension-type headache: a multi-centre controlled study.\n\nAbstract sentences:\n[0] Amitriptyline is the medication of first choice in the treatment of chronic tension-type headache.\n[1] In 197 patients with chronic tension-type headache (87M and 110F with a mean age of 38 +/-\n[2] 13 (18-68)) efficacy and tolerability of 60-90 mg amitriptylinoxide (AO) were compared with 50-75 mg amitriptyline (AM) and placebo (PL) in a double-blind, parallel-group trial consisting of a four weeks' baseline phase and 12 weeks of treatment.\n[3] The primary study endpoint was a reduction of at least 50% of the product of headache duration and frequency and a reduction of at least 50% in headache intensity.\n[4] Statistics used were Fisher's exact test and analysis of variance.\n[5] No significant difference emerged between AO, AM and PL with respect to the primary study endpoint.\n[6] Treatment response occurred in 30.3% of the AO, 22.4% of the AM and 21.9% of the PL group.\n[7] A reduction in headache duration and frequency of at least 50% was found in 39.4% on AO, in 25.4% on AM and in 26.6% on PL (PAO-PL = .1384, PAM-PL = 1.000, PAO-AM = .0973).\n[8] A reduction in headache intensity of at least 50% was found in 31.8% on AO, in 26.9% on AM and in 26.6% on PL (PAO-PL = .5657, PAM-PL = 1.000, PAO-AM = .5715).\n[9] Trend analysis with respect to a significant reduction of headache intensity (p < 0.05) and the product of headache duration and frequency revealed a superior effect of AO.(ABSTRACT TRUNCATED AT 250 WORDS)"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"A reduction in headache duration and frequency of at least 50% was found in 39.4% on AO, in 25.4% on AM and in 26.6% on PL (PAO-PL = .1384, PAM-PL = 1.000, PAO-AM = .0973).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 108, "doc_id": 23865182, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [6191684, 22995579, 23865182], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Amitriptyline is an effective treatment for chronic tension-type headaches.\n\nDocument title: Efficacy and tolerability of amitriptylinoxide in the treatment of chronic tension-type headache: a multi-centre controlled study.\n\nAbstract sentences:\n[0] Amitriptyline is the medication of first choice in the treatment of chronic tension-type headache.\n[1] In 197 patients with chronic tension-type headache (87M and 110F with a mean age of 38 +/-\n[2] 13 (18-68)) efficacy and tolerability of 60-90 mg amitriptylinoxide (AO) were compared with 50-75 mg amitriptyline (AM) and placebo (PL) in a double-blind, parallel-group trial consisting of a four weeks' baseline phase and 12 weeks of treatment.\n[3] The primary study endpoint was a reduction of at least 50% of the product of headache duration and frequency and a reduction of at least 50% in headache intensity.\n[4] Statistics used were Fisher's exact test and analysis of variance.\n[5] No significant difference emerged between AO, AM and PL with respect to the primary study endpoint.\n[6] Treatment response occurred in 30.3% of the AO, 22.4% of the AM and 21.9% of the PL group.\n[7] A reduction in headache duration and frequency of at least 50% was found in 39.4% on AO, in 25.4% on AM and in 26.6% on PL (PAO-PL = .1384, PAM-PL = 1.000, PAO-AM = .0973).\n[8] A reduction in headache intensity of at least 50% was found in 31.8% on AO, in 26.9% on AM and in 26.6% on PL (PAO-PL = .5657, PAM-PL = 1.000, PAO-AM = .5715).\n[9] Trend analysis with respect to a significant reduction of headache intensity (p < 0.05) and the product of headache duration and frequency revealed a superior effect of AO.(ABSTRACT TRUNCATED AT 250 WORDS)"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"A reduction in headache intensity of at least 50% was found in 31.8% on AO, in 26.9% on AM and in 26.6% on PL (PAO-PL = .5657, PAM-PL = 1.000, PAO-AM = .5715).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 108, "doc_id": 23865182, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [6191684, 22995579, 23865182], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: An M2-like phenotype in brown adipose tissue macrophages is quickly induced by cold exposure.\n\nDocument title: Alternatively activated macrophages produce catecholamines to sustain adaptive thermogenesis\n\nAbstract sentences:\n[0] All homeotherms use thermogenesis to maintain their core body temperature, ensuring that cellular functions and physiological processes can continue in cold environments.\n[1] In the prevailing model of thermogenesis, when the hypothalamus senses cold temperatures it triggers sympathetic discharge, resulting in the release of noradrenaline in brown adipose tissue and white adipose tissue.\n[2] Acting via the β(3)-adrenergic receptors, noradrenaline induces lipolysis in white adipocytes, whereas it stimulates the expression of thermogenic genes, such as PPAR-γ coactivator 1a (Ppargc1a), uncoupling protein 1 (Ucp1) and acyl-CoA synthetase long-chain family member 1 (Acsl1), in brown adipocytes.\n[3] However, the precise nature of all the cell types involved in this efferent loop is not well established.\n[4] Here we report in mice an unexpected requirement for the interleukin-4 (IL-4)-stimulated program of alternative macrophage activation in adaptive thermogenesis.\n[5] Exposure to cold temperature rapidly promoted alternative activation of adipose tissue macrophages, which secrete catecholamines to induce thermogenic gene expression in brown adipose tissue and lipolysis in white adipose tissue.\n[6] Absence of alternatively activated macrophages impaired metabolic adaptations to cold, whereas administration of IL-4 increased thermogenic gene expression, fatty acid mobilization and energy expenditure, all in a macrophage-dependent manner.\n[7] Thus, we have discovered a role for alternatively activated macrophages in the orchestration of an important mammalian stress response, the response to cold."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Exposure to cold temperature rapidly promoted alternative activation of adipose tissue macrophages, which secrete catecholamines to induce thermogenic gene expression in brown adipose tissue and lipolysis in white adipose tissue.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 109, "doc_id": 4319174, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [4319174], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Androgenetic haploid mouse embryonic stem cells (ESCs) can be derived and genetically manipulated in vitro.\n\nDocument title: Generation of Genetically Modified Mice by Oocyte Injection of Androgenetic Haploid Embryonic Stem Cells\n\nAbstract sentences:\n[0] Haploid cells are amenable for genetic analysis.\n[1] Recent success in the derivation of mouse haploid embryonic stem cells (haESCs) via parthenogenesis has enabled genetic screening in mammalian cells.\n[2] However, successful generation of live animals from these haESCs, which is needed to extend the genetic analysis to the organism level, has not been achieved.\n[3] Here, we report the derivation of haESCs from androgenetic blastocysts.\n[4] These cells, designated as AG-haESCs, partially maintain paternal imprints, express classical ESC pluripotency markers, and contribute to various tissues, including the germline, upon injection into diploid blastocysts.\n[5] Strikingly, live mice can be obtained upon injection of AG-haESCs into MII oocytes, and these mice bear haESC-carried genetic traits and develop into fertile adults.\n[6] Furthermore, gene targeting via homologous recombination is feasible in the AG-haESCs.\n[7] Our results demonstrate that AG-haESCs can be used as a genetically tractable fertilization agent for the production of live animals via injection into oocytes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Strikingly, live mice can be obtained upon injection of AG-haESCs into MII oocytes, and these mice bear haESC-carried genetic traits and develop into fertile adults.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 111, "doc_id": 13513790, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [13513790], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Androgenetic haploid mouse embryonic stem cells (ESCs) can be derived and genetically manipulated in vitro.\n\nDocument title: Generation of Genetically Modified Mice by Oocyte Injection of Androgenetic Haploid Embryonic Stem Cells\n\nAbstract sentences:\n[0] Haploid cells are amenable for genetic analysis.\n[1] Recent success in the derivation of mouse haploid embryonic stem cells (haESCs) via parthenogenesis has enabled genetic screening in mammalian cells.\n[2] However, successful generation of live animals from these haESCs, which is needed to extend the genetic analysis to the organism level, has not been achieved.\n[3] Here, we report the derivation of haESCs from androgenetic blastocysts.\n[4] These cells, designated as AG-haESCs, partially maintain paternal imprints, express classical ESC pluripotency markers, and contribute to various tissues, including the germline, upon injection into diploid blastocysts.\n[5] Strikingly, live mice can be obtained upon injection of AG-haESCs into MII oocytes, and these mice bear haESC-carried genetic traits and develop into fertile adults.\n[6] Furthermore, gene targeting via homologous recombination is feasible in the AG-haESCs.\n[7] Our results demonstrate that AG-haESCs can be used as a genetically tractable fertilization agent for the production of live animals via injection into oocytes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Our results demonstrate that AG-haESCs can be used as a genetically tractable fertilization agent for the production of live animals via injection into oocytes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 111, "doc_id": 13513790, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [13513790], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Angiotensin converting enzyme inhibitors are associated with decreased risk for functional renal insufficiency.\n\nDocument title: Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association.\n\nAbstract sentences:\n[0] Angiotensin converting enzyme (ACE) inhibitors are now one of the most frequently used classes of antihypertensive drugs.\n[1] Beyond their utility in the management of hypertension, their use has been extended to the long-term management of patients with congestive heart failure (CHF), as well as diabetic and nondiabetic nephropathies.\n[2] Although ACE inhibitor therapy usually improves renal blood flow (RBF) and sodium excretion rates in CHF and reduces the rate of progressive renal injury in chronic renal disease, its use can also be associated with a syndrome of “functional renal insufficiency” and/or hyperkalemia.\n[3] This form of acute renal failure (ARF) most commonly develops shortly after initiation of ACE inhibitor therapy but can be observed after months or years of therapy, even in the absence of prior ill effects.\n[4] ARF is most likely to occur when renal perfusion pressure cannot be sustained because of substantial decreases in mean arterial pressure (MAP) or when glomerular filtration rate (GFR) is highly angiotensin II (Ang II) dependent.\n[5] Conditions that predict an adverse hemodynamic effect of ACE inhibitors in patients with CHF are preexisting hypotension and low cardiac filling pressures.\n[6] The GFR is especially dependent on Ang II during extracellular fluid (ECF) volume depletion, high-grade bilateral renal artery stenosis, or stenosis of a dominant or single kidney, as in a renal transplant recipient.\n[7] Understanding the pathophysiological mechanisms and the common risk factors for ACE inhibitor–induced functional ARF is critical, because preventive strategies for ARF exist, and if effectively used, they may permit use of these compounds in a less restricted fashion.\n[8] Under normal physiological conditions, renal autoregulation adjusts renal vascular resistance, so that RBF and GFR remain constant over a wide range of MAPs.1 The intrinsic renal autoregulation mechanism is adjusted by Ang II and the sympathetic nervous system.\n[9] When renal perfusion pressure falls (as in …"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Although ACE inhibitor therapy usually improves renal blood flow (RBF) and sodium excretion rates in CHF and reduces the rate of progressive renal injury in chronic renal disease, its use can also be associated with a syndrome of “functional renal insufficiency” and/or hyperkalemia.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 112, "doc_id": 6157837, "label": "CONTRADICTS", "evidence_sentence_ids": [2], "cited_doc_ids": [6157837], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Angiotensin converting enzyme inhibitors are associated with decreased risk for functional renal insufficiency.\n\nDocument title: Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association.\n\nAbstract sentences:\n[0] Angiotensin converting enzyme (ACE) inhibitors are now one of the most frequently used classes of antihypertensive drugs.\n[1] Beyond their utility in the management of hypertension, their use has been extended to the long-term management of patients with congestive heart failure (CHF), as well as diabetic and nondiabetic nephropathies.\n[2] Although ACE inhibitor therapy usually improves renal blood flow (RBF) and sodium excretion rates in CHF and reduces the rate of progressive renal injury in chronic renal disease, its use can also be associated with a syndrome of “functional renal insufficiency” and/or hyperkalemia.\n[3] This form of acute renal failure (ARF) most commonly develops shortly after initiation of ACE inhibitor therapy but can be observed after months or years of therapy, even in the absence of prior ill effects.\n[4] ARF is most likely to occur when renal perfusion pressure cannot be sustained because of substantial decreases in mean arterial pressure (MAP) or when glomerular filtration rate (GFR) is highly angiotensin II (Ang II) dependent.\n[5] Conditions that predict an adverse hemodynamic effect of ACE inhibitors in patients with CHF are preexisting hypotension and low cardiac filling pressures.\n[6] The GFR is especially dependent on Ang II during extracellular fluid (ECF) volume depletion, high-grade bilateral renal artery stenosis, or stenosis of a dominant or single kidney, as in a renal transplant recipient.\n[7] Understanding the pathophysiological mechanisms and the common risk factors for ACE inhibitor–induced functional ARF is critical, because preventive strategies for ARF exist, and if effectively used, they may permit use of these compounds in a less restricted fashion.\n[8] Under normal physiological conditions, renal autoregulation adjusts renal vascular resistance, so that RBF and GFR remain constant over a wide range of MAPs.1 The intrinsic renal autoregulation mechanism is adjusted by Ang II and the sympathetic nervous system.\n[9] When renal perfusion pressure falls (as in …"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Understanding the pathophysiological mechanisms and the common risk factors for ACE inhibitor–induced functional ARF is critical, because preventive strategies for ARF exist, and if effectively used, they may permit use of these compounds in a less restricted fashion.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 112, "doc_id": 6157837, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [6157837], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Anthrax spores are very difficult to dispose once they are dispersed.\n\nDocument title: Secondary aerosolization of viable Bacillus anthracis spores in a contaminated US Senate Office.\n\nAbstract sentences:\n[0] CONTEXT Bioterrorist attacks involving letters and mail-handling systems in Washington, DC, resulted in Bacillus anthracis (anthrax) spore contamination in the Hart Senate Office Building and other facilities in the US Capitol's vicinity.\n[1] OBJECTIVE To provide information about the nature and extent of indoor secondary aerosolization of B anthracis spores.\n[2] DESIGN Stationary and personal air samples, surface dust, and swab samples were collected under semiquiescent (minimal activities) and then simulated active office conditions to estimate secondary aerosolization of B anthracis spores.\n[3] Nominal size characteristics, airborne concentrations, and surface contamination of B anthracis particles (colony-forming units) were evaluated.\n[4] RESULTS Viable B anthracis spores reaerosolized under semiquiescent conditions, with a marked increase in reaerosolization during simulated active office conditions.\n[5] Increases were observed for B anthracis collected on open sheep blood agar plates (P<.001) and personal air monitors (P =.01) during active office conditions.\n[6] More than 80% of the B anthracis particles collected on stationary monitors were within an alveolar respirable size range of 0.95 to 3.5 micro m.   CONCLUSIONS Bacillus anthracis spores used in a recent terrorist incident reaerosolized under common office activities.\n[7] These findings have important implications for appropriate respiratory protection, remediation, and reoccupancy of contaminated office environments."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"More than 80% of the B anthracis particles collected on stationary monitors were within an alveolar respirable size range of 0.95 to 3.5 micro m.   CONCLUSIONS Bacillus anthracis spores used in a recent terrorist incident reaerosolized under common office activities.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 114, "doc_id": 33872649, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [33872649], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Anthrax spores remain deadly until affected areas are decontaminated.\n\nDocument title: Secondary aerosolization of viable Bacillus anthracis spores in a contaminated US Senate Office.\n\nAbstract sentences:\n[0] CONTEXT Bioterrorist attacks involving letters and mail-handling systems in Washington, DC, resulted in Bacillus anthracis (anthrax) spore contamination in the Hart Senate Office Building and other facilities in the US Capitol's vicinity.\n[1] OBJECTIVE To provide information about the nature and extent of indoor secondary aerosolization of B anthracis spores.\n[2] DESIGN Stationary and personal air samples, surface dust, and swab samples were collected under semiquiescent (minimal activities) and then simulated active office conditions to estimate secondary aerosolization of B anthracis spores.\n[3] Nominal size characteristics, airborne concentrations, and surface contamination of B anthracis particles (colony-forming units) were evaluated.\n[4] RESULTS Viable B anthracis spores reaerosolized under semiquiescent conditions, with a marked increase in reaerosolization during simulated active office conditions.\n[5] Increases were observed for B anthracis collected on open sheep blood agar plates (P<.001) and personal air monitors (P =.01) during active office conditions.\n[6] More than 80% of the B anthracis particles collected on stationary monitors were within an alveolar respirable size range of 0.95 to 3.5 micro m.   CONCLUSIONS Bacillus anthracis spores used in a recent terrorist incident reaerosolized under common office activities.\n[7] These findings have important implications for appropriate respiratory protection, remediation, and reoccupancy of contaminated office environments."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"More than 80% of the B anthracis particles collected on stationary monitors were within an alveolar respirable size range of 0.95 to 3.5 micro m.   CONCLUSIONS Bacillus anthracis spores used in a recent terrorist incident reaerosolized under common office activities.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 116, "doc_id": 33872649, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [33872649], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Antidepressants increase the severity of migraines.\n\nDocument title: Tricyclic antidepressants and headaches: systematic review and meta-analysis\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate the efficacy and relative adverse effects of tricyclic antidepressants in the treatment of migraine, tension-type, and mixed headaches.\n[1] DESIGN Meta-analysis.\n[2] DATA SOURCES Medline, Embase, the Cochrane Trials Registry, and PsycLIT.\n[3] Studies reviewed Randomised trials of adults receiving tricyclics as only treatment for a minimum of four weeks.\n[4] DATA EXTRACTION Frequency of headaches (number of headache attacks for migraine and number of days with headache for tension-type headaches), intensity of headache, and headache index.\n[5] RESULTS 37 studies met the inclusion criteria.\n[6] Tricyclics significantly reduced the number of days with tension-type headache and number of headache attacks from migraine than placebo (average standardised mean difference -1.29, 95% confidence interval -2.18 to -0.39 and -0.70, -0.93 to -0.48) but not compared with selective serotonin reuptake inhibitors (-0.80, -2.63 to 0.02 and -0.20, -0.60 to 0.19).\n[7] The effect of tricyclics increased with longer duration of treatment (β=-0.11, 95% confidence interval -0.63 to -0.15; P<0.0005).\n[8] Tricyclics were also more likely to reduce the intensity of headaches by at least 50% than either placebo (tension-type: relative risk 1.41, 95% confidence interval 1.02 to 1.89; migraine: 1.80, 1.24 to 2.62) or selective serotonin reuptake inhibitors (1.73, 1.34 to 2.22 and 1.72, 1.15 to 2.55).\n[9] Tricyclics were more likely to cause adverse effects than placebo (1.53, 95% confidence interval 1.11 to 2.12) and selective serotonin reuptake inhibitors (2.22, 1.52 to 3.32), including dry mouth (P<0.0005 for both), drowsiness (P<0.0005 for both), and weight gain (P<0.001 for both), but did not increase dropout rates (placebo: 1.22, 0.83 to 1.80, selective serotonin reuptake inhibitors: 1.16, 0.81 to 2.97).\n[10] CONCLUSIONS Tricyclic antidepressants are effective in preventing migraine and tension-type headaches and are more effective than selective serotonin reuptake inhibitors, although with greater adverse effects.\n[11] The effectiveness of tricyclics seems to increase over time."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Tricyclics significantly reduced the number of days with tension-type headache and number of headache attacks from migraine than placebo (average standardised mean difference -1.29, 95% confidence interval -2.18 to -0.39 and -0.70, -0.93 to -0.48) but not compared with selective serotonin reuptake inhibitors (-0.80, -2.63 to 0.02 and -0.20, -0.60 to 0.19).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 119, "doc_id": 14606752, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [14606752], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Antidepressants increase the severity of migraines.\n\nDocument title: Tricyclic antidepressants and headaches: systematic review and meta-analysis\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate the efficacy and relative adverse effects of tricyclic antidepressants in the treatment of migraine, tension-type, and mixed headaches.\n[1] DESIGN Meta-analysis.\n[2] DATA SOURCES Medline, Embase, the Cochrane Trials Registry, and PsycLIT.\n[3] Studies reviewed Randomised trials of adults receiving tricyclics as only treatment for a minimum of four weeks.\n[4] DATA EXTRACTION Frequency of headaches (number of headache attacks for migraine and number of days with headache for tension-type headaches), intensity of headache, and headache index.\n[5] RESULTS 37 studies met the inclusion criteria.\n[6] Tricyclics significantly reduced the number of days with tension-type headache and number of headache attacks from migraine than placebo (average standardised mean difference -1.29, 95% confidence interval -2.18 to -0.39 and -0.70, -0.93 to -0.48) but not compared with selective serotonin reuptake inhibitors (-0.80, -2.63 to 0.02 and -0.20, -0.60 to 0.19).\n[7] The effect of tricyclics increased with longer duration of treatment (β=-0.11, 95% confidence interval -0.63 to -0.15; P<0.0005).\n[8] Tricyclics were also more likely to reduce the intensity of headaches by at least 50% than either placebo (tension-type: relative risk 1.41, 95% confidence interval 1.02 to 1.89; migraine: 1.80, 1.24 to 2.62) or selective serotonin reuptake inhibitors (1.73, 1.34 to 2.22 and 1.72, 1.15 to 2.55).\n[9] Tricyclics were more likely to cause adverse effects than placebo (1.53, 95% confidence interval 1.11 to 2.12) and selective serotonin reuptake inhibitors (2.22, 1.52 to 3.32), including dry mouth (P<0.0005 for both), drowsiness (P<0.0005 for both), and weight gain (P<0.001 for both), but did not increase dropout rates (placebo: 1.22, 0.83 to 1.80, selective serotonin reuptake inhibitors: 1.16, 0.81 to 2.97).\n[10] CONCLUSIONS Tricyclic antidepressants are effective in preventing migraine and tension-type headaches and are more effective than selective serotonin reuptake inhibitors, although with greater adverse effects.\n[11] The effectiveness of tricyclics seems to increase over time."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Tricyclics were also more likely to reduce the intensity of headaches by at least 50% than either placebo (tension-type: relative risk 1.41, 95% confidence interval 1.02 to 1.89; migraine: 1.80, 1.24 to 2.62) or selective serotonin reuptake inhibitors (1.73, 1.34 to 2.22 and 1.72, 1.15 to 2.55).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 119, "doc_id": 14606752, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [14606752], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Antidepressants increase the severity of migraines.\n\nDocument title: Tricyclic antidepressants and headaches: systematic review and meta-analysis\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate the efficacy and relative adverse effects of tricyclic antidepressants in the treatment of migraine, tension-type, and mixed headaches.\n[1] DESIGN Meta-analysis.\n[2] DATA SOURCES Medline, Embase, the Cochrane Trials Registry, and PsycLIT.\n[3] Studies reviewed Randomised trials of adults receiving tricyclics as only treatment for a minimum of four weeks.\n[4] DATA EXTRACTION Frequency of headaches (number of headache attacks for migraine and number of days with headache for tension-type headaches), intensity of headache, and headache index.\n[5] RESULTS 37 studies met the inclusion criteria.\n[6] Tricyclics significantly reduced the number of days with tension-type headache and number of headache attacks from migraine than placebo (average standardised mean difference -1.29, 95% confidence interval -2.18 to -0.39 and -0.70, -0.93 to -0.48) but not compared with selective serotonin reuptake inhibitors (-0.80, -2.63 to 0.02 and -0.20, -0.60 to 0.19).\n[7] The effect of tricyclics increased with longer duration of treatment (β=-0.11, 95% confidence interval -0.63 to -0.15; P<0.0005).\n[8] Tricyclics were also more likely to reduce the intensity of headaches by at least 50% than either placebo (tension-type: relative risk 1.41, 95% confidence interval 1.02 to 1.89; migraine: 1.80, 1.24 to 2.62) or selective serotonin reuptake inhibitors (1.73, 1.34 to 2.22 and 1.72, 1.15 to 2.55).\n[9] Tricyclics were more likely to cause adverse effects than placebo (1.53, 95% confidence interval 1.11 to 2.12) and selective serotonin reuptake inhibitors (2.22, 1.52 to 3.32), including dry mouth (P<0.0005 for both), drowsiness (P<0.0005 for both), and weight gain (P<0.001 for both), but did not increase dropout rates (placebo: 1.22, 0.83 to 1.80, selective serotonin reuptake inhibitors: 1.16, 0.81 to 2.97).\n[10] CONCLUSIONS Tricyclic antidepressants are effective in preventing migraine and tension-type headaches and are more effective than selective serotonin reuptake inhibitors, although with greater adverse effects.\n[11] The effectiveness of tricyclics seems to increase over time."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"CONCLUSIONS Tricyclic antidepressants are effective in preventing migraine and tension-type headaches and are more effective than selective serotonin reuptake inhibitors, although with greater adverse effects.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 119, "doc_id": 14606752, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [14606752], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Antidepressants reduce the severity of migraines.\n\nDocument title: Tricyclic antidepressants and headaches: systematic review and meta-analysis\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate the efficacy and relative adverse effects of tricyclic antidepressants in the treatment of migraine, tension-type, and mixed headaches.\n[1] DESIGN Meta-analysis.\n[2] DATA SOURCES Medline, Embase, the Cochrane Trials Registry, and PsycLIT.\n[3] Studies reviewed Randomised trials of adults receiving tricyclics as only treatment for a minimum of four weeks.\n[4] DATA EXTRACTION Frequency of headaches (number of headache attacks for migraine and number of days with headache for tension-type headaches), intensity of headache, and headache index.\n[5] RESULTS 37 studies met the inclusion criteria.\n[6] Tricyclics significantly reduced the number of days with tension-type headache and number of headache attacks from migraine than placebo (average standardised mean difference -1.29, 95% confidence interval -2.18 to -0.39 and -0.70, -0.93 to -0.48) but not compared with selective serotonin reuptake inhibitors (-0.80, -2.63 to 0.02 and -0.20, -0.60 to 0.19).\n[7] The effect of tricyclics increased with longer duration of treatment (β=-0.11, 95% confidence interval -0.63 to -0.15; P<0.0005).\n[8] Tricyclics were also more likely to reduce the intensity of headaches by at least 50% than either placebo (tension-type: relative risk 1.41, 95% confidence interval 1.02 to 1.89; migraine: 1.80, 1.24 to 2.62) or selective serotonin reuptake inhibitors (1.73, 1.34 to 2.22 and 1.72, 1.15 to 2.55).\n[9] Tricyclics were more likely to cause adverse effects than placebo (1.53, 95% confidence interval 1.11 to 2.12) and selective serotonin reuptake inhibitors (2.22, 1.52 to 3.32), including dry mouth (P<0.0005 for both), drowsiness (P<0.0005 for both), and weight gain (P<0.001 for both), but did not increase dropout rates (placebo: 1.22, 0.83 to 1.80, selective serotonin reuptake inhibitors: 1.16, 0.81 to 2.97).\n[10] CONCLUSIONS Tricyclic antidepressants are effective in preventing migraine and tension-type headaches and are more effective than selective serotonin reuptake inhibitors, although with greater adverse effects.\n[11] The effectiveness of tricyclics seems to increase over time."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Tricyclics significantly reduced the number of days with tension-type headache and number of headache attacks from migraine than placebo (average standardised mean difference -1.29, 95% confidence interval -2.18 to -0.39 and -0.70, -0.93 to -0.48) but not compared with selective serotonin reuptake inhibitors (-0.80, -2.63 to 0.02 and -0.20, -0.60 to 0.19).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 120, "doc_id": 14606752, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [14606752], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Antidepressants reduce the severity of migraines.\n\nDocument title: Tricyclic antidepressants and headaches: systematic review and meta-analysis\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate the efficacy and relative adverse effects of tricyclic antidepressants in the treatment of migraine, tension-type, and mixed headaches.\n[1] DESIGN Meta-analysis.\n[2] DATA SOURCES Medline, Embase, the Cochrane Trials Registry, and PsycLIT.\n[3] Studies reviewed Randomised trials of adults receiving tricyclics as only treatment for a minimum of four weeks.\n[4] DATA EXTRACTION Frequency of headaches (number of headache attacks for migraine and number of days with headache for tension-type headaches), intensity of headache, and headache index.\n[5] RESULTS 37 studies met the inclusion criteria.\n[6] Tricyclics significantly reduced the number of days with tension-type headache and number of headache attacks from migraine than placebo (average standardised mean difference -1.29, 95% confidence interval -2.18 to -0.39 and -0.70, -0.93 to -0.48) but not compared with selective serotonin reuptake inhibitors (-0.80, -2.63 to 0.02 and -0.20, -0.60 to 0.19).\n[7] The effect of tricyclics increased with longer duration of treatment (β=-0.11, 95% confidence interval -0.63 to -0.15; P<0.0005).\n[8] Tricyclics were also more likely to reduce the intensity of headaches by at least 50% than either placebo (tension-type: relative risk 1.41, 95% confidence interval 1.02 to 1.89; migraine: 1.80, 1.24 to 2.62) or selective serotonin reuptake inhibitors (1.73, 1.34 to 2.22 and 1.72, 1.15 to 2.55).\n[9] Tricyclics were more likely to cause adverse effects than placebo (1.53, 95% confidence interval 1.11 to 2.12) and selective serotonin reuptake inhibitors (2.22, 1.52 to 3.32), including dry mouth (P<0.0005 for both), drowsiness (P<0.0005 for both), and weight gain (P<0.001 for both), but did not increase dropout rates (placebo: 1.22, 0.83 to 1.80, selective serotonin reuptake inhibitors: 1.16, 0.81 to 2.97).\n[10] CONCLUSIONS Tricyclic antidepressants are effective in preventing migraine and tension-type headaches and are more effective than selective serotonin reuptake inhibitors, although with greater adverse effects.\n[11] The effectiveness of tricyclics seems to increase over time."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Tricyclics were also more likely to reduce the intensity of headaches by at least 50% than either placebo (tension-type: relative risk 1.41, 95% confidence interval 1.02 to 1.89; migraine: 1.80, 1.24 to 2.62) or selective serotonin reuptake inhibitors (1.73, 1.34 to 2.22 and 1.72, 1.15 to 2.55).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 120, "doc_id": 14606752, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [14606752], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Antidepressants reduce the severity of migraines.\n\nDocument title: Tricyclic antidepressants and headaches: systematic review and meta-analysis\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate the efficacy and relative adverse effects of tricyclic antidepressants in the treatment of migraine, tension-type, and mixed headaches.\n[1] DESIGN Meta-analysis.\n[2] DATA SOURCES Medline, Embase, the Cochrane Trials Registry, and PsycLIT.\n[3] Studies reviewed Randomised trials of adults receiving tricyclics as only treatment for a minimum of four weeks.\n[4] DATA EXTRACTION Frequency of headaches (number of headache attacks for migraine and number of days with headache for tension-type headaches), intensity of headache, and headache index.\n[5] RESULTS 37 studies met the inclusion criteria.\n[6] Tricyclics significantly reduced the number of days with tension-type headache and number of headache attacks from migraine than placebo (average standardised mean difference -1.29, 95% confidence interval -2.18 to -0.39 and -0.70, -0.93 to -0.48) but not compared with selective serotonin reuptake inhibitors (-0.80, -2.63 to 0.02 and -0.20, -0.60 to 0.19).\n[7] The effect of tricyclics increased with longer duration of treatment (β=-0.11, 95% confidence interval -0.63 to -0.15; P<0.0005).\n[8] Tricyclics were also more likely to reduce the intensity of headaches by at least 50% than either placebo (tension-type: relative risk 1.41, 95% confidence interval 1.02 to 1.89; migraine: 1.80, 1.24 to 2.62) or selective serotonin reuptake inhibitors (1.73, 1.34 to 2.22 and 1.72, 1.15 to 2.55).\n[9] Tricyclics were more likely to cause adverse effects than placebo (1.53, 95% confidence interval 1.11 to 2.12) and selective serotonin reuptake inhibitors (2.22, 1.52 to 3.32), including dry mouth (P<0.0005 for both), drowsiness (P<0.0005 for both), and weight gain (P<0.001 for both), but did not increase dropout rates (placebo: 1.22, 0.83 to 1.80, selective serotonin reuptake inhibitors: 1.16, 0.81 to 2.97).\n[10] CONCLUSIONS Tricyclic antidepressants are effective in preventing migraine and tension-type headaches and are more effective than selective serotonin reuptake inhibitors, although with greater adverse effects.\n[11] The effectiveness of tricyclics seems to increase over time."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"CONCLUSIONS Tricyclic antidepressants are effective in preventing migraine and tension-type headaches and are more effective than selective serotonin reuptake inhibitors, although with greater adverse effects.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 120, "doc_id": 14606752, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [14606752], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Antimicrobial agents are less effective due to the pressure of antimicrobial usage.\n\nDocument title: Resistance to antimicrobials in humans and animals.\n\nAbstract sentences:\n[0] Overusing antibiotics is not the only cause and reducing use is not the only solution   W arning signs of antimicrobial resistance, chinks in the antimicrobial armour, began to appear in the middle of the last century, and by the 1990s various reports had signalled the dangers of excessive or inappropriate use of antibiotics in clinical medicine and of the use of antibiotics in animal feed as growth promoters.1–3 Overuse of antimicrobials emerged as the main culprit, and reducing their use was seen as the answer.\n[1] But it may not be that simple.\n[2] The idea that reducing antibiotic use would redress the problem formed part of a positive response on the part of the United Kingdom government to the House of Lords report,1 including a public information campaign, surveillance of resistance along the food chain, targets with respect to hospital acquired infections, and setting up of an overarching advisory body on all aspects of antibiotic use.\n[3] However, the concept of overuse has proved too simplistic, for, although the evidence of overprescribing as the …"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Overusing antibiotics is not the only cause and reducing use is not the only solution   W arning signs of antimicrobial resistance, chinks in the antimicrobial armour, began to appear in the middle of the last century, and by the 1990s various reports had signalled the dangers of excessive or inappropriate use of antibiotics in clinical medicine and of the use of antibiotics in animal feed as growth promoters.1–3 Overuse of antimicrobials emerged as the main culprit, and reducing their use was seen as the answer.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 121, "doc_id": 31460499, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [31460499], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Antimicrobial agents are more effective due to the pressure of antimicrobial usage.\n\nDocument title: Resistance to antimicrobials in humans and animals.\n\nAbstract sentences:\n[0] Overusing antibiotics is not the only cause and reducing use is not the only solution   W arning signs of antimicrobial resistance, chinks in the antimicrobial armour, began to appear in the middle of the last century, and by the 1990s various reports had signalled the dangers of excessive or inappropriate use of antibiotics in clinical medicine and of the use of antibiotics in animal feed as growth promoters.1–3 Overuse of antimicrobials emerged as the main culprit, and reducing their use was seen as the answer.\n[1] But it may not be that simple.\n[2] The idea that reducing antibiotic use would redress the problem formed part of a positive response on the part of the United Kingdom government to the House of Lords report,1 including a public information campaign, surveillance of resistance along the food chain, targets with respect to hospital acquired infections, and setting up of an overarching advisory body on all aspects of antibiotic use.\n[3] However, the concept of overuse has proved too simplistic, for, although the evidence of overprescribing as the …"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Overusing antibiotics is not the only cause and reducing use is not the only solution   W arning signs of antimicrobial resistance, chinks in the antimicrobial armour, began to appear in the middle of the last century, and by the 1990s various reports had signalled the dangers of excessive or inappropriate use of antibiotics in clinical medicine and of the use of antibiotics in animal feed as growth promoters.1–3 Overuse of antimicrobials emerged as the main culprit, and reducing their use was seen as the answer.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 122, "doc_id": 31460499, "label": "CONTRADICTS", "evidence_sentence_ids": [0], "cited_doc_ids": [31460499], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Antiretroviral therapy increases rates of tuberculosis across a broad range of CD4 strata.\n\nDocument title: Antiretroviral Therapy for Prevention of Tuberculosis in Adults with HIV: A Systematic Review and Meta-Analysis\n\nAbstract sentences:\n[0] BACKGROUND Human immunodeficiency virus (HIV) infection is the strongest risk factor for developing tuberculosis and has fuelled its resurgence, especially in sub-Saharan Africa.\n[1] In 2010, there were an estimated 1.1 million incident cases of tuberculosis among the 34 million people living with HIV worldwide.\n[2] Antiretroviral therapy has substantial potential to prevent HIV-associated tuberculosis.\n[3] We conducted a systematic review of studies that analysed the impact of antiretroviral therapy on the incidence of tuberculosis in adults with HIV infection.\n[4] METHODS AND FINDINGS PubMed, Embase, African Index Medicus, LILACS, and clinical trial registries were systematically searched.\n[5] Randomised controlled trials, prospective cohort studies, and retrospective cohort studies were included if they compared tuberculosis incidence by antiretroviral therapy status in HIV-infected adults for a median of over 6 mo in developing countries.\n[6] For the meta-analyses there were four categories based on CD4 counts at antiretroviral therapy initiation: (1) less than 200 cells/µl, (2) 200 to 350 cells/µl, (3) greater than 350 cells/µl, and (4) any CD4 count.\n[7] Eleven studies met the inclusion criteria.\n[8] Antiretroviral therapy is strongly associated with a reduction in the incidence of tuberculosis in all baseline CD4 count categories: (1) less than 200 cells/µl (hazard ratio [HR] 0.16, 95% confidence interval [CI] 0.07 to 0.36), (2) 200 to 350 cells/µl (HR 0.34, 95% CI 0.19 to 0.60), (3) greater than 350 cells/µl (HR 0.43, 95% CI 0.30 to 0.63), and (4) any CD4 count (HR 0.35, 95% CI 0.28 to 0.44).\n[9] There was no evidence of hazard ratio modification with respect to baseline CD4 count category (p = 0.20).\n[10] CONCLUSIONS Antiretroviral therapy is strongly associated with a reduction in the incidence of tuberculosis across all CD4 count strata.\n[11] Earlier initiation of antiretroviral therapy may be a key component of global and national strategies to control the HIV-associated tuberculosis syndemic.\n[12] REVIEW REGISTRATION International Prospective Register of Systematic Reviews CRD42011001209 Please see later in the article for the Editors' Summary."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Antiretroviral therapy is strongly associated with a reduction in the incidence of tuberculosis in all baseline CD4 count categories: (1) less than 200 cells/µl (hazard ratio [HR] 0.16, 95% confidence interval [CI] 0.07 to 0.36), (2) 200 to 350 cells/µl (HR 0.34, 95% CI 0.19 to 0.60), (3) greater than 350 cells/µl (HR 0.43, 95% CI 0.30 to 0.63), and (4) any CD4 count (HR 0.35, 95% CI 0.28 to 0.44).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 123, "doc_id": 4883040, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [4883040], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Antiretroviral therapy increases rates of tuberculosis across a broad range of CD4 strata.\n\nDocument title: Antiretroviral Therapy for Prevention of Tuberculosis in Adults with HIV: A Systematic Review and Meta-Analysis\n\nAbstract sentences:\n[0] BACKGROUND Human immunodeficiency virus (HIV) infection is the strongest risk factor for developing tuberculosis and has fuelled its resurgence, especially in sub-Saharan Africa.\n[1] In 2010, there were an estimated 1.1 million incident cases of tuberculosis among the 34 million people living with HIV worldwide.\n[2] Antiretroviral therapy has substantial potential to prevent HIV-associated tuberculosis.\n[3] We conducted a systematic review of studies that analysed the impact of antiretroviral therapy on the incidence of tuberculosis in adults with HIV infection.\n[4] METHODS AND FINDINGS PubMed, Embase, African Index Medicus, LILACS, and clinical trial registries were systematically searched.\n[5] Randomised controlled trials, prospective cohort studies, and retrospective cohort studies were included if they compared tuberculosis incidence by antiretroviral therapy status in HIV-infected adults for a median of over 6 mo in developing countries.\n[6] For the meta-analyses there were four categories based on CD4 counts at antiretroviral therapy initiation: (1) less than 200 cells/µl, (2) 200 to 350 cells/µl, (3) greater than 350 cells/µl, and (4) any CD4 count.\n[7] Eleven studies met the inclusion criteria.\n[8] Antiretroviral therapy is strongly associated with a reduction in the incidence of tuberculosis in all baseline CD4 count categories: (1) less than 200 cells/µl (hazard ratio [HR] 0.16, 95% confidence interval [CI] 0.07 to 0.36), (2) 200 to 350 cells/µl (HR 0.34, 95% CI 0.19 to 0.60), (3) greater than 350 cells/µl (HR 0.43, 95% CI 0.30 to 0.63), and (4) any CD4 count (HR 0.35, 95% CI 0.28 to 0.44).\n[9] There was no evidence of hazard ratio modification with respect to baseline CD4 count category (p = 0.20).\n[10] CONCLUSIONS Antiretroviral therapy is strongly associated with a reduction in the incidence of tuberculosis across all CD4 count strata.\n[11] Earlier initiation of antiretroviral therapy may be a key component of global and national strategies to control the HIV-associated tuberculosis syndemic.\n[12] REVIEW REGISTRATION International Prospective Register of Systematic Reviews CRD42011001209 Please see later in the article for the Editors' Summary."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"CONCLUSIONS Antiretroviral therapy is strongly associated with a reduction in the incidence of tuberculosis across all CD4 count strata.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 123, "doc_id": 4883040, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [4883040], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Approximately 250,000 people are infected with human T-cell lymphotropic virus type 1 in the United Kingdom.\n\nDocument title: HTLV-I/II associated disease in England and Wales, 1993-7: retrospective review of serology requests.\n\nAbstract sentences:\n[0] Apart from HIV two exogenous retroviruses (human T cell leukaemia viruses type I (HTLV-I) and type II (HTLV-II)) infect humans.\n[1] HTLV-I infection is endemic in Japan, the Caribbean, Africa, and Melanesia and is found among immigrants from these regions in Europe.\n[2] HTLV-I infection is associated with a 1-5% lifetime risk of adult T cell leukaemia/lymphoma, 1 a 0.25% lifetime risk of HTLV-I associated myelopathy, 2 and other inflammatory conditions (uveitis, alveolitis, and arthritis).1 HTLV-II infection is endemic in some native American and African peoples and among injecting drug users and has been associated with neurological disease.1 Between 1986 and 1992, 100 cases of HTLV-I associated myelopathy and 44 cases of adult T cell leukaemia/lymphoma were diagnosed in the United Kingdom.3 Adult T cell leukaemia/lymphoma was first described in 1977 and patients with it have a mean life expectancy of only six months, so most of the 44 cases were probably incident cases.\n[3] …"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 126, "doc_id": 24512064, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [24512064], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Assessing treatment adherence is more beneficial to clinical practice than measuring routine outcomes.\n\nDocument title: Anxiety\n\nAbstract sentences:\n[0] OBJECTIVES To examine the effect of routinely administered psychiatric questionnaires on the recognition, management, and outcome of psychiatric disorders in non-psychiatric settings.\n[1] DATA SOURCES Embase, Medline, PsycLIT, Cinahl, Cochrane Controlled Trials Register, and hand searches of key journals.\n[2] METHODS A systematic review of randomised controlled trials of the administration and routine feedback of psychiatric screening and outcome questionnaires to clinicians in non-psychiatric settings.\n[3] Narrative overview of key design features and end points, together with a random effects quantitative synthesis of comparable studies.\n[4] MAIN OUTCOME MEASURES Recognition of psychiatric disorders after feedback of questionnaire results; interventions for psychiatric disorders; and outcome of psychiatric disorders.\n[5] RESULTS Nine randomised studies were identified that examined the use of common psychiatric instruments in primary care and general hospital settings.\n[6] Studies compared the effect of the administration of these instruments followed by the feedback of the results to clinicians, with administration with no feedback.\n[7] Meta-analytic pooling was possible for four of these studies (2457 participants), which measured the effect of feedback on the recognition of depressive disorders.\n[8] Routine administration and feedback of scores for all patients (irrespective of score) did not increase the overall rate of recognition of mental disorders such as anxiety and depression (relative risk of detection of depression by clinician after feedback 0.95, 95% confidence interval 0.83 to 1.09).\n[9] Two studies showed that routine administration followed by selective feedback for only high scorers increased the rate of recognition of depression (relative risk of detection of depression after feedback 2.64, 1.62 to 4.31).\n[10] This increased recognition, however, did not translate into an increased rate of intervention.\n[11] Overall, studies of routine administration of psychiatric measures did not show an effect on patient outcome.\n[12] CONCLUSIONS The routine measurement of outcome is a costly exercise.\n[13] Little evidence shows that it is of benefit in improving psychosocial outcomes of those with psychiatric disorder managed in non-psychiatric settings."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 134, "doc_id": 4695046, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4695046], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Asymptomatic visual impairment screening in elderly populations leads to improved vision.\n\nDocument title: Effectiveness of screening older people for impaired vision in community setting: systematic review of evidence from randomised controlled trials.\n\nAbstract sentences:\n[0] OBJECTIVE To assess whether population screening for impaired vision among older people in the community leads to improvements in vision.\n[1] DESIGN Systematic review of randomised controlled trials of population screening in the community that included any assessment of vision or visual function with at least 6 months' follow up.\n[2] SUBJECTS Adults aged 65 or over.\n[3] MAIN OUTCOME MEASURE Proportions with visual impairment in intervention and control groups with any method of assessing visual impairment.\n[4] RESULTS There were no trials that primarily assessed visual screening.\n[5] Outcome data on vision were available for 3494 people in five trials of multiphasic assessment.\n[6] All the trials used self reported measures for vision impairment, both as screening tools and as outcome measures.\n[7] The inclusion of a visual screening component in the assessment did not result in improvements in self reported visual problems (pooled odds ratio 1.04:95% confidence interval 0.89 to 1.22).\n[8] A small reduction (11%) in the number of older people with self reported visual problems cannot be excluded.\n[9] CONCLUSIONS Screening of asymptomatic older people in the community is not justified on present evidence.\n[10] Visual impairment in this age group can usually be reduced with treatment.\n[11] It is unclear why no benefit was seen.\n[12] Further work is needed to clarify what interventions are appropriate for older people with unreported impairment of vision."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7, 9]\nExplanation: Evidence states: \"The inclusion of a visual screening component in the assessment did not result in improvements in self reported visual problems (pooled odds ratio 1.04:95% confidence interval 0.89 to 1.22). CONCLUSIONS Screening of asymptomatic older people in the community is not justified on present evidence.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 138, "doc_id": 26016929, "label": "CONTRADICTS", "evidence_sentence_ids": [7, 9], "cited_doc_ids": [26016929], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: At least 85% of patients exposed to radiation have activated markers of myofibroblasts.\n\nDocument title: KLF4-dependent phenotypic modulation of smooth muscle cells has a key role in atherosclerotic plaque pathogenesis\n\nAbstract sentences:\n[0] Previous studies investigating the role of smooth muscle cells (SMCs) and macrophages in the pathogenesis of atherosclerosis have provided controversial results owing to the use of unreliable methods for clearly identifying each of these cell types.\n[1] Here, using Myh11-CreERT2 ROSA floxed STOP eYFP Apoe−/− mice to perform SMC lineage tracing, we find that traditional methods for detecting SMCs based on immunostaining for SMC markers fail to detect >80% of SMC-derived cells within advanced atherosclerotic lesions.\n[2] These unidentified SMC-derived cells exhibit phenotypes of other cell lineages, including macrophages and mesenchymal stem cells (MSCs).\n[3] SMC-specific conditional knockout of Krüppel-like factor 4 (Klf4) resulted in reduced numbers of SMC-derived MSC- and macrophage-like cells, a marked reduction in lesion size, and increases in multiple indices of plaque stability, including an increase in fibrous cap thickness as compared to wild-type controls.\n[4] On the basis of in vivo KLF4 chromatin immunoprecipitation–sequencing (ChIP-seq) analyses and studies of cholesterol-treated cultured SMCs, we identified >800 KLF4 target genes, including many that regulate pro-inflammatory responses of SMCs.\n[5] Our findings indicate that the contribution of SMCs to atherosclerotic plaques has been greatly underestimated, and that KLF4-dependent transitions in SMC phenotype are critical in lesion pathogenesis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 139, "doc_id": 22080671, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [22080671], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Autologous transplantation of mesenchymal stem cells has better graft function than induction therapy with anti-interleukin-2 receptor antibodies.\n\nDocument title: Induction therapy with autologous mesenchymal stem cells in living-related kidney transplants: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Antibody-based induction therapy plus calcineurin inhibitors (CNIs) reduce acute rejection rates in kidney recipients; however, opportunistic infections and toxic CNI effects remain challenging.\n[1] Reportedly, mesenchymal stem cells (MSCs) have successfully treated graft-vs-host disease.\n[2] OBJECTIVE To assess autologous MSCs as replacement of antibody induction for patients with end-stage renal disease who undergo ABO-compatible, cross-match-negative kidney transplants from a living-related donor.\n[3] DESIGN, SETTING, AND PATIENTS One hundred fifty-nine patients were enrolled in this single-site, prospective, open-label, randomized study from February 2008-May 2009, when recruitment was completed.\n[4] INTERVENTION Patients were inoculated with marrow-derived autologous MSC (1-2 x 10(6)/kg) at kidney reperfusion and two weeks later.\n[5] Fifty-three patients received standard-dose and 52 patients received low-dose CNIs (80% of standard); 51 patients in the control group received anti-IL-2 receptor antibody plus standard-dose CNIs.\n[6] MAIN OUTCOME MEASURES The primary measure was 1-year incidence of acute rejection and renal function (estimated glomerular filtration rate [eGFR]); the secondary measure was patient and graft survival and incidence of adverse events.\n[7] RESULTS Patient and graft survival at 13 to 30 months was similar in all groups.\n[8] After 6 months, 4 of 53 patients (7.5%) in the autologous MSC plus standard-dose CNI group (95% CI, 0.4%-14.7%; P = .04) and 4 of 52 patients (7.7%) in the low-dose group (95% CI, 0.5%-14.9%; P = .046) compared with 11 of 51 controls (21.6%; 95% CI, 10.5%-32.6%) had biopsy-confirmed acute rejection.\n[9] None of the patients in either autologous MSC group had glucorticoid-resistant rejection, whereas 4 patients (7.8%) in the control group did (95% CI, 0.6%-15.1%; overall P = .02).\n[10] Renal function recovered faster among both MSC groups showing increased eGFR levels during the first month after surgery than the control group.\n[11] Patients receiving standard-dose CNI had a mean difference of 6.2 mL/min per 1.73 m(2) (95% CI, 0.4-11.9; P=.04) and those in the low-dose CNI of 10.0 mL/min per 1.73 m(2) (95% CI, 3.8-16.2; P=.002).\n[12] Also, during the 1-year follow-up, combined analysis of MSC-treated groups revealed significantly decreased risk of opportunistic infections than the control group (hazard ratio, 0.42; 95% CI, 0.20-0.85, P=.02)   CONCLUSION Among patients undergoing renal transplant, the use of autologous MSCs compared with anti-IL-2 receptor antibody induction therapy resulted in lower incidence of acute rejection, decreased risk of opportunistic infection, and better estimated renal function at 1 year.\n[13] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00658073."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"After 6 months, 4 of 53 patients (7.5%) in the autologous MSC plus standard-dose CNI group (95% CI, 0.4%-14.7%; P = .04) and 4 of 52 patients (7.7%) in the low-dose group (95% CI, 0.5%-14.9%; P = .046) compared with 11 of 51 controls (21.6%; 95% CI, 10.5%-32.6%) had biopsy-confirmed acute rejection.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 144, "doc_id": 10582939, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [10582939], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Autologous transplantation of mesenchymal stem cells has better graft function than induction therapy with anti-interleukin-2 receptor antibodies.\n\nDocument title: Induction therapy with autologous mesenchymal stem cells in living-related kidney transplants: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Antibody-based induction therapy plus calcineurin inhibitors (CNIs) reduce acute rejection rates in kidney recipients; however, opportunistic infections and toxic CNI effects remain challenging.\n[1] Reportedly, mesenchymal stem cells (MSCs) have successfully treated graft-vs-host disease.\n[2] OBJECTIVE To assess autologous MSCs as replacement of antibody induction for patients with end-stage renal disease who undergo ABO-compatible, cross-match-negative kidney transplants from a living-related donor.\n[3] DESIGN, SETTING, AND PATIENTS One hundred fifty-nine patients were enrolled in this single-site, prospective, open-label, randomized study from February 2008-May 2009, when recruitment was completed.\n[4] INTERVENTION Patients were inoculated with marrow-derived autologous MSC (1-2 x 10(6)/kg) at kidney reperfusion and two weeks later.\n[5] Fifty-three patients received standard-dose and 52 patients received low-dose CNIs (80% of standard); 51 patients in the control group received anti-IL-2 receptor antibody plus standard-dose CNIs.\n[6] MAIN OUTCOME MEASURES The primary measure was 1-year incidence of acute rejection and renal function (estimated glomerular filtration rate [eGFR]); the secondary measure was patient and graft survival and incidence of adverse events.\n[7] RESULTS Patient and graft survival at 13 to 30 months was similar in all groups.\n[8] After 6 months, 4 of 53 patients (7.5%) in the autologous MSC plus standard-dose CNI group (95% CI, 0.4%-14.7%; P = .04) and 4 of 52 patients (7.7%) in the low-dose group (95% CI, 0.5%-14.9%; P = .046) compared with 11 of 51 controls (21.6%; 95% CI, 10.5%-32.6%) had biopsy-confirmed acute rejection.\n[9] None of the patients in either autologous MSC group had glucorticoid-resistant rejection, whereas 4 patients (7.8%) in the control group did (95% CI, 0.6%-15.1%; overall P = .02).\n[10] Renal function recovered faster among both MSC groups showing increased eGFR levels during the first month after surgery than the control group.\n[11] Patients receiving standard-dose CNI had a mean difference of 6.2 mL/min per 1.73 m(2) (95% CI, 0.4-11.9; P=.04) and those in the low-dose CNI of 10.0 mL/min per 1.73 m(2) (95% CI, 3.8-16.2; P=.002).\n[12] Also, during the 1-year follow-up, combined analysis of MSC-treated groups revealed significantly decreased risk of opportunistic infections than the control group (hazard ratio, 0.42; 95% CI, 0.20-0.85, P=.02)   CONCLUSION Among patients undergoing renal transplant, the use of autologous MSCs compared with anti-IL-2 receptor antibody induction therapy resulted in lower incidence of acute rejection, decreased risk of opportunistic infection, and better estimated renal function at 1 year.\n[13] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00658073."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Renal function recovered faster among both MSC groups showing increased eGFR levels during the first month after surgery than the control group.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 144, "doc_id": 10582939, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [10582939], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Autologous transplantation of mesenchymal stem cells has better graft function than induction therapy with anti-interleukin-2 receptor antibodies.\n\nDocument title: Induction therapy with autologous mesenchymal stem cells in living-related kidney transplants: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Antibody-based induction therapy plus calcineurin inhibitors (CNIs) reduce acute rejection rates in kidney recipients; however, opportunistic infections and toxic CNI effects remain challenging.\n[1] Reportedly, mesenchymal stem cells (MSCs) have successfully treated graft-vs-host disease.\n[2] OBJECTIVE To assess autologous MSCs as replacement of antibody induction for patients with end-stage renal disease who undergo ABO-compatible, cross-match-negative kidney transplants from a living-related donor.\n[3] DESIGN, SETTING, AND PATIENTS One hundred fifty-nine patients were enrolled in this single-site, prospective, open-label, randomized study from February 2008-May 2009, when recruitment was completed.\n[4] INTERVENTION Patients were inoculated with marrow-derived autologous MSC (1-2 x 10(6)/kg) at kidney reperfusion and two weeks later.\n[5] Fifty-three patients received standard-dose and 52 patients received low-dose CNIs (80% of standard); 51 patients in the control group received anti-IL-2 receptor antibody plus standard-dose CNIs.\n[6] MAIN OUTCOME MEASURES The primary measure was 1-year incidence of acute rejection and renal function (estimated glomerular filtration rate [eGFR]); the secondary measure was patient and graft survival and incidence of adverse events.\n[7] RESULTS Patient and graft survival at 13 to 30 months was similar in all groups.\n[8] After 6 months, 4 of 53 patients (7.5%) in the autologous MSC plus standard-dose CNI group (95% CI, 0.4%-14.7%; P = .04) and 4 of 52 patients (7.7%) in the low-dose group (95% CI, 0.5%-14.9%; P = .046) compared with 11 of 51 controls (21.6%; 95% CI, 10.5%-32.6%) had biopsy-confirmed acute rejection.\n[9] None of the patients in either autologous MSC group had glucorticoid-resistant rejection, whereas 4 patients (7.8%) in the control group did (95% CI, 0.6%-15.1%; overall P = .02).\n[10] Renal function recovered faster among both MSC groups showing increased eGFR levels during the first month after surgery than the control group.\n[11] Patients receiving standard-dose CNI had a mean difference of 6.2 mL/min per 1.73 m(2) (95% CI, 0.4-11.9; P=.04) and those in the low-dose CNI of 10.0 mL/min per 1.73 m(2) (95% CI, 3.8-16.2; P=.002).\n[12] Also, during the 1-year follow-up, combined analysis of MSC-treated groups revealed significantly decreased risk of opportunistic infections than the control group (hazard ratio, 0.42; 95% CI, 0.20-0.85, P=.02)   CONCLUSION Among patients undergoing renal transplant, the use of autologous MSCs compared with anti-IL-2 receptor antibody induction therapy resulted in lower incidence of acute rejection, decreased risk of opportunistic infection, and better estimated renal function at 1 year.\n[13] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00658073."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"Also, during the 1-year follow-up, combined analysis of MSC-treated groups revealed significantly decreased risk of opportunistic infections than the control group (hazard ratio, 0.42; 95% CI, 0.20-0.85, P=.02)   CONCLUSION Among patients undergoing renal transplant, the use of autologous MSCs compared with anti-IL-2 receptor antibody induction therapy resulted in lower incidence of acute rejection, decreased risk of opportunistic infection, and better estimated renal function at 1 year.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 144, "doc_id": 10582939, "label": "SUPPORTS", "evidence_sentence_ids": [12], "cited_doc_ids": [10582939], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Autophagy deficiency in the liver increases vulnerability to insulin resistance.\n\nDocument title: Autophagy deficiency leads to protection from obesity and insulin resistance by inducing Fgf21 as a mitokine\n\nAbstract sentences:\n[0] Despite growing interest and a recent surge in papers, the role of autophagy in glucose and lipid metabolism is unclear.\n[1] We produced mice with skeletal muscle–specific deletion of Atg7 (encoding autophagy-related 7).\n[2] Unexpectedly, these mice showed decreased fat mass and were protected from diet-induced obesity and insulin resistance; this phenotype was accompanied by increased fatty acid oxidation and browning of white adipose tissue (WAT) owing to induction of fibroblast growth factor 21 (Fgf21).\n[3] Mitochondrial dysfunction induced by autophagy deficiency increased Fgf21 expression through induction of Atf4, a master regulator of the integrated stress response.\n[4] Mitochondrial respiratory chain inhibitors also induced Fgf21 in an Atf4-dependent manner.\n[5] We also observed induction of Fgf21, resistance to diet-induced obesity and amelioration of insulin resistance in mice with autophagy deficiency in the liver, another insulin target tissue.\n[6] These findings suggest that autophagy deficiency and subsequent mitochondrial dysfunction promote Fgf21 expression, a hormone we consequently term a 'mitokine', and together these processes promote protection from diet-induced obesity and insulin resistance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Unexpectedly, these mice showed decreased fat mass and were protected from diet-induced obesity and insulin resistance; this phenotype was accompanied by increased fatty acid oxidation and browning of white adipose tissue (WAT) owing to induction of fibroblast growth factor 21 (Fgf21).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 149, "doc_id": 6227220, "label": "CONTRADICTS", "evidence_sentence_ids": [2], "cited_doc_ids": [6227220], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Autophagy deficiency in the liver increases vulnerability to insulin resistance.\n\nDocument title: Autophagy deficiency leads to protection from obesity and insulin resistance by inducing Fgf21 as a mitokine\n\nAbstract sentences:\n[0] Despite growing interest and a recent surge in papers, the role of autophagy in glucose and lipid metabolism is unclear.\n[1] We produced mice with skeletal muscle–specific deletion of Atg7 (encoding autophagy-related 7).\n[2] Unexpectedly, these mice showed decreased fat mass and were protected from diet-induced obesity and insulin resistance; this phenotype was accompanied by increased fatty acid oxidation and browning of white adipose tissue (WAT) owing to induction of fibroblast growth factor 21 (Fgf21).\n[3] Mitochondrial dysfunction induced by autophagy deficiency increased Fgf21 expression through induction of Atf4, a master regulator of the integrated stress response.\n[4] Mitochondrial respiratory chain inhibitors also induced Fgf21 in an Atf4-dependent manner.\n[5] We also observed induction of Fgf21, resistance to diet-induced obesity and amelioration of insulin resistance in mice with autophagy deficiency in the liver, another insulin target tissue.\n[6] These findings suggest that autophagy deficiency and subsequent mitochondrial dysfunction promote Fgf21 expression, a hormone we consequently term a 'mitokine', and together these processes promote protection from diet-induced obesity and insulin resistance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"We also observed induction of Fgf21, resistance to diet-induced obesity and amelioration of insulin resistance in mice with autophagy deficiency in the liver, another insulin target tissue.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 149, "doc_id": 6227220, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [6227220], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Autophagy deficiency in the liver increases vulnerability to insulin resistance.\n\nDocument title: Autophagy deficiency leads to protection from obesity and insulin resistance by inducing Fgf21 as a mitokine\n\nAbstract sentences:\n[0] Despite growing interest and a recent surge in papers, the role of autophagy in glucose and lipid metabolism is unclear.\n[1] We produced mice with skeletal muscle–specific deletion of Atg7 (encoding autophagy-related 7).\n[2] Unexpectedly, these mice showed decreased fat mass and were protected from diet-induced obesity and insulin resistance; this phenotype was accompanied by increased fatty acid oxidation and browning of white adipose tissue (WAT) owing to induction of fibroblast growth factor 21 (Fgf21).\n[3] Mitochondrial dysfunction induced by autophagy deficiency increased Fgf21 expression through induction of Atf4, a master regulator of the integrated stress response.\n[4] Mitochondrial respiratory chain inhibitors also induced Fgf21 in an Atf4-dependent manner.\n[5] We also observed induction of Fgf21, resistance to diet-induced obesity and amelioration of insulin resistance in mice with autophagy deficiency in the liver, another insulin target tissue.\n[6] These findings suggest that autophagy deficiency and subsequent mitochondrial dysfunction promote Fgf21 expression, a hormone we consequently term a 'mitokine', and together these processes promote protection from diet-induced obesity and insulin resistance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"These findings suggest that autophagy deficiency and subsequent mitochondrial dysfunction promote Fgf21 expression, a hormone we consequently term a 'mitokine', and together these processes promote protection from diet-induced obesity and insulin resistance.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 149, "doc_id": 6227220, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [6227220], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: B cells go though plasmablast differentiation and antibody production by continuous expression of EBI2.\n\nDocument title: Guidance of B cells by the orphan G protein-coupled receptor EBI2 shapes humoral immune responses.\n\nAbstract sentences:\n[0] Humoral immunity depends on both rapid and long-term antibody production against invading pathogens.\n[1] This is achieved by the generation of spatially distinct extrafollicular plasmablast and follicular germinal center (GC) B cell populations, but the signals that guide responding B cells to these alternative compartments have not been fully elucidated.\n[2] Here, we show that expression of the orphan G protein-coupled receptor Epstein-Barr virus-induced gene 2 (EBI2, also known as GPR183) by activated B cells was essential for their movement to extrafollicular sites and induction of early plasmablast responses.\n[3] Conversely, downregulation of EBI2 enabled B cells to access the center of follicles and promoted efficient GC formation.\n[4] EBI2 therefore provides a previously uncharacterized dimension to B cell migration that is crucial for coordinating rapid versus long-term antibody responses."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here, we show that expression of the orphan G protein-coupled receptor Epstein-Barr virus-induced gene 2 (EBI2, also known as GPR183) by activated B cells was essential for their movement to extrafollicular sites and induction of early plasmablast responses.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 152, "doc_id": 15488881, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [15488881], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: B cells go though plasmablast differentiation and antibody production by continuous expression of EBI2.\n\nDocument title: Guidance of B cells by the orphan G protein-coupled receptor EBI2 shapes humoral immune responses.\n\nAbstract sentences:\n[0] Humoral immunity depends on both rapid and long-term antibody production against invading pathogens.\n[1] This is achieved by the generation of spatially distinct extrafollicular plasmablast and follicular germinal center (GC) B cell populations, but the signals that guide responding B cells to these alternative compartments have not been fully elucidated.\n[2] Here, we show that expression of the orphan G protein-coupled receptor Epstein-Barr virus-induced gene 2 (EBI2, also known as GPR183) by activated B cells was essential for their movement to extrafollicular sites and induction of early plasmablast responses.\n[3] Conversely, downregulation of EBI2 enabled B cells to access the center of follicles and promoted efficient GC formation.\n[4] EBI2 therefore provides a previously uncharacterized dimension to B cell migration that is crucial for coordinating rapid versus long-term antibody responses."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"EBI2 therefore provides a previously uncharacterized dimension to B cell migration that is crucial for coordinating rapid versus long-term antibody responses.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 152, "doc_id": 15488881, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [15488881], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: B3-Galectin decreases cell resistance to tyrosine kinase inhibitors (TKIs) by engaging the alternate KRAS-RalB signaling complex downstream of EGFR.\n\nDocument title: An integrin β3–KRAS–RalB complex drives tumour stemness and resistance to EGFR inhibition\n\nAbstract sentences:\n[0] Tumour cells, with stem-like properties, are highly aggressive and often show drug resistance.\n[1] Here, we reveal that integrin αvβ3 serves as a marker of breast, lung and pancreatic carcinomas with stem-like properties that are highly resistant to receptor tyrosine kinase inhibitors such as erlotinib.\n[2] This was observed in vitro and in mice bearing patient-derived tumour xenografts or in clinical specimens from lung cancer patients who had progressed on erlotinib.\n[3] Mechanistically, αvβ3, in the unliganded state, recruits KRAS and RalB to the tumour cell plasma membrane, leading to the activation of TBK1 and NF-κB. In fact, αvβ3 expression and the resulting KRAS–RalB–NF-κB pathway were both necessary and sufficient for tumour initiation, anchorage independence, self-renewal and erlotinib resistance.\n[4] Pharmacological targeting of this pathway with bortezomib reversed both tumour stemness and erlotinib resistance.\n[5] These findings not only identify αvβ3 as a marker/driver of carcinoma stemness but also reveal a therapeutic strategy to sensitize such tumours to RTK inhibition."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 153, "doc_id": 4702639, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4702639], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: B3-Galectin increases cell resistance to tyrosine kinase inhibitors (TKIs) by engaging the alternate KRAS-RalB signaling complex downstream of EGFR.\n\nDocument title: An integrin β3–KRAS–RalB complex drives tumour stemness and resistance to EGFR inhibition\n\nAbstract sentences:\n[0] Tumour cells, with stem-like properties, are highly aggressive and often show drug resistance.\n[1] Here, we reveal that integrin αvβ3 serves as a marker of breast, lung and pancreatic carcinomas with stem-like properties that are highly resistant to receptor tyrosine kinase inhibitors such as erlotinib.\n[2] This was observed in vitro and in mice bearing patient-derived tumour xenografts or in clinical specimens from lung cancer patients who had progressed on erlotinib.\n[3] Mechanistically, αvβ3, in the unliganded state, recruits KRAS and RalB to the tumour cell plasma membrane, leading to the activation of TBK1 and NF-κB. In fact, αvβ3 expression and the resulting KRAS–RalB–NF-κB pathway were both necessary and sufficient for tumour initiation, anchorage independence, self-renewal and erlotinib resistance.\n[4] Pharmacological targeting of this pathway with bortezomib reversed both tumour stemness and erlotinib resistance.\n[5] These findings not only identify αvβ3 as a marker/driver of carcinoma stemness but also reveal a therapeutic strategy to sensitize such tumours to RTK inhibition."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 154, "doc_id": 4702639, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4702639], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: BCL-2 activation antagonizes the apoptotic effects of c-Myc.\n\nDocument title: Antiapoptotic BCL-2 is required for maintenance of a model leukemia.\n\nAbstract sentences:\n[0] Resistance to apoptosis, often achieved by the overexpression of antiapoptotic proteins, is common and perhaps required in the genesis of cancer.\n[1] However, it remains uncertain whether apoptotic defects are essential for tumor maintenance.\n[2] To test this, we generated mice expressing a conditional BCL-2 gene and constitutive c-myc that develop lymphoblastic leukemia.\n[3] Eliminating BCL-2 yielded rapid loss of leukemic cells and significantly prolonged survival, formally validating BCL-2 as a rational target for cancer therapy.\n[4] Loss of this single molecule resulted in cell death, despite or perhaps attributable to the presence of other oncogenic events.\n[5] This suggests a generalizable model in which aberrations inherent to cancer generate tonic death signals that would otherwise kill the cell if not opposed by a requisite apoptotic defect(s)."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Eliminating BCL-2 yielded rapid loss of leukemic cells and significantly prolonged survival, formally validating BCL-2 as a rational target for cancer therapy.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 155, "doc_id": 37549932, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [37549932], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: BCL-2 promotes the apoptotic effects of c-Myc.\n\nDocument title: Antiapoptotic BCL-2 is required for maintenance of a model leukemia.\n\nAbstract sentences:\n[0] Resistance to apoptosis, often achieved by the overexpression of antiapoptotic proteins, is common and perhaps required in the genesis of cancer.\n[1] However, it remains uncertain whether apoptotic defects are essential for tumor maintenance.\n[2] To test this, we generated mice expressing a conditional BCL-2 gene and constitutive c-myc that develop lymphoblastic leukemia.\n[3] Eliminating BCL-2 yielded rapid loss of leukemic cells and significantly prolonged survival, formally validating BCL-2 as a rational target for cancer therapy.\n[4] Loss of this single molecule resulted in cell death, despite or perhaps attributable to the presence of other oncogenic events.\n[5] This suggests a generalizable model in which aberrations inherent to cancer generate tonic death signals that would otherwise kill the cell if not opposed by a requisite apoptotic defect(s)."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Eliminating BCL-2 yielded rapid loss of leukemic cells and significantly prolonged survival, formally validating BCL-2 as a rational target for cancer therapy.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 156, "doc_id": 37549932, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [37549932], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: BLM gene encodes RecQ-class DNA helicase.\n\nDocument title: The Bloom's syndrome gene product is homologous to RecQ helicases\n\nAbstract sentences:\n[0] The Bloom's syndrome (BS) gene, BLM, plays an important role in the maintenance of genomic stability in somatic cells.\n[1] A candidate for BLM was identified by direct selection of a cDNA derived from a 250 kb segment of the genome to which BLM had been assigned by somatic crossover point mapping.\n[2] In this novel mapping method, cells were used from persons with BS that had undergone intragenic recombination within BLM.\n[3] cDNA analysis of the candidate gene identified a 4437 bp cDNA that encodes a 1417 amino acid peptide with homology to the RecQ helicases, a subfamily of DExH box-containing DNA and RNA helicases.\n[4] The presence of chain-terminating mutations in the candidate gene in persons with BS proved that it was BLM."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"cDNA analysis of the candidate gene identified a 4437 bp cDNA that encodes a 1417 amino acid peptide with homology to the RecQ helicases, a subfamily of DExH box-containing DNA and RNA helicases.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 157, "doc_id": 13439128, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [13439128], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: BRCA 1 mutation carriers' risk of breast and ovarian cancer depends on where the mutation is located.\n\nDocument title: Association of type and location of BRCA1 and BRCA2 mutations with risk of breast and ovarian cancer.\n\nAbstract sentences:\n[0] IMPORTANCE Limited information about the relationship between specific mutations in BRCA1 or BRCA2 (BRCA1/2) and cancer risk exists.\n[1] OBJECTIVE To identify mutation-specific cancer risks for carriers of BRCA1/2.\n[2] DESIGN, SETTING, AND PARTICIPANTS Observational study of women who were ascertained between 1937 and 2011 (median, 1999) and found to carry disease-associated BRCA1 or BRCA2 mutations.\n[3] The international sample comprised 19,581 carriers of BRCA1 mutations and 11,900 carriers of BRCA2 mutations from 55 centers in 33 countries on 6 continents.\n[4] We estimated hazard ratios for breast and ovarian cancer based on mutation type, function, and nucleotide position.\n[5] We also estimated RHR, the ratio of breast vs ovarian cancer hazard ratios.\n[6] A value of RHR greater than 1 indicated elevated breast cancer risk; a value of RHR less than 1 indicated elevated ovarian cancer risk.\n[7] EXPOSURES Mutations of BRCA1 or BRCA2.\n[8] MAIN OUTCOMES AND MEASURES Breast and ovarian cancer risks.\n[9] RESULTS Among BRCA1 mutation carriers, 9052 women (46%) were diagnosed with breast cancer, 2317 (12%) with ovarian cancer, 1041 (5%) with breast and ovarian cancer, and 7171 (37%) without cancer.\n[10] Among BRCA2 mutation carriers, 6180 women (52%) were diagnosed with breast cancer, 682 (6%) with ovarian cancer, 272 (2%) with breast and ovarian cancer, and 4766 (40%) without cancer.\n[11] In BRCA1, we identified 3 breast cancer cluster regions (BCCRs) located at c.179 to c.505 (BCCR1; RHR = 1.46; 95% CI, 1.22-1.74; P = 2 × 10(-6)), c.4328 to c.4945 (BCCR2; RHR = 1.34; 95% CI, 1.01-1.78; P = .04), and c. 5261 to c.5563 (BCCR2', RHR = 1.38; 95% CI, 1.22-1.55; P = 6 × 10(-9)).\n[12] We also identified an ovarian cancer cluster region (OCCR) from c.1380 to c.4062 (approximately exon 11) with RHR = 0.62 (95% CI, 0.56-0.70; P = 9 × 10(-17)).\n[13] In BRCA2, we observed multiple BCCRs spanning c.1 to c.596 (BCCR1; RHR = 1.71; 95% CI, 1.06-2.78; P = .03), c.772 to c.1806 (BCCR1'; RHR = 1.63; 95% CI, 1.10-2.40; P = .01), and c.7394 to c.8904 (BCCR2; RHR = 2.31; 95% CI, 1.69-3.16; P = .00002).\n[14] We also identified 3 OCCRs: the first (OCCR1) spanned c.3249 to c.5681 that was adjacent to c.5946delT (6174delT; RHR = 0.51; 95% CI, 0.44-0.60; P = 6 × 10(-17)).\n[15] The second OCCR spanned c.6645 to c.7471 (OCCR2; RHR = 0.57; 95% CI, 0.41-0.80; P = .001).\n[16] Mutations conferring nonsense-mediated decay were associated with differential breast or ovarian cancer risks and an earlier age of breast cancer diagnosis for both BRCA1 and BRCA2 mutation carriers.\n[17] CONCLUSIONS AND RELEVANCE Breast and ovarian cancer risks varied by type and location of BRCA1/2 mutations.\n[18] With appropriate validation, these data may have implications for risk assessment and cancer prevention decision making for carriers of BRCA1 and BRCA2 mutations."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [16]\nExplanation: Evidence states: \"Mutations conferring nonsense-mediated decay were associated with differential breast or ovarian cancer risks and an earlier age of breast cancer diagnosis for both BRCA1 and BRCA2 mutation carriers.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 159, "doc_id": 9394119, "label": "SUPPORTS", "evidence_sentence_ids": [16], "cited_doc_ids": [9394119], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: BRCA 1 mutation carriers' risk of breast and ovarian cancer depends on where the mutation is located.\n\nDocument title: Association of type and location of BRCA1 and BRCA2 mutations with risk of breast and ovarian cancer.\n\nAbstract sentences:\n[0] IMPORTANCE Limited information about the relationship between specific mutations in BRCA1 or BRCA2 (BRCA1/2) and cancer risk exists.\n[1] OBJECTIVE To identify mutation-specific cancer risks for carriers of BRCA1/2.\n[2] DESIGN, SETTING, AND PARTICIPANTS Observational study of women who were ascertained between 1937 and 2011 (median, 1999) and found to carry disease-associated BRCA1 or BRCA2 mutations.\n[3] The international sample comprised 19,581 carriers of BRCA1 mutations and 11,900 carriers of BRCA2 mutations from 55 centers in 33 countries on 6 continents.\n[4] We estimated hazard ratios for breast and ovarian cancer based on mutation type, function, and nucleotide position.\n[5] We also estimated RHR, the ratio of breast vs ovarian cancer hazard ratios.\n[6] A value of RHR greater than 1 indicated elevated breast cancer risk; a value of RHR less than 1 indicated elevated ovarian cancer risk.\n[7] EXPOSURES Mutations of BRCA1 or BRCA2.\n[8] MAIN OUTCOMES AND MEASURES Breast and ovarian cancer risks.\n[9] RESULTS Among BRCA1 mutation carriers, 9052 women (46%) were diagnosed with breast cancer, 2317 (12%) with ovarian cancer, 1041 (5%) with breast and ovarian cancer, and 7171 (37%) without cancer.\n[10] Among BRCA2 mutation carriers, 6180 women (52%) were diagnosed with breast cancer, 682 (6%) with ovarian cancer, 272 (2%) with breast and ovarian cancer, and 4766 (40%) without cancer.\n[11] In BRCA1, we identified 3 breast cancer cluster regions (BCCRs) located at c.179 to c.505 (BCCR1; RHR = 1.46; 95% CI, 1.22-1.74; P = 2 × 10(-6)), c.4328 to c.4945 (BCCR2; RHR = 1.34; 95% CI, 1.01-1.78; P = .04), and c. 5261 to c.5563 (BCCR2', RHR = 1.38; 95% CI, 1.22-1.55; P = 6 × 10(-9)).\n[12] We also identified an ovarian cancer cluster region (OCCR) from c.1380 to c.4062 (approximately exon 11) with RHR = 0.62 (95% CI, 0.56-0.70; P = 9 × 10(-17)).\n[13] In BRCA2, we observed multiple BCCRs spanning c.1 to c.596 (BCCR1; RHR = 1.71; 95% CI, 1.06-2.78; P = .03), c.772 to c.1806 (BCCR1'; RHR = 1.63; 95% CI, 1.10-2.40; P = .01), and c.7394 to c.8904 (BCCR2; RHR = 2.31; 95% CI, 1.69-3.16; P = .00002).\n[14] We also identified 3 OCCRs: the first (OCCR1) spanned c.3249 to c.5681 that was adjacent to c.5946delT (6174delT; RHR = 0.51; 95% CI, 0.44-0.60; P = 6 × 10(-17)).\n[15] The second OCCR spanned c.6645 to c.7471 (OCCR2; RHR = 0.57; 95% CI, 0.41-0.80; P = .001).\n[16] Mutations conferring nonsense-mediated decay were associated with differential breast or ovarian cancer risks and an earlier age of breast cancer diagnosis for both BRCA1 and BRCA2 mutation carriers.\n[17] CONCLUSIONS AND RELEVANCE Breast and ovarian cancer risks varied by type and location of BRCA1/2 mutations.\n[18] With appropriate validation, these data may have implications for risk assessment and cancer prevention decision making for carriers of BRCA1 and BRCA2 mutations."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [17]\nExplanation: Evidence states: \"CONCLUSIONS AND RELEVANCE Breast and ovarian cancer risks varied by type and location of BRCA1/2 mutations.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 159, "doc_id": 9394119, "label": "SUPPORTS", "evidence_sentence_ids": [17], "cited_doc_ids": [9394119], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Bacterial meningitis can be diagnosed on the basis of positive cerebrospinal fluid (CSF) cultures.\n\nDocument title: How do I perform a lumbar puncture and analyze the results to diagnose bacterial meningitis?\n\nAbstract sentences:\n[0] CONTEXT Diagnostic lumbar punctures (LPs), commonly used to rule out meningitis, are associated with adverse events.\n[1] OBJECTIVE To systematically review the evidence about diagnostic LP techniques that may decrease the risk of adverse events and the evidence about test accuracy of cerebrospinal fluid (CSF) analysis in adult patients with suspected bacterial meningitis.\n[2] DATA SOURCES We searched the Cochrane Library, MEDLINE (using Ovid and PubMed) from 1966 to January 2006 and EMBASE from 1980 to January 2006 without language restrictions to identify relevant studies and identified others from the bibliographies of retrieved articles.\n[3] STUDY SELECTION We included randomized trials of patients aged 18 years or older undergoing interventions to facilitate a successful diagnostic LP or to potentially reduce adverse events.\n[4] Studies assessing the accuracy of biochemical analysis of the CSF for possible bacterial meningitis were also identified.\n[5] DATA EXTRACTION Two investigators independently appraised study quality and extracted relevant data.\n[6] For studies of the LP technique, data on the intervention and the outcome were extracted.\n[7] For studies of the laboratory diagnosis of bacterial meningitis, data on the reference standard and test accuracy were extracted.\n[8] DATA SYNTHESIS We found 15 randomized trials.\n[9] A random-effects model was used for quantitative synthesis.\n[10] Five studies of 587 patients compared atraumatic needles with standard needles and found a nonsignificant decrease in the odds of headache with an atraumatic needle (absolute risk reduction [ARR], 12.3%; 95% confidence interval [CI], -1.72% to 26.2%).\n[11] Reinsertion of the stylet before needle removal decreased the risk of headache (ARR, 11.3%; 95% CI, 6.50%-16.2%).\n[12] The combined results from 4 studies of 717 patients showed a nonsignificant decrease in headache in patients who were mobilized after LP (ARR, 2.9%; 95% CI, -3.4 to 9.3%).\n[13] Four studies on the accuracy of biochemical analysis of CSF in patients with suspected meningitis met inclusion criteria.\n[14] A CSF-blood glucose ratio of 0.4 or less (likelihood ratio [LR], 18; 95% CI, 12-27]), CSF white blood cell count of 500/muL or higher (LR, 15; 95% CI, 10-22), and CSF lactate level of 31.53 mg/dL or more (> or =3.5 mmol/L; LR, 21; 95% CI, 14-32) accurately diagnosed bacterial meningitis.\n[15] CONCLUSIONS These data suggest that small-gauge, atraumatic needles may decrease the risk of headache after diagnostic LP.\n[16] Reinsertion of the stylet before needle removal should occur and patients do not require bed rest after the procedure.\n[17] Future research should focus on evaluating interventions to optimize the success of a diagnostic LP and to enhance training in procedural skills."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [14]\nExplanation: Evidence states: \"A CSF-blood glucose ratio of 0.4 or less (likelihood ratio [LR], 18; 95% CI, 12-27]), CSF white blood cell count of 500/muL or higher (LR, 15; 95% CI, 10-22), and CSF lactate level of 31.53 mg/dL or more (> or =3.5 mmol/L; LR, 21; 95% CI, 14-32) accurately diagnosed bacterial meningitis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 160, "doc_id": 52874170, "label": "SUPPORTS", "evidence_sentence_ids": [14], "cited_doc_ids": [52874170], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Bacteriophagaes MS2 and Qβ are members of the Leviviridae.\n\nDocument title: Asymmetric cryo-EM reconstruction of phage MS2 reveals genome structure in situ\n\nAbstract sentences:\n[0] In single-stranded ribonucleic acid (RNA) viruses, virus capsid assembly and genome packaging are intertwined processes.\n[1] Using cryo-electron microscopy and single particle analysis we determined the asymmetric virion structure of bacteriophage MS2, which includes 178 copies of the coat protein, a single copy of the A-protein and the RNA genome.\n[2] This reveals that in situ, the viral RNA genome can adopt a defined conformation.\n[3] The RNA forms a branched network of stem-loops that almost all allocate near the capsid inner surface, while predominantly binding to coat protein dimers that are located in one-half of the capsid.\n[4] This suggests that genomic RNA is highly involved in genome packaging and virion assembly."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 161, "doc_id": 6903077, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [6903077], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Bariatric surgery increases rates of colorectal cancer.\n\nDocument title: Bariatric Surgery in the United Kingdom: A Cohort Study of Weight Loss and Clinical Outcomes in Routine Clinical Care.\n\nAbstract sentences:\n[0] BACKGROUND Bariatric surgery is becoming a more widespread treatment for obesity.\n[1] Comprehensive evidence of the long-term effects of contemporary surgery on a broad range of clinical outcomes in large populations treated in routine clinical practice is lacking.\n[2] The objective of this study was to measure the association between bariatric surgery, weight, body mass index, and obesity-related co-morbidities.\n[3] METHODS AND FINDINGS This was an observational retrospective cohort study using data from the United Kingdom Clinical Practice Research Datalink.\n[4] All 3,882 patients registered in the database and with bariatric surgery on or before 31 December 2014 were included and matched by propensity score to 3,882 obese patients without surgery.\n[5] The main outcome measures were change in weight and body mass index over 4 y; incident diagnoses of type 2 diabetes mellitus (T2DM), hypertension, angina, myocardial infarction (MI), stroke, fractures, obstructive sleep apnoea, and cancer; mortality; and resolution of hypertension and T2DM.\n[6] Weight measures were available for 3,847 patients between 1 and 4 mo, 2,884 patients between 5 and 12 mo, and 2,258 patients between 13 and 48 mo post-procedure.\n[7] Bariatric surgery patients exhibited rapid weight loss for the first four postoperative months, at a rate of 4.98 kg/mo (95% CI 4.88-5.08).\n[8] Slower weight loss was sustained to the end of 4 y. Gastric bypass (6.56 kg/mo) and sleeve gastrectomy (6.29 kg/mo) were associated with greater initial weight reduction than gastric banding (2.77 kg/mo).\n[9] Protective hazard ratios (HRs) were detected for bariatric surgery for incident T2DM, 0.68 (95% CI 0.55-0.83); hypertension, 0.35 (95% CI 0.27-0.45); angina, 0.59 (95% CI 0.40-0.87);MI, 0.28 (95% CI 0.10-0.74); and obstructive sleep apnoea, 0.55 (95% CI 0.40-0.87).\n[10] Strong associations were found between bariatric surgery and the resolution of T2DM, with a HR of 9.29 (95% CI 6.84-12.62), and between bariatric surgery and the resolution of hypertension, with a HR of 5.64 (95% CI 2.65-11.99).\n[11] No association was detected between bariatric surgery and fractures, cancer, or stroke.\n[12] Effect estimates for mortality found no protective association with bariatric surgery overall, with a HR of 0.97 (95% CI 0.66-1.43).\n[13] The data used were recorded for the management of patients in primary care and may be subject to inaccuracy, which would tend to lead to underestimates of true relative effect sizes.\n[14] CONCLUSIONS Bariatric surgery as delivered in the UK healthcare system is associated with dramatic weight loss, sustained at least 4 y after surgery.\n[15] This weight loss is accompanied by substantial improvements in pre-existing T2DM and hypertension, as well as a reduced risk of incident T2DM, hypertension, angina, MI, and obstructive sleep apnoea.\n[16] Widening the availability of bariatric surgery could lead to substantial health benefits for many people who are morbidly obese."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"No association was detected between bariatric surgery and fractures, cancer, or stroke.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 164, "doc_id": 5824985, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [5824985], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Bariatric surgery increases rates of postmenopausal breast cancer.\n\nDocument title: Bariatric Surgery in the United Kingdom: A Cohort Study of Weight Loss and Clinical Outcomes in Routine Clinical Care.\n\nAbstract sentences:\n[0] BACKGROUND Bariatric surgery is becoming a more widespread treatment for obesity.\n[1] Comprehensive evidence of the long-term effects of contemporary surgery on a broad range of clinical outcomes in large populations treated in routine clinical practice is lacking.\n[2] The objective of this study was to measure the association between bariatric surgery, weight, body mass index, and obesity-related co-morbidities.\n[3] METHODS AND FINDINGS This was an observational retrospective cohort study using data from the United Kingdom Clinical Practice Research Datalink.\n[4] All 3,882 patients registered in the database and with bariatric surgery on or before 31 December 2014 were included and matched by propensity score to 3,882 obese patients without surgery.\n[5] The main outcome measures were change in weight and body mass index over 4 y; incident diagnoses of type 2 diabetes mellitus (T2DM), hypertension, angina, myocardial infarction (MI), stroke, fractures, obstructive sleep apnoea, and cancer; mortality; and resolution of hypertension and T2DM.\n[6] Weight measures were available for 3,847 patients between 1 and 4 mo, 2,884 patients between 5 and 12 mo, and 2,258 patients between 13 and 48 mo post-procedure.\n[7] Bariatric surgery patients exhibited rapid weight loss for the first four postoperative months, at a rate of 4.98 kg/mo (95% CI 4.88-5.08).\n[8] Slower weight loss was sustained to the end of 4 y. Gastric bypass (6.56 kg/mo) and sleeve gastrectomy (6.29 kg/mo) were associated with greater initial weight reduction than gastric banding (2.77 kg/mo).\n[9] Protective hazard ratios (HRs) were detected for bariatric surgery for incident T2DM, 0.68 (95% CI 0.55-0.83); hypertension, 0.35 (95% CI 0.27-0.45); angina, 0.59 (95% CI 0.40-0.87);MI, 0.28 (95% CI 0.10-0.74); and obstructive sleep apnoea, 0.55 (95% CI 0.40-0.87).\n[10] Strong associations were found between bariatric surgery and the resolution of T2DM, with a HR of 9.29 (95% CI 6.84-12.62), and between bariatric surgery and the resolution of hypertension, with a HR of 5.64 (95% CI 2.65-11.99).\n[11] No association was detected between bariatric surgery and fractures, cancer, or stroke.\n[12] Effect estimates for mortality found no protective association with bariatric surgery overall, with a HR of 0.97 (95% CI 0.66-1.43).\n[13] The data used were recorded for the management of patients in primary care and may be subject to inaccuracy, which would tend to lead to underestimates of true relative effect sizes.\n[14] CONCLUSIONS Bariatric surgery as delivered in the UK healthcare system is associated with dramatic weight loss, sustained at least 4 y after surgery.\n[15] This weight loss is accompanied by substantial improvements in pre-existing T2DM and hypertension, as well as a reduced risk of incident T2DM, hypertension, angina, MI, and obstructive sleep apnoea.\n[16] Widening the availability of bariatric surgery could lead to substantial health benefits for many people who are morbidly obese."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"No association was detected between bariatric surgery and fractures, cancer, or stroke.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 165, "doc_id": 5824985, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [5824985], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Bariatric surgery leads to negative outcomes in mental health.\n\nDocument title: Mental Health Conditions Among Patients Seeking and Undergoing Bariatric Surgery: A Meta-analysis.\n\nAbstract sentences:\n[0] IMPORTANCE Bariatric surgery is associated with sustained weight loss and improved physical health status for severely obese individuals.\n[1] Mental health conditions may be common among patients seeking bariatric surgery; however, the prevalence of these conditions and whether they are associated with postoperative outcomes remains unknown.\n[2] OBJECTIVE To determine the prevalence of mental health conditions among bariatric surgery candidates and recipients, to evaluate the association between preoperative mental health conditions and health outcomes following bariatric surgery, and to evaluate the association between surgery and the clinical course of mental health conditions.\n[3] DATA SOURCES We searched PubMed, MEDLINE on OVID, and PsycINFO for studies published between January 1988 and November 2015.\n[4] Study quality was assessed using an adapted tool for risk of bias; quality of evidence was rated based on GRADE (Grading of Recommendations Assessment, Development and Evaluation) criteria.\n[5] FINDINGS We identified 68 publications meeting inclusion criteria: 59 reporting the prevalence of preoperative mental health conditions (65,363 patients) and 27 reporting associations between preoperative mental health conditions and postoperative outcomes (50,182 patients).\n[6] Among patients seeking and undergoing bariatric surgery, the most common mental health conditions, based on random-effects estimates of prevalence, were depression (19% [95% CI, 14%-25%]) and binge eating disorder (17% [95% CI, 13%-21%]).\n[7] There was conflicting evidence regarding the association between preoperative mental health conditions and postoperative weight loss.\n[8] Neither depression nor binge eating disorder was consistently associated with differences in weight outcomes.\n[9] Bariatric surgery was, however, consistently associated with postoperative decreases in the prevalence of depression (7 studies; 8%-74% decrease) and the severity of depressive symptoms (6 studies; 40%-70% decrease).\n[10] CONCLUSIONS AND RELEVANCE Mental health conditions are common among bariatric surgery patients-in particular, depression and binge eating disorder.\n[11] There is inconsistent evidence regarding the association between preoperative mental health conditions and postoperative weight loss.\n[12] Moderate-quality evidence supports an association between bariatric surgery and lower rates of depression postoperatively."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Bariatric surgery was, however, consistently associated with postoperative decreases in the prevalence of depression (7 studies; 8%-74% decrease) and the severity of depressive symptoms (6 studies; 40%-70% decrease).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 166, "doc_id": 18872233, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [18872233], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Bariatric surgery leads to negative outcomes in mental health.\n\nDocument title: Mental Health Conditions Among Patients Seeking and Undergoing Bariatric Surgery: A Meta-analysis.\n\nAbstract sentences:\n[0] IMPORTANCE Bariatric surgery is associated with sustained weight loss and improved physical health status for severely obese individuals.\n[1] Mental health conditions may be common among patients seeking bariatric surgery; however, the prevalence of these conditions and whether they are associated with postoperative outcomes remains unknown.\n[2] OBJECTIVE To determine the prevalence of mental health conditions among bariatric surgery candidates and recipients, to evaluate the association between preoperative mental health conditions and health outcomes following bariatric surgery, and to evaluate the association between surgery and the clinical course of mental health conditions.\n[3] DATA SOURCES We searched PubMed, MEDLINE on OVID, and PsycINFO for studies published between January 1988 and November 2015.\n[4] Study quality was assessed using an adapted tool for risk of bias; quality of evidence was rated based on GRADE (Grading of Recommendations Assessment, Development and Evaluation) criteria.\n[5] FINDINGS We identified 68 publications meeting inclusion criteria: 59 reporting the prevalence of preoperative mental health conditions (65,363 patients) and 27 reporting associations between preoperative mental health conditions and postoperative outcomes (50,182 patients).\n[6] Among patients seeking and undergoing bariatric surgery, the most common mental health conditions, based on random-effects estimates of prevalence, were depression (19% [95% CI, 14%-25%]) and binge eating disorder (17% [95% CI, 13%-21%]).\n[7] There was conflicting evidence regarding the association between preoperative mental health conditions and postoperative weight loss.\n[8] Neither depression nor binge eating disorder was consistently associated with differences in weight outcomes.\n[9] Bariatric surgery was, however, consistently associated with postoperative decreases in the prevalence of depression (7 studies; 8%-74% decrease) and the severity of depressive symptoms (6 studies; 40%-70% decrease).\n[10] CONCLUSIONS AND RELEVANCE Mental health conditions are common among bariatric surgery patients-in particular, depression and binge eating disorder.\n[11] There is inconsistent evidence regarding the association between preoperative mental health conditions and postoperative weight loss.\n[12] Moderate-quality evidence supports an association between bariatric surgery and lower rates of depression postoperatively."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"Moderate-quality evidence supports an association between bariatric surgery and lower rates of depression postoperatively.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 166, "doc_id": 18872233, "label": "CONTRADICTS", "evidence_sentence_ids": [12], "cited_doc_ids": [18872233], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Bariatric surgery leads to positive outcomes in mental health.\n\nDocument title: Mental Health Conditions Among Patients Seeking and Undergoing Bariatric Surgery: A Meta-analysis.\n\nAbstract sentences:\n[0] IMPORTANCE Bariatric surgery is associated with sustained weight loss and improved physical health status for severely obese individuals.\n[1] Mental health conditions may be common among patients seeking bariatric surgery; however, the prevalence of these conditions and whether they are associated with postoperative outcomes remains unknown.\n[2] OBJECTIVE To determine the prevalence of mental health conditions among bariatric surgery candidates and recipients, to evaluate the association between preoperative mental health conditions and health outcomes following bariatric surgery, and to evaluate the association between surgery and the clinical course of mental health conditions.\n[3] DATA SOURCES We searched PubMed, MEDLINE on OVID, and PsycINFO for studies published between January 1988 and November 2015.\n[4] Study quality was assessed using an adapted tool for risk of bias; quality of evidence was rated based on GRADE (Grading of Recommendations Assessment, Development and Evaluation) criteria.\n[5] FINDINGS We identified 68 publications meeting inclusion criteria: 59 reporting the prevalence of preoperative mental health conditions (65,363 patients) and 27 reporting associations between preoperative mental health conditions and postoperative outcomes (50,182 patients).\n[6] Among patients seeking and undergoing bariatric surgery, the most common mental health conditions, based on random-effects estimates of prevalence, were depression (19% [95% CI, 14%-25%]) and binge eating disorder (17% [95% CI, 13%-21%]).\n[7] There was conflicting evidence regarding the association between preoperative mental health conditions and postoperative weight loss.\n[8] Neither depression nor binge eating disorder was consistently associated with differences in weight outcomes.\n[9] Bariatric surgery was, however, consistently associated with postoperative decreases in the prevalence of depression (7 studies; 8%-74% decrease) and the severity of depressive symptoms (6 studies; 40%-70% decrease).\n[10] CONCLUSIONS AND RELEVANCE Mental health conditions are common among bariatric surgery patients-in particular, depression and binge eating disorder.\n[11] There is inconsistent evidence regarding the association between preoperative mental health conditions and postoperative weight loss.\n[12] Moderate-quality evidence supports an association between bariatric surgery and lower rates of depression postoperatively."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Bariatric surgery was, however, consistently associated with postoperative decreases in the prevalence of depression (7 studies; 8%-74% decrease) and the severity of depressive symptoms (6 studies; 40%-70% decrease).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 167, "doc_id": 18872233, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [18872233], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Bariatric surgery leads to positive outcomes in mental health.\n\nDocument title: Mental Health Conditions Among Patients Seeking and Undergoing Bariatric Surgery: A Meta-analysis.\n\nAbstract sentences:\n[0] IMPORTANCE Bariatric surgery is associated with sustained weight loss and improved physical health status for severely obese individuals.\n[1] Mental health conditions may be common among patients seeking bariatric surgery; however, the prevalence of these conditions and whether they are associated with postoperative outcomes remains unknown.\n[2] OBJECTIVE To determine the prevalence of mental health conditions among bariatric surgery candidates and recipients, to evaluate the association between preoperative mental health conditions and health outcomes following bariatric surgery, and to evaluate the association between surgery and the clinical course of mental health conditions.\n[3] DATA SOURCES We searched PubMed, MEDLINE on OVID, and PsycINFO for studies published between January 1988 and November 2015.\n[4] Study quality was assessed using an adapted tool for risk of bias; quality of evidence was rated based on GRADE (Grading of Recommendations Assessment, Development and Evaluation) criteria.\n[5] FINDINGS We identified 68 publications meeting inclusion criteria: 59 reporting the prevalence of preoperative mental health conditions (65,363 patients) and 27 reporting associations between preoperative mental health conditions and postoperative outcomes (50,182 patients).\n[6] Among patients seeking and undergoing bariatric surgery, the most common mental health conditions, based on random-effects estimates of prevalence, were depression (19% [95% CI, 14%-25%]) and binge eating disorder (17% [95% CI, 13%-21%]).\n[7] There was conflicting evidence regarding the association between preoperative mental health conditions and postoperative weight loss.\n[8] Neither depression nor binge eating disorder was consistently associated with differences in weight outcomes.\n[9] Bariatric surgery was, however, consistently associated with postoperative decreases in the prevalence of depression (7 studies; 8%-74% decrease) and the severity of depressive symptoms (6 studies; 40%-70% decrease).\n[10] CONCLUSIONS AND RELEVANCE Mental health conditions are common among bariatric surgery patients-in particular, depression and binge eating disorder.\n[11] There is inconsistent evidence regarding the association between preoperative mental health conditions and postoperative weight loss.\n[12] Moderate-quality evidence supports an association between bariatric surgery and lower rates of depression postoperatively."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"Moderate-quality evidence supports an association between bariatric surgery and lower rates of depression postoperatively.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 167, "doc_id": 18872233, "label": "SUPPORTS", "evidence_sentence_ids": [12], "cited_doc_ids": [18872233], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Bariatric surgery reduces colorectal cancer.\n\nDocument title: Bariatric Surgery in the United Kingdom: A Cohort Study of Weight Loss and Clinical Outcomes in Routine Clinical Care.\n\nAbstract sentences:\n[0] BACKGROUND Bariatric surgery is becoming a more widespread treatment for obesity.\n[1] Comprehensive evidence of the long-term effects of contemporary surgery on a broad range of clinical outcomes in large populations treated in routine clinical practice is lacking.\n[2] The objective of this study was to measure the association between bariatric surgery, weight, body mass index, and obesity-related co-morbidities.\n[3] METHODS AND FINDINGS This was an observational retrospective cohort study using data from the United Kingdom Clinical Practice Research Datalink.\n[4] All 3,882 patients registered in the database and with bariatric surgery on or before 31 December 2014 were included and matched by propensity score to 3,882 obese patients without surgery.\n[5] The main outcome measures were change in weight and body mass index over 4 y; incident diagnoses of type 2 diabetes mellitus (T2DM), hypertension, angina, myocardial infarction (MI), stroke, fractures, obstructive sleep apnoea, and cancer; mortality; and resolution of hypertension and T2DM.\n[6] Weight measures were available for 3,847 patients between 1 and 4 mo, 2,884 patients between 5 and 12 mo, and 2,258 patients between 13 and 48 mo post-procedure.\n[7] Bariatric surgery patients exhibited rapid weight loss for the first four postoperative months, at a rate of 4.98 kg/mo (95% CI 4.88-5.08).\n[8] Slower weight loss was sustained to the end of 4 y. Gastric bypass (6.56 kg/mo) and sleeve gastrectomy (6.29 kg/mo) were associated with greater initial weight reduction than gastric banding (2.77 kg/mo).\n[9] Protective hazard ratios (HRs) were detected for bariatric surgery for incident T2DM, 0.68 (95% CI 0.55-0.83); hypertension, 0.35 (95% CI 0.27-0.45); angina, 0.59 (95% CI 0.40-0.87);MI, 0.28 (95% CI 0.10-0.74); and obstructive sleep apnoea, 0.55 (95% CI 0.40-0.87).\n[10] Strong associations were found between bariatric surgery and the resolution of T2DM, with a HR of 9.29 (95% CI 6.84-12.62), and between bariatric surgery and the resolution of hypertension, with a HR of 5.64 (95% CI 2.65-11.99).\n[11] No association was detected between bariatric surgery and fractures, cancer, or stroke.\n[12] Effect estimates for mortality found no protective association with bariatric surgery overall, with a HR of 0.97 (95% CI 0.66-1.43).\n[13] The data used were recorded for the management of patients in primary care and may be subject to inaccuracy, which would tend to lead to underestimates of true relative effect sizes.\n[14] CONCLUSIONS Bariatric surgery as delivered in the UK healthcare system is associated with dramatic weight loss, sustained at least 4 y after surgery.\n[15] This weight loss is accompanied by substantial improvements in pre-existing T2DM and hypertension, as well as a reduced risk of incident T2DM, hypertension, angina, MI, and obstructive sleep apnoea.\n[16] Widening the availability of bariatric surgery could lead to substantial health benefits for many people who are morbidly obese."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"No association was detected between bariatric surgery and fractures, cancer, or stroke.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 168, "doc_id": 5824985, "label": "CONTRADICTS", "evidence_sentence_ids": [11], "cited_doc_ids": [5824985], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Bariatric surgery reduces postmenopausal breast cancer.\n\nDocument title: Bariatric Surgery in the United Kingdom: A Cohort Study of Weight Loss and Clinical Outcomes in Routine Clinical Care.\n\nAbstract sentences:\n[0] BACKGROUND Bariatric surgery is becoming a more widespread treatment for obesity.\n[1] Comprehensive evidence of the long-term effects of contemporary surgery on a broad range of clinical outcomes in large populations treated in routine clinical practice is lacking.\n[2] The objective of this study was to measure the association between bariatric surgery, weight, body mass index, and obesity-related co-morbidities.\n[3] METHODS AND FINDINGS This was an observational retrospective cohort study using data from the United Kingdom Clinical Practice Research Datalink.\n[4] All 3,882 patients registered in the database and with bariatric surgery on or before 31 December 2014 were included and matched by propensity score to 3,882 obese patients without surgery.\n[5] The main outcome measures were change in weight and body mass index over 4 y; incident diagnoses of type 2 diabetes mellitus (T2DM), hypertension, angina, myocardial infarction (MI), stroke, fractures, obstructive sleep apnoea, and cancer; mortality; and resolution of hypertension and T2DM.\n[6] Weight measures were available for 3,847 patients between 1 and 4 mo, 2,884 patients between 5 and 12 mo, and 2,258 patients between 13 and 48 mo post-procedure.\n[7] Bariatric surgery patients exhibited rapid weight loss for the first four postoperative months, at a rate of 4.98 kg/mo (95% CI 4.88-5.08).\n[8] Slower weight loss was sustained to the end of 4 y. Gastric bypass (6.56 kg/mo) and sleeve gastrectomy (6.29 kg/mo) were associated with greater initial weight reduction than gastric banding (2.77 kg/mo).\n[9] Protective hazard ratios (HRs) were detected for bariatric surgery for incident T2DM, 0.68 (95% CI 0.55-0.83); hypertension, 0.35 (95% CI 0.27-0.45); angina, 0.59 (95% CI 0.40-0.87);MI, 0.28 (95% CI 0.10-0.74); and obstructive sleep apnoea, 0.55 (95% CI 0.40-0.87).\n[10] Strong associations were found between bariatric surgery and the resolution of T2DM, with a HR of 9.29 (95% CI 6.84-12.62), and between bariatric surgery and the resolution of hypertension, with a HR of 5.64 (95% CI 2.65-11.99).\n[11] No association was detected between bariatric surgery and fractures, cancer, or stroke.\n[12] Effect estimates for mortality found no protective association with bariatric surgery overall, with a HR of 0.97 (95% CI 0.66-1.43).\n[13] The data used were recorded for the management of patients in primary care and may be subject to inaccuracy, which would tend to lead to underestimates of true relative effect sizes.\n[14] CONCLUSIONS Bariatric surgery as delivered in the UK healthcare system is associated with dramatic weight loss, sustained at least 4 y after surgery.\n[15] This weight loss is accompanied by substantial improvements in pre-existing T2DM and hypertension, as well as a reduced risk of incident T2DM, hypertension, angina, MI, and obstructive sleep apnoea.\n[16] Widening the availability of bariatric surgery could lead to substantial health benefits for many people who are morbidly obese."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"No association was detected between bariatric surgery and fractures, cancer, or stroke.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 169, "doc_id": 5824985, "label": "CONTRADICTS", "evidence_sentence_ids": [11], "cited_doc_ids": [5824985], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Basophils promote disease development in patients with systemic lupus erythematosus (SLE).\n\nDocument title: BASOPHILS AND THE T HELPER 2 ENVIRONMENT CAN PROMOTE THE DEVELOPMENT OF LUPUS NEPHRITIS\n\nAbstract sentences:\n[0] In systemic lupus erythematosus (SLE), self-reactive antibodies can target the kidney (lupus nephritis), leading to functional failure and possible mortality.\n[1] We report that activation of basophils by autoreactive IgE causes their homing to lymph nodes, promoting T helper type 2 (T(H)2) cell differentiation and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in mice lacking the Src family protein tyrosine kinase Lyn (Lyn(-/-) mice).\n[2] Individuals with SLE also have elevated serum IgE, self-reactive IgEs and activated basophils that express CD62 ligand (CD62L) and the major histocompatibility complex (MHC) class II molecule human leukocyte antigen-DR (HLA-DR), parameters that are associated with increased disease activity and active lupus nephritis.\n[3] Basophils were also present in the lymph nodes and spleen of subjects with SLE.\n[4] Thus, in Lyn(-/-) mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in individuals with SLE IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"We report that activation of basophils by autoreactive IgE causes their homing to lymph nodes, promoting T helper type 2 (T(H)2) cell differentiation and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in mice lacking the Src family protein tyrosine kinase Lyn (Lyn(-/-) mice).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 172, "doc_id": 12670680, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [12670680], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Basophils promote disease development in patients with systemic lupus erythematosus (SLE).\n\nDocument title: BASOPHILS AND THE T HELPER 2 ENVIRONMENT CAN PROMOTE THE DEVELOPMENT OF LUPUS NEPHRITIS\n\nAbstract sentences:\n[0] In systemic lupus erythematosus (SLE), self-reactive antibodies can target the kidney (lupus nephritis), leading to functional failure and possible mortality.\n[1] We report that activation of basophils by autoreactive IgE causes their homing to lymph nodes, promoting T helper type 2 (T(H)2) cell differentiation and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in mice lacking the Src family protein tyrosine kinase Lyn (Lyn(-/-) mice).\n[2] Individuals with SLE also have elevated serum IgE, self-reactive IgEs and activated basophils that express CD62 ligand (CD62L) and the major histocompatibility complex (MHC) class II molecule human leukocyte antigen-DR (HLA-DR), parameters that are associated with increased disease activity and active lupus nephritis.\n[3] Basophils were also present in the lymph nodes and spleen of subjects with SLE.\n[4] Thus, in Lyn(-/-) mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in individuals with SLE IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Individuals with SLE also have elevated serum IgE, self-reactive IgEs and activated basophils that express CD62 ligand (CD62L) and the major histocompatibility complex (MHC) class II molecule human leukocyte antigen-DR (HLA-DR), parameters that are associated with increased disease activity and active lupus nephritis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 172, "doc_id": 12670680, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [12670680], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Basophils promote disease development in patients with systemic lupus erythematosus (SLE).\n\nDocument title: BASOPHILS AND THE T HELPER 2 ENVIRONMENT CAN PROMOTE THE DEVELOPMENT OF LUPUS NEPHRITIS\n\nAbstract sentences:\n[0] In systemic lupus erythematosus (SLE), self-reactive antibodies can target the kidney (lupus nephritis), leading to functional failure and possible mortality.\n[1] We report that activation of basophils by autoreactive IgE causes their homing to lymph nodes, promoting T helper type 2 (T(H)2) cell differentiation and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in mice lacking the Src family protein tyrosine kinase Lyn (Lyn(-/-) mice).\n[2] Individuals with SLE also have elevated serum IgE, self-reactive IgEs and activated basophils that express CD62 ligand (CD62L) and the major histocompatibility complex (MHC) class II molecule human leukocyte antigen-DR (HLA-DR), parameters that are associated with increased disease activity and active lupus nephritis.\n[3] Basophils were also present in the lymph nodes and spleen of subjects with SLE.\n[4] Thus, in Lyn(-/-) mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in individuals with SLE IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Thus, in Lyn(-/-) mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in individuals with SLE IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 172, "doc_id": 12670680, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [12670680], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Bcp1 is a chaperone for Rpl23.\n\nDocument title: Rational Extension of the Ribosome Biogenesis Pathway Using Network-Guided Genetics\n\nAbstract sentences:\n[0] Biogenesis of ribosomes is an essential cellular process conserved across all eukaryotes and is known to require >170 genes for the assembly, modification, and trafficking of ribosome components through multiple cellular compartments.\n[1] Despite intensive study, this pathway likely involves many additional genes.\n[2] Here, we employ network-guided genetics-an approach for associating candidate genes with biological processes that capitalizes on recent advances in functional genomic and proteomic studies-to computationally identify additional ribosomal biogenesis genes.\n[3] We experimentally evaluated >100 candidate yeast genes in a battery of assays, confirming involvement of at least 15 new genes, including previously uncharacterized genes (YDL063C, YIL091C, YOR287C, YOR006C/TSR3, YOL022C/TSR4).\n[4] We associate the new genes with specific aspects of ribosomal subunit maturation, ribosomal particle association, and ribosomal subunit nuclear export, and we identify genes specifically required for the processing of 5S, 7S, 20S, 27S, and 35S rRNAs.\n[5] These results reveal new connections between ribosome biogenesis and mRNA splicing and add >10% new genes-most with human orthologs-to the biogenesis pathway, significantly extending our understanding of a universally conserved eukaryotic process."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 173, "doc_id": 8126244, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [8126244], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Beta-band coherence is diminished for visible stimuli over invisible stimuli.\n\nDocument title: Converging Intracranial Markers of Conscious Access\n\nAbstract sentences:\n[0] We compared conscious and nonconscious processing of briefly flashed words using a visual masking procedure while recording intracranial electroencephalogram (iEEG) in ten patients.\n[1] Nonconscious processing of masked words was observed in multiple cortical areas, mostly within an early time window (<300 ms), accompanied by induced gamma-band activity, but without coherent long-distance neural activity, suggesting a quickly dissipating feedforward wave.\n[2] In contrast, conscious processing of unmasked words was characterized by the convergence of four distinct neurophysiological markers: sustained voltage changes, particularly in prefrontal cortex, large increases in spectral power in the gamma band, increases in long-distance phase synchrony in the beta range, and increases in long-range Granger causality.\n[3] We argue that all of those measures provide distinct windows into the same distributed state of conscious processing.\n[4] These results have a direct impact on current theoretical discussions concerning the neural correlates of conscious access."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 174, "doc_id": 1710116, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [1710116], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Beta-band coherence is enhanced for visible stimuli over invisible stimuli.\n\nDocument title: Converging Intracranial Markers of Conscious Access\n\nAbstract sentences:\n[0] We compared conscious and nonconscious processing of briefly flashed words using a visual masking procedure while recording intracranial electroencephalogram (iEEG) in ten patients.\n[1] Nonconscious processing of masked words was observed in multiple cortical areas, mostly within an early time window (<300 ms), accompanied by induced gamma-band activity, but without coherent long-distance neural activity, suggesting a quickly dissipating feedforward wave.\n[2] In contrast, conscious processing of unmasked words was characterized by the convergence of four distinct neurophysiological markers: sustained voltage changes, particularly in prefrontal cortex, large increases in spectral power in the gamma band, increases in long-distance phase synchrony in the beta range, and increases in long-range Granger causality.\n[3] We argue that all of those measures provide distinct windows into the same distributed state of conscious processing.\n[4] These results have a direct impact on current theoretical discussions concerning the neural correlates of conscious access."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 175, "doc_id": 1710116, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [1710116], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: BiP is a general endoplasmic reticulum stress marker.\n\nDocument title: Wolfram syndrome 1 and adenylyl cyclase 8 interact at the plasma membrane to regulate insulin production and secretion\n\nAbstract sentences:\n[0] Endoplasmic reticulum (ER) stress causes pancreatic β-cell dysfunction and contributes to β-cell loss and the progression of type 2 diabetes.\n[1] Wolfram syndrome 1 (WFS1) has been shown to be an important regulator of the ER stress signalling pathway; however, its role in β-cell function remains unclear.\n[2] Here we provide evidence that WFS1 is essential for glucose- and glucagon-like peptide 1 (GLP-1)-stimulated cyclic AMP production and regulation of insulin biosynthesis and secretion.\n[3] Stimulation with glucose causes WFS1 translocation from the ER to the plasma membrane, where it forms a complex with adenylyl cyclase 8 (AC8), an essential cAMP-generating enzyme in the β-cell that integrates glucose and GLP-1 signalling.\n[4] ER stress and mutant WFS1 inhibit complex formation and activation of AC8, reducing cAMP synthesis and insulin secretion.\n[5] These findings reveal that an ER-stress-related protein has a distinct role outside the ER regulating both insulin biosynthesis and secretion.\n[6] The reduction of WFS1 protein on the plasma membrane during ER stress is a contributing factor for β-cell dysfunction and progression of type 2 diabetes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 176, "doc_id": 32587939, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [32587939], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Binding of p53 to enhancer regions (p53BERs) regulates the activity of p53 transcription and cell cycle arrest through the production of p53-dependent eRNAs.\n\nDocument title: eRNAs are required for p53-dependent enhancer activity and gene transcription.\n\nAbstract sentences:\n[0] Binding within or nearby target genes involved in cell proliferation and survival enables the p53 tumor suppressor gene to regulate their transcription and cell-cycle progression.\n[1] Using genome-wide chromatin-binding profiles, we describe binding of p53 also to regions located distantly from any known p53 target gene.\n[2] Interestingly, many of these regions possess conserved p53-binding sites and all known hallmarks of enhancer regions.\n[3] We demonstrate that these p53-bound enhancer regions (p53BERs) indeed contain enhancer activity and interact intrachromosomally with multiple neighboring genes to convey long-distance p53-dependent transcription regulation.\n[4] Furthermore, p53BERs produce, in a p53-dependent manner, enhancer RNAs (eRNAs) that are required for efficient transcriptional enhancement of interacting target genes and induction of a p53-dependent cell-cycle arrest.\n[5] Thus, our results ascribe transcription enhancement activity to p53 with the capacity to regulate multiple genes from a single genomic binding site.\n[6] Moreover, eRNA production from p53BERs is required for efficient p53 transcription enhancement."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Furthermore, p53BERs produce, in a p53-dependent manner, enhancer RNAs (eRNAs) that are required for efficient transcriptional enhancement of interacting target genes and induction of a p53-dependent cell-cycle arrest.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 177, "doc_id": 9669099, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [9669099], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Binding of p53 to enhancer regions (p53BERs) regulates the activity of p53 transcription and cell cycle arrest through the production of p53-dependent eRNAs.\n\nDocument title: eRNAs are required for p53-dependent enhancer activity and gene transcription.\n\nAbstract sentences:\n[0] Binding within or nearby target genes involved in cell proliferation and survival enables the p53 tumor suppressor gene to regulate their transcription and cell-cycle progression.\n[1] Using genome-wide chromatin-binding profiles, we describe binding of p53 also to regions located distantly from any known p53 target gene.\n[2] Interestingly, many of these regions possess conserved p53-binding sites and all known hallmarks of enhancer regions.\n[3] We demonstrate that these p53-bound enhancer regions (p53BERs) indeed contain enhancer activity and interact intrachromosomally with multiple neighboring genes to convey long-distance p53-dependent transcription regulation.\n[4] Furthermore, p53BERs produce, in a p53-dependent manner, enhancer RNAs (eRNAs) that are required for efficient transcriptional enhancement of interacting target genes and induction of a p53-dependent cell-cycle arrest.\n[5] Thus, our results ascribe transcription enhancement activity to p53 with the capacity to regulate multiple genes from a single genomic binding site.\n[6] Moreover, eRNA production from p53BERs is required for efficient p53 transcription enhancement."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Moreover, eRNA production from p53BERs is required for efficient p53 transcription enhancement.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 177, "doc_id": 9669099, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [9669099], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Birth-weight is negatively associated with breast cancer.\n\nDocument title: Birth Size and Breast Cancer Risk: Re-analysis of Individual Participant Data from 32 Studies\n\nAbstract sentences:\n[0] BACKGROUND Birth size, perhaps a proxy for prenatal environment, might be a correlate of subsequent breast cancer risk, but findings from epidemiological studies have been inconsistent.\n[1] We re-analysed individual participant data from published and unpublished studies to obtain more precise estimates of the magnitude and shape of the birth size-breast cancer association.\n[2] METHODS AND FINDINGS Studies were identified through computer-assisted and manual searches, and personal communication with investigators.\n[3] Individual participant data from 32 studies, comprising 22,058 breast cancer cases, were obtained.\n[4] Random effect models were used, if appropriate, to combine study-specific estimates of effect.\n[5] Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003).\n[6] Relative to women who weighed 3.000-3.499 kg, the risk was 0.96 (CI 0.80-1.16) in those who weighed < 2.500 kg, and 1.12 (95% CI 1.00-1.25) in those who weighed > or = 4.000 kg (p for linear trend = 0.001) in birth record data.\n[7] Birth length and head circumference from birth records were also positively associated with breast cancer risk (pooled RR per one SD increment: 1.06 [95% CI 1.03-1.10] and 1.09 [95% CI 1.03-1.15], respectively).\n[8] Simultaneous adjustment for these three birth size variables showed that length was the strongest independent predictor of risk.\n[9] The birth size effects did not appear to be confounded or mediated by established breast cancer risk factors and were not modified by age or menopausal status.\n[10] The cumulative incidence of breast cancer per 100 women by age 80 y in the study populations was estimated to be 10.0, 10.0, 10.4, and 11.5 in those who were, respectively, in the bottom, second, third, and top fourths of the birth length distribution.\n[11] CONCLUSIONS This pooled analysis of individual participant data is consistent with birth size, and in particular birth length, being an independent correlate of breast cancer risk in adulthood."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 178, "doc_id": 16322674, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [16322674, 27123743, 23557241, 17450673], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Birth-weight is negatively associated with breast cancer.\n\nDocument title: Birth Size and Breast Cancer Risk: Re-analysis of Individual Participant Data from 32 Studies\n\nAbstract sentences:\n[0] BACKGROUND Birth size, perhaps a proxy for prenatal environment, might be a correlate of subsequent breast cancer risk, but findings from epidemiological studies have been inconsistent.\n[1] We re-analysed individual participant data from published and unpublished studies to obtain more precise estimates of the magnitude and shape of the birth size-breast cancer association.\n[2] METHODS AND FINDINGS Studies were identified through computer-assisted and manual searches, and personal communication with investigators.\n[3] Individual participant data from 32 studies, comprising 22,058 breast cancer cases, were obtained.\n[4] Random effect models were used, if appropriate, to combine study-specific estimates of effect.\n[5] Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003).\n[6] Relative to women who weighed 3.000-3.499 kg, the risk was 0.96 (CI 0.80-1.16) in those who weighed < 2.500 kg, and 1.12 (95% CI 1.00-1.25) in those who weighed > or = 4.000 kg (p for linear trend = 0.001) in birth record data.\n[7] Birth length and head circumference from birth records were also positively associated with breast cancer risk (pooled RR per one SD increment: 1.06 [95% CI 1.03-1.10] and 1.09 [95% CI 1.03-1.15], respectively).\n[8] Simultaneous adjustment for these three birth size variables showed that length was the strongest independent predictor of risk.\n[9] The birth size effects did not appear to be confounded or mediated by established breast cancer risk factors and were not modified by age or menopausal status.\n[10] The cumulative incidence of breast cancer per 100 women by age 80 y in the study populations was estimated to be 10.0, 10.0, 10.4, and 11.5 in those who were, respectively, in the bottom, second, third, and top fourths of the birth length distribution.\n[11] CONCLUSIONS This pooled analysis of individual participant data is consistent with birth size, and in particular birth length, being an independent correlate of breast cancer risk in adulthood."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Relative to women who weighed 3.000-3.499 kg, the risk was 0.96 (CI 0.80-1.16) in those who weighed < 2.500 kg, and 1.12 (95% CI 1.00-1.25) in those who weighed > or = 4.000 kg (p for linear trend = 0.001) in birth record data.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 178, "doc_id": 16322674, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [16322674, 27123743, 23557241, 17450673], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Birth-weight is negatively associated with breast cancer.\n\nDocument title: Birth Size and Breast Cancer Risk: Re-analysis of Individual Participant Data from 32 Studies\n\nAbstract sentences:\n[0] BACKGROUND Birth size, perhaps a proxy for prenatal environment, might be a correlate of subsequent breast cancer risk, but findings from epidemiological studies have been inconsistent.\n[1] We re-analysed individual participant data from published and unpublished studies to obtain more precise estimates of the magnitude and shape of the birth size-breast cancer association.\n[2] METHODS AND FINDINGS Studies were identified through computer-assisted and manual searches, and personal communication with investigators.\n[3] Individual participant data from 32 studies, comprising 22,058 breast cancer cases, were obtained.\n[4] Random effect models were used, if appropriate, to combine study-specific estimates of effect.\n[5] Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003).\n[6] Relative to women who weighed 3.000-3.499 kg, the risk was 0.96 (CI 0.80-1.16) in those who weighed < 2.500 kg, and 1.12 (95% CI 1.00-1.25) in those who weighed > or = 4.000 kg (p for linear trend = 0.001) in birth record data.\n[7] Birth length and head circumference from birth records were also positively associated with breast cancer risk (pooled RR per one SD increment: 1.06 [95% CI 1.03-1.10] and 1.09 [95% CI 1.03-1.15], respectively).\n[8] Simultaneous adjustment for these three birth size variables showed that length was the strongest independent predictor of risk.\n[9] The birth size effects did not appear to be confounded or mediated by established breast cancer risk factors and were not modified by age or menopausal status.\n[10] The cumulative incidence of breast cancer per 100 women by age 80 y in the study populations was estimated to be 10.0, 10.0, 10.4, and 11.5 in those who were, respectively, in the bottom, second, third, and top fourths of the birth length distribution.\n[11] CONCLUSIONS This pooled analysis of individual participant data is consistent with birth size, and in particular birth length, being an independent correlate of breast cancer risk in adulthood."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"CONCLUSIONS This pooled analysis of individual participant data is consistent with birth size, and in particular birth length, being an independent correlate of breast cancer risk in adulthood.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 178, "doc_id": 16322674, "label": "CONTRADICTS", "evidence_sentence_ids": [11], "cited_doc_ids": [16322674, 27123743, 23557241, 17450673], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Birth-weight is negatively associated with breast cancer.\n\nDocument title: Role of birthweight in the etiology of breast cancer.\n\nAbstract sentences:\n[0] Breast cancer may originate in utero.\n[1] We reviewed the available evidence on the association between birthweight and the risk of breast cancer.\n[2] To date, 26 research papers addressing this issue have been published.\n[3] The majority of studies identified a positive link between birthweight and premenopausal, but not postmenopausal, breast cancer.\n[4] The relative risk estimate for breast cancer comparing women with high birthweight to women with low birthweight combining all studies including both pre- and postmenopausal breast cancer was 1.23 (95% confidence interval 1.13-1.34).\n[5] The mechanisms underlying this association likely include elevated levels of growth factors that may increase the number of susceptible stem cells in the mammary gland or initiate tumors through DNA mutations.\n[6] Loss of imprinting (LOI) of growth hormone genes relevant for intrauterine growth, such as insulin-like growth factor 2 (IGF2), leads to abnormally high levels of these hormones evidenced by high birthweight.\n[7] LOI of IGF2 has also been found in mammary tumor tissue.\n[8] The role of environmental factors that stimulate such epigenetic regulation of gene expression remains to be elucidated."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"The relative risk estimate for breast cancer comparing women with high birthweight to women with low birthweight combining all studies including both pre- and postmenopausal breast cancer was 1.23 (95% confidence interval 1.13-1.34).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 178, "doc_id": 27123743, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [16322674, 27123743, 23557241, 17450673], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Birth-weight is negatively associated with breast cancer.\n\nDocument title: Intrauterine factors and risk of breast cancer: a systematic review and meta-analysis of current evidence.\n\nAbstract sentences:\n[0] BACKGROUND Emerging evidence suggests an association between female prenatal experience and her subsequent risk of developing breast cancer.\n[1] Potential underlying mechanisms include variation in amounts of maternal endogenous sex hormones and growth hormones, germ-cell mutations, formation of cancer stem-cells, and other genetic or epigenetic events.\n[2] We reviewed and summarised quantitatively the available data on intrauterine exposures and risk of breast cancer.\n[3] METHODS We systematically searched for studies that assessed association between perinatal factors and risk of breast cancer.\n[4] We reviewed separately each of the perinatal factors, including birthweight, birth length, parental age at delivery, gestational age, intrauterine exposure to diethylstilbestrol, twin membership, maternal pre-eclampsia or eclampsia, and other factors.\n[5] FINDINGS We identified 57 studies published between Oct 1, 1980, and June 21, 2007.\n[6] Increased risk of breast cancer was noted with increased birthweight (relative risk [RR] 1.15 [95% CI 1.09-1.21]), birth length (1.28 [1.11-1.48]), higher maternal age (1.13 [1.02-1.25]), and paternal age (1.12 [1.05-1.19]).\n[7] Decreased risk of breast cancer was noted for maternal pre-eclampsia and eclampsia (0.48 [0.30-0.78]) and twin membership (0.93 [0.87-1.00]).\n[8] No association was noted between risk of breast cancer and gestational age at birth (0.95 [0.71-1.26]) or maternal diethylstilbestrol treatment (1.40 [0.86-2.28]).\n[9] INTERPRETATION The intrauterine environment contributes to the predisposition of women to breast cancer in adulthood.\n[10] The in-utero mechanisms responsible for such predisposition need to be elucidated."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Increased risk of breast cancer was noted with increased birthweight (relative risk [RR] 1.15 [95% CI 1.09-1.21]), birth length (1.28 [1.11-1.48]), higher maternal age (1.13 [1.02-1.25]), and paternal age (1.12 [1.05-1.19]).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 178, "doc_id": 23557241, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [16322674, 27123743, 23557241, 17450673], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Birth-weight is negatively associated with breast cancer.\n\nDocument title: Intrauterine environments and breast cancer risk: meta-analysis and systematic review\n\nAbstract sentences:\n[0] INTRODUCTION Various perinatal factors, including birth weight, birth order, maternal age, gestational age, twin status, and parental smoking, have been postulated to affect breast cancer risk in daughters by altering the hormonal environment of the developing fetal mammary glands.\n[1] Despite ample biologic plausibility, epidemiologic studies to date have yielded conflicting results.\n[2] We investigated the associations between perinatal factors and subsequent breast cancer risk through meta-analyses.\n[3] METHODS We reviewed breast cancer studies published from January 1966 to February 2007 that included data on birth weight, birth order, maternal age, gestational age, twin status, and maternal or paternal smoking.\n[4] Meta-analyses using random effect models were employed to summarize the results.\n[5] RESULTS We found that heavier birth weights were associated with increased breast cancer risk, with studies involving five categories of birth weight identifying odds ratios (ORs) of 1.24 (95% confidence interval [CI] 1.04 to 1.48) for 4,000 g or more and 1.15 (95% CI 1.04 to 1.26) for 3,500 g to 3,999 g, relative to a birth weight of 2,500 to 2,599 g. These studies provided no support for a J-shaped relationship of birthweight to risk.\n[6] Support for an association with birthweight was also derived from studies based on three birth weight categories (OR 1.15 [95% CI 1.01 to 1.31] for > or =4,000 g relative to <3,000 g) and two birth weight categories (OR 1.09 [95% CI 1.02 to 1.18] for > or =3,000 g relative to <3,000 g).\n[7] Women born to older mothers and twins were also at some increased risk, but the results were heterogeneous across studies and publication years.\n[8] Birth order, prematurity, and maternal smoking were unrelated to breast cancer risk.\n[9] CONCLUSION Our findings provide some support for the hypothesis that in utero exposures reflective of higher endogenous hormone levels could affect risk for development of breast cancer in adulthood."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"RESULTS We found that heavier birth weights were associated with increased breast cancer risk, with studies involving five categories of birth weight identifying odds ratios (ORs) of 1.24 (95% confidence interval [CI] 1.04 to 1.48) for 4,000 g or more and 1.15 (95% CI 1.04 to 1.26) for 3,500 g to 3,999 g, relative to a birth weight of 2,500 to 2,599 g. These studies provided no support for a J-shaped relationship of birthweight to risk.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 178, "doc_id": 17450673, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [16322674, 27123743, 23557241, 17450673], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Birth-weight is negatively associated with breast cancer.\n\nDocument title: Intrauterine environments and breast cancer risk: meta-analysis and systematic review\n\nAbstract sentences:\n[0] INTRODUCTION Various perinatal factors, including birth weight, birth order, maternal age, gestational age, twin status, and parental smoking, have been postulated to affect breast cancer risk in daughters by altering the hormonal environment of the developing fetal mammary glands.\n[1] Despite ample biologic plausibility, epidemiologic studies to date have yielded conflicting results.\n[2] We investigated the associations between perinatal factors and subsequent breast cancer risk through meta-analyses.\n[3] METHODS We reviewed breast cancer studies published from January 1966 to February 2007 that included data on birth weight, birth order, maternal age, gestational age, twin status, and maternal or paternal smoking.\n[4] Meta-analyses using random effect models were employed to summarize the results.\n[5] RESULTS We found that heavier birth weights were associated with increased breast cancer risk, with studies involving five categories of birth weight identifying odds ratios (ORs) of 1.24 (95% confidence interval [CI] 1.04 to 1.48) for 4,000 g or more and 1.15 (95% CI 1.04 to 1.26) for 3,500 g to 3,999 g, relative to a birth weight of 2,500 to 2,599 g. These studies provided no support for a J-shaped relationship of birthweight to risk.\n[6] Support for an association with birthweight was also derived from studies based on three birth weight categories (OR 1.15 [95% CI 1.01 to 1.31] for > or =4,000 g relative to <3,000 g) and two birth weight categories (OR 1.09 [95% CI 1.02 to 1.18] for > or =3,000 g relative to <3,000 g).\n[7] Women born to older mothers and twins were also at some increased risk, but the results were heterogeneous across studies and publication years.\n[8] Birth order, prematurity, and maternal smoking were unrelated to breast cancer risk.\n[9] CONCLUSION Our findings provide some support for the hypothesis that in utero exposures reflective of higher endogenous hormone levels could affect risk for development of breast cancer in adulthood."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"CONCLUSION Our findings provide some support for the hypothesis that in utero exposures reflective of higher endogenous hormone levels could affect risk for development of breast cancer in adulthood.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 178, "doc_id": 17450673, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [16322674, 27123743, 23557241, 17450673], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Blocking the interaction between TDP-43 and respiratory complex I proteins ND3 and ND6 prevents TDP-43-induced neuronal loss.\n\nDocument title: The Inhibition of TDP-43 Mitochondrial Localization Blocks Its Neuronal Toxicity\n\nAbstract sentences:\n[0] Genetic mutations in TAR DNA-binding protein 43 (TARDBP, also known as TDP-43) cause amyotrophic lateral sclerosis (ALS), and an increase in the presence of TDP-43 (encoded by TARDBP) in the cytoplasm is a prominent histopathological feature of degenerating neurons in various neurodegenerative diseases.\n[1] However, the molecular mechanisms by which TDP-43 contributes to ALS pathophysiology remain elusive.\n[2] Here we have found that TDP-43 accumulates in the mitochondria of neurons in subjects with ALS or frontotemporal dementia (FTD).\n[3] Disease-associated mutations increase TDP-43 mitochondrial localization.\n[4] In mitochondria, wild-type (WT) and mutant TDP-43 preferentially bind mitochondria-transcribed messenger RNAs (mRNAs) encoding respiratory complex I subunits ND3 and ND6, impair their expression and specifically cause complex I disassembly.\n[5] The suppression of TDP-43 mitochondrial localization abolishes WT and mutant TDP-43-induced mitochondrial dysfunction and neuronal loss, and improves phenotypes of transgenic mutant TDP-43 mice.\n[6] Thus, our studies link TDP-43 toxicity directly to mitochondrial bioenergetics and propose the targeting of TDP-43 mitochondrial localization as a promising therapeutic approach for neurodegeneration."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"The suppression of TDP-43 mitochondrial localization abolishes WT and mutant TDP-43-induced mitochondrial dysfunction and neuronal loss, and improves phenotypes of transgenic mutant TDP-43 mice.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 181, "doc_id": 16966326, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [16966326], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Bone Marrow (BM) transplantation is used to treat acute myeloid leukemia (AML)\n\nDocument title: Tetraspanin 3 Is Required for the Development and Propagation of Acute Myelogenous Leukemia.\n\nAbstract sentences:\n[0] Acute Myelogenous Leukemia (AML) is an aggressive cancer that strikes both adults and children and is frequently resistant to therapy.\n[1] Thus, identifying signals needed for AML propagation is a critical step toward developing new approaches for treating this disease.\n[2] Here, we show that Tetraspanin 3 is a target of the RNA binding protein Musashi 2, which plays a key role in AML.\n[3] We generated Tspan3 knockout mice that were born without overt defects.\n[4] However, Tspan3 deletion impaired leukemia stem cell self-renewal and disease propagation and markedly improved survival in mouse models of AML.\n[5] Additionally, Tspan3 inhibition blocked growth of AML patient samples, suggesting that Tspan3 is also important in human disease.\n[6] As part of the mechanism, we show that Tspan3 deficiency disabled responses to CXCL12/SDF-1 and led to defects in AML localization within the niche.\n[7] These identify Tspan3 as an important regulator of aggressive leukemias and highlight a role for Tspan3 in oncogenesis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 182, "doc_id": 11369420, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [11369420], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Bone marrow cells don't contribute to adult macrophage compartments.\n\nDocument title: Tissue-resident macrophages self-maintain locally throughout adult life with minimal contribution from circulating monocytes.\n\nAbstract sentences:\n[0] Despite accumulating evidence suggesting local self-maintenance of tissue macrophages in the steady state, the dogma remains that tissue macrophages derive from monocytes.\n[1] Using parabiosis and fate-mapping approaches, we confirmed that monocytes do not show significant contribution to tissue macrophages in the steady state.\n[2] Similarly, we found that after depletion of lung macrophages, the majority of repopulation occurred by stochastic cellular proliferation in situ in a macrophage colony-stimulating factor (M-Csf)- and granulocyte macrophage (GM)-CSF-dependent manner but independently of interleukin-4.\n[3] We also found that after bone marrow transplantation, host macrophages retained the capacity to expand when the development of donor macrophages was compromised.\n[4] Expansion of host macrophages was functional and prevented the development of alveolar proteinosis in mice transplanted with GM-Csf-receptor-deficient progenitors.\n[5] Collectively, these results indicate that tissue-resident macrophages and circulating monocytes should be classified as mononuclear phagocyte lineages that are independently maintained in the steady state."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"We also found that after bone marrow transplantation, host macrophages retained the capacity to expand when the development of donor macrophages was compromised.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 184, "doc_id": 12827098, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [12827098], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: British female students are bullied more than British male students.\n\nDocument title: Bullying in school: are short pupils at risk? Questionnaire study in a cohort.\n\nAbstract sentences:\n[0] Bullying is still prevalent in schools and is clearly stressful for victims.\n[1] 1 2 It may also have undesirable consequences for bullies, with antisocial behaviour persisting into adulthood.\n[2] Victims are generally reported to be weaker than the bullies.\n[3] 2 3 This would suggest that very short pupils are more likely to be victims and less likely to be the aggressors.\n[4] The Wessex growth study allowed us to examine the prevalence of bullying, as experienced or perpetrated by pupils of different heights.\n[5] Ninety two short normal adolescents who had been below the third centile for height at school entry4 and 117 controls matched for age and sex completed a bullying questionnaire, derived from work by Whitney and Smith.5 There were no refusals or any significant differences in sex or social class between the groups.\n[6] Mean age (range) was 14.7 (13.4-15.7) years.\n[7] Mean height SD scores were: short pupils −1.90 (−3.53 to −0.01), controls 0.31 (−1.41 …"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 186, "doc_id": 16855829, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [16855829], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: British male students are bullied more than British female students.\n\nDocument title: Bullying in school: are short pupils at risk? Questionnaire study in a cohort.\n\nAbstract sentences:\n[0] Bullying is still prevalent in schools and is clearly stressful for victims.\n[1] 1 2 It may also have undesirable consequences for bullies, with antisocial behaviour persisting into adulthood.\n[2] Victims are generally reported to be weaker than the bullies.\n[3] 2 3 This would suggest that very short pupils are more likely to be victims and less likely to be the aggressors.\n[4] The Wessex growth study allowed us to examine the prevalence of bullying, as experienced or perpetrated by pupils of different heights.\n[5] Ninety two short normal adolescents who had been below the third centile for height at school entry4 and 117 controls matched for age and sex completed a bullying questionnaire, derived from work by Whitney and Smith.5 There were no refusals or any significant differences in sex or social class between the groups.\n[6] Mean age (range) was 14.7 (13.4-15.7) years.\n[7] Mean height SD scores were: short pupils −1.90 (−3.53 to −0.01), controls 0.31 (−1.41 …"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 187, "doc_id": 16855829, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [16855829], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Broadly HIV-1 Neutralizing Antibodies (bnAb) 10EB have no affinity for phospholipids.\n\nDocument title: Broad and potent neutralization of HIV-1 by a gp41-specific human antibody\n\nAbstract sentences:\n[0] Characterization of human monoclonal antibodies is providing considerable insight into mechanisms of broad HIV-1 neutralization.\n[1] Here we report an HIV-1 gp41 membrane-proximal external region (MPER)-specific antibody, named 10E8, which neutralizes ∼98% of tested viruses.\n[2] An analysis of sera from 78 healthy HIV-1-infected donors demonstrated that 27% contained MPER-specific antibodies and 8% contained 10E8-like specificities.\n[3] In contrast to other neutralizing MPER antibodies, 10E8 did not bind phospholipids, was not autoreactive, and bound cell-surface envelope.\n[4] The structure of 10E8 in complex with the complete MPER revealed a site of vulnerability comprising a narrow stretch of highly conserved gp41-hydrophobic residues and a critical arginine or lysine just before the transmembrane region.\n[5] Analysis of resistant HIV-1 variants confirmed the importance of these residues for neutralization.\n[6] The highly conserved MPER is a target of potent, non-self-reactive neutralizing antibodies, suggesting that HIV-1 vaccines should aim to induce antibodies to this region of HIV-1 envelope glycoprotein."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"In contrast to other neutralizing MPER antibodies, 10E8 did not bind phospholipids, was not autoreactive, and bound cell-surface envelope.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 189, "doc_id": 4421578, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [4421578], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: C2 works synergistically with A-769662 to activate dephosphorylated AMPK.\n\nDocument title: Structural basis of allosteric and synergistic activation of AMPK by furan-2-phosphonic derivative C2 binding.\n\nAbstract sentences:\n[0] The metabolic stress-sensing enzyme AMP-activated protein kinase (AMPK) is responsible for regulating metabolism in response to energy supply and demand.\n[1] Drugs that activate AMPK may be useful in the treatment of metabolic diseases including type 2 diabetes.\n[2] We have determined the crystal structure of AMPK in complex with its activator 5-(5-hydroxyl-isoxazol-3-yl)-furan-2-phosphonic acid (C2), revealing two C2-binding sites in the γ-subunit distinct from nucleotide sites.\n[3] C2 acts synergistically with the drug A769662 to activate AMPK α1-containing complexes independent of upstream kinases.\n[4] Our results show that dual drug therapies could be effective AMPK-targeting strategies to treat metabolic diseases."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"C2 acts synergistically with the drug A769662 to activate AMPK α1-containing complexes independent of upstream kinases.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 196, "doc_id": 19313533, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [19313533], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CCL19 is a ligand for CCR7.\n\nDocument title: Immobilized chemokine fields and soluble chemokine gradients cooperatively shape migration patterns of dendritic cells.\n\nAbstract sentences:\n[0] Chemokines orchestrate immune cell trafficking by eliciting either directed or random migration and by activating integrins in order to induce cell adhesion.\n[1] Analyzing dendritic cell (DC) migration, we showed that these distinct cellular responses depended on the mode of chemokine presentation within tissues.\n[2] The surface-immobilized form of the chemokine CCL21, the heparan sulfate-anchoring ligand of the CC-chemokine receptor 7 (CCR7), caused random movement of DCs that was confined to the chemokine-presenting surface because it triggered integrin-mediated adhesion.\n[3] Upon direct contact with CCL21, DCs truncated the anchoring residues of CCL21, thereby releasing it from the solid phase.\n[4] Soluble CCL21 functionally resembles the second CCR7 ligand, CCL19, which lacks anchoring residues and forms soluble gradients.\n[5] Both soluble CCR7 ligands triggered chemotactic movement, but not surface adhesion.\n[6] Adhesive random migration and directional steering cooperate to produce dynamic but spatially restricted locomotion patterns closely resembling the cellular dynamics observed in secondary lymphoid organs."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Soluble CCL21 functionally resembles the second CCR7 ligand, CCL19, which lacks anchoring residues and forms soluble gradients.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 197, "doc_id": 2177022, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [2177022], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CCL19 is predominantly present within dLNs.\n\nDocument title: Immobilized chemokine fields and soluble chemokine gradients cooperatively shape migration patterns of dendritic cells.\n\nAbstract sentences:\n[0] Chemokines orchestrate immune cell trafficking by eliciting either directed or random migration and by activating integrins in order to induce cell adhesion.\n[1] Analyzing dendritic cell (DC) migration, we showed that these distinct cellular responses depended on the mode of chemokine presentation within tissues.\n[2] The surface-immobilized form of the chemokine CCL21, the heparan sulfate-anchoring ligand of the CC-chemokine receptor 7 (CCR7), caused random movement of DCs that was confined to the chemokine-presenting surface because it triggered integrin-mediated adhesion.\n[3] Upon direct contact with CCL21, DCs truncated the anchoring residues of CCL21, thereby releasing it from the solid phase.\n[4] Soluble CCL21 functionally resembles the second CCR7 ligand, CCL19, which lacks anchoring residues and forms soluble gradients.\n[5] Both soluble CCR7 ligands triggered chemotactic movement, but not surface adhesion.\n[6] Adhesive random migration and directional steering cooperate to produce dynamic but spatially restricted locomotion patterns closely resembling the cellular dynamics observed in secondary lymphoid organs."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 199, "doc_id": 2177022, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [2177022], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CD28 initiates tonic signaling in conventional T cells, which causes an exhaustion phenotype and limited efficiency.\n\nDocument title: 4-1BB Costimulation Ameliorates T Cell Exhaustion Induced by Tonic Signaling of Chimeric Antigen Receptors\n\nAbstract sentences:\n[0] Chimeric antigen receptors (CARs) targeting CD19 have mediated dramatic antitumor responses in hematologic malignancies, but tumor regression has rarely occurred using CARs targeting other antigens.\n[1] It remains unknown whether the impressive effects of CD19 CARs relate to greater susceptibility of hematologic malignancies to CAR therapies, or superior functionality of the CD19 CAR itself.\n[2] We show that tonic CAR CD3-ζ phosphorylation, triggered by antigen-independent clustering of CAR single-chain variable fragments, can induce early exhaustion of CAR T cells that limits antitumor efficacy.\n[3] Such activation is present to varying degrees in all CARs studied, except the highly effective CD19 CAR.\n[4] We further determine that CD28 costimulation augments, whereas 4-1BB costimulation reduces, exhaustion induced by persistent CAR signaling.\n[5] Our results provide biological explanations for the antitumor effects of CD19 CARs and for the observations that CD19 CAR T cells incorporating the 4-1BB costimulatory domain are more persistent than those incorporating CD28 in clinical trials."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"We further determine that CD28 costimulation augments, whereas 4-1BB costimulation reduces, exhaustion induced by persistent CAR signaling.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 200, "doc_id": 18231807, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [18231807], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CD28 signals regulate trafficking of murine auto-reactive T cells into target tissues.\n\nDocument title: CD28 and ITK signals regulate autoreactive T cell trafficking\n\nAbstract sentences:\n[0] Activation of self-reactive T cells and their trafficking to target tissues leads to autoimmune organ destruction.\n[1] Mice lacking the co-inhibitory receptor cytotoxic T lymphocyte antigen-4 (CTLA-4) develop fatal autoimmunity characterized by lymphocytic infiltration into nonlymphoid tissues.\n[2] Here, we demonstrate that the CD28 co-stimulatory pathway regulates the trafficking of self-reactive Ctla4(-/-) T cells to tissues.\n[3] Concurrent ablation of the CD28-activated Tec family kinase ITK does not block spontaneous T cell activation but instead causes self-reactive Ctla4(-/-) T cells to accumulate in secondary lymphoid organs.\n[4] Despite excessive spontaneous T cell activation and proliferation in lymphoid organs, Itk(-/-); Ctla4(-/-) mice are otherwise healthy, mount antiviral immune responses and exhibit a long lifespan.\n[5] We propose that ITK specifically licenses autoreactive T cells to enter tissues to mount destructive immune responses.\n[6] Notably, ITK inhibitors mimic the null mutant phenotype and also prevent pancreatic islet infiltration by diabetogenic T cells in mouse models of type 1 diabetes, highlighting their potential utility for the treatment of human autoimmune disorders."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here, we demonstrate that the CD28 co-stimulatory pathway regulates the trafficking of self-reactive Ctla4(-/-) T cells to tissues.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 201, "doc_id": 2462673, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [2462673], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CD28 signals regulate trafficking of murine auto-reactive T cells into target tissues.\n\nDocument title: CD28 and ITK signals regulate autoreactive T cell trafficking\n\nAbstract sentences:\n[0] Activation of self-reactive T cells and their trafficking to target tissues leads to autoimmune organ destruction.\n[1] Mice lacking the co-inhibitory receptor cytotoxic T lymphocyte antigen-4 (CTLA-4) develop fatal autoimmunity characterized by lymphocytic infiltration into nonlymphoid tissues.\n[2] Here, we demonstrate that the CD28 co-stimulatory pathway regulates the trafficking of self-reactive Ctla4(-/-) T cells to tissues.\n[3] Concurrent ablation of the CD28-activated Tec family kinase ITK does not block spontaneous T cell activation but instead causes self-reactive Ctla4(-/-) T cells to accumulate in secondary lymphoid organs.\n[4] Despite excessive spontaneous T cell activation and proliferation in lymphoid organs, Itk(-/-); Ctla4(-/-) mice are otherwise healthy, mount antiviral immune responses and exhibit a long lifespan.\n[5] We propose that ITK specifically licenses autoreactive T cells to enter tissues to mount destructive immune responses.\n[6] Notably, ITK inhibitors mimic the null mutant phenotype and also prevent pancreatic islet infiltration by diabetogenic T cells in mouse models of type 1 diabetes, highlighting their potential utility for the treatment of human autoimmune disorders."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Concurrent ablation of the CD28-activated Tec family kinase ITK does not block spontaneous T cell activation but instead causes self-reactive Ctla4(-/-) T cells to accumulate in secondary lymphoid organs.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 201, "doc_id": 2462673, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [2462673], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CD44v6 is not associated with constitutive and reprogrammed cancer stem cells driving cancer metastasis.\n\nDocument title: CD44v6 is a marker of constitutive and reprogrammed cancer stem cells driving colon cancer metastasis.\n\nAbstract sentences:\n[0] Cancer stem cells drive tumor formation and metastasis, but how they acquire metastatic traits is not well understood.\n[1] Here, we show that all colorectal cancer stem cells (CR-CSCs) express CD44v6, which is required for their migration and generation of metastatic tumors.\n[2] CD44v6 expression is low in primary tumors but demarcated clonogenic CR-CSC populations.\n[3] Cytokines hepatocyte growth factor (HGF), osteopontin (OPN), and stromal-derived factor 1α (SDF-1), secreted from tumor associated cells, increase CD44v6 expression in CR-CSCs by activating the Wnt/β-catenin pathway, which promotes migration and metastasis.\n[4] CD44v6(-) progenitor cells do not give rise to metastatic lesions but, when treated with cytokines, acquire CD44v6 expression and metastatic capacity.\n[5] Importantly, phosphatidylinositol 3-kinase (PI3K) inhibition selectively killed CD44v6 CR-CSCs and reduced metastatic growth.\n[6] In patient cohorts, low levels of CD44v6 predict increased probability of survival.\n[7] Thus, the metastatic process in colorectal cancer is initiated by CSCs through the expression of CD44v6, which is both a functional biomarker and therapeutic target."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Here, we show that all colorectal cancer stem cells (CR-CSCs) express CD44v6, which is required for their migration and generation of metastatic tumors.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 203, "doc_id": 9558539, "label": "CONTRADICTS", "evidence_sentence_ids": [1], "cited_doc_ids": [9558539], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CD44v6 is not associated with constitutive and reprogrammed cancer stem cells driving cancer metastasis.\n\nDocument title: CD44v6 is a marker of constitutive and reprogrammed cancer stem cells driving colon cancer metastasis.\n\nAbstract sentences:\n[0] Cancer stem cells drive tumor formation and metastasis, but how they acquire metastatic traits is not well understood.\n[1] Here, we show that all colorectal cancer stem cells (CR-CSCs) express CD44v6, which is required for their migration and generation of metastatic tumors.\n[2] CD44v6 expression is low in primary tumors but demarcated clonogenic CR-CSC populations.\n[3] Cytokines hepatocyte growth factor (HGF), osteopontin (OPN), and stromal-derived factor 1α (SDF-1), secreted from tumor associated cells, increase CD44v6 expression in CR-CSCs by activating the Wnt/β-catenin pathway, which promotes migration and metastasis.\n[4] CD44v6(-) progenitor cells do not give rise to metastatic lesions but, when treated with cytokines, acquire CD44v6 expression and metastatic capacity.\n[5] Importantly, phosphatidylinositol 3-kinase (PI3K) inhibition selectively killed CD44v6 CR-CSCs and reduced metastatic growth.\n[6] In patient cohorts, low levels of CD44v6 predict increased probability of survival.\n[7] Thus, the metastatic process in colorectal cancer is initiated by CSCs through the expression of CD44v6, which is both a functional biomarker and therapeutic target."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Cytokines hepatocyte growth factor (HGF), osteopontin (OPN), and stromal-derived factor 1α (SDF-1), secreted from tumor associated cells, increase CD44v6 expression in CR-CSCs by activating the Wnt/β-catenin pathway, which promotes migration and metastasis.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 203, "doc_id": 9558539, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [9558539], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CD44v6 is not associated with constitutive and reprogrammed cancer stem cells driving cancer metastasis.\n\nDocument title: CD44v6 is a marker of constitutive and reprogrammed cancer stem cells driving colon cancer metastasis.\n\nAbstract sentences:\n[0] Cancer stem cells drive tumor formation and metastasis, but how they acquire metastatic traits is not well understood.\n[1] Here, we show that all colorectal cancer stem cells (CR-CSCs) express CD44v6, which is required for their migration and generation of metastatic tumors.\n[2] CD44v6 expression is low in primary tumors but demarcated clonogenic CR-CSC populations.\n[3] Cytokines hepatocyte growth factor (HGF), osteopontin (OPN), and stromal-derived factor 1α (SDF-1), secreted from tumor associated cells, increase CD44v6 expression in CR-CSCs by activating the Wnt/β-catenin pathway, which promotes migration and metastasis.\n[4] CD44v6(-) progenitor cells do not give rise to metastatic lesions but, when treated with cytokines, acquire CD44v6 expression and metastatic capacity.\n[5] Importantly, phosphatidylinositol 3-kinase (PI3K) inhibition selectively killed CD44v6 CR-CSCs and reduced metastatic growth.\n[6] In patient cohorts, low levels of CD44v6 predict increased probability of survival.\n[7] Thus, the metastatic process in colorectal cancer is initiated by CSCs through the expression of CD44v6, which is both a functional biomarker and therapeutic target."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"CD44v6(-) progenitor cells do not give rise to metastatic lesions but, when treated with cytokines, acquire CD44v6 expression and metastatic capacity.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 203, "doc_id": 9558539, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [9558539], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CD44v6 is not associated with constitutive and reprogrammed cancer stem cells driving cancer metastasis.\n\nDocument title: CD44v6 is a marker of constitutive and reprogrammed cancer stem cells driving colon cancer metastasis.\n\nAbstract sentences:\n[0] Cancer stem cells drive tumor formation and metastasis, but how they acquire metastatic traits is not well understood.\n[1] Here, we show that all colorectal cancer stem cells (CR-CSCs) express CD44v6, which is required for their migration and generation of metastatic tumors.\n[2] CD44v6 expression is low in primary tumors but demarcated clonogenic CR-CSC populations.\n[3] Cytokines hepatocyte growth factor (HGF), osteopontin (OPN), and stromal-derived factor 1α (SDF-1), secreted from tumor associated cells, increase CD44v6 expression in CR-CSCs by activating the Wnt/β-catenin pathway, which promotes migration and metastasis.\n[4] CD44v6(-) progenitor cells do not give rise to metastatic lesions but, when treated with cytokines, acquire CD44v6 expression and metastatic capacity.\n[5] Importantly, phosphatidylinositol 3-kinase (PI3K) inhibition selectively killed CD44v6 CR-CSCs and reduced metastatic growth.\n[6] In patient cohorts, low levels of CD44v6 predict increased probability of survival.\n[7] Thus, the metastatic process in colorectal cancer is initiated by CSCs through the expression of CD44v6, which is both a functional biomarker and therapeutic target."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Importantly, phosphatidylinositol 3-kinase (PI3K) inhibition selectively killed CD44v6 CR-CSCs and reduced metastatic growth.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 203, "doc_id": 9558539, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [9558539], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CD44v6 is not associated with constitutive and reprogrammed cancer stem cells driving cancer metastasis.\n\nDocument title: CD44v6 is a marker of constitutive and reprogrammed cancer stem cells driving colon cancer metastasis.\n\nAbstract sentences:\n[0] Cancer stem cells drive tumor formation and metastasis, but how they acquire metastatic traits is not well understood.\n[1] Here, we show that all colorectal cancer stem cells (CR-CSCs) express CD44v6, which is required for their migration and generation of metastatic tumors.\n[2] CD44v6 expression is low in primary tumors but demarcated clonogenic CR-CSC populations.\n[3] Cytokines hepatocyte growth factor (HGF), osteopontin (OPN), and stromal-derived factor 1α (SDF-1), secreted from tumor associated cells, increase CD44v6 expression in CR-CSCs by activating the Wnt/β-catenin pathway, which promotes migration and metastasis.\n[4] CD44v6(-) progenitor cells do not give rise to metastatic lesions but, when treated with cytokines, acquire CD44v6 expression and metastatic capacity.\n[5] Importantly, phosphatidylinositol 3-kinase (PI3K) inhibition selectively killed CD44v6 CR-CSCs and reduced metastatic growth.\n[6] In patient cohorts, low levels of CD44v6 predict increased probability of survival.\n[7] Thus, the metastatic process in colorectal cancer is initiated by CSCs through the expression of CD44v6, which is both a functional biomarker and therapeutic target."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Thus, the metastatic process in colorectal cancer is initiated by CSCs through the expression of CD44v6, which is both a functional biomarker and therapeutic target.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 203, "doc_id": 9558539, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [9558539], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CDK6 shows impaired binding to loss-of-function variants of p18 INK4C.\n\nDocument title: Feedback Circuit among INK4 Tumor Suppressors Constrains Human Glioblastoma Development\n\nAbstract sentences:\n[0] We have developed a nonheuristic genome topography scan (GTS) algorithm to characterize the patterns of genomic alterations in human glioblastoma (GBM), identifying frequent p18(INK4C) and p16(INK4A) codeletion.\n[1] Functional reconstitution of p18(INK4C) in GBM cells null for both p16(INK4A) and p18(INK4C) resulted in impaired cell-cycle progression and tumorigenic potential.\n[2] Conversely, RNAi-mediated depletion of p18(INK4C) in p16(INK4A)-deficient primary astrocytes or established GBM cells enhanced tumorigenicity in vitro and in vivo.\n[3] Furthermore, acute suppression of p16(INK4A) in primary astrocytes induced a concomitant increase in p18(INK4C).\n[4] Together, these findings uncover a feedback regulatory circuit in the astrocytic lineage and demonstrate a bona fide tumor suppressor role for p18(INK4C) in human GBM wherein it functions cooperatively with other INK4 family members to constrain inappropriate proliferation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 204, "doc_id": 7898952, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [7898952], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CDK6 shows improved binding to loss-of-function variants of p18 INK4C.\n\nDocument title: Feedback Circuit among INK4 Tumor Suppressors Constrains Human Glioblastoma Development\n\nAbstract sentences:\n[0] We have developed a nonheuristic genome topography scan (GTS) algorithm to characterize the patterns of genomic alterations in human glioblastoma (GBM), identifying frequent p18(INK4C) and p16(INK4A) codeletion.\n[1] Functional reconstitution of p18(INK4C) in GBM cells null for both p16(INK4A) and p18(INK4C) resulted in impaired cell-cycle progression and tumorigenic potential.\n[2] Conversely, RNAi-mediated depletion of p18(INK4C) in p16(INK4A)-deficient primary astrocytes or established GBM cells enhanced tumorigenicity in vitro and in vivo.\n[3] Furthermore, acute suppression of p16(INK4A) in primary astrocytes induced a concomitant increase in p18(INK4C).\n[4] Together, these findings uncover a feedback regulatory circuit in the astrocytic lineage and demonstrate a bona fide tumor suppressor role for p18(INK4C) in human GBM wherein it functions cooperatively with other INK4 family members to constrain inappropriate proliferation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 205, "doc_id": 7898952, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [7898952, 470625], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CHOP is a general endoplasmic reticulum stress marker.\n\nDocument title: Wolfram syndrome 1 and adenylyl cyclase 8 interact at the plasma membrane to regulate insulin production and secretion\n\nAbstract sentences:\n[0] Endoplasmic reticulum (ER) stress causes pancreatic β-cell dysfunction and contributes to β-cell loss and the progression of type 2 diabetes.\n[1] Wolfram syndrome 1 (WFS1) has been shown to be an important regulator of the ER stress signalling pathway; however, its role in β-cell function remains unclear.\n[2] Here we provide evidence that WFS1 is essential for glucose- and glucagon-like peptide 1 (GLP-1)-stimulated cyclic AMP production and regulation of insulin biosynthesis and secretion.\n[3] Stimulation with glucose causes WFS1 translocation from the ER to the plasma membrane, where it forms a complex with adenylyl cyclase 8 (AC8), an essential cAMP-generating enzyme in the β-cell that integrates glucose and GLP-1 signalling.\n[4] ER stress and mutant WFS1 inhibit complex formation and activation of AC8, reducing cAMP synthesis and insulin secretion.\n[5] These findings reveal that an ER-stress-related protein has a distinct role outside the ER regulating both insulin biosynthesis and secretion.\n[6] The reduction of WFS1 protein on the plasma membrane during ER stress is a contributing factor for β-cell dysfunction and progression of type 2 diabetes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 209, "doc_id": 32587939, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [32587939], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: COPI coatmer is involved in lipid homeostasis.\n\nDocument title: COPI Complex Is a Regulator of Lipid Homeostasis\n\nAbstract sentences:\n[0] Lipid droplets are ubiquitous triglyceride and sterol ester storage organelles required for energy storage homeostasis and biosynthesis.\n[1] Although little is known about lipid droplet formation and regulation, it is clear that members of the PAT (perilipin, adipocyte differentiation related protein, tail interacting protein of 47 kDa) protein family coat the droplet surface and mediate interactions with lipases that remobilize the stored lipids.\n[2] We identified key Drosophila candidate genes for lipid droplet regulation by RNA interference (RNAi) screening with an image segmentation-based optical read-out system, and show that these regulatory functions are conserved in the mouse.\n[3] Those include the vesicle-mediated Coat Protein Complex I (COPI) transport complex, which is required for limiting lipid storage.\n[4] We found that COPI components regulate the PAT protein composition at the lipid droplet surface, and promote the association of adipocyte triglyceride lipase (ATGL) with the lipid droplet surface to mediate lipolysis.\n[5] Two compounds known to inhibit COPI function, Exo1 and Brefeldin A, phenocopy COPI knockdowns.\n[6] Furthermore, RNAi inhibition of ATGL and simultaneous drug treatment indicate that COPI and ATGL function in the same pathway.\n[7] These data indicate that the COPI complex is an evolutionarily conserved regulator of lipid homeostasis, and highlight an interaction between vesicle transport systems and lipid droplets."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Those include the vesicle-mediated Coat Protein Complex I (COPI) transport complex, which is required for limiting lipid storage.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 210, "doc_id": 13794374, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [13794374], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: COPI coatmer is involved in lipid homeostasis.\n\nDocument title: COPI Complex Is a Regulator of Lipid Homeostasis\n\nAbstract sentences:\n[0] Lipid droplets are ubiquitous triglyceride and sterol ester storage organelles required for energy storage homeostasis and biosynthesis.\n[1] Although little is known about lipid droplet formation and regulation, it is clear that members of the PAT (perilipin, adipocyte differentiation related protein, tail interacting protein of 47 kDa) protein family coat the droplet surface and mediate interactions with lipases that remobilize the stored lipids.\n[2] We identified key Drosophila candidate genes for lipid droplet regulation by RNA interference (RNAi) screening with an image segmentation-based optical read-out system, and show that these regulatory functions are conserved in the mouse.\n[3] Those include the vesicle-mediated Coat Protein Complex I (COPI) transport complex, which is required for limiting lipid storage.\n[4] We found that COPI components regulate the PAT protein composition at the lipid droplet surface, and promote the association of adipocyte triglyceride lipase (ATGL) with the lipid droplet surface to mediate lipolysis.\n[5] Two compounds known to inhibit COPI function, Exo1 and Brefeldin A, phenocopy COPI knockdowns.\n[6] Furthermore, RNAi inhibition of ATGL and simultaneous drug treatment indicate that COPI and ATGL function in the same pathway.\n[7] These data indicate that the COPI complex is an evolutionarily conserved regulator of lipid homeostasis, and highlight an interaction between vesicle transport systems and lipid droplets."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"We found that COPI components regulate the PAT protein composition at the lipid droplet surface, and promote the association of adipocyte triglyceride lipase (ATGL) with the lipid droplet surface to mediate lipolysis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 210, "doc_id": 13794374, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [13794374], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: COPI coatmer is involved in lipid homeostasis.\n\nDocument title: COPI Complex Is a Regulator of Lipid Homeostasis\n\nAbstract sentences:\n[0] Lipid droplets are ubiquitous triglyceride and sterol ester storage organelles required for energy storage homeostasis and biosynthesis.\n[1] Although little is known about lipid droplet formation and regulation, it is clear that members of the PAT (perilipin, adipocyte differentiation related protein, tail interacting protein of 47 kDa) protein family coat the droplet surface and mediate interactions with lipases that remobilize the stored lipids.\n[2] We identified key Drosophila candidate genes for lipid droplet regulation by RNA interference (RNAi) screening with an image segmentation-based optical read-out system, and show that these regulatory functions are conserved in the mouse.\n[3] Those include the vesicle-mediated Coat Protein Complex I (COPI) transport complex, which is required for limiting lipid storage.\n[4] We found that COPI components regulate the PAT protein composition at the lipid droplet surface, and promote the association of adipocyte triglyceride lipase (ATGL) with the lipid droplet surface to mediate lipolysis.\n[5] Two compounds known to inhibit COPI function, Exo1 and Brefeldin A, phenocopy COPI knockdowns.\n[6] Furthermore, RNAi inhibition of ATGL and simultaneous drug treatment indicate that COPI and ATGL function in the same pathway.\n[7] These data indicate that the COPI complex is an evolutionarily conserved regulator of lipid homeostasis, and highlight an interaction between vesicle transport systems and lipid droplets."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"These data indicate that the COPI complex is an evolutionarily conserved regulator of lipid homeostasis, and highlight an interaction between vesicle transport systems and lipid droplets.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 210, "doc_id": 13794374, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [13794374], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: COPI coatmer is involved in viral replication.\n\nDocument title: COPI Complex Is a Regulator of Lipid Homeostasis\n\nAbstract sentences:\n[0] Lipid droplets are ubiquitous triglyceride and sterol ester storage organelles required for energy storage homeostasis and biosynthesis.\n[1] Although little is known about lipid droplet formation and regulation, it is clear that members of the PAT (perilipin, adipocyte differentiation related protein, tail interacting protein of 47 kDa) protein family coat the droplet surface and mediate interactions with lipases that remobilize the stored lipids.\n[2] We identified key Drosophila candidate genes for lipid droplet regulation by RNA interference (RNAi) screening with an image segmentation-based optical read-out system, and show that these regulatory functions are conserved in the mouse.\n[3] Those include the vesicle-mediated Coat Protein Complex I (COPI) transport complex, which is required for limiting lipid storage.\n[4] We found that COPI components regulate the PAT protein composition at the lipid droplet surface, and promote the association of adipocyte triglyceride lipase (ATGL) with the lipid droplet surface to mediate lipolysis.\n[5] Two compounds known to inhibit COPI function, Exo1 and Brefeldin A, phenocopy COPI knockdowns.\n[6] Furthermore, RNAi inhibition of ATGL and simultaneous drug treatment indicate that COPI and ATGL function in the same pathway.\n[7] These data indicate that the COPI complex is an evolutionarily conserved regulator of lipid homeostasis, and highlight an interaction between vesicle transport systems and lipid droplets."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 211, "doc_id": 13794374, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [13794374], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CRP is positively correlated with postoperative mortality following Coronary Artery Bypass Graft (CABG) surgery.\n\nDocument title: Assessing the cost effectiveness of using prognostic biomarkers with decision models: case study in prioritising patients waiting for coronary artery surgery\n\nAbstract sentences:\n[0] OBJECTIVE To determine the effectiveness and cost effectiveness of using information from circulating biomarkers to inform the prioritisation process of patients with stable angina awaiting coronary artery bypass graft surgery.\n[1] DESIGN Decision analytical model comparing four prioritisation strategies without biomarkers (no formal prioritisation, two urgency scores, and a risk score) and three strategies based on a risk score using biomarkers: a routinely assessed biomarker (estimated glomerular filtration rate), a novel biomarker (C reactive protein), or both.\n[2] The order in which to perform coronary artery bypass grafting in a cohort of patients was determined by each prioritisation strategy, and mean lifetime costs and quality adjusted life years (QALYs) were compared.\n[3] DATA SOURCES Swedish Coronary Angiography and Angioplasty Registry (9935 patients with stable angina awaiting coronary artery bypass grafting and then followed up for cardiovascular events after the procedure for 3.8 years), and meta-analyses of prognostic effects (relative risks) of biomarkers.\n[4] RESULTS The observed risk of cardiovascular events while on the waiting list for coronary artery bypass grafting was 3 per 10,000 patients per day within the first 90 days (184 events in 9935 patients).\n[5] Using a cost effectiveness threshold of pound20,000- pound30,000 (euro22,000-euro33,000; $32,000-$48,000) per additional QALY, a prioritisation strategy using a risk score with estimated glomerular filtration rate was the most cost effective strategy (cost per additional QALY was < pound410 compared with the Ontario urgency score).\n[6] The impact on population health of implementing this strategy was 800 QALYs per 100,000 patients at an additional cost of pound 245,000 to the National Health Service.\n[7] The prioritisation strategy using a risk score with C reactive protein was associated with lower QALYs and higher costs compared with a risk score using estimated glomerular filtration rate.\n[8] CONCLUSION Evaluating the cost effectiveness of prognostic biomarkers is important even when effects at an individual level are small.\n[9] Formal prioritisation of patients awaiting coronary artery bypass grafting using a routinely assessed biomarker (estimated glomerular filtration rate) along with simple, routinely collected clinical information was cost effective.\n[10] Prioritisation strategies based on the prognostic information conferred by C reactive protein, which is not currently measured in this context, or a combination of C reactive protein and estimated glomerular filtration rate, is unlikely to be cost effective.\n[11] The widespread practice of using only implicit or informal means of clinically ordering the waiting list may be harmful and should be replaced with formal prioritisation approaches."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 214, "doc_id": 13625993, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [13625993], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ca2+ cycling controls whole-body energy homeostasis in beige fat.\n\nDocument title: UCP1-independent signaling involving SERCA2b-mediated calcium cycling regulates beige fat thermogenesis and systemic glucose homeostasis\n\nAbstract sentences:\n[0] Uncoupling protein 1 (UCP1) plays a central role in nonshivering thermogenesis in brown fat; however, its role in beige fat remains unclear.\n[1] Here we report a robust UCP1-independent thermogenic mechanism in beige fat that involves enhanced ATP-dependent Ca2+ cycling by sarco/endoplasmic reticulum Ca2+-ATPase 2b (SERCA2b) and ryanodine receptor 2 (RyR2).\n[2] Inhibition of SERCA2b impairs UCP1-independent beige fat thermogenesis in humans and mice as well as in pigs, a species that lacks a functional UCP1 protein.\n[3] Conversely, enhanced Ca2+ cycling by activation of α1- and/or β3-adrenergic receptors or the SERCA2b-RyR2 pathway stimulates UCP1-independent thermogenesis in beige adipocytes.\n[4] In the absence of UCP1, beige fat dynamically expends glucose through enhanced glycolysis, tricarboxylic acid metabolism and pyruvate dehydrogenase activity for ATP-dependent thermogenesis through the SERCA2b pathway; beige fat thereby functions as a 'glucose sink' and improves glucose tolerance independently of body weight loss.\n[5] Our study uncovers a noncanonical thermogenic mechanism through which beige fat controls whole-body energy homeostasis via Ca2+ cycling."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3, 4]\nExplanation: Evidence states: \"Conversely, enhanced Ca2+ cycling by activation of α1- and/or β3-adrenergic receptors or the SERCA2b-RyR2 pathway stimulates UCP1-independent thermogenesis in beige adipocytes. In the absence of UCP1, beige fat dynamically expends glucose through enhanced glycolysis, tricarboxylic acid metabolism and pyruvate dehydrogenase activity for ATP-dependent thermogenesis through the SERCA2b pathway; beige fat thereby functions as a 'glucose sink' and improves glucose tolerance independently of body weight loss.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 220, "doc_id": 19205437, "label": "SUPPORTS", "evidence_sentence_ids": [3, 4], "cited_doc_ids": [19205437], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ca2+ cycling controls whole-body energy homeostasis in beige fat.\n\nDocument title: UCP1-independent signaling involving SERCA2b-mediated calcium cycling regulates beige fat thermogenesis and systemic glucose homeostasis\n\nAbstract sentences:\n[0] Uncoupling protein 1 (UCP1) plays a central role in nonshivering thermogenesis in brown fat; however, its role in beige fat remains unclear.\n[1] Here we report a robust UCP1-independent thermogenic mechanism in beige fat that involves enhanced ATP-dependent Ca2+ cycling by sarco/endoplasmic reticulum Ca2+-ATPase 2b (SERCA2b) and ryanodine receptor 2 (RyR2).\n[2] Inhibition of SERCA2b impairs UCP1-independent beige fat thermogenesis in humans and mice as well as in pigs, a species that lacks a functional UCP1 protein.\n[3] Conversely, enhanced Ca2+ cycling by activation of α1- and/or β3-adrenergic receptors or the SERCA2b-RyR2 pathway stimulates UCP1-independent thermogenesis in beige adipocytes.\n[4] In the absence of UCP1, beige fat dynamically expends glucose through enhanced glycolysis, tricarboxylic acid metabolism and pyruvate dehydrogenase activity for ATP-dependent thermogenesis through the SERCA2b pathway; beige fat thereby functions as a 'glucose sink' and improves glucose tolerance independently of body weight loss.\n[5] Our study uncovers a noncanonical thermogenic mechanism through which beige fat controls whole-body energy homeostasis via Ca2+ cycling."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Our study uncovers a noncanonical thermogenic mechanism through which beige fat controls whole-body energy homeostasis via Ca2+ cycling.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 220, "doc_id": 19205437, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [19205437], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ca2+ cycling is a UCP1-dependent thermogenic mechanism.\n\nDocument title: UCP1-independent signaling involving SERCA2b-mediated calcium cycling regulates beige fat thermogenesis and systemic glucose homeostasis\n\nAbstract sentences:\n[0] Uncoupling protein 1 (UCP1) plays a central role in nonshivering thermogenesis in brown fat; however, its role in beige fat remains unclear.\n[1] Here we report a robust UCP1-independent thermogenic mechanism in beige fat that involves enhanced ATP-dependent Ca2+ cycling by sarco/endoplasmic reticulum Ca2+-ATPase 2b (SERCA2b) and ryanodine receptor 2 (RyR2).\n[2] Inhibition of SERCA2b impairs UCP1-independent beige fat thermogenesis in humans and mice as well as in pigs, a species that lacks a functional UCP1 protein.\n[3] Conversely, enhanced Ca2+ cycling by activation of α1- and/or β3-adrenergic receptors or the SERCA2b-RyR2 pathway stimulates UCP1-independent thermogenesis in beige adipocytes.\n[4] In the absence of UCP1, beige fat dynamically expends glucose through enhanced glycolysis, tricarboxylic acid metabolism and pyruvate dehydrogenase activity for ATP-dependent thermogenesis through the SERCA2b pathway; beige fat thereby functions as a 'glucose sink' and improves glucose tolerance independently of body weight loss.\n[5] Our study uncovers a noncanonical thermogenic mechanism through which beige fat controls whole-body energy homeostasis via Ca2+ cycling."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Here we report a robust UCP1-independent thermogenic mechanism in beige fat that involves enhanced ATP-dependent Ca2+ cycling by sarco/endoplasmic reticulum Ca2+-ATPase 2b (SERCA2b) and ryanodine receptor 2 (RyR2).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 221, "doc_id": 19205437, "label": "CONTRADICTS", "evidence_sentence_ids": [1], "cited_doc_ids": [19205437], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ca2+ cycling is a UCP1-dependent thermogenic mechanism.\n\nDocument title: UCP1-independent signaling involving SERCA2b-mediated calcium cycling regulates beige fat thermogenesis and systemic glucose homeostasis\n\nAbstract sentences:\n[0] Uncoupling protein 1 (UCP1) plays a central role in nonshivering thermogenesis in brown fat; however, its role in beige fat remains unclear.\n[1] Here we report a robust UCP1-independent thermogenic mechanism in beige fat that involves enhanced ATP-dependent Ca2+ cycling by sarco/endoplasmic reticulum Ca2+-ATPase 2b (SERCA2b) and ryanodine receptor 2 (RyR2).\n[2] Inhibition of SERCA2b impairs UCP1-independent beige fat thermogenesis in humans and mice as well as in pigs, a species that lacks a functional UCP1 protein.\n[3] Conversely, enhanced Ca2+ cycling by activation of α1- and/or β3-adrenergic receptors or the SERCA2b-RyR2 pathway stimulates UCP1-independent thermogenesis in beige adipocytes.\n[4] In the absence of UCP1, beige fat dynamically expends glucose through enhanced glycolysis, tricarboxylic acid metabolism and pyruvate dehydrogenase activity for ATP-dependent thermogenesis through the SERCA2b pathway; beige fat thereby functions as a 'glucose sink' and improves glucose tolerance independently of body weight loss.\n[5] Our study uncovers a noncanonical thermogenic mechanism through which beige fat controls whole-body energy homeostasis via Ca2+ cycling."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Conversely, enhanced Ca2+ cycling by activation of α1- and/or β3-adrenergic receptors or the SERCA2b-RyR2 pathway stimulates UCP1-independent thermogenesis in beige adipocytes.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 221, "doc_id": 19205437, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [19205437], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ca2+ cycling is a UCP1-independent thermogenic mechanism.\n\nDocument title: UCP1-independent signaling involving SERCA2b-mediated calcium cycling regulates beige fat thermogenesis and systemic glucose homeostasis\n\nAbstract sentences:\n[0] Uncoupling protein 1 (UCP1) plays a central role in nonshivering thermogenesis in brown fat; however, its role in beige fat remains unclear.\n[1] Here we report a robust UCP1-independent thermogenic mechanism in beige fat that involves enhanced ATP-dependent Ca2+ cycling by sarco/endoplasmic reticulum Ca2+-ATPase 2b (SERCA2b) and ryanodine receptor 2 (RyR2).\n[2] Inhibition of SERCA2b impairs UCP1-independent beige fat thermogenesis in humans and mice as well as in pigs, a species that lacks a functional UCP1 protein.\n[3] Conversely, enhanced Ca2+ cycling by activation of α1- and/or β3-adrenergic receptors or the SERCA2b-RyR2 pathway stimulates UCP1-independent thermogenesis in beige adipocytes.\n[4] In the absence of UCP1, beige fat dynamically expends glucose through enhanced glycolysis, tricarboxylic acid metabolism and pyruvate dehydrogenase activity for ATP-dependent thermogenesis through the SERCA2b pathway; beige fat thereby functions as a 'glucose sink' and improves glucose tolerance independently of body weight loss.\n[5] Our study uncovers a noncanonical thermogenic mechanism through which beige fat controls whole-body energy homeostasis via Ca2+ cycling."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Here we report a robust UCP1-independent thermogenic mechanism in beige fat that involves enhanced ATP-dependent Ca2+ cycling by sarco/endoplasmic reticulum Ca2+-ATPase 2b (SERCA2b) and ryanodine receptor 2 (RyR2).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 222, "doc_id": 19205437, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [19205437], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ca2+ cycling is a UCP1-independent thermogenic mechanism.\n\nDocument title: UCP1-independent signaling involving SERCA2b-mediated calcium cycling regulates beige fat thermogenesis and systemic glucose homeostasis\n\nAbstract sentences:\n[0] Uncoupling protein 1 (UCP1) plays a central role in nonshivering thermogenesis in brown fat; however, its role in beige fat remains unclear.\n[1] Here we report a robust UCP1-independent thermogenic mechanism in beige fat that involves enhanced ATP-dependent Ca2+ cycling by sarco/endoplasmic reticulum Ca2+-ATPase 2b (SERCA2b) and ryanodine receptor 2 (RyR2).\n[2] Inhibition of SERCA2b impairs UCP1-independent beige fat thermogenesis in humans and mice as well as in pigs, a species that lacks a functional UCP1 protein.\n[3] Conversely, enhanced Ca2+ cycling by activation of α1- and/or β3-adrenergic receptors or the SERCA2b-RyR2 pathway stimulates UCP1-independent thermogenesis in beige adipocytes.\n[4] In the absence of UCP1, beige fat dynamically expends glucose through enhanced glycolysis, tricarboxylic acid metabolism and pyruvate dehydrogenase activity for ATP-dependent thermogenesis through the SERCA2b pathway; beige fat thereby functions as a 'glucose sink' and improves glucose tolerance independently of body weight loss.\n[5] Our study uncovers a noncanonical thermogenic mechanism through which beige fat controls whole-body energy homeostasis via Ca2+ cycling."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Conversely, enhanced Ca2+ cycling by activation of α1- and/or β3-adrenergic receptors or the SERCA2b-RyR2 pathway stimulates UCP1-independent thermogenesis in beige adipocytes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 222, "doc_id": 19205437, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [19205437], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cancer cells can stimulate the accumulation of intra-tumoural myeloid-derived suppressor cells by promoting granulocyte colony stimulating factor production.\n\nDocument title: Oncogenic mTOR signaling recruits myeloid-derived suppressor cells to promote tumor initiation\n\nAbstract sentences:\n[0] Myeloid-derived suppressor cells (MDSCs) play critical roles in primary and metastatic cancer progression.\n[1] MDSC regulation is widely variable even among patients harbouring the same type of malignancy, and the mechanisms governing such heterogeneity are largely unknown.\n[2] Here, integrating human tumour genomics and syngeneic mammary tumour models, we demonstrate that mTOR signalling in cancer cells dictates a mammary tumour's ability to stimulate MDSC accumulation through regulating G-CSF.\n[3] Inhibiting this pathway or its activators (for example, FGFR) impairs tumour progression, which is partially rescued by restoring MDSCs or G-CSF.\n[4] Tumour-initiating cells (TICs) exhibit elevated G-CSF.\n[5] MDSCs reciprocally increase TIC frequency through activating Notch in tumour cells, forming a feedforward loop.\n[6] Analyses of primary breast cancers and patient-derived xenografts corroborate these mechanisms in patients.\n[7] These findings establish a non-canonical oncogenic role of mTOR signalling in recruiting pro-tumorigenic MDSCs and show how defined cancer subsets may evolve to promote and depend on a distinct immune microenvironment."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here, integrating human tumour genomics and syngeneic mammary tumour models, we demonstrate that mTOR signalling in cancer cells dictates a mammary tumour's ability to stimulate MDSC accumulation through regulating G-CSF.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 223, "doc_id": 2014909, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [2014909], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cancer-associated fibroblasts (CAFs) are constituents of tumor microenvironments\n\nDocument title: Microenvironmental regulation of tumor progression and metastasis\n\nAbstract sentences:\n[0] Cancers develop in complex tissue environments, which they depend on for sustained growth, invasion and metastasis.\n[1] Unlike tumor cells, stromal cell types within the tumor microenvironment (TME) are genetically stable and thus represent an attractive therapeutic target with reduced risk of resistance and tumor recurrence.\n[2] However, specifically disrupting the pro-tumorigenic TME is a challenging undertaking, as the TME has diverse capacities to induce both beneficial and adverse consequences for tumorigenesis.\n[3] Furthermore, many studies have shown that the microenvironment is capable of normalizing tumor cells, suggesting that re-education of stromal cells, rather than targeted ablation per se, may be an effective strategy for treating cancer.\n[4] Here we discuss the paradoxical roles of the TME during specific stages of cancer progression and metastasis, as well as recent therapeutic attempts to re-educate stromal cells within the TME to have anti-tumorigenic effects."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 224, "doc_id": 6944800, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [6944800], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cancer-associated fibroblasts (CAFs) have no known interaction with cancer cells in the formation and activation of CAFs.\n\nDocument title: Microenvironmental regulation of tumor progression and metastasis\n\nAbstract sentences:\n[0] Cancers develop in complex tissue environments, which they depend on for sustained growth, invasion and metastasis.\n[1] Unlike tumor cells, stromal cell types within the tumor microenvironment (TME) are genetically stable and thus represent an attractive therapeutic target with reduced risk of resistance and tumor recurrence.\n[2] However, specifically disrupting the pro-tumorigenic TME is a challenging undertaking, as the TME has diverse capacities to induce both beneficial and adverse consequences for tumorigenesis.\n[3] Furthermore, many studies have shown that the microenvironment is capable of normalizing tumor cells, suggesting that re-education of stromal cells, rather than targeted ablation per se, may be an effective strategy for treating cancer.\n[4] Here we discuss the paradoxical roles of the TME during specific stages of cancer progression and metastasis, as well as recent therapeutic attempts to re-educate stromal cells within the TME to have anti-tumorigenic effects."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 225, "doc_id": 6944800, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [6944800], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cancer-associated fibroblasts (CAFs) interact with cancer cells to mediate formation and activation of CAFs.\n\nDocument title: Microenvironmental regulation of tumor progression and metastasis\n\nAbstract sentences:\n[0] Cancers develop in complex tissue environments, which they depend on for sustained growth, invasion and metastasis.\n[1] Unlike tumor cells, stromal cell types within the tumor microenvironment (TME) are genetically stable and thus represent an attractive therapeutic target with reduced risk of resistance and tumor recurrence.\n[2] However, specifically disrupting the pro-tumorigenic TME is a challenging undertaking, as the TME has diverse capacities to induce both beneficial and adverse consequences for tumorigenesis.\n[3] Furthermore, many studies have shown that the microenvironment is capable of normalizing tumor cells, suggesting that re-education of stromal cells, rather than targeted ablation per se, may be an effective strategy for treating cancer.\n[4] Here we discuss the paradoxical roles of the TME during specific stages of cancer progression and metastasis, as well as recent therapeutic attempts to re-educate stromal cells within the TME to have anti-tumorigenic effects."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 226, "doc_id": 6944800, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [6944800], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cancers that initially benefit from epidermal growth factor receptor targeted therapies later become refractory through several mechanisms.\n\nDocument title: The quest to overcome resistance to EGFR-targeted therapies in cancer\n\nAbstract sentences:\n[0] All patients with metastatic lung, colorectal, pancreatic or head and neck cancers who initially benefit from epidermal growth factor receptor (EGFR)-targeted therapies eventually develop resistance.\n[1] An increasing understanding of the number and complexity of resistance mechanisms highlights the Herculean challenge of killing tumors that are resistant to EGFR inhibitors.\n[2] Our growing knowledge of resistance pathways provides an opportunity to develop new mechanism-based inhibitors and combination therapies to prevent or overcome therapeutic resistance in tumors.\n[3] We present a comprehensive review of resistance pathways to EGFR-targeted therapies in lung, colorectal and head and neck cancers and discuss therapeutic strategies that are designed to circumvent resistance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"All patients with metastatic lung, colorectal, pancreatic or head and neck cancers who initially benefit from epidermal growth factor receptor (EGFR)-targeted therapies eventually develop resistance.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 227, "doc_id": 26973393, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [26973393], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cardiac tissue-resident macrophages directly contribute to electrical activity.\n\nDocument title: Macrophages Facilitate Electrical Conduction in the Heart\n\nAbstract sentences:\n[0] Organ-specific functions of tissue-resident macrophages in the steady-state heart are unknown.\n[1] Here, we show that cardiac macrophages facilitate electrical conduction through the distal atrioventricular node, where conducting cells densely intersperse with elongated macrophages expressing connexin 43.\n[2] When coupled to spontaneously beating cardiomyocytes via connexin-43-containing gap junctions, cardiac macrophages have a negative resting membrane potential and depolarize in synchrony with cardiomyocytes.\n[3] Conversely, macrophages render the resting membrane potential of cardiomyocytes more positive and, according to computational modeling, accelerate their repolarization.\n[4] Photostimulation of channelrhodopsin-2-expressing macrophages improves atrioventricular conduction, whereas conditional deletion of connexin 43 in macrophages and congenital lack of macrophages delay atrioventricular conduction.\n[5] In the Cd11bDTR mouse, macrophage ablation induces progressive atrioventricular block.\n[6] These observations implicate macrophages in normal and aberrant cardiac conduction."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Here, we show that cardiac macrophages facilitate electrical conduction through the distal atrioventricular node, where conducting cells densely intersperse with elongated macrophages expressing connexin 43.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 228, "doc_id": 4928057, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [4928057], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cardiac tissue-resident macrophages directly contribute to electrical activity.\n\nDocument title: Macrophages Facilitate Electrical Conduction in the Heart\n\nAbstract sentences:\n[0] Organ-specific functions of tissue-resident macrophages in the steady-state heart are unknown.\n[1] Here, we show that cardiac macrophages facilitate electrical conduction through the distal atrioventricular node, where conducting cells densely intersperse with elongated macrophages expressing connexin 43.\n[2] When coupled to spontaneously beating cardiomyocytes via connexin-43-containing gap junctions, cardiac macrophages have a negative resting membrane potential and depolarize in synchrony with cardiomyocytes.\n[3] Conversely, macrophages render the resting membrane potential of cardiomyocytes more positive and, according to computational modeling, accelerate their repolarization.\n[4] Photostimulation of channelrhodopsin-2-expressing macrophages improves atrioventricular conduction, whereas conditional deletion of connexin 43 in macrophages and congenital lack of macrophages delay atrioventricular conduction.\n[5] In the Cd11bDTR mouse, macrophage ablation induces progressive atrioventricular block.\n[6] These observations implicate macrophages in normal and aberrant cardiac conduction."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Conversely, macrophages render the resting membrane potential of cardiomyocytes more positive and, according to computational modeling, accelerate their repolarization.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 228, "doc_id": 4928057, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [4928057], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cardiac tissue-resident macrophages directly contribute to electrical activity.\n\nDocument title: Macrophages Facilitate Electrical Conduction in the Heart\n\nAbstract sentences:\n[0] Organ-specific functions of tissue-resident macrophages in the steady-state heart are unknown.\n[1] Here, we show that cardiac macrophages facilitate electrical conduction through the distal atrioventricular node, where conducting cells densely intersperse with elongated macrophages expressing connexin 43.\n[2] When coupled to spontaneously beating cardiomyocytes via connexin-43-containing gap junctions, cardiac macrophages have a negative resting membrane potential and depolarize in synchrony with cardiomyocytes.\n[3] Conversely, macrophages render the resting membrane potential of cardiomyocytes more positive and, according to computational modeling, accelerate their repolarization.\n[4] Photostimulation of channelrhodopsin-2-expressing macrophages improves atrioventricular conduction, whereas conditional deletion of connexin 43 in macrophages and congenital lack of macrophages delay atrioventricular conduction.\n[5] In the Cd11bDTR mouse, macrophage ablation induces progressive atrioventricular block.\n[6] These observations implicate macrophages in normal and aberrant cardiac conduction."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Photostimulation of channelrhodopsin-2-expressing macrophages improves atrioventricular conduction, whereas conditional deletion of connexin 43 in macrophages and congenital lack of macrophages delay atrioventricular conduction.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 228, "doc_id": 4928057, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [4928057], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cardiac tissue-resident macrophages directly contribute to electrical activity.\n\nDocument title: Macrophages Facilitate Electrical Conduction in the Heart\n\nAbstract sentences:\n[0] Organ-specific functions of tissue-resident macrophages in the steady-state heart are unknown.\n[1] Here, we show that cardiac macrophages facilitate electrical conduction through the distal atrioventricular node, where conducting cells densely intersperse with elongated macrophages expressing connexin 43.\n[2] When coupled to spontaneously beating cardiomyocytes via connexin-43-containing gap junctions, cardiac macrophages have a negative resting membrane potential and depolarize in synchrony with cardiomyocytes.\n[3] Conversely, macrophages render the resting membrane potential of cardiomyocytes more positive and, according to computational modeling, accelerate their repolarization.\n[4] Photostimulation of channelrhodopsin-2-expressing macrophages improves atrioventricular conduction, whereas conditional deletion of connexin 43 in macrophages and congenital lack of macrophages delay atrioventricular conduction.\n[5] In the Cd11bDTR mouse, macrophage ablation induces progressive atrioventricular block.\n[6] These observations implicate macrophages in normal and aberrant cardiac conduction."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"These observations implicate macrophages in normal and aberrant cardiac conduction.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 228, "doc_id": 4928057, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [4928057], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Carriers of HNF4A mutations are at reduced risk for diabetes.\n\nDocument title: Macrosomia and Hyperinsulinaemic Hypoglycaemia in Patients with Heterozygous Mutations in the HNF4A Gene\n\nAbstract sentences:\n[0] Background  Macrosomia is associated with considerable neonatal and maternal morbidity.\n[1] Factors that predict macrosomia are poorly understood.\n[2] The increased rate of macrosomia in the offspring of pregnant women with diabetes and in congenital hyperinsulinaemia is mediated by increased foetal insulin secretion.\n[3] We assessed the in utero and neonatal role of two key regulators of pancreatic insulin secretion by studying birthweight and the incidence of neonatal hypoglycaemia in patients with heterozygous mutations in the maturity-onset diabetes of the young (MODY) genes HNF4A (encoding HNF-4α) and HNF1A/TCF1 (encoding HNF-1α), and the effect of pancreatic deletion of Hnf4a on foetal and neonatal insulin secretion in mice."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 229, "doc_id": 56893404, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [56893404], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cell autonomous sex determination in somatic cells occurs in Galliformes.\n\nDocument title: Somatic sex identity is cell-autonomous in the chicken\n\nAbstract sentences:\n[0] In the mammalian model of sex determination, embryos are considered to be sexually indifferent until the transient action of a sex-determining gene initiates gonadal differentiation.\n[1] Although this model is thought to apply to all vertebrates, this has yet to be established.\n[2] Here we have examined three lateral gynandromorph chickens (a rare, naturally occurring phenomenon in which one side of the animal appears male and the other female) to investigate the sex-determining mechanism in birds.\n[3] These studies demonstrated that gynandromorph birds are genuine male:female chimaeras, and indicated that male and female avian somatic cells may have an inherent sex identity.\n[4] To test this hypothesis, we transplanted presumptive mesoderm between embryos of reciprocal sexes to generate embryos containing male:female chimaeric gonads.\n[5] In contrast to the outcome for mammalian mixed-sex chimaeras, in chicken mixed-sex chimaeras the donor cells were excluded from the functional structures of the host gonad.\n[6] In an example where female tissue was transplanted into a male host, donor cells contributing to the developing testis retained a female identity and expressed a marker of female function.\n[7] Our study demonstrates that avian somatic cells possess an inherent sex identity and that, in birds, sexual differentiation is substantively cell autonomous."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"These studies demonstrated that gynandromorph birds are genuine male:female chimaeras, and indicated that male and female avian somatic cells may have an inherent sex identity.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 235, "doc_id": 4388470, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [4388470], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cell autonomous sex determination in somatic cells occurs in Galliformes.\n\nDocument title: Somatic sex identity is cell-autonomous in the chicken\n\nAbstract sentences:\n[0] In the mammalian model of sex determination, embryos are considered to be sexually indifferent until the transient action of a sex-determining gene initiates gonadal differentiation.\n[1] Although this model is thought to apply to all vertebrates, this has yet to be established.\n[2] Here we have examined three lateral gynandromorph chickens (a rare, naturally occurring phenomenon in which one side of the animal appears male and the other female) to investigate the sex-determining mechanism in birds.\n[3] These studies demonstrated that gynandromorph birds are genuine male:female chimaeras, and indicated that male and female avian somatic cells may have an inherent sex identity.\n[4] To test this hypothesis, we transplanted presumptive mesoderm between embryos of reciprocal sexes to generate embryos containing male:female chimaeric gonads.\n[5] In contrast to the outcome for mammalian mixed-sex chimaeras, in chicken mixed-sex chimaeras the donor cells were excluded from the functional structures of the host gonad.\n[6] In an example where female tissue was transplanted into a male host, donor cells contributing to the developing testis retained a female identity and expressed a marker of female function.\n[7] Our study demonstrates that avian somatic cells possess an inherent sex identity and that, in birds, sexual differentiation is substantively cell autonomous."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"In an example where female tissue was transplanted into a male host, donor cells contributing to the developing testis retained a female identity and expressed a marker of female function.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 235, "doc_id": 4388470, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [4388470], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cell autonomous sex determination in somatic cells occurs in Galliformes.\n\nDocument title: Somatic sex identity is cell-autonomous in the chicken\n\nAbstract sentences:\n[0] In the mammalian model of sex determination, embryos are considered to be sexually indifferent until the transient action of a sex-determining gene initiates gonadal differentiation.\n[1] Although this model is thought to apply to all vertebrates, this has yet to be established.\n[2] Here we have examined three lateral gynandromorph chickens (a rare, naturally occurring phenomenon in which one side of the animal appears male and the other female) to investigate the sex-determining mechanism in birds.\n[3] These studies demonstrated that gynandromorph birds are genuine male:female chimaeras, and indicated that male and female avian somatic cells may have an inherent sex identity.\n[4] To test this hypothesis, we transplanted presumptive mesoderm between embryos of reciprocal sexes to generate embryos containing male:female chimaeric gonads.\n[5] In contrast to the outcome for mammalian mixed-sex chimaeras, in chicken mixed-sex chimaeras the donor cells were excluded from the functional structures of the host gonad.\n[6] In an example where female tissue was transplanted into a male host, donor cells contributing to the developing testis retained a female identity and expressed a marker of female function.\n[7] Our study demonstrates that avian somatic cells possess an inherent sex identity and that, in birds, sexual differentiation is substantively cell autonomous."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Our study demonstrates that avian somatic cells possess an inherent sex identity and that, in birds, sexual differentiation is substantively cell autonomous.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 235, "doc_id": 4388470, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [4388470], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cellular clocks are associated with mitosis timing in NIH 3T3 cells.\n\nDocument title: Robust synchronization of coupled circadian and cell cycle oscillators in single mammalian cells\n\nAbstract sentences:\n[0] Circadian cycles and cell cycles are two fundamental periodic processes with a period in the range of 1 day.\n[1] Consequently, coupling between such cycles can lead to synchronization.\n[2] Here, we estimated the mutual interactions between the two oscillators by time-lapse imaging of single mammalian NIH3T3 fibroblasts during several days.\n[3] The analysis of thousands of circadian cycles in dividing cells clearly indicated that both oscillators tick in a 1:1 mode-locked state, with cell divisions occurring tightly 5 h before the peak in circadian Rev-Erbα-YFP reporter expression.\n[4] In principle, such synchrony may be caused by either unidirectional or bidirectional coupling.\n[5] While gating of cell division by the circadian cycle has been most studied, our data combined with stochastic modeling unambiguously show that the reverse coupling is predominant in NIH3T3 cells.\n[6] Moreover, temperature, genetic, and pharmacological perturbations showed that the two interacting cellular oscillators adopt a synchronized state that is highly robust over a wide range of parameters.\n[7] These findings have implications for circadian function in proliferative tissues, including epidermis, immune cells, and cancer."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"The analysis of thousands of circadian cycles in dividing cells clearly indicated that both oscillators tick in a 1:1 mode-locked state, with cell divisions occurring tightly 5 h before the peak in circadian Rev-Erbα-YFP reporter expression.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 241, "doc_id": 2212067, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [2212067, 10608822], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cellular clocks are not predictive of mitosis timing in NIH 3T3 cells.\n\nDocument title: Robust synchronization of coupled circadian and cell cycle oscillators in single mammalian cells\n\nAbstract sentences:\n[0] Circadian cycles and cell cycles are two fundamental periodic processes with a period in the range of 1 day.\n[1] Consequently, coupling between such cycles can lead to synchronization.\n[2] Here, we estimated the mutual interactions between the two oscillators by time-lapse imaging of single mammalian NIH3T3 fibroblasts during several days.\n[3] The analysis of thousands of circadian cycles in dividing cells clearly indicated that both oscillators tick in a 1:1 mode-locked state, with cell divisions occurring tightly 5 h before the peak in circadian Rev-Erbα-YFP reporter expression.\n[4] In principle, such synchrony may be caused by either unidirectional or bidirectional coupling.\n[5] While gating of cell division by the circadian cycle has been most studied, our data combined with stochastic modeling unambiguously show that the reverse coupling is predominant in NIH3T3 cells.\n[6] Moreover, temperature, genetic, and pharmacological perturbations showed that the two interacting cellular oscillators adopt a synchronized state that is highly robust over a wide range of parameters.\n[7] These findings have implications for circadian function in proliferative tissues, including epidermis, immune cells, and cancer."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"The analysis of thousands of circadian cycles in dividing cells clearly indicated that both oscillators tick in a 1:1 mode-locked state, with cell divisions occurring tightly 5 h before the peak in circadian Rev-Erbα-YFP reporter expression.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 242, "doc_id": 2212067, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [2212067, 10608822], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cellular differentiation of embryonic stem cells is accompanied by changes in replication timing, transcription and nuclear localization.\n\nDocument title: Global Reorganization of Replication Domains During Embryonic Stem Cell Differentiation\n\nAbstract sentences:\n[0] DNA replication in mammals is regulated via the coordinate firing of clusters of replicons that duplicate megabase-sized chromosome segments at specific times during S-phase.\n[1] Cytogenetic studies show that these \"replicon clusters\" coalesce as subchromosomal units that persist through multiple cell generations, but the molecular boundaries of such units have remained elusive.\n[2] Moreover, the extent to which changes in replication timing occur during differentiation and their relationship to transcription changes has not been rigorously investigated.\n[3] We have constructed high-resolution replication-timing profiles in mouse embryonic stem cells (mESCs) before and after differentiation to neural precursor cells.\n[4] We demonstrate that chromosomes can be segmented into multimegabase domains of coordinate replication, which we call \"replication domains,\" separated by transition regions whose replication kinetics are consistent with large originless segments.\n[5] The molecular boundaries of replication domains are remarkably well conserved between distantly related ESC lines and induced pluripotent stem cells.\n[6] Unexpectedly, ESC differentiation was accompanied by the consolidation of smaller differentially replicating domains into larger coordinately replicated units whose replication time was more aligned to isochore GC content and the density of LINE-1 transposable elements, but not gene density.\n[7] Replication-timing changes were coordinated with transcription changes for weak promoters more than strong promoters, and were accompanied by rearrangements in subnuclear position.\n[8] We conclude that replication profiles are cell-type specific, and changes in these profiles reveal chromosome segments that undergo large changes in organization during differentiation.\n[9] Moreover, smaller replication domains and a higher density of timing transition regions that interrupt isochore replication timing define a novel characteristic of the pluripotent state."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Replication-timing changes were coordinated with transcription changes for weak promoters more than strong promoters, and were accompanied by rearrangements in subnuclear position.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 243, "doc_id": 8148122, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [8148122], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Certain immunomodulator-human dialyzable leukocyte extract (hDLE) peptides are recognized by toll-like receptors (TLRs) on macrophages and dendritic cells.\n\nDocument title: TLR activation triggers the rapid differentiation of monocytes into macrophages and dendritic cells\n\nAbstract sentences:\n[0] Leprosy enables investigation of mechanisms by which the innate immune system contributes to host defense against infection, because in one form, the disease progresses, and in the other, the infection is limited.\n[1] We report that Toll-like receptor (TLR) activation of human monocytes induces rapid differentiation into two distinct subsets: DC-SIGN+ CD16+ macrophages and CD1b+ DC-SIGN− dendritic cells.\n[2] DC-SIGN+ phagocytic macrophages were expanded by TLR-mediated upregulation of interleukin (IL)-15 and IL-15 receptor.\n[3] CD1b+ dendritic cells were expanded by TLR-mediated upregulation of granulocyte-macrophage colony-stimulating factor (GM-CSF) and its receptor, promoted T cell activation and secreted proinflammatory cytokines.\n[4] Whereas DC-SIGN+ macrophages were detected in lesions and after TLR activation in all leprosy patients, CD1b+ dendritic cells were not detected in lesions or after TLR activation of peripheral monocytes in individuals with the progressive lepromatous form, except during reversal reactions in which bacilli were cleared by T helper type 1 (TH1) responses.\n[5] In tuberculoid lepromatous lesions, DC-SIGN+ cells were positive for macrophage markers, but negative for dendritic cell markers.\n[6] Thus, TLR-induced differentiation of monocytes into either macrophages or dendritic cells seems to crucially influence effective host defenses in human infectious disease."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 244, "doc_id": 21498497, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [21498497], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Charcoal is an effective treatment for acute paraquat poisoning.\n\nDocument title: Effect of activated charcoal hemoperfusion on renal function in patients with paraquat poisoning.\n\nAbstract sentences:\n[0] The present study retrospectively analyzed 19 patients diagnosed with paraquat (PQ) poisoning with the aim to investigate the effect of activated charcoal hemoperfusion on renal function and PQ elimination.\n[1] The results indicated that 7 patients died and 12 survived.\n[2] Non-oliguric renal failure occurred in all of the 7 patients who died.\n[3] Among the 12 surviving patients, 10 had normal renal function and 2 developed non-oliguric renal failure.\n[4] There was a linear correlation between plasma and urine paraquat concentration prior to and during activated charcoal hemoperfusion.\n[5] The equation parameters together with the correlation coefficient on admission were as follows: Y=0.5820+1.7348X (R2=0.678; F=35.768; P<0.0001).\n[6] The equation parameters together with the correlation coefficient were as follows during activated charcoal hemoperfusion: Y=0.6827+1.2649X (R2=0.626; F=50.308; P<0.0001).\n[7] Therefore, it was concluded that in patients with normal renal function, the elimination kinetics of PQ by the kidneys were only associated with the plasma PQ concentration.\n[8] Activated charcoal hemoperfusion had little effect on avoiding acute kidney injury in patients with severe PQ poisoning."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Activated charcoal hemoperfusion had little effect on avoiding acute kidney injury in patients with severe PQ poisoning.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 245, "doc_id": 3430789, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [8447873, 3430789], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Charcoal shows no benefit for acute paraquat poisoning.\n\nDocument title: Effect of activated charcoal hemoperfusion on renal function in patients with paraquat poisoning.\n\nAbstract sentences:\n[0] The present study retrospectively analyzed 19 patients diagnosed with paraquat (PQ) poisoning with the aim to investigate the effect of activated charcoal hemoperfusion on renal function and PQ elimination.\n[1] The results indicated that 7 patients died and 12 survived.\n[2] Non-oliguric renal failure occurred in all of the 7 patients who died.\n[3] Among the 12 surviving patients, 10 had normal renal function and 2 developed non-oliguric renal failure.\n[4] There was a linear correlation between plasma and urine paraquat concentration prior to and during activated charcoal hemoperfusion.\n[5] The equation parameters together with the correlation coefficient on admission were as follows: Y=0.5820+1.7348X (R2=0.678; F=35.768; P<0.0001).\n[6] The equation parameters together with the correlation coefficient were as follows during activated charcoal hemoperfusion: Y=0.6827+1.2649X (R2=0.626; F=50.308; P<0.0001).\n[7] Therefore, it was concluded that in patients with normal renal function, the elimination kinetics of PQ by the kidneys were only associated with the plasma PQ concentration.\n[8] Activated charcoal hemoperfusion had little effect on avoiding acute kidney injury in patients with severe PQ poisoning."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Activated charcoal hemoperfusion had little effect on avoiding acute kidney injury in patients with severe PQ poisoning.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 246, "doc_id": 3430789, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [8447873, 3430789], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Chemical injury represses transglutaminase 2 activity.\n\nDocument title: Transglutaminase 2 Undergoes a Large Conformational Change upon Activation \n\nAbstract sentences:\n[0] Human transglutaminase 2 (TG2), a member of a large family of enzymes that catalyze protein crosslinking, plays an important role in the extracellular matrix biology of many tissues and is implicated in the gluten-induced pathogenesis of celiac sprue.\n[1] Although vertebrate transglutaminases have been studied extensively, thus far all structurally characterized members of this family have been crystallized in conformations with inaccessible active sites.\n[2] We have trapped human TG2 in complex with an inhibitor that mimics inflammatory gluten peptide substrates and have solved, at 2-A resolution, its x-ray crystal structure.\n[3] The inhibitor stabilizes TG2 in an extended conformation that is dramatically different from earlier transglutaminase structures.\n[4] The active site is exposed, revealing that catalysis takes place in a tunnel, bridged by two tryptophan residues that separate acyl-donor from acyl-acceptor and stabilize the tetrahedral reaction intermediates.\n[5] Site-directed mutagenesis was used to investigate the acyl-acceptor side of the tunnel, yielding mutants with a marked increase in preference for hydrolysis over transamidation.\n[6] By providing the ability to visualize this activated conformer, our results create a foundation for understanding the catalytic as well as the non-catalytic roles of TG2 in biology, and for dissecting the process by which the autoantibody response to TG2 is induced in celiac sprue patients."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 247, "doc_id": 13578199, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [13578199], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Chenodeoxycholic acid treatment decreases brown adipose tissue activity.\n\nDocument title: The Bile Acid Chenodeoxycholic Acid Increases Human Brown Adipose Tissue Activity.\n\nAbstract sentences:\n[0] The interest in brown adipose tissue (BAT) as a target to combat metabolic disease has recently been renewed with the discovery of functional BAT in humans.\n[1] In rodents, BAT can be activated by bile acids, which activate type 2 iodothyronine deiodinase (D2) in BAT via the G-coupled protein receptor TGR5, resulting in increased oxygen consumption and energy expenditure.\n[2] Here we examined the effects of oral supplementation of the bile acid chenodeoxycholic acid (CDCA) on human BAT activity.\n[3] Treatment of 12 healthy female subjects with CDCA for 2 days resulted in increased BAT activity.\n[4] Whole-body energy expenditure was also increased upon CDCA treatment.\n[5] In vitro treatment of primary human brown adipocytes derived with CDCA or specific TGR5 agonists increased mitochondrial uncoupling and D2 expression, an effect that was absent in human primary white adipocytes.\n[6] These findings identify bile acids as a target to activate BAT in humans."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Treatment of 12 healthy female subjects with CDCA for 2 days resulted in increased BAT activity.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 250, "doc_id": 1568684, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [1568684], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Chenodeoxycholic acid treatment increases brown adipose tissue activity.\n\nDocument title: The Bile Acid Chenodeoxycholic Acid Increases Human Brown Adipose Tissue Activity.\n\nAbstract sentences:\n[0] The interest in brown adipose tissue (BAT) as a target to combat metabolic disease has recently been renewed with the discovery of functional BAT in humans.\n[1] In rodents, BAT can be activated by bile acids, which activate type 2 iodothyronine deiodinase (D2) in BAT via the G-coupled protein receptor TGR5, resulting in increased oxygen consumption and energy expenditure.\n[2] Here we examined the effects of oral supplementation of the bile acid chenodeoxycholic acid (CDCA) on human BAT activity.\n[3] Treatment of 12 healthy female subjects with CDCA for 2 days resulted in increased BAT activity.\n[4] Whole-body energy expenditure was also increased upon CDCA treatment.\n[5] In vitro treatment of primary human brown adipocytes derived with CDCA or specific TGR5 agonists increased mitochondrial uncoupling and D2 expression, an effect that was absent in human primary white adipocytes.\n[6] These findings identify bile acids as a target to activate BAT in humans."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Treatment of 12 healthy female subjects with CDCA for 2 days resulted in increased BAT activity.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 251, "doc_id": 1568684, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [1568684], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Chinese individuals with TT homozygosity in the MTHFR gene are less vulnerable to strokes caused by low levels of folate intake.\n\nDocument title: The effect of folate fortification on folic acid-based homocysteine-lowering intervention and stroke risk: a meta-analysis.\n\nAbstract sentences:\n[0] OBJECTIVE Folate and vitamin B12 are two vital regulators in the metabolic process of homocysteine, which is a risk factor of atherothrombotic events.\n[1] Low folate intake or low plasma folate concentration is associated with increased stroke risk.\n[2] Previous randomized controlled trials presented discordant findings in the effect of folic acid supplementation-based homocysteine lowering on stroke risk.\n[3] The aim of the present review was to perform a meta-analysis of relevant randomized controlled trials to check the how different folate fortification status might affect the effects of folic acid supplementation in lowering homocysteine and reducing stroke risk.\n[4] DESIGN Relevant randomized controlled trials were identified through formal literature search.\n[5] Homocysteine reduction was compared in subgroups stratified by folate fortification status.\n[6] Relative risks with 95 % confidence intervals were used as a measure to assess the association between folic acid supplementation and stroke risk.\n[7] SETTING The meta-analysis included fourteen randomized controlled trials,   SUBJECTS A total of 39 420 patients.\n[8] RESULTS Homocysteine reductions were 26·99 (sd 1·91) %, 18·38 (sd 3·82) % and 21·30 (sd 1·98) %, respectively, in the subgroups without folate fortification, with folate fortification and with partial folate fortification.\n[9] Significant difference was observed between the subgroups with folate fortification and without folate fortification (P=0·05).\n[10] The relative risk of stroke was 0·88 (95 % CI 0·77, 1·00, P=0·05) in the subgroup without folate fortification, 0·94 (95 % CI 0·58, 1·54, P=0·82) in the subgroup with folate fortification and 0·91 (95 % CI 0·82, 1·01, P=0·09) in the subgroup with partial folate fortification.\n[11] CONCLUSIONS Folic acid supplementation might have a modest benefit on stroke prevention in regions without folate fortification."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 253, "doc_id": 37424881, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [37424881], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Chinese individuals with TT homozygosity in the MTHFR gene are more vulnerable to strokes caused by low levels of folate intake.\n\nDocument title: The effect of folate fortification on folic acid-based homocysteine-lowering intervention and stroke risk: a meta-analysis.\n\nAbstract sentences:\n[0] OBJECTIVE Folate and vitamin B12 are two vital regulators in the metabolic process of homocysteine, which is a risk factor of atherothrombotic events.\n[1] Low folate intake or low plasma folate concentration is associated with increased stroke risk.\n[2] Previous randomized controlled trials presented discordant findings in the effect of folic acid supplementation-based homocysteine lowering on stroke risk.\n[3] The aim of the present review was to perform a meta-analysis of relevant randomized controlled trials to check the how different folate fortification status might affect the effects of folic acid supplementation in lowering homocysteine and reducing stroke risk.\n[4] DESIGN Relevant randomized controlled trials were identified through formal literature search.\n[5] Homocysteine reduction was compared in subgroups stratified by folate fortification status.\n[6] Relative risks with 95 % confidence intervals were used as a measure to assess the association between folic acid supplementation and stroke risk.\n[7] SETTING The meta-analysis included fourteen randomized controlled trials,   SUBJECTS A total of 39 420 patients.\n[8] RESULTS Homocysteine reductions were 26·99 (sd 1·91) %, 18·38 (sd 3·82) % and 21·30 (sd 1·98) %, respectively, in the subgroups without folate fortification, with folate fortification and with partial folate fortification.\n[9] Significant difference was observed between the subgroups with folate fortification and without folate fortification (P=0·05).\n[10] The relative risk of stroke was 0·88 (95 % CI 0·77, 1·00, P=0·05) in the subgroup without folate fortification, 0·94 (95 % CI 0·58, 1·54, P=0·82) in the subgroup with folate fortification and 0·91 (95 % CI 0·82, 1·01, P=0·09) in the subgroup with partial folate fortification.\n[11] CONCLUSIONS Folic acid supplementation might have a modest benefit on stroke prevention in regions without folate fortification."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 254, "doc_id": 37424881, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [37424881], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Chlamydia trachomatis is most prevalent in the UK among individuals in their 50s and 60s.\n\nDocument title: Prevalence, risk factors, and uptake of interventions for sexually transmitted infections in Britain: findings from the National Surveys of Sexual Attitudes and Lifestyles (Natsal)\n\nAbstract sentences:\n[0] BACKGROUND Population-based estimates of prevalence, risk distribution, and intervention uptake inform delivery of control programmes for sexually transmitted infections (STIs).\n[1] We undertook the third National Survey of Sexual Attitudes and Lifestyles (Natsal-3) after implementation of national sexual health strategies, and describe the epidemiology of four STIs in Britain (England, Scotland, and Wales) and the uptake of interventions.\n[2] METHODS Between Sept 6, 2010 and Aug 31, 2012\n[3] , we did a probability sample survey of 15,162 women and men aged 16-74 years in Britain.\n[4] Participants were interviewed with computer-assisted face-to-face and self-completion questionnaires.\n[5] Urine from a sample of participants aged 16-44 years who reported at least one sexual partner over the lifetime was tested for the presence of Chlamydia trachomatis, type-specific human papillomavirus (HPV), Neisseria gonorrhoeae, and HIV antibody.\n[6] We describe age-specific and sex-specific prevalences of infection and intervention uptake, in relation to demographic and behavioural factors, and explore changes since Natsal-1 (1990-91) and Natsal-2 (1999-2001).\n[7] FINDINGS Of 8047 eligible participants invited to provide a urine sample, 4828 (60%) agreed.\n[8] We excluded 278 samples, leaving 4550 (94%) participants with STI test results.\n[9] Chlamydia prevalence was 1·5% (95% CI 1·1-2·0) in women and 1·1% (0·7-1·6) in men.\n[10] Prevalences in individuals aged 16-24 years were 3·1% (2·2-4·3) in women and 2·3% (1·5-3·4) in men.\n[11] Area-level deprivation and higher numbers of partners, especially without use of condoms, were risk factors.\n[12] However, 60·4% (45·5-73·7) of chlamydia in women and 43·3% (25·9-62·5) in men was in individuals who had had one partner in the past year.\n[13] Among sexually active 16-24-year-olds, 54·2% (51·4-56·9) of women and 34·6% (31·8-37·4) of men reported testing for chlamydia in the past year, with testing higher in those with more partners.\n[14] High-risk HPV was detected in 15·9% (14·4-17·5) of women, similar to in Natsal-2.\n[15] Coverage of HPV catch-up vaccination was 61·5% (58·2-64·7).\n[16] Prevalence of HPV types 16 and 18 in women aged 18-20 years was lower in Natsal-3 than Natsal-2 (5·8% [3·9-8·6] vs 11·3% [6·8-18·2]; age-adjusted odds ratio 0·44 [0·21-0·94]).\n[17] Gonorrhoea (<0·1% prevalence in women and men) and HIV (0·1% prevalence in women and 0·2% in men) were uncommon and restricted to participants with recognised high-risk factors.\n[18] Since Natsal-2, substantial increases were noted in attendance at sexual health clinics (from 6·7% to 21·4% in women and from 7·7% to 19·6% in men) and HIV testing (from 8·7% to 27·6% in women and from 9·2% to 16·9% in men) in the past 5 years.\n[19] INTERPRETATION STIs were distributed heterogeneously, requiring general and infection-specific interventions.\n[20] Increases in testing and attendance at sexual health clinics, especially in people at highest risk, are encouraging.\n[21] However, STIs persist both in individuals accessing and those not accessing services.\n[22] Our findings provide empirical evidence to inform future sexual health interventions and services.\n[23] FUNDING Grants from the UK Medical Research Council and the Wellcome Trust, with support from the Economic and Social Research Council and the Department of Health."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 255, "doc_id": 5850219, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [5850219], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Chlamydia trachomatis is most prevalent in the UK among sexually-experienced individuals aged 16 to 24.\n\nDocument title: Prevalence, risk factors, and uptake of interventions for sexually transmitted infections in Britain: findings from the National Surveys of Sexual Attitudes and Lifestyles (Natsal)\n\nAbstract sentences:\n[0] BACKGROUND Population-based estimates of prevalence, risk distribution, and intervention uptake inform delivery of control programmes for sexually transmitted infections (STIs).\n[1] We undertook the third National Survey of Sexual Attitudes and Lifestyles (Natsal-3) after implementation of national sexual health strategies, and describe the epidemiology of four STIs in Britain (England, Scotland, and Wales) and the uptake of interventions.\n[2] METHODS Between Sept 6, 2010 and Aug 31, 2012\n[3] , we did a probability sample survey of 15,162 women and men aged 16-74 years in Britain.\n[4] Participants were interviewed with computer-assisted face-to-face and self-completion questionnaires.\n[5] Urine from a sample of participants aged 16-44 years who reported at least one sexual partner over the lifetime was tested for the presence of Chlamydia trachomatis, type-specific human papillomavirus (HPV), Neisseria gonorrhoeae, and HIV antibody.\n[6] We describe age-specific and sex-specific prevalences of infection and intervention uptake, in relation to demographic and behavioural factors, and explore changes since Natsal-1 (1990-91) and Natsal-2 (1999-2001).\n[7] FINDINGS Of 8047 eligible participants invited to provide a urine sample, 4828 (60%) agreed.\n[8] We excluded 278 samples, leaving 4550 (94%) participants with STI test results.\n[9] Chlamydia prevalence was 1·5% (95% CI 1·1-2·0) in women and 1·1% (0·7-1·6) in men.\n[10] Prevalences in individuals aged 16-24 years were 3·1% (2·2-4·3) in women and 2·3% (1·5-3·4) in men.\n[11] Area-level deprivation and higher numbers of partners, especially without use of condoms, were risk factors.\n[12] However, 60·4% (45·5-73·7) of chlamydia in women and 43·3% (25·9-62·5) in men was in individuals who had had one partner in the past year.\n[13] Among sexually active 16-24-year-olds, 54·2% (51·4-56·9) of women and 34·6% (31·8-37·4) of men reported testing for chlamydia in the past year, with testing higher in those with more partners.\n[14] High-risk HPV was detected in 15·9% (14·4-17·5) of women, similar to in Natsal-2.\n[15] Coverage of HPV catch-up vaccination was 61·5% (58·2-64·7).\n[16] Prevalence of HPV types 16 and 18 in women aged 18-20 years was lower in Natsal-3 than Natsal-2 (5·8% [3·9-8·6] vs 11·3% [6·8-18·2]; age-adjusted odds ratio 0·44 [0·21-0·94]).\n[17] Gonorrhoea (<0·1% prevalence in women and men) and HIV (0·1% prevalence in women and 0·2% in men) were uncommon and restricted to participants with recognised high-risk factors.\n[18] Since Natsal-2, substantial increases were noted in attendance at sexual health clinics (from 6·7% to 21·4% in women and from 7·7% to 19·6% in men) and HIV testing (from 8·7% to 27·6% in women and from 9·2% to 16·9% in men) in the past 5 years.\n[19] INTERPRETATION STIs were distributed heterogeneously, requiring general and infection-specific interventions.\n[20] Increases in testing and attendance at sexual health clinics, especially in people at highest risk, are encouraging.\n[21] However, STIs persist both in individuals accessing and those not accessing services.\n[22] Our findings provide empirical evidence to inform future sexual health interventions and services.\n[23] FUNDING Grants from the UK Medical Research Council and the Wellcome Trust, with support from the Economic and Social Research Council and the Department of Health."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Prevalences in individuals aged 16-24 years were 3·1% (2·2-4·3) in women and 2·3% (1·5-3·4) in men.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 256, "doc_id": 5850219, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [5850219], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cholesterol loading induces KLF4 expression in VSMCs, resulting in the expression of pro-inflammatory cytokines.\n\nDocument title: KLF4-dependent phenotypic modulation of smooth muscle cells has a key role in atherosclerotic plaque pathogenesis\n\nAbstract sentences:\n[0] Previous studies investigating the role of smooth muscle cells (SMCs) and macrophages in the pathogenesis of atherosclerosis have provided controversial results owing to the use of unreliable methods for clearly identifying each of these cell types.\n[1] Here, using Myh11-CreERT2 ROSA floxed STOP eYFP Apoe−/− mice to perform SMC lineage tracing, we find that traditional methods for detecting SMCs based on immunostaining for SMC markers fail to detect >80% of SMC-derived cells within advanced atherosclerotic lesions.\n[2] These unidentified SMC-derived cells exhibit phenotypes of other cell lineages, including macrophages and mesenchymal stem cells (MSCs).\n[3] SMC-specific conditional knockout of Krüppel-like factor 4 (Klf4) resulted in reduced numbers of SMC-derived MSC- and macrophage-like cells, a marked reduction in lesion size, and increases in multiple indices of plaque stability, including an increase in fibrous cap thickness as compared to wild-type controls.\n[4] On the basis of in vivo KLF4 chromatin immunoprecipitation–sequencing (ChIP-seq) analyses and studies of cholesterol-treated cultured SMCs, we identified >800 KLF4 target genes, including many that regulate pro-inflammatory responses of SMCs.\n[5] Our findings indicate that the contribution of SMCs to atherosclerotic plaques has been greatly underestimated, and that KLF4-dependent transitions in SMC phenotype are critical in lesion pathogenesis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4, 5]\nExplanation: Evidence states: \"On the basis of in vivo KLF4 chromatin immunoprecipitation–sequencing (ChIP-seq) analyses and studies of cholesterol-treated cultured SMCs, we identified >800 KLF4 target genes, including many that regulate pro-inflammatory responses of SMCs. Our findings indicate that the contribution of SMCs to atherosclerotic plaques has been greatly underestimated, and that KLF4-dependent transitions in SMC phenotype are critical in lesion pathogenesis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 258, "doc_id": 22080671, "label": "SUPPORTS", "evidence_sentence_ids": [4, 5], "cited_doc_ids": [22080671], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Chronic HIV stimulation of B cells leads to the premature exhaustion of B cells.\n\nDocument title: Antibody-Based HIV-1 Vaccines: Recent Developments and Future Directions\n\nAbstract sentences:\n[0] The Global HIV Vaccine Enterprise convened a two-day workshop in May of 2007 to discuss humoral immune responses to HIV and approaches to design vaccines that induce viral neutralizing and other potentially protective antibody responses.\n[1] The goals of this workshop were to identify key scientific issues, gaps, and opportunities that have emerged since the Enterprise Strategic Plan was first published in 2005 [1], and to make recommendations that Enterprise stakeholders can use to plan new activities.\n[2] Most effective viral vaccines work, at least in part, by generating antibodies that inactivate or neutralize the invading virus, and the existing data strongly suggest that an optimally effective HIV-1 vaccine should elicit potent antiviral neutralizing antibodies.\n[3] However, unlike acute viral pathogens, HIV-1 chronically replicates in the host and evades the antibody response.\n[4] This immune evasion, along with the large genetic variation among HIV-1 strains worldwide, has posed major obstacles to vaccine development.\n[5] Current HIV vaccine candidates do not elicit neutralizing antibodies against most circulating virus strains, and thus the induction of a protective antibody response remains a major priority for HIV-1 vaccine development.\n[6] For an antibody-based HIV-1 vaccine, progress in vaccine design is generally gauged by in vitro assays that measure the ability of vaccine-induced antibodies to neutralize a broad spectrum of viral isolates representing the major genetic subtypes (clades) of HIV-1 [2].\n[7] Although it is not known what magnitude and breadth of neutralization will predict protection in vaccine recipients, it is clear that current vaccine immunogens elicit antibodies that neutralize only a minority of circulating isolates.\n[8] Thus, much progress needs to be made in this area.\n[9] Also, though virus neutralization is considered a critical benchmark for a vaccine, this may not be the only benchmark for predicting success with antibody-based HIV-1 vaccine immunogens.\n[10] The main targets for neutralizing antibodies to HIV-1 are the surface gp120 and trans-membrane gp41 envelope glycoproteins (Env) that mediate receptor and coreceptor binding and the subsequent membrane fusion events that allow the virus to gain entry into cells [3].\n[11] Antibodies neutralize the virus by binding these viral spikes and blocking virus entry into susceptible cells, such as CD4+ T cells [4,5].\n[12] In order to chronically replicate in the host, the virus exploits several mechanisms to shield itself against antibody recognition, including a dense outer coating of sugar molecules (N-linked glycans) and the strategic positioning of cysteine–cysteine loop structures on the gp120 molecule [6–8].\n[13] These shielding mechanisms, although highly effective, have vulnerabilities imposed by fitness constraints.\n[14] Information on the precise location and molecular structure of these vulnerable regions could be valuable for the rational design of improved vaccine immunogens.\n[15] Participants in the workshop identified four areas that, if given proper attention, could provide key information that would bring the field closer to an effective antibody-based HIV-1 vaccine: (1) structure-assisted immunogen design, (2) role of Fc receptors and complement, (3) assay standardization and validation, and (4) immunoregulation of B cell responses."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 259, "doc_id": 8883846, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [8883846], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cis-acting lncRNAs control the expression of genes that are positioned in the vicinity of their transcription sites.\n\nDocument title: Functional Consequences of Splicing of the Antisense Transcript COOLAIR on FLC Transcription\n\nAbstract sentences:\n[0] Antisense transcription is widespread in many genomes; however, how much is functional is hotly debated.\n[1] We are investigating functionality of a set of long noncoding antisense transcripts, collectively called COOLAIR, produced at Arabidopsis FLOWERING LOCUS C (FLC).\n[2] COOLAIR initiates just downstream of the major sense transcript poly(A) site and terminates either early or extends into the FLC promoter region.\n[3] We now show that splicing of COOLAIR is functionally important.\n[4] This was revealed through analysis of a hypomorphic mutation in the core spliceosome component PRP8.\n[5] The prp8 mutation perturbs a cotranscriptional feedback mechanism linking COOLAIR processing to FLC gene body histone demethylation and reduced FLC transcription.\n[6] The importance of COOLAIR splicing in this repression mechanism was confirmed by disrupting COOLAIR production and mutating the COOLAIR proximal splice acceptor site.\n[7] Our findings suggest that altered splicing of a long noncoding transcript can quantitatively modulate gene expression through cotranscriptional coupling mechanisms."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 262, "doc_id": 14610165, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14610165], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Citrullinated proteins externalized in neutrophil extracellular traps act indirectly to disrupt the inflammatory cycle.\n\nDocument title: NETs are a source of citrullinated autoantigens and stimulate inflammatory responses in rheumatoid arthritis.\n\nAbstract sentences:\n[0] The early events leading to the development of rheumatoid arthritis (RA) remain unclear, but formation of autoantibodies to citrullinated protein antigens (ACPAs) is considered a key pathogenic event.\n[1] Neutrophils isolated from patients with various autoimmune diseases display enhanced neutrophil extracellular trap (NET) formation, a phenomenon that exposes autoantigens in the context of immunostimulatory molecules.\n[2] We investigated whether aberrant NETosis occurs in RA, determined its triggers, and examined its deleterious inflammatory consequences.\n[3] Enhanced NETosis was observed in circulating and RA synovial fluid neutrophils compared to neutrophils from healthy controls and from patients with osteoarthritis (OA).\n[4] Further, netting neutrophils infiltrated RA synovial tissue, rheumatoid nodules, and skin.\n[5] NETosis correlated with ACPA presence and levels and with systemic inflammatory markers.\n[6] RA sera and immunoglobulin fractions from RA patients with high levels of ACPA and/or rheumatoid factor significantly enhanced NETosis, and the NETs induced by these autoantibodies displayed distinct protein content.\n[7] Indeed, during NETosis, neutrophils externalized the citrullinated autoantigens implicated in RA pathogenesis, and anti-citrullinated vimentin antibodies potently induced NET formation.\n[8] Moreover, the inflammatory cytokines interleukin-17A (IL-17A) and tumor necrosis factor-α (TNF-α) induced NETosis in RA neutrophils.\n[9] In turn, NETs significantly augmented inflammatory responses in RA and OA synovial fibroblasts, including induction of IL-6, IL-8, chemokines, and adhesion molecules.\n[10] These observations implicate accelerated NETosis in RA pathogenesis, through externalization of citrullinated autoantigens and immunostimulatory molecules that may promote aberrant adaptive and innate immune responses in the joint and in the periphery, and perpetuate pathogenic mechanisms in this disease."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7, 9]\nExplanation: Evidence states: \"Indeed, during NETosis, neutrophils externalized the citrullinated autoantigens implicated in RA pathogenesis, and anti-citrullinated vimentin antibodies potently induced NET formation. In turn, NETs significantly augmented inflammatory responses in RA and OA synovial fibroblasts, including induction of IL-6, IL-8, chemokines, and adhesion molecules.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 263, "doc_id": 11328820, "label": "CONTRADICTS", "evidence_sentence_ids": [7, 9], "cited_doc_ids": [11328820, 30041340, 14853989], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Citrullinated proteins externalized in neutrophil extracellular traps act indirectly to disrupt the inflammatory cycle.\n\nDocument title: Antibodies from patients with rheumatoid arthritis target citrullinated histone 4 contained in neutrophils extracellular traps.\n\nAbstract sentences:\n[0] BACKGROUND Histone deimination regulates gene function and contributes to antimicrobial response, allowing the formation of neutrophil extracellular traps (NETs).\n[1] Deiminated proteins are target of anti-citrullinated peptides antibodies (ACPA) in rheumatoid arthritis (RA).\n[2] OBJECTIVE The objective of this paper is to test the hypothesis that RA sera react with deiminated histones contained in NETs.\n[3] METHODS Neutrophils from peripheral blood were stimulated with A23187 and acid treated; NETosis was induced by phorbol myristate acetate, and NET proteins were isolated.\n[4] Sera were tested by immunoblot on acid extracted proteins from neutrophils and from NETs, and by ELISA on deiminated histone H4 or H4-derived peptides.\n[5] Bands reactive with RA sera were excised from gels, digested with trypsin and subjected to matrix-assisted laser desorption/ionisation time of flight (MALDI-TOF) analysis, before and after derivatisation to detect citrullinated peptides.\n[6] RESULTS RA sera reacted with a deiminated antigen of 11 KDa from activated neutrophils, recognised also by anti-H4 and antideiminated H4 antibodies.\n[7] A similar reactivity was observed with NET proteins.\n[8] The antigen from neutrophils or NETs was identified as citrullinated H4 by MALDI-TOF analysis.\n[9] By ELISA, RA sera bound in vitro citrullinated H4.\n[10] Citrullinated H4 14-34 and 31-50 peptides detected antibodies in 67% and 63% of RA sera and in less than 5% of controls; antibody titre was correlated with anti-CCP2.\n[11] CONCLUSIONS Citrullinated H4 from activated neutrophils and NETs is a target of antibodies in RA, and synthetic citrullinated H4-derived peptides are a new substrate for ACPA detection.\n[12] As NETosis can generate antigens for ACPA, these data suggest a novel connection between innate and adaptive immunity in RA."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [0, 1]\nExplanation: Evidence states: \"BACKGROUND Histone deimination regulates gene function and contributes to antimicrobial response, allowing the formation of neutrophil extracellular traps (NETs). Deiminated proteins are target of anti-citrullinated peptides antibodies (ACPA) in rheumatoid arthritis (RA).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 263, "doc_id": 30041340, "label": "CONTRADICTS", "evidence_sentence_ids": [0, 1], "cited_doc_ids": [11328820, 30041340, 14853989], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Citrullinated proteins externalized in neutrophil extracellular traps act indirectly to disrupt the inflammatory cycle.\n\nDocument title: Antibodies from patients with rheumatoid arthritis target citrullinated histone 4 contained in neutrophils extracellular traps.\n\nAbstract sentences:\n[0] BACKGROUND Histone deimination regulates gene function and contributes to antimicrobial response, allowing the formation of neutrophil extracellular traps (NETs).\n[1] Deiminated proteins are target of anti-citrullinated peptides antibodies (ACPA) in rheumatoid arthritis (RA).\n[2] OBJECTIVE The objective of this paper is to test the hypothesis that RA sera react with deiminated histones contained in NETs.\n[3] METHODS Neutrophils from peripheral blood were stimulated with A23187 and acid treated; NETosis was induced by phorbol myristate acetate, and NET proteins were isolated.\n[4] Sera were tested by immunoblot on acid extracted proteins from neutrophils and from NETs, and by ELISA on deiminated histone H4 or H4-derived peptides.\n[5] Bands reactive with RA sera were excised from gels, digested with trypsin and subjected to matrix-assisted laser desorption/ionisation time of flight (MALDI-TOF) analysis, before and after derivatisation to detect citrullinated peptides.\n[6] RESULTS RA sera reacted with a deiminated antigen of 11 KDa from activated neutrophils, recognised also by anti-H4 and antideiminated H4 antibodies.\n[7] A similar reactivity was observed with NET proteins.\n[8] The antigen from neutrophils or NETs was identified as citrullinated H4 by MALDI-TOF analysis.\n[9] By ELISA, RA sera bound in vitro citrullinated H4.\n[10] Citrullinated H4 14-34 and 31-50 peptides detected antibodies in 67% and 63% of RA sera and in less than 5% of controls; antibody titre was correlated with anti-CCP2.\n[11] CONCLUSIONS Citrullinated H4 from activated neutrophils and NETs is a target of antibodies in RA, and synthetic citrullinated H4-derived peptides are a new substrate for ACPA detection.\n[12] As NETosis can generate antigens for ACPA, these data suggest a novel connection between innate and adaptive immunity in RA."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"CONCLUSIONS Citrullinated H4 from activated neutrophils and NETs is a target of antibodies in RA, and synthetic citrullinated H4-derived peptides are a new substrate for ACPA detection.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 263, "doc_id": 30041340, "label": "CONTRADICTS", "evidence_sentence_ids": [11], "cited_doc_ids": [11328820, 30041340, 14853989], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Citrullinated proteins externalized in neutrophil extracellular traps act indirectly to perpetuate the inflammatory cycle via induction of autoantibodies.\n\nDocument title: NETs are a source of citrullinated autoantigens and stimulate inflammatory responses in rheumatoid arthritis.\n\nAbstract sentences:\n[0] The early events leading to the development of rheumatoid arthritis (RA) remain unclear, but formation of autoantibodies to citrullinated protein antigens (ACPAs) is considered a key pathogenic event.\n[1] Neutrophils isolated from patients with various autoimmune diseases display enhanced neutrophil extracellular trap (NET) formation, a phenomenon that exposes autoantigens in the context of immunostimulatory molecules.\n[2] We investigated whether aberrant NETosis occurs in RA, determined its triggers, and examined its deleterious inflammatory consequences.\n[3] Enhanced NETosis was observed in circulating and RA synovial fluid neutrophils compared to neutrophils from healthy controls and from patients with osteoarthritis (OA).\n[4] Further, netting neutrophils infiltrated RA synovial tissue, rheumatoid nodules, and skin.\n[5] NETosis correlated with ACPA presence and levels and with systemic inflammatory markers.\n[6] RA sera and immunoglobulin fractions from RA patients with high levels of ACPA and/or rheumatoid factor significantly enhanced NETosis, and the NETs induced by these autoantibodies displayed distinct protein content.\n[7] Indeed, during NETosis, neutrophils externalized the citrullinated autoantigens implicated in RA pathogenesis, and anti-citrullinated vimentin antibodies potently induced NET formation.\n[8] Moreover, the inflammatory cytokines interleukin-17A (IL-17A) and tumor necrosis factor-α (TNF-α) induced NETosis in RA neutrophils.\n[9] In turn, NETs significantly augmented inflammatory responses in RA and OA synovial fibroblasts, including induction of IL-6, IL-8, chemokines, and adhesion molecules.\n[10] These observations implicate accelerated NETosis in RA pathogenesis, through externalization of citrullinated autoantigens and immunostimulatory molecules that may promote aberrant adaptive and innate immune responses in the joint and in the periphery, and perpetuate pathogenic mechanisms in this disease."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7, 8, 9, 10]\nExplanation: Evidence states: \"Indeed, during NETosis, neutrophils externalized the citrullinated autoantigens implicated in RA pathogenesis, and anti-citrullinated vimentin antibodies potently induced NET formation. Moreover, the inflammatory cytokines interleukin-17A (IL-17A) and tumor necrosis factor-α (TNF-α) induced NETosis in RA neutrophils. In turn, NETs significantly augmented inflammatory responses in RA and OA synovial fibroblasts, including induction of IL-6, IL-8, chemokines, and adhesion molecules. These observations implicate accelerated NETosis in RA pathogenesis, through externalization of citrullinated autoantigens and immunostimulatory molecules that may promote aberrant adaptive and innate immune responses in the joint and in the periphery, and perpetuate pathogenic mechanisms in this disease.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 264, "doc_id": 11328820, "label": "SUPPORTS", "evidence_sentence_ids": [7, 8, 9, 10], "cited_doc_ids": [11328820], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Clathrin stabilizes the spindle fiber apparatus during mitosis.\n\nDocument title: Clathrin is required for the function of the mitotic spindle\n\nAbstract sentences:\n[0] Clathrin has an established function in the generation of vesicles that transfer membrane and proteins around the cell.\n[1] The formation of clathrin-coated vesicles occurs continuously in non-dividing cells, but is shut down during mitosis, when clathrin concentrates at the spindle apparatus.\n[2] Here, we show that clathrin stabilizes fibres of the mitotic spindle to aid congression of chromosomes.\n[3] Clathrin bound to the spindle directly by the amino-terminal domain of clathrin heavy chain.\n[4] Depletion of clathrin heavy chain using RNA interference prolonged mitosis; kinetochore fibres were destabilized, leading to defective congression of chromosomes to the metaphase plate and persistent activation of the spindle checkpoint.\n[5] Normal mitosis was rescued by clathrin triskelia but not the N-terminal domain of clathrin heavy chain, indicating that stabilization of kinetochore fibres was dependent on the unique structure of clathrin.\n[6] The importance of clathrin for normal mitosis may be relevant to understanding human cancers that involve gene fusions of clathrin heavy chain."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here, we show that clathrin stabilizes fibres of the mitotic spindle to aid congression of chromosomes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 265, "doc_id": 2033917, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [2033917], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Clathrin stabilizes the spindle fiber apparatus during mitosis.\n\nDocument title: Clathrin is required for the function of the mitotic spindle\n\nAbstract sentences:\n[0] Clathrin has an established function in the generation of vesicles that transfer membrane and proteins around the cell.\n[1] The formation of clathrin-coated vesicles occurs continuously in non-dividing cells, but is shut down during mitosis, when clathrin concentrates at the spindle apparatus.\n[2] Here, we show that clathrin stabilizes fibres of the mitotic spindle to aid congression of chromosomes.\n[3] Clathrin bound to the spindle directly by the amino-terminal domain of clathrin heavy chain.\n[4] Depletion of clathrin heavy chain using RNA interference prolonged mitosis; kinetochore fibres were destabilized, leading to defective congression of chromosomes to the metaphase plate and persistent activation of the spindle checkpoint.\n[5] Normal mitosis was rescued by clathrin triskelia but not the N-terminal domain of clathrin heavy chain, indicating that stabilization of kinetochore fibres was dependent on the unique structure of clathrin.\n[6] The importance of clathrin for normal mitosis may be relevant to understanding human cancers that involve gene fusions of clathrin heavy chain."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Depletion of clathrin heavy chain using RNA interference prolonged mitosis; kinetochore fibres were destabilized, leading to defective congression of chromosomes to the metaphase plate and persistent activation of the spindle checkpoint.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 265, "doc_id": 2033917, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [2033917], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Clathrin stabilizes the spindle fiber apparatus during mitosis.\n\nDocument title: Clathrin is required for the function of the mitotic spindle\n\nAbstract sentences:\n[0] Clathrin has an established function in the generation of vesicles that transfer membrane and proteins around the cell.\n[1] The formation of clathrin-coated vesicles occurs continuously in non-dividing cells, but is shut down during mitosis, when clathrin concentrates at the spindle apparatus.\n[2] Here, we show that clathrin stabilizes fibres of the mitotic spindle to aid congression of chromosomes.\n[3] Clathrin bound to the spindle directly by the amino-terminal domain of clathrin heavy chain.\n[4] Depletion of clathrin heavy chain using RNA interference prolonged mitosis; kinetochore fibres were destabilized, leading to defective congression of chromosomes to the metaphase plate and persistent activation of the spindle checkpoint.\n[5] Normal mitosis was rescued by clathrin triskelia but not the N-terminal domain of clathrin heavy chain, indicating that stabilization of kinetochore fibres was dependent on the unique structure of clathrin.\n[6] The importance of clathrin for normal mitosis may be relevant to understanding human cancers that involve gene fusions of clathrin heavy chain."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Normal mitosis was rescued by clathrin triskelia but not the N-terminal domain of clathrin heavy chain, indicating that stabilization of kinetochore fibres was dependent on the unique structure of clathrin.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 265, "doc_id": 2033917, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [2033917], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cnn1 recruitment varies with cell cycle timing.\n\nDocument title: Cnn1 inhibits the interactions between the KMN complexes of the yeast kinetochore\n\nAbstract sentences:\n[0] Kinetochores attach the replicated chromosomes to the mitotic spindle and orchestrate their transmission to the daughter cells.\n[1] Kinetochore–spindle binding and chromosome segregation are mediated by the multi-copy KNL1Spc105, MIS12Mtw1 and NDC80Ndc80 complexes that form the so-called KMN network.\n[2] KMN–spindle attachment is regulated by the Aurora BIpl1 and MPS1Mps1 kinases.\n[3] It is unclear whether other mechanisms exist that support KMN activity during the cell cycle.\n[4] Using budding yeast, we show that kinetochore protein Cnn1 localizes to the base of the Ndc80 complex and promotes a functionally competent configuration of the KMN network.\n[5] Cnn1 regulates KMN activity in a spatiotemporal manner by inhibiting the interaction between its complexes.\n[6] Cnn1 activity peaks in anaphase and is driven by the Cdc28, Mps1 and Ipl1 kinases."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Cnn1 regulates KMN activity in a spatiotemporal manner by inhibiting the interaction between its complexes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 266, "doc_id": 22405338, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [22405338], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cnn1 recruitment varies with cell cycle timing.\n\nDocument title: Cnn1 inhibits the interactions between the KMN complexes of the yeast kinetochore\n\nAbstract sentences:\n[0] Kinetochores attach the replicated chromosomes to the mitotic spindle and orchestrate their transmission to the daughter cells.\n[1] Kinetochore–spindle binding and chromosome segregation are mediated by the multi-copy KNL1Spc105, MIS12Mtw1 and NDC80Ndc80 complexes that form the so-called KMN network.\n[2] KMN–spindle attachment is regulated by the Aurora BIpl1 and MPS1Mps1 kinases.\n[3] It is unclear whether other mechanisms exist that support KMN activity during the cell cycle.\n[4] Using budding yeast, we show that kinetochore protein Cnn1 localizes to the base of the Ndc80 complex and promotes a functionally competent configuration of the KMN network.\n[5] Cnn1 regulates KMN activity in a spatiotemporal manner by inhibiting the interaction between its complexes.\n[6] Cnn1 activity peaks in anaphase and is driven by the Cdc28, Mps1 and Ipl1 kinases."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Cnn1 activity peaks in anaphase and is driven by the Cdc28, Mps1 and Ipl1 kinases.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 266, "doc_id": 22405338, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [22405338], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cognitive behavioral therapy is an ineffective treatment for insomnia\n\nDocument title: Cognitive behavioral therapy vs zopiclone for treatment of chronic primary insomnia in older adults: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Insomnia is a common condition in older adults and is associated with a number of adverse medical, social, and psychological consequences.\n[1] Previous research has suggested beneficial outcomes of both psychological and pharmacological treatments, but blinded placebo-controlled trials comparing the effects of these treatments are lacking.\n[2] OBJECTIVE To examine short- and long-term clinical efficacy of cognitive behavioral therapy (CBT) and pharmacological treatment in older adults experiencing chronic primary insomnia.\n[3] DESIGN, SETTING, AND PARTICIPANTS A randomized, double-blinded, placebo-controlled trial of 46 adults (mean age, 60.8 y; 22 women) with chronic primary insomnia conducted between January 2004 and December 2005 in a single Norwegian university-based outpatient clinic for adults and elderly patients.\n[4] INTERVENTION CBT (sleep hygiene, sleep restriction, stimulus control, cognitive therapy, and relaxation; n = 18), sleep medication (7.5-mg zopiclone each night; n = 16), or placebo medication (n = 12).\n[5] All treatment duration was 6 weeks, and the 2 active treatments were followed up at 6 months.\n[6] MAIN OUTCOME MEASURES Ambulant clinical polysomnographic data and sleep diaries were used to determine total wake time, total sleep time, sleep efficiency, and slow-wave sleep (only assessed using polysomnography) on all 3 assessment points.\n[7] RESULTS CBT resulted in improved short- and long-term outcomes compared with zopiclone on 3 out of 4 outcome measures.\n[8] For most outcomes, zopiclone did not differ from placebo.\n[9] Participants receiving CBT improved their sleep efficiency from 81.4% at pretreatment to 90.1% at 6-month follow-up compared with a decrease from 82.3% to 81.9% in the zopiclone group.\n[10] Participants in the CBT group spent much more time in slow-wave sleep (stages 3 and 4) compared with those in other groups, and spent less time awake during the night.\n[11] Total sleep time was similar in all 3 groups; at 6 months, patients receiving CBT had better sleep efficiency using polysomnography than those taking zopiclone.\n[12] CONCLUSION These results suggest that interventions based on CBT are superior to zopiclone treatment both in short- and long-term management of insomnia in older adults.\n[13] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00295386."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"RESULTS CBT resulted in improved short- and long-term outcomes compared with zopiclone on 3 out of 4 outcome measures.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 267, "doc_id": 5912283, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [5912283, 31554917], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cognitive behavioral therapy is an ineffective treatment for insomnia\n\nDocument title: Cognitive behavioral therapy vs zopiclone for treatment of chronic primary insomnia in older adults: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Insomnia is a common condition in older adults and is associated with a number of adverse medical, social, and psychological consequences.\n[1] Previous research has suggested beneficial outcomes of both psychological and pharmacological treatments, but blinded placebo-controlled trials comparing the effects of these treatments are lacking.\n[2] OBJECTIVE To examine short- and long-term clinical efficacy of cognitive behavioral therapy (CBT) and pharmacological treatment in older adults experiencing chronic primary insomnia.\n[3] DESIGN, SETTING, AND PARTICIPANTS A randomized, double-blinded, placebo-controlled trial of 46 adults (mean age, 60.8 y; 22 women) with chronic primary insomnia conducted between January 2004 and December 2005 in a single Norwegian university-based outpatient clinic for adults and elderly patients.\n[4] INTERVENTION CBT (sleep hygiene, sleep restriction, stimulus control, cognitive therapy, and relaxation; n = 18), sleep medication (7.5-mg zopiclone each night; n = 16), or placebo medication (n = 12).\n[5] All treatment duration was 6 weeks, and the 2 active treatments were followed up at 6 months.\n[6] MAIN OUTCOME MEASURES Ambulant clinical polysomnographic data and sleep diaries were used to determine total wake time, total sleep time, sleep efficiency, and slow-wave sleep (only assessed using polysomnography) on all 3 assessment points.\n[7] RESULTS CBT resulted in improved short- and long-term outcomes compared with zopiclone on 3 out of 4 outcome measures.\n[8] For most outcomes, zopiclone did not differ from placebo.\n[9] Participants receiving CBT improved their sleep efficiency from 81.4% at pretreatment to 90.1% at 6-month follow-up compared with a decrease from 82.3% to 81.9% in the zopiclone group.\n[10] Participants in the CBT group spent much more time in slow-wave sleep (stages 3 and 4) compared with those in other groups, and spent less time awake during the night.\n[11] Total sleep time was similar in all 3 groups; at 6 months, patients receiving CBT had better sleep efficiency using polysomnography than those taking zopiclone.\n[12] CONCLUSION These results suggest that interventions based on CBT are superior to zopiclone treatment both in short- and long-term management of insomnia in older adults.\n[13] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00295386."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Participants receiving CBT improved their sleep efficiency from 81.4% at pretreatment to 90.1% at 6-month follow-up compared with a decrease from 82.3% to 81.9% in the zopiclone group.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 267, "doc_id": 5912283, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [5912283, 31554917], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cognitive behavioral therapy is an ineffective treatment for insomnia\n\nDocument title: Cognitive behavioral therapy vs zopiclone for treatment of chronic primary insomnia in older adults: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Insomnia is a common condition in older adults and is associated with a number of adverse medical, social, and psychological consequences.\n[1] Previous research has suggested beneficial outcomes of both psychological and pharmacological treatments, but blinded placebo-controlled trials comparing the effects of these treatments are lacking.\n[2] OBJECTIVE To examine short- and long-term clinical efficacy of cognitive behavioral therapy (CBT) and pharmacological treatment in older adults experiencing chronic primary insomnia.\n[3] DESIGN, SETTING, AND PARTICIPANTS A randomized, double-blinded, placebo-controlled trial of 46 adults (mean age, 60.8 y; 22 women) with chronic primary insomnia conducted between January 2004 and December 2005 in a single Norwegian university-based outpatient clinic for adults and elderly patients.\n[4] INTERVENTION CBT (sleep hygiene, sleep restriction, stimulus control, cognitive therapy, and relaxation; n = 18), sleep medication (7.5-mg zopiclone each night; n = 16), or placebo medication (n = 12).\n[5] All treatment duration was 6 weeks, and the 2 active treatments were followed up at 6 months.\n[6] MAIN OUTCOME MEASURES Ambulant clinical polysomnographic data and sleep diaries were used to determine total wake time, total sleep time, sleep efficiency, and slow-wave sleep (only assessed using polysomnography) on all 3 assessment points.\n[7] RESULTS CBT resulted in improved short- and long-term outcomes compared with zopiclone on 3 out of 4 outcome measures.\n[8] For most outcomes, zopiclone did not differ from placebo.\n[9] Participants receiving CBT improved their sleep efficiency from 81.4% at pretreatment to 90.1% at 6-month follow-up compared with a decrease from 82.3% to 81.9% in the zopiclone group.\n[10] Participants in the CBT group spent much more time in slow-wave sleep (stages 3 and 4) compared with those in other groups, and spent less time awake during the night.\n[11] Total sleep time was similar in all 3 groups; at 6 months, patients receiving CBT had better sleep efficiency using polysomnography than those taking zopiclone.\n[12] CONCLUSION These results suggest that interventions based on CBT are superior to zopiclone treatment both in short- and long-term management of insomnia in older adults.\n[13] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00295386."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Participants in the CBT group spent much more time in slow-wave sleep (stages 3 and 4) compared with those in other groups, and spent less time awake during the night.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 267, "doc_id": 5912283, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [5912283, 31554917], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cognitive behavioral therapy is an ineffective treatment for insomnia\n\nDocument title: Cognitive behavioral therapy vs zopiclone for treatment of chronic primary insomnia in older adults: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Insomnia is a common condition in older adults and is associated with a number of adverse medical, social, and psychological consequences.\n[1] Previous research has suggested beneficial outcomes of both psychological and pharmacological treatments, but blinded placebo-controlled trials comparing the effects of these treatments are lacking.\n[2] OBJECTIVE To examine short- and long-term clinical efficacy of cognitive behavioral therapy (CBT) and pharmacological treatment in older adults experiencing chronic primary insomnia.\n[3] DESIGN, SETTING, AND PARTICIPANTS A randomized, double-blinded, placebo-controlled trial of 46 adults (mean age, 60.8 y; 22 women) with chronic primary insomnia conducted between January 2004 and December 2005 in a single Norwegian university-based outpatient clinic for adults and elderly patients.\n[4] INTERVENTION CBT (sleep hygiene, sleep restriction, stimulus control, cognitive therapy, and relaxation; n = 18), sleep medication (7.5-mg zopiclone each night; n = 16), or placebo medication (n = 12).\n[5] All treatment duration was 6 weeks, and the 2 active treatments were followed up at 6 months.\n[6] MAIN OUTCOME MEASURES Ambulant clinical polysomnographic data and sleep diaries were used to determine total wake time, total sleep time, sleep efficiency, and slow-wave sleep (only assessed using polysomnography) on all 3 assessment points.\n[7] RESULTS CBT resulted in improved short- and long-term outcomes compared with zopiclone on 3 out of 4 outcome measures.\n[8] For most outcomes, zopiclone did not differ from placebo.\n[9] Participants receiving CBT improved their sleep efficiency from 81.4% at pretreatment to 90.1% at 6-month follow-up compared with a decrease from 82.3% to 81.9% in the zopiclone group.\n[10] Participants in the CBT group spent much more time in slow-wave sleep (stages 3 and 4) compared with those in other groups, and spent less time awake during the night.\n[11] Total sleep time was similar in all 3 groups; at 6 months, patients receiving CBT had better sleep efficiency using polysomnography than those taking zopiclone.\n[12] CONCLUSION These results suggest that interventions based on CBT are superior to zopiclone treatment both in short- and long-term management of insomnia in older adults.\n[13] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00295386."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"CONCLUSION These results suggest that interventions based on CBT are superior to zopiclone treatment both in short- and long-term management of insomnia in older adults.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 267, "doc_id": 5912283, "label": "CONTRADICTS", "evidence_sentence_ids": [12], "cited_doc_ids": [5912283, 31554917], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Combination nicotine replacement therapies with varenicline or bupropion are more effective after 12 weeks of reatment compared to varenicline monotherapy.\n\nDocument title: Combination varenicline and bupropion SR for tobacco-dependence treatment in cigarette smokers: a randomized trial.\n\nAbstract sentences:\n[0] IMPORTANCE Combining pharmacotherapies for tobacco-dependence treatment may increase smoking abstinence.\n[1] OBJECTIVE To determine efficacy and safety of varenicline and bupropion sustained-release (SR; combination therapy) compared with varenicline (monotherapy) in cigarette smokers.\n[2] DESIGN, SETTING, AND PARTICIPANTS Randomized, blinded, placebo-controlled multicenter clinical trial with a 12-week treatment period and follow-up through week 52 conducted between October 2009 and April 2013 at 3 midwestern clinical research sites.\n[3] Five hundred six adult (≥18 years) cigarette smokers were randomly assigned and 315 (62%) completed the study.\n[4] INTERVENTIONS Twelve weeks of varenicline and bupropion SR or varenicline and placebo.\n[5] MAIN OUTCOMES AND MEASURES Primary outcome was abstinence rates at week 12, defined as prolonged (no smoking from 2 weeks after the target quit date) abstinence and 7-day point-prevalence (no smoking past 7 days) abstinence.\n[6] Secondary outcomes were prolonged and point-prevalence smoking abstinence rates at weeks 26 and 52.\n[7] Outcomes were biochemically confirmed.\n[8] RESULTS At 12 weeks, 53.0% of the combination therapy group achieved prolonged smoking abstinence and 56.2% achieved 7-day point-prevalence smoking abstinence compared with 43.2% and 48.6% in varenicline monotherapy (odds ratio [OR], 1.49; 95% CI, 1.05-2.12; P = .03 and OR, 1.36; 95% CI, 0.95-1.93; P = .09, respectively).\n[9] At 26 weeks, 36.6% of the combination therapy group achieved prolonged and 38.2% achieved 7-day point-prevalence smoking abstinence compared with 27.6% and 31.9% in varenicline monotherapy (OR, 1.52; 95% CI, 1.04-2.22; P = .03 and OR, 1.32; 95% CI, 0.91-1.91; P = .14, respectively).\n[10] At 52 weeks, 30.9% of the combination therapy group achieved prolonged and 36.6% achieved 7-day point-prevalence smoking abstinence compared with 24.5% and 29.2% in varenicline monotherapy (OR, 1.39; 95% CI, 0.93-2.07; P = .11 and OR, 1.40; 95% CI, 0.96-2.05; P = .08, respectively).\n[11] Participants receiving combination therapy reported more anxiety (7.2% vs 3.1%; P = .04) and depressive symptoms (3.6% vs 0.8%; P = .03).\n[12] CONCLUSIONS AND RELEVANCE Among cigarette smokers, combined use of varenicline and bupropion, compared with varenicline alone, increased prolonged abstinence but not 7-day point prevalence at 12 and 26 weeks.\n[13] Neither outcome was significantly different at 52 weeks.\n[14] Further research is required to determine the role of combination therapy in smoking cessation.\n[15] TRIAL REGISTRATION clinicaltrials.gov Identifier: http://clinicaltrials.gov/show/NCT00935818."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"RESULTS At 12 weeks, 53.0% of the combination therapy group achieved prolonged smoking abstinence and 56.2% achieved 7-day point-prevalence smoking abstinence compared with 43.2% and 48.6% in varenicline monotherapy (odds ratio [OR], 1.49; 95% CI, 1.05-2.12; P = .03 and OR, 1.36; 95% CI, 0.95-1.93; P = .09, respectively).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 272, "doc_id": 11614737, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [11614737], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Commelina yellow mottle virus (ComYMV) has three typical badnavirus ORFs, capable of encoding proteins 23, 15, and 216 kD.\n\nDocument title: Properties of Commelina yellow mottle virus's complete DNA sequence, genomic discontinuities and transcript suggest that it is a pararetrovirus.\n\nAbstract sentences:\n[0] The non-enveloped bacilliform viruses are the second group of plant viruses known to possess a genome consisting of circular double-stranded DNA.\n[1] We have characterized the viral transcript and determined the complete sequence of the genome of Commelina mellow mottle virus (CoYMV), a member of this group.\n[2] Analysis of the viral transcript indicates that the virus encodes a single terminally-redundant genome-length plus 120 nucleotide transcript.\n[3] A fraction of the transcripts is polyadenylated, although the majority of the transcript is not polyadenylated.\n[4] Analysis of the genome sequence indicates that the genome is 7489 bp in size and that the transcribed strand contains three open reading frames capable of encoding proteins of 23, 15 and 216 kd.\n[5] The function of the 25 and 15 kd proteins is unknown.\n[6] Similarities between the 216 kd polypeptide and the cauliflower mosaic virus coat protein and protease/reverse transcriptase polyprotein suggest that the 216 kd polypeptide is a polyprotein that is proteolytically processed to yield the virion coat protein, a protease, and replicase (reverse transcriptase and ribonuclease H).\n[7] Each strand of the CoYMV genome is interrupted by site-specific discontinuities.\n[8] The locations of the 5'-ends of these discontinuities, and the presence and location of a region on the CoYMV transcript capable of annealing with the 3'-end of cytosolic initiator methionine tRNA are consistent with replication by reverse transcription.\n[9] We have demonstrated that a construct containing 1.3 CoYMV genomes is infective when introduced into Commelina diffusa, the host for CoYMV, using Agrobacterium-mediated infection."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Analysis of the genome sequence indicates that the genome is 7489 bp in size and that the transcribed strand contains three open reading frames capable of encoding proteins of 23, 15 and 216 kd.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 277, "doc_id": 14376683, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [14376683], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Commelina yellow mottle virus' (ComYMV) genome consists of 2140 baise pairs.\n\nDocument title: Properties of Commelina yellow mottle virus's complete DNA sequence, genomic discontinuities and transcript suggest that it is a pararetrovirus.\n\nAbstract sentences:\n[0] The non-enveloped bacilliform viruses are the second group of plant viruses known to possess a genome consisting of circular double-stranded DNA.\n[1] We have characterized the viral transcript and determined the complete sequence of the genome of Commelina mellow mottle virus (CoYMV), a member of this group.\n[2] Analysis of the viral transcript indicates that the virus encodes a single terminally-redundant genome-length plus 120 nucleotide transcript.\n[3] A fraction of the transcripts is polyadenylated, although the majority of the transcript is not polyadenylated.\n[4] Analysis of the genome sequence indicates that the genome is 7489 bp in size and that the transcribed strand contains three open reading frames capable of encoding proteins of 23, 15 and 216 kd.\n[5] The function of the 25 and 15 kd proteins is unknown.\n[6] Similarities between the 216 kd polypeptide and the cauliflower mosaic virus coat protein and protease/reverse transcriptase polyprotein suggest that the 216 kd polypeptide is a polyprotein that is proteolytically processed to yield the virion coat protein, a protease, and replicase (reverse transcriptase and ribonuclease H).\n[7] Each strand of the CoYMV genome is interrupted by site-specific discontinuities.\n[8] The locations of the 5'-ends of these discontinuities, and the presence and location of a region on the CoYMV transcript capable of annealing with the 3'-end of cytosolic initiator methionine tRNA are consistent with replication by reverse transcription.\n[9] We have demonstrated that a construct containing 1.3 CoYMV genomes is infective when introduced into Commelina diffusa, the host for CoYMV, using Agrobacterium-mediated infection."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Analysis of the genome sequence indicates that the genome is 7489 bp in size and that the transcribed strand contains three open reading frames capable of encoding proteins of 23, 15 and 216 kd.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 278, "doc_id": 14376683, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [14376683], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Comparative transcriptome analysis identified new platelet proteins with structural features suggesting a role in platelet function.\n\nDocument title: Comparative gene expression profiling of in vitro differentiated megakaryocytes and erythroblasts identifies novel activatory and inhibitory platelet membrane proteins.\n\nAbstract sentences:\n[0] To identify previously unknown platelet receptors we compared the transcriptomes of in vitro differentiated megakaryocytes (MKs) and erythroblasts (EBs).\n[1] RNA was obtained from purified, biologically paired MK and EB cultures and compared using cDNA microarrays.\n[2] Bioinformatical analysis of MK-up-regulated genes identified 151 transcripts encoding transmembrane domain-containing proteins.\n[3] Although many of these were known platelet genes, a number of previously unidentified or poorly characterized transcripts were also detected.\n[4] Many of these transcripts, including G6b, G6f, LRRC32, LAT2, and the G protein-coupled receptor SUCNR1, encode proteins with structural features or functions that suggest they may be involved in the modulation of platelet function.\n[5] Immunoblotting on platelets confirmed the presence of the encoded proteins, and flow cytometric analysis confirmed the expression of G6b, G6f, and LRRC32 on the surface of platelets.\n[6] Through comparative analysis of expression in platelets and other blood cells we demonstrated that G6b, G6f, and LRRC32 are restricted to the platelet lineage, whereas LAT2 and SUCNR1 were also detected in other blood cells.\n[7] The identification of the succinate receptor SUCNR1 in platelets is of particular interest, because physiologically relevant concentrations of succinate were shown to potentiate the effect of low doses of a variety of platelet agonists."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6, 7]\nExplanation: Evidence states: \"Through comparative analysis of expression in platelets and other blood cells we demonstrated that G6b, G6f, and LRRC32 are restricted to the platelet lineage, whereas LAT2 and SUCNR1 were also detected in other blood cells. The identification of the succinate receptor SUCNR1 in platelets is of particular interest, because physiologically relevant concentrations of succinate were shown to potentiate the effect of low doses of a variety of platelet agonists.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 280, "doc_id": 25001628, "label": "SUPPORTS", "evidence_sentence_ids": [6, 7], "cited_doc_ids": [25001628], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Concentrations of SNV and CNV in stem-cell regulatory elements and binding sites of transcription factors in iPSC-lines are distinct from their founding cells.\n\nDocument title: Large-Scale Profiling Reveals the Influence of Genetic Variation on Gene Expression in Human Induced Pluripotent Stem Cells.\n\nAbstract sentences:\n[0] In this study, we used whole-genome sequencing and gene expression profiling of 215 human induced pluripotent stem cell (iPSC) lines from different donors to identify genetic variants associated with RNA expression for 5,746 genes.\n[1] We were able to predict causal variants for these expression quantitative trait loci (eQTLs) that disrupt transcription factor binding and validated a subset of them experimentally.\n[2] We also identified copy-number variant (CNV) eQTLs, including some that appear to affect gene expression by altering the copy number of intergenic regulatory regions.\n[3] In addition, we were able to identify effects on gene expression of rare genic CNVs and regulatory single-nucleotide variants and found that reactivation of gene expression on the X chromosome depends on gene chromosomal position.\n[4] Our work highlights the value of iPSCs for genetic association analyses and provides a unique resource for investigating the genetic regulation of gene expression in pluripotent cells."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 281, "doc_id": 4632921, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4632921], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Consumption of whole fruits increases the risk of type 2 diabetes.\n\nDocument title: Fruit consumption and risk of type 2 diabetes: results from three prospective longitudinal cohort studies\n\nAbstract sentences:\n[0] OBJECTIVE To determine whether individual fruits are differentially associated with risk of type 2 diabetes.\n[1] DESIGN Prospective longitudinal cohort study.\n[2] SETTING Health professionals in the United States.\n[3] PARTICIPANTS 66,105 women from the Nurses' Health Study (1984-2008), 85,104 women from the Nurses' Health Study II (1991-2009), and 36,173 men from the Health Professionals Follow-up Study (1986-2008) who were free of major chronic diseases at baseline in these studies.\n[4] MAIN OUTCOME MEASURE Incident cases of type 2 diabetes, identified through self report and confirmed by supplementary questionnaires.\n[5] RESULTS During 3,464,641 person years of follow-up, 12,198 participants developed type 2 diabetes.\n[6] After adjustment for personal, lifestyle, and dietary risk factors of diabetes, the pooled hazard ratio of type 2 diabetes for every three servings/week of total whole fruit consumption was 0.98 (95% confidence interval 0.97 [corrected] to 0.99).\n[7] With mutual adjustment of individual fruits, the pooled hazard ratios of type 2 diabetes for every three servings/week were 0.74 (0.66 to 0.83) for blueberries, 0.88 (0.83 to 0.93) for grapes and raisins, 0.89 (0.79 to 1.01) for prunes, 0.93 (0.90 to 0.96) for apples and pears, 0.95 (0.91 to 0.98) for bananas, 0.95 (0.91 to 0.99) for grapefruit, 0.97 (0.92 to 1.02) for peaches, plums, and apricots, 0.99 (0.95 to 1.03) for oranges, 1.03 (0.96 to 1.10) for strawberries, and 1.10 (1.02 to 1.18) for cantaloupe.\n[8] The pooled hazard ratio for the same increment in fruit juice consumption was 1.08 (1.05 to 1.11).\n[9] The associations with risk of type 2 diabetes differed significantly among individual fruits (P<0.001 in all cohorts).\n[10] CONCLUSION Our findings suggest the presence of heterogeneity in the associations between individual fruit consumption and risk of type 2 diabetes.\n[11] Greater consumption of specific whole fruits, particularly blueberries, grapes, and apples, is significantly associated with a lower risk of type 2 diabetes, whereas greater consumption of fruit juice is associated with a higher risk."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"Greater consumption of specific whole fruits, particularly blueberries, grapes, and apples, is significantly associated with a lower risk of type 2 diabetes, whereas greater consumption of fruit juice is associated with a higher risk.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 283, "doc_id": 1974176, "label": "CONTRADICTS", "evidence_sentence_ids": [11], "cited_doc_ids": [1974176], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Continued HHV-8 transmission among MSM in San Francisco may be explained by urogenital contact.\n\nDocument title: Prevalence of Kaposi sarcoma-associated herpesvirus infection in homosexual men at beginning of and during the HIV epidemic.\n\nAbstract sentences:\n[0] CONTEXT Some studies have inferred that an epidemic of Kaposi sarcoma-associated herpesvirus (KSHV) infection in homosexual men in the United States occurred concurrently with that of human immunodeficiency virus (HIV), but there have been no direct measurements of KSHV prevalence at the beginning of the HIV epidemic.\n[1] OBJECTIVES To determine the prevalence of KSHV infection in homosexual men in San Francisco, Calif, at the beginning of the HIV epidemic in 1978 and 1979 and to examine changes in prevalence of KSHV at time points from 1978 through 1996 in light of changes in sexual behavior.\n[2] DESIGN, SETTING, AND PARTICIPANTS Analysis of a clinic-based sample (n = 398) derived from the San Francisco City Clinic Cohort (ages 18-66 years) (n = 2666 for analyses herein) and from population-based samples from the San Francisco Men's Health Study (MHS) (ages 25-54 years) (n = 825 and 252) and the San Francisco Young Men's Health Study (YMHS) (ages 18-29 years) (n = 428-976, and 557); behavioral studies were longitudinal and KSHV prevalence studies were cross-sectional.\n[3] MAIN OUTCOME MEASURES Antibodies against KSHV and HIV; sexual behaviors.\n[4] RESULTS The prevalence of KSHV infection in 1978 and 1979 was 26.5% of 235 (a random sample) overall (weighted for HIV infection) vs 6.9% (128/1842) for HIV in the San Francisco City Clinic Cohort sample.\n[5] The prevalence of KSHV infection remained essentially unchanged between an MHS sample of 252 in 1984 and 1985 (29.6%) and a YMHS sample of 557 in 1995 and 1996 (26.4%), while HIV prevalence dropped from 49.5% of 825 in 1984 and 1985 (MHS) to 17.6% of 428 in 1992 and 1993 (YMHS).\n[6] The proportion of men practicing unprotected receptive anal intercourse with 1 or more partners declined from 54% to 11% during the 1984 through 1993 period (MHS) with similar though slightly higher values in the YMHS in 1992 and 1993; whereas for unprotected oral intercourse it ranged between 60% and 90% in the 1984 through 1996 period (MHS and YMHS).\n[7] CONCLUSIONS Infection with KSHV was already highly prevalent in homosexual men when the HIV epidemic began in San Francisco, and its prevalence has been maintained at a nearly constant level.\n[8] Any declines in the incidence of Kaposi sarcoma do not appear to be caused by a decline in KSHV transmission."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 285, "doc_id": 5548081, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [5548081], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Converting apoE4 to apoE3 by gene editing prevents the pathology associated with apoE4 in human iPSCderived neurons.\n\nDocument title: Gain of toxic Apolipoprotein E4 effects in Human iPSC-Derived Neurons Is Ameliorated by a Small-Molecule Structure Corrector\n\nAbstract sentences:\n[0] Efforts to develop drugs for Alzheimer's disease (AD) have shown promise in animal studies, only to fail in human trials, suggesting a pressing need to study AD in human model systems.\n[1] Using human neurons derived from induced pluripotent stem cells that expressed apolipoprotein E4 (ApoE4), a variant of the APOE gene product and the major genetic risk factor for AD, we demonstrated that ApoE4-expressing neurons had higher levels of tau phosphorylation, unrelated to their increased production of amyloid-β (Aβ) peptides, and that they displayed GABAergic neuron degeneration.\n[2] ApoE4 increased Aβ production in human, but not in mouse, neurons.\n[3] Converting ApoE4 to ApoE3 by gene editing rescued these phenotypes, indicating the specific effects of ApoE4.\n[4] Neurons that lacked APOE behaved similarly to those expressing ApoE3, and the introduction of ApoE4 expression recapitulated the pathological phenotypes, suggesting a gain of toxic effects from ApoE4.\n[5] Treatment of ApoE4-expressing neurons with a small-molecule structure corrector ameliorated the detrimental effects, thus showing that correcting the pathogenic conformation of ApoE4 is a viable therapeutic approach for ApoE4-related AD."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Converting ApoE4 to ApoE3 by gene editing rescued these phenotypes, indicating the specific effects of ApoE4.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 286, "doc_id": 4709641, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [4709641], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Converting apoE4 to apoE3 by gene editing worsens the pathology associated with apoE4 in human iPSCderived neurons.\n\nDocument title: Gain of toxic Apolipoprotein E4 effects in Human iPSC-Derived Neurons Is Ameliorated by a Small-Molecule Structure Corrector\n\nAbstract sentences:\n[0] Efforts to develop drugs for Alzheimer's disease (AD) have shown promise in animal studies, only to fail in human trials, suggesting a pressing need to study AD in human model systems.\n[1] Using human neurons derived from induced pluripotent stem cells that expressed apolipoprotein E4 (ApoE4), a variant of the APOE gene product and the major genetic risk factor for AD, we demonstrated that ApoE4-expressing neurons had higher levels of tau phosphorylation, unrelated to their increased production of amyloid-β (Aβ) peptides, and that they displayed GABAergic neuron degeneration.\n[2] ApoE4 increased Aβ production in human, but not in mouse, neurons.\n[3] Converting ApoE4 to ApoE3 by gene editing rescued these phenotypes, indicating the specific effects of ApoE4.\n[4] Neurons that lacked APOE behaved similarly to those expressing ApoE3, and the introduction of ApoE4 expression recapitulated the pathological phenotypes, suggesting a gain of toxic effects from ApoE4.\n[5] Treatment of ApoE4-expressing neurons with a small-molecule structure corrector ameliorated the detrimental effects, thus showing that correcting the pathogenic conformation of ApoE4 is a viable therapeutic approach for ApoE4-related AD."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Converting ApoE4 to ApoE3 by gene editing rescued these phenotypes, indicating the specific effects of ApoE4.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 287, "doc_id": 4709641, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [4709641], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cost effectiveness evaluations based on cRCT data accurately reflect prices for patients in actual clinical practice.\n\nDocument title: A Comparison of Cost Effectiveness Using Data from Randomized Trials or Actual Clinical Practice: Selective Cox-2 Inhibitors as an Example\n\nAbstract sentences:\n[0] BACKGROUND Data on absolute risks of outcomes and patterns of drug use in cost-effectiveness analyses are often based on randomised clinical trials (RCTs).\n[1] The objective of this study was to evaluate the external validity of published cost-effectiveness studies by comparing the data used in these studies (typically based on RCTs) to observational data from actual clinical practice.\n[2] Selective Cox-2 inhibitors (coxibs) were used as an example.\n[3] METHODS AND FINDINGS The UK General Practice Research Database (GPRD) was used to estimate the exposure characteristics and individual probabilities of upper gastrointestinal (GI) events during current exposure to nonsteroidal anti-inflammatory drugs (NSAIDs) or coxibs.\n[4] A basic cost-effectiveness model was developed evaluating two alternative strategies: prescription of a conventional NSAID or coxib.\n[5] Outcomes included upper GI events as recorded in GPRD and hospitalisation for upper GI events recorded in the national registry of hospitalisations (Hospital Episode Statistics) linked to GPRD.\n[6] Prescription costs were based on the prescribed number of tables as recorded in GPRD and the 2006 cost data from the British National Formulary.\n[7] The study population included over 1 million patients prescribed conventional NSAIDs or coxibs.\n[8] Only a minority of patients used the drugs long-term and daily (34.5% of conventional NSAIDs and 44.2% of coxibs), whereas coxib RCTs required daily use for at least 6-9 months.\n[9] The mean cost of preventing one upper GI event as recorded in GPRD was US$104k (ranging from US$64k with long-term daily use to US$182k with intermittent use) and US$298k for hospitalizations.\n[10] The mean costs (for GPRD events) over calendar time were US$58k during 1990-1993 and US$174k during 2002-2005.\n[11] Using RCT data rather than GPRD data for event probabilities, the mean cost was US$16k with the VIGOR RCT and US$20k with the CLASS RCT.\n[12] CONCLUSIONS The published cost-effectiveness analyses of coxibs lacked external validity, did not represent patients in actual clinical practice, and should not have been used to inform prescribing policies.\n[13] External validity should be an explicit requirement for cost-effectiveness analyses."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10, 11]\nExplanation: Evidence states: \"The mean costs (for GPRD events) over calendar time were US$58k during 1990-1993 and US$174k during 2002-2005. Using RCT data rather than GPRD data for event probabilities, the mean cost was US$16k with the VIGOR RCT and US$20k with the CLASS RCT.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 290, "doc_id": 15048300, "label": "CONTRADICTS", "evidence_sentence_ids": [10, 11], "cited_doc_ids": [15048300], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cost effectiveness evaluations based on cRCT data accurately reflect prices for patients in actual clinical practice.\n\nDocument title: A Comparison of Cost Effectiveness Using Data from Randomized Trials or Actual Clinical Practice: Selective Cox-2 Inhibitors as an Example\n\nAbstract sentences:\n[0] BACKGROUND Data on absolute risks of outcomes and patterns of drug use in cost-effectiveness analyses are often based on randomised clinical trials (RCTs).\n[1] The objective of this study was to evaluate the external validity of published cost-effectiveness studies by comparing the data used in these studies (typically based on RCTs) to observational data from actual clinical practice.\n[2] Selective Cox-2 inhibitors (coxibs) were used as an example.\n[3] METHODS AND FINDINGS The UK General Practice Research Database (GPRD) was used to estimate the exposure characteristics and individual probabilities of upper gastrointestinal (GI) events during current exposure to nonsteroidal anti-inflammatory drugs (NSAIDs) or coxibs.\n[4] A basic cost-effectiveness model was developed evaluating two alternative strategies: prescription of a conventional NSAID or coxib.\n[5] Outcomes included upper GI events as recorded in GPRD and hospitalisation for upper GI events recorded in the national registry of hospitalisations (Hospital Episode Statistics) linked to GPRD.\n[6] Prescription costs were based on the prescribed number of tables as recorded in GPRD and the 2006 cost data from the British National Formulary.\n[7] The study population included over 1 million patients prescribed conventional NSAIDs or coxibs.\n[8] Only a minority of patients used the drugs long-term and daily (34.5% of conventional NSAIDs and 44.2% of coxibs), whereas coxib RCTs required daily use for at least 6-9 months.\n[9] The mean cost of preventing one upper GI event as recorded in GPRD was US$104k (ranging from US$64k with long-term daily use to US$182k with intermittent use) and US$298k for hospitalizations.\n[10] The mean costs (for GPRD events) over calendar time were US$58k during 1990-1993 and US$174k during 2002-2005.\n[11] Using RCT data rather than GPRD data for event probabilities, the mean cost was US$16k with the VIGOR RCT and US$20k with the CLASS RCT.\n[12] CONCLUSIONS The published cost-effectiveness analyses of coxibs lacked external validity, did not represent patients in actual clinical practice, and should not have been used to inform prescribing policies.\n[13] External validity should be an explicit requirement for cost-effectiveness analyses."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"CONCLUSIONS The published cost-effectiveness analyses of coxibs lacked external validity, did not represent patients in actual clinical practice, and should not have been used to inform prescribing policies.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 290, "doc_id": 15048300, "label": "CONTRADICTS", "evidence_sentence_ids": [12], "cited_doc_ids": [15048300], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cost effectiveness evaluations based on cRCT data lack external validity.\n\nDocument title: A Comparison of Cost Effectiveness Using Data from Randomized Trials or Actual Clinical Practice: Selective Cox-2 Inhibitors as an Example\n\nAbstract sentences:\n[0] BACKGROUND Data on absolute risks of outcomes and patterns of drug use in cost-effectiveness analyses are often based on randomised clinical trials (RCTs).\n[1] The objective of this study was to evaluate the external validity of published cost-effectiveness studies by comparing the data used in these studies (typically based on RCTs) to observational data from actual clinical practice.\n[2] Selective Cox-2 inhibitors (coxibs) were used as an example.\n[3] METHODS AND FINDINGS The UK General Practice Research Database (GPRD) was used to estimate the exposure characteristics and individual probabilities of upper gastrointestinal (GI) events during current exposure to nonsteroidal anti-inflammatory drugs (NSAIDs) or coxibs.\n[4] A basic cost-effectiveness model was developed evaluating two alternative strategies: prescription of a conventional NSAID or coxib.\n[5] Outcomes included upper GI events as recorded in GPRD and hospitalisation for upper GI events recorded in the national registry of hospitalisations (Hospital Episode Statistics) linked to GPRD.\n[6] Prescription costs were based on the prescribed number of tables as recorded in GPRD and the 2006 cost data from the British National Formulary.\n[7] The study population included over 1 million patients prescribed conventional NSAIDs or coxibs.\n[8] Only a minority of patients used the drugs long-term and daily (34.5% of conventional NSAIDs and 44.2% of coxibs), whereas coxib RCTs required daily use for at least 6-9 months.\n[9] The mean cost of preventing one upper GI event as recorded in GPRD was US$104k (ranging from US$64k with long-term daily use to US$182k with intermittent use) and US$298k for hospitalizations.\n[10] The mean costs (for GPRD events) over calendar time were US$58k during 1990-1993 and US$174k during 2002-2005.\n[11] Using RCT data rather than GPRD data for event probabilities, the mean cost was US$16k with the VIGOR RCT and US$20k with the CLASS RCT.\n[12] CONCLUSIONS The published cost-effectiveness analyses of coxibs lacked external validity, did not represent patients in actual clinical practice, and should not have been used to inform prescribing policies.\n[13] External validity should be an explicit requirement for cost-effectiveness analyses."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Only a minority of patients used the drugs long-term and daily (34.5% of conventional NSAIDs and 44.2% of coxibs), whereas coxib RCTs required daily use for at least 6-9 months.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 292, "doc_id": 15048300, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [15048300], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cost effectiveness evaluations based on cRCT data lack external validity.\n\nDocument title: A Comparison of Cost Effectiveness Using Data from Randomized Trials or Actual Clinical Practice: Selective Cox-2 Inhibitors as an Example\n\nAbstract sentences:\n[0] BACKGROUND Data on absolute risks of outcomes and patterns of drug use in cost-effectiveness analyses are often based on randomised clinical trials (RCTs).\n[1] The objective of this study was to evaluate the external validity of published cost-effectiveness studies by comparing the data used in these studies (typically based on RCTs) to observational data from actual clinical practice.\n[2] Selective Cox-2 inhibitors (coxibs) were used as an example.\n[3] METHODS AND FINDINGS The UK General Practice Research Database (GPRD) was used to estimate the exposure characteristics and individual probabilities of upper gastrointestinal (GI) events during current exposure to nonsteroidal anti-inflammatory drugs (NSAIDs) or coxibs.\n[4] A basic cost-effectiveness model was developed evaluating two alternative strategies: prescription of a conventional NSAID or coxib.\n[5] Outcomes included upper GI events as recorded in GPRD and hospitalisation for upper GI events recorded in the national registry of hospitalisations (Hospital Episode Statistics) linked to GPRD.\n[6] Prescription costs were based on the prescribed number of tables as recorded in GPRD and the 2006 cost data from the British National Formulary.\n[7] The study population included over 1 million patients prescribed conventional NSAIDs or coxibs.\n[8] Only a minority of patients used the drugs long-term and daily (34.5% of conventional NSAIDs and 44.2% of coxibs), whereas coxib RCTs required daily use for at least 6-9 months.\n[9] The mean cost of preventing one upper GI event as recorded in GPRD was US$104k (ranging from US$64k with long-term daily use to US$182k with intermittent use) and US$298k for hospitalizations.\n[10] The mean costs (for GPRD events) over calendar time were US$58k during 1990-1993 and US$174k during 2002-2005.\n[11] Using RCT data rather than GPRD data for event probabilities, the mean cost was US$16k with the VIGOR RCT and US$20k with the CLASS RCT.\n[12] CONCLUSIONS The published cost-effectiveness analyses of coxibs lacked external validity, did not represent patients in actual clinical practice, and should not have been used to inform prescribing policies.\n[13] External validity should be an explicit requirement for cost-effectiveness analyses."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10, 11]\nExplanation: Evidence states: \"The mean costs (for GPRD events) over calendar time were US$58k during 1990-1993 and US$174k during 2002-2005. Using RCT data rather than GPRD data for event probabilities, the mean cost was US$16k with the VIGOR RCT and US$20k with the CLASS RCT.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 292, "doc_id": 15048300, "label": "SUPPORTS", "evidence_sentence_ids": [10, 11], "cited_doc_ids": [15048300], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cost effectiveness evaluations based on cRCT data lack external validity.\n\nDocument title: A Comparison of Cost Effectiveness Using Data from Randomized Trials or Actual Clinical Practice: Selective Cox-2 Inhibitors as an Example\n\nAbstract sentences:\n[0] BACKGROUND Data on absolute risks of outcomes and patterns of drug use in cost-effectiveness analyses are often based on randomised clinical trials (RCTs).\n[1] The objective of this study was to evaluate the external validity of published cost-effectiveness studies by comparing the data used in these studies (typically based on RCTs) to observational data from actual clinical practice.\n[2] Selective Cox-2 inhibitors (coxibs) were used as an example.\n[3] METHODS AND FINDINGS The UK General Practice Research Database (GPRD) was used to estimate the exposure characteristics and individual probabilities of upper gastrointestinal (GI) events during current exposure to nonsteroidal anti-inflammatory drugs (NSAIDs) or coxibs.\n[4] A basic cost-effectiveness model was developed evaluating two alternative strategies: prescription of a conventional NSAID or coxib.\n[5] Outcomes included upper GI events as recorded in GPRD and hospitalisation for upper GI events recorded in the national registry of hospitalisations (Hospital Episode Statistics) linked to GPRD.\n[6] Prescription costs were based on the prescribed number of tables as recorded in GPRD and the 2006 cost data from the British National Formulary.\n[7] The study population included over 1 million patients prescribed conventional NSAIDs or coxibs.\n[8] Only a minority of patients used the drugs long-term and daily (34.5% of conventional NSAIDs and 44.2% of coxibs), whereas coxib RCTs required daily use for at least 6-9 months.\n[9] The mean cost of preventing one upper GI event as recorded in GPRD was US$104k (ranging from US$64k with long-term daily use to US$182k with intermittent use) and US$298k for hospitalizations.\n[10] The mean costs (for GPRD events) over calendar time were US$58k during 1990-1993 and US$174k during 2002-2005.\n[11] Using RCT data rather than GPRD data for event probabilities, the mean cost was US$16k with the VIGOR RCT and US$20k with the CLASS RCT.\n[12] CONCLUSIONS The published cost-effectiveness analyses of coxibs lacked external validity, did not represent patients in actual clinical practice, and should not have been used to inform prescribing policies.\n[13] External validity should be an explicit requirement for cost-effectiveness analyses."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"CONCLUSIONS The published cost-effectiveness analyses of coxibs lacked external validity, did not represent patients in actual clinical practice, and should not have been used to inform prescribing policies.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 292, "doc_id": 15048300, "label": "SUPPORTS", "evidence_sentence_ids": [12], "cited_doc_ids": [15048300], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Crossover hot spots are found within gene promoters in Saccharomyces cerevisiae.\n\nDocument title: Mapping Meiotic Single-Strand DNA Reveals a New Landscape of DNA Double-Strand Breaks in Saccharomyces cerevisiae\n\nAbstract sentences:\n[0] DNA double-strand breaks (DSBs), which are formed by the Spo11 protein, initiate meiotic recombination.\n[1] Previous DSB-mapping studies have used rad50S or sae2Δ mutants, which are defective in break processing, to accumulate Spo11-linked DSBs, and report large (≥ 50 kb) “DSB-hot” regions that are separated by “DSB-cold” domains of similar size.\n[2] Substantial recombination occurs in some DSB-cold regions, suggesting that DSB patterns are not normal in rad50S or sae2Δ mutants.\n[3] We therefore developed a novel method to map genome-wide, single-strand DNA (ssDNA)–associated DSBs that accumulate in processing-capable, repair-defective dmc1Δ and dmc1Δ rad51Δ mutants.\n[4] DSBs were observed at known hot spots, but also in most previously identified “DSB-cold” regions, including near centromeres and telomeres.\n[5] Although approximately 40% of the genome is DSB-cold in rad50S mutants, analysis of meiotic ssDNA from dmc1Δ shows that most of these regions have substantial DSB activity.\n[6] Southern blot assays of DSBs in selected regions in dmc1Δ, rad50S, and wild-type cells confirm these findings.\n[7] Thus, DSBs are distributed much more uniformly than was previously believed.\n[8] Comparisons of DSB signals in dmc1, dmc1 rad51, and dmc1 spo11 mutant strains identify Dmc1 as a critical strand-exchange activity genome-wide, and confirm previous conclusions that Spo11-induced lesions initiate all meiotic recombination."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 293, "doc_id": 10874408, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [10874408], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cyclin A2 destruction is necessary to switch from unstable to stable kt-mt attachments in mitosis.\n\nDocument title: Cyclin A Regulates Kinetochore-Microtubules to Promote Faithful Chromosome Segregation\n\nAbstract sentences:\n[0] The most conspicuous event in the cell cycle is the alignment of chromosomes in metaphase.\n[1] Chromosome alignment fosters faithful segregation through the formation of bi-oriented attachments of kinetochores to spindle microtubules.\n[2] Notably, numerous kinetochore-microtubule (k-MT) attachment errors are present in early mitosis (prometaphase), and the persistence of those errors is the leading cause of chromosome mis-segregation in aneuploid human tumour cells that continually mis-segregate whole chromosomes and display chromosomal instability.\n[3] How robust error correction is achieved in prometaphase to ensure error-free mitosis remains unknown.\n[4] Here we show that k-MT attachments in prometaphase cells are considerably less stable than in metaphase cells.\n[5] The switch to more stable k-MT attachments in metaphase requires the proteasome-dependent destruction of cyclin A in prometaphase.\n[6] Persistent cyclin A expression prevents k-MT stabilization even in cells with aligned chromosomes.\n[7] By contrast, k-MTs are prematurely stabilized in cyclin-A-deficient cells.\n[8] Consequently, cells lacking cyclin A display higher rates of chromosome mis-segregation.\n[9] Thus, the stability of k-MT attachments increases decisively in a coordinated fashion among all chromosomes as cells transit from prometaphase to metaphase.\n[10] Cyclin A creates a cellular environment that promotes microtubule detachment from kinetochores in prometaphase to ensure efficient error correction and faithful chromosome segregation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"The switch to more stable k-MT attachments in metaphase requires the proteasome-dependent destruction of cyclin A in prometaphase.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 296, "doc_id": 4398832, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [4398832], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cyclin A2 destruction is necessary to switch from unstable to stable kt-mt attachments in mitosis.\n\nDocument title: Cyclin A Regulates Kinetochore-Microtubules to Promote Faithful Chromosome Segregation\n\nAbstract sentences:\n[0] The most conspicuous event in the cell cycle is the alignment of chromosomes in metaphase.\n[1] Chromosome alignment fosters faithful segregation through the formation of bi-oriented attachments of kinetochores to spindle microtubules.\n[2] Notably, numerous kinetochore-microtubule (k-MT) attachment errors are present in early mitosis (prometaphase), and the persistence of those errors is the leading cause of chromosome mis-segregation in aneuploid human tumour cells that continually mis-segregate whole chromosomes and display chromosomal instability.\n[3] How robust error correction is achieved in prometaphase to ensure error-free mitosis remains unknown.\n[4] Here we show that k-MT attachments in prometaphase cells are considerably less stable than in metaphase cells.\n[5] The switch to more stable k-MT attachments in metaphase requires the proteasome-dependent destruction of cyclin A in prometaphase.\n[6] Persistent cyclin A expression prevents k-MT stabilization even in cells with aligned chromosomes.\n[7] By contrast, k-MTs are prematurely stabilized in cyclin-A-deficient cells.\n[8] Consequently, cells lacking cyclin A display higher rates of chromosome mis-segregation.\n[9] Thus, the stability of k-MT attachments increases decisively in a coordinated fashion among all chromosomes as cells transit from prometaphase to metaphase.\n[10] Cyclin A creates a cellular environment that promotes microtubule detachment from kinetochores in prometaphase to ensure efficient error correction and faithful chromosome segregation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Persistent cyclin A expression prevents k-MT stabilization even in cells with aligned chromosomes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 296, "doc_id": 4398832, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [4398832], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cyclin A2 destruction is necessary to switch from unstable to stable kt-mt attachments in mitosis.\n\nDocument title: Cyclin A Regulates Kinetochore-Microtubules to Promote Faithful Chromosome Segregation\n\nAbstract sentences:\n[0] The most conspicuous event in the cell cycle is the alignment of chromosomes in metaphase.\n[1] Chromosome alignment fosters faithful segregation through the formation of bi-oriented attachments of kinetochores to spindle microtubules.\n[2] Notably, numerous kinetochore-microtubule (k-MT) attachment errors are present in early mitosis (prometaphase), and the persistence of those errors is the leading cause of chromosome mis-segregation in aneuploid human tumour cells that continually mis-segregate whole chromosomes and display chromosomal instability.\n[3] How robust error correction is achieved in prometaphase to ensure error-free mitosis remains unknown.\n[4] Here we show that k-MT attachments in prometaphase cells are considerably less stable than in metaphase cells.\n[5] The switch to more stable k-MT attachments in metaphase requires the proteasome-dependent destruction of cyclin A in prometaphase.\n[6] Persistent cyclin A expression prevents k-MT stabilization even in cells with aligned chromosomes.\n[7] By contrast, k-MTs are prematurely stabilized in cyclin-A-deficient cells.\n[8] Consequently, cells lacking cyclin A display higher rates of chromosome mis-segregation.\n[9] Thus, the stability of k-MT attachments increases decisively in a coordinated fashion among all chromosomes as cells transit from prometaphase to metaphase.\n[10] Cyclin A creates a cellular environment that promotes microtubule detachment from kinetochores in prometaphase to ensure efficient error correction and faithful chromosome segregation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"By contrast, k-MTs are prematurely stabilized in cyclin-A-deficient cells.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 296, "doc_id": 4398832, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [4398832], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cytochrome c is transferred from cytosol to the mitochondrial intermembrane space during apoptosis.\n\nDocument title: At the gates of death.\n\nAbstract sentences:\n[0] Apoptosis that proceeds via the mitochondrial pathway involves mitochondrial outer membrane permeabilization (MOMP), responsible for the release of cytochrome c and other proteins of the mitochondrial intermembrane space.\n[1] This essential step is controlled and mediated by proteins of the Bcl-2 family.\n[2] The proapoptotic proteins Bax and Bak are required for MOMP, while the antiapoptotic Bcl-2 proteins, including Bcl-2, Bcl-xL, Mcl-1, and others, prevent MOMP.\n[3] Different proapoptotic BH3-only proteins act to interfere with the function of the antiapoptotic Bcl-2 members and/or activate Bax and Bak.\n[4] Here, we discuss an emerging view, proposed by Certo et al. in this issue of Cancer Cell, on how these interactions result in MOMP and apoptosis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Apoptosis that proceeds via the mitochondrial pathway involves mitochondrial outer membrane permeabilization (MOMP), responsible for the release of cytochrome c and other proteins of the mitochondrial intermembrane space.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 299, "doc_id": 39381118, "label": "CONTRADICTS", "evidence_sentence_ids": [0], "cited_doc_ids": [39381118], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cytosolic proteins bind to iron-responsive elements on mRNAs coding for TFRC1.\n\nDocument title: Mitochondrial iron chelation ameliorates cigarette-smoke induced bronchitis and emphysema in mice\n\nAbstract sentences:\n[0] Chronic obstructive pulmonary disease (COPD) is linked to both cigarette smoking and genetic determinants.\n[1] We have previously identified iron-responsive element-binding protein 2 (IRP2) as an important COPD susceptibility gene and have shown that IRP2 protein is increased in the lungs of individuals with COPD.\n[2] Here we demonstrate that mice deficient in Irp2 were protected from cigarette smoke (CS)-induced experimental COPD.\n[3] By integrating RNA immunoprecipitation followed by sequencing (RIP-seq), RNA sequencing (RNA-seq), and gene expression and functional enrichment clustering analysis, we identified Irp2 as a regulator of mitochondrial function in the lungs of mice.\n[4] Irp2 increased mitochondrial iron loading and levels of cytochrome c oxidase (COX), which led to mitochondrial dysfunction and subsequent experimental COPD.\n[5] Frataxin-deficient mice, which had higher mitochondrial iron loading, showed impaired airway mucociliary clearance (MCC) and higher pulmonary inflammation at baseline, whereas mice deficient in the synthesis of cytochrome c oxidase, which have reduced COX, were protected from CS-induced pulmonary inflammation and impairment of MCC.\n[6] Mice treated with a mitochondrial iron chelator or mice fed a low-iron diet were protected from CS-induced COPD.\n[7] Mitochondrial iron chelation also alleviated CS-induced impairment of MCC, CS-induced pulmonary inflammation and CS-associated lung injury in mice with established COPD, suggesting a critical functional role and potential therapeutic intervention for the mitochondrial-iron axis in COPD."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 301, "doc_id": 3553087, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [3553087], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: DMS3 protein enables Pol V transcription in vivo.\n\nDocument title: Noncoding Transcription by RNA Polymerase Pol IVb/Pol V Mediates Transcriptional Silencing of Overlapping and Adjacent Genes\n\nAbstract sentences:\n[0] Nuclear transcription is not restricted to genes but occurs throughout the intergenic and noncoding space of eukaryotic genomes.\n[1] The functional significance of this widespread noncoding transcription is mostly unknown.\n[2] We show that Arabidopsis RNA polymerase IVb/Pol V, a multisubunit nuclear enzyme required for siRNA-mediated gene silencing of transposons and other repeats, transcribes intergenic and noncoding sequences, thereby facilitating heterochromatin formation and silencing of overlapping and adjacent genes.\n[3] Pol IVb/Pol V transcription requires the chromatin-remodeling protein DRD1 but is independent of siRNA biogenesis.\n[4] However, Pol IVb/Pol V transcription and siRNA production are both required to silence transposons, suggesting that Pol IVb/Pol V generates RNAs or chromatin structures that serve as scaffolds for siRNA-mediated heterochromatin-forming complexes.\n[5] Pol IVb/Pol V function provides a solution to a paradox of epigenetic control: the need for transcription in order to transcriptionally silence the same region."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 304, "doc_id": 14797520, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14797520], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: DRD1 proteins enable Pol V transcription in vivo.\n\nDocument title: Noncoding Transcription by RNA Polymerase Pol IVb/Pol V Mediates Transcriptional Silencing of Overlapping and Adjacent Genes\n\nAbstract sentences:\n[0] Nuclear transcription is not restricted to genes but occurs throughout the intergenic and noncoding space of eukaryotic genomes.\n[1] The functional significance of this widespread noncoding transcription is mostly unknown.\n[2] We show that Arabidopsis RNA polymerase IVb/Pol V, a multisubunit nuclear enzyme required for siRNA-mediated gene silencing of transposons and other repeats, transcribes intergenic and noncoding sequences, thereby facilitating heterochromatin formation and silencing of overlapping and adjacent genes.\n[3] Pol IVb/Pol V transcription requires the chromatin-remodeling protein DRD1 but is independent of siRNA biogenesis.\n[4] However, Pol IVb/Pol V transcription and siRNA production are both required to silence transposons, suggesting that Pol IVb/Pol V generates RNAs or chromatin structures that serve as scaffolds for siRNA-mediated heterochromatin-forming complexes.\n[5] Pol IVb/Pol V function provides a solution to a paradox of epigenetic control: the need for transcription in order to transcriptionally silence the same region."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Pol IVb/Pol V transcription requires the chromatin-remodeling protein DRD1 but is independent of siRNA biogenesis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 305, "doc_id": 14797520, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [14797520], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: DUSP4 decreases apoptosis.\n\nDocument title: Profiling of residual breast cancers after neoadjuvant chemotherapy identifies DUSP4 deficiency as a mechanism of drug resistance\n\nAbstract sentences:\n[0] Neoadjuvant chemotherapy (NAC) induces a pathological complete response (pCR) in ∼30% of patients with breast cancer.\n[1] However, many patients have residual cancer after chemotherapy, which correlates with a higher risk of metastatic recurrence and poorer outcome than those who achieve a pCR.\n[2] We hypothesized that molecular profiling of tumors after NAC would identify genes associated with drug resistance.\n[3] Digital transcript counting was used to profile surgically resected breast cancers after NAC.\n[4] Low concentrations of dual specificity protein phosphatase 4 (DUSP4), an ERK phosphatase, correlated with high post-NAC tumor cell proliferation and with basal-like breast cancer (BLBC) status.\n[5] BLBC had higher DUSP4 promoter methylation and gene expression patterns of Ras-ERK pathway activation relative to other breast cancer subtypes.\n[6] DUSP4 overexpression increased chemotherapy-induced apoptosis, whereas DUSP4 depletion dampened the response to chemotherapy.\n[7] Reduced DUSP4 expression in primary tumors after NAC was associated with treatment-refractory high Ki-67 scores and shorter recurrence-free survival.\n[8] Finally, inhibition of mitogen-activated protein kinase kinase (MEK) synergized with docetaxel treatment in BLBC xenografts.\n[9] Thus, DUSP4 downregulation activates the Ras-ERK pathway in BLBC, resulting in an attenuated response to anti-cancer chemotherapy."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"DUSP4 overexpression increased chemotherapy-induced apoptosis, whereas DUSP4 depletion dampened the response to chemotherapy.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 306, "doc_id": 7821634, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [7821634], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: DUSP4 downregulation deactivates the Ras-ERK pathway\n\nDocument title: Profiling of residual breast cancers after neoadjuvant chemotherapy identifies DUSP4 deficiency as a mechanism of drug resistance\n\nAbstract sentences:\n[0] Neoadjuvant chemotherapy (NAC) induces a pathological complete response (pCR) in ∼30% of patients with breast cancer.\n[1] However, many patients have residual cancer after chemotherapy, which correlates with a higher risk of metastatic recurrence and poorer outcome than those who achieve a pCR.\n[2] We hypothesized that molecular profiling of tumors after NAC would identify genes associated with drug resistance.\n[3] Digital transcript counting was used to profile surgically resected breast cancers after NAC.\n[4] Low concentrations of dual specificity protein phosphatase 4 (DUSP4), an ERK phosphatase, correlated with high post-NAC tumor cell proliferation and with basal-like breast cancer (BLBC) status.\n[5] BLBC had higher DUSP4 promoter methylation and gene expression patterns of Ras-ERK pathway activation relative to other breast cancer subtypes.\n[6] DUSP4 overexpression increased chemotherapy-induced apoptosis, whereas DUSP4 depletion dampened the response to chemotherapy.\n[7] Reduced DUSP4 expression in primary tumors after NAC was associated with treatment-refractory high Ki-67 scores and shorter recurrence-free survival.\n[8] Finally, inhibition of mitogen-activated protein kinase kinase (MEK) synergized with docetaxel treatment in BLBC xenografts.\n[9] Thus, DUSP4 downregulation activates the Ras-ERK pathway in BLBC, resulting in an attenuated response to anti-cancer chemotherapy."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4, 5]\nExplanation: Evidence states: \"Low concentrations of dual specificity protein phosphatase 4 (DUSP4), an ERK phosphatase, correlated with high post-NAC tumor cell proliferation and with basal-like breast cancer (BLBC) status. BLBC had higher DUSP4 promoter methylation and gene expression patterns of Ras-ERK pathway activation relative to other breast cancer subtypes.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 308, "doc_id": 7821634, "label": "CONTRADICTS", "evidence_sentence_ids": [4, 5], "cited_doc_ids": [7821634], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: DUSP4 downregulation deactivates the Ras-ERK pathway\n\nDocument title: Profiling of residual breast cancers after neoadjuvant chemotherapy identifies DUSP4 deficiency as a mechanism of drug resistance\n\nAbstract sentences:\n[0] Neoadjuvant chemotherapy (NAC) induces a pathological complete response (pCR) in ∼30% of patients with breast cancer.\n[1] However, many patients have residual cancer after chemotherapy, which correlates with a higher risk of metastatic recurrence and poorer outcome than those who achieve a pCR.\n[2] We hypothesized that molecular profiling of tumors after NAC would identify genes associated with drug resistance.\n[3] Digital transcript counting was used to profile surgically resected breast cancers after NAC.\n[4] Low concentrations of dual specificity protein phosphatase 4 (DUSP4), an ERK phosphatase, correlated with high post-NAC tumor cell proliferation and with basal-like breast cancer (BLBC) status.\n[5] BLBC had higher DUSP4 promoter methylation and gene expression patterns of Ras-ERK pathway activation relative to other breast cancer subtypes.\n[6] DUSP4 overexpression increased chemotherapy-induced apoptosis, whereas DUSP4 depletion dampened the response to chemotherapy.\n[7] Reduced DUSP4 expression in primary tumors after NAC was associated with treatment-refractory high Ki-67 scores and shorter recurrence-free survival.\n[8] Finally, inhibition of mitogen-activated protein kinase kinase (MEK) synergized with docetaxel treatment in BLBC xenografts.\n[9] Thus, DUSP4 downregulation activates the Ras-ERK pathway in BLBC, resulting in an attenuated response to anti-cancer chemotherapy."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Thus, DUSP4 downregulation activates the Ras-ERK pathway in BLBC, resulting in an attenuated response to anti-cancer chemotherapy.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 308, "doc_id": 7821634, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [7821634], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: DUSP4 increases apoptosis.\n\nDocument title: Profiling of residual breast cancers after neoadjuvant chemotherapy identifies DUSP4 deficiency as a mechanism of drug resistance\n\nAbstract sentences:\n[0] Neoadjuvant chemotherapy (NAC) induces a pathological complete response (pCR) in ∼30% of patients with breast cancer.\n[1] However, many patients have residual cancer after chemotherapy, which correlates with a higher risk of metastatic recurrence and poorer outcome than those who achieve a pCR.\n[2] We hypothesized that molecular profiling of tumors after NAC would identify genes associated with drug resistance.\n[3] Digital transcript counting was used to profile surgically resected breast cancers after NAC.\n[4] Low concentrations of dual specificity protein phosphatase 4 (DUSP4), an ERK phosphatase, correlated with high post-NAC tumor cell proliferation and with basal-like breast cancer (BLBC) status.\n[5] BLBC had higher DUSP4 promoter methylation and gene expression patterns of Ras-ERK pathway activation relative to other breast cancer subtypes.\n[6] DUSP4 overexpression increased chemotherapy-induced apoptosis, whereas DUSP4 depletion dampened the response to chemotherapy.\n[7] Reduced DUSP4 expression in primary tumors after NAC was associated with treatment-refractory high Ki-67 scores and shorter recurrence-free survival.\n[8] Finally, inhibition of mitogen-activated protein kinase kinase (MEK) synergized with docetaxel treatment in BLBC xenografts.\n[9] Thus, DUSP4 downregulation activates the Ras-ERK pathway in BLBC, resulting in an attenuated response to anti-cancer chemotherapy."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"DUSP4 overexpression increased chemotherapy-induced apoptosis, whereas DUSP4 depletion dampened the response to chemotherapy.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 309, "doc_id": 7821634, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [7821634], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: De novo assembly of sequence data has fewer specific contigs than unassembled sequence data.\n\nDocument title: A culture-independent sequence-based metagenomics approach to the investigation of an outbreak of Shiga-toxigenic Escherichia coli O104:H4.\n\nAbstract sentences:\n[0] IMPORTANCE Identification of the bacterium responsible for an outbreak can aid in disease management.\n[1] However, traditional culture-based diagnosis can be difficult, particularly if no specific diagnostic test is available for an outbreak strain.\n[2] OBJECTIVE To explore the potential of metagenomics, which is the direct sequencing of DNA extracted from microbiologically complex samples, as an open-ended clinical discovery platform capable of identifying and characterizing bacterial strains from an outbreak without laboratory culture.\n[3] DESIGN, SETTING, AND PATIENTS In a retrospective investigation, 45 samples were selected from fecal specimens obtained from patients with diarrhea during the 2011 outbreak of Shiga-toxigenic Escherichia coli (STEC) O104:H4 in Germany.\n[4] Samples were subjected to high-throughput sequencing (August-September 2012), followed by a 3-phase analysis (November 2012-February 2013).\n[5] In phase 1, a de novo assembly approach was developed to obtain a draft genome of the outbreak strain.\n[6] In phase 2, the depth of coverage of the outbreak strain genome was determined in each sample.\n[7] In phase 3, sequences from each sample were compared with sequences from known bacteria to identify pathogens other than the outbreak strain.\n[8] MAIN OUTCOMES AND MEASURES The recovery of genome sequence data for the purposes of identification and characterization of the outbreak strain and other pathogens from fecal samples.\n[9] RESULTS During phase 1, a draft genome of the STEC outbreak strain was obtained.\n[10] During phase 2, the outbreak strain genome was recovered from 10 samples at greater than 10-fold coverage and from 26 samples at greater than 1-fold coverage.\n[11] Sequences from the Shiga-toxin genes were detected in 27 of 40 STEC-positive samples (67%).\n[12] In phase 3, sequences from Clostridium difficile, Campylobacter jejuni, Campylobacter concisus, and Salmonella enterica were recovered.\n[13] CONCLUSIONS AND RELEVANCE These results suggest the potential of metagenomics as a culture-independent approach for the identification of bacterial pathogens during an outbreak of diarrheal disease.\n[14] Challenges include improving diagnostic sensitivity, speeding up and simplifying workflows, and reducing costs."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 310, "doc_id": 6173523, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [6173523], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: De novo assembly of sequence data has shorter contigs than unassembled sequence data.\n\nDocument title: A culture-independent sequence-based metagenomics approach to the investigation of an outbreak of Shiga-toxigenic Escherichia coli O104:H4.\n\nAbstract sentences:\n[0] IMPORTANCE Identification of the bacterium responsible for an outbreak can aid in disease management.\n[1] However, traditional culture-based diagnosis can be difficult, particularly if no specific diagnostic test is available for an outbreak strain.\n[2] OBJECTIVE To explore the potential of metagenomics, which is the direct sequencing of DNA extracted from microbiologically complex samples, as an open-ended clinical discovery platform capable of identifying and characterizing bacterial strains from an outbreak without laboratory culture.\n[3] DESIGN, SETTING, AND PATIENTS In a retrospective investigation, 45 samples were selected from fecal specimens obtained from patients with diarrhea during the 2011 outbreak of Shiga-toxigenic Escherichia coli (STEC) O104:H4 in Germany.\n[4] Samples were subjected to high-throughput sequencing (August-September 2012), followed by a 3-phase analysis (November 2012-February 2013).\n[5] In phase 1, a de novo assembly approach was developed to obtain a draft genome of the outbreak strain.\n[6] In phase 2, the depth of coverage of the outbreak strain genome was determined in each sample.\n[7] In phase 3, sequences from each sample were compared with sequences from known bacteria to identify pathogens other than the outbreak strain.\n[8] MAIN OUTCOMES AND MEASURES The recovery of genome sequence data for the purposes of identification and characterization of the outbreak strain and other pathogens from fecal samples.\n[9] RESULTS During phase 1, a draft genome of the STEC outbreak strain was obtained.\n[10] During phase 2, the outbreak strain genome was recovered from 10 samples at greater than 10-fold coverage and from 26 samples at greater than 1-fold coverage.\n[11] Sequences from the Shiga-toxin genes were detected in 27 of 40 STEC-positive samples (67%).\n[12] In phase 3, sequences from Clostridium difficile, Campylobacter jejuni, Campylobacter concisus, and Salmonella enterica were recovered.\n[13] CONCLUSIONS AND RELEVANCE These results suggest the potential of metagenomics as a culture-independent approach for the identification of bacterial pathogens during an outbreak of diarrheal disease.\n[14] Challenges include improving diagnostic sensitivity, speeding up and simplifying workflows, and reducing costs."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 313, "doc_id": 6173523, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [6173523], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Decrease of p62 in prostate tumor stroma results in defective autophagy.\n\nDocument title: p62/SQSTM1 by Binding to Vitamin D Receptor Inhibits Hepatic Stellate Cell Activity, Fibrosis, and Liver Cancer.\n\nAbstract sentences:\n[0] Hepatic stellate cells (HSCs) play critical roles in liver fibrosis and hepatocellular carcinoma (HCC).\n[1] Vitamin D receptor (VDR) activation in HSCs inhibits liver inflammation and fibrosis.\n[2] We found that p62/SQSTM1, a protein upregulated in liver parenchymal cells but downregulated in HCC-associated HSCs, negatively controls HSC activation.\n[3] Total body or HSC-specific p62 ablation potentiates HSCs and enhances inflammation, fibrosis, and HCC progression.\n[4] p62 directly interacts with VDR and RXR promoting their heterodimerization, which is critical for VDR:RXR target gene recruitment.\n[5] Loss of p62 in HSCs impairs the repression of fibrosis and inflammation by VDR agonists.\n[6] This demonstrates that p62 is a negative regulator of liver inflammation and fibrosis through its ability to promote VDR signaling in HSCs, whose activation supports HCC."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 315, "doc_id": 3701541, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [3701541], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Decreased conversion of PGE 2 to PPARy ligand 15-ket-PGE 2 causes accumulation of PGE.\n\nDocument title: Pharmacological correction of a defect in PPARγ signaling ameliorates disease severity in Cftr-deficient mice\n\nAbstract sentences:\n[0] Cystic fibrosis is caused by mutations in the cystic fibrosis transmembrane conductance regulator (encoded by Cftr) that impair its role as an apical chloride channel that supports bicarbonate transport.\n[1] Individuals with cystic fibrosis show retained, thickened mucus that plugs airways and obstructs luminal organs as well as numerous other abnormalities that include inflammation of affected organs, alterations in lipid metabolism and insulin resistance.\n[2] Here we show that colonic epithelial cells and whole lung tissue from Cftr-deficient mice show a defect in peroxisome proliferator-activated receptor-gamma (PPAR-gamma, encoded by Pparg) function that contributes to a pathological program of gene expression.\n[3] Lipidomic analysis of colonic epithelial cells suggests that this defect results in part from reduced amounts of the endogenous PPAR-gamma ligand 15-keto-prostaglandin E(2) (15-keto-PGE(2)).\n[4] Treatment of Cftr-deficient mice with the synthetic PPAR-gamma ligand rosiglitazone partially normalizes the altered gene expression pattern associated with Cftr deficiency and reduces disease severity.\n[5] Rosiglitazone has no effect on chloride secretion in the colon, but it increases expression of the genes encoding carbonic anhydrases 4 and 2 (Car4 and Car2), increases bicarbonate secretion and reduces mucus retention.\n[6] These studies reveal a reversible defect in PPAR-gamma signaling in Cftr-deficient cells that can be pharmacologically corrected to ameliorate the severity of the cystic fibrosis phenotype in mice."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 316, "doc_id": 712078, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [712078], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Decreased diastolic blood pressure (DBP) is associated with abdominal aortic aneurysm.\n\nDocument title: Blood pressure and incidence of twelve cardiovascular diseases: lifetime risks, healthy life-years lost, and age-specific associations in 1·25 million people\n\nAbstract sentences:\n[0] BACKGROUND The associations of blood pressure with the different manifestations of incident cardiovascular disease in a contemporary population have not been compared.\n[1] In this study, we aimed to analyse the associations of blood pressure with 12 different presentations of cardiovascular disease.\n[2] METHODS We used linked electronic health records from 1997 to 2010 in the CALIBER (CArdiovascular research using LInked Bespoke studies and Electronic health Records) programme to assemble a cohort of 1·25 million patients, 30 years of age or older and initially free from cardiovascular disease, a fifth of whom received blood pressure-lowering treatments.\n[3] We studied the heterogeneity in the age-specific associations of clinically measured blood pressure with 12 acute and chronic cardiovascular diseases, and estimated the lifetime risks (up to 95 years of age) and cardiovascular disease-free life-years lost adjusted for other risk factors at index ages 30, 60, and 80 years.\n[4] This study is registered at ClinicalTrials.gov, number NCT01164371.\n[5] FINDINGS During 5·2 years median follow-up, we recorded 83,098 initial cardiovascular disease presentations.\n[6] In each age group, the lowest risk for cardiovascular disease was in people with systolic blood pressure of 90-114 mm Hg and diastolic blood pressure of 60-74 mm Hg, with no evidence of a J-shaped increased risk at lower blood pressures.\n[7] The effect of high blood pressure varied by cardiovascular disease endpoint, from strongly positive to no effect.\n[8] Associations with high systolic blood pressure were strongest for intracerebral haemorrhage (hazard ratio 1·44 [95% CI 1·32-1·58]), subarachnoid haemorrhage (1·43 [1·25-1·63]), and stable angina (1·41 [1·36-1·46]), and weakest for abdominal aortic aneurysm (1·08 [1·00-1·17]).\n[9] Compared with diastolic blood pressure, raised systolic blood pressure had a greater effect on angina, myocardial infarction, and peripheral arterial disease, whereas raised diastolic blood pressure had a greater effect on abdominal aortic aneurysm than did raised systolic pressure.\n[10] Pulse pressure associations were inverse for abdominal aortic aneurysm (HR per 10 mm Hg 0·91 [95% CI 0·86-0·98]) and strongest for peripheral arterial disease (1·23 [1·20-1·27]).\n[11] People with hypertension (blood pressure ≥140/90 mm Hg or those receiving blood pressure-lowering drugs) had a lifetime risk of overall cardiovascular disease at 30 years of age of 63·3% (95% CI 62·9-63·8) compared with 46·1% (45·5-46·8) for those with normal blood pressure, and developed cardiovascular disease 5·0 years earlier (95% CI 4·8-5·2).\n[12] Stable and unstable angina accounted for most (43%) of the cardiovascular disease-free years of life lost associated with hypertension from index age 30 years, whereas heart failure and stable angina accounted for the largest proportion (19% each) of years of life lost from index age 80 years.\n[13] INTERPRETATION The widely held assumptions that blood pressure has strong associations with the occurrence of all cardiovascular diseases across a wide age range, and that diastolic and systolic associations are concordant, are not supported by the findings of this high-resolution study.\n[14] Despite modern treatments, the lifetime burden of hypertension is substantial.\n[15] These findings emphasise the need for new blood pressure-lowering strategies, and will help to inform the design of randomised trials to assess them.\n[16] FUNDING Medical Research Council, National Institute for Health Research, and Wellcome Trust."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Compared with diastolic blood pressure, raised systolic blood pressure had a greater effect on angina, myocardial infarction, and peripheral arterial disease, whereas raised diastolic blood pressure had a greater effect on abdominal aortic aneurysm than did raised systolic pressure.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 317, "doc_id": 4506414, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [4506414], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Deleting Raptor increases G-CSF levels.\n\nDocument title: Oncogenic mTOR signaling recruits myeloid-derived suppressor cells to promote tumor initiation\n\nAbstract sentences:\n[0] Myeloid-derived suppressor cells (MDSCs) play critical roles in primary and metastatic cancer progression.\n[1] MDSC regulation is widely variable even among patients harbouring the same type of malignancy, and the mechanisms governing such heterogeneity are largely unknown.\n[2] Here, integrating human tumour genomics and syngeneic mammary tumour models, we demonstrate that mTOR signalling in cancer cells dictates a mammary tumour's ability to stimulate MDSC accumulation through regulating G-CSF.\n[3] Inhibiting this pathway or its activators (for example, FGFR) impairs tumour progression, which is partially rescued by restoring MDSCs or G-CSF.\n[4] Tumour-initiating cells (TICs) exhibit elevated G-CSF.\n[5] MDSCs reciprocally increase TIC frequency through activating Notch in tumour cells, forming a feedforward loop.\n[6] Analyses of primary breast cancers and patient-derived xenografts corroborate these mechanisms in patients.\n[7] These findings establish a non-canonical oncogenic role of mTOR signalling in recruiting pro-tumorigenic MDSCs and show how defined cancer subsets may evolve to promote and depend on a distinct immune microenvironment."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 323, "doc_id": 2014909, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [2014909], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Deletion of ATM and Rad3 related protein is not predictive of acute tissue loss.\n\nDocument title: Deletion of the developmentally essential gene ATR in adult mice leads to age-related phenotypes and stem cell loss.\n\nAbstract sentences:\n[0] Developmental abnormalities, cancer, and premature aging each have been linked to defects in the DNA damage response (DDR).\n[1] Mutations in the ATR checkpoint regulator cause developmental defects in mice (pregastrulation lethality) and humans (Seckel syndrome).\n[2] Here we show that eliminating ATR in adult mice leads to defects in tissue homeostasis and the rapid appearance of age-related phenotypes, such as hair graying, alopecia, kyphosis, osteoporosis, thymic involution, fibrosis, and other abnormalities.\n[3] Histological and genetic analyses indicate that ATR deletion causes acute cellular loss in tissues in which continuous cell proliferation is required for maintenance.\n[4] Importantly, thymic involution, alopecia, and hair graying in ATR knockout mice were associated with dramatic reductions in tissue-specific stem and progenitor cells and exhaustion of tissue renewal and homeostatic capacity.\n[5] In aggregate, these studies suggest that reduced regenerative capacity in adults via deletion of a developmentally essential DDR gene is sufficient to cause the premature appearance of age-related phenotypes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 325, "doc_id": 40349336, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [40349336], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Deletion of ATM and Rad3 related protein leads to acute tissue loss.\n\nDocument title: Deletion of the developmentally essential gene ATR in adult mice leads to age-related phenotypes and stem cell loss.\n\nAbstract sentences:\n[0] Developmental abnormalities, cancer, and premature aging each have been linked to defects in the DNA damage response (DDR).\n[1] Mutations in the ATR checkpoint regulator cause developmental defects in mice (pregastrulation lethality) and humans (Seckel syndrome).\n[2] Here we show that eliminating ATR in adult mice leads to defects in tissue homeostasis and the rapid appearance of age-related phenotypes, such as hair graying, alopecia, kyphosis, osteoporosis, thymic involution, fibrosis, and other abnormalities.\n[3] Histological and genetic analyses indicate that ATR deletion causes acute cellular loss in tissues in which continuous cell proliferation is required for maintenance.\n[4] Importantly, thymic involution, alopecia, and hair graying in ATR knockout mice were associated with dramatic reductions in tissue-specific stem and progenitor cells and exhaustion of tissue renewal and homeostatic capacity.\n[5] In aggregate, these studies suggest that reduced regenerative capacity in adults via deletion of a developmentally essential DDR gene is sufficient to cause the premature appearance of age-related phenotypes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 326, "doc_id": 40349336, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [40349336], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Deltex has no known interactions with eIF3f.\n\nDocument title: The Translation Initiation Factor 3f (eIF3f) Exhibits a Deubiquitinase Activity Regulating Notch Activation\n\nAbstract sentences:\n[0] Activation of the mammalian Notch receptor after ligand binding relies on a succession of events including metalloprotease-cleavage, endocytosis, monoubiquitination, and eventually processing by the gamma-secretase, giving rise to a soluble, transcriptionally active molecule.\n[1] The Notch1 receptor was proposed to be monoubiquitinated before its gamma-secretase cleavage; the targeted lysine has been localized to its submembrane domain.\n[2] Investigating how this step might be regulated by a deubiquitinase (DUB) activity will provide new insight for understanding Notch receptor activation and downstream signaling.\n[3] An immunofluorescence-based screening of an shRNA library allowed us to identify eIF3f, previously known as one of the subunits of the translation initiation factor eIF3, as a DUB targeting the activated Notch receptor.\n[4] We show that eIF3f has an intrinsic DUB activity.\n[5] Knocking down eIF3f leads to an accumulation of monoubiquitinated forms of activated Notch, an effect counteracted by murine WT eIF3f but not by a catalytically inactive mutant.\n[6] We also show that eIF3f is recruited to activated Notch on endocytic vesicles by the putative E3 ubiquitin ligase Deltex1, which serves as a bridging factor.\n[7] Finally, catalytically inactive forms of eIF3f as well as shRNAs targeting eIF3f repress Notch activation in a coculture assay, showing that eIF3f is a new positive regulator of the Notch pathway.\n[8] Our results support two new and provocative conclusions: (1) The activated form of Notch needs to be deubiquitinated before being processed by the gamma-secretase activity and entering the nucleus, where it fulfills its transcriptional function.\n[9] (2) The enzyme accounting for this deubiquitinase activity is eIF3f, known so far as a translation initiation factor.\n[10] These data improve our knowledge of Notch signaling but also open new avenues of research on the Zomes family and the translation initiation factors."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"We also show that eIF3f is recruited to activated Notch on endocytic vesicles by the putative E3 ubiquitin ligase Deltex1, which serves as a bridging factor.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 330, "doc_id": 9505448, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [9505448], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Deltex interacts with eIF3. There is no known interaction between Deltex and elF3\n\nDocument title: The Translation Initiation Factor 3f (eIF3f) Exhibits a Deubiquitinase Activity Regulating Notch Activation\n\nAbstract sentences:\n[0] Activation of the mammalian Notch receptor after ligand binding relies on a succession of events including metalloprotease-cleavage, endocytosis, monoubiquitination, and eventually processing by the gamma-secretase, giving rise to a soluble, transcriptionally active molecule.\n[1] The Notch1 receptor was proposed to be monoubiquitinated before its gamma-secretase cleavage; the targeted lysine has been localized to its submembrane domain.\n[2] Investigating how this step might be regulated by a deubiquitinase (DUB) activity will provide new insight for understanding Notch receptor activation and downstream signaling.\n[3] An immunofluorescence-based screening of an shRNA library allowed us to identify eIF3f, previously known as one of the subunits of the translation initiation factor eIF3, as a DUB targeting the activated Notch receptor.\n[4] We show that eIF3f has an intrinsic DUB activity.\n[5] Knocking down eIF3f leads to an accumulation of monoubiquitinated forms of activated Notch, an effect counteracted by murine WT eIF3f but not by a catalytically inactive mutant.\n[6] We also show that eIF3f is recruited to activated Notch on endocytic vesicles by the putative E3 ubiquitin ligase Deltex1, which serves as a bridging factor.\n[7] Finally, catalytically inactive forms of eIF3f as well as shRNAs targeting eIF3f repress Notch activation in a coculture assay, showing that eIF3f is a new positive regulator of the Notch pathway.\n[8] Our results support two new and provocative conclusions: (1) The activated form of Notch needs to be deubiquitinated before being processed by the gamma-secretase activity and entering the nucleus, where it fulfills its transcriptional function.\n[9] (2) The enzyme accounting for this deubiquitinase activity is eIF3f, known so far as a translation initiation factor.\n[10] These data improve our knowledge of Notch signaling but also open new avenues of research on the Zomes family and the translation initiation factors."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"We also show that eIF3f is recruited to activated Notch on endocytic vesicles by the putative E3 ubiquitin ligase Deltex1, which serves as a bridging factor.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 331, "doc_id": 9505448, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [9505448], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Depletion of T-helper 17 (Th17) cells during simian immunodeficiency virus (SIV) infection decreases dissemination of Salmonella Typhimurium from the gut.\n\nDocument title: Simian immunodeficiency virus–induced mucosal interleukin-17 deficiency promotes Salmonella dissemination from the gut\n\nAbstract sentences:\n[0] Salmonella typhimurium causes a localized enteric infection in immunocompetent individuals, whereas HIV-infected individuals develop a life-threatening bacteremia.\n[1] Here we show that simian immunodeficiency virus (SIV) infection results in depletion of T helper type 17 (TH17) cells in the ileal mucosa of rhesus macaques, thereby impairing mucosal barrier functions to S. typhimurium dissemination.\n[2] In SIV-negative macaques, the gene expression profile induced by S. typhimurium in ligated ileal loops was dominated by TH17 responses, including the expression of interleukin-17 (IL-17) and IL-22.\n[3] TH17 cells were markedly depleted in SIV-infected rhesus macaques, resulting in blunted TH17 responses to S. typhimurium infection and increased bacterial dissemination.\n[4] IL-17 receptor–deficient mice showed increased systemic dissemination of S. typhimurium from the gut, suggesting that IL-17 deficiency causes defects in mucosal barrier function.\n[5] We conclude that SIV infection impairs the IL-17 axis, an arm of the mucosal immune response preventing systemic microbial dissemination from the gastrointestinal tract."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Here we show that simian immunodeficiency virus (SIV) infection results in depletion of T helper type 17 (TH17) cells in the ileal mucosa of rhesus macaques, thereby impairing mucosal barrier functions to S. typhimurium dissemination.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 332, "doc_id": 29023309, "label": "CONTRADICTS", "evidence_sentence_ids": [1], "cited_doc_ids": [29023309], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Depletion of T-helper 17 (Th17) cells during simian immunodeficiency virus (SIV) infection decreases dissemination of Salmonella Typhimurium from the gut.\n\nDocument title: Simian immunodeficiency virus–induced mucosal interleukin-17 deficiency promotes Salmonella dissemination from the gut\n\nAbstract sentences:\n[0] Salmonella typhimurium causes a localized enteric infection in immunocompetent individuals, whereas HIV-infected individuals develop a life-threatening bacteremia.\n[1] Here we show that simian immunodeficiency virus (SIV) infection results in depletion of T helper type 17 (TH17) cells in the ileal mucosa of rhesus macaques, thereby impairing mucosal barrier functions to S. typhimurium dissemination.\n[2] In SIV-negative macaques, the gene expression profile induced by S. typhimurium in ligated ileal loops was dominated by TH17 responses, including the expression of interleukin-17 (IL-17) and IL-22.\n[3] TH17 cells were markedly depleted in SIV-infected rhesus macaques, resulting in blunted TH17 responses to S. typhimurium infection and increased bacterial dissemination.\n[4] IL-17 receptor–deficient mice showed increased systemic dissemination of S. typhimurium from the gut, suggesting that IL-17 deficiency causes defects in mucosal barrier function.\n[5] We conclude that SIV infection impairs the IL-17 axis, an arm of the mucosal immune response preventing systemic microbial dissemination from the gastrointestinal tract."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"TH17 cells were markedly depleted in SIV-infected rhesus macaques, resulting in blunted TH17 responses to S. typhimurium infection and increased bacterial dissemination.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 332, "doc_id": 29023309, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [29023309], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Depletion of T-helper 17 (Th17) cells during simian immunodeficiency virus (SIV) infection increases dissemination of Salmonella Typhimurium from the gut.\n\nDocument title: Simian immunodeficiency virus–induced mucosal interleukin-17 deficiency promotes Salmonella dissemination from the gut\n\nAbstract sentences:\n[0] Salmonella typhimurium causes a localized enteric infection in immunocompetent individuals, whereas HIV-infected individuals develop a life-threatening bacteremia.\n[1] Here we show that simian immunodeficiency virus (SIV) infection results in depletion of T helper type 17 (TH17) cells in the ileal mucosa of rhesus macaques, thereby impairing mucosal barrier functions to S. typhimurium dissemination.\n[2] In SIV-negative macaques, the gene expression profile induced by S. typhimurium in ligated ileal loops was dominated by TH17 responses, including the expression of interleukin-17 (IL-17) and IL-22.\n[3] TH17 cells were markedly depleted in SIV-infected rhesus macaques, resulting in blunted TH17 responses to S. typhimurium infection and increased bacterial dissemination.\n[4] IL-17 receptor–deficient mice showed increased systemic dissemination of S. typhimurium from the gut, suggesting that IL-17 deficiency causes defects in mucosal barrier function.\n[5] We conclude that SIV infection impairs the IL-17 axis, an arm of the mucosal immune response preventing systemic microbial dissemination from the gastrointestinal tract."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Here we show that simian immunodeficiency virus (SIV) infection results in depletion of T helper type 17 (TH17) cells in the ileal mucosa of rhesus macaques, thereby impairing mucosal barrier functions to S. typhimurium dissemination.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 333, "doc_id": 29023309, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [29023309], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Depletion of T-helper 17 (Th17) cells during simian immunodeficiency virus (SIV) infection increases dissemination of Salmonella Typhimurium from the gut.\n\nDocument title: Simian immunodeficiency virus–induced mucosal interleukin-17 deficiency promotes Salmonella dissemination from the gut\n\nAbstract sentences:\n[0] Salmonella typhimurium causes a localized enteric infection in immunocompetent individuals, whereas HIV-infected individuals develop a life-threatening bacteremia.\n[1] Here we show that simian immunodeficiency virus (SIV) infection results in depletion of T helper type 17 (TH17) cells in the ileal mucosa of rhesus macaques, thereby impairing mucosal barrier functions to S. typhimurium dissemination.\n[2] In SIV-negative macaques, the gene expression profile induced by S. typhimurium in ligated ileal loops was dominated by TH17 responses, including the expression of interleukin-17 (IL-17) and IL-22.\n[3] TH17 cells were markedly depleted in SIV-infected rhesus macaques, resulting in blunted TH17 responses to S. typhimurium infection and increased bacterial dissemination.\n[4] IL-17 receptor–deficient mice showed increased systemic dissemination of S. typhimurium from the gut, suggesting that IL-17 deficiency causes defects in mucosal barrier function.\n[5] We conclude that SIV infection impairs the IL-17 axis, an arm of the mucosal immune response preventing systemic microbial dissemination from the gastrointestinal tract."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"TH17 cells were markedly depleted in SIV-infected rhesus macaques, resulting in blunted TH17 responses to S. typhimurium infection and increased bacterial dissemination.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 333, "doc_id": 29023309, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [29023309], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Depletion of nitric oxide is responsible for vasospasm.\n\nDocument title: Nitrite infusions to prevent delayed cerebral vasospasm in a primate model of subarachnoid hemorrhage.\n\nAbstract sentences:\n[0] CONTEXT Delayed cerebral vasospasm causes permanent neurological deficits or death in at least 15% of patients following otherwise successful treatment for ruptured intracranial aneurysm.\n[1] Decreased bioavailability of nitric oxide has been associated with the development of cerebral vasospasm.\n[2] OBJECTIVE To determine whether infusions of nitrite will prevent delayed cerebral vasospasm.\n[3] DESIGN, SETTING, AND SUBJECTS A total of 14 anesthetized cynomolgus monkeys had an autologous blood clot placed around the right middle cerebral artery.\n[4] Cerebral arteriography was performed before clot placement and on days 7 and 14 to assess vasospasm.\n[5] The study was conducted from August 2003 to February 2004.\n[6] INTERVENTIONS A 90-mg sodium nitrite intravenous solution infused over 24 hours plus a 45-mg sodium nitrite bolus daily (n = 3); a 180-mg sodium nitrite intravenous solution infused over 24 hours (n = 3); or a control saline solution infusion (n = 8).\n[7] Each was infused continuously for 14 days.\n[8] MAIN OUTCOME MEASURES Nitrite, S-nitrosothiol, and methemoglobin levels in blood and cerebrospinal fluid and degree of arteriographic vasospasm.\n[9] RESULTS In control monkeys, mean (SD) cerebrospinal fluid nitrite levels decreased from 3.1 (1.5) micromol/L to 0.4 (0.1) micromol/L at day 7 and to 0.4 (0.4) micromol/L at day 14 (P = .03).\n[10] All 8 control monkeys developed significant vasospasm of the right middle cerebral artery, which was complicated by stroke and death in 1 animal.\n[11] Sodium nitrite infusions increased the nitrite and methemoglobin levels (<2.1% of total hemoglobin) in the blood and cerebrospinal fluid without evoking systemic hypotension.\n[12] Nitrite infusion prevented development of vasospasm (no animals developed significant vasospasm; mean [SD] reduction in right middle cerebral artery area on day 7 after subarachnoid hemorrhage of 8% [9%] in nitrite-treated monkeys vs 47% [5%] in saline-treated controls; P<.001).\n[13] There was a negative correlation between the concentration of nitrite in cerebrospinal fluid and the degree of cerebral vasospasm (P<.001).\n[14] Pharmacological effects of nitrite infusion were also associated with the formation of S-nitrosothiol in cerebrospinal fluid.\n[15] There was no clinical or pathological evidence of nitrite toxicity.\n[16] CONCLUSION Subacute sodium nitrite infusions prevented delayed cerebral vasospasm in a primate model of subarachnoid hemorrhage."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Decreased bioavailability of nitric oxide has been associated with the development of cerebral vasospasm.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 334, "doc_id": 25079962, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [25079962], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Depletion of nitric oxide is responsible for vasospasm.\n\nDocument title: Nitrite infusions to prevent delayed cerebral vasospasm in a primate model of subarachnoid hemorrhage.\n\nAbstract sentences:\n[0] CONTEXT Delayed cerebral vasospasm causes permanent neurological deficits or death in at least 15% of patients following otherwise successful treatment for ruptured intracranial aneurysm.\n[1] Decreased bioavailability of nitric oxide has been associated with the development of cerebral vasospasm.\n[2] OBJECTIVE To determine whether infusions of nitrite will prevent delayed cerebral vasospasm.\n[3] DESIGN, SETTING, AND SUBJECTS A total of 14 anesthetized cynomolgus monkeys had an autologous blood clot placed around the right middle cerebral artery.\n[4] Cerebral arteriography was performed before clot placement and on days 7 and 14 to assess vasospasm.\n[5] The study was conducted from August 2003 to February 2004.\n[6] INTERVENTIONS A 90-mg sodium nitrite intravenous solution infused over 24 hours plus a 45-mg sodium nitrite bolus daily (n = 3); a 180-mg sodium nitrite intravenous solution infused over 24 hours (n = 3); or a control saline solution infusion (n = 8).\n[7] Each was infused continuously for 14 days.\n[8] MAIN OUTCOME MEASURES Nitrite, S-nitrosothiol, and methemoglobin levels in blood and cerebrospinal fluid and degree of arteriographic vasospasm.\n[9] RESULTS In control monkeys, mean (SD) cerebrospinal fluid nitrite levels decreased from 3.1 (1.5) micromol/L to 0.4 (0.1) micromol/L at day 7 and to 0.4 (0.4) micromol/L at day 14 (P = .03).\n[10] All 8 control monkeys developed significant vasospasm of the right middle cerebral artery, which was complicated by stroke and death in 1 animal.\n[11] Sodium nitrite infusions increased the nitrite and methemoglobin levels (<2.1% of total hemoglobin) in the blood and cerebrospinal fluid without evoking systemic hypotension.\n[12] Nitrite infusion prevented development of vasospasm (no animals developed significant vasospasm; mean [SD] reduction in right middle cerebral artery area on day 7 after subarachnoid hemorrhage of 8% [9%] in nitrite-treated monkeys vs 47% [5%] in saline-treated controls; P<.001).\n[13] There was a negative correlation between the concentration of nitrite in cerebrospinal fluid and the degree of cerebral vasospasm (P<.001).\n[14] Pharmacological effects of nitrite infusion were also associated with the formation of S-nitrosothiol in cerebrospinal fluid.\n[15] There was no clinical or pathological evidence of nitrite toxicity.\n[16] CONCLUSION Subacute sodium nitrite infusions prevented delayed cerebral vasospasm in a primate model of subarachnoid hemorrhage."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"All 8 control monkeys developed significant vasospasm of the right middle cerebral artery, which was complicated by stroke and death in 1 animal.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 334, "doc_id": 25079962, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [25079962], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Depletion of nitric oxide is responsible for vasospasm.\n\nDocument title: Nitrite infusions to prevent delayed cerebral vasospasm in a primate model of subarachnoid hemorrhage.\n\nAbstract sentences:\n[0] CONTEXT Delayed cerebral vasospasm causes permanent neurological deficits or death in at least 15% of patients following otherwise successful treatment for ruptured intracranial aneurysm.\n[1] Decreased bioavailability of nitric oxide has been associated with the development of cerebral vasospasm.\n[2] OBJECTIVE To determine whether infusions of nitrite will prevent delayed cerebral vasospasm.\n[3] DESIGN, SETTING, AND SUBJECTS A total of 14 anesthetized cynomolgus monkeys had an autologous blood clot placed around the right middle cerebral artery.\n[4] Cerebral arteriography was performed before clot placement and on days 7 and 14 to assess vasospasm.\n[5] The study was conducted from August 2003 to February 2004.\n[6] INTERVENTIONS A 90-mg sodium nitrite intravenous solution infused over 24 hours plus a 45-mg sodium nitrite bolus daily (n = 3); a 180-mg sodium nitrite intravenous solution infused over 24 hours (n = 3); or a control saline solution infusion (n = 8).\n[7] Each was infused continuously for 14 days.\n[8] MAIN OUTCOME MEASURES Nitrite, S-nitrosothiol, and methemoglobin levels in blood and cerebrospinal fluid and degree of arteriographic vasospasm.\n[9] RESULTS In control monkeys, mean (SD) cerebrospinal fluid nitrite levels decreased from 3.1 (1.5) micromol/L to 0.4 (0.1) micromol/L at day 7 and to 0.4 (0.4) micromol/L at day 14 (P = .03).\n[10] All 8 control monkeys developed significant vasospasm of the right middle cerebral artery, which was complicated by stroke and death in 1 animal.\n[11] Sodium nitrite infusions increased the nitrite and methemoglobin levels (<2.1% of total hemoglobin) in the blood and cerebrospinal fluid without evoking systemic hypotension.\n[12] Nitrite infusion prevented development of vasospasm (no animals developed significant vasospasm; mean [SD] reduction in right middle cerebral artery area on day 7 after subarachnoid hemorrhage of 8% [9%] in nitrite-treated monkeys vs 47% [5%] in saline-treated controls; P<.001).\n[13] There was a negative correlation between the concentration of nitrite in cerebrospinal fluid and the degree of cerebral vasospasm (P<.001).\n[14] Pharmacological effects of nitrite infusion were also associated with the formation of S-nitrosothiol in cerebrospinal fluid.\n[15] There was no clinical or pathological evidence of nitrite toxicity.\n[16] CONCLUSION Subacute sodium nitrite infusions prevented delayed cerebral vasospasm in a primate model of subarachnoid hemorrhage."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"Nitrite infusion prevented development of vasospasm (no animals developed significant vasospasm; mean [SD] reduction in right middle cerebral artery area on day 7 after subarachnoid hemorrhage of 8% [9%] in nitrite-treated monkeys vs 47% [5%] in saline-treated controls; P<.001).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 334, "doc_id": 25079962, "label": "SUPPORTS", "evidence_sentence_ids": [12], "cited_doc_ids": [25079962], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Deregulation of HAND2 is a crucial step in endometrial carcinogenesis in mice.\n\nDocument title: Role of DNA Methylation and Epigenetic Silencing of HAND2 in Endometrial Cancer Development\n\nAbstract sentences:\n[0] BACKGROUND Endometrial cancer incidence is continuing to rise in the wake of the current ageing and obesity epidemics.\n[1] Much of the risk for endometrial cancer development is influenced by the environment and lifestyle.\n[2] Accumulating evidence suggests that the epigenome serves as the interface between the genome and the environment and that hypermethylation of stem cell polycomb group target genes is an epigenetic hallmark of cancer.\n[3] The objective of this study was to determine the functional role of epigenetic factors in endometrial cancer development.\n[4] METHODS AND FINDINGS Epigenome-wide methylation analysis of >27,000 CpG sites in endometrial cancer tissue samples (n = 64) and control samples (n = 23) revealed that HAND2 (a gene encoding a transcription factor expressed in the endometrial stroma) is one of the most commonly hypermethylated and silenced genes in endometrial cancer.\n[5] A novel integrative epigenome-transcriptome-interactome analysis further revealed that HAND2 is the hub of the most highly ranked differential methylation hotspot in endometrial cancer.\n[6] These findings were validated using candidate gene methylation analysis in multiple clinical sample sets of tissue samples from a total of 272 additional women.\n[7] Increased HAND2 methylation was a feature of premalignant endometrial lesions and was seen to parallel a decrease in RNA and protein levels.\n[8] Furthermore, women with high endometrial HAND2 methylation in their premalignant lesions were less likely to respond to progesterone treatment.\n[9] HAND2 methylation analysis of endometrial secretions collected using high vaginal swabs taken from women with postmenopausal bleeding specifically identified those patients with early stage endometrial cancer with both high sensitivity and high specificity (receiver operating characteristics area under the curve = 0.91 for stage 1A and 0.97 for higher than stage 1A).\n[10] Finally, mice harbouring a Hand2 knock-out specifically in their endometrium were shown to develop precancerous endometrial lesions with increasing age, and these lesions also demonstrated a lack of PTEN expression.\n[11] CONCLUSIONS HAND2 methylation is a common and crucial molecular alteration in endometrial cancer that could potentially be employed as a biomarker for early detection of endometrial cancer and as a predictor of treatment response.\n[12] The true clinical utility of HAND2 DNA methylation, however, requires further validation in prospective studies.\n[13] Please see later in the article for the Editors' Summary."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Finally, mice harbouring a Hand2 knock-out specifically in their endometrium were shown to develop precancerous endometrial lesions with increasing age, and these lesions also demonstrated a lack of PTEN expression.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 335, "doc_id": 1780819, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [1780819], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Destination container port throughput(CPT) is negatively related to dengue virus (DENV-1) diffusion in air traffic shipments.\n\nDocument title: Population Density, Water Supply, and the Risk of Dengue Fever in Vietnam: Cohort Study and Spatial Analysis\n\nAbstract sentences:\n[0] BACKGROUND Aedes aegypti, the major vector of dengue viruses, often breeds in water storage containers used by households without tap water supply, and occurs in high numbers even in dense urban areas.\n[1] We analysed the interaction between human population density and lack of tap water as a cause of dengue fever outbreaks with the aim of identifying geographic areas at highest risk.\n[2] METHODS AND FINDINGS We conducted an individual-level cohort study in a population of 75,000 geo-referenced households in Vietnam over the course of two epidemics, on the basis of dengue hospital admissions (n = 3,013).\n[3] We applied space-time scan statistics and mathematical models to confirm the findings.\n[4] We identified a surprisingly narrow range of critical human population densities between around 3,000 to 7,000 people/km² prone to dengue outbreaks.\n[5] In the study area, this population density was typical of villages and some peri-urban areas.\n[6] Scan statistics showed that areas with a high population density or adequate water supply did not experience severe outbreaks.\n[7] The risk of dengue was higher in rural than in urban areas, largely explained by lack of piped water supply, and in human population densities more often falling within the critical range.\n[8] Mathematical modeling suggests that simple assumptions regarding area-level vector/host ratios may explain the occurrence of outbreaks.\n[9] CONCLUSIONS Rural areas may contribute at least as much to the dissemination of dengue fever as cities.\n[10] Improving water supply and vector control in areas with a human population density critical for dengue transmission could increase the efficiency of control efforts.\n[11] Please see later in the article for the Editors' Summary."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 336, "doc_id": 2097256, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [2097256], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Destination container port throughput(CPT) is positively related to dengue virus (DENV-1) diffusion in air traffic shipments.\n\nDocument title: Population Density, Water Supply, and the Risk of Dengue Fever in Vietnam: Cohort Study and Spatial Analysis\n\nAbstract sentences:\n[0] BACKGROUND Aedes aegypti, the major vector of dengue viruses, often breeds in water storage containers used by households without tap water supply, and occurs in high numbers even in dense urban areas.\n[1] We analysed the interaction between human population density and lack of tap water as a cause of dengue fever outbreaks with the aim of identifying geographic areas at highest risk.\n[2] METHODS AND FINDINGS We conducted an individual-level cohort study in a population of 75,000 geo-referenced households in Vietnam over the course of two epidemics, on the basis of dengue hospital admissions (n = 3,013).\n[3] We applied space-time scan statistics and mathematical models to confirm the findings.\n[4] We identified a surprisingly narrow range of critical human population densities between around 3,000 to 7,000 people/km² prone to dengue outbreaks.\n[5] In the study area, this population density was typical of villages and some peri-urban areas.\n[6] Scan statistics showed that areas with a high population density or adequate water supply did not experience severe outbreaks.\n[7] The risk of dengue was higher in rural than in urban areas, largely explained by lack of piped water supply, and in human population densities more often falling within the critical range.\n[8] Mathematical modeling suggests that simple assumptions regarding area-level vector/host ratios may explain the occurrence of outbreaks.\n[9] CONCLUSIONS Rural areas may contribute at least as much to the dissemination of dengue fever as cities.\n[10] Improving water supply and vector control in areas with a human population density critical for dengue transmission could increase the efficiency of control efforts.\n[11] Please see later in the article for the Editors' Summary."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 337, "doc_id": 2097256, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [2097256], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Dexamethasone increases risk of postoperative bleeding.\n\nDocument title: Dexamethasone and risk of nausea and vomiting and postoperative bleeding after tonsillectomy in children: a randomized trial.\n\nAbstract sentences:\n[0] CONTEXT Dexamethasone is widely used to prevent postoperative nausea and vomiting (PONV) in pediatric tonsillectomy.\n[1] OBJECTIVE To assess whether dexamethasone dose-dependently reduces the risk of PONV at 24 hours after tonsillectomy.\n[2] DESIGN, SETTING, AND PATIENTS Randomized placebo-controlled trial conducted among 215 children undergoing elective tonsillectomy at a major public teaching hospital in Switzerland from February 2005 to December 2007.\n[3] INTERVENTIONS Children were randomly assigned to receive dexamethasone (0.05, 0.15, or 0.5 mg/kg) or placebo intravenously after induction of anesthesia.\n[4] Acetaminophen-codeine and ibuprofen were given as postoperative analgesia.\n[5] Follow-up continued until the 10th postoperative day.\n[6] MAIN OUTCOME MEASURES The primary end point was prevention of PONV at 24 hours; secondary end points were decrease in the need for ibuprofen at 24 hours and evaluation of adverse effects.\n[7] RESULTS At 24 hours, 24 of 54 participants who received placebo (44%; 95% confidence interval [CI], 31%-59%) had experienced PONV compared with 20 of 53 (38%; 95% CI, 25%-52%), 13 of 54 (24%; 95% CI, 13%-38%), and 6 of 52 (12%; 95% CI, 4%-23%) who received dexamethasone at 0.05, 0.15, and 0.5 mg/kg, respectively (P<.001 for linear trend).\n[8] Children who received dexamethasone received significantly less ibuprofen.\n[9] There were 26 postoperative bleeding episodes in 22 children.\n[10] Two of 53 (4%; 95% CI, 0.5%-13%)\n[11] children who received placebo had bleeding compared with 6 of 53 (11%; 95% CI, 4%-23%), 2 of 51 (4%; 95% CI, 0.5%-13%), and 12 of 50 (24%; 95% CI, 13%-38%) who received dexamethasone at 0.05, 0.15, and 0.5 mg/kg, respectively (P = .003).\n[12] Dexamethasone, 0.5 mg/kg, was associated with the highest bleeding risk (adjusted relative risk, 6.80; 95% CI, 1.77-16.5).\n[13] Eight children had to undergo emergency reoperation because of bleeding, all of whom had received dexamethasone.\n[14] The trial was stopped early for safety reasons.\n[15] CONCLUSION In this study of children undergoing tonsillectomy, dexamethasone decreased the risk of PONV dose dependently but was associated with an increased risk of postoperative bleeding.\n[16] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00403806."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10, 11]\nExplanation: Evidence states: \"Two of 53 (4%; 95% CI, 0.5%-13%) children who received placebo had bleeding compared with 6 of 53 (11%; 95% CI, 4%-23%), 2 of 51 (4%; 95% CI, 0.5%-13%), and 12 of 50 (24%; 95% CI, 13%-38%) who received dexamethasone at 0.05, 0.15, and 0.5 mg/kg, respectively (P = .003).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 339, "doc_id": 23349986, "label": "SUPPORTS", "evidence_sentence_ids": [10, 11], "cited_doc_ids": [23349986], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Dexamethasone increases risk of postoperative bleeding.\n\nDocument title: Dexamethasone and risk of nausea and vomiting and postoperative bleeding after tonsillectomy in children: a randomized trial.\n\nAbstract sentences:\n[0] CONTEXT Dexamethasone is widely used to prevent postoperative nausea and vomiting (PONV) in pediatric tonsillectomy.\n[1] OBJECTIVE To assess whether dexamethasone dose-dependently reduces the risk of PONV at 24 hours after tonsillectomy.\n[2] DESIGN, SETTING, AND PATIENTS Randomized placebo-controlled trial conducted among 215 children undergoing elective tonsillectomy at a major public teaching hospital in Switzerland from February 2005 to December 2007.\n[3] INTERVENTIONS Children were randomly assigned to receive dexamethasone (0.05, 0.15, or 0.5 mg/kg) or placebo intravenously after induction of anesthesia.\n[4] Acetaminophen-codeine and ibuprofen were given as postoperative analgesia.\n[5] Follow-up continued until the 10th postoperative day.\n[6] MAIN OUTCOME MEASURES The primary end point was prevention of PONV at 24 hours; secondary end points were decrease in the need for ibuprofen at 24 hours and evaluation of adverse effects.\n[7] RESULTS At 24 hours, 24 of 54 participants who received placebo (44%; 95% confidence interval [CI], 31%-59%) had experienced PONV compared with 20 of 53 (38%; 95% CI, 25%-52%), 13 of 54 (24%; 95% CI, 13%-38%), and 6 of 52 (12%; 95% CI, 4%-23%) who received dexamethasone at 0.05, 0.15, and 0.5 mg/kg, respectively (P<.001 for linear trend).\n[8] Children who received dexamethasone received significantly less ibuprofen.\n[9] There were 26 postoperative bleeding episodes in 22 children.\n[10] Two of 53 (4%; 95% CI, 0.5%-13%)\n[11] children who received placebo had bleeding compared with 6 of 53 (11%; 95% CI, 4%-23%), 2 of 51 (4%; 95% CI, 0.5%-13%), and 12 of 50 (24%; 95% CI, 13%-38%) who received dexamethasone at 0.05, 0.15, and 0.5 mg/kg, respectively (P = .003).\n[12] Dexamethasone, 0.5 mg/kg, was associated with the highest bleeding risk (adjusted relative risk, 6.80; 95% CI, 1.77-16.5).\n[13] Eight children had to undergo emergency reoperation because of bleeding, all of whom had received dexamethasone.\n[14] The trial was stopped early for safety reasons.\n[15] CONCLUSION In this study of children undergoing tonsillectomy, dexamethasone decreased the risk of PONV dose dependently but was associated with an increased risk of postoperative bleeding.\n[16] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00403806."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"Dexamethasone, 0.5 mg/kg, was associated with the highest bleeding risk (adjusted relative risk, 6.80; 95% CI, 1.77-16.5).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 339, "doc_id": 23349986, "label": "SUPPORTS", "evidence_sentence_ids": [12], "cited_doc_ids": [23349986], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Dexamethasone increases risk of postoperative bleeding.\n\nDocument title: Dexamethasone and risk of nausea and vomiting and postoperative bleeding after tonsillectomy in children: a randomized trial.\n\nAbstract sentences:\n[0] CONTEXT Dexamethasone is widely used to prevent postoperative nausea and vomiting (PONV) in pediatric tonsillectomy.\n[1] OBJECTIVE To assess whether dexamethasone dose-dependently reduces the risk of PONV at 24 hours after tonsillectomy.\n[2] DESIGN, SETTING, AND PATIENTS Randomized placebo-controlled trial conducted among 215 children undergoing elective tonsillectomy at a major public teaching hospital in Switzerland from February 2005 to December 2007.\n[3] INTERVENTIONS Children were randomly assigned to receive dexamethasone (0.05, 0.15, or 0.5 mg/kg) or placebo intravenously after induction of anesthesia.\n[4] Acetaminophen-codeine and ibuprofen were given as postoperative analgesia.\n[5] Follow-up continued until the 10th postoperative day.\n[6] MAIN OUTCOME MEASURES The primary end point was prevention of PONV at 24 hours; secondary end points were decrease in the need for ibuprofen at 24 hours and evaluation of adverse effects.\n[7] RESULTS At 24 hours, 24 of 54 participants who received placebo (44%; 95% confidence interval [CI], 31%-59%) had experienced PONV compared with 20 of 53 (38%; 95% CI, 25%-52%), 13 of 54 (24%; 95% CI, 13%-38%), and 6 of 52 (12%; 95% CI, 4%-23%) who received dexamethasone at 0.05, 0.15, and 0.5 mg/kg, respectively (P<.001 for linear trend).\n[8] Children who received dexamethasone received significantly less ibuprofen.\n[9] There were 26 postoperative bleeding episodes in 22 children.\n[10] Two of 53 (4%; 95% CI, 0.5%-13%)\n[11] children who received placebo had bleeding compared with 6 of 53 (11%; 95% CI, 4%-23%), 2 of 51 (4%; 95% CI, 0.5%-13%), and 12 of 50 (24%; 95% CI, 13%-38%) who received dexamethasone at 0.05, 0.15, and 0.5 mg/kg, respectively (P = .003).\n[12] Dexamethasone, 0.5 mg/kg, was associated with the highest bleeding risk (adjusted relative risk, 6.80; 95% CI, 1.77-16.5).\n[13] Eight children had to undergo emergency reoperation because of bleeding, all of whom had received dexamethasone.\n[14] The trial was stopped early for safety reasons.\n[15] CONCLUSION In this study of children undergoing tonsillectomy, dexamethasone decreased the risk of PONV dose dependently but was associated with an increased risk of postoperative bleeding.\n[16] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00403806."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [15]\nExplanation: Evidence states: \"CONCLUSION In this study of children undergoing tonsillectomy, dexamethasone decreased the risk of PONV dose dependently but was associated with an increased risk of postoperative bleeding.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 339, "doc_id": 23349986, "label": "SUPPORTS", "evidence_sentence_ids": [15], "cited_doc_ids": [23349986], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Diabetes remission occurs less in people treated with conventional therapy than in people treated with laparoscopic adjustable gastric banding surgery.\n\nDocument title: Adjustable gastric banding and conventional therapy for type 2 diabetes: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Observational studies suggest that surgically induced loss of weight may be effective therapy for type 2 diabetes.\n[1] OBJECTIVE To determine if surgically induced weight loss results in better glycemic control and less need for diabetes medications than conventional approaches to weight loss and diabetes control.\n[2] DESIGN, SETTING, AND PARTICIPANTS Unblinded randomized controlled trial conducted from December 2002 through December 2006 at the University Obesity Research Center in Australia, with general community recruitment to established treatment programs.\n[3] Participants were 60 obese patients (BMI >30 and <40) with recently diagnosed (<2 years) type 2 diabetes.\n[4] INTERVENTIONS Conventional diabetes therapy with a focus on weight loss by lifestyle change vs laparoscopic adjustable gastric banding with conventional diabetes care.\n[5] MAIN OUTCOME MEASURES Remission of type 2 diabetes (fasting glucose level <126 mg/dL [7.0 mmol/L] and glycated hemoglobin [HbA1c] value <6.2% while taking no glycemic therapy).\n[6] Secondary measures included weight and components of the metabolic syndrome.\n[7] Analysis was by intention-to-treat.\n[8] RESULTS Of the 60 patients enrolled, 55 (92%) completed the 2-year follow-up.\n[9] Remission of type 2 diabetes was achieved by 22 (73%) in the surgical group and 4 (13%) in the conventional-therapy group.\n[10] Relative risk of remission for the surgical group was 5.5 (95% confidence interval, 2.2-14.0).\n[11] Surgical and conventional-therapy groups lost a mean (SD) of 20.7% (8.6%) and 1.7% (5.2%) of weight, respectively, at 2 years (P < .001).\n[12] Remission of type 2 diabetes was related to weight loss (R2 = 0.46, P < .001) and lower baseline HbA1c levels (combined R2 = 0.52, P < .001).\n[13] There were no serious complications in either group.\n[14] CONCLUSIONS Participants randomized to surgical therapy were more likely to achieve remission of type 2 diabetes through greater weight loss.\n[15] These results need to be confirmed in a larger, more diverse population and have long-term efficacy assessed.\n[16] TRIAL REGISTRATION actr.org Identifier: ACTRN012605000159651."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Remission of type 2 diabetes was achieved by 22 (73%) in the surgical group and 4 (13%) in the conventional-therapy group.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 340, "doc_id": 7098463, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [7098463], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Diabetes remission occurs less in people treated with conventional therapy than in people treated with laparoscopic adjustable gastric banding surgery.\n\nDocument title: Adjustable gastric banding and conventional therapy for type 2 diabetes: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Observational studies suggest that surgically induced loss of weight may be effective therapy for type 2 diabetes.\n[1] OBJECTIVE To determine if surgically induced weight loss results in better glycemic control and less need for diabetes medications than conventional approaches to weight loss and diabetes control.\n[2] DESIGN, SETTING, AND PARTICIPANTS Unblinded randomized controlled trial conducted from December 2002 through December 2006 at the University Obesity Research Center in Australia, with general community recruitment to established treatment programs.\n[3] Participants were 60 obese patients (BMI >30 and <40) with recently diagnosed (<2 years) type 2 diabetes.\n[4] INTERVENTIONS Conventional diabetes therapy with a focus on weight loss by lifestyle change vs laparoscopic adjustable gastric banding with conventional diabetes care.\n[5] MAIN OUTCOME MEASURES Remission of type 2 diabetes (fasting glucose level <126 mg/dL [7.0 mmol/L] and glycated hemoglobin [HbA1c] value <6.2% while taking no glycemic therapy).\n[6] Secondary measures included weight and components of the metabolic syndrome.\n[7] Analysis was by intention-to-treat.\n[8] RESULTS Of the 60 patients enrolled, 55 (92%) completed the 2-year follow-up.\n[9] Remission of type 2 diabetes was achieved by 22 (73%) in the surgical group and 4 (13%) in the conventional-therapy group.\n[10] Relative risk of remission for the surgical group was 5.5 (95% confidence interval, 2.2-14.0).\n[11] Surgical and conventional-therapy groups lost a mean (SD) of 20.7% (8.6%) and 1.7% (5.2%) of weight, respectively, at 2 years (P < .001).\n[12] Remission of type 2 diabetes was related to weight loss (R2 = 0.46, P < .001) and lower baseline HbA1c levels (combined R2 = 0.52, P < .001).\n[13] There were no serious complications in either group.\n[14] CONCLUSIONS Participants randomized to surgical therapy were more likely to achieve remission of type 2 diabetes through greater weight loss.\n[15] These results need to be confirmed in a larger, more diverse population and have long-term efficacy assessed.\n[16] TRIAL REGISTRATION actr.org Identifier: ACTRN012605000159651."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Relative risk of remission for the surgical group was 5.5 (95% confidence interval, 2.2-14.0).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 340, "doc_id": 7098463, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [7098463], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Diabetes remission occurs less in people treated with conventional therapy than in people treated with laparoscopic adjustable gastric banding surgery.\n\nDocument title: Adjustable gastric banding and conventional therapy for type 2 diabetes: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Observational studies suggest that surgically induced loss of weight may be effective therapy for type 2 diabetes.\n[1] OBJECTIVE To determine if surgically induced weight loss results in better glycemic control and less need for diabetes medications than conventional approaches to weight loss and diabetes control.\n[2] DESIGN, SETTING, AND PARTICIPANTS Unblinded randomized controlled trial conducted from December 2002 through December 2006 at the University Obesity Research Center in Australia, with general community recruitment to established treatment programs.\n[3] Participants were 60 obese patients (BMI >30 and <40) with recently diagnosed (<2 years) type 2 diabetes.\n[4] INTERVENTIONS Conventional diabetes therapy with a focus on weight loss by lifestyle change vs laparoscopic adjustable gastric banding with conventional diabetes care.\n[5] MAIN OUTCOME MEASURES Remission of type 2 diabetes (fasting glucose level <126 mg/dL [7.0 mmol/L] and glycated hemoglobin [HbA1c] value <6.2% while taking no glycemic therapy).\n[6] Secondary measures included weight and components of the metabolic syndrome.\n[7] Analysis was by intention-to-treat.\n[8] RESULTS Of the 60 patients enrolled, 55 (92%) completed the 2-year follow-up.\n[9] Remission of type 2 diabetes was achieved by 22 (73%) in the surgical group and 4 (13%) in the conventional-therapy group.\n[10] Relative risk of remission for the surgical group was 5.5 (95% confidence interval, 2.2-14.0).\n[11] Surgical and conventional-therapy groups lost a mean (SD) of 20.7% (8.6%) and 1.7% (5.2%) of weight, respectively, at 2 years (P < .001).\n[12] Remission of type 2 diabetes was related to weight loss (R2 = 0.46, P < .001) and lower baseline HbA1c levels (combined R2 = 0.52, P < .001).\n[13] There were no serious complications in either group.\n[14] CONCLUSIONS Participants randomized to surgical therapy were more likely to achieve remission of type 2 diabetes through greater weight loss.\n[15] These results need to be confirmed in a larger, more diverse population and have long-term efficacy assessed.\n[16] TRIAL REGISTRATION actr.org Identifier: ACTRN012605000159651."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [14]\nExplanation: Evidence states: \"CONCLUSIONS Participants randomized to surgical therapy were more likely to achieve remission of type 2 diabetes through greater weight loss.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 340, "doc_id": 7098463, "label": "SUPPORTS", "evidence_sentence_ids": [14], "cited_doc_ids": [7098463], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Diabetes remission occurs more in people treated with conventional therapy than in people treated with laparoscopic adjustable gastric banding surgery.\n\nDocument title: Adjustable gastric banding and conventional therapy for type 2 diabetes: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Observational studies suggest that surgically induced loss of weight may be effective therapy for type 2 diabetes.\n[1] OBJECTIVE To determine if surgically induced weight loss results in better glycemic control and less need for diabetes medications than conventional approaches to weight loss and diabetes control.\n[2] DESIGN, SETTING, AND PARTICIPANTS Unblinded randomized controlled trial conducted from December 2002 through December 2006 at the University Obesity Research Center in Australia, with general community recruitment to established treatment programs.\n[3] Participants were 60 obese patients (BMI >30 and <40) with recently diagnosed (<2 years) type 2 diabetes.\n[4] INTERVENTIONS Conventional diabetes therapy with a focus on weight loss by lifestyle change vs laparoscopic adjustable gastric banding with conventional diabetes care.\n[5] MAIN OUTCOME MEASURES Remission of type 2 diabetes (fasting glucose level <126 mg/dL [7.0 mmol/L] and glycated hemoglobin [HbA1c] value <6.2% while taking no glycemic therapy).\n[6] Secondary measures included weight and components of the metabolic syndrome.\n[7] Analysis was by intention-to-treat.\n[8] RESULTS Of the 60 patients enrolled, 55 (92%) completed the 2-year follow-up.\n[9] Remission of type 2 diabetes was achieved by 22 (73%) in the surgical group and 4 (13%) in the conventional-therapy group.\n[10] Relative risk of remission for the surgical group was 5.5 (95% confidence interval, 2.2-14.0).\n[11] Surgical and conventional-therapy groups lost a mean (SD) of 20.7% (8.6%) and 1.7% (5.2%) of weight, respectively, at 2 years (P < .001).\n[12] Remission of type 2 diabetes was related to weight loss (R2 = 0.46, P < .001) and lower baseline HbA1c levels (combined R2 = 0.52, P < .001).\n[13] There were no serious complications in either group.\n[14] CONCLUSIONS Participants randomized to surgical therapy were more likely to achieve remission of type 2 diabetes through greater weight loss.\n[15] These results need to be confirmed in a larger, more diverse population and have long-term efficacy assessed.\n[16] TRIAL REGISTRATION actr.org Identifier: ACTRN012605000159651."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Remission of type 2 diabetes was achieved by 22 (73%) in the surgical group and 4 (13%) in the conventional-therapy group.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 341, "doc_id": 7098463, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [7098463], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Diabetes remission occurs more in people treated with conventional therapy than in people treated with laparoscopic adjustable gastric banding surgery.\n\nDocument title: Adjustable gastric banding and conventional therapy for type 2 diabetes: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Observational studies suggest that surgically induced loss of weight may be effective therapy for type 2 diabetes.\n[1] OBJECTIVE To determine if surgically induced weight loss results in better glycemic control and less need for diabetes medications than conventional approaches to weight loss and diabetes control.\n[2] DESIGN, SETTING, AND PARTICIPANTS Unblinded randomized controlled trial conducted from December 2002 through December 2006 at the University Obesity Research Center in Australia, with general community recruitment to established treatment programs.\n[3] Participants were 60 obese patients (BMI >30 and <40) with recently diagnosed (<2 years) type 2 diabetes.\n[4] INTERVENTIONS Conventional diabetes therapy with a focus on weight loss by lifestyle change vs laparoscopic adjustable gastric banding with conventional diabetes care.\n[5] MAIN OUTCOME MEASURES Remission of type 2 diabetes (fasting glucose level <126 mg/dL [7.0 mmol/L] and glycated hemoglobin [HbA1c] value <6.2% while taking no glycemic therapy).\n[6] Secondary measures included weight and components of the metabolic syndrome.\n[7] Analysis was by intention-to-treat.\n[8] RESULTS Of the 60 patients enrolled, 55 (92%) completed the 2-year follow-up.\n[9] Remission of type 2 diabetes was achieved by 22 (73%) in the surgical group and 4 (13%) in the conventional-therapy group.\n[10] Relative risk of remission for the surgical group was 5.5 (95% confidence interval, 2.2-14.0).\n[11] Surgical and conventional-therapy groups lost a mean (SD) of 20.7% (8.6%) and 1.7% (5.2%) of weight, respectively, at 2 years (P < .001).\n[12] Remission of type 2 diabetes was related to weight loss (R2 = 0.46, P < .001) and lower baseline HbA1c levels (combined R2 = 0.52, P < .001).\n[13] There were no serious complications in either group.\n[14] CONCLUSIONS Participants randomized to surgical therapy were more likely to achieve remission of type 2 diabetes through greater weight loss.\n[15] These results need to be confirmed in a larger, more diverse population and have long-term efficacy assessed.\n[16] TRIAL REGISTRATION actr.org Identifier: ACTRN012605000159651."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Relative risk of remission for the surgical group was 5.5 (95% confidence interval, 2.2-14.0).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 341, "doc_id": 7098463, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [7098463], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Diabetes remission occurs more in people treated with conventional therapy than in people treated with laparoscopic adjustable gastric banding surgery.\n\nDocument title: Adjustable gastric banding and conventional therapy for type 2 diabetes: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Observational studies suggest that surgically induced loss of weight may be effective therapy for type 2 diabetes.\n[1] OBJECTIVE To determine if surgically induced weight loss results in better glycemic control and less need for diabetes medications than conventional approaches to weight loss and diabetes control.\n[2] DESIGN, SETTING, AND PARTICIPANTS Unblinded randomized controlled trial conducted from December 2002 through December 2006 at the University Obesity Research Center in Australia, with general community recruitment to established treatment programs.\n[3] Participants were 60 obese patients (BMI >30 and <40) with recently diagnosed (<2 years) type 2 diabetes.\n[4] INTERVENTIONS Conventional diabetes therapy with a focus on weight loss by lifestyle change vs laparoscopic adjustable gastric banding with conventional diabetes care.\n[5] MAIN OUTCOME MEASURES Remission of type 2 diabetes (fasting glucose level <126 mg/dL [7.0 mmol/L] and glycated hemoglobin [HbA1c] value <6.2% while taking no glycemic therapy).\n[6] Secondary measures included weight and components of the metabolic syndrome.\n[7] Analysis was by intention-to-treat.\n[8] RESULTS Of the 60 patients enrolled, 55 (92%) completed the 2-year follow-up.\n[9] Remission of type 2 diabetes was achieved by 22 (73%) in the surgical group and 4 (13%) in the conventional-therapy group.\n[10] Relative risk of remission for the surgical group was 5.5 (95% confidence interval, 2.2-14.0).\n[11] Surgical and conventional-therapy groups lost a mean (SD) of 20.7% (8.6%) and 1.7% (5.2%) of weight, respectively, at 2 years (P < .001).\n[12] Remission of type 2 diabetes was related to weight loss (R2 = 0.46, P < .001) and lower baseline HbA1c levels (combined R2 = 0.52, P < .001).\n[13] There were no serious complications in either group.\n[14] CONCLUSIONS Participants randomized to surgical therapy were more likely to achieve remission of type 2 diabetes through greater weight loss.\n[15] These results need to be confirmed in a larger, more diverse population and have long-term efficacy assessed.\n[16] TRIAL REGISTRATION actr.org Identifier: ACTRN012605000159651."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [14]\nExplanation: Evidence states: \"CONCLUSIONS Participants randomized to surgical therapy were more likely to achieve remission of type 2 diabetes through greater weight loss.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 341, "doc_id": 7098463, "label": "CONTRADICTS", "evidence_sentence_ids": [14], "cited_doc_ids": [7098463], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Diabetic patients with acute coronary syndrome experience decreased short-term and long-term risk for bleeding events.\n\nDocument title: Impact of diabetes on long-term prognosis in patients with unstable angina and non-Q-wave myocardial infarction: results of the OASIS (Organization to Assess Strategies for Ischemic Syndromes) Registry.\n\nAbstract sentences:\n[0] BACKGROUND Although unstable coronary artery disease is the most common reason for admission to a coronary care unit, the long-term prognosis of patients with this diagnosis is unknown.\n[1] This is particularly true for patients with diabetes mellitus, who are known to have a high morbidity and mortality after an acute myocardial infarction.\n[2] METHODS AND RESULTS Prospectively collected data from 6 different countries in the Organization to Assess Strategies for Ischemic Syndromes (OASIS) registry were analyzed to determine the 2-year prognosis of diabetic and nondiabetic patients who were hospitalized with unstable angina or non-Q-wave myocardial infarction.\n[3] Overall, 1718 of 8013 registry patients (21%) had diabetes.\n[4] Diabetic patients had a higher rate of coronary bypass surgery than nondiabetic patients (23% versus 20%, P:<0.001) but had similar rates of catheterization and angioplasty.\n[5] Diabetes independently predicted mortality (relative risk [RR], 1.57; 95% CI, 1.38 to 1.81; P:<0.001), as well as cardiovascular death, new myocardial infarction, stroke, and new congestive heart failure.\n[6] Moreover, compared with their nondiabetic counterparts, women had a significantly higher risk than men (RR, 1.98; 95% CI, 1.60 to 2.44; and RR, 1.28; 95% CI, 1.06 to 1.56, respectively).\n[7] Interestingly, diabetic patients without prior cardiovascular disease had the same event rates for all outcomes as nondiabetic patients with previous vascular disease.\n[8] CONCLUSIONS Hospitalization for unstable angina or non-Q-wave myocardial infarction predicts a high 2-year morbidity and mortality; this is especially evident for patients with diabetes.\n[9] Diabetic patients with no previous cardiovascular disease have the same long-term morbidity and mortality as nondiabetic patients with established cardiovascular disease after hospitalization for unstable coronary artery disease."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Diabetes independently predicted mortality (relative risk [RR], 1.57; 95% CI, 1.38 to 1.81; P:<0.001), as well as cardiovascular death, new myocardial infarction, stroke, and new congestive heart failure.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 342, "doc_id": 5884524, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [7873737, 5884524], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Differentiated E2f-1, -2, -3 TKO cells in the intestine do not exhibit apoptosis.\n\nDocument title: E2F1-3 Switch from Activators in Progenitor Cells to Repressors in Differentiating Cells\n\nAbstract sentences:\n[0] In the established model of mammalian cell cycle control, the retinoblastoma protein (Rb) functions to restrict cells from entering S phase by binding and sequestering E2f activators (E2f1, E2f2 and E2f3), which are invariably portrayed as the ultimate effectors of a transcriptional program that commit cells to enter and progress through S phase.\n[1] Using a panel of tissue-specific cre-transgenic mice and conditional E2f alleles we examined the effects of E2f1, E2f2 and E2f3 triple deficiency in murine embryonic stem cells, embryos and small intestines.\n[2] We show that in normal dividing progenitor cells E2f1-3 function as transcriptional activators, but contrary to the current view, are dispensable for cell division and instead are necessary for cell survival.\n[3] In differentiating cells E2f1-3 function in a complex with Rb as repressors to silence E2f targets and facilitate exit from the cell cycle.\n[4] The inactivation of Rb in differentiating cells resulted in a switch of E2f1-3 from repressors to activators, leading to the superactivation of E2f responsive targets and ectopic cell divisions.\n[5] Loss of E2f1-3 completely suppressed these phenotypes caused by Rb deficiency.\n[6] This work contextualizes the activator versus repressor functions of E2f1-3 in vivo, revealing distinct roles in dividing versus differentiating cells and in normal versus cancer-like cell cycles."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 345, "doc_id": 4394817, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4394817], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Differentiation of progenitor cells to myeloid cells is skewed upon activation of insulin signaling.\n\nDocument title: Direct sensing of systemic and nutritional signals by hematopoietic progenitors in Drosophila\n\nAbstract sentences:\n[0] The Drosophila lymph gland is a haematopoietic organ in which progenitor cells, which are most akin to the common myeloid progenitor in mammals, proliferate and differentiate into three types of mature cell--plasmatocytes, crystal cells and lamellocytes--the functions of which are reminiscent of mammalian myeloid cells.\n[1] During the first and early second instars of larval development, the lymph gland contains only progenitors, whereas in the third instar, a medial region of the primary lobe of the lymph gland called the medullary zone contains these progenitors, and maturing blood cells are found juxtaposed in a peripheral region designated the cortical zone.\n[2] A third group of cells referred to as the posterior signalling centre functions as a haematopoietic niche.\n[3] Similarly to mammalian myeloid cells, Drosophila blood cells respond to multiple stresses including hypoxia, infection and oxidative stress.\n[4] However, how systemic signals are sensed by myeloid progenitors to regulate cell-fate determination has not been well described.\n[5] Here, we show that the haematopoietic progenitors of Drosophila are direct targets of systemic (insulin) and nutritional (essential amino acid) signals, and that these systemic signals maintain the progenitors by promoting Wingless (WNT in mammals) signalling.\n[6] We expect that this study will promote investigation of such possible direct signal sensing mechanisms by mammalian myeloid progenitors."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Here, we show that the haematopoietic progenitors of Drosophila are direct targets of systemic (insulin) and nutritional (essential amino acid) signals, and that these systemic signals maintain the progenitors by promoting Wingless (WNT in mammals) signalling.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 346, "doc_id": 11902109, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [11902109], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Differentiation of progenitor cells to myeloid cells is skewed when insulin signaling is suppressed.\n\nDocument title: Direct sensing of systemic and nutritional signals by hematopoietic progenitors in Drosophila\n\nAbstract sentences:\n[0] The Drosophila lymph gland is a haematopoietic organ in which progenitor cells, which are most akin to the common myeloid progenitor in mammals, proliferate and differentiate into three types of mature cell--plasmatocytes, crystal cells and lamellocytes--the functions of which are reminiscent of mammalian myeloid cells.\n[1] During the first and early second instars of larval development, the lymph gland contains only progenitors, whereas in the third instar, a medial region of the primary lobe of the lymph gland called the medullary zone contains these progenitors, and maturing blood cells are found juxtaposed in a peripheral region designated the cortical zone.\n[2] A third group of cells referred to as the posterior signalling centre functions as a haematopoietic niche.\n[3] Similarly to mammalian myeloid cells, Drosophila blood cells respond to multiple stresses including hypoxia, infection and oxidative stress.\n[4] However, how systemic signals are sensed by myeloid progenitors to regulate cell-fate determination has not been well described.\n[5] Here, we show that the haematopoietic progenitors of Drosophila are direct targets of systemic (insulin) and nutritional (essential amino acid) signals, and that these systemic signals maintain the progenitors by promoting Wingless (WNT in mammals) signalling.\n[6] We expect that this study will promote investigation of such possible direct signal sensing mechanisms by mammalian myeloid progenitors."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Here, we show that the haematopoietic progenitors of Drosophila are direct targets of systemic (insulin) and nutritional (essential amino acid) signals, and that these systemic signals maintain the progenitors by promoting Wingless (WNT in mammals) signalling.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 347, "doc_id": 11902109, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [11902109], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Diminished ovarian reserve is a reliable indicator of infertility in a non-infertile population.\n\nDocument title: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\n\nAbstract sentences:\n[0] Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential.\n[1] Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age.\n[2] Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area.\n[3] Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH.\n[4] Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle).\n[5] Conception was defined as a positive pregnancy test result.\n[6] Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis.\n[7] After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively).\n[8] Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (63%; 95% CI, 50%-73%) compared with women (n = 654) with normal values (62%; 95% CI, 57%-66%) or after 12 cycles of attempt (82% [95% CI, 70%-89%] vs 75% [95% CI, 70%-78%], respectively).\n[9] Women with high urinary FSH values (>11.5 mIU/mg creatinine [n = 69]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (61%; 95% CI, 46%-74%) compared with women (n = 660) with normal values (62%; 95% CI, 58%-66%) or after 12 cycles of attempt (70% [95% CI, 54%-80%] vs 76% [95% CI, 72%-80%], respectively).\n[10] Inhibin B levels (n = 737) were not associated with the probability of conceiving in a given cycle (hazard ratio per 1-pg/mL increase, 0.999; 95% CI, 0.997-1.001).\n[11] Conclusions and Relevance Among women aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, biomarkers indicating diminished ovarian reserve compared with normal ovarian reserve were not associated with reduced fertility.\n[12] These findings do not support the use of urinary or blood follicle-stimulating hormone tests or antimüllerian hormone levels to assess natural fertility for women with these characteristics."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 349, "doc_id": 13497630, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [13497630], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Diminished ovarian reserve is a reliable indicator of infertility in a non-infertile population.\n\nDocument title: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\n\nAbstract sentences:\n[0] Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential.\n[1] Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age.\n[2] Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area.\n[3] Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH.\n[4] Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle).\n[5] Conception was defined as a positive pregnancy test result.\n[6] Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis.\n[7] After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively).\n[8] Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (63%; 95% CI, 50%-73%) compared with women (n = 654) with normal values (62%; 95% CI, 57%-66%) or after 12 cycles of attempt (82% [95% CI, 70%-89%] vs 75% [95% CI, 70%-78%], respectively).\n[9] Women with high urinary FSH values (>11.5 mIU/mg creatinine [n = 69]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (61%; 95% CI, 46%-74%) compared with women (n = 660) with normal values (62%; 95% CI, 58%-66%) or after 12 cycles of attempt (70% [95% CI, 54%-80%] vs 76% [95% CI, 72%-80%], respectively).\n[10] Inhibin B levels (n = 737) were not associated with the probability of conceiving in a given cycle (hazard ratio per 1-pg/mL increase, 0.999; 95% CI, 0.997-1.001).\n[11] Conclusions and Relevance Among women aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, biomarkers indicating diminished ovarian reserve compared with normal ovarian reserve were not associated with reduced fertility.\n[12] These findings do not support the use of urinary or blood follicle-stimulating hormone tests or antimüllerian hormone levels to assess natural fertility for women with these characteristics."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (63%; 95% CI, 50%-73%) compared with women (n = 654) with normal values (62%; 95% CI, 57%-66%) or after 12 cycles of attempt (82% [95% CI, 70%-89%] vs 75% [95% CI, 70%-78%], respectively).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 349, "doc_id": 13497630, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [13497630], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Diminished ovarian reserve is a reliable indicator of infertility in a non-infertile population.\n\nDocument title: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\n\nAbstract sentences:\n[0] Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential.\n[1] Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age.\n[2] Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area.\n[3] Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH.\n[4] Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle).\n[5] Conception was defined as a positive pregnancy test result.\n[6] Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis.\n[7] After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively).\n[8] Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (63%; 95% CI, 50%-73%) compared with women (n = 654) with normal values (62%; 95% CI, 57%-66%) or after 12 cycles of attempt (82% [95% CI, 70%-89%] vs 75% [95% CI, 70%-78%], respectively).\n[9] Women with high urinary FSH values (>11.5 mIU/mg creatinine [n = 69]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (61%; 95% CI, 46%-74%) compared with women (n = 660) with normal values (62%; 95% CI, 58%-66%) or after 12 cycles of attempt (70% [95% CI, 54%-80%] vs 76% [95% CI, 72%-80%], respectively).\n[10] Inhibin B levels (n = 737) were not associated with the probability of conceiving in a given cycle (hazard ratio per 1-pg/mL increase, 0.999; 95% CI, 0.997-1.001).\n[11] Conclusions and Relevance Among women aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, biomarkers indicating diminished ovarian reserve compared with normal ovarian reserve were not associated with reduced fertility.\n[12] These findings do not support the use of urinary or blood follicle-stimulating hormone tests or antimüllerian hormone levels to assess natural fertility for women with these characteristics."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Women with high urinary FSH values (>11.5 mIU/mg creatinine [n = 69]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (61%; 95% CI, 46%-74%) compared with women (n = 660) with normal values (62%; 95% CI, 58%-66%) or after 12 cycles of attempt (70% [95% CI, 54%-80%] vs 76% [95% CI, 72%-80%], respectively).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 349, "doc_id": 13497630, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [13497630], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Diminished ovarian reserve is a reliable indicator of infertility in a non-infertile population.\n\nDocument title: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\n\nAbstract sentences:\n[0] Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential.\n[1] Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age.\n[2] Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area.\n[3] Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH.\n[4] Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle).\n[5] Conception was defined as a positive pregnancy test result.\n[6] Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis.\n[7] After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively).\n[8] Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (63%; 95% CI, 50%-73%) compared with women (n = 654) with normal values (62%; 95% CI, 57%-66%) or after 12 cycles of attempt (82% [95% CI, 70%-89%] vs 75% [95% CI, 70%-78%], respectively).\n[9] Women with high urinary FSH values (>11.5 mIU/mg creatinine [n = 69]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (61%; 95% CI, 46%-74%) compared with women (n = 660) with normal values (62%; 95% CI, 58%-66%) or after 12 cycles of attempt (70% [95% CI, 54%-80%] vs 76% [95% CI, 72%-80%], respectively).\n[10] Inhibin B levels (n = 737) were not associated with the probability of conceiving in a given cycle (hazard ratio per 1-pg/mL increase, 0.999; 95% CI, 0.997-1.001).\n[11] Conclusions and Relevance Among women aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, biomarkers indicating diminished ovarian reserve compared with normal ovarian reserve were not associated with reduced fertility.\n[12] These findings do not support the use of urinary or blood follicle-stimulating hormone tests or antimüllerian hormone levels to assess natural fertility for women with these characteristics."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"Conclusions and Relevance Among women aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, biomarkers indicating diminished ovarian reserve compared with normal ovarian reserve were not associated with reduced fertility.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 349, "doc_id": 13497630, "label": "CONTRADICTS", "evidence_sentence_ids": [11], "cited_doc_ids": [13497630], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Distant CREs are important for transcriptional regulation.\n\nDocument title: Enhancer Evolution across 20 Mammalian Species\n\nAbstract sentences:\n[0] The mammalian radiation has corresponded with rapid changes in noncoding regions of the genome, but we lack a comprehensive understanding of regulatory evolution in mammals.\n[1] Here, we track the evolution of promoters and enhancers active in liver across 20 mammalian species from six diverse orders by profiling genomic enrichment of H3K27 acetylation and H3K4 trimethylation.\n[2] We report that rapid evolution of enhancers is a universal feature of mammalian genomes.\n[3] Most of the recently evolved enhancers arise from ancestral DNA exaptation, rather than lineage-specific expansions of repeat elements.\n[4] In contrast, almost all liver promoters are partially or fully conserved across these species.\n[5] Our data further reveal that recently evolved enhancers can be associated with genes under positive selection, demonstrating the power of this approach for annotating regulatory adaptations in genomic sequences.\n[6] These results provide important insight into the functional genetics underpinning mammalian regulatory evolution."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 351, "doc_id": 14658685, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14658685], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Distant CREs are less conserved among species.\n\nDocument title: Enhancer Evolution across 20 Mammalian Species\n\nAbstract sentences:\n[0] The mammalian radiation has corresponded with rapid changes in noncoding regions of the genome, but we lack a comprehensive understanding of regulatory evolution in mammals.\n[1] Here, we track the evolution of promoters and enhancers active in liver across 20 mammalian species from six diverse orders by profiling genomic enrichment of H3K27 acetylation and H3K4 trimethylation.\n[2] We report that rapid evolution of enhancers is a universal feature of mammalian genomes.\n[3] Most of the recently evolved enhancers arise from ancestral DNA exaptation, rather than lineage-specific expansions of repeat elements.\n[4] In contrast, almost all liver promoters are partially or fully conserved across these species.\n[5] Our data further reveal that recently evolved enhancers can be associated with genes under positive selection, demonstrating the power of this approach for annotating regulatory adaptations in genomic sequences.\n[6] These results provide important insight into the functional genetics underpinning mammalian regulatory evolution."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 352, "doc_id": 14658685, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14658685], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Drosophila supracellular actomyosin structures are found at boundaries in wing imaginal discs.\n\nDocument title: Increased Cell Bond Tension Governs Cell Sorting at the Drosophila Anteroposterior Compartment Boundary\n\nAbstract sentences:\n[0] Subdividing proliferating tissues into compartments is an evolutionarily conserved strategy of animal development [1-6].\n[1] Signals across boundaries between compartments can result in local expression of secreted proteins organizing growth and patterning of tissues [1-6].\n[2] Sharp and straight interfaces between compartments are crucial for stabilizing the position of such organizers and therefore for precise implementation of body plans.\n[3] Maintaining boundaries in proliferating tissues requires mechanisms to counteract cell rearrangements caused by cell division; however, the nature of such mechanisms remains unclear.\n[4] Here we quantitatively analyzed cell morphology and the response to the laser ablation of cell bonds in the vicinity of the anteroposterior compartment boundary in developing Drosophila wings.\n[5] We found that mechanical tension is approximately 2.5-fold increased on cell bonds along this compartment boundary as compared to the remaining tissue.\n[6] Cell bond tension is decreased in the presence of Y-27632 [7], an inhibitor of Rho-kinase whose main effector is Myosin II [8].\n[7] Simulations using a vertex model [9] demonstrate that a 2.5-fold increase in local cell bond tension suffices to guide the rearrangement of cells after cell division to maintain compartment boundaries.\n[8] Our results provide a physical mechanism in which the local increase in Myosin II-dependent cell bond tension directs cell sorting at compartment boundaries."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Our results provide a physical mechanism in which the local increase in Myosin II-dependent cell bond tension directs cell sorting at compartment boundaries.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 355, "doc_id": 12800122, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [12800122, 38380061], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Drosophila supracellular actomyosin structures are found at boundaries in wing imaginal discs.\n\nDocument title: Localization and requirement for Myosin II at the dorsal-ventral compartment boundary of the Drosophila wing.\n\nAbstract sentences:\n[0] As organisms develop, their tissues can become separated into distinct cell populations through the establishment of compartment boundaries.\n[1] Compartment boundaries have been discovered in a wide variety of tissues, but in many cases the molecular mechanisms that separate cells remain poorly understood.\n[2] In the Drosophila wing, a stripe of Notch activation maintains the dorsal-ventral compartment boundary, through a process that depends on the actin cytoskeleton.\n[3] Here, we show that the dorsal-ventral boundary exhibits a distinct accumulation of Myosin II, and that this accumulation is regulated downstream of Notch signaling.\n[4] Conversely, the dorsal-ventral boundary is depleted for the Par-3 homologue Bazooka.\n[5] We further show that mutations in the Myosin heavy chain subunit encoded by zipper can impair dorsal-ventral compartmentalization without affecting anterior-posterior compartmentalization.\n[6] These observations identify a distinct accumulation and requirement for Myosin activity in dorsal-ventral compartmentalization, and suggest a novel mechanism in which contractile tension along an F-actin cable at the compartment boundary contributes to compartmentalization."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Here, we show that the dorsal-ventral boundary exhibits a distinct accumulation of Myosin II, and that this accumulation is regulated downstream of Notch signaling.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 355, "doc_id": 38380061, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [12800122, 38380061], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Dscam1 acts as a hypervariable pattern-recognition receptor for the immune system.\n\nDocument title: AgDscam, a Hypervariable Immunoglobulin Domain-Containing Receptor of the       Anopheles gambiae Innate Immune System     \n\nAbstract sentences:\n[0] Activation of the insect innate immune system is dependent on a limited number of pattern recognition receptors (PRRs) capable of interacting with pathogen-associated molecular pattern.\n[1] Here we report a novel role of an alternatively spliced hypervariable immunoglobulin domain-encoding gene, Dscam, in generating a broad range of PRRs implicated in immune defense in the malaria vector Anopheles gambiae.\n[2] The mosquito Down syndrome cell adhesion molecule gene, AgDscam, has a complex genome organization with 101 exons that can produce over 31,000 potential alternative splice forms with different combinations of adhesive domains and interaction specificities.\n[3] AgDscam responds to infection by producing pathogen challenge-specific splice form repertoires.\n[4] Transient silencing of AgDscam compromises the mosquito's resistance to infections with bacteria and the malaria parasite Plasmodium.\n[5] AgDscam is mediating phagocytosis of bacteria with which it can associate and defend against in a splice form–specific manner.\n[6] AgDscam is a hypervariable PRR of the A. gambiae innate immune system."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Here we report a novel role of an alternatively spliced hypervariable immunoglobulin domain-encoding gene, Dscam, in generating a broad range of PRRs implicated in immune defense in the malaria vector Anopheles gambiae.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 356, "doc_id": 6144337, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [6144337], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Dscam1 acts as a hypervariable pattern-recognition receptor for the immune system.\n\nDocument title: AgDscam, a Hypervariable Immunoglobulin Domain-Containing Receptor of the       Anopheles gambiae Innate Immune System     \n\nAbstract sentences:\n[0] Activation of the insect innate immune system is dependent on a limited number of pattern recognition receptors (PRRs) capable of interacting with pathogen-associated molecular pattern.\n[1] Here we report a novel role of an alternatively spliced hypervariable immunoglobulin domain-encoding gene, Dscam, in generating a broad range of PRRs implicated in immune defense in the malaria vector Anopheles gambiae.\n[2] The mosquito Down syndrome cell adhesion molecule gene, AgDscam, has a complex genome organization with 101 exons that can produce over 31,000 potential alternative splice forms with different combinations of adhesive domains and interaction specificities.\n[3] AgDscam responds to infection by producing pathogen challenge-specific splice form repertoires.\n[4] Transient silencing of AgDscam compromises the mosquito's resistance to infections with bacteria and the malaria parasite Plasmodium.\n[5] AgDscam is mediating phagocytosis of bacteria with which it can associate and defend against in a splice form–specific manner.\n[6] AgDscam is a hypervariable PRR of the A. gambiae innate immune system."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"AgDscam responds to infection by producing pathogen challenge-specific splice form repertoires.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 356, "doc_id": 6144337, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [6144337], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Dscam1 acts as a hypervariable pattern-recognition receptor for the immune system.\n\nDocument title: AgDscam, a Hypervariable Immunoglobulin Domain-Containing Receptor of the       Anopheles gambiae Innate Immune System     \n\nAbstract sentences:\n[0] Activation of the insect innate immune system is dependent on a limited number of pattern recognition receptors (PRRs) capable of interacting with pathogen-associated molecular pattern.\n[1] Here we report a novel role of an alternatively spliced hypervariable immunoglobulin domain-encoding gene, Dscam, in generating a broad range of PRRs implicated in immune defense in the malaria vector Anopheles gambiae.\n[2] The mosquito Down syndrome cell adhesion molecule gene, AgDscam, has a complex genome organization with 101 exons that can produce over 31,000 potential alternative splice forms with different combinations of adhesive domains and interaction specificities.\n[3] AgDscam responds to infection by producing pathogen challenge-specific splice form repertoires.\n[4] Transient silencing of AgDscam compromises the mosquito's resistance to infections with bacteria and the malaria parasite Plasmodium.\n[5] AgDscam is mediating phagocytosis of bacteria with which it can associate and defend against in a splice form–specific manner.\n[6] AgDscam is a hypervariable PRR of the A. gambiae innate immune system."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"AgDscam is mediating phagocytosis of bacteria with which it can associate and defend against in a splice form–specific manner.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 356, "doc_id": 6144337, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [6144337], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Dscam1 acts as a hypervariable pattern-recognition receptor for the immune system.\n\nDocument title: AgDscam, a Hypervariable Immunoglobulin Domain-Containing Receptor of the       Anopheles gambiae Innate Immune System     \n\nAbstract sentences:\n[0] Activation of the insect innate immune system is dependent on a limited number of pattern recognition receptors (PRRs) capable of interacting with pathogen-associated molecular pattern.\n[1] Here we report a novel role of an alternatively spliced hypervariable immunoglobulin domain-encoding gene, Dscam, in generating a broad range of PRRs implicated in immune defense in the malaria vector Anopheles gambiae.\n[2] The mosquito Down syndrome cell adhesion molecule gene, AgDscam, has a complex genome organization with 101 exons that can produce over 31,000 potential alternative splice forms with different combinations of adhesive domains and interaction specificities.\n[3] AgDscam responds to infection by producing pathogen challenge-specific splice form repertoires.\n[4] Transient silencing of AgDscam compromises the mosquito's resistance to infections with bacteria and the malaria parasite Plasmodium.\n[5] AgDscam is mediating phagocytosis of bacteria with which it can associate and defend against in a splice form–specific manner.\n[6] AgDscam is a hypervariable PRR of the A. gambiae innate immune system."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"AgDscam is a hypervariable PRR of the A. gambiae innate immune system.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 356, "doc_id": 6144337, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [6144337], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: During non-homologous end joining, the ligation step is not as tolerant of disrepairs and other distortions when joining 3' of strand breaks as compared to 5' strand breaks.\n\nDocument title: The fidelity of the ligation step determines how ends are resolved during Nonhomologous end joining\n\nAbstract sentences:\n[0] Nonhomologous end joining (NHEJ) can effectively resolve chromosome breaks despite diverse end structures; however, it is unclear how the steps employed for resolution are determined.\n[1] We sought to address this question by analysing cellular NHEJ of ends with systematically mispaired and damaged termini.\n[2] We show NHEJ is uniquely proficient at bypassing subtle terminal mispairs and radiomimetic damage by direct ligation.\n[3] Nevertheless, bypass ability varies widely, with increases in mispair severity gradually reducing bypass products from 85 to 6%.\n[4] End-processing by nucleases and polymerases is increased to compensate, although paths with the fewest number of steps to generate a substrate suitable for ligation are favoured.\n[5] Thus, both the frequency and nature of end processing are tailored to meet the needs of the ligation step.\n[6] We propose a model where the ligase organizes all steps during NHEJ within the stable paired-end complex to limit end processing and associated errors."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 357, "doc_id": 18111172, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [18111172], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: During non-homologous end joining, the ligation step is not as tolerant of disrepairs and other distortions when joining 5' of strand breaks as compared to 3' strand breaks.\n\nDocument title: The fidelity of the ligation step determines how ends are resolved during Nonhomologous end joining\n\nAbstract sentences:\n[0] Nonhomologous end joining (NHEJ) can effectively resolve chromosome breaks despite diverse end structures; however, it is unclear how the steps employed for resolution are determined.\n[1] We sought to address this question by analysing cellular NHEJ of ends with systematically mispaired and damaged termini.\n[2] We show NHEJ is uniquely proficient at bypassing subtle terminal mispairs and radiomimetic damage by direct ligation.\n[3] Nevertheless, bypass ability varies widely, with increases in mispair severity gradually reducing bypass products from 85 to 6%.\n[4] End-processing by nucleases and polymerases is increased to compensate, although paths with the fewest number of steps to generate a substrate suitable for ligation are favoured.\n[5] Thus, both the frequency and nature of end processing are tailored to meet the needs of the ligation step.\n[6] We propose a model where the ligase organizes all steps during NHEJ within the stable paired-end complex to limit end processing and associated errors."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 358, "doc_id": 18111172, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [18111172], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: During the primary early antibody response activated B cells migrate toward the inner-and outer follicular areas where oxysterol accumulation is generated by stromal cells.\n\nDocument title: Finding the right niche: B-cell migration in the early phases of T-dependent antibody responses.\n\nAbstract sentences:\n[0] Humoral immune responses depend on B cells encountering antigen, interacting with helper T cells, proliferating and differentiating into low-affinity plasma cells or, after organizing into a germinal center (GC), high-affinity plasma cells and memory B cells.\n[1] Remarkably, each of these events occurs in association with distinct stromal cells in separate subcompartments of the lymphoid tissue.\n[2] B cells must migrate from niche to niche in a rapid and highly regulated manner to successfully mount a response.\n[3] The chemokine, CXCL13, plays a central role in guiding B cells to follicles whereas T-zone chemokines guide activated B cells to the T zone.\n[4] Sphingosine-1-phosphate (S1P) promotes cell egress from the tissue, as well as marginal-zone B-cell positioning in the spleen.\n[5] Recent studies have identified a role for the orphan receptor, EBV-induced molecule 2 (EBI2; GPR183), in guiding activated B cells to inter and outer follicular niche(s) and down-regulation of this receptor is essential for organizing cells into GCs.\n[6] In this review, we discuss current understanding of the roles played by chemokines, S1P and EBI2 in the migration events that underlie humoral immune responses."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 361, "doc_id": 38587347, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [38587347], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: EG7 tumors can be killed by systemic oxaliplatin primed CD8+ T cells from the tumor-draining lymph node cells.\n\nDocument title: Activation of the NLRP3 inflammasome in dendritic cells induces IL-1β–dependent adaptive immunity against tumors\n\nAbstract sentences:\n[0] The therapeutic efficacy of anticancer chemotherapies may depend on dendritic cells (DCs), which present antigens from dying cancer cells to prime tumor-specific interferon-γ (IFN-γ)–producing T lymphocytes.\n[1] Here we show that dying tumor cells release ATP, which then acts on P2X7 purinergic receptors from DCs and triggers the NOD-like receptor family, pyrin domain containing-3 protein (NLRP3)-dependent caspase-1 activation complex ('inflammasome'), allowing for the secretion of interleukin-1β (IL-1β).\n[2] The priming of IFN-γ–producing CD8+ T cells by dying tumor cells fails in the absence of a functional IL-1 receptor 1 and in Nlpr3-deficient (Nlrp3−/−) or caspase-1–deficient (Casp-1−/−) mice unless exogenous IL-1β is provided.\n[3] Accordingly, anticancer chemotherapy turned out to be inefficient against tumors established in purinergic receptor P2rx7−/− or Nlrp3−/− or Casp1−/− hosts.\n[4] Anthracycline-treated individuals with breast cancer carrying a loss-of-function allele of P2RX7 developed metastatic disease more rapidly than individuals bearing the normal allele.\n[5] These results indicate that the NLRP3 inflammasome links the innate and adaptive immune responses against dying tumor cells."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 363, "doc_id": 5386514, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [5386514], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: EGR2 is important to myelination of the peripheral nervous system.\n\nDocument title: The Transcription Factors Egr2 and Egr3 Are Essential for the Control of Inflammation and Antigen-Induced Proliferation of B and T Cells\n\nAbstract sentences:\n[0] Lymphocytes provide optimal responses against pathogens with minimal inflammatory pathology.\n[1] However, the intrinsic mechanisms regulating these responses are unknown.\n[2] Here, we report that deletion of both transcription factors Egr2 and Egr3 in lymphocytes resulted in a lethal autoimmune syndrome with excessive serum proinflammatory cytokines but also impaired antigen receptor-induced proliferation of B and T cells.\n[3] Egr2- and Egr3-defective B and T cells had hyperactive signal transducer and activator of transcription-1 (STAT1) and STAT3 while antigen receptor-induced activation of transcription factor AP-1 was severely impaired.\n[4] We discovered that Egr2 and/or Egr3 directly induced expression of suppressor of cytokine signaling-1 (SOCS1) and SOCS3, inhibitors of STAT1 and STAT3, and also blocked the function of Batf, an AP-1 inhibitor, in B and T cells.\n[5] Thus, Egr2 and Egr3 regulate B and T cell function in adaptive immune responses and homeostasis by promoting antigen receptor signaling and controlling inflammation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 364, "doc_id": 1550937, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [1550937], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: ER-localized phosphatase Sac1 processes PI4P through coordination with OSBP and the endosome-localized protein sorting nexin 2.\n\nDocument title: Endosome-ER Contacts Control Actin Nucleation and Retromer Function through VAP-Dependent Regulation of PI4P\n\nAbstract sentences:\n[0] VAP (VAPA and VAPB) is an evolutionarily conserved endoplasmic reticulum (ER)-anchored protein that helps generate tethers between the ER and other membranes through which lipids are exchanged across adjacent bilayers.\n[1] Here, we report that by regulating PI4P levels on endosomes, VAP affects WASH-dependent actin nucleation on these organelles and the function of the retromer, a protein coat responsible for endosome-to-Golgi traffic.\n[2] VAP is recruited to retromer budding sites on endosomes via an interaction with the retromer SNX2 subunit.\n[3] Cells lacking VAP accumulate high levels of PI4P, actin comets, and trans-Golgi proteins on endosomes.\n[4] Such defects are mimicked by downregulation of OSBP, a VAP interactor and PI4P transporter that participates in VAP-dependent ER-endosomes tethers.\n[5] These results reveal a role of PI4P in retromer-/WASH-dependent budding from endosomes.\n[6] Collectively, our data show how the ER can control budding dynamics and association with the cytoskeleton of another membrane by direct contacts leading to bilayer lipid modifications."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 365, "doc_id": 600437, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [600437], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: ERAP1 SNPs are epistatic to HLA alleles for ankylosing spondylitis.\n\nDocument title: Major histocompatibility complex associations of ankylosing spondylitis are complex and involve further epistasis with ERAP1\n\nAbstract sentences:\n[0] Ankylosing spondylitis (AS) is a common, highly heritable, inflammatory arthritis for which HLA-B*27 is the major genetic risk factor, although its role in the aetiology of AS remains elusive.\n[1] To better understand the genetic basis of the MHC susceptibility loci, we genotyped 7,264 MHC SNPs in 22,647 AS cases and controls of European descent.\n[2] We impute SNPs, classical HLA alleles and amino-acid residues within HLA proteins, and tested these for association to AS status.\n[3] Here we show that in addition to effects due to HLA-B*27 alleles, several other HLA-B alleles also affect susceptibility.\n[4] After controlling for the associated haplotypes in HLA-B, we observe independent associations with variants in the HLA-A, HLA-DPB1 and HLA-DRB1 loci.\n[5] We also demonstrate that the ERAP1 SNP rs30187 association is not restricted only to carriers of HLA-B*27 but also found in HLA-B*40:01 carriers independently of HLA-B*27 genotype."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"We also demonstrate that the ERAP1 SNP rs30187 association is not restricted only to carriers of HLA-B*27 but also found in HLA-B*40:01 carriers independently of HLA-B*27 genotype.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 366, "doc_id": 13956305, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [13956305], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Early patent ductus ateriosus (PDA) screening decreases in-hospital mortality.\n\nDocument title: Association Between Early Screening for Patent Ductus Arteriosus and In-Hospital Mortality Among Extremely Preterm Infants.\n\nAbstract sentences:\n[0] IMPORTANCE There is currently no consensus for the screening and treatment of patent ductus arteriosus (PDA) in extremely preterm infants.\n[1] Less pharmacological closure and more supportive management have been observed without evidence to support these changes.\n[2] OBJECTIVE To evaluate the association between early screening echocardiography for PDA and in-hospital mortality.\n[3] DESIGN, SETTING, AND PARTICIPANTS Comparison of screened and not screened preterm infants enrolled in the EPIPAGE 2 national prospective population-based cohort study that included all preterm infants born at less than 29 weeks of gestation and hospitalized in 68 neonatal intensive care units in France from April through December 2011.\n[4] Two main analyses were performed to adjust for potential selection bias, one using propensity score matching and one using neonatal unit preference for early screening echocardiography as an instrumental variable.\n[5] EXPOSURES Early screening echocardiography before day 3 of life.\n[6] MAIN OUTCOMES AND MEASURES The primary outcome was death between day 3 and discharge.\n[7] The secondary outcomes were major neonatal morbidities (pulmonary hemorrhage, severe bronchopulmonary dysplasia, severe cerebral lesions, and necrotizing enterocolitis).\n[8] RESULTS Among the 1513 preterm infants with data available to determine exposure, 847 were screened for PDA and 666 were not; 605 infants from each group could be paired.\n[9] Exposed infants were treated for PDA more frequently during their hospitalization than nonexposed infants (55.1% vs 43.1%; odds ratio [OR], 1.62 [95% CI, 1.31 to 2.00]; absolute risk reduction [ARR] in events per 100 infants, -12.0 [95% CI, -17.3 to -6.7).\n[10] Exposed infants had a lower hospital death rate (14.2% vs 18.5% ; OR, 0.73 [95% CI, 0.54 to 0.98]; ARR, 4.3 [95% CI, 0.3 to 8.3]) and a lower rate of pulmonary hemorrhage (5.6% vs 8.9%; OR, 0.60 [95% CI, 0.38 to 0.95]; ARR, 3.3 [95% CI, 0.4 to 6.3]).\n[11] No differences in rates of necrotizing enterocolitis, severe bronchopulmonary dysplasia, or severe cerebral lesions were observed.\n[12] In the overall cohort, instrumental variable analysis yielded an adjusted OR for in-hospital mortality of 0.62 [95% CI, 0.37 to 1.04].\n[13] CONCLUSIONS AND RELEVANCE In this national population-based cohort of extremely preterm infants, screening echocardiography before day 3 of life was associated with lower in-hospital mortality and likelihood of pulmonary hemorrhage but not with differences in necrotizing enterocolitis, severe bronchopulmonary dysplasia, or severe cerebral lesions.\n[14] However, results of the instrumental variable analysis leave some ambiguity in the interpretation, and longer-term evaluation is needed to provide clarity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Exposed infants had a lower hospital death rate (14.2% vs 18.5% ; OR, 0.73 [95% CI, 0.54 to 0.98]; ARR, 4.3 [95% CI, 0.3 to 8.3]) and a lower rate of pulmonary hemorrhage (5.6% vs 8.9%; OR, 0.60 [95% CI, 0.38 to 0.95]; ARR, 3.3 [95% CI, 0.4 to 6.3]).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 367, "doc_id": 27099731, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [27099731], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Early patent ductus ateriosus (PDA) screening decreases in-hospital mortality.\n\nDocument title: Association Between Early Screening for Patent Ductus Arteriosus and In-Hospital Mortality Among Extremely Preterm Infants.\n\nAbstract sentences:\n[0] IMPORTANCE There is currently no consensus for the screening and treatment of patent ductus arteriosus (PDA) in extremely preterm infants.\n[1] Less pharmacological closure and more supportive management have been observed without evidence to support these changes.\n[2] OBJECTIVE To evaluate the association between early screening echocardiography for PDA and in-hospital mortality.\n[3] DESIGN, SETTING, AND PARTICIPANTS Comparison of screened and not screened preterm infants enrolled in the EPIPAGE 2 national prospective population-based cohort study that included all preterm infants born at less than 29 weeks of gestation and hospitalized in 68 neonatal intensive care units in France from April through December 2011.\n[4] Two main analyses were performed to adjust for potential selection bias, one using propensity score matching and one using neonatal unit preference for early screening echocardiography as an instrumental variable.\n[5] EXPOSURES Early screening echocardiography before day 3 of life.\n[6] MAIN OUTCOMES AND MEASURES The primary outcome was death between day 3 and discharge.\n[7] The secondary outcomes were major neonatal morbidities (pulmonary hemorrhage, severe bronchopulmonary dysplasia, severe cerebral lesions, and necrotizing enterocolitis).\n[8] RESULTS Among the 1513 preterm infants with data available to determine exposure, 847 were screened for PDA and 666 were not; 605 infants from each group could be paired.\n[9] Exposed infants were treated for PDA more frequently during their hospitalization than nonexposed infants (55.1% vs 43.1%; odds ratio [OR], 1.62 [95% CI, 1.31 to 2.00]; absolute risk reduction [ARR] in events per 100 infants, -12.0 [95% CI, -17.3 to -6.7).\n[10] Exposed infants had a lower hospital death rate (14.2% vs 18.5% ; OR, 0.73 [95% CI, 0.54 to 0.98]; ARR, 4.3 [95% CI, 0.3 to 8.3]) and a lower rate of pulmonary hemorrhage (5.6% vs 8.9%; OR, 0.60 [95% CI, 0.38 to 0.95]; ARR, 3.3 [95% CI, 0.4 to 6.3]).\n[11] No differences in rates of necrotizing enterocolitis, severe bronchopulmonary dysplasia, or severe cerebral lesions were observed.\n[12] In the overall cohort, instrumental variable analysis yielded an adjusted OR for in-hospital mortality of 0.62 [95% CI, 0.37 to 1.04].\n[13] CONCLUSIONS AND RELEVANCE In this national population-based cohort of extremely preterm infants, screening echocardiography before day 3 of life was associated with lower in-hospital mortality and likelihood of pulmonary hemorrhage but not with differences in necrotizing enterocolitis, severe bronchopulmonary dysplasia, or severe cerebral lesions.\n[14] However, results of the instrumental variable analysis leave some ambiguity in the interpretation, and longer-term evaluation is needed to provide clarity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"CONCLUSIONS AND RELEVANCE In this national population-based cohort of extremely preterm infants, screening echocardiography before day 3 of life was associated with lower in-hospital mortality and likelihood of pulmonary hemorrhage but not with differences in necrotizing enterocolitis, severe bronchopulmonary dysplasia, or severe cerebral lesions.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 367, "doc_id": 27099731, "label": "SUPPORTS", "evidence_sentence_ids": [13], "cited_doc_ids": [27099731], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Early patent ductus ateriosus (PDA) screening increases in-hospital mortality.\n\nDocument title: Association Between Early Screening for Patent Ductus Arteriosus and In-Hospital Mortality Among Extremely Preterm Infants.\n\nAbstract sentences:\n[0] IMPORTANCE There is currently no consensus for the screening and treatment of patent ductus arteriosus (PDA) in extremely preterm infants.\n[1] Less pharmacological closure and more supportive management have been observed without evidence to support these changes.\n[2] OBJECTIVE To evaluate the association between early screening echocardiography for PDA and in-hospital mortality.\n[3] DESIGN, SETTING, AND PARTICIPANTS Comparison of screened and not screened preterm infants enrolled in the EPIPAGE 2 national prospective population-based cohort study that included all preterm infants born at less than 29 weeks of gestation and hospitalized in 68 neonatal intensive care units in France from April through December 2011.\n[4] Two main analyses were performed to adjust for potential selection bias, one using propensity score matching and one using neonatal unit preference for early screening echocardiography as an instrumental variable.\n[5] EXPOSURES Early screening echocardiography before day 3 of life.\n[6] MAIN OUTCOMES AND MEASURES The primary outcome was death between day 3 and discharge.\n[7] The secondary outcomes were major neonatal morbidities (pulmonary hemorrhage, severe bronchopulmonary dysplasia, severe cerebral lesions, and necrotizing enterocolitis).\n[8] RESULTS Among the 1513 preterm infants with data available to determine exposure, 847 were screened for PDA and 666 were not; 605 infants from each group could be paired.\n[9] Exposed infants were treated for PDA more frequently during their hospitalization than nonexposed infants (55.1% vs 43.1%; odds ratio [OR], 1.62 [95% CI, 1.31 to 2.00]; absolute risk reduction [ARR] in events per 100 infants, -12.0 [95% CI, -17.3 to -6.7).\n[10] Exposed infants had a lower hospital death rate (14.2% vs 18.5% ; OR, 0.73 [95% CI, 0.54 to 0.98]; ARR, 4.3 [95% CI, 0.3 to 8.3]) and a lower rate of pulmonary hemorrhage (5.6% vs 8.9%; OR, 0.60 [95% CI, 0.38 to 0.95]; ARR, 3.3 [95% CI, 0.4 to 6.3]).\n[11] No differences in rates of necrotizing enterocolitis, severe bronchopulmonary dysplasia, or severe cerebral lesions were observed.\n[12] In the overall cohort, instrumental variable analysis yielded an adjusted OR for in-hospital mortality of 0.62 [95% CI, 0.37 to 1.04].\n[13] CONCLUSIONS AND RELEVANCE In this national population-based cohort of extremely preterm infants, screening echocardiography before day 3 of life was associated with lower in-hospital mortality and likelihood of pulmonary hemorrhage but not with differences in necrotizing enterocolitis, severe bronchopulmonary dysplasia, or severe cerebral lesions.\n[14] However, results of the instrumental variable analysis leave some ambiguity in the interpretation, and longer-term evaluation is needed to provide clarity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Exposed infants had a lower hospital death rate (14.2% vs 18.5% ; OR, 0.73 [95% CI, 0.54 to 0.98]; ARR, 4.3 [95% CI, 0.3 to 8.3]) and a lower rate of pulmonary hemorrhage (5.6% vs 8.9%; OR, 0.60 [95% CI, 0.38 to 0.95]; ARR, 3.3 [95% CI, 0.4 to 6.3]).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 368, "doc_id": 27099731, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [27099731], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Early patent ductus ateriosus (PDA) screening increases in-hospital mortality.\n\nDocument title: Association Between Early Screening for Patent Ductus Arteriosus and In-Hospital Mortality Among Extremely Preterm Infants.\n\nAbstract sentences:\n[0] IMPORTANCE There is currently no consensus for the screening and treatment of patent ductus arteriosus (PDA) in extremely preterm infants.\n[1] Less pharmacological closure and more supportive management have been observed without evidence to support these changes.\n[2] OBJECTIVE To evaluate the association between early screening echocardiography for PDA and in-hospital mortality.\n[3] DESIGN, SETTING, AND PARTICIPANTS Comparison of screened and not screened preterm infants enrolled in the EPIPAGE 2 national prospective population-based cohort study that included all preterm infants born at less than 29 weeks of gestation and hospitalized in 68 neonatal intensive care units in France from April through December 2011.\n[4] Two main analyses were performed to adjust for potential selection bias, one using propensity score matching and one using neonatal unit preference for early screening echocardiography as an instrumental variable.\n[5] EXPOSURES Early screening echocardiography before day 3 of life.\n[6] MAIN OUTCOMES AND MEASURES The primary outcome was death between day 3 and discharge.\n[7] The secondary outcomes were major neonatal morbidities (pulmonary hemorrhage, severe bronchopulmonary dysplasia, severe cerebral lesions, and necrotizing enterocolitis).\n[8] RESULTS Among the 1513 preterm infants with data available to determine exposure, 847 were screened for PDA and 666 were not; 605 infants from each group could be paired.\n[9] Exposed infants were treated for PDA more frequently during their hospitalization than nonexposed infants (55.1% vs 43.1%; odds ratio [OR], 1.62 [95% CI, 1.31 to 2.00]; absolute risk reduction [ARR] in events per 100 infants, -12.0 [95% CI, -17.3 to -6.7).\n[10] Exposed infants had a lower hospital death rate (14.2% vs 18.5% ; OR, 0.73 [95% CI, 0.54 to 0.98]; ARR, 4.3 [95% CI, 0.3 to 8.3]) and a lower rate of pulmonary hemorrhage (5.6% vs 8.9%; OR, 0.60 [95% CI, 0.38 to 0.95]; ARR, 3.3 [95% CI, 0.4 to 6.3]).\n[11] No differences in rates of necrotizing enterocolitis, severe bronchopulmonary dysplasia, or severe cerebral lesions were observed.\n[12] In the overall cohort, instrumental variable analysis yielded an adjusted OR for in-hospital mortality of 0.62 [95% CI, 0.37 to 1.04].\n[13] CONCLUSIONS AND RELEVANCE In this national population-based cohort of extremely preterm infants, screening echocardiography before day 3 of life was associated with lower in-hospital mortality and likelihood of pulmonary hemorrhage but not with differences in necrotizing enterocolitis, severe bronchopulmonary dysplasia, or severe cerebral lesions.\n[14] However, results of the instrumental variable analysis leave some ambiguity in the interpretation, and longer-term evaluation is needed to provide clarity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"CONCLUSIONS AND RELEVANCE In this national population-based cohort of extremely preterm infants, screening echocardiography before day 3 of life was associated with lower in-hospital mortality and likelihood of pulmonary hemorrhage but not with differences in necrotizing enterocolitis, severe bronchopulmonary dysplasia, or severe cerebral lesions.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 368, "doc_id": 27099731, "label": "CONTRADICTS", "evidence_sentence_ids": [13], "cited_doc_ids": [27099731], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ectopic expression of Sall4, Nanog, Esrrb, and Lin28 generates induced pluripotent stem cells from mouse embryonic fibroblasts more efficiently than other factor combinations.\n\nDocument title: The developmental potential of iPSCs is greatly influenced by reprogramming factor selection.\n\nAbstract sentences:\n[0] Induced pluripotent stem cells (iPSCs) are commonly generated by transduction of Oct4, Sox2, Klf4, and Myc (OSKM) into cells.\n[1] Although iPSCs are pluripotent, they frequently exhibit high variation in terms of quality, as measured in mice by chimera contribution and tetraploid complementation.\n[2] Reliably high-quality iPSCs will be needed for future therapeutic applications.\n[3] Here, we show that one major determinant of iPSC quality is the combination of reprogramming factors used.\n[4] Based on tetraploid complementation, we found that ectopic expression of Sall4, Nanog, Esrrb, and Lin28 (SNEL) in mouse embryonic fibroblasts (MEFs) generated high-quality iPSCs more efficiently than other combinations of factors including OSKM.\n[5] Although differentially methylated regions, transcript number of master regulators, establishment of specific superenhancers, and global aneuploidy were comparable between high- and low-quality lines, aberrant gene expression, trisomy of chromosome 8, and abnormal H2A.X deposition were distinguishing features that could potentially also be applicable to human."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Based on tetraploid complementation, we found that ectopic expression of Sall4, Nanog, Esrrb, and Lin28 (SNEL) in mouse embryonic fibroblasts (MEFs) generated high-quality iPSCs more efficiently than other combinations of factors including OSKM.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 369, "doc_id": 6826100, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [6826100], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Egr2 regulates the homeostasis of B and T cells.\n\nDocument title: The Transcription Factors Egr2 and Egr3 Are Essential for the Control of Inflammation and Antigen-Induced Proliferation of B and T Cells\n\nAbstract sentences:\n[0] Lymphocytes provide optimal responses against pathogens with minimal inflammatory pathology.\n[1] However, the intrinsic mechanisms regulating these responses are unknown.\n[2] Here, we report that deletion of both transcription factors Egr2 and Egr3 in lymphocytes resulted in a lethal autoimmune syndrome with excessive serum proinflammatory cytokines but also impaired antigen receptor-induced proliferation of B and T cells.\n[3] Egr2- and Egr3-defective B and T cells had hyperactive signal transducer and activator of transcription-1 (STAT1) and STAT3 while antigen receptor-induced activation of transcription factor AP-1 was severely impaired.\n[4] We discovered that Egr2 and/or Egr3 directly induced expression of suppressor of cytokine signaling-1 (SOCS1) and SOCS3, inhibitors of STAT1 and STAT3, and also blocked the function of Batf, an AP-1 inhibitor, in B and T cells.\n[5] Thus, Egr2 and Egr3 regulate B and T cell function in adaptive immune responses and homeostasis by promoting antigen receptor signaling and controlling inflammation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here, we report that deletion of both transcription factors Egr2 and Egr3 in lymphocytes resulted in a lethal autoimmune syndrome with excessive serum proinflammatory cytokines but also impaired antigen receptor-induced proliferation of B and T cells.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 370, "doc_id": 1550937, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [1550937], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Egr2 regulates the homeostasis of B and T cells.\n\nDocument title: The Transcription Factors Egr2 and Egr3 Are Essential for the Control of Inflammation and Antigen-Induced Proliferation of B and T Cells\n\nAbstract sentences:\n[0] Lymphocytes provide optimal responses against pathogens with minimal inflammatory pathology.\n[1] However, the intrinsic mechanisms regulating these responses are unknown.\n[2] Here, we report that deletion of both transcription factors Egr2 and Egr3 in lymphocytes resulted in a lethal autoimmune syndrome with excessive serum proinflammatory cytokines but also impaired antigen receptor-induced proliferation of B and T cells.\n[3] Egr2- and Egr3-defective B and T cells had hyperactive signal transducer and activator of transcription-1 (STAT1) and STAT3 while antigen receptor-induced activation of transcription factor AP-1 was severely impaired.\n[4] We discovered that Egr2 and/or Egr3 directly induced expression of suppressor of cytokine signaling-1 (SOCS1) and SOCS3, inhibitors of STAT1 and STAT3, and also blocked the function of Batf, an AP-1 inhibitor, in B and T cells.\n[5] Thus, Egr2 and Egr3 regulate B and T cell function in adaptive immune responses and homeostasis by promoting antigen receptor signaling and controlling inflammation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Egr2- and Egr3-defective B and T cells had hyperactive signal transducer and activator of transcription-1 (STAT1) and STAT3 while antigen receptor-induced activation of transcription factor AP-1 was severely impaired.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 370, "doc_id": 1550937, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [1550937], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Egr2 regulates the homeostasis of B and T cells.\n\nDocument title: The Transcription Factors Egr2 and Egr3 Are Essential for the Control of Inflammation and Antigen-Induced Proliferation of B and T Cells\n\nAbstract sentences:\n[0] Lymphocytes provide optimal responses against pathogens with minimal inflammatory pathology.\n[1] However, the intrinsic mechanisms regulating these responses are unknown.\n[2] Here, we report that deletion of both transcription factors Egr2 and Egr3 in lymphocytes resulted in a lethal autoimmune syndrome with excessive serum proinflammatory cytokines but also impaired antigen receptor-induced proliferation of B and T cells.\n[3] Egr2- and Egr3-defective B and T cells had hyperactive signal transducer and activator of transcription-1 (STAT1) and STAT3 while antigen receptor-induced activation of transcription factor AP-1 was severely impaired.\n[4] We discovered that Egr2 and/or Egr3 directly induced expression of suppressor of cytokine signaling-1 (SOCS1) and SOCS3, inhibitors of STAT1 and STAT3, and also blocked the function of Batf, an AP-1 inhibitor, in B and T cells.\n[5] Thus, Egr2 and Egr3 regulate B and T cell function in adaptive immune responses and homeostasis by promoting antigen receptor signaling and controlling inflammation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"We discovered that Egr2 and/or Egr3 directly induced expression of suppressor of cytokine signaling-1 (SOCS1) and SOCS3, inhibitors of STAT1 and STAT3, and also blocked the function of Batf, an AP-1 inhibitor, in B and T cells.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 370, "doc_id": 1550937, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [1550937], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Egr2 regulates the homeostasis of B and T cells.\n\nDocument title: The Transcription Factors Egr2 and Egr3 Are Essential for the Control of Inflammation and Antigen-Induced Proliferation of B and T Cells\n\nAbstract sentences:\n[0] Lymphocytes provide optimal responses against pathogens with minimal inflammatory pathology.\n[1] However, the intrinsic mechanisms regulating these responses are unknown.\n[2] Here, we report that deletion of both transcription factors Egr2 and Egr3 in lymphocytes resulted in a lethal autoimmune syndrome with excessive serum proinflammatory cytokines but also impaired antigen receptor-induced proliferation of B and T cells.\n[3] Egr2- and Egr3-defective B and T cells had hyperactive signal transducer and activator of transcription-1 (STAT1) and STAT3 while antigen receptor-induced activation of transcription factor AP-1 was severely impaired.\n[4] We discovered that Egr2 and/or Egr3 directly induced expression of suppressor of cytokine signaling-1 (SOCS1) and SOCS3, inhibitors of STAT1 and STAT3, and also blocked the function of Batf, an AP-1 inhibitor, in B and T cells.\n[5] Thus, Egr2 and Egr3 regulate B and T cell function in adaptive immune responses and homeostasis by promoting antigen receptor signaling and controlling inflammation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Thus, Egr2 and Egr3 regulate B and T cell function in adaptive immune responses and homeostasis by promoting antigen receptor signaling and controlling inflammation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 370, "doc_id": 1550937, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [1550937], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Egr3 regulates the homeostasis of B and T cells.\n\nDocument title: The Transcription Factors Egr2 and Egr3 Are Essential for the Control of Inflammation and Antigen-Induced Proliferation of B and T Cells\n\nAbstract sentences:\n[0] Lymphocytes provide optimal responses against pathogens with minimal inflammatory pathology.\n[1] However, the intrinsic mechanisms regulating these responses are unknown.\n[2] Here, we report that deletion of both transcription factors Egr2 and Egr3 in lymphocytes resulted in a lethal autoimmune syndrome with excessive serum proinflammatory cytokines but also impaired antigen receptor-induced proliferation of B and T cells.\n[3] Egr2- and Egr3-defective B and T cells had hyperactive signal transducer and activator of transcription-1 (STAT1) and STAT3 while antigen receptor-induced activation of transcription factor AP-1 was severely impaired.\n[4] We discovered that Egr2 and/or Egr3 directly induced expression of suppressor of cytokine signaling-1 (SOCS1) and SOCS3, inhibitors of STAT1 and STAT3, and also blocked the function of Batf, an AP-1 inhibitor, in B and T cells.\n[5] Thus, Egr2 and Egr3 regulate B and T cell function in adaptive immune responses and homeostasis by promoting antigen receptor signaling and controlling inflammation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here, we report that deletion of both transcription factors Egr2 and Egr3 in lymphocytes resulted in a lethal autoimmune syndrome with excessive serum proinflammatory cytokines but also impaired antigen receptor-induced proliferation of B and T cells.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 371, "doc_id": 1550937, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [1550937], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Egr3 regulates the homeostasis of B and T cells.\n\nDocument title: The Transcription Factors Egr2 and Egr3 Are Essential for the Control of Inflammation and Antigen-Induced Proliferation of B and T Cells\n\nAbstract sentences:\n[0] Lymphocytes provide optimal responses against pathogens with minimal inflammatory pathology.\n[1] However, the intrinsic mechanisms regulating these responses are unknown.\n[2] Here, we report that deletion of both transcription factors Egr2 and Egr3 in lymphocytes resulted in a lethal autoimmune syndrome with excessive serum proinflammatory cytokines but also impaired antigen receptor-induced proliferation of B and T cells.\n[3] Egr2- and Egr3-defective B and T cells had hyperactive signal transducer and activator of transcription-1 (STAT1) and STAT3 while antigen receptor-induced activation of transcription factor AP-1 was severely impaired.\n[4] We discovered that Egr2 and/or Egr3 directly induced expression of suppressor of cytokine signaling-1 (SOCS1) and SOCS3, inhibitors of STAT1 and STAT3, and also blocked the function of Batf, an AP-1 inhibitor, in B and T cells.\n[5] Thus, Egr2 and Egr3 regulate B and T cell function in adaptive immune responses and homeostasis by promoting antigen receptor signaling and controlling inflammation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Egr2- and Egr3-defective B and T cells had hyperactive signal transducer and activator of transcription-1 (STAT1) and STAT3 while antigen receptor-induced activation of transcription factor AP-1 was severely impaired.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 371, "doc_id": 1550937, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [1550937], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Egr3 regulates the homeostasis of B and T cells.\n\nDocument title: The Transcription Factors Egr2 and Egr3 Are Essential for the Control of Inflammation and Antigen-Induced Proliferation of B and T Cells\n\nAbstract sentences:\n[0] Lymphocytes provide optimal responses against pathogens with minimal inflammatory pathology.\n[1] However, the intrinsic mechanisms regulating these responses are unknown.\n[2] Here, we report that deletion of both transcription factors Egr2 and Egr3 in lymphocytes resulted in a lethal autoimmune syndrome with excessive serum proinflammatory cytokines but also impaired antigen receptor-induced proliferation of B and T cells.\n[3] Egr2- and Egr3-defective B and T cells had hyperactive signal transducer and activator of transcription-1 (STAT1) and STAT3 while antigen receptor-induced activation of transcription factor AP-1 was severely impaired.\n[4] We discovered that Egr2 and/or Egr3 directly induced expression of suppressor of cytokine signaling-1 (SOCS1) and SOCS3, inhibitors of STAT1 and STAT3, and also blocked the function of Batf, an AP-1 inhibitor, in B and T cells.\n[5] Thus, Egr2 and Egr3 regulate B and T cell function in adaptive immune responses and homeostasis by promoting antigen receptor signaling and controlling inflammation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"We discovered that Egr2 and/or Egr3 directly induced expression of suppressor of cytokine signaling-1 (SOCS1) and SOCS3, inhibitors of STAT1 and STAT3, and also blocked the function of Batf, an AP-1 inhibitor, in B and T cells.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 371, "doc_id": 1550937, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [1550937], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Egr3 regulates the homeostasis of B and T cells.\n\nDocument title: The Transcription Factors Egr2 and Egr3 Are Essential for the Control of Inflammation and Antigen-Induced Proliferation of B and T Cells\n\nAbstract sentences:\n[0] Lymphocytes provide optimal responses against pathogens with minimal inflammatory pathology.\n[1] However, the intrinsic mechanisms regulating these responses are unknown.\n[2] Here, we report that deletion of both transcription factors Egr2 and Egr3 in lymphocytes resulted in a lethal autoimmune syndrome with excessive serum proinflammatory cytokines but also impaired antigen receptor-induced proliferation of B and T cells.\n[3] Egr2- and Egr3-defective B and T cells had hyperactive signal transducer and activator of transcription-1 (STAT1) and STAT3 while antigen receptor-induced activation of transcription factor AP-1 was severely impaired.\n[4] We discovered that Egr2 and/or Egr3 directly induced expression of suppressor of cytokine signaling-1 (SOCS1) and SOCS3, inhibitors of STAT1 and STAT3, and also blocked the function of Batf, an AP-1 inhibitor, in B and T cells.\n[5] Thus, Egr2 and Egr3 regulate B and T cell function in adaptive immune responses and homeostasis by promoting antigen receptor signaling and controlling inflammation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Thus, Egr2 and Egr3 regulate B and T cell function in adaptive immune responses and homeostasis by promoting antigen receptor signaling and controlling inflammation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 371, "doc_id": 1550937, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [1550937], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Eilat virus (EILV) produced in mosquitos elicits rapid and long-lasting neutralizing antibodies in nonhuman primates.\n\nDocument title: A chikungunya fever vaccine utilizing an insect-specific virus platform\n\nAbstract sentences:\n[0] Traditionally, vaccine development involves tradeoffs between immunogenicity and safety.\n[1] Live-attenuated vaccines typically offer rapid and durable immunity but have reduced safety when compared to inactivated vaccines.\n[2] In contrast, the inability of inactivated vaccines to replicate enhances safety at the expense of immunogenicity, often necessitating multiple doses and boosters.\n[3] To overcome these tradeoffs, we developed the insect-specific alphavirus, Eilat virus (EILV), as a vaccine platform.\n[4] To address the chikungunya fever (CHIKF) pandemic, we used an EILV cDNA clone to design a chimeric virus containing the chikungunya virus (CHIKV) structural proteins.\n[5] The recombinant EILV/CHIKV was structurally identical at 10 Å to wild-type CHIKV, as determined by single-particle cryo-electron microscopy, and it mimicked the early stages of CHIKV replication in vertebrate cells from attachment and entry to viral RNA delivery.\n[6] Yet the recombinant virus remained completely defective for productive replication, providing a high degree of safety.\n[7] A single dose of EILV/CHIKV produced in mosquito cells elicited rapid (within 4 d) and long-lasting (>290 d) neutralizing antibodies that provided complete protection in two different mouse models.\n[8] In nonhuman primates, EILV/CHIKV elicited rapid and robust immunity that protected against viremia and telemetrically monitored fever.\n[9] Our EILV platform represents the first structurally native application of an insect-specific virus in preclinical vaccine development and highlights the potential application of such viruses in vaccinology."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7, 8]\nExplanation: Evidence states: \"A single dose of EILV/CHIKV produced in mosquito cells elicited rapid (within 4 d) and long-lasting (>290 d) neutralizing antibodies that provided complete protection in two different mouse models. In nonhuman primates, EILV/CHIKV elicited rapid and robust immunity that protected against viremia and telemetrically monitored fever.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 372, "doc_id": 24922825, "label": "SUPPORTS", "evidence_sentence_ids": [7, 8], "cited_doc_ids": [24922825], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Elevated cell-free mitochondrial DNA levels are associated with mortality.\n\nDocument title: Circulating Mitochondrial DNA in Patients in the ICU as a Marker of Mortality: Derivation and Validation\n\nAbstract sentences:\n[0] BACKGROUND Mitochondrial DNA (mtDNA) is a critical activator of inflammation and the innate immune system.\n[1] However, mtDNA level has not been tested for its role as a biomarker in the intensive care unit (ICU).\n[2] We hypothesized that circulating cell-free mtDNA levels would be associated with mortality and improve risk prediction in ICU patients.\n[3] METHODS AND FINDINGS Analyses of mtDNA levels were performed on blood samples obtained from two prospective observational cohort studies of ICU patients (the Brigham and Women's Hospital Registry of Critical Illness [BWH RoCI, n = 200] and Molecular Epidemiology of Acute Respiratory Distress Syndrome [ME ARDS, n = 243]).\n[4] mtDNA levels in plasma were assessed by measuring the copy number of the NADH dehydrogenase 1 gene using quantitative real-time PCR.\n[5] Medical ICU patients with an elevated mtDNA level (≥3,200 copies/µl plasma) had increased odds of dying within 28 d of ICU admission in both the BWH RoCI (odds ratio [OR] 7.5, 95% CI 3.6-15.8, p = 1×10(-7)) and ME ARDS (OR 8.4, 95% CI 2.9-24.2, p = 9×10(-5)) cohorts, while no evidence for association was noted in non-medical ICU patients.\n[6] The addition of an elevated mtDNA level improved the net reclassification index (NRI) of 28-d mortality among medical ICU patients when added to clinical models in both the BWH RoCI (NRI 79%, standard error 14%, p<1×10(-4)) and ME ARDS (NRI 55%, standard error 20%, p = 0.007) cohorts.\n[7] In the BWH RoCI cohort, those with an elevated mtDNA level had an increased risk of death, even in analyses limited to patients with sepsis or acute respiratory distress syndrome.\n[8] Study limitations include the lack of data elucidating the concise pathological roles of mtDNA in the patients, and the limited numbers of measurements for some of biomarkers.\n[9] CONCLUSIONS Increased mtDNA levels are associated with ICU mortality, and inclusion of mtDNA level improves risk prediction in medical ICU patients.\n[10] Our data suggest that mtDNA could serve as a viable plasma biomarker in medical ICU patients."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Medical ICU patients with an elevated mtDNA level (≥3,200 copies/µl plasma) had increased odds of dying within 28 d of ICU admission in both the BWH RoCI (odds ratio [OR] 7.5, 95% CI 3.6-15.8, p = 1×10(-7)) and ME ARDS (OR 8.4, 95% CI 2.9-24.2, p = 9×10(-5)) cohorts, while no evidence for association was noted in non-medical ICU patients.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 375, "doc_id": 1522647, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [1522647], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Elevated cell-free mitochondrial DNA levels are associated with mortality.\n\nDocument title: Circulating Mitochondrial DNA in Patients in the ICU as a Marker of Mortality: Derivation and Validation\n\nAbstract sentences:\n[0] BACKGROUND Mitochondrial DNA (mtDNA) is a critical activator of inflammation and the innate immune system.\n[1] However, mtDNA level has not been tested for its role as a biomarker in the intensive care unit (ICU).\n[2] We hypothesized that circulating cell-free mtDNA levels would be associated with mortality and improve risk prediction in ICU patients.\n[3] METHODS AND FINDINGS Analyses of mtDNA levels were performed on blood samples obtained from two prospective observational cohort studies of ICU patients (the Brigham and Women's Hospital Registry of Critical Illness [BWH RoCI, n = 200] and Molecular Epidemiology of Acute Respiratory Distress Syndrome [ME ARDS, n = 243]).\n[4] mtDNA levels in plasma were assessed by measuring the copy number of the NADH dehydrogenase 1 gene using quantitative real-time PCR.\n[5] Medical ICU patients with an elevated mtDNA level (≥3,200 copies/µl plasma) had increased odds of dying within 28 d of ICU admission in both the BWH RoCI (odds ratio [OR] 7.5, 95% CI 3.6-15.8, p = 1×10(-7)) and ME ARDS (OR 8.4, 95% CI 2.9-24.2, p = 9×10(-5)) cohorts, while no evidence for association was noted in non-medical ICU patients.\n[6] The addition of an elevated mtDNA level improved the net reclassification index (NRI) of 28-d mortality among medical ICU patients when added to clinical models in both the BWH RoCI (NRI 79%, standard error 14%, p<1×10(-4)) and ME ARDS (NRI 55%, standard error 20%, p = 0.007) cohorts.\n[7] In the BWH RoCI cohort, those with an elevated mtDNA level had an increased risk of death, even in analyses limited to patients with sepsis or acute respiratory distress syndrome.\n[8] Study limitations include the lack of data elucidating the concise pathological roles of mtDNA in the patients, and the limited numbers of measurements for some of biomarkers.\n[9] CONCLUSIONS Increased mtDNA levels are associated with ICU mortality, and inclusion of mtDNA level improves risk prediction in medical ICU patients.\n[10] Our data suggest that mtDNA could serve as a viable plasma biomarker in medical ICU patients."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"In the BWH RoCI cohort, those with an elevated mtDNA level had an increased risk of death, even in analyses limited to patients with sepsis or acute respiratory distress syndrome.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 375, "doc_id": 1522647, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [1522647], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Elevated cell-free mitochondrial DNA levels are associated with mortality.\n\nDocument title: Circulating Mitochondrial DNA in Patients in the ICU as a Marker of Mortality: Derivation and Validation\n\nAbstract sentences:\n[0] BACKGROUND Mitochondrial DNA (mtDNA) is a critical activator of inflammation and the innate immune system.\n[1] However, mtDNA level has not been tested for its role as a biomarker in the intensive care unit (ICU).\n[2] We hypothesized that circulating cell-free mtDNA levels would be associated with mortality and improve risk prediction in ICU patients.\n[3] METHODS AND FINDINGS Analyses of mtDNA levels were performed on blood samples obtained from two prospective observational cohort studies of ICU patients (the Brigham and Women's Hospital Registry of Critical Illness [BWH RoCI, n = 200] and Molecular Epidemiology of Acute Respiratory Distress Syndrome [ME ARDS, n = 243]).\n[4] mtDNA levels in plasma were assessed by measuring the copy number of the NADH dehydrogenase 1 gene using quantitative real-time PCR.\n[5] Medical ICU patients with an elevated mtDNA level (≥3,200 copies/µl plasma) had increased odds of dying within 28 d of ICU admission in both the BWH RoCI (odds ratio [OR] 7.5, 95% CI 3.6-15.8, p = 1×10(-7)) and ME ARDS (OR 8.4, 95% CI 2.9-24.2, p = 9×10(-5)) cohorts, while no evidence for association was noted in non-medical ICU patients.\n[6] The addition of an elevated mtDNA level improved the net reclassification index (NRI) of 28-d mortality among medical ICU patients when added to clinical models in both the BWH RoCI (NRI 79%, standard error 14%, p<1×10(-4)) and ME ARDS (NRI 55%, standard error 20%, p = 0.007) cohorts.\n[7] In the BWH RoCI cohort, those with an elevated mtDNA level had an increased risk of death, even in analyses limited to patients with sepsis or acute respiratory distress syndrome.\n[8] Study limitations include the lack of data elucidating the concise pathological roles of mtDNA in the patients, and the limited numbers of measurements for some of biomarkers.\n[9] CONCLUSIONS Increased mtDNA levels are associated with ICU mortality, and inclusion of mtDNA level improves risk prediction in medical ICU patients.\n[10] Our data suggest that mtDNA could serve as a viable plasma biomarker in medical ICU patients."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"CONCLUSIONS Increased mtDNA levels are associated with ICU mortality, and inclusion of mtDNA level improves risk prediction in medical ICU patients.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 375, "doc_id": 1522647, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [1522647], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Eliminating the last sporadic cases of malaria requires considerable funding.\n\nDocument title: Costs and financial feasibility of malaria elimination\n\nAbstract sentences:\n[0] The marginal costs and benefits of converting malaria programmes from a control to an elimination goal are central to strategic decisions, but empirical evidence is scarce.\n[1] We present a conceptual framework to assess the economics of elimination and analyse a central component of that framework-potential short-term to medium-term financial savings.\n[2] After a review that showed a dearth of existing evidence, the net present value of elimination in five sites was calculated and compared with effective control.\n[3] The probability that elimination would be cost-saving over 50 years ranged from 0% to 42%, with only one site achieving cost-savings in the base case.\n[4] These findings show that financial savings should not be a primary rationale for elimination, but that elimination might still be a worthy investment if total benefits are sufficient to outweigh marginal costs.\n[5] Robust research into these elimination benefits is urgently needed."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 376, "doc_id": 22401061, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [22401061], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Emodin forms hydrogen bonds with residues involved in PGAM1 substrate binding.\n\nDocument title: Tyr26 phosphorylation of PGAM1 provides a metabolic advantage to tumours by stabilizing the active conformation\n\nAbstract sentences:\n[0] How oncogenic signalling coordinates glycolysis and anabolic biosynthesis in cancer cells remains unclear.\n[1] We recently reported that the glycolytic enzyme phosphoglycerate mutase 1 (PGAM1) regulates anabolic biosynthesis by controlling intracellular levels of its substrate 3-phosphoglycerate and product 2-phosphoglycerate.\n[2] Here we report a novel mechanism in which Y26 phosphorylation enhances PGAM1 activation through release of inhibitory E19 that blocks the active site, stabilising cofactor 2,3-bisphosphoglycerate binding and H11 phosphorylation.\n[3] We also report the crystal structure of H11-phosphorylated PGAM1 and find that phospho-H11 activates PGAM1 at least in part by promoting substrate 3-phosphoglycerate binding.\n[4] Moreover, Y26 phosphorylation of PGAM1 is common in human cancer cells and contributes to regulation of 3-phosphoglycerate and 2-phosphoglycerate levels, promoting cancer cell proliferation and tumour growth.\n[5] As PGAM1 is a negative transcriptional target of TP53, and is therefore commonly upregulated in human cancers, these findings suggest that Y26 phosphorylation represents an additional acute mechanism underlying phosphoglycerate mutase 1 upregulation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 377, "doc_id": 18810195, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [18810195], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Energy balance requires hypothalamic glutamate neurotransmission.\n\nDocument title: Glutamate mediates the function of melanocortin receptor 4 on Sim1 neurons in body weight regulation.\n\nAbstract sentences:\n[0] The melanocortin receptor 4 (MC4R) is a well-established mediator of body weight homeostasis.\n[1] However, the neurotransmitter(s) that mediate MC4R function remain largely unknown; as a result, little is known about the second-order neurons of the MC4R neural pathway.\n[2] Single-minded 1 (Sim1)-expressing brain regions, which include the paraventricular nucleus of hypothalamus (PVH), represent key brain sites that mediate melanocortin action.\n[3] We conditionally restored MC4R expression in Sim1 neurons in the background of Mc4r-null mice.\n[4] The restoration dramatically reduced obesity in Mc4r-null mice.\n[5] The anti-obesity effect was completely reversed by selective disruption of glutamate release from those same Sim1 neurons.\n[6] The reversal was caused by lower energy expenditure and hyperphagia.\n[7] Corroboratively, selective disruption of glutamate release from adult PVH neurons led to rapid obesity development via reduced energy expenditure and hyperphagia.\n[8] Thus, this study establishes glutamate as the primary neurotransmitter that mediates MC4Rs on Sim1 neurons in body weight regulation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"The anti-obesity effect was completely reversed by selective disruption of glutamate release from those same Sim1 neurons.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 378, "doc_id": 45154987, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [45154987, 10534299, 11886686, 25007443, 17150648], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Energy balance requires hypothalamic glutamate neurotransmission.\n\nDocument title: Glutamate mediates the function of melanocortin receptor 4 on Sim1 neurons in body weight regulation.\n\nAbstract sentences:\n[0] The melanocortin receptor 4 (MC4R) is a well-established mediator of body weight homeostasis.\n[1] However, the neurotransmitter(s) that mediate MC4R function remain largely unknown; as a result, little is known about the second-order neurons of the MC4R neural pathway.\n[2] Single-minded 1 (Sim1)-expressing brain regions, which include the paraventricular nucleus of hypothalamus (PVH), represent key brain sites that mediate melanocortin action.\n[3] We conditionally restored MC4R expression in Sim1 neurons in the background of Mc4r-null mice.\n[4] The restoration dramatically reduced obesity in Mc4r-null mice.\n[5] The anti-obesity effect was completely reversed by selective disruption of glutamate release from those same Sim1 neurons.\n[6] The reversal was caused by lower energy expenditure and hyperphagia.\n[7] Corroboratively, selective disruption of glutamate release from adult PVH neurons led to rapid obesity development via reduced energy expenditure and hyperphagia.\n[8] Thus, this study establishes glutamate as the primary neurotransmitter that mediates MC4Rs on Sim1 neurons in body weight regulation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Corroboratively, selective disruption of glutamate release from adult PVH neurons led to rapid obesity development via reduced energy expenditure and hyperphagia.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 378, "doc_id": 45154987, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [45154987, 10534299, 11886686, 25007443, 17150648], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Energy balance requires hypothalamic glutamate neurotransmission.\n\nDocument title: Glutamate mediates the function of melanocortin receptor 4 on Sim1 neurons in body weight regulation.\n\nAbstract sentences:\n[0] The melanocortin receptor 4 (MC4R) is a well-established mediator of body weight homeostasis.\n[1] However, the neurotransmitter(s) that mediate MC4R function remain largely unknown; as a result, little is known about the second-order neurons of the MC4R neural pathway.\n[2] Single-minded 1 (Sim1)-expressing brain regions, which include the paraventricular nucleus of hypothalamus (PVH), represent key brain sites that mediate melanocortin action.\n[3] We conditionally restored MC4R expression in Sim1 neurons in the background of Mc4r-null mice.\n[4] The restoration dramatically reduced obesity in Mc4r-null mice.\n[5] The anti-obesity effect was completely reversed by selective disruption of glutamate release from those same Sim1 neurons.\n[6] The reversal was caused by lower energy expenditure and hyperphagia.\n[7] Corroboratively, selective disruption of glutamate release from adult PVH neurons led to rapid obesity development via reduced energy expenditure and hyperphagia.\n[8] Thus, this study establishes glutamate as the primary neurotransmitter that mediates MC4Rs on Sim1 neurons in body weight regulation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Thus, this study establishes glutamate as the primary neurotransmitter that mediates MC4Rs on Sim1 neurons in body weight regulation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 378, "doc_id": 45154987, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [45154987, 10534299, 11886686, 25007443, 17150648], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Energy balance requires hypothalamic glutamate neurotransmission.\n\nDocument title: Fasting Activation of AgRP Neurons Requires NMDA Receptors and Involves Spinogenesis and Increased Excitatory Tone\n\nAbstract sentences:\n[0] AgRP neuron activity drives feeding and weight gain whereas that of nearby POMC neurons does the opposite.\n[1] However, the role of excitatory glutamatergic input in controlling these neurons is unknown.\n[2] To address this question, we generated mice lacking NMDA receptors (NMDARs) on either AgRP or POMC neurons.\n[3] Deletion of NMDARs from AgRP neurons markedly reduced weight, body fat and food intake whereas deletion from POMC neurons had no effect.\n[4] Activation of AgRP neurons by fasting, as assessed by c-Fos, Agrp and Npy mRNA expression, AMPA receptor-mediated EPSCs, depolarization and firing rates, required NMDARs.\n[5] Furthermore, AgRP but not POMC neurons have dendritic spines and increased glutamatergic input onto AgRP neurons caused by fasting was paralleled by an increase in spines, suggesting fasting induced synaptogenesis and spinogenesis.\n[6] Thus glutamatergic synaptic transmission and its modulation by NMDARs play key roles in controlling AgRP neurons and determining the cellular and behavioral response to fasting."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Deletion of NMDARs from AgRP neurons markedly reduced weight, body fat and food intake whereas deletion from POMC neurons had no effect.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 378, "doc_id": 10534299, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [45154987, 10534299, 11886686, 25007443, 17150648], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Energy balance requires hypothalamic glutamate neurotransmission.\n\nDocument title: Fasting Activation of AgRP Neurons Requires NMDA Receptors and Involves Spinogenesis and Increased Excitatory Tone\n\nAbstract sentences:\n[0] AgRP neuron activity drives feeding and weight gain whereas that of nearby POMC neurons does the opposite.\n[1] However, the role of excitatory glutamatergic input in controlling these neurons is unknown.\n[2] To address this question, we generated mice lacking NMDA receptors (NMDARs) on either AgRP or POMC neurons.\n[3] Deletion of NMDARs from AgRP neurons markedly reduced weight, body fat and food intake whereas deletion from POMC neurons had no effect.\n[4] Activation of AgRP neurons by fasting, as assessed by c-Fos, Agrp and Npy mRNA expression, AMPA receptor-mediated EPSCs, depolarization and firing rates, required NMDARs.\n[5] Furthermore, AgRP but not POMC neurons have dendritic spines and increased glutamatergic input onto AgRP neurons caused by fasting was paralleled by an increase in spines, suggesting fasting induced synaptogenesis and spinogenesis.\n[6] Thus glutamatergic synaptic transmission and its modulation by NMDARs play key roles in controlling AgRP neurons and determining the cellular and behavioral response to fasting."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Activation of AgRP neurons by fasting, as assessed by c-Fos, Agrp and Npy mRNA expression, AMPA receptor-mediated EPSCs, depolarization and firing rates, required NMDARs.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 378, "doc_id": 10534299, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [45154987, 10534299, 11886686, 25007443, 17150648], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Energy balance requires hypothalamic glutamate neurotransmission.\n\nDocument title: Fasting Activation of AgRP Neurons Requires NMDA Receptors and Involves Spinogenesis and Increased Excitatory Tone\n\nAbstract sentences:\n[0] AgRP neuron activity drives feeding and weight gain whereas that of nearby POMC neurons does the opposite.\n[1] However, the role of excitatory glutamatergic input in controlling these neurons is unknown.\n[2] To address this question, we generated mice lacking NMDA receptors (NMDARs) on either AgRP or POMC neurons.\n[3] Deletion of NMDARs from AgRP neurons markedly reduced weight, body fat and food intake whereas deletion from POMC neurons had no effect.\n[4] Activation of AgRP neurons by fasting, as assessed by c-Fos, Agrp and Npy mRNA expression, AMPA receptor-mediated EPSCs, depolarization and firing rates, required NMDARs.\n[5] Furthermore, AgRP but not POMC neurons have dendritic spines and increased glutamatergic input onto AgRP neurons caused by fasting was paralleled by an increase in spines, suggesting fasting induced synaptogenesis and spinogenesis.\n[6] Thus glutamatergic synaptic transmission and its modulation by NMDARs play key roles in controlling AgRP neurons and determining the cellular and behavioral response to fasting."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Furthermore, AgRP but not POMC neurons have dendritic spines and increased glutamatergic input onto AgRP neurons caused by fasting was paralleled by an increase in spines, suggesting fasting induced synaptogenesis and spinogenesis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 378, "doc_id": 10534299, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [45154987, 10534299, 11886686, 25007443, 17150648], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Energy balance requires hypothalamic glutamate neurotransmission.\n\nDocument title: Fasting Activation of AgRP Neurons Requires NMDA Receptors and Involves Spinogenesis and Increased Excitatory Tone\n\nAbstract sentences:\n[0] AgRP neuron activity drives feeding and weight gain whereas that of nearby POMC neurons does the opposite.\n[1] However, the role of excitatory glutamatergic input in controlling these neurons is unknown.\n[2] To address this question, we generated mice lacking NMDA receptors (NMDARs) on either AgRP or POMC neurons.\n[3] Deletion of NMDARs from AgRP neurons markedly reduced weight, body fat and food intake whereas deletion from POMC neurons had no effect.\n[4] Activation of AgRP neurons by fasting, as assessed by c-Fos, Agrp and Npy mRNA expression, AMPA receptor-mediated EPSCs, depolarization and firing rates, required NMDARs.\n[5] Furthermore, AgRP but not POMC neurons have dendritic spines and increased glutamatergic input onto AgRP neurons caused by fasting was paralleled by an increase in spines, suggesting fasting induced synaptogenesis and spinogenesis.\n[6] Thus glutamatergic synaptic transmission and its modulation by NMDARs play key roles in controlling AgRP neurons and determining the cellular and behavioral response to fasting."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Thus glutamatergic synaptic transmission and its modulation by NMDARs play key roles in controlling AgRP neurons and determining the cellular and behavioral response to fasting.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 378, "doc_id": 10534299, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [45154987, 10534299, 11886686, 25007443, 17150648], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Energy balance requires hypothalamic glutamate neurotransmission.\n\nDocument title: Synaptic glutamate release by ventromedial hypothalamic neurons is part of the neurocircuitry that prevents hypoglycemia.\n\nAbstract sentences:\n[0] The importance of neuropeptides in the hypothalamus has been experimentally established.\n[1] Due to difficulties in assessing function in vivo, the roles of the fast-acting neurotransmitters glutamate and GABA are largely unknown.\n[2] Synaptic vesicular transporters (VGLUTs for glutamate and VGAT for GABA) are required for vesicular uptake and, consequently, synaptic release of neurotransmitters.\n[3] Ventromedial hypothalamic (VMH) neurons are predominantly glutamatergic and express VGLUT2.\n[4] To evaluate the role of glutamate release from VMH neurons, we generated mice lacking VGLUT2 selectively in SF1 neurons (a major subset of VMH neurons).\n[5] These mice have hypoglycemia during fasting secondary to impaired fasting-induced increases in the glucose-raising pancreatic hormone glucagon and impaired induction in liver of mRNAs encoding PGC-1alpha and the gluconeogenic enzymes PEPCK and G6Pase.\n[6] Similarly, these mice have defective counterregulatory responses to insulin-induced hypoglycemia and 2-deoxyglucose (an antimetabolite).\n[7] Thus, glutamate release from VMH neurons is an important component of the neurocircuitry that functions to prevent hypoglycemia."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Thus, glutamate release from VMH neurons is an important component of the neurocircuitry that functions to prevent hypoglycemia.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 378, "doc_id": 11886686, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [45154987, 10534299, 11886686, 25007443, 17150648], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Energy balance requires hypothalamic glutamate neurotransmission.\n\nDocument title: Leptin regulates glutamate and glucose transporters in hypothalamic astrocytes.\n\nAbstract sentences:\n[0] Glial cells perform critical functions that alter the metabolism and activity of neurons, and there is increasing interest in their role in appetite and energy balance.\n[1] Leptin, a key regulator of appetite and metabolism, has previously been reported to influence glial structural proteins and morphology.\n[2] Here, we demonstrate that metabolic status and leptin also modify astrocyte-specific glutamate and glucose transporters, indicating that metabolic signals influence synaptic efficacy and glucose uptake and, ultimately, neuronal function.\n[3] We found that basal and glucose-stimulated electrical activity of hypothalamic proopiomelanocortin (POMC) neurons in mice were altered in the offspring of mothers fed a high-fat diet.\n[4] In adulthood, increased body weight and fasting also altered the expression of glucose and glutamate transporters.\n[5] These results demonstrate that whole-organism metabolism alters hypothalamic glial cell activity and suggest that these cells play an important role in the pathology of obesity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here, we demonstrate that metabolic status and leptin also modify astrocyte-specific glutamate and glucose transporters, indicating that metabolic signals influence synaptic efficacy and glucose uptake and, ultimately, neuronal function.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 378, "doc_id": 17150648, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [45154987, 10534299, 11886686, 25007443, 17150648], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Energy balance requires hypothalamic glutamate neurotransmission.\n\nDocument title: Leptin regulates glutamate and glucose transporters in hypothalamic astrocytes.\n\nAbstract sentences:\n[0] Glial cells perform critical functions that alter the metabolism and activity of neurons, and there is increasing interest in their role in appetite and energy balance.\n[1] Leptin, a key regulator of appetite and metabolism, has previously been reported to influence glial structural proteins and morphology.\n[2] Here, we demonstrate that metabolic status and leptin also modify astrocyte-specific glutamate and glucose transporters, indicating that metabolic signals influence synaptic efficacy and glucose uptake and, ultimately, neuronal function.\n[3] We found that basal and glucose-stimulated electrical activity of hypothalamic proopiomelanocortin (POMC) neurons in mice were altered in the offspring of mothers fed a high-fat diet.\n[4] In adulthood, increased body weight and fasting also altered the expression of glucose and glutamate transporters.\n[5] These results demonstrate that whole-organism metabolism alters hypothalamic glial cell activity and suggest that these cells play an important role in the pathology of obesity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"We found that basal and glucose-stimulated electrical activity of hypothalamic proopiomelanocortin (POMC) neurons in mice were altered in the offspring of mothers fed a high-fat diet.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 378, "doc_id": 17150648, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [45154987, 10534299, 11886686, 25007443, 17150648], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Energy balance requires hypothalamic glutamate neurotransmission.\n\nDocument title: Leptin regulates glutamate and glucose transporters in hypothalamic astrocytes.\n\nAbstract sentences:\n[0] Glial cells perform critical functions that alter the metabolism and activity of neurons, and there is increasing interest in their role in appetite and energy balance.\n[1] Leptin, a key regulator of appetite and metabolism, has previously been reported to influence glial structural proteins and morphology.\n[2] Here, we demonstrate that metabolic status and leptin also modify astrocyte-specific glutamate and glucose transporters, indicating that metabolic signals influence synaptic efficacy and glucose uptake and, ultimately, neuronal function.\n[3] We found that basal and glucose-stimulated electrical activity of hypothalamic proopiomelanocortin (POMC) neurons in mice were altered in the offspring of mothers fed a high-fat diet.\n[4] In adulthood, increased body weight and fasting also altered the expression of glucose and glutamate transporters.\n[5] These results demonstrate that whole-organism metabolism alters hypothalamic glial cell activity and suggest that these cells play an important role in the pathology of obesity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"In adulthood, increased body weight and fasting also altered the expression of glucose and glutamate transporters.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 378, "doc_id": 17150648, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [45154987, 10534299, 11886686, 25007443, 17150648], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Enhanced early production of inflammatory chemokines damages viral control in the lung.\n\nDocument title: Memory CD4+ T cells induce innate responses independently of pathogen\n\nAbstract sentences:\n[0] Inflammation induced by recognition of pathogen-associated molecular patterns markedly affects subsequent adaptive responses.\n[1] We asked whether the adaptive immune system can also affect the character and magnitude of innate inflammatory responses.\n[2] We found that the response of memory, but not naive, CD4+ T cells enhances production of multiple innate inflammatory cytokines and chemokines (IICs) in the lung and that, during influenza infection, this leads to early control of virus.\n[3] Memory CD4+ T cell–induced IICs and viral control require cognate antigen recognition and are optimal when memory cells are either T helper type 1 (TH1) or TH17 polarized but are independent of interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) production and do not require activation of conserved pathogen recognition pathways.\n[4] This represents a previously undescribed mechanism by which memory CD4+ T cells induce an early innate response that enhances immune protection against pathogens."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"We found that the response of memory, but not naive, CD4+ T cells enhances production of multiple innate inflammatory cytokines and chemokines (IICs) in the lung and that, during influenza infection, this leads to early control of virus.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 379, "doc_id": 19005293, "label": "CONTRADICTS", "evidence_sentence_ids": [2], "cited_doc_ids": [19005293], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Environmental factors can influence the development of breast cancer.\n\nDocument title: Gene–environment interactions in 7610 women with breast cancer: prospective evidence from the Million Women Study\n\nAbstract sentences:\n[0] BACKGROUND Information is scarce about the combined effects on breast cancer incidence of low-penetrance genetic susceptibility polymorphisms and environmental factors (reproductive, behavioural, and anthropometric risk factors for breast cancer).\n[1] To test for evidence of gene-environment interactions, we compared genotypic relative risks for breast cancer across the other risk factors in a large UK prospective study.\n[2] METHODS We tested gene-environment interactions in 7610 women who developed breast cancer and 10 196 controls without the disease, studying the effects of 12 polymorphisms (FGFR2-rs2981582, TNRC9-rs3803662, 2q35-rs13387042, MAP3K1-rs889312, 8q24-rs13281615, 2p-rs4666451, 5p12-rs981782, CASP8-rs1045485, LSP1-rs3817198, 5q-rs30099, TGFB1-rs1982073, and ATM-rs1800054) in relation to prospectively collected information about ten established environmental risk factors (age at menarche, parity, age at first birth, breastfeeding, menopausal status, age at menopause, use of hormone replacement therapy, body-mass index, height, and alcohol consumption).\n[3] FINDINGS After allowance for multiple testing none of the 120 comparisons yielded significant evidence of a gene-environment interaction.\n[4] By contrast with previous suggestions, there was little evidence that the genotypic relative risks were affected by use of hormone replacement therapy, either overall or for oestrogen-receptor-positive disease.\n[5] Only one of the 12 polymorphisms was correlated with any of the ten other risk factors: carriers of the high-risk C allele of MAP3K1-rs889312 were significantly shorter than non-carriers (mean height 162.4 cm [95% CI 162.1-162.7] vs 163.1 cm [162.9-163.2]; p=0.01 after allowance for multiple testing).\n[6] INTERPRETATION Risks of breast cancer associated with low-penetrance susceptibility polymorphisms do not vary significantly with these ten established environmental risk factors.\n[7] FUNDING Cancer Research UK and the UK Medical Research Council."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"METHODS We tested gene-environment interactions in 7610 women who developed breast cancer and 10 196 controls without the disease, studying the effects of 12 polymorphisms (FGFR2-rs2981582, TNRC9-rs3803662, 2q35-rs13387042, MAP3K1-rs889312, 8q24-rs13281615, 2p-rs4666451, 5p12-rs981782, CASP8-rs1045485, LSP1-rs3817198, 5q-rs30099, TGFB1-rs1982073, and ATM-rs1800054) in relation to prospectively collected information about ten established environmental risk factors (age at menarche, parity, age at first birth, breastfeeding, menopausal status, age at menopause, use of hormone replacement therapy, body-mass index, height, and alcohol consumption).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 381, "doc_id": 18340282, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [18340282], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Environmental factors can influence the development of breast cancer.\n\nDocument title: Gene–environment interactions in 7610 women with breast cancer: prospective evidence from the Million Women Study\n\nAbstract sentences:\n[0] BACKGROUND Information is scarce about the combined effects on breast cancer incidence of low-penetrance genetic susceptibility polymorphisms and environmental factors (reproductive, behavioural, and anthropometric risk factors for breast cancer).\n[1] To test for evidence of gene-environment interactions, we compared genotypic relative risks for breast cancer across the other risk factors in a large UK prospective study.\n[2] METHODS We tested gene-environment interactions in 7610 women who developed breast cancer and 10 196 controls without the disease, studying the effects of 12 polymorphisms (FGFR2-rs2981582, TNRC9-rs3803662, 2q35-rs13387042, MAP3K1-rs889312, 8q24-rs13281615, 2p-rs4666451, 5p12-rs981782, CASP8-rs1045485, LSP1-rs3817198, 5q-rs30099, TGFB1-rs1982073, and ATM-rs1800054) in relation to prospectively collected information about ten established environmental risk factors (age at menarche, parity, age at first birth, breastfeeding, menopausal status, age at menopause, use of hormone replacement therapy, body-mass index, height, and alcohol consumption).\n[3] FINDINGS After allowance for multiple testing none of the 120 comparisons yielded significant evidence of a gene-environment interaction.\n[4] By contrast with previous suggestions, there was little evidence that the genotypic relative risks were affected by use of hormone replacement therapy, either overall or for oestrogen-receptor-positive disease.\n[5] Only one of the 12 polymorphisms was correlated with any of the ten other risk factors: carriers of the high-risk C allele of MAP3K1-rs889312 were significantly shorter than non-carriers (mean height 162.4 cm [95% CI 162.1-162.7] vs 163.1 cm [162.9-163.2]; p=0.01 after allowance for multiple testing).\n[6] INTERPRETATION Risks of breast cancer associated with low-penetrance susceptibility polymorphisms do not vary significantly with these ten established environmental risk factors.\n[7] FUNDING Cancer Research UK and the UK Medical Research Council."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"INTERPRETATION Risks of breast cancer associated with low-penetrance susceptibility polymorphisms do not vary significantly with these ten established environmental risk factors.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 381, "doc_id": 18340282, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [18340282], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Environmentally-induced senescence is mimicked in disease modeling by adding specific molecules to the culture system.\n\nDocument title: Human iPSC-based modeling of late-onset disease via progerin-induced aging.\n\nAbstract sentences:\n[0] Reprogramming somatic cells to induced pluripotent stem cells (iPSCs) resets their identity back to an embryonic age and, thus, presents a significant hurdle for modeling late-onset disorders.\n[1] In this study, we describe a strategy for inducing aging-related features in human iPSC-derived lineages and apply it to the modeling of Parkinson's disease (PD).\n[2] Our approach involves expression of progerin, a truncated form of lamin A associated with premature aging.\n[3] We found that expression of progerin in iPSC-derived fibroblasts and neurons induces multiple aging-related markers and characteristics, including dopamine-specific phenotypes such as neuromelanin accumulation.\n[4] Induced aging in PD iPSC-derived dopamine neurons revealed disease phenotypes that require both aging and genetic susceptibility, such as pronounced dendrite degeneration, progressive loss of tyrosine hydroxylase (TH) expression, and enlarged mitochondria or Lewy-body-precursor inclusions.\n[5] Thus, our study suggests that progerin-induced aging can be used to reveal late-onset age-related disease features in hiPSC-based disease models."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1, 2]\nExplanation: Evidence states: \"In this study, we describe a strategy for inducing aging-related features in human iPSC-derived lineages and apply it to the modeling of Parkinson's disease (PD). Our approach involves expression of progerin, a truncated form of lamin A associated with premature aging.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 382, "doc_id": 11659421, "label": "SUPPORTS", "evidence_sentence_ids": [1, 2], "cited_doc_ids": [11659421], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Environmentally-induced senescence is mimicked in disease modeling by adding specific molecules to the culture system.\n\nDocument title: Human iPSC-based modeling of late-onset disease via progerin-induced aging.\n\nAbstract sentences:\n[0] Reprogramming somatic cells to induced pluripotent stem cells (iPSCs) resets their identity back to an embryonic age and, thus, presents a significant hurdle for modeling late-onset disorders.\n[1] In this study, we describe a strategy for inducing aging-related features in human iPSC-derived lineages and apply it to the modeling of Parkinson's disease (PD).\n[2] Our approach involves expression of progerin, a truncated form of lamin A associated with premature aging.\n[3] We found that expression of progerin in iPSC-derived fibroblasts and neurons induces multiple aging-related markers and characteristics, including dopamine-specific phenotypes such as neuromelanin accumulation.\n[4] Induced aging in PD iPSC-derived dopamine neurons revealed disease phenotypes that require both aging and genetic susceptibility, such as pronounced dendrite degeneration, progressive loss of tyrosine hydroxylase (TH) expression, and enlarged mitochondria or Lewy-body-precursor inclusions.\n[5] Thus, our study suggests that progerin-induced aging can be used to reveal late-onset age-related disease features in hiPSC-based disease models."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4, 5]\nExplanation: Evidence states: \"Induced aging in PD iPSC-derived dopamine neurons revealed disease phenotypes that require both aging and genetic susceptibility, such as pronounced dendrite degeneration, progressive loss of tyrosine hydroxylase (TH) expression, and enlarged mitochondria or Lewy-body-precursor inclusions. Thus, our study suggests that progerin-induced aging can be used to reveal late-onset age-related disease features in hiPSC-based disease models.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 382, "doc_id": 11659421, "label": "SUPPORTS", "evidence_sentence_ids": [4, 5], "cited_doc_ids": [11659421], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Epidemiological disease burden from noncommunicable diseases is more prevalent in high economic settings.\n\nDocument title: Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015\n\nAbstract sentences:\n[0] BACKGROUND The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease.\n[1] By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context.\n[2] METHODS We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015.\n[3] This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence.\n[4] We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources.\n[5] We used statistical models to pool data, adjust for bias, and incorporate covariates.\n[6] We developed a metric that allows comparisons of exposure across risk factors-the summary exposure value.\n[7] Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk.\n[8] We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates.\n[9] We characterised risk exposure in relation to a Socio-demographic Index (SDI).\n[10] FINDINGS Between 1990 and 2015, global exposure to unsafe sanitation, household air pollution, childhood underweight, childhood stunting, and smoking each decreased by more than 25%.\n[11] Global exposure for several occupational risks, high body-mass index (BMI), and drug use increased by more than 25% over the same period.\n[12] All risks jointly evaluated in 2015 accounted for 57·8% (95% CI 56·6-58·8) of global deaths and 41·2% (39·8-42·8) of DALYs.\n[13] In 2015, the ten largest contributors to global DALYs among Level 3 risks were high systolic blood pressure (211·8 million [192·7 million to 231·1 million] global DALYs), smoking (148·6 million [134·2 million to 163·1 million]), high fasting plasma glucose (143·1 million [125·1 million to 163·5 million]), high BMI (120·1 million [83·8 million to 158·4 million]), childhood undernutrition (113·3 million [103·9 million to 123·4 million]), ambient particulate matter (103·1 million [90·8 million to 115·1 million]), high total cholesterol (88·7 million [74·6 million to 105·7 million]), household air pollution (85·6 million [66·7 million to 106·1 million]), alcohol use (85·0 million [77·2 million to 93·0 million]), and diets high in sodium (83·0 million [49·3 million to 127·5 million]).\n[14] From 1990 to 2015, attributable DALYs declined for micronutrient deficiencies, childhood undernutrition, unsafe sanitation and water, and household air pollution; reductions in risk-deleted DALY rates rather than reductions in exposure drove these declines.\n[15] Rising exposure contributed to notable increases in attributable DALYs from high BMI, high fasting plasma glucose, occupational carcinogens, and drug use.\n[16] Environmental risks and childhood undernutrition declined steadily with SDI; low physical activity, high BMI, and high fasting plasma glucose increased with SDI.\n[17] In 119 countries, metabolic risks, such as high BMI and fasting plasma glucose, contributed the most attributable DALYs in 2015.\n[18] Regionally, smoking still ranked among the leading five risk factors for attributable DALYs in 109 countries; childhood underweight and unsafe sex remained primary drivers of early death and disability in much of sub-Saharan Africa.\n[19] INTERPRETATION Declines in some key environmental risks have contributed to declines in critical infectious diseases.\n[20] Some risks appear to be invariant to SDI.\n[21] Increasing risks, including high BMI, high fasting plasma glucose, drug use, and some occupational exposures, contribute to rising burden from some conditions, but also provide opportunities for intervention.\n[22] Some highly preventable risks, such as smoking, remain major causes of attributable DALYs, even as exposure is declining.\n[23] Public policy makers need to pay attention to the risks that are increasingly major contributors to global burden.\n[24] FUNDING Bill & Melinda Gates Foundation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 383, "doc_id": 13770184, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [13770184], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ethanol stress increases the expression of IBP in bacteria.\n\nDocument title: Regulatory and metabolic rewiring during laboratory evolution of ethanol tolerance in E. coli\n\nAbstract sentences:\n[0] Understanding the genetic basis of adaptation is a central problem in biology.\n[1] However, revealing the underlying molecular mechanisms has been challenging as changes in fitness may result from perturbations to many pathways, any of which may contribute relatively little.\n[2] We have developed a combined experimental/computational framework to address this problem and used it to understand the genetic basis of ethanol tolerance in Escherichia coli.\n[3] We used fitness profiling to measure the consequences of single-locus perturbations in the context of ethanol exposure.\n[4] A module-level computational analysis was then used to reveal the organization of the contributing loci into cellular processes and regulatory pathways (e.g. osmoregulation and cell-wall biogenesis) whose modifications significantly affect ethanol tolerance.\n[5] Strikingly, we discovered that a dominant component of adaptation involves metabolic rewiring that boosts intracellular ethanol degradation and assimilation.\n[6] Through phenotypic and metabolomic analysis of laboratory-evolved ethanol-tolerant strains, we investigated naturally accessible pathways of ethanol tolerance.\n[7] Remarkably, these laboratory-evolved strains, by and large, follow the same adaptive paths as inferred from our coarse-grained search of the fitness landscape."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 389, "doc_id": 1148122, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [1148122], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ethanol stress increases the expression of PSP in bacteria.\n\nDocument title: Regulatory and metabolic rewiring during laboratory evolution of ethanol tolerance in E. coli\n\nAbstract sentences:\n[0] Understanding the genetic basis of adaptation is a central problem in biology.\n[1] However, revealing the underlying molecular mechanisms has been challenging as changes in fitness may result from perturbations to many pathways, any of which may contribute relatively little.\n[2] We have developed a combined experimental/computational framework to address this problem and used it to understand the genetic basis of ethanol tolerance in Escherichia coli.\n[3] We used fitness profiling to measure the consequences of single-locus perturbations in the context of ethanol exposure.\n[4] A module-level computational analysis was then used to reveal the organization of the contributing loci into cellular processes and regulatory pathways (e.g. osmoregulation and cell-wall biogenesis) whose modifications significantly affect ethanol tolerance.\n[5] Strikingly, we discovered that a dominant component of adaptation involves metabolic rewiring that boosts intracellular ethanol degradation and assimilation.\n[6] Through phenotypic and metabolomic analysis of laboratory-evolved ethanol-tolerant strains, we investigated naturally accessible pathways of ethanol tolerance.\n[7] Remarkably, these laboratory-evolved strains, by and large, follow the same adaptive paths as inferred from our coarse-grained search of the fitness landscape."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 390, "doc_id": 1148122, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [1148122], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ethanol stress increases the expression of SRL in bacteria.\n\nDocument title: Regulatory and metabolic rewiring during laboratory evolution of ethanol tolerance in E. coli\n\nAbstract sentences:\n[0] Understanding the genetic basis of adaptation is a central problem in biology.\n[1] However, revealing the underlying molecular mechanisms has been challenging as changes in fitness may result from perturbations to many pathways, any of which may contribute relatively little.\n[2] We have developed a combined experimental/computational framework to address this problem and used it to understand the genetic basis of ethanol tolerance in Escherichia coli.\n[3] We used fitness profiling to measure the consequences of single-locus perturbations in the context of ethanol exposure.\n[4] A module-level computational analysis was then used to reveal the organization of the contributing loci into cellular processes and regulatory pathways (e.g. osmoregulation and cell-wall biogenesis) whose modifications significantly affect ethanol tolerance.\n[5] Strikingly, we discovered that a dominant component of adaptation involves metabolic rewiring that boosts intracellular ethanol degradation and assimilation.\n[6] Through phenotypic and metabolomic analysis of laboratory-evolved ethanol-tolerant strains, we investigated naturally accessible pathways of ethanol tolerance.\n[7] Remarkably, these laboratory-evolved strains, by and large, follow the same adaptive paths as inferred from our coarse-grained search of the fitness landscape."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 391, "doc_id": 1148122, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [1148122], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ethanol stress lowers the expression of PSP in bacteria.\n\nDocument title: Regulatory and metabolic rewiring during laboratory evolution of ethanol tolerance in E. coli\n\nAbstract sentences:\n[0] Understanding the genetic basis of adaptation is a central problem in biology.\n[1] However, revealing the underlying molecular mechanisms has been challenging as changes in fitness may result from perturbations to many pathways, any of which may contribute relatively little.\n[2] We have developed a combined experimental/computational framework to address this problem and used it to understand the genetic basis of ethanol tolerance in Escherichia coli.\n[3] We used fitness profiling to measure the consequences of single-locus perturbations in the context of ethanol exposure.\n[4] A module-level computational analysis was then used to reveal the organization of the contributing loci into cellular processes and regulatory pathways (e.g. osmoregulation and cell-wall biogenesis) whose modifications significantly affect ethanol tolerance.\n[5] Strikingly, we discovered that a dominant component of adaptation involves metabolic rewiring that boosts intracellular ethanol degradation and assimilation.\n[6] Through phenotypic and metabolomic analysis of laboratory-evolved ethanol-tolerant strains, we investigated naturally accessible pathways of ethanol tolerance.\n[7] Remarkably, these laboratory-evolved strains, by and large, follow the same adaptive paths as inferred from our coarse-grained search of the fitness landscape."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 392, "doc_id": 1148122, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [1148122], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ethanol stress reduces the expression of SRL in bacteria.\n\nDocument title: Regulatory and metabolic rewiring during laboratory evolution of ethanol tolerance in E. coli\n\nAbstract sentences:\n[0] Understanding the genetic basis of adaptation is a central problem in biology.\n[1] However, revealing the underlying molecular mechanisms has been challenging as changes in fitness may result from perturbations to many pathways, any of which may contribute relatively little.\n[2] We have developed a combined experimental/computational framework to address this problem and used it to understand the genetic basis of ethanol tolerance in Escherichia coli.\n[3] We used fitness profiling to measure the consequences of single-locus perturbations in the context of ethanol exposure.\n[4] A module-level computational analysis was then used to reveal the organization of the contributing loci into cellular processes and regulatory pathways (e.g. osmoregulation and cell-wall biogenesis) whose modifications significantly affect ethanol tolerance.\n[5] Strikingly, we discovered that a dominant component of adaptation involves metabolic rewiring that boosts intracellular ethanol degradation and assimilation.\n[6] Through phenotypic and metabolomic analysis of laboratory-evolved ethanol-tolerant strains, we investigated naturally accessible pathways of ethanol tolerance.\n[7] Remarkably, these laboratory-evolved strains, by and large, follow the same adaptive paths as inferred from our coarse-grained search of the fitness landscape."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 393, "doc_id": 1148122, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [1148122], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Excess gestational weight gain is associated with obesity-related pregnancy outcomes.\n\nDocument title: Effects of interventions in pregnancy on maternal weight and obstetric outcomes: meta-analysis of randomised evidence\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate the effects of dietary and lifestyle interventions in pregnancy on maternal and fetal weight and to quantify the effects of these interventions on obstetric outcomes.\n[1] DESIGN Systematic review and meta-analysis.\n[2] DATA SOURCES Major databases from inception to January 2012 without language restrictions.\n[3] STUDY SELECTION Randomised controlled trials that evaluated any dietary or lifestyle interventions with potential to influence maternal weight during pregnancy and outcomes of pregnancy.\n[4] DATA SYNTHESIS Results summarised as relative risks for dichotomous data and mean differences for continuous data.\n[5] RESULTS We identified 44 relevant randomised controlled trials (7278 women) evaluating three categories of interventions: diet, physical activity, and a mixed approach.\n[6] Overall, there was 1.42 kg reduction (95% confidence interval 0.95 to 1.89 kg) in gestational weight gain with any intervention compared with control.\n[7] With all interventions combined, there were no significant differences in birth weight (mean difference -50 g, -100 to 0 g) and the incidence of large for gestational age (relative risk 0.85, 0.66 to 1.09) or small for gestational age (1.00, 0.78 to 1.28) babies between the groups, though by itself physical activity was associated with reduced birth weight (mean difference -60 g, -120 to -10 g).\n[8] Interventions were associated with a reduced the risk of pre-eclampsia (0.74, 0.60 to 0.92) and shoulder dystocia (0.39, 0.22 to 0.70), with no significant effect on other critically important outcomes.\n[9] Dietary intervention resulted in the largest reduction in maternal gestational weight gain (3.84 kg, 2.45 to 5.22 kg), with improved pregnancy outcomes compared with other interventions.\n[10] The overall evidence rating was low to very low for important outcomes such as pre-eclampsia, gestational diabetes, gestational hypertension, and preterm delivery.\n[11] CONCLUSIONS Dietary and lifestyle interventions in pregnancy can reduce maternal gestational weight gain and improve outcomes for both mother and baby.\n[12] Among the interventions, those based on diet are the most effective and are associated with reductions in maternal gestational weight gain and improved obstetric outcomes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Interventions were associated with a reduced the risk of pre-eclampsia (0.74, 0.60 to 0.92) and shoulder dystocia (0.39, 0.22 to 0.70), with no significant effect on other critically important outcomes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 394, "doc_id": 11360768, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [11360768], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Excess gestational weight gain is associated with obesity-related pregnancy outcomes.\n\nDocument title: Effects of interventions in pregnancy on maternal weight and obstetric outcomes: meta-analysis of randomised evidence\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate the effects of dietary and lifestyle interventions in pregnancy on maternal and fetal weight and to quantify the effects of these interventions on obstetric outcomes.\n[1] DESIGN Systematic review and meta-analysis.\n[2] DATA SOURCES Major databases from inception to January 2012 without language restrictions.\n[3] STUDY SELECTION Randomised controlled trials that evaluated any dietary or lifestyle interventions with potential to influence maternal weight during pregnancy and outcomes of pregnancy.\n[4] DATA SYNTHESIS Results summarised as relative risks for dichotomous data and mean differences for continuous data.\n[5] RESULTS We identified 44 relevant randomised controlled trials (7278 women) evaluating three categories of interventions: diet, physical activity, and a mixed approach.\n[6] Overall, there was 1.42 kg reduction (95% confidence interval 0.95 to 1.89 kg) in gestational weight gain with any intervention compared with control.\n[7] With all interventions combined, there were no significant differences in birth weight (mean difference -50 g, -100 to 0 g) and the incidence of large for gestational age (relative risk 0.85, 0.66 to 1.09) or small for gestational age (1.00, 0.78 to 1.28) babies between the groups, though by itself physical activity was associated with reduced birth weight (mean difference -60 g, -120 to -10 g).\n[8] Interventions were associated with a reduced the risk of pre-eclampsia (0.74, 0.60 to 0.92) and shoulder dystocia (0.39, 0.22 to 0.70), with no significant effect on other critically important outcomes.\n[9] Dietary intervention resulted in the largest reduction in maternal gestational weight gain (3.84 kg, 2.45 to 5.22 kg), with improved pregnancy outcomes compared with other interventions.\n[10] The overall evidence rating was low to very low for important outcomes such as pre-eclampsia, gestational diabetes, gestational hypertension, and preterm delivery.\n[11] CONCLUSIONS Dietary and lifestyle interventions in pregnancy can reduce maternal gestational weight gain and improve outcomes for both mother and baby.\n[12] Among the interventions, those based on diet are the most effective and are associated with reductions in maternal gestational weight gain and improved obstetric outcomes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"CONCLUSIONS Dietary and lifestyle interventions in pregnancy can reduce maternal gestational weight gain and improve outcomes for both mother and baby.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 394, "doc_id": 11360768, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [11360768], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Excess gestational weight gain is associated with obesity-related pregnancy outcomes.\n\nDocument title: Effects of interventions in pregnancy on maternal weight and obstetric outcomes: meta-analysis of randomised evidence\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate the effects of dietary and lifestyle interventions in pregnancy on maternal and fetal weight and to quantify the effects of these interventions on obstetric outcomes.\n[1] DESIGN Systematic review and meta-analysis.\n[2] DATA SOURCES Major databases from inception to January 2012 without language restrictions.\n[3] STUDY SELECTION Randomised controlled trials that evaluated any dietary or lifestyle interventions with potential to influence maternal weight during pregnancy and outcomes of pregnancy.\n[4] DATA SYNTHESIS Results summarised as relative risks for dichotomous data and mean differences for continuous data.\n[5] RESULTS We identified 44 relevant randomised controlled trials (7278 women) evaluating three categories of interventions: diet, physical activity, and a mixed approach.\n[6] Overall, there was 1.42 kg reduction (95% confidence interval 0.95 to 1.89 kg) in gestational weight gain with any intervention compared with control.\n[7] With all interventions combined, there were no significant differences in birth weight (mean difference -50 g, -100 to 0 g) and the incidence of large for gestational age (relative risk 0.85, 0.66 to 1.09) or small for gestational age (1.00, 0.78 to 1.28) babies between the groups, though by itself physical activity was associated with reduced birth weight (mean difference -60 g, -120 to -10 g).\n[8] Interventions were associated with a reduced the risk of pre-eclampsia (0.74, 0.60 to 0.92) and shoulder dystocia (0.39, 0.22 to 0.70), with no significant effect on other critically important outcomes.\n[9] Dietary intervention resulted in the largest reduction in maternal gestational weight gain (3.84 kg, 2.45 to 5.22 kg), with improved pregnancy outcomes compared with other interventions.\n[10] The overall evidence rating was low to very low for important outcomes such as pre-eclampsia, gestational diabetes, gestational hypertension, and preterm delivery.\n[11] CONCLUSIONS Dietary and lifestyle interventions in pregnancy can reduce maternal gestational weight gain and improve outcomes for both mother and baby.\n[12] Among the interventions, those based on diet are the most effective and are associated with reductions in maternal gestational weight gain and improved obstetric outcomes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"Among the interventions, those based on diet are the most effective and are associated with reductions in maternal gestational weight gain and improved obstetric outcomes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 394, "doc_id": 11360768, "label": "SUPPORTS", "evidence_sentence_ids": [12], "cited_doc_ids": [11360768], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Exercise increases cancer mortality rates among Chinese citizens.\n\nDocument title: Combined Impact of Lifestyle-Related Factors on Total and Cause-Specific Mortality among Chinese Women: Prospective Cohort Study\n\nAbstract sentences:\n[0] BACKGROUND Although cigarette smoking, excessive alcohol drinking, obesity, and several other well-studied unhealthy lifestyle-related factors each have been linked to the risk of multiple chronic diseases and premature death, little is known about the combined impact on mortality outcomes, in particular among Chinese and other non-Western populations.\n[1] The objective of this study was to quantify the overall impact of lifestyle-related factors beyond that of active cigarette smoking and alcohol consumption on all-cause and cause-specific mortality in Chinese women.\n[2] METHODS AND FINDINGS We used data from the Shanghai Women's Health Study, an ongoing population-based prospective cohort study in China.\n[3] Participants included 71,243 women aged 40 to 70 years enrolled during 1996-2000 who never smoked or drank alcohol regularly.\n[4] A healthy lifestyle score was created on the basis of five lifestyle-related factors shown to be independently associated with mortality outcomes (normal weight, lower waist-hip ratio, daily exercise, never exposed to spouse's smoking, higher daily fruit and vegetable intake).\n[5] The score ranged from zero (least healthy) to five (most healthy) points.\n[6] During an average follow-up of 9 years, 2,860 deaths occurred, including 775 from cardiovascular disease (CVD) and 1,351 from cancer.\n[7] Adjusted hazard ratios for mortality decreased progressively with an increasing number of healthy lifestyle factors.\n[8] Compared to women with a score of zero, hazard ratios (95% confidence intervals) for women with four to five factors were 0.57 (0.44-0.74) for total mortality, 0.29 (0.16-0.54) for CVD mortality, and 0.76 (0.54-1.06) for cancer mortality.\n[9] The inverse association between the healthy lifestyle score and mortality was seen consistently regardless of chronic disease status at baseline.\n[10] The population attributable risks for not having 4-5 healthy lifestyle factors were 33% for total deaths, 59% for CVD deaths, and 19% for cancer deaths.\n[11] CONCLUSIONS In this first study, to our knowledge, to quantify the combined impact of lifestyle-related factors on mortality outcomes in Chinese women, a healthier lifestyle pattern-including being of normal weight, lower central adiposity, participation in physical activity, nonexposure to spousal smoking, and higher fruit and vegetable intake-was associated with reductions in total and cause-specific mortality among lifetime nonsmoking and nondrinking women, supporting the importance of overall lifestyle modification in disease prevention.\n[12] Please see later in the article for the Editors' Summary."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Compared to women with a score of zero, hazard ratios (95% confidence intervals) for women with four to five factors were 0.57 (0.44-0.74) for total mortality, 0.29 (0.16-0.54) for CVD mortality, and 0.76 (0.54-1.06) for cancer mortality.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 396, "doc_id": 1456068, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [1456068], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Exercise increases cancer mortality rates among Chinese citizens.\n\nDocument title: Combined Impact of Lifestyle-Related Factors on Total and Cause-Specific Mortality among Chinese Women: Prospective Cohort Study\n\nAbstract sentences:\n[0] BACKGROUND Although cigarette smoking, excessive alcohol drinking, obesity, and several other well-studied unhealthy lifestyle-related factors each have been linked to the risk of multiple chronic diseases and premature death, little is known about the combined impact on mortality outcomes, in particular among Chinese and other non-Western populations.\n[1] The objective of this study was to quantify the overall impact of lifestyle-related factors beyond that of active cigarette smoking and alcohol consumption on all-cause and cause-specific mortality in Chinese women.\n[2] METHODS AND FINDINGS We used data from the Shanghai Women's Health Study, an ongoing population-based prospective cohort study in China.\n[3] Participants included 71,243 women aged 40 to 70 years enrolled during 1996-2000 who never smoked or drank alcohol regularly.\n[4] A healthy lifestyle score was created on the basis of five lifestyle-related factors shown to be independently associated with mortality outcomes (normal weight, lower waist-hip ratio, daily exercise, never exposed to spouse's smoking, higher daily fruit and vegetable intake).\n[5] The score ranged from zero (least healthy) to five (most healthy) points.\n[6] During an average follow-up of 9 years, 2,860 deaths occurred, including 775 from cardiovascular disease (CVD) and 1,351 from cancer.\n[7] Adjusted hazard ratios for mortality decreased progressively with an increasing number of healthy lifestyle factors.\n[8] Compared to women with a score of zero, hazard ratios (95% confidence intervals) for women with four to five factors were 0.57 (0.44-0.74) for total mortality, 0.29 (0.16-0.54) for CVD mortality, and 0.76 (0.54-1.06) for cancer mortality.\n[9] The inverse association between the healthy lifestyle score and mortality was seen consistently regardless of chronic disease status at baseline.\n[10] The population attributable risks for not having 4-5 healthy lifestyle factors were 33% for total deaths, 59% for CVD deaths, and 19% for cancer deaths.\n[11] CONCLUSIONS In this first study, to our knowledge, to quantify the combined impact of lifestyle-related factors on mortality outcomes in Chinese women, a healthier lifestyle pattern-including being of normal weight, lower central adiposity, participation in physical activity, nonexposure to spousal smoking, and higher fruit and vegetable intake-was associated with reductions in total and cause-specific mortality among lifetime nonsmoking and nondrinking women, supporting the importance of overall lifestyle modification in disease prevention.\n[12] Please see later in the article for the Editors' Summary."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"The population attributable risks for not having 4-5 healthy lifestyle factors were 33% for total deaths, 59% for CVD deaths, and 19% for cancer deaths.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 396, "doc_id": 1456068, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [1456068], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Exercise increases cancer mortality rates among Chinese citizens.\n\nDocument title: Combined Impact of Lifestyle-Related Factors on Total and Cause-Specific Mortality among Chinese Women: Prospective Cohort Study\n\nAbstract sentences:\n[0] BACKGROUND Although cigarette smoking, excessive alcohol drinking, obesity, and several other well-studied unhealthy lifestyle-related factors each have been linked to the risk of multiple chronic diseases and premature death, little is known about the combined impact on mortality outcomes, in particular among Chinese and other non-Western populations.\n[1] The objective of this study was to quantify the overall impact of lifestyle-related factors beyond that of active cigarette smoking and alcohol consumption on all-cause and cause-specific mortality in Chinese women.\n[2] METHODS AND FINDINGS We used data from the Shanghai Women's Health Study, an ongoing population-based prospective cohort study in China.\n[3] Participants included 71,243 women aged 40 to 70 years enrolled during 1996-2000 who never smoked or drank alcohol regularly.\n[4] A healthy lifestyle score was created on the basis of five lifestyle-related factors shown to be independently associated with mortality outcomes (normal weight, lower waist-hip ratio, daily exercise, never exposed to spouse's smoking, higher daily fruit and vegetable intake).\n[5] The score ranged from zero (least healthy) to five (most healthy) points.\n[6] During an average follow-up of 9 years, 2,860 deaths occurred, including 775 from cardiovascular disease (CVD) and 1,351 from cancer.\n[7] Adjusted hazard ratios for mortality decreased progressively with an increasing number of healthy lifestyle factors.\n[8] Compared to women with a score of zero, hazard ratios (95% confidence intervals) for women with four to five factors were 0.57 (0.44-0.74) for total mortality, 0.29 (0.16-0.54) for CVD mortality, and 0.76 (0.54-1.06) for cancer mortality.\n[9] The inverse association between the healthy lifestyle score and mortality was seen consistently regardless of chronic disease status at baseline.\n[10] The population attributable risks for not having 4-5 healthy lifestyle factors were 33% for total deaths, 59% for CVD deaths, and 19% for cancer deaths.\n[11] CONCLUSIONS In this first study, to our knowledge, to quantify the combined impact of lifestyle-related factors on mortality outcomes in Chinese women, a healthier lifestyle pattern-including being of normal weight, lower central adiposity, participation in physical activity, nonexposure to spousal smoking, and higher fruit and vegetable intake-was associated with reductions in total and cause-specific mortality among lifetime nonsmoking and nondrinking women, supporting the importance of overall lifestyle modification in disease prevention.\n[12] Please see later in the article for the Editors' Summary."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"CONCLUSIONS In this first study, to our knowledge, to quantify the combined impact of lifestyle-related factors on mortality outcomes in Chinese women, a healthier lifestyle pattern-including being of normal weight, lower central adiposity, participation in physical activity, nonexposure to spousal smoking, and higher fruit and vegetable intake-was associated with reductions in total and cause-specific mortality among lifetime nonsmoking and nondrinking women, supporting the importance of overall lifestyle modification in disease prevention.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 396, "doc_id": 1456068, "label": "CONTRADICTS", "evidence_sentence_ids": [11], "cited_doc_ids": [1456068], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Exercise reduces cancer mortality rates among Chinese citizens.\n\nDocument title: Combined Impact of Lifestyle-Related Factors on Total and Cause-Specific Mortality among Chinese Women: Prospective Cohort Study\n\nAbstract sentences:\n[0] BACKGROUND Although cigarette smoking, excessive alcohol drinking, obesity, and several other well-studied unhealthy lifestyle-related factors each have been linked to the risk of multiple chronic diseases and premature death, little is known about the combined impact on mortality outcomes, in particular among Chinese and other non-Western populations.\n[1] The objective of this study was to quantify the overall impact of lifestyle-related factors beyond that of active cigarette smoking and alcohol consumption on all-cause and cause-specific mortality in Chinese women.\n[2] METHODS AND FINDINGS We used data from the Shanghai Women's Health Study, an ongoing population-based prospective cohort study in China.\n[3] Participants included 71,243 women aged 40 to 70 years enrolled during 1996-2000 who never smoked or drank alcohol regularly.\n[4] A healthy lifestyle score was created on the basis of five lifestyle-related factors shown to be independently associated with mortality outcomes (normal weight, lower waist-hip ratio, daily exercise, never exposed to spouse's smoking, higher daily fruit and vegetable intake).\n[5] The score ranged from zero (least healthy) to five (most healthy) points.\n[6] During an average follow-up of 9 years, 2,860 deaths occurred, including 775 from cardiovascular disease (CVD) and 1,351 from cancer.\n[7] Adjusted hazard ratios for mortality decreased progressively with an increasing number of healthy lifestyle factors.\n[8] Compared to women with a score of zero, hazard ratios (95% confidence intervals) for women with four to five factors were 0.57 (0.44-0.74) for total mortality, 0.29 (0.16-0.54) for CVD mortality, and 0.76 (0.54-1.06) for cancer mortality.\n[9] The inverse association between the healthy lifestyle score and mortality was seen consistently regardless of chronic disease status at baseline.\n[10] The population attributable risks for not having 4-5 healthy lifestyle factors were 33% for total deaths, 59% for CVD deaths, and 19% for cancer deaths.\n[11] CONCLUSIONS In this first study, to our knowledge, to quantify the combined impact of lifestyle-related factors on mortality outcomes in Chinese women, a healthier lifestyle pattern-including being of normal weight, lower central adiposity, participation in physical activity, nonexposure to spousal smoking, and higher fruit and vegetable intake-was associated with reductions in total and cause-specific mortality among lifetime nonsmoking and nondrinking women, supporting the importance of overall lifestyle modification in disease prevention.\n[12] Please see later in the article for the Editors' Summary."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Compared to women with a score of zero, hazard ratios (95% confidence intervals) for women with four to five factors were 0.57 (0.44-0.74) for total mortality, 0.29 (0.16-0.54) for CVD mortality, and 0.76 (0.54-1.06) for cancer mortality.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 397, "doc_id": 1456068, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [1456068], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Exercise reduces cancer mortality rates among Chinese citizens.\n\nDocument title: Combined Impact of Lifestyle-Related Factors on Total and Cause-Specific Mortality among Chinese Women: Prospective Cohort Study\n\nAbstract sentences:\n[0] BACKGROUND Although cigarette smoking, excessive alcohol drinking, obesity, and several other well-studied unhealthy lifestyle-related factors each have been linked to the risk of multiple chronic diseases and premature death, little is known about the combined impact on mortality outcomes, in particular among Chinese and other non-Western populations.\n[1] The objective of this study was to quantify the overall impact of lifestyle-related factors beyond that of active cigarette smoking and alcohol consumption on all-cause and cause-specific mortality in Chinese women.\n[2] METHODS AND FINDINGS We used data from the Shanghai Women's Health Study, an ongoing population-based prospective cohort study in China.\n[3] Participants included 71,243 women aged 40 to 70 years enrolled during 1996-2000 who never smoked or drank alcohol regularly.\n[4] A healthy lifestyle score was created on the basis of five lifestyle-related factors shown to be independently associated with mortality outcomes (normal weight, lower waist-hip ratio, daily exercise, never exposed to spouse's smoking, higher daily fruit and vegetable intake).\n[5] The score ranged from zero (least healthy) to five (most healthy) points.\n[6] During an average follow-up of 9 years, 2,860 deaths occurred, including 775 from cardiovascular disease (CVD) and 1,351 from cancer.\n[7] Adjusted hazard ratios for mortality decreased progressively with an increasing number of healthy lifestyle factors.\n[8] Compared to women with a score of zero, hazard ratios (95% confidence intervals) for women with four to five factors were 0.57 (0.44-0.74) for total mortality, 0.29 (0.16-0.54) for CVD mortality, and 0.76 (0.54-1.06) for cancer mortality.\n[9] The inverse association between the healthy lifestyle score and mortality was seen consistently regardless of chronic disease status at baseline.\n[10] The population attributable risks for not having 4-5 healthy lifestyle factors were 33% for total deaths, 59% for CVD deaths, and 19% for cancer deaths.\n[11] CONCLUSIONS In this first study, to our knowledge, to quantify the combined impact of lifestyle-related factors on mortality outcomes in Chinese women, a healthier lifestyle pattern-including being of normal weight, lower central adiposity, participation in physical activity, nonexposure to spousal smoking, and higher fruit and vegetable intake-was associated with reductions in total and cause-specific mortality among lifetime nonsmoking and nondrinking women, supporting the importance of overall lifestyle modification in disease prevention.\n[12] Please see later in the article for the Editors' Summary."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"The population attributable risks for not having 4-5 healthy lifestyle factors were 33% for total deaths, 59% for CVD deaths, and 19% for cancer deaths.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 397, "doc_id": 1456068, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [1456068], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Exercise reduces cancer mortality rates among Chinese citizens.\n\nDocument title: Combined Impact of Lifestyle-Related Factors on Total and Cause-Specific Mortality among Chinese Women: Prospective Cohort Study\n\nAbstract sentences:\n[0] BACKGROUND Although cigarette smoking, excessive alcohol drinking, obesity, and several other well-studied unhealthy lifestyle-related factors each have been linked to the risk of multiple chronic diseases and premature death, little is known about the combined impact on mortality outcomes, in particular among Chinese and other non-Western populations.\n[1] The objective of this study was to quantify the overall impact of lifestyle-related factors beyond that of active cigarette smoking and alcohol consumption on all-cause and cause-specific mortality in Chinese women.\n[2] METHODS AND FINDINGS We used data from the Shanghai Women's Health Study, an ongoing population-based prospective cohort study in China.\n[3] Participants included 71,243 women aged 40 to 70 years enrolled during 1996-2000 who never smoked or drank alcohol regularly.\n[4] A healthy lifestyle score was created on the basis of five lifestyle-related factors shown to be independently associated with mortality outcomes (normal weight, lower waist-hip ratio, daily exercise, never exposed to spouse's smoking, higher daily fruit and vegetable intake).\n[5] The score ranged from zero (least healthy) to five (most healthy) points.\n[6] During an average follow-up of 9 years, 2,860 deaths occurred, including 775 from cardiovascular disease (CVD) and 1,351 from cancer.\n[7] Adjusted hazard ratios for mortality decreased progressively with an increasing number of healthy lifestyle factors.\n[8] Compared to women with a score of zero, hazard ratios (95% confidence intervals) for women with four to five factors were 0.57 (0.44-0.74) for total mortality, 0.29 (0.16-0.54) for CVD mortality, and 0.76 (0.54-1.06) for cancer mortality.\n[9] The inverse association between the healthy lifestyle score and mortality was seen consistently regardless of chronic disease status at baseline.\n[10] The population attributable risks for not having 4-5 healthy lifestyle factors were 33% for total deaths, 59% for CVD deaths, and 19% for cancer deaths.\n[11] CONCLUSIONS In this first study, to our knowledge, to quantify the combined impact of lifestyle-related factors on mortality outcomes in Chinese women, a healthier lifestyle pattern-including being of normal weight, lower central adiposity, participation in physical activity, nonexposure to spousal smoking, and higher fruit and vegetable intake-was associated with reductions in total and cause-specific mortality among lifetime nonsmoking and nondrinking women, supporting the importance of overall lifestyle modification in disease prevention.\n[12] Please see later in the article for the Editors' Summary."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"CONCLUSIONS In this first study, to our knowledge, to quantify the combined impact of lifestyle-related factors on mortality outcomes in Chinese women, a healthier lifestyle pattern-including being of normal weight, lower central adiposity, participation in physical activity, nonexposure to spousal smoking, and higher fruit and vegetable intake-was associated with reductions in total and cause-specific mortality among lifetime nonsmoking and nondrinking women, supporting the importance of overall lifestyle modification in disease prevention.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 397, "doc_id": 1456068, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [1456068], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Exhaustion of B cells contributes to poor Ab response in HIV-infected individuals.\n\nDocument title: Antibody-Based HIV-1 Vaccines: Recent Developments and Future Directions\n\nAbstract sentences:\n[0] The Global HIV Vaccine Enterprise convened a two-day workshop in May of 2007 to discuss humoral immune responses to HIV and approaches to design vaccines that induce viral neutralizing and other potentially protective antibody responses.\n[1] The goals of this workshop were to identify key scientific issues, gaps, and opportunities that have emerged since the Enterprise Strategic Plan was first published in 2005 [1], and to make recommendations that Enterprise stakeholders can use to plan new activities.\n[2] Most effective viral vaccines work, at least in part, by generating antibodies that inactivate or neutralize the invading virus, and the existing data strongly suggest that an optimally effective HIV-1 vaccine should elicit potent antiviral neutralizing antibodies.\n[3] However, unlike acute viral pathogens, HIV-1 chronically replicates in the host and evades the antibody response.\n[4] This immune evasion, along with the large genetic variation among HIV-1 strains worldwide, has posed major obstacles to vaccine development.\n[5] Current HIV vaccine candidates do not elicit neutralizing antibodies against most circulating virus strains, and thus the induction of a protective antibody response remains a major priority for HIV-1 vaccine development.\n[6] For an antibody-based HIV-1 vaccine, progress in vaccine design is generally gauged by in vitro assays that measure the ability of vaccine-induced antibodies to neutralize a broad spectrum of viral isolates representing the major genetic subtypes (clades) of HIV-1 [2].\n[7] Although it is not known what magnitude and breadth of neutralization will predict protection in vaccine recipients, it is clear that current vaccine immunogens elicit antibodies that neutralize only a minority of circulating isolates.\n[8] Thus, much progress needs to be made in this area.\n[9] Also, though virus neutralization is considered a critical benchmark for a vaccine, this may not be the only benchmark for predicting success with antibody-based HIV-1 vaccine immunogens.\n[10] The main targets for neutralizing antibodies to HIV-1 are the surface gp120 and trans-membrane gp41 envelope glycoproteins (Env) that mediate receptor and coreceptor binding and the subsequent membrane fusion events that allow the virus to gain entry into cells [3].\n[11] Antibodies neutralize the virus by binding these viral spikes and blocking virus entry into susceptible cells, such as CD4+ T cells [4,5].\n[12] In order to chronically replicate in the host, the virus exploits several mechanisms to shield itself against antibody recognition, including a dense outer coating of sugar molecules (N-linked glycans) and the strategic positioning of cysteine–cysteine loop structures on the gp120 molecule [6–8].\n[13] These shielding mechanisms, although highly effective, have vulnerabilities imposed by fitness constraints.\n[14] Information on the precise location and molecular structure of these vulnerable regions could be valuable for the rational design of improved vaccine immunogens.\n[15] Participants in the workshop identified four areas that, if given proper attention, could provide key information that would bring the field closer to an effective antibody-based HIV-1 vaccine: (1) structure-assisted immunogen design, (2) role of Fc receptors and complement, (3) assay standardization and validation, and (4) immunoregulation of B cell responses."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 398, "doc_id": 8883846, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [8883846], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Exposure to fine particulate air pollution is unrelated to anxiety prevalence.\n\nDocument title: The relation between past exposure to fine particulate air pollution and prevalent anxiety: observational cohort study\n\nAbstract sentences:\n[0] OBJECTIVE To determine whether higher past exposure to particulate air pollution is associated with prevalent high symptoms of anxiety.\n[1] DESIGN Observational cohort study.\n[2] SETTING Nurses' Health Study.\n[3] PARTICIPANTS 71,271 women enrolled in the Nurses' Health Study residing throughout the contiguous United States who had valid estimates on exposure to particulate matter for at least one exposure period of interest and data on anxiety symptoms.\n[4] MAIN OUTCOME MEASURES Meaningfully high symptoms of anxiety, defined as a score of 6 points or greater on the phobic anxiety subscale of the Crown-Crisp index, administered in 2004.\n[5] RESULTS The 71,271 eligible women were aged between 57 and 85 years (mean 70 years) at the time of assessment of anxiety symptoms, with a prevalence of high anxiety symptoms of 15%.\n[6] Exposure to particulate matter was characterized using estimated average exposure to particulate matter <2.5 μm in diameter (PM2.5) and 2.5 to 10 μm in diameter (PM2.5-10) in the one month, three months, six months, one year, and 15 years prior to assessment of anxiety symptoms, and residential distance to the nearest major road two years prior to assessment.\n[7] Significantly increased odds of high anxiety symptoms were observed with higher exposure to PM2.5 for multiple averaging periods (for example, odds ratio per 10 µg/m(3) increase in prior one month average PM2.5: 1.12, 95% confidence interval 1.06 to 1.19; in prior 12 month average PM2.5: 1.15, 1.06 to 1.26).\n[8] Models including multiple exposure windows suggested short term averaging periods were more relevant than long term averaging periods.\n[9] There was no association between anxiety and exposure to PM2.5-10.\n[10] Residential proximity to major roads was not related to anxiety symptoms in a dose dependent manner.\n[11] CONCLUSIONS Exposure to fine particulate matter (PM2.5) was associated with high symptoms of anxiety, with more recent exposures potentially more relevant than more distant exposures.\n[12] Research evaluating whether reductions in exposure to ambient PM2.5 would reduce the population level burden of clinically relevant symptoms of anxiety is warranted."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Significantly increased odds of high anxiety symptoms were observed with higher exposure to PM2.5 for multiple averaging periods (for example, odds ratio per 10 µg/m(3) increase in prior one month average PM2.5: 1.12, 95% confidence interval 1.06 to 1.19; in prior 12 month average PM2.5: 1.15, 1.06 to 1.26).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 400, "doc_id": 791050, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [791050], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Exposure to fine particulate air pollution is unrelated to anxiety prevalence.\n\nDocument title: The relation between past exposure to fine particulate air pollution and prevalent anxiety: observational cohort study\n\nAbstract sentences:\n[0] OBJECTIVE To determine whether higher past exposure to particulate air pollution is associated with prevalent high symptoms of anxiety.\n[1] DESIGN Observational cohort study.\n[2] SETTING Nurses' Health Study.\n[3] PARTICIPANTS 71,271 women enrolled in the Nurses' Health Study residing throughout the contiguous United States who had valid estimates on exposure to particulate matter for at least one exposure period of interest and data on anxiety symptoms.\n[4] MAIN OUTCOME MEASURES Meaningfully high symptoms of anxiety, defined as a score of 6 points or greater on the phobic anxiety subscale of the Crown-Crisp index, administered in 2004.\n[5] RESULTS The 71,271 eligible women were aged between 57 and 85 years (mean 70 years) at the time of assessment of anxiety symptoms, with a prevalence of high anxiety symptoms of 15%.\n[6] Exposure to particulate matter was characterized using estimated average exposure to particulate matter <2.5 μm in diameter (PM2.5) and 2.5 to 10 μm in diameter (PM2.5-10) in the one month, three months, six months, one year, and 15 years prior to assessment of anxiety symptoms, and residential distance to the nearest major road two years prior to assessment.\n[7] Significantly increased odds of high anxiety symptoms were observed with higher exposure to PM2.5 for multiple averaging periods (for example, odds ratio per 10 µg/m(3) increase in prior one month average PM2.5: 1.12, 95% confidence interval 1.06 to 1.19; in prior 12 month average PM2.5: 1.15, 1.06 to 1.26).\n[8] Models including multiple exposure windows suggested short term averaging periods were more relevant than long term averaging periods.\n[9] There was no association between anxiety and exposure to PM2.5-10.\n[10] Residential proximity to major roads was not related to anxiety symptoms in a dose dependent manner.\n[11] CONCLUSIONS Exposure to fine particulate matter (PM2.5) was associated with high symptoms of anxiety, with more recent exposures potentially more relevant than more distant exposures.\n[12] Research evaluating whether reductions in exposure to ambient PM2.5 would reduce the population level burden of clinically relevant symptoms of anxiety is warranted."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"CONCLUSIONS Exposure to fine particulate matter (PM2.5) was associated with high symptoms of anxiety, with more recent exposures potentially more relevant than more distant exposures.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 400, "doc_id": 791050, "label": "CONTRADICTS", "evidence_sentence_ids": [11], "cited_doc_ids": [791050], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Expression of MSX2 is induced 3 hours after the addition of BMP4, which is earlier than T and CDX2.\n\nDocument title: BRACHYURY and CDX2 Mediate BMP-Induced Differentiation of Human and Mouse Pluripotent Stem Cells into Embryonic and Extraembryonic Lineages\n\nAbstract sentences:\n[0] BMP is thought to induce hESC differentiation toward multiple lineages including mesoderm and trophoblast.\n[1] The BMP-induced trophoblast phenotype is a long-standing paradox in stem cell biology.\n[2] Here we readdressed BMP function in hESCs and mouse epiblast-derived cells.\n[3] We found that BMP4 cooperates with FGF2 (via ERK) to induce mesoderm and to inhibit endoderm differentiation.\n[4] These conditions induced cells with high levels of BRACHYURY (BRA) that coexpressed CDX2.\n[5] BRA was necessary for and preceded CDX2 expression; both genes were essential for expression not only of mesodermal genes but also of trophoblast-associated genes.\n[6] Maximal expression of the latter was seen in the absence of FGF but these cells coexpressed mesodermal genes and moreover they differed in cell surface and epigenetic properties from placental trophoblast.\n[7] We conclude that BMP induces human and mouse pluripotent stem cells primarily to form mesoderm, rather than trophoblast, acting through BRA and CDX2."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 401, "doc_id": 5633876, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [5633876], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Expression of oncolytic virus antigens as peptides makes relapse more likely.\n\nDocument title: Detecting and targeting tumor relapse by its resistance to innate effectors at early recurrence\n\nAbstract sentences:\n[0] Tumor recurrence represents a major clinical challenge.\n[1] Our data show that emergent recurrent tumors acquire a phenotype radically different from that of their originating primary tumors.\n[2] This phenotype allows them to evade a host-derived innate immune response elicited by the progression from minimal residual disease (MRD) to actively growing recurrence.\n[3] Screening for this innate response predicted accurately in which mice recurrence would occur.\n[4] Premature induction of recurrence resensitized MRD to the primary therapy, suggesting a possible paradigm shift for clinical treatment of dormant disease in which the current expectant approach is replaced with active attempts to uncover MRD before evolution of the escape phenotype is complete.\n[5] By combining screening with second-line treatments targeting innate insensitivity, up to 100% of mice that would have otherwise relapsed were cured.\n[6] These data may open new avenues for early detection and appropriately timed, highly targeted treatment of tumor recurrence irrespective of tumor type or frontline treatment."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 403, "doc_id": 1921218, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [1921218], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Expression of oncolytic virus antigens as peptides permits additional protection against relapse.\n\nDocument title: Detecting and targeting tumor relapse by its resistance to innate effectors at early recurrence\n\nAbstract sentences:\n[0] Tumor recurrence represents a major clinical challenge.\n[1] Our data show that emergent recurrent tumors acquire a phenotype radically different from that of their originating primary tumors.\n[2] This phenotype allows them to evade a host-derived innate immune response elicited by the progression from minimal residual disease (MRD) to actively growing recurrence.\n[3] Screening for this innate response predicted accurately in which mice recurrence would occur.\n[4] Premature induction of recurrence resensitized MRD to the primary therapy, suggesting a possible paradigm shift for clinical treatment of dormant disease in which the current expectant approach is replaced with active attempts to uncover MRD before evolution of the escape phenotype is complete.\n[5] By combining screening with second-line treatments targeting innate insensitivity, up to 100% of mice that would have otherwise relapsed were cured.\n[6] These data may open new avenues for early detection and appropriately timed, highly targeted treatment of tumor recurrence irrespective of tumor type or frontline treatment."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 404, "doc_id": 1921218, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [1921218], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: F4/80+ macrophages regulate mature osteoblast maintenance.\n\nDocument title: PDGF-BB secreted by preosteoclasts induces angiogenesis during coupling with osteogenesis\n\nAbstract sentences:\n[0] Osteogenesis during bone modeling and remodeling is coupled with angiogenesis.\n[1] A recent study showed that a specific vessel subtype, strongly positive for CD31 and endomucin (CD31hiEmcnhi), couples angiogenesis and osteogenesis.\n[2] Here, we found that platelet-derived growth factor-BB (PDGF-BB) secreted by preosteoclasts induces CD31hiEmcnhi vessel formation during bone modeling and remodeling.\n[3] Mice with depletion of PDGF-BB in the tartrate-resistant acid phosphatase–positive cell lineage show significantly lower trabecular and cortical bone mass, serum and bone marrow PDGF-BB concentrations, and fewer CD31hiEmcnhi vessels compared to wild-type mice.\n[4] In the ovariectomy (OVX)-induced osteoporotic mouse model, serum and bone marrow levels of PDGF-BB and numbers of CD31hiEmcnhi vessels are significantly lower compared to sham-operated controls.\n[5] Treatment with exogenous PDGF-BB or inhibition of cathepsin K to increase the number of preosteoclasts, and thus the endogenous levels of PDGF-BB, increases CD31hiEmcnhi vessel number and stimulates bone formation in OVX mice.\n[6] Thus, pharmacotherapies that increase PDGF-BB secretion from preosteoclasts offer a new therapeutic target for treating osteoporosis by promoting angiogenesis and thus bone formation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 406, "doc_id": 6796297, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [6796297], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: FACT and other histone chaperone(s) compensate for Histone 2A (H2A)-histone 2B (H2B) dimer eviction during the histone exchange process.\n\nDocument title: FACT Disrupts Nucleosome Structure by Binding H2A-H2B with Conserved Peptide Motifs.\n\nAbstract sentences:\n[0] FACT, a heterodimer of Spt16 and Pob3, is an essential histone chaperone.\n[1] We show that the H2A-H2B binding activity that is central to FACT function resides in short acidic regions near the C termini of each subunit.\n[2] Mutations throughout these regions affect binding and cause correlated phenotypes that range from mild to lethal, with the largest individual contributions unexpectedly coming from an aromatic residue and a nearby carboxylate residue within each domain.\n[3] Spt16 and Pob3 bind overlapping sites on H2A-H2B, and Spt16-Pob3 heterodimers simultaneously bind two H2A-H2B dimers, the same stoichiometry as the components of a nucleosome.\n[4] An Spt16:H2A-H2B crystal structure explains the biochemical and genetic data, provides a model for Pob3 binding, and implies a mechanism for FACT reorganization that we confirm biochemically.\n[5] Moreover, unexpected similarity to binding of ANP32E and Swr1 with H2A.Z-H2B reveals that diverse H2A-H2B chaperones use common mechanisms of histone binding and regulating nucleosome functions."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 407, "doc_id": 9889151, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [9889151], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Female carriers of the Apolipoprotein E4 (APOE4) allele have decreased risk for dementia.\n\nDocument title: Reproductive period and risk of dementia in postmenopausal women.\n\nAbstract sentences:\n[0] CONTEXT Exogenous estrogen use may lower risk of dementia in postmenopausal women.\n[1] A relationship between long-term exposure to endogenous estrogens and incident dementia has been hypothesized but not studied.\n[2] OBJECTIVE To determine whether a longer reproductive period, as an indicator of longer exposure to endogenous estrogens, is associated with lower risk of dementia and Alzheimer disease (AD) in women who have natural menopause.\n[3] DESIGN AND SETTING The Rotterdam Study, a population-based prospective cohort study conducted in the Netherlands.\n[4] PARTICIPANTS A total of 3601 women aged 55 years or older who did not have dementia at baseline (1990-1993) and had information on age at menarche, age at menopause, and type of menopause.\n[5] Participants were reexamined in 1993-1994 and 1997-1999 and were continuously monitored for development of dementia.\n[6] MAIN OUTCOME MEASURES Incidence of dementia, based on Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition criteria, and AD, based on National Institute of Neurological Disorders and Stroke/Alzheimer's Disease and Related Disorders Association criteria, compared by quartiles of reproductive period among women with natural menopause.\n[7] RESULTS During 21 046 person-years of follow-up (median follow-up, 6.3 years), 199 women developed dementia, including 159 who developed AD.\n[8] After adjusting for age, dementia was not clearly associated with length of reproductive period.\n[9] However, after adjusting for multiple covariates, women with natural menopause and more reproductive years had an increased risk of dementia (adjusted rate ratio [RR] for women with >39 reproductive years [highest quartile] compared with <34 reproductive years [lowest quartile], 1.78; 95% confidence interval [CI], 1.12-2.84).\n[10] The adjusted RR per year of increase was 1.04 (95% CI, 1.01-1.08).\n[11] For risk of AD, the adjusted RRs were 1.51 (95% CI, 0.91-2.50) and 1.03 (95% CI, 1.00-1.07), respectively.\n[12] Risk of dementia associated with a longer reproductive period was most pronounced in APOE epsilon4 carriers (adjusted RR for >39 reproductive years compared with <34 reproductive years, 4.20 [95% CI, 1.97-8.92] for dementia and 3.42 [95% CI, 1.51-7.75] for AD), whereas in noncarriers, no clear association with dementia or AD was observed.\n[13] CONCLUSION Our findings do not support the hypothesis that a longer reproductive period reduces risk of dementia in women who have natural menopause."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"Risk of dementia associated with a longer reproductive period was most pronounced in APOE epsilon4 carriers (adjusted RR for >39 reproductive years compared with <34 reproductive years, 4.20 [95% CI, 1.97-8.92] for dementia and 3.42 [95% CI, 1.51-7.75] for AD), whereas in noncarriers, no clear association with dementia or AD was observed.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 413, "doc_id": 6309659, "label": "CONTRADICTS", "evidence_sentence_ids": [12], "cited_doc_ids": [6309659], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Female carriers of the Apolipoprotein E4 (APOE4) allele have increased risk for Alzheimer's disease.\n\nDocument title: Reproductive period and risk of dementia in postmenopausal women.\n\nAbstract sentences:\n[0] CONTEXT Exogenous estrogen use may lower risk of dementia in postmenopausal women.\n[1] A relationship between long-term exposure to endogenous estrogens and incident dementia has been hypothesized but not studied.\n[2] OBJECTIVE To determine whether a longer reproductive period, as an indicator of longer exposure to endogenous estrogens, is associated with lower risk of dementia and Alzheimer disease (AD) in women who have natural menopause.\n[3] DESIGN AND SETTING The Rotterdam Study, a population-based prospective cohort study conducted in the Netherlands.\n[4] PARTICIPANTS A total of 3601 women aged 55 years or older who did not have dementia at baseline (1990-1993) and had information on age at menarche, age at menopause, and type of menopause.\n[5] Participants were reexamined in 1993-1994 and 1997-1999 and were continuously monitored for development of dementia.\n[6] MAIN OUTCOME MEASURES Incidence of dementia, based on Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition criteria, and AD, based on National Institute of Neurological Disorders and Stroke/Alzheimer's Disease and Related Disorders Association criteria, compared by quartiles of reproductive period among women with natural menopause.\n[7] RESULTS During 21 046 person-years of follow-up (median follow-up, 6.3 years), 199 women developed dementia, including 159 who developed AD.\n[8] After adjusting for age, dementia was not clearly associated with length of reproductive period.\n[9] However, after adjusting for multiple covariates, women with natural menopause and more reproductive years had an increased risk of dementia (adjusted rate ratio [RR] for women with >39 reproductive years [highest quartile] compared with <34 reproductive years [lowest quartile], 1.78; 95% confidence interval [CI], 1.12-2.84).\n[10] The adjusted RR per year of increase was 1.04 (95% CI, 1.01-1.08).\n[11] For risk of AD, the adjusted RRs were 1.51 (95% CI, 0.91-2.50) and 1.03 (95% CI, 1.00-1.07), respectively.\n[12] Risk of dementia associated with a longer reproductive period was most pronounced in APOE epsilon4 carriers (adjusted RR for >39 reproductive years compared with <34 reproductive years, 4.20 [95% CI, 1.97-8.92] for dementia and 3.42 [95% CI, 1.51-7.75] for AD), whereas in noncarriers, no clear association with dementia or AD was observed.\n[13] CONCLUSION Our findings do not support the hypothesis that a longer reproductive period reduces risk of dementia in women who have natural menopause."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"Risk of dementia associated with a longer reproductive period was most pronounced in APOE epsilon4 carriers (adjusted RR for >39 reproductive years compared with <34 reproductive years, 4.20 [95% CI, 1.97-8.92] for dementia and 3.42 [95% CI, 1.51-7.75] for AD), whereas in noncarriers, no clear association with dementia or AD was observed.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 414, "doc_id": 6309659, "label": "SUPPORTS", "evidence_sentence_ids": [12], "cited_doc_ids": [6309659], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Female carriers of the Apolipoprotein E4 (APOE4) allele have longer lifetime exposure to estrogen due to an increased reproductive period.\n\nDocument title: Reproductive period and risk of dementia in postmenopausal women.\n\nAbstract sentences:\n[0] CONTEXT Exogenous estrogen use may lower risk of dementia in postmenopausal women.\n[1] A relationship between long-term exposure to endogenous estrogens and incident dementia has been hypothesized but not studied.\n[2] OBJECTIVE To determine whether a longer reproductive period, as an indicator of longer exposure to endogenous estrogens, is associated with lower risk of dementia and Alzheimer disease (AD) in women who have natural menopause.\n[3] DESIGN AND SETTING The Rotterdam Study, a population-based prospective cohort study conducted in the Netherlands.\n[4] PARTICIPANTS A total of 3601 women aged 55 years or older who did not have dementia at baseline (1990-1993) and had information on age at menarche, age at menopause, and type of menopause.\n[5] Participants were reexamined in 1993-1994 and 1997-1999 and were continuously monitored for development of dementia.\n[6] MAIN OUTCOME MEASURES Incidence of dementia, based on Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition criteria, and AD, based on National Institute of Neurological Disorders and Stroke/Alzheimer's Disease and Related Disorders Association criteria, compared by quartiles of reproductive period among women with natural menopause.\n[7] RESULTS During 21 046 person-years of follow-up (median follow-up, 6.3 years), 199 women developed dementia, including 159 who developed AD.\n[8] After adjusting for age, dementia was not clearly associated with length of reproductive period.\n[9] However, after adjusting for multiple covariates, women with natural menopause and more reproductive years had an increased risk of dementia (adjusted rate ratio [RR] for women with >39 reproductive years [highest quartile] compared with <34 reproductive years [lowest quartile], 1.78; 95% confidence interval [CI], 1.12-2.84).\n[10] The adjusted RR per year of increase was 1.04 (95% CI, 1.01-1.08).\n[11] For risk of AD, the adjusted RRs were 1.51 (95% CI, 0.91-2.50) and 1.03 (95% CI, 1.00-1.07), respectively.\n[12] Risk of dementia associated with a longer reproductive period was most pronounced in APOE epsilon4 carriers (adjusted RR for >39 reproductive years compared with <34 reproductive years, 4.20 [95% CI, 1.97-8.92] for dementia and 3.42 [95% CI, 1.51-7.75] for AD), whereas in noncarriers, no clear association with dementia or AD was observed.\n[13] CONCLUSION Our findings do not support the hypothesis that a longer reproductive period reduces risk of dementia in women who have natural menopause."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"Risk of dementia associated with a longer reproductive period was most pronounced in APOE epsilon4 carriers (adjusted RR for >39 reproductive years compared with <34 reproductive years, 4.20 [95% CI, 1.97-8.92] for dementia and 3.42 [95% CI, 1.51-7.75] for AD), whereas in noncarriers, no clear association with dementia or AD was observed.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 416, "doc_id": 6309659, "label": "SUPPORTS", "evidence_sentence_ids": [12], "cited_doc_ids": [6309659], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Female carriers of the Apolipoprotein E4 (APOE4) allele have shorter lifetime exposure to estrogen due to a decreased reproductive period.\n\nDocument title: Reproductive period and risk of dementia in postmenopausal women.\n\nAbstract sentences:\n[0] CONTEXT Exogenous estrogen use may lower risk of dementia in postmenopausal women.\n[1] A relationship between long-term exposure to endogenous estrogens and incident dementia has been hypothesized but not studied.\n[2] OBJECTIVE To determine whether a longer reproductive period, as an indicator of longer exposure to endogenous estrogens, is associated with lower risk of dementia and Alzheimer disease (AD) in women who have natural menopause.\n[3] DESIGN AND SETTING The Rotterdam Study, a population-based prospective cohort study conducted in the Netherlands.\n[4] PARTICIPANTS A total of 3601 women aged 55 years or older who did not have dementia at baseline (1990-1993) and had information on age at menarche, age at menopause, and type of menopause.\n[5] Participants were reexamined in 1993-1994 and 1997-1999 and were continuously monitored for development of dementia.\n[6] MAIN OUTCOME MEASURES Incidence of dementia, based on Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition criteria, and AD, based on National Institute of Neurological Disorders and Stroke/Alzheimer's Disease and Related Disorders Association criteria, compared by quartiles of reproductive period among women with natural menopause.\n[7] RESULTS During 21 046 person-years of follow-up (median follow-up, 6.3 years), 199 women developed dementia, including 159 who developed AD.\n[8] After adjusting for age, dementia was not clearly associated with length of reproductive period.\n[9] However, after adjusting for multiple covariates, women with natural menopause and more reproductive years had an increased risk of dementia (adjusted rate ratio [RR] for women with >39 reproductive years [highest quartile] compared with <34 reproductive years [lowest quartile], 1.78; 95% confidence interval [CI], 1.12-2.84).\n[10] The adjusted RR per year of increase was 1.04 (95% CI, 1.01-1.08).\n[11] For risk of AD, the adjusted RRs were 1.51 (95% CI, 0.91-2.50) and 1.03 (95% CI, 1.00-1.07), respectively.\n[12] Risk of dementia associated with a longer reproductive period was most pronounced in APOE epsilon4 carriers (adjusted RR for >39 reproductive years compared with <34 reproductive years, 4.20 [95% CI, 1.97-8.92] for dementia and 3.42 [95% CI, 1.51-7.75] for AD), whereas in noncarriers, no clear association with dementia or AD was observed.\n[13] CONCLUSION Our findings do not support the hypothesis that a longer reproductive period reduces risk of dementia in women who have natural menopause."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"Risk of dementia associated with a longer reproductive period was most pronounced in APOE epsilon4 carriers (adjusted RR for >39 reproductive years compared with <34 reproductive years, 4.20 [95% CI, 1.97-8.92] for dementia and 3.42 [95% CI, 1.51-7.75] for AD), whereas in noncarriers, no clear association with dementia or AD was observed.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 417, "doc_id": 6309659, "label": "CONTRADICTS", "evidence_sentence_ids": [12], "cited_doc_ids": [6309659], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Fibroblast Growth Factor is a ligand which signals through receptor tyrosine kinases.\n\nDocument title: Sprouty1 Regulates Reversible Quiescence of a Self-Renewing Adult Muscle Stem Cell Pool during Regeneration\n\nAbstract sentences:\n[0] Satellite cells are skeletal muscle stem cells capable of self-renewal and differentiation after transplantation, but whether they contribute to endogenous muscle fiber repair has been unclear.\n[1] The transcription factor Pax7 marks satellite cells and is critical for establishing the adult satellite cell pool.\n[2] By using a lineage tracing approach, we show that after injury, quiescent adult Pax7(+) cells enter the cell cycle; a subpopulation returns to quiescence to replenish the satellite cell compartment, while others contribute to muscle fiber formation.\n[3] We demonstrate that Sprouty1 (Spry1), a receptor tyrosine kinase signaling inhibitor, is expressed in quiescent Pax7(+) satellite cells in uninjured muscle, downregulated in proliferating myogenic cells after injury, and reinduced as Pax7(+) cells re-enter quiescence.\n[4] We show that Spry1 is required for the return to quiescence and homeostasis of the satellite cell pool during repair.\n[5] Our results therefore define a role for Spry1 in adult muscle stem cell biology and tissue repair."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 418, "doc_id": 16660256, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [16660256], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Fibroblast growth factor 21 protects against atherosclerosis by modulating adiponectin and SREBP2 levels.\n\nDocument title: Fibroblast Growth Factor 21 Prevents Atherosclerosis by Suppression of Hepatic Sterol Regulatory Element-Binding Protein-2 and Induction of Adiponectin in Mice\n\nAbstract sentences:\n[0] BACKGROUND Fibroblast growth factor 21 (FGF21) is a metabolic hormone with pleiotropic effects on glucose and lipid metabolism and insulin sensitivity.\n[1] It acts as a key downstream target of both peroxisome proliferator-activated receptor α and γ, the agonists of which have been used for lipid lowering and insulin sensitization, respectively.\n[2] However, the role of FGF21 in the cardiovascular system remains elusive.\n[3] METHODS AND RESULTS The roles of FGF21 in atherosclerosis were investigated by evaluating the impact of FGF21 deficiency and replenishment with recombinant FGF21 in apolipoprotein E(-/-) mice.\n[4] FGF21 deficiency causes a marked exacerbation of atherosclerotic plaque formation and premature death in apolipoprotein E(-/-) mice, which is accompanied by hypoadiponectinemia and severe hypercholesterolemia.\n[5] Replenishment of FGF21 protects against atherosclerosis in apolipoprotein E(-/-)mice via 2 independent mechanisms, inducing the adipocyte production of adiponectin, which in turn acts on the blood vessels to inhibit neointima formation and macrophage inflammation, and suppressing the hepatic expression of the transcription factor sterol regulatory element-binding protein-2, thereby leading to reduced cholesterol synthesis and attenuation of hypercholesterolemia.\n[6] Chronic treatment with adiponectin partially reverses atherosclerosis without obvious effects on hypercholesterolemia in FGF21-deficient apolipoprotein E(-/-) mice.\n[7] By contrast, the cholesterol-lowering effects of FGF21 are abrogated by hepatic expression of sterol regulatory element-binding protein-2.\n[8] CONCLUSIONS FGF21 protects against atherosclerosis via fine tuning the multiorgan crosstalk among liver, adipose tissue, and blood vessels."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Replenishment of FGF21 protects against atherosclerosis in apolipoprotein E(-/-)mice via 2 independent mechanisms, inducing the adipocyte production of adiponectin, which in turn acts on the blood vessels to inhibit neointima formation and macrophage inflammation, and suppressing the hepatic expression of the transcription factor sterol regulatory element-binding protein-2, thereby leading to reduced cholesterol synthesis and attenuation of hypercholesterolemia.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 420, "doc_id": 9315213, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [9315213], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Flexible molecules experience less steric hindrance in the tumor microenviroment than rigid molecules.\n\nDocument title: Quantum dots spectrally distinguish multiple species within the tumor milieu in vivo\n\nAbstract sentences:\n[0] A solid tumor is an organ composed of cancer and host cells embedded in an extracellular matrix and nourished by blood vessels.\n[1] A prerequisite to understanding tumor pathophysiology is the ability to distinguish and monitor each component in dynamic studies.\n[2] Standard fluorophores hamper simultaneous intravital imaging of these components.\n[3] Here, we used multiphoton microscopy techniques and transgenic mice that expressed green fluorescent protein, and combined them with the use of quantum dot preparations.\n[4] We show that these fluorescent semiconductor nanocrystals can be customized to concurrently image and differentiate tumor vessels from both the perivascular cells and the matrix.\n[5] Moreover, we used them to measure the ability of particles of different sizes to access the tumor.\n[6] Finally, we successfully monitored the recruitment of quantum dot–labeled bone marrow–derived precursor cells to the tumor vasculature.\n[7] These examples show the versatility of quantum dots for studying tumor pathophysiology and creating avenues for treatment."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 422, "doc_id": 11172205, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [11172205], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Folate and vitamin B12 levels influence the association between homocysteine and preeclampsia.\n\nDocument title: Effect modification by population dietary folate on the association between MTHFR genotype, homocysteine, and stroke risk: a meta-analysis of genetic studies and randomised trials\n\nAbstract sentences:\n[0] BACKGROUND The MTHFR 677C→T polymorphism has been associated with raised homocysteine concentration and increased risk of stroke.\n[1] A previous overview showed that the effects were greatest in regions with low dietary folate consumption, but differentiation between the effect of folate and small-study bias was difficult.\n[2] A meta-analysis of randomised trials of homocysteine-lowering interventions showed no reduction in coronary heart disease events or stroke, but the trials were generally set in populations with high folate consumption.\n[3] We aimed to reduce the effect of small-study bias and investigate whether folate status modifies the association between MTHFR 677C→T and stroke in a genetic analysis and meta-analysis of randomised controlled trials.\n[4] METHODS We established a collaboration of genetic studies consisting of 237 datasets including 59,995 individuals with data for homocysteine and 20,885 stroke events.\n[5] We compared the genetic findings with a meta-analysis of 13 randomised trials of homocysteine-lowering treatments and stroke risk (45,549 individuals, 2314 stroke events, 269 transient ischaemic attacks).\n[6] FINDINGS The effect of the MTHFR 677C→T variant on homocysteine concentration was larger in low folate regions (Asia; difference between individuals with TT versus CC genotype, 3·12 μmol/L, 95% CI 2·23 to 4·01) than in areas with folate fortification (America, Australia, and New Zealand, high; 0·13 μmol/L, -0·85 to 1·11).\n[7] The odds ratio (OR) for stroke was also higher in Asia (1·68, 95% CI 1·44 to 1·97) than in America, Australia, and New Zealand, high (1·03, 0·84 to 1·25).\n[8] Most randomised trials took place in regions with high or increasing population folate concentrations.\n[9] The summary relative risk (RR) of stroke in trials of homocysteine-lowering interventions (0·94, 95% CI 0·85 to 1·04) was similar to that predicted for the same extent of homocysteine reduction in large genetic studies in populations with similar folate status (predicted RR 1·00, 95% CI 0·90 to 1·11).\n[10] Although the predicted effect of homocysteine reduction from large genetic studies in low folate regions (Asia) was larger (RR 0·78, 95% CI 0·68 to 0·90), no trial has evaluated the effect of lowering of homocysteine on stroke risk exclusively in a low folate region.\n[11] INTERPRETATION In regions with increasing levels or established policies of population folate supplementation, evidence from genetic studies and randomised trials is concordant in suggesting an absence of benefit from lowering of homocysteine for prevention of stroke.\n[12] Further large-scale genetic studies of the association between MTHFR 677C→T and stroke in low folate settings are needed to distinguish effect modification by folate from small-study bias.\n[13] If future randomised trials of homocysteine-lowering interventions for stroke prevention are undertaken, they should take place in regions with low folate consumption.\n[14] FUNDING Full funding sources listed at end of paper (see Acknowledgments)."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 423, "doc_id": 8595678, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [8595678], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: For every 1,000 children with cerebral palsy, more than 300 of them are premature or underweight at birth.\n\nDocument title: Changes in the prevalence of cerebral palsy for children born very prematurely within a population-based program over 30 years.\n\nAbstract sentences:\n[0] CONTEXT Although cerebral palsy (CP) among extremely premature infants has been reported as a major morbidity outcome, there are difficulties comparing published CP rates from many sites over various birth years.\n[1] OBJECTIVE To assess the changes in population-based, gestational age-specific prevalence rates of CP among extremely premature infants over 30 years.\n[2] DESIGN Prospective population-based longitudinal outcome study.\n[3] SETTING AND PARTICIPANTS In Northern Alberta, 2318 infants 20 to 27 weeks' gestational age with birth weights of 500 to 1249 g were liveborn from 1974 through 2003.\n[4] By 2 years of age, 1437 (62%) had died, 23 (1%) were lost to follow-up, and 858 (37%) had received multidisciplinary neurodevelopmental assessment.\n[5] MAIN OUTCOME MEASURE Population-based prevalence rates of CP were determined.\n[6] Logistic regression with linear spline was used to assess changes in CP prevalence over time.\n[7] RESULTS At age 2 years, 122 (14.2%) of 858 survivors had CP.\n[8] This diagnosis was confirmed for each child by age 3 years or older.\n[9] Among those whose gestational age was 20 to 25 weeks, population-based survival increased from 4% to 31% (P<.001), while CP prevalence per 1000 live births increased monotonically from 0 to 110 until the years 1992-1994 (P<.001) and decreased thereafter to 22 in the years 2001-2003 (P<.001).\n[10] Among those whose gestational age was 26 to 27 weeks, population-based survival increased from 23% to between 75% and 80% (P<.001), while CP prevalence per 1000 live births increased monotonically from 15 to 155 until the years 1992-1994 (P<.001) and then decreased to 16 in the years 2001-2003 (P<.001).\n[11] For all survivors born in the years 2001-2003, CP prevalence was 19 per 1000 live births.\n[12] CONCLUSION Population-based CP prevalence rates for children whose gestational age was 20 to 27 weeks and whose birth weight ranged from 500 to 1249 g show steady reductions in the last decade with stable or reducing mortality, reversing trends prior to 1992-1994."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 425, "doc_id": 33257464, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [33257464], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Forkhead 0 (fox0) transcription factors are involved in apoptosis.\n\nDocument title: Cell Stem Cell Review FoxO Transcription Factors and Stem Cell Homeostasis: Insights from the Hematopoietic System\n\nAbstract sentences:\n[0] The forkhead O (FoxO) family of transcription factors participates in diverse physiologic processes, including induction of cell-cycle arrest, stress resistance, differentiation, apoptosis, and metabolism.\n[1] Several recent studies indicate that FoxO-dependent signaling is required for long-term regenerative potential of the hematopoietic stem cell (HSC) compartment through regulation of HSC response to physiologic oxidative stress, quiescence, and survival.\n[2] These observations link FoxO function in mammalian systems with the evolutionarily conserved role of FoxO in promotion of stress resistance and longevity in lower phylogenetic systems.\n[3] Furthermore, these findings have implications for aging in higher organisms and in malignant stem cell biology, and suggest that FoxOs may play an important role in the maintenance and integrity of stem cell compartments in a broad spectrum of tissues."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"The forkhead O (FoxO) family of transcription factors participates in diverse physiologic processes, including induction of cell-cycle arrest, stress resistance, differentiation, apoptosis, and metabolism.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 426, "doc_id": 16728949, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [16728949], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Forkhead 0 (fox0) transcription factors are involved in cellular differentiation.\n\nDocument title: Cell Stem Cell Review FoxO Transcription Factors and Stem Cell Homeostasis: Insights from the Hematopoietic System\n\nAbstract sentences:\n[0] The forkhead O (FoxO) family of transcription factors participates in diverse physiologic processes, including induction of cell-cycle arrest, stress resistance, differentiation, apoptosis, and metabolism.\n[1] Several recent studies indicate that FoxO-dependent signaling is required for long-term regenerative potential of the hematopoietic stem cell (HSC) compartment through regulation of HSC response to physiologic oxidative stress, quiescence, and survival.\n[2] These observations link FoxO function in mammalian systems with the evolutionarily conserved role of FoxO in promotion of stress resistance and longevity in lower phylogenetic systems.\n[3] Furthermore, these findings have implications for aging in higher organisms and in malignant stem cell biology, and suggest that FoxOs may play an important role in the maintenance and integrity of stem cell compartments in a broad spectrum of tissues."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"The forkhead O (FoxO) family of transcription factors participates in diverse physiologic processes, including induction of cell-cycle arrest, stress resistance, differentiation, apoptosis, and metabolism.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 428, "doc_id": 16728949, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [16728949], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Formation of N-terminal pyroglutamate by glutamine cyclase (GC) competes with NTAQ1 for Nt-Gln substrates.\n\nDocument title: Glutamine-specific N-terminal amidase, a component of the N-end rule pathway.\n\nAbstract sentences:\n[0] Deamidation of N-terminal Gln by Nt(Q)-amidase, an N-terminal amidohydrolase, is a part of the N-end rule pathway of protein degradation.\n[1] We detected the activity of Nt(Q)-amidase, termed Ntaq1, in mouse tissues, purified Ntaq1 from bovine brains, identified its gene, and began analyzing this enzyme.\n[2] Ntaq1 is highly conserved among animals, plants, and some fungi, but its sequence is dissimilar to sequences of other amidases.\n[3] An earlier mutant in the Drosophila Cg8253 gene that we show here to encode Nt(Q)-amidase has defective long-term memory.\n[4] Other studies identified protein ligands of the uncharacterized human C8orf32 protein that we show here to be the Ntaq1 Nt(Q)-amidase.\n[5] Remarkably, \"high-throughput\" studies have recently solved the crystal structure of C8orf32 (Ntaq1).\n[6] Our site-directed mutagenesis of Ntaq1 and its crystal structure indicate that the active site and catalytic mechanism of Nt(Q)-amidase are similar to those of transglutaminases."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 429, "doc_id": 36540079, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [36540079], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: FoxO3a activation in neuronal death is inhibited by reactive oxygen species (ROS).\n\nDocument title: Stress-dependent regulation of FOXO transcription factors by the SIRT1 deacetylase.\n\nAbstract sentences:\n[0] The Sir2 deacetylase modulates organismal life-span in various species.\n[1] However, the molecular mechanisms by which Sir2 increases longevity are largely unknown.\n[2] We show that in mammalian cells, the Sir2 homolog SIRT1 appears to control the cellular response to stress by regulating the FOXO family of Forkhead transcription factors, a family of proteins that function as sensors of the insulin signaling pathway and as regulators of organismal longevity.\n[3] SIRT1 and the FOXO transcription factor FOXO3 formed a complex in cells in response to oxidative stress, and SIRT1 deacetylated FOXO3 in vitro and within cells.\n[4] SIRT1 had a dual effect on FOXO3 function: SIRT1 increased FOXO3's ability to induce cell cycle arrest and resistance to oxidative stress but inhibited FOXO3's ability to induce cell death.\n[5] Thus, one way in which members of the Sir2 family of proteins may increase organismal longevity is by tipping FOXO-dependent responses away from apoptosis and toward stress resistance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Thus, one way in which members of the Sir2 family of proteins may increase organismal longevity is by tipping FOXO-dependent responses away from apoptosis and toward stress resistance.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 430, "doc_id": 28937856, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [28937856], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Foxk2 regulates autophagy genes in muscle cells and fibroblast cells.\n\nDocument title: Foxk proteins repress the initiation of starvation-induced atrophy and autophagy programs\n\nAbstract sentences:\n[0] Autophagy is the primary catabolic process triggered in response to starvation.\n[1] Although autophagic regulation within the cytosolic compartment is well established, it is becoming clear that nuclear events also regulate the induction or repression of autophagy.\n[2] Nevertheless, a thorough understanding of the mechanisms by which sequence-specific transcription factors modulate expression of genes required for autophagy is lacking.\n[3] Here, we identify Foxk proteins (Foxk1 and Foxk2) as transcriptional repressors of autophagy in muscle cells and fibroblasts.\n[4] Interestingly, Foxk1/2 serve to counter-balance another forkhead transcription factor, Foxo3, which induces an overlapping set of autophagic and atrophic targets in muscle.\n[5] Foxk1/2 specifically recruits Sin3A-HDAC complexes to restrict acetylation of histone H4 and expression of critical autophagy genes.\n[6] Remarkably, mTOR promotes the transcriptional activity of Foxk1 by facilitating nuclear entry to specifically limit basal levels of autophagy in nutrient-rich conditions.\n[7] Our study highlights an ancient, conserved mechanism whereby nutritional status is interpreted by mTOR to restrict autophagy by repressing essential autophagy genes through Foxk-Sin3-mediated transcriptional control."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Here, we identify Foxk proteins (Foxk1 and Foxk2) as transcriptional repressors of autophagy in muscle cells and fibroblasts.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 432, "doc_id": 8002887, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [8002887], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Foxk2 regulates autophagy genes in muscle cells and fibroblast cells.\n\nDocument title: Foxk proteins repress the initiation of starvation-induced atrophy and autophagy programs\n\nAbstract sentences:\n[0] Autophagy is the primary catabolic process triggered in response to starvation.\n[1] Although autophagic regulation within the cytosolic compartment is well established, it is becoming clear that nuclear events also regulate the induction or repression of autophagy.\n[2] Nevertheless, a thorough understanding of the mechanisms by which sequence-specific transcription factors modulate expression of genes required for autophagy is lacking.\n[3] Here, we identify Foxk proteins (Foxk1 and Foxk2) as transcriptional repressors of autophagy in muscle cells and fibroblasts.\n[4] Interestingly, Foxk1/2 serve to counter-balance another forkhead transcription factor, Foxo3, which induces an overlapping set of autophagic and atrophic targets in muscle.\n[5] Foxk1/2 specifically recruits Sin3A-HDAC complexes to restrict acetylation of histone H4 and expression of critical autophagy genes.\n[6] Remarkably, mTOR promotes the transcriptional activity of Foxk1 by facilitating nuclear entry to specifically limit basal levels of autophagy in nutrient-rich conditions.\n[7] Our study highlights an ancient, conserved mechanism whereby nutritional status is interpreted by mTOR to restrict autophagy by repressing essential autophagy genes through Foxk-Sin3-mediated transcriptional control."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Foxk1/2 specifically recruits Sin3A-HDAC complexes to restrict acetylation of histone H4 and expression of critical autophagy genes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 432, "doc_id": 8002887, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [8002887], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Foxp3 enables the expression of transcriptional regulators implicated in memory T cell development.\n\nDocument title: Extrathymic Generation of Regulatory T Cells in Placental Mammals Mitigates Maternal-Fetal Conflict\n\nAbstract sentences:\n[0] Regulatory T (Treg) cells, whose differentiation and function are controlled by X chromosome-encoded transcription factor Foxp3, are generated in the thymus (tTreg) and extrathymically (peripheral, pTreg), and their deficiency results in fatal autoimmunity.\n[1] Here, we demonstrate that a Foxp3 enhancer, conserved noncoding sequence 1 (CNS1), essential for pTreg but dispensable for tTreg cell generation, is present only in placental mammals.\n[2] CNS1 is largely composed of mammalian-wide interspersed repeats (MIR) that have undergone retrotransposition during early mammalian radiation.\n[3] During pregnancy, pTreg cells specific to a model paternal alloantigen were generated in a CNS1-dependent manner and accumulated in the placenta.\n[4] Furthermore, when mated with allogeneic, but not syngeneic, males, CNS1-deficient females showed increased fetal resorption accompanied by increased immune cell infiltration and defective remodeling of spiral arteries.\n[5] Our results suggest that, during evolution, a CNS1-dependent mechanism of extrathymic differentiation of Treg cells emerged in placental animals to enforce maternal-fetal tolerance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 434, "doc_id": 9500590, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [9500590], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Foxp3 represses the expression of transcriptional regulators implicated in memory T cell development.\n\nDocument title: Extrathymic Generation of Regulatory T Cells in Placental Mammals Mitigates Maternal-Fetal Conflict\n\nAbstract sentences:\n[0] Regulatory T (Treg) cells, whose differentiation and function are controlled by X chromosome-encoded transcription factor Foxp3, are generated in the thymus (tTreg) and extrathymically (peripheral, pTreg), and their deficiency results in fatal autoimmunity.\n[1] Here, we demonstrate that a Foxp3 enhancer, conserved noncoding sequence 1 (CNS1), essential for pTreg but dispensable for tTreg cell generation, is present only in placental mammals.\n[2] CNS1 is largely composed of mammalian-wide interspersed repeats (MIR) that have undergone retrotransposition during early mammalian radiation.\n[3] During pregnancy, pTreg cells specific to a model paternal alloantigen were generated in a CNS1-dependent manner and accumulated in the placenta.\n[4] Furthermore, when mated with allogeneic, but not syngeneic, males, CNS1-deficient females showed increased fetal resorption accompanied by increased immune cell infiltration and defective remodeling of spiral arteries.\n[5] Our results suggest that, during evolution, a CNS1-dependent mechanism of extrathymic differentiation of Treg cells emerged in placental animals to enforce maternal-fetal tolerance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 435, "doc_id": 9500590, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [9500590], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: G-CSF increases the expansion and infiltration of MDSCs into tumors.\n\nDocument title: Oncogenic mTOR signaling recruits myeloid-derived suppressor cells to promote tumor initiation\n\nAbstract sentences:\n[0] Myeloid-derived suppressor cells (MDSCs) play critical roles in primary and metastatic cancer progression.\n[1] MDSC regulation is widely variable even among patients harbouring the same type of malignancy, and the mechanisms governing such heterogeneity are largely unknown.\n[2] Here, integrating human tumour genomics and syngeneic mammary tumour models, we demonstrate that mTOR signalling in cancer cells dictates a mammary tumour's ability to stimulate MDSC accumulation through regulating G-CSF.\n[3] Inhibiting this pathway or its activators (for example, FGFR) impairs tumour progression, which is partially rescued by restoring MDSCs or G-CSF.\n[4] Tumour-initiating cells (TICs) exhibit elevated G-CSF.\n[5] MDSCs reciprocally increase TIC frequency through activating Notch in tumour cells, forming a feedforward loop.\n[6] Analyses of primary breast cancers and patient-derived xenografts corroborate these mechanisms in patients.\n[7] These findings establish a non-canonical oncogenic role of mTOR signalling in recruiting pro-tumorigenic MDSCs and show how defined cancer subsets may evolve to promote and depend on a distinct immune microenvironment."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here, integrating human tumour genomics and syngeneic mammary tumour models, we demonstrate that mTOR signalling in cancer cells dictates a mammary tumour's ability to stimulate MDSC accumulation through regulating G-CSF.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 441, "doc_id": 2014909, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [2014909], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: GATA3 regulates cell cycle progression in bone marrow hematopoietic stem cells.\n\nDocument title: GATA-3 regulates hematopoietic stem cell maintenance and cell-cycle entry.\n\nAbstract sentences:\n[0] Maintaining hematopoietic stem cell (HSC) quiescence is a critical property for the life-long generation of blood cells.\n[1] Approximately 75% of cells in a highly enriched long-term repopulating HSC (LT-HSC) pool (Lin(-)Sca1(+)c-Kit(hi)CD150(+)CD48(-)) are quiescent, with only a small percentage of the LT-HSCs in cycle.\n[2] Transcription factor GATA-3 is known to be vital for the development of T cells at multiple stages in the thymus and for Th2 differentiation in the peripheral organs.\n[3] Although it is well documented that GATA-3 is expressed in HSCs, a role for GATA-3 in any prethymic progenitor cell has not been established.\n[4] In the present study, we show that Gata3-null mutant mice generate fewer LT-HSCs and that fewer Gata3-null LT-HSCs are in cycle.\n[5] Furthermore, Gata3 mutant hematopoietic progenitor cells fail to be recruited into an increased cycling state after 5-fluorouracil-induced myelosuppression.\n[6] Therefore, GATA-3 is required for the maintenance of a normal number of LT-HSCs and for their entry into the cell cycle."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5, 6]\nExplanation: Evidence states: \"Furthermore, Gata3 mutant hematopoietic progenitor cells fail to be recruited into an increased cycling state after 5-fluorouracil-induced myelosuppression. Therefore, GATA-3 is required for the maintenance of a normal number of LT-HSCs and for their entry into the cell cycle.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 444, "doc_id": 10165258, "label": "SUPPORTS", "evidence_sentence_ids": [5, 6], "cited_doc_ids": [10165258], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: GATA3 regulates self-renewal capacity in bone marrow hematopoietic stem cells.\n\nDocument title: GATA-3 regulates hematopoietic stem cell maintenance and cell-cycle entry.\n\nAbstract sentences:\n[0] Maintaining hematopoietic stem cell (HSC) quiescence is a critical property for the life-long generation of blood cells.\n[1] Approximately 75% of cells in a highly enriched long-term repopulating HSC (LT-HSC) pool (Lin(-)Sca1(+)c-Kit(hi)CD150(+)CD48(-)) are quiescent, with only a small percentage of the LT-HSCs in cycle.\n[2] Transcription factor GATA-3 is known to be vital for the development of T cells at multiple stages in the thymus and for Th2 differentiation in the peripheral organs.\n[3] Although it is well documented that GATA-3 is expressed in HSCs, a role for GATA-3 in any prethymic progenitor cell has not been established.\n[4] In the present study, we show that Gata3-null mutant mice generate fewer LT-HSCs and that fewer Gata3-null LT-HSCs are in cycle.\n[5] Furthermore, Gata3 mutant hematopoietic progenitor cells fail to be recruited into an increased cycling state after 5-fluorouracil-induced myelosuppression.\n[6] Therefore, GATA-3 is required for the maintenance of a normal number of LT-HSCs and for their entry into the cell cycle."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"In the present study, we show that Gata3-null mutant mice generate fewer LT-HSCs and that fewer Gata3-null LT-HSCs are in cycle.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 445, "doc_id": 10165258, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [10165258], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: GATA3 regulates self-renewal capacity in bone marrow hematopoietic stem cells.\n\nDocument title: GATA-3 regulates hematopoietic stem cell maintenance and cell-cycle entry.\n\nAbstract sentences:\n[0] Maintaining hematopoietic stem cell (HSC) quiescence is a critical property for the life-long generation of blood cells.\n[1] Approximately 75% of cells in a highly enriched long-term repopulating HSC (LT-HSC) pool (Lin(-)Sca1(+)c-Kit(hi)CD150(+)CD48(-)) are quiescent, with only a small percentage of the LT-HSCs in cycle.\n[2] Transcription factor GATA-3 is known to be vital for the development of T cells at multiple stages in the thymus and for Th2 differentiation in the peripheral organs.\n[3] Although it is well documented that GATA-3 is expressed in HSCs, a role for GATA-3 in any prethymic progenitor cell has not been established.\n[4] In the present study, we show that Gata3-null mutant mice generate fewer LT-HSCs and that fewer Gata3-null LT-HSCs are in cycle.\n[5] Furthermore, Gata3 mutant hematopoietic progenitor cells fail to be recruited into an increased cycling state after 5-fluorouracil-induced myelosuppression.\n[6] Therefore, GATA-3 is required for the maintenance of a normal number of LT-HSCs and for their entry into the cell cycle."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Therefore, GATA-3 is required for the maintenance of a normal number of LT-HSCs and for their entry into the cell cycle.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 445, "doc_id": 10165258, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [10165258], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Gastric infection with Helicobacter pylori decreases risk of gastric cancer in humans.\n\nDocument title: Association between infection with Helicobacter pylori and risk of gastric cancer: evidence from a prospective investigation.\n\nAbstract sentences:\n[0] OBJECTIVE To investigate the association between gastric cancer and prior infection with Helicobacter pylori.\n[1] DESIGN Case-control comparison of prevalence of IgG antibodies to H pylori in blood samples collected prospectively, before diagnosis of gastric cancer in the cases.\n[2] Presence of H pylori antibody (greater than 10 micrograms IgG/ml) determined by enzyme linked immunosorbent assay (ELISA).\n[3] SUBJECTS 29 men with a subsequent diagnosis of gastric cancer and 116 aged matched controls selected from over 22,000 middle aged men participating in two ongoing cohort studies (the British United Provident Association study and the Caerphilly collaborative heart disease study), who had provided blood samples during 1975-1982.\n[4] RESULTS 20 of the 29 cases (69%) and 54 of the 116 controls (47%) were positive for H pylori specific antibody.\n[5] The median specific IgG concentration was significantly higher in the cases than controls (90 micrograms/ml v 3.6 micrograms/ml, p less than 0.01).\n[6] The estimated odds ratio for the risk of gastric cancer in those with a history of infection with H pylori was 2.77 (95% confidence interval 1.04 to 7.97, 2p = 0.039).\n[7] CONCLUSIONS H pylori infection may be an important cause of gastric cancer; between 35% and 55% of all cases may be associated with such an infection."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"The estimated odds ratio for the risk of gastric cancer in those with a history of infection with H pylori was 2.77 (95% confidence interval 1.04 to 7.97, 2p = 0.039).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 447, "doc_id": 2052720, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [2052720], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Gastric infection with Helicobacter pylori decreases risk of gastric cancer in humans.\n\nDocument title: Association between infection with Helicobacter pylori and risk of gastric cancer: evidence from a prospective investigation.\n\nAbstract sentences:\n[0] OBJECTIVE To investigate the association between gastric cancer and prior infection with Helicobacter pylori.\n[1] DESIGN Case-control comparison of prevalence of IgG antibodies to H pylori in blood samples collected prospectively, before diagnosis of gastric cancer in the cases.\n[2] Presence of H pylori antibody (greater than 10 micrograms IgG/ml) determined by enzyme linked immunosorbent assay (ELISA).\n[3] SUBJECTS 29 men with a subsequent diagnosis of gastric cancer and 116 aged matched controls selected from over 22,000 middle aged men participating in two ongoing cohort studies (the British United Provident Association study and the Caerphilly collaborative heart disease study), who had provided blood samples during 1975-1982.\n[4] RESULTS 20 of the 29 cases (69%) and 54 of the 116 controls (47%) were positive for H pylori specific antibody.\n[5] The median specific IgG concentration was significantly higher in the cases than controls (90 micrograms/ml v 3.6 micrograms/ml, p less than 0.01).\n[6] The estimated odds ratio for the risk of gastric cancer in those with a history of infection with H pylori was 2.77 (95% confidence interval 1.04 to 7.97, 2p = 0.039).\n[7] CONCLUSIONS H pylori infection may be an important cause of gastric cancer; between 35% and 55% of all cases may be associated with such an infection."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"CONCLUSIONS H pylori infection may be an important cause of gastric cancer; between 35% and 55% of all cases may be associated with such an infection.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 447, "doc_id": 2052720, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [2052720], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Gastric infection with Helicobacter pylori increases risk of gastric cancer in humans.\n\nDocument title: Association between infection with Helicobacter pylori and risk of gastric cancer: evidence from a prospective investigation.\n\nAbstract sentences:\n[0] OBJECTIVE To investigate the association between gastric cancer and prior infection with Helicobacter pylori.\n[1] DESIGN Case-control comparison of prevalence of IgG antibodies to H pylori in blood samples collected prospectively, before diagnosis of gastric cancer in the cases.\n[2] Presence of H pylori antibody (greater than 10 micrograms IgG/ml) determined by enzyme linked immunosorbent assay (ELISA).\n[3] SUBJECTS 29 men with a subsequent diagnosis of gastric cancer and 116 aged matched controls selected from over 22,000 middle aged men participating in two ongoing cohort studies (the British United Provident Association study and the Caerphilly collaborative heart disease study), who had provided blood samples during 1975-1982.\n[4] RESULTS 20 of the 29 cases (69%) and 54 of the 116 controls (47%) were positive for H pylori specific antibody.\n[5] The median specific IgG concentration was significantly higher in the cases than controls (90 micrograms/ml v 3.6 micrograms/ml, p less than 0.01).\n[6] The estimated odds ratio for the risk of gastric cancer in those with a history of infection with H pylori was 2.77 (95% confidence interval 1.04 to 7.97, 2p = 0.039).\n[7] CONCLUSIONS H pylori infection may be an important cause of gastric cancer; between 35% and 55% of all cases may be associated with such an infection."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"The estimated odds ratio for the risk of gastric cancer in those with a history of infection with H pylori was 2.77 (95% confidence interval 1.04 to 7.97, 2p = 0.039).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 448, "doc_id": 2052720, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [2052720], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Gastric infection with Helicobacter pylori increases risk of gastric cancer in humans.\n\nDocument title: Association between infection with Helicobacter pylori and risk of gastric cancer: evidence from a prospective investigation.\n\nAbstract sentences:\n[0] OBJECTIVE To investigate the association between gastric cancer and prior infection with Helicobacter pylori.\n[1] DESIGN Case-control comparison of prevalence of IgG antibodies to H pylori in blood samples collected prospectively, before diagnosis of gastric cancer in the cases.\n[2] Presence of H pylori antibody (greater than 10 micrograms IgG/ml) determined by enzyme linked immunosorbent assay (ELISA).\n[3] SUBJECTS 29 men with a subsequent diagnosis of gastric cancer and 116 aged matched controls selected from over 22,000 middle aged men participating in two ongoing cohort studies (the British United Provident Association study and the Caerphilly collaborative heart disease study), who had provided blood samples during 1975-1982.\n[4] RESULTS 20 of the 29 cases (69%) and 54 of the 116 controls (47%) were positive for H pylori specific antibody.\n[5] The median specific IgG concentration was significantly higher in the cases than controls (90 micrograms/ml v 3.6 micrograms/ml, p less than 0.01).\n[6] The estimated odds ratio for the risk of gastric cancer in those with a history of infection with H pylori was 2.77 (95% confidence interval 1.04 to 7.97, 2p = 0.039).\n[7] CONCLUSIONS H pylori infection may be an important cause of gastric cancer; between 35% and 55% of all cases may be associated with such an infection."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"CONCLUSIONS H pylori infection may be an important cause of gastric cancer; between 35% and 55% of all cases may be associated with such an infection.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 448, "doc_id": 2052720, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [2052720], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Gastric lavage is an effective treatment for acute paraquat poisoning.\n\nDocument title: Multiple-dose activated charcoal in acute self-poisoning: a randomised controlled trial\n\nAbstract sentences:\n[0] BACKGROUND The case-fatality for intentional self-poisoning in the rural developing world is 10-50-fold higher than that in industrialised countries, mostly because of the use of highly toxic pesticides and plants.\n[1] We therefore aimed to assess whether routine treatment with multiple-dose activated charcoal, to interrupt enterovascular or enterohepatic circulations, offers benefit compared with no charcoal in such an environment.\n[2] METHODS We did an open-label, parallel group, randomised, controlled trial of six 50 g doses of activated charcoal at 4-h intervals versus no charcoal versus one 50 g dose of activated charcoal in three Sri Lankan hospitals.\n[3] 4632 patients were randomised to receive no charcoal (n=1554), one dose of charcoal (n=1545), or six doses of charcoal (n=1533); outcomes were available for 4629 patients.\n[4] 2338 (51%) individuals had ingested pesticides, whereas 1647 (36%) had ingested yellow oleander (Thevetia peruviana) seeds.\n[5] Mortality was the primary outcome measure.\n[6] Analysis was by intention to treat.\n[7] The trial is registered with controlled-trials.com as ISRCTN02920054.\n[8] FINDINGS Mortality did not differ between the groups.\n[9] 97 (6.3%) of 1531 participants in the multiple-dose group died, compared with 105 (6.8%) of 1554 in the no charcoal group (adjusted odds ratio 0.96, 95% CI 0.70-1.33).\n[10] No differences were noted for patients who took particular poisons, were severely ill on admission, or who presented early.\n[11] INTERPRETATION We cannot recommend the routine use of multiple-dose activated charcoal in rural Asia Pacific; although further studies of early charcoal administration might be useful, effective affordable treatments are urgently needed."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 449, "doc_id": 12209494, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [12209494, 3430789], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: General exercise therapy is more effective than rotator cuff exercises in reducing pain and improving function of the shoulder.\n\nDocument title: Effect of specific exercise strategy on need for surgery in patients with subacromial impingement syndrome: randomised controlled study\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate if a specific exercise strategy, targeting the rotator cuff and scapula stabilisers, improves shoulder function and pain more than unspecific exercises in patients with subacromial impingement syndrome, thereby decreasing the need for arthroscopic subacromial decompression.\n[1] DESIGN Randomised, participant and single assessor blinded, controlled study.\n[2] SETTING Department of orthopaedics in a Swedish university hospital.\n[3] PARTICIPANTS 102 patients with long standing (over six months) persistent subacromial impingement syndrome in whom earlier conservative treatment had failed, recruited through orthopaedic specialists.\n[4] INTERVENTIONS The specific exercise strategy consisted of strengthening eccentric exercises for the rotator cuff and concentric/eccentric exercises for the scapula stabilisers in combination with manual mobilisation.\n[5] The control exercise programme consisted of unspecific movement exercises for the neck and shoulder.\n[6] Patients in both groups received five to six individual guided treatment sessions during 12 weeks.\n[7] In between these supervised sessions the participants performed home exercises once or twice a day for 12 weeks.\n[8] MAIN OUTCOME MEASURES The primary outcome was the Constant-Murley shoulder assessment score evaluating shoulder function and pain.\n[9] Secondary outcomes were patients' global impression of change because of treatment and decision regarding surgery.\n[10] RESULTS Most (97, 95%) participants completed the 12 week study.\n[11] There was a significantly greater improvement in the Constant-Murley score in the specific exercise group than in the control exercise group (24 points (95% confidence interval 19 to 28.0) v 9 points (5 to 13); mean difference between group: 15 points (8.5 to 20.6)).\n[12] Significantly more patients in the specific exercise group reported successful outcome (defined as large improvement or recovered) in the patients' global assessment of change because of treatment: 69% (35/51) v 24% (11/46); odds ratio 7.6, 3.1 to 18.9; P<0.001.\n[13] A significantly lower proportion of patients in the specific exercise group subsequently chose to undergo surgery: 20% (10/51) v 63% (29/46); odds ratio 7.7, 3.1 to 19.4; P<0.001).\n[14] CONCLUSION A specific exercise strategy, focusing on strengthening eccentric exercises for the rotator cuff and concentric/eccentric exercises for the scapula stabilisers, is effective in reducing pain and improving shoulder function in patients with persistent subacromial impingement syndrome.\n[15] By extension, this exercise strategy reduces the need for arthroscopic subacromial decompression within the three month timeframe used in the study.\n[16] TRIAL REGISTRATION Clinical trials NCT01037673."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"There was a significantly greater improvement in the Constant-Murley score in the specific exercise group than in the control exercise group (24 points (95% confidence interval 19 to 28.0) v 9 points (5 to 13); mean difference between group: 15 points (8.5 to 20.6)).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 453, "doc_id": 4200695, "label": "CONTRADICTS", "evidence_sentence_ids": [11], "cited_doc_ids": [4200695], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: General exercise therapy is more effective than scapular stabilizer exercises in reducing pain and improving function of the shoulder.\n\nDocument title: Effect of specific exercise strategy on need for surgery in patients with subacromial impingement syndrome: randomised controlled study\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate if a specific exercise strategy, targeting the rotator cuff and scapula stabilisers, improves shoulder function and pain more than unspecific exercises in patients with subacromial impingement syndrome, thereby decreasing the need for arthroscopic subacromial decompression.\n[1] DESIGN Randomised, participant and single assessor blinded, controlled study.\n[2] SETTING Department of orthopaedics in a Swedish university hospital.\n[3] PARTICIPANTS 102 patients with long standing (over six months) persistent subacromial impingement syndrome in whom earlier conservative treatment had failed, recruited through orthopaedic specialists.\n[4] INTERVENTIONS The specific exercise strategy consisted of strengthening eccentric exercises for the rotator cuff and concentric/eccentric exercises for the scapula stabilisers in combination with manual mobilisation.\n[5] The control exercise programme consisted of unspecific movement exercises for the neck and shoulder.\n[6] Patients in both groups received five to six individual guided treatment sessions during 12 weeks.\n[7] In between these supervised sessions the participants performed home exercises once or twice a day for 12 weeks.\n[8] MAIN OUTCOME MEASURES The primary outcome was the Constant-Murley shoulder assessment score evaluating shoulder function and pain.\n[9] Secondary outcomes were patients' global impression of change because of treatment and decision regarding surgery.\n[10] RESULTS Most (97, 95%) participants completed the 12 week study.\n[11] There was a significantly greater improvement in the Constant-Murley score in the specific exercise group than in the control exercise group (24 points (95% confidence interval 19 to 28.0) v 9 points (5 to 13); mean difference between group: 15 points (8.5 to 20.6)).\n[12] Significantly more patients in the specific exercise group reported successful outcome (defined as large improvement or recovered) in the patients' global assessment of change because of treatment: 69% (35/51) v 24% (11/46); odds ratio 7.6, 3.1 to 18.9; P<0.001.\n[13] A significantly lower proportion of patients in the specific exercise group subsequently chose to undergo surgery: 20% (10/51) v 63% (29/46); odds ratio 7.7, 3.1 to 19.4; P<0.001).\n[14] CONCLUSION A specific exercise strategy, focusing on strengthening eccentric exercises for the rotator cuff and concentric/eccentric exercises for the scapula stabilisers, is effective in reducing pain and improving shoulder function in patients with persistent subacromial impingement syndrome.\n[15] By extension, this exercise strategy reduces the need for arthroscopic subacromial decompression within the three month timeframe used in the study.\n[16] TRIAL REGISTRATION Clinical trials NCT01037673."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"There was a significantly greater improvement in the Constant-Murley score in the specific exercise group than in the control exercise group (24 points (95% confidence interval 19 to 28.0) v 9 points (5 to 13); mean difference between group: 15 points (8.5 to 20.6)).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 454, "doc_id": 4200695, "label": "CONTRADICTS", "evidence_sentence_ids": [11], "cited_doc_ids": [4200695], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: General exercise therapy is more effective than scapular stabilizer exercises in reducing pain and improving function of the shoulder.\n\nDocument title: Effect of specific exercise strategy on need for surgery in patients with subacromial impingement syndrome: randomised controlled study\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate if a specific exercise strategy, targeting the rotator cuff and scapula stabilisers, improves shoulder function and pain more than unspecific exercises in patients with subacromial impingement syndrome, thereby decreasing the need for arthroscopic subacromial decompression.\n[1] DESIGN Randomised, participant and single assessor blinded, controlled study.\n[2] SETTING Department of orthopaedics in a Swedish university hospital.\n[3] PARTICIPANTS 102 patients with long standing (over six months) persistent subacromial impingement syndrome in whom earlier conservative treatment had failed, recruited through orthopaedic specialists.\n[4] INTERVENTIONS The specific exercise strategy consisted of strengthening eccentric exercises for the rotator cuff and concentric/eccentric exercises for the scapula stabilisers in combination with manual mobilisation.\n[5] The control exercise programme consisted of unspecific movement exercises for the neck and shoulder.\n[6] Patients in both groups received five to six individual guided treatment sessions during 12 weeks.\n[7] In between these supervised sessions the participants performed home exercises once or twice a day for 12 weeks.\n[8] MAIN OUTCOME MEASURES The primary outcome was the Constant-Murley shoulder assessment score evaluating shoulder function and pain.\n[9] Secondary outcomes were patients' global impression of change because of treatment and decision regarding surgery.\n[10] RESULTS Most (97, 95%) participants completed the 12 week study.\n[11] There was a significantly greater improvement in the Constant-Murley score in the specific exercise group than in the control exercise group (24 points (95% confidence interval 19 to 28.0) v 9 points (5 to 13); mean difference between group: 15 points (8.5 to 20.6)).\n[12] Significantly more patients in the specific exercise group reported successful outcome (defined as large improvement or recovered) in the patients' global assessment of change because of treatment: 69% (35/51) v 24% (11/46); odds ratio 7.6, 3.1 to 18.9; P<0.001.\n[13] A significantly lower proportion of patients in the specific exercise group subsequently chose to undergo surgery: 20% (10/51) v 63% (29/46); odds ratio 7.7, 3.1 to 19.4; P<0.001).\n[14] CONCLUSION A specific exercise strategy, focusing on strengthening eccentric exercises for the rotator cuff and concentric/eccentric exercises for the scapula stabilisers, is effective in reducing pain and improving shoulder function in patients with persistent subacromial impingement syndrome.\n[15] By extension, this exercise strategy reduces the need for arthroscopic subacromial decompression within the three month timeframe used in the study.\n[16] TRIAL REGISTRATION Clinical trials NCT01037673."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"Significantly more patients in the specific exercise group reported successful outcome (defined as large improvement or recovered) in the patients' global assessment of change because of treatment: 69% (35/51) v 24% (11/46); odds ratio 7.6, 3.1 to 18.9; P<0.001.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 454, "doc_id": 4200695, "label": "CONTRADICTS", "evidence_sentence_ids": [12], "cited_doc_ids": [4200695], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: General exercise therapy is more effective than scapular stabilizer exercises in reducing pain and improving function of the shoulder.\n\nDocument title: Effect of specific exercise strategy on need for surgery in patients with subacromial impingement syndrome: randomised controlled study\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate if a specific exercise strategy, targeting the rotator cuff and scapula stabilisers, improves shoulder function and pain more than unspecific exercises in patients with subacromial impingement syndrome, thereby decreasing the need for arthroscopic subacromial decompression.\n[1] DESIGN Randomised, participant and single assessor blinded, controlled study.\n[2] SETTING Department of orthopaedics in a Swedish university hospital.\n[3] PARTICIPANTS 102 patients with long standing (over six months) persistent subacromial impingement syndrome in whom earlier conservative treatment had failed, recruited through orthopaedic specialists.\n[4] INTERVENTIONS The specific exercise strategy consisted of strengthening eccentric exercises for the rotator cuff and concentric/eccentric exercises for the scapula stabilisers in combination with manual mobilisation.\n[5] The control exercise programme consisted of unspecific movement exercises for the neck and shoulder.\n[6] Patients in both groups received five to six individual guided treatment sessions during 12 weeks.\n[7] In between these supervised sessions the participants performed home exercises once or twice a day for 12 weeks.\n[8] MAIN OUTCOME MEASURES The primary outcome was the Constant-Murley shoulder assessment score evaluating shoulder function and pain.\n[9] Secondary outcomes were patients' global impression of change because of treatment and decision regarding surgery.\n[10] RESULTS Most (97, 95%) participants completed the 12 week study.\n[11] There was a significantly greater improvement in the Constant-Murley score in the specific exercise group than in the control exercise group (24 points (95% confidence interval 19 to 28.0) v 9 points (5 to 13); mean difference between group: 15 points (8.5 to 20.6)).\n[12] Significantly more patients in the specific exercise group reported successful outcome (defined as large improvement or recovered) in the patients' global assessment of change because of treatment: 69% (35/51) v 24% (11/46); odds ratio 7.6, 3.1 to 18.9; P<0.001.\n[13] A significantly lower proportion of patients in the specific exercise group subsequently chose to undergo surgery: 20% (10/51) v 63% (29/46); odds ratio 7.7, 3.1 to 19.4; P<0.001).\n[14] CONCLUSION A specific exercise strategy, focusing on strengthening eccentric exercises for the rotator cuff and concentric/eccentric exercises for the scapula stabilisers, is effective in reducing pain and improving shoulder function in patients with persistent subacromial impingement syndrome.\n[15] By extension, this exercise strategy reduces the need for arthroscopic subacromial decompression within the three month timeframe used in the study.\n[16] TRIAL REGISTRATION Clinical trials NCT01037673."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [14]\nExplanation: Evidence states: \"CONCLUSION A specific exercise strategy, focusing on strengthening eccentric exercises for the rotator cuff and concentric/eccentric exercises for the scapula stabilisers, is effective in reducing pain and improving shoulder function in patients with persistent subacromial impingement syndrome.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 454, "doc_id": 4200695, "label": "CONTRADICTS", "evidence_sentence_ids": [14], "cited_doc_ids": [4200695], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Genes involved in pre-mRNA splicing have a significant impact on genome stability.\n\nDocument title: A genome-wide siRNA screen reveals diverse cellular processes and pathways that mediate genome stability.\n\nAbstract sentences:\n[0] Signaling pathways that respond to DNA damage are essential for the maintenance of genome stability and are linked to many diseases, including cancer.\n[1] Here, a genome-wide siRNA screen was employed to identify additional genes involved in genome stabilization by monitoring phosphorylation of the histone variant H2AX, an early mark of DNA damage.\n[2] We identified hundreds of genes whose downregulation led to elevated levels of H2AX phosphorylation (gammaH2AX) and revealed links to cellular complexes and to genes with unclassified functions.\n[3] We demonstrate a widespread role for mRNA-processing factors in preventing DNA damage, which in some cases is caused by aberrant RNA-DNA structures.\n[4] Furthermore, we connect increased gammaH2AX levels to the neurological disorder Charcot-Marie-Tooth (CMT) syndrome, and we find a role for several CMT proteins in the DNA-damage response.\n[5] These data indicate that preservation of genome stability is mediated by a larger network of biological processes than previously appreciated."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"We demonstrate a widespread role for mRNA-processing factors in preventing DNA damage, which in some cases is caused by aberrant RNA-DNA structures.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 455, "doc_id": 12643937, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [12643937], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Genes regulated by Esrrb transcription factor are sensitive to Mbd3 function.\n\nDocument title: An Oct4-Centered Protein Interaction Network in Embryonic Stem Cells\n\nAbstract sentences:\n[0] Transcription factors, such as Oct4, are critical for establishing and maintaining pluripotent cell identity.\n[1] Whereas the genomic locations of several pluripotency transcription factors have been reported, the spectrum of their interaction partners is underexplored.\n[2] Here, we use an improved affinity protocol to purify Oct4-interacting proteins from mouse embryonic stem cells (ESCs).\n[3] Subsequent purification of Oct4 partners Sall4, Tcfcp2l1, Dax1, and Esrrb resulted in an Oct4 interactome of 166 proteins, including transcription factors and chromatin-modifying complexes with documented roles in self-renewal, but also many factors not previously associated with the ESC network.\n[4] We find that Esrrb associated with the basal transcription machinery and also detect interactions between transcription factors and components of the TGF-beta, Notch, and Wnt signaling pathways.\n[5] Acute depletion of Oct4 reduced binding of Tcfcp2l1, Dax1, and Esrrb to several target genes.\n[6] In conclusion, our purification protocol allowed us to bring greater definition to the circuitry controlling pluripotent cell identity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 456, "doc_id": 30507607, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [30507607], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Genetic deficiency of mast cells leads to decreased weight gain in a mouse model of diet-induced obesity.\n\nDocument title: Deficiency and pharmacological stabilization of mast cells reduce diet-induced obesity and diabetes in mice\n\nAbstract sentences:\n[0] Although mast cell functions have classically been related to allergic responses, recent studies indicate that these cells contribute to other common diseases such as multiple sclerosis, rheumatoid arthritis, atherosclerosis, aortic aneurysm and cancer.\n[1] This study presents evidence that mast cells also contribute to diet-induced obesity and diabetes.\n[2] For example, white adipose tissue (WAT) from obese humans and mice contain more mast cells than WAT from their lean counterparts.\n[3] Furthermore, in the context of mice on a Western diet, genetically induced deficiency of mast cells, or their pharmacological stabilization, reduces body weight gain and levels of inflammatory cytokines, chemokines and proteases in serum and WAT, in concert with improved glucose homeostasis and energy expenditure.\n[4] Mechanistic studies reveal that mast cells contribute to WAT and muscle angiogenesis and associated cell apoptosis and cathepsin activity.\n[5] Adoptive transfer experiments of cytokine-deficient mast cells show that these cells, by producing interleukin-6 (IL-6) and interferon-gamma (IFN-gamma), contribute to mouse adipose tissue cysteine protease cathepsin expression, apoptosis and angiogenesis, thereby promoting diet-induced obesity and glucose intolerance.\n[6] Our results showing reduced obesity and diabetes in mice treated with clinically available mast cell-stabilizing agents suggest the potential of developing new therapies for these common human metabolic disorders."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Furthermore, in the context of mice on a Western diet, genetically induced deficiency of mast cells, or their pharmacological stabilization, reduces body weight gain and levels of inflammatory cytokines, chemokines and proteases in serum and WAT, in concert with improved glucose homeostasis and energy expenditure.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 458, "doc_id": 597790, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [597790], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Genetic deletion of JAM-A increases gut permeability.\n\nDocument title: Compromised intestinal epithelial barrier induces adaptive immune compensation that protects from colitis.\n\nAbstract sentences:\n[0] Mice lacking junctional adhesion molecule A (JAM-A, encoded by F11r) exhibit enhanced intestinal epithelial permeability, bacterial translocation, and elevated colonic lymphocyte numbers, yet do not develop colitis.\n[1] To investigate the contribution of adaptive immune compensation in response to increased intestinal epithelial permeability, we examined the susceptibility of F11r(-/-)Rag1(-/-) mice to acute colitis.\n[2] Although negligible contributions of adaptive immunity in F11r(+/+)Rag1(-/-) mice were observed, F11r(-/-)Rag1(-/-) mice exhibited increased microflora-dependent colitis.\n[3] Elimination of T cell subsets and cytokine analyses revealed a protective role for TGF-β-producing CD4(+) T cells in F11r(-/-) mice.\n[4] Additionally, loss of JAM-A resulted in elevated mucosal and serum IgA that was dependent upon CD4(+) T cells and TGF-β.\n[5] Absence of IgA in F11r(+/+)Igha(-/-) mice did not affect disease, whereas F11r(-/-)Igha(-/-) mice displayed markedly increased susceptibility to acute injury-induced colitis.\n[6] These data establish a role for adaptive immune-mediated protection from acute colitis under conditions of intestinal epithelial barrier compromise."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Mice lacking junctional adhesion molecule A (JAM-A, encoded by F11r) exhibit enhanced intestinal epithelial permeability, bacterial translocation, and elevated colonic lymphocyte numbers, yet do not develop colitis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 461, "doc_id": 40096222, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [40096222], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Genomic aberrations of metastases provide information for targeted therapy.\n\nDocument title: Evolution of metastasis revealed by mutational landscapes of chemically induced skin cancers\n\nAbstract sentences:\n[0] Human tumors show a high level of genetic heterogeneity, but the processes that influence the timing and route of metastatic dissemination of the subclones are unknown.\n[1] Here we have used whole-exome sequencing of 103 matched benign, malignant and metastatic skin tumors from genetically heterogeneous mice to demonstrate that most metastases disseminate synchronously from the primary tumor, supporting parallel rather than linear evolution as the predominant model of metastasis.\n[2] Shared mutations between primary carcinomas and their matched metastases have the distinct A-to-T signature of the initiating carcinogen dimethylbenzanthracene, but non-shared mutations are primarily G-to-T, a signature associated with oxidative stress.\n[3] The existence of carcinomas that either did or did not metastasize in the same host animal suggests that there are tumor-intrinsic factors that influence metastatic seeding.\n[4] We also demonstrate the importance of germline polymorphisms in determining allele-specific mutations, and we identify somatic genetic alterations that are specifically related to initiation of carcinogenesis by Hras or Kras mutations.\n[5] Mouse tumors that mimic the genetic heterogeneity of human cancers can aid our understanding of the clonal evolution of metastasis and provide a realistic model for the testing of novel therapies."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Mouse tumors that mimic the genetic heterogeneity of human cancers can aid our understanding of the clonal evolution of metastasis and provide a realistic model for the testing of novel therapies.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 463, "doc_id": 19736671, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [19736671], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Genomic sequences involved in alternative splicing responsible for Hutchinson-Gilford progeria syndrome (HGPS) are abundant in the ''progerinonly'' allele of Lmna knock-in models.\n\nDocument title: Reversal of the cellular phenotype in the premature aging disease Hutchinson-Gilford progeria syndrome\n\nAbstract sentences:\n[0] Hutchinson-Gilford progeria syndrome (HGPS) is a childhood premature aging disease caused by a spontaneous point mutation in lamin A (encoded by LMNA), one of the major architectural elements of the mammalian cell nucleus.\n[1] The HGPS mutation activates an aberrant cryptic splice site in LMNA pre-mRNA, leading to synthesis of a truncated lamin A protein and concomitant reduction in wild-type lamin A. Fibroblasts from individuals with HGPS have severe morphological abnormalities in nuclear envelope structure.\n[2] Here we show that the cellular disease phenotype is reversible in cells from individuals with HGPS.\n[3] Introduction of wild-type lamin A protein does not rescue the cellular disease symptoms.\n[4] The mutant LMNA mRNA and lamin A protein can be efficiently eliminated by correction of the aberrant splicing event using a modified oligonucleotide targeted to the activated cryptic splice site.\n[5] Upon splicing correction, HGPS fibroblasts assume normal nuclear morphology, the aberrant nuclear distribution and cellular levels of lamina-associated proteins are rescued, defects in heterochromatin-specific histone modifications are corrected and proper expression of several misregulated genes is reestablished.\n[6] Our results establish proof of principle for the correction of the premature aging phenotype in individuals with HGPS."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [0, 4, 5]\nExplanation: Evidence states: \"Hutchinson-Gilford progeria syndrome (HGPS) is a childhood premature aging disease caused by a spontaneous point mutation in lamin A (encoded by LMNA), one of the major architectural elements of the mammalian cell nucleus. The mutant LMNA mRNA and lamin A protein can be efficiently eliminated by correction of the aberrant splicing event using a modified oligonucleotide targeted to the activated cryptic splice site. Upon splicing correction, HGPS fibroblasts assume normal nuclear morphology, the aberrant nuclear distribution and cellular levels of lamina-associated proteins are rescued, defects in heterochromatin-specific histone modifications are corrected and proper expression of several misregulated genes is reestablished.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 466, "doc_id": 22544171, "label": "CONTRADICTS", "evidence_sentence_ids": [0, 4, 5], "cited_doc_ids": [22544171], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Glial calcium waves influence seizures.\n\nDocument title: An Excitatory Loop with Astrocytes Contributes to Drive Neurons to Seizure Threshold\n\nAbstract sentences:\n[0] Seizures in focal epilepsies are sustained by a highly synchronous neuronal discharge that arises at restricted brain sites and subsequently spreads to large portions of the brain.\n[1] Despite intense experimental research in this field, the earlier cellular events that initiate and sustain a focal seizure are still not well defined.\n[2] Their identification is central to understand the pathophysiology of focal epilepsies and to develop new pharmacological therapies for drug-resistant forms of epilepsy.\n[3] The prominent involvement of astrocytes in ictogenesis was recently proposed.\n[4] We test here whether a cooperation between astrocytes and neurons is a prerequisite to support ictal (seizure-like) and interictal epileptiform events.\n[5] Simultaneous patch-clamp recording and Ca2+ imaging techniques were performed in a new in vitro model of focal seizures induced by local applications of N-methyl-D-aspartic acid (NMDA) in rat entorhinal cortex slices.\n[6] We found that a Ca2+ elevation in astrocytes correlates with both the initial development and the maintenance of a focal, seizure-like discharge.\n[7] A delayed astrocyte activation during ictal discharges was also observed in other models (including the whole in vitro isolated guinea pig brain) in which the site of generation of seizure activity cannot be precisely monitored.\n[8] In contrast, interictal discharges were not associated with Ca2+ changes in astrocytes.\n[9] Selective inhibition or stimulation of astrocyte Ca2+ signalling blocked or enhanced, respectively, ictal discharges, but did not affect interictal discharge generation.\n[10] Our data reveal that neurons engage astrocytes in a recurrent excitatory loop (possibly involving gliotransmission) that promotes seizure ignition and sustains the ictal discharge.\n[11] This neuron-astrocyte interaction may represent a novel target to develop effective therapeutic strategies to control seizures."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6, 10]\nExplanation: Evidence states: \"We found that a Ca2+ elevation in astrocytes correlates with both the initial development and the maintenance of a focal, seizure-like discharge. Our data reveal that neurons engage astrocytes in a recurrent excitatory loop (possibly involving gliotransmission) that promotes seizure ignition and sustains the ictal discharge.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 469, "doc_id": 1410197, "label": "SUPPORTS", "evidence_sentence_ids": [6, 10], "cited_doc_ids": [1410197], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Glioblastoma multiforme (GBM) is characterized by extensive invasion, rapid growth, necrosis, and angiogenesis.\n\nDocument title: Guanylate binding protein 1 is a novel effector of EGFR-driven invasion in glioblastoma\n\nAbstract sentences:\n[0] Although GBP1 (guanylate binding protein 1) was among the first interferon-inducible proteins identified, its function is still largely unknown.\n[1] Epidermal growth factor receptor (EGFR) activation by amplification or mutation is one of the most frequent genetic lesions in a variety of human tumors.\n[2] These include glioblastoma multiforme (GBM), which is characterized by independent but interrelated features of extensive invasion into normal brain parenchyma, rapid growth, necrosis, and angiogenesis.\n[3] In this study, we show that EGFR activation promoted GBP1 expression in GBM cell lines through a signaling pathway involving Src and p38 mitogen-activated protein kinase.\n[4] Moreover, we identified YY1 (Yin Yang 1) as the downstream transcriptional regulator regulating EGFR-driven GBP1 expression.\n[5] GBP1 was required for EGFR-mediated MMP1 (matrix metalloproteinase 1) expression and glioma cell invasion in vitro.\n[6] Although deregulation of GBP1 expression did not affect glioma cell proliferation, overexpression of GBP1 enhanced glioma cell invasion through MMP1 induction, which required its C-terminal helical domain and was independent of its GTPase activity.\n[7] Reducing GBP1 levels by RNA interference in invasive GBM cells also markedly inhibited their ability to infiltrate the brain parenchyma of mice.\n[8] GBP1 expression was high and positively correlated with EGFR expression in human GBM tumors and cell lines, particularly those of the neural subtype.\n[9] Together, these findings establish GBP1 as a previously unknown link between EGFR activity and MMP1 expression and nominate it as a novel potential therapeutic target for inhibiting GBM invasion."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"These include glioblastoma multiforme (GBM), which is characterized by independent but interrelated features of extensive invasion into normal brain parenchyma, rapid growth, necrosis, and angiogenesis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 470, "doc_id": 12685434, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [12685434], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Glucose restriction to 0.05% reduces RLS (replicative life span) by 20-40% in S. cerevisiae.\n\nDocument title: Sir2-Independent Life Span Extension by Calorie Restriction in Yeast\n\nAbstract sentences:\n[0] Calorie restriction slows aging and increases life span in many organisms.\n[1] In yeast, a mechanistic explanation has been proposed whereby calorie restriction slows aging by activating Sir2.\n[2] Here we report the identification of a Sir2-independent pathway responsible for a majority of the longevity benefit associated with calorie restriction.\n[3] Deletion of FOB1 and overexpression of SIR2 have been previously found to increase life span by reducing the levels of toxic rDNA circles in aged mother cells.\n[4] We find that combining calorie restriction with either of these genetic interventions dramatically enhances longevity, resulting in the longest-lived yeast strain reported thus far.\n[5] Further, calorie restriction results in a greater life span extension in cells lacking both Sir2 and Fob1 than in cells where Sir2 is present.\n[6] These findings indicate that Sir2 and calorie restriction act in parallel pathways to promote longevity in yeast and, perhaps, higher eukaryotes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 472, "doc_id": 7185591, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [7185591, 26330861, 4414481], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Glycan adaptation involves insertion-deletion events.\n\nDocument title: Broad neutralization coverage of HIV by multiple highly potent antibodies\n\nAbstract sentences:\n[0] Broadly neutralizing antibodies against highly variable viral pathogens are much sought after to treat or protect against global circulating viruses.\n[1] Here we probed the neutralizing antibody repertoires of four human immunodeficiency virus (HIV)-infected donors with remarkably broad and potent neutralizing responses and rescued 17 new monoclonal antibodies that neutralize broadly across clades.\n[2] Many of the new monoclonal antibodies are almost tenfold more potent than the recently described PG9, PG16 and VRC01 broadly neutralizing monoclonal antibodies and 100-fold more potent than the original prototype HIV broadly neutralizing monoclonal antibodies.\n[3] The monoclonal antibodies largely recapitulate the neutralization breadth found in the corresponding donor serum and many recognize novel epitopes on envelope (Env) glycoprotein gp120, illuminating new targets for vaccine design.\n[4] Analysis of neutralization by the full complement of anti-HIV broadly neutralizing monoclonal antibodies now available reveals that certain combinations of antibodies should offer markedly more favourable coverage of the enormous diversity of global circulating viruses than others and these combinations might be sought in active or passive immunization regimes.\n[5] Overall, the isolation of multiple HIV broadly neutralizing monoclonal antibodies from several donors that, in aggregate, provide broad coverage at low concentrations is a highly positive indicator for the eventual design of an effective antibody-based HIV vaccine."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 473, "doc_id": 4373433, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4373433], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Glycan adaptation is rarely observed in the B-cell repertoire.\n\nDocument title: Broad neutralization coverage of HIV by multiple highly potent antibodies\n\nAbstract sentences:\n[0] Broadly neutralizing antibodies against highly variable viral pathogens are much sought after to treat or protect against global circulating viruses.\n[1] Here we probed the neutralizing antibody repertoires of four human immunodeficiency virus (HIV)-infected donors with remarkably broad and potent neutralizing responses and rescued 17 new monoclonal antibodies that neutralize broadly across clades.\n[2] Many of the new monoclonal antibodies are almost tenfold more potent than the recently described PG9, PG16 and VRC01 broadly neutralizing monoclonal antibodies and 100-fold more potent than the original prototype HIV broadly neutralizing monoclonal antibodies.\n[3] The monoclonal antibodies largely recapitulate the neutralization breadth found in the corresponding donor serum and many recognize novel epitopes on envelope (Env) glycoprotein gp120, illuminating new targets for vaccine design.\n[4] Analysis of neutralization by the full complement of anti-HIV broadly neutralizing monoclonal antibodies now available reveals that certain combinations of antibodies should offer markedly more favourable coverage of the enormous diversity of global circulating viruses than others and these combinations might be sought in active or passive immunization regimes.\n[5] Overall, the isolation of multiple HIV broadly neutralizing monoclonal antibodies from several donors that, in aggregate, provide broad coverage at low concentrations is a highly positive indicator for the eventual design of an effective antibody-based HIV vaccine."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 474, "doc_id": 4373433, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4373433], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Gpr124 increases BBB breakdown in mouse models of ischemic stroke.\n\nDocument title: Gpr124 is essential for blood–brain barrier integrity in central nervous system disease\n\nAbstract sentences:\n[0] Although blood–brain barrier (BBB) compromise is central to the etiology of diverse central nervous system (CNS) disorders, endothelial receptor proteins that control BBB function are poorly defined.\n[1] The endothelial G-protein-coupled receptor (GPCR) Gpr124 has been reported to be required for normal forebrain angiogenesis and BBB function in mouse embryos, but the role of this receptor in adult animals is unknown.\n[2] Here Gpr124 conditional knockout (CKO) in the endothelia of adult mice did not affect homeostatic BBB integrity, but resulted in BBB disruption and microvascular hemorrhage in mouse models of both ischemic stroke and glioblastoma, accompanied by reduced cerebrovascular canonical Wnt–β-catenin signaling.\n[3] Constitutive activation of Wnt–β-catenin signaling fully corrected the BBB disruption and hemorrhage defects of Gpr124-CKO mice, with rescue of the endothelial gene tight junction, pericyte coverage and extracellular-matrix deficits.\n[4] We thus identify Gpr124 as an endothelial GPCR specifically required for endothelial Wnt signaling and BBB integrity under pathological conditions in adult mice.\n[5] This finding implicates Gpr124 as a potential therapeutic target for human CNS disorders characterized by BBB disruption."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here Gpr124 conditional knockout (CKO) in the endothelia of adult mice did not affect homeostatic BBB integrity, but resulted in BBB disruption and microvascular hemorrhage in mouse models of both ischemic stroke and glioblastoma, accompanied by reduced cerebrovascular canonical Wnt–β-catenin signaling.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 479, "doc_id": 6325527, "label": "CONTRADICTS", "evidence_sentence_ids": [2], "cited_doc_ids": [6325527], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Gpr124 suppresses BBB breakdown in mouse models of ischemic stroke.\n\nDocument title: Gpr124 is essential for blood–brain barrier integrity in central nervous system disease\n\nAbstract sentences:\n[0] Although blood–brain barrier (BBB) compromise is central to the etiology of diverse central nervous system (CNS) disorders, endothelial receptor proteins that control BBB function are poorly defined.\n[1] The endothelial G-protein-coupled receptor (GPCR) Gpr124 has been reported to be required for normal forebrain angiogenesis and BBB function in mouse embryos, but the role of this receptor in adult animals is unknown.\n[2] Here Gpr124 conditional knockout (CKO) in the endothelia of adult mice did not affect homeostatic BBB integrity, but resulted in BBB disruption and microvascular hemorrhage in mouse models of both ischemic stroke and glioblastoma, accompanied by reduced cerebrovascular canonical Wnt–β-catenin signaling.\n[3] Constitutive activation of Wnt–β-catenin signaling fully corrected the BBB disruption and hemorrhage defects of Gpr124-CKO mice, with rescue of the endothelial gene tight junction, pericyte coverage and extracellular-matrix deficits.\n[4] We thus identify Gpr124 as an endothelial GPCR specifically required for endothelial Wnt signaling and BBB integrity under pathological conditions in adult mice.\n[5] This finding implicates Gpr124 as a potential therapeutic target for human CNS disorders characterized by BBB disruption."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here Gpr124 conditional knockout (CKO) in the endothelia of adult mice did not affect homeostatic BBB integrity, but resulted in BBB disruption and microvascular hemorrhage in mouse models of both ischemic stroke and glioblastoma, accompanied by reduced cerebrovascular canonical Wnt–β-catenin signaling.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 480, "doc_id": 6325527, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [6325527], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Guanine nucleotide dissociation inhibitor (Rho-GDI) interacts with the p75 NTR death domain\n\nDocument title: Gamma-Secretase Represents a Therapeutic Target for the Treatment of Invasive Glioma Mediated by the p75 Neurotrophin Receptor\n\nAbstract sentences:\n[0] The multifunctional signaling protein p75 neurotrophin receptor (p75(NTR)) is a central regulator and major contributor to the highly invasive nature of malignant gliomas.\n[1] Here, we show that neurotrophin-dependent regulated intramembrane proteolysis (RIP) of p75(NTR) is required for p75(NTR)-mediated glioma invasion, and identify a previously unnamed process for targeted glioma therapy.\n[2] Expression of cleavage-resistant chimeras of p75(NTR) or treatment of animals bearing p75(NTR)-positive intracranial tumors with clinically applicable gamma-secretase inhibitors resulted in dramatically decreased glioma invasion and prolonged survival.\n[3] Importantly, proteolytic processing of p75(NTR) was observed in p75(NTR)-positive patient tumor specimens and brain tumor initiating cells.\n[4] This work highlights the importance of p75(NTR) as a therapeutic target, suggesting that gamma-secretase inhibitors may have direct clinical application for the treatment of malignant glioma."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 481, "doc_id": 14706752, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14706752], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Guanine nucleotide exchange factors (GEFs) mediate RhoA activation in response to tensional forces on fibronectin-binding integrins.\n\nDocument title: The Rho GEFs LARG and GEF-H1 regulate the mechanical response to force on integrins\n\nAbstract sentences:\n[0] How individual cells respond to mechanical forces is of considerable interest to biologists as force affects many aspects of cell behaviour.\n[1] The application of force on integrins triggers cytoskeletal rearrangements and growth of the associated adhesion complex, resulting in increased cellular stiffness, also known as reinforcement.\n[2] Although RhoA has been shown to play a role during reinforcement, the molecular mechanisms that regulate its activity are unknown.\n[3] By combining biochemical and biophysical approaches, we identified two guanine nucleotide exchange factors (GEFs), LARG and GEF-H1, as key molecules that regulate the cellular adaptation to force.\n[4] We show that stimulation of integrins with tensional force triggers activation of these two GEFs and their recruitment to adhesion complexes.\n[5] Surprisingly, activation of LARG and GEF-H1 involves distinct signalling pathways.\n[6] Our results reveal that LARG is activated by the Src family tyrosine kinase Fyn, whereas GEF-H1 catalytic activity is enhanced by ERK downstream of a signalling cascade that includes FAK and Ras."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"By combining biochemical and biophysical approaches, we identified two guanine nucleotide exchange factors (GEFs), LARG and GEF-H1, as key molecules that regulate the cellular adaptation to force.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 482, "doc_id": 10991183, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [10991183], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: H.pylori-mediated gastric cancer occurs due to the accumulation of mutations in host epithelial cells.\n\nDocument title: Helicobacter pylori infection triggers aberrant expression of activation-induced cytidine deaminase in gastric epithelium\n\nAbstract sentences:\n[0] Infection with Helicobacter pylori (H. pylori) is a risk factor for the development of gastric cancer.\n[1] Here we show that infection of gastric epithelial cells with 'cag' pathogenicity island (cagPAI)-positive H. pylori induced aberrant expression of activation-induced cytidine deaminase (AID), a member of the cytidine-deaminase family that acts as a DNA- and RNA-editing enzyme, via the IκB kinase–dependent nuclear factor-κB activation pathway.\n[2] H. pylori–mediated upregulation of AID resulted in the accumulation of nucleotide alterations in the TP53 tumor suppressor gene in gastric cells in vitro.\n[3] Our findings provide evidence that aberrant AID expression caused by H. pylori infection might be a mechanism of mutation accumulation in the gastric mucosa during H. pylori–associated gastric carcinogenesis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"H. pylori–mediated upregulation of AID resulted in the accumulation of nucleotide alterations in the TP53 tumor suppressor gene in gastric cells in vitro.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 483, "doc_id": 22703082, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [22703082], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: H.pylori-mediated gastric cancer occurs due to the accumulation of mutations in host epithelial cells.\n\nDocument title: Helicobacter pylori infection triggers aberrant expression of activation-induced cytidine deaminase in gastric epithelium\n\nAbstract sentences:\n[0] Infection with Helicobacter pylori (H. pylori) is a risk factor for the development of gastric cancer.\n[1] Here we show that infection of gastric epithelial cells with 'cag' pathogenicity island (cagPAI)-positive H. pylori induced aberrant expression of activation-induced cytidine deaminase (AID), a member of the cytidine-deaminase family that acts as a DNA- and RNA-editing enzyme, via the IκB kinase–dependent nuclear factor-κB activation pathway.\n[2] H. pylori–mediated upregulation of AID resulted in the accumulation of nucleotide alterations in the TP53 tumor suppressor gene in gastric cells in vitro.\n[3] Our findings provide evidence that aberrant AID expression caused by H. pylori infection might be a mechanism of mutation accumulation in the gastric mucosa during H. pylori–associated gastric carcinogenesis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Our findings provide evidence that aberrant AID expression caused by H. pylori infection might be a mechanism of mutation accumulation in the gastric mucosa during H. pylori–associated gastric carcinogenesis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 483, "doc_id": 22703082, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [22703082], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: H4 G94P proteins induce chromatin assembly, which increases free histones.\n\nDocument title: Histone levels are regulated by phosphorylation and ubiquitylation dependent proteolysis\n\nAbstract sentences:\n[0] Histone levels are tightly regulated to prevent harmful effects such as genomic instability and hypersensitivity to DNA-damaging agents due to the accumulation of these highly basic proteins when DNA replication slows down or stops.\n[1] Although chromosomal histones are stable, excess (non-chromatin bound) histones are rapidly degraded in a Rad53 (radiation sensitive 53) kinase-dependent manner in Saccharomyces cerevisiae.\n[2] Here we demonstrate that excess histones associate with Rad53 in vivo and seem to undergo modifications such as tyrosine phosphorylation and polyubiquitylation, before their proteolysis by the proteasome.\n[3] We have identified the Tyr 99 residue of histone H3 as being critical for the efficient ubiquitylation and degradation of this histone.\n[4] We have also identified the ubiquitin conjugating enzymes (E2) Ubc4 and Ubc5, as well as the ubiquitin ligase (E3) Tom1 (temperature dependent organization in mitotic nucleus 1), as enzymes involved in the ubiquitylation of excess histones.\n[5] Regulated histone proteolysis has major implications for the maintenance of epigenetic marks on chromatin, genomic stability and the packaging of sperm DNA."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 484, "doc_id": 14637235, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14637235], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: H4 G94P proteins induce degradation of free histones via Rad53-dependent mechanisms.\n\nDocument title: Histone levels are regulated by phosphorylation and ubiquitylation dependent proteolysis\n\nAbstract sentences:\n[0] Histone levels are tightly regulated to prevent harmful effects such as genomic instability and hypersensitivity to DNA-damaging agents due to the accumulation of these highly basic proteins when DNA replication slows down or stops.\n[1] Although chromosomal histones are stable, excess (non-chromatin bound) histones are rapidly degraded in a Rad53 (radiation sensitive 53) kinase-dependent manner in Saccharomyces cerevisiae.\n[2] Here we demonstrate that excess histones associate with Rad53 in vivo and seem to undergo modifications such as tyrosine phosphorylation and polyubiquitylation, before their proteolysis by the proteasome.\n[3] We have identified the Tyr 99 residue of histone H3 as being critical for the efficient ubiquitylation and degradation of this histone.\n[4] We have also identified the ubiquitin conjugating enzymes (E2) Ubc4 and Ubc5, as well as the ubiquitin ligase (E3) Tom1 (temperature dependent organization in mitotic nucleus 1), as enzymes involved in the ubiquitylation of excess histones.\n[5] Regulated histone proteolysis has major implications for the maintenance of epigenetic marks on chromatin, genomic stability and the packaging of sperm DNA."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 485, "doc_id": 14637235, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14637235], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: H4 G94P proteins inhibit chromatin assembly, which decreases free histones.\n\nDocument title: Histone levels are regulated by phosphorylation and ubiquitylation dependent proteolysis\n\nAbstract sentences:\n[0] Histone levels are tightly regulated to prevent harmful effects such as genomic instability and hypersensitivity to DNA-damaging agents due to the accumulation of these highly basic proteins when DNA replication slows down or stops.\n[1] Although chromosomal histones are stable, excess (non-chromatin bound) histones are rapidly degraded in a Rad53 (radiation sensitive 53) kinase-dependent manner in Saccharomyces cerevisiae.\n[2] Here we demonstrate that excess histones associate with Rad53 in vivo and seem to undergo modifications such as tyrosine phosphorylation and polyubiquitylation, before their proteolysis by the proteasome.\n[3] We have identified the Tyr 99 residue of histone H3 as being critical for the efficient ubiquitylation and degradation of this histone.\n[4] We have also identified the ubiquitin conjugating enzymes (E2) Ubc4 and Ubc5, as well as the ubiquitin ligase (E3) Tom1 (temperature dependent organization in mitotic nucleus 1), as enzymes involved in the ubiquitylation of excess histones.\n[5] Regulated histone proteolysis has major implications for the maintenance of epigenetic marks on chromatin, genomic stability and the packaging of sperm DNA."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 486, "doc_id": 14637235, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14637235], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: H4 G94P proteins suppress degradation of free histones via Rad53-dependent mechanisms.\n\nDocument title: Histone levels are regulated by phosphorylation and ubiquitylation dependent proteolysis\n\nAbstract sentences:\n[0] Histone levels are tightly regulated to prevent harmful effects such as genomic instability and hypersensitivity to DNA-damaging agents due to the accumulation of these highly basic proteins when DNA replication slows down or stops.\n[1] Although chromosomal histones are stable, excess (non-chromatin bound) histones are rapidly degraded in a Rad53 (radiation sensitive 53) kinase-dependent manner in Saccharomyces cerevisiae.\n[2] Here we demonstrate that excess histones associate with Rad53 in vivo and seem to undergo modifications such as tyrosine phosphorylation and polyubiquitylation, before their proteolysis by the proteasome.\n[3] We have identified the Tyr 99 residue of histone H3 as being critical for the efficient ubiquitylation and degradation of this histone.\n[4] We have also identified the ubiquitin conjugating enzymes (E2) Ubc4 and Ubc5, as well as the ubiquitin ligase (E3) Tom1 (temperature dependent organization in mitotic nucleus 1), as enzymes involved in the ubiquitylation of excess histones.\n[5] Regulated histone proteolysis has major implications for the maintenance of epigenetic marks on chromatin, genomic stability and the packaging of sperm DNA."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 487, "doc_id": 14637235, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14637235], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: HAND2 methylation is a key step in early endometrial carcinogenesis.\n\nDocument title: Role of DNA Methylation and Epigenetic Silencing of HAND2 in Endometrial Cancer Development\n\nAbstract sentences:\n[0] BACKGROUND Endometrial cancer incidence is continuing to rise in the wake of the current ageing and obesity epidemics.\n[1] Much of the risk for endometrial cancer development is influenced by the environment and lifestyle.\n[2] Accumulating evidence suggests that the epigenome serves as the interface between the genome and the environment and that hypermethylation of stem cell polycomb group target genes is an epigenetic hallmark of cancer.\n[3] The objective of this study was to determine the functional role of epigenetic factors in endometrial cancer development.\n[4] METHODS AND FINDINGS Epigenome-wide methylation analysis of >27,000 CpG sites in endometrial cancer tissue samples (n = 64) and control samples (n = 23) revealed that HAND2 (a gene encoding a transcription factor expressed in the endometrial stroma) is one of the most commonly hypermethylated and silenced genes in endometrial cancer.\n[5] A novel integrative epigenome-transcriptome-interactome analysis further revealed that HAND2 is the hub of the most highly ranked differential methylation hotspot in endometrial cancer.\n[6] These findings were validated using candidate gene methylation analysis in multiple clinical sample sets of tissue samples from a total of 272 additional women.\n[7] Increased HAND2 methylation was a feature of premalignant endometrial lesions and was seen to parallel a decrease in RNA and protein levels.\n[8] Furthermore, women with high endometrial HAND2 methylation in their premalignant lesions were less likely to respond to progesterone treatment.\n[9] HAND2 methylation analysis of endometrial secretions collected using high vaginal swabs taken from women with postmenopausal bleeding specifically identified those patients with early stage endometrial cancer with both high sensitivity and high specificity (receiver operating characteristics area under the curve = 0.91 for stage 1A and 0.97 for higher than stage 1A).\n[10] Finally, mice harbouring a Hand2 knock-out specifically in their endometrium were shown to develop precancerous endometrial lesions with increasing age, and these lesions also demonstrated a lack of PTEN expression.\n[11] CONCLUSIONS HAND2 methylation is a common and crucial molecular alteration in endometrial cancer that could potentially be employed as a biomarker for early detection of endometrial cancer and as a predictor of treatment response.\n[12] The true clinical utility of HAND2 DNA methylation, however, requires further validation in prospective studies.\n[13] Please see later in the article for the Editors' Summary."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"METHODS AND FINDINGS Epigenome-wide methylation analysis of >27,000 CpG sites in endometrial cancer tissue samples (n = 64) and control samples (n = 23) revealed that HAND2 (a gene encoding a transcription factor expressed in the endometrial stroma) is one of the most commonly hypermethylated and silenced genes in endometrial cancer.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 488, "doc_id": 1780819, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [1780819], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: HAND2 methylation is a key step in early endometrial carcinogenesis.\n\nDocument title: Role of DNA Methylation and Epigenetic Silencing of HAND2 in Endometrial Cancer Development\n\nAbstract sentences:\n[0] BACKGROUND Endometrial cancer incidence is continuing to rise in the wake of the current ageing and obesity epidemics.\n[1] Much of the risk for endometrial cancer development is influenced by the environment and lifestyle.\n[2] Accumulating evidence suggests that the epigenome serves as the interface between the genome and the environment and that hypermethylation of stem cell polycomb group target genes is an epigenetic hallmark of cancer.\n[3] The objective of this study was to determine the functional role of epigenetic factors in endometrial cancer development.\n[4] METHODS AND FINDINGS Epigenome-wide methylation analysis of >27,000 CpG sites in endometrial cancer tissue samples (n = 64) and control samples (n = 23) revealed that HAND2 (a gene encoding a transcription factor expressed in the endometrial stroma) is one of the most commonly hypermethylated and silenced genes in endometrial cancer.\n[5] A novel integrative epigenome-transcriptome-interactome analysis further revealed that HAND2 is the hub of the most highly ranked differential methylation hotspot in endometrial cancer.\n[6] These findings were validated using candidate gene methylation analysis in multiple clinical sample sets of tissue samples from a total of 272 additional women.\n[7] Increased HAND2 methylation was a feature of premalignant endometrial lesions and was seen to parallel a decrease in RNA and protein levels.\n[8] Furthermore, women with high endometrial HAND2 methylation in their premalignant lesions were less likely to respond to progesterone treatment.\n[9] HAND2 methylation analysis of endometrial secretions collected using high vaginal swabs taken from women with postmenopausal bleeding specifically identified those patients with early stage endometrial cancer with both high sensitivity and high specificity (receiver operating characteristics area under the curve = 0.91 for stage 1A and 0.97 for higher than stage 1A).\n[10] Finally, mice harbouring a Hand2 knock-out specifically in their endometrium were shown to develop precancerous endometrial lesions with increasing age, and these lesions also demonstrated a lack of PTEN expression.\n[11] CONCLUSIONS HAND2 methylation is a common and crucial molecular alteration in endometrial cancer that could potentially be employed as a biomarker for early detection of endometrial cancer and as a predictor of treatment response.\n[12] The true clinical utility of HAND2 DNA methylation, however, requires further validation in prospective studies.\n[13] Please see later in the article for the Editors' Summary."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Increased HAND2 methylation was a feature of premalignant endometrial lesions and was seen to parallel a decrease in RNA and protein levels.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 488, "doc_id": 1780819, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [1780819], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: HAND2 methylation is a key step in early endometrial carcinogenesis.\n\nDocument title: Role of DNA Methylation and Epigenetic Silencing of HAND2 in Endometrial Cancer Development\n\nAbstract sentences:\n[0] BACKGROUND Endometrial cancer incidence is continuing to rise in the wake of the current ageing and obesity epidemics.\n[1] Much of the risk for endometrial cancer development is influenced by the environment and lifestyle.\n[2] Accumulating evidence suggests that the epigenome serves as the interface between the genome and the environment and that hypermethylation of stem cell polycomb group target genes is an epigenetic hallmark of cancer.\n[3] The objective of this study was to determine the functional role of epigenetic factors in endometrial cancer development.\n[4] METHODS AND FINDINGS Epigenome-wide methylation analysis of >27,000 CpG sites in endometrial cancer tissue samples (n = 64) and control samples (n = 23) revealed that HAND2 (a gene encoding a transcription factor expressed in the endometrial stroma) is one of the most commonly hypermethylated and silenced genes in endometrial cancer.\n[5] A novel integrative epigenome-transcriptome-interactome analysis further revealed that HAND2 is the hub of the most highly ranked differential methylation hotspot in endometrial cancer.\n[6] These findings were validated using candidate gene methylation analysis in multiple clinical sample sets of tissue samples from a total of 272 additional women.\n[7] Increased HAND2 methylation was a feature of premalignant endometrial lesions and was seen to parallel a decrease in RNA and protein levels.\n[8] Furthermore, women with high endometrial HAND2 methylation in their premalignant lesions were less likely to respond to progesterone treatment.\n[9] HAND2 methylation analysis of endometrial secretions collected using high vaginal swabs taken from women with postmenopausal bleeding specifically identified those patients with early stage endometrial cancer with both high sensitivity and high specificity (receiver operating characteristics area under the curve = 0.91 for stage 1A and 0.97 for higher than stage 1A).\n[10] Finally, mice harbouring a Hand2 knock-out specifically in their endometrium were shown to develop precancerous endometrial lesions with increasing age, and these lesions also demonstrated a lack of PTEN expression.\n[11] CONCLUSIONS HAND2 methylation is a common and crucial molecular alteration in endometrial cancer that could potentially be employed as a biomarker for early detection of endometrial cancer and as a predictor of treatment response.\n[12] The true clinical utility of HAND2 DNA methylation, however, requires further validation in prospective studies.\n[13] Please see later in the article for the Editors' Summary."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"HAND2 methylation analysis of endometrial secretions collected using high vaginal swabs taken from women with postmenopausal bleeding specifically identified those patients with early stage endometrial cancer with both high sensitivity and high specificity (receiver operating characteristics area under the curve = 0.91 for stage 1A and 0.97 for higher than stage 1A).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 488, "doc_id": 1780819, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [1780819], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: HAND2 methylation is a key step in early endometrial carcinogenesis.\n\nDocument title: Role of DNA Methylation and Epigenetic Silencing of HAND2 in Endometrial Cancer Development\n\nAbstract sentences:\n[0] BACKGROUND Endometrial cancer incidence is continuing to rise in the wake of the current ageing and obesity epidemics.\n[1] Much of the risk for endometrial cancer development is influenced by the environment and lifestyle.\n[2] Accumulating evidence suggests that the epigenome serves as the interface between the genome and the environment and that hypermethylation of stem cell polycomb group target genes is an epigenetic hallmark of cancer.\n[3] The objective of this study was to determine the functional role of epigenetic factors in endometrial cancer development.\n[4] METHODS AND FINDINGS Epigenome-wide methylation analysis of >27,000 CpG sites in endometrial cancer tissue samples (n = 64) and control samples (n = 23) revealed that HAND2 (a gene encoding a transcription factor expressed in the endometrial stroma) is one of the most commonly hypermethylated and silenced genes in endometrial cancer.\n[5] A novel integrative epigenome-transcriptome-interactome analysis further revealed that HAND2 is the hub of the most highly ranked differential methylation hotspot in endometrial cancer.\n[6] These findings were validated using candidate gene methylation analysis in multiple clinical sample sets of tissue samples from a total of 272 additional women.\n[7] Increased HAND2 methylation was a feature of premalignant endometrial lesions and was seen to parallel a decrease in RNA and protein levels.\n[8] Furthermore, women with high endometrial HAND2 methylation in their premalignant lesions were less likely to respond to progesterone treatment.\n[9] HAND2 methylation analysis of endometrial secretions collected using high vaginal swabs taken from women with postmenopausal bleeding specifically identified those patients with early stage endometrial cancer with both high sensitivity and high specificity (receiver operating characteristics area under the curve = 0.91 for stage 1A and 0.97 for higher than stage 1A).\n[10] Finally, mice harbouring a Hand2 knock-out specifically in their endometrium were shown to develop precancerous endometrial lesions with increasing age, and these lesions also demonstrated a lack of PTEN expression.\n[11] CONCLUSIONS HAND2 methylation is a common and crucial molecular alteration in endometrial cancer that could potentially be employed as a biomarker for early detection of endometrial cancer and as a predictor of treatment response.\n[12] The true clinical utility of HAND2 DNA methylation, however, requires further validation in prospective studies.\n[13] Please see later in the article for the Editors' Summary."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"CONCLUSIONS HAND2 methylation is a common and crucial molecular alteration in endometrial cancer that could potentially be employed as a biomarker for early detection of endometrial cancer and as a predictor of treatment response.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 488, "doc_id": 1780819, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [1780819], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: HIV trans-activator protein (TAT) effectively transports large and small molecules across cellular membranes into larger populations of neurons.\n\nDocument title: Suppression of inflammatory and neuropathic pain by uncoupling CRMP-2 from the presynaptic Ca2+ channel complex\n\nAbstract sentences:\n[0] The use of N-type voltage-gated calcium channel (CaV2.2) blockers to treat pain is limited by many physiological side effects.\n[1] Here we report that inflammatory and neuropathic hypersensitivity can be suppressed by inhibiting the binding of collapsin response mediator protein 2 (CRMP-2) to CaV2.2 and thereby reducing channel function.\n[2] A peptide of CRMP-2 fused to the HIV transactivator of transcription (TAT) protein (TAT-CBD3) decreased neuropeptide release from sensory neurons and excitatory synaptic transmission in dorsal horn neurons, reduced meningeal blood flow, reduced nocifensive behavior induced by formalin injection or corneal capsaicin application and reversed neuropathic hypersensitivity produced by an antiretroviral drug.\n[3] TAT-CBD3 was mildly anxiolytic without affecting memory retrieval, sensorimotor function or depression.\n[4] At doses tenfold higher than that required to reduce hypersensitivity in vivo, TAT-CBD3 caused a transient episode of tail kinking and body contortion.\n[5] By preventing CRMP-2–mediated enhancement of CaV2.2 function, TAT-CBD3 alleviated inflammatory and neuropathic hypersensitivity, an approach that may prove useful in managing chronic pain."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 489, "doc_id": 6625693, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [6625693], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: HNF4A mutations are associated with macrosomia in infancy.\n\nDocument title: Macrosomia and Hyperinsulinaemic Hypoglycaemia in Patients with Heterozygous Mutations in the HNF4A Gene\n\nAbstract sentences:\n[0] Background  Macrosomia is associated with considerable neonatal and maternal morbidity.\n[1] Factors that predict macrosomia are poorly understood.\n[2] The increased rate of macrosomia in the offspring of pregnant women with diabetes and in congenital hyperinsulinaemia is mediated by increased foetal insulin secretion.\n[3] We assessed the in utero and neonatal role of two key regulators of pancreatic insulin secretion by studying birthweight and the incidence of neonatal hypoglycaemia in patients with heterozygous mutations in the maturity-onset diabetes of the young (MODY) genes HNF4A (encoding HNF-4α) and HNF1A/TCF1 (encoding HNF-1α), and the effect of pancreatic deletion of Hnf4a on foetal and neonatal insulin secretion in mice."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 490, "doc_id": 56893404, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [56893404], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: HOXB4 facilitates HSC expansion when co-cultured with HSCs.\n\nDocument title: Angiopoietin-like proteins stimulate ex vivo expansion of hematopoietic stem cells\n\nAbstract sentences:\n[0] Successful ex vivo expansion of hematopoietic stem cells (HSCs) would greatly benefit the treatment of disease and the understanding of crucial questions of stem cell biology.\n[1] Here we show, using microarray studies, that the HSC-supportive mouse fetal liver CD3+ cells specifically express the proteins angiopoietin-like 2 (Angptl2) and angiopoietin-like 3 (Angptl3).\n[2] We observed a 24- or 30-fold net expansion of long-term HSCs by reconstitution analysis when we cultured highly enriched HSCs for 10 days in the presence of Angptl2 or Angptl3 together with saturating levels of other growth factors.\n[3] The coiled-coil domain of Angptl2 was capable of stimulating expansion of HSCs.\n[4] Furthermore, angiopoietin-like 5, angiopoietin-like 7 and microfibril-associated glycoprotein 4 also supported expansion of HSCs in culture."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 492, "doc_id": 19583924, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [19583924], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: HOXB4 is a highly expressed component of cellular secretome from fetal liver cell populations.\n\nDocument title: Angiopoietin-like proteins stimulate ex vivo expansion of hematopoietic stem cells\n\nAbstract sentences:\n[0] Successful ex vivo expansion of hematopoietic stem cells (HSCs) would greatly benefit the treatment of disease and the understanding of crucial questions of stem cell biology.\n[1] Here we show, using microarray studies, that the HSC-supportive mouse fetal liver CD3+ cells specifically express the proteins angiopoietin-like 2 (Angptl2) and angiopoietin-like 3 (Angptl3).\n[2] We observed a 24- or 30-fold net expansion of long-term HSCs by reconstitution analysis when we cultured highly enriched HSCs for 10 days in the presence of Angptl2 or Angptl3 together with saturating levels of other growth factors.\n[3] The coiled-coil domain of Angptl2 was capable of stimulating expansion of HSCs.\n[4] Furthermore, angiopoietin-like 5, angiopoietin-like 7 and microfibril-associated glycoprotein 4 also supported expansion of HSCs in culture."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 493, "doc_id": 19583924, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [19583924], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: HSCT-T dosage may not be diagnostic if the onset of symptoms occurs less than 3 hours before AMI.\n\nDocument title: Diagnostic accuracy of single baseline measurement of Elecsys Troponin T high-sensitive assay for diagnosis of acute myocardial infarction in emergency department: systematic review and meta-analysis\n\nAbstract sentences:\n[0] OBJECTIVE To obtain summary estimates of the accuracy of a single baseline measurement of the Elecsys Troponin T high-sensitive assay (Roche Diagnostics) for the diagnosis of acute myocardial infarction in patients presenting to the emergency department.\n[1] DESIGN Systematic review and meta-analysis of diagnostic test accuracy studies.\n[2] DATA SOURCES Medline, Embase, and other relevant electronic databases were searched for papers published between January 2006 and December 2013.\n[3] STUDY SELECTION Studies were included if they evaluated the diagnostic accuracy of a single baseline measurement of Elecsys Troponin T high-sensitive assay for the diagnosis of acute myocardial infarction in patients presenting to the emergency department with suspected acute coronary syndrome.\n[4] STUDY APPRAISAL AND DATA SYNTHESIS The first author screened all titles and abstracts identified through the searches and selected all potentially relevant papers.\n[5] The screening of the full texts, the data extraction, and the methodological quality assessment, using the adapted QUADAS-2 tool, were conducted independently by two reviewers with disagreements being resolved through discussion or arbitration.\n[6] If appropriate, meta-analysis was conducted using the hierarchical bivariate model.\n[7] RESULTS Twenty three studies reported the performance of the evaluated assay at presentation.\n[8] The results for 14 ng/L and 3-5 ng/L cut-off values were pooled separately.\n[9] At 14 ng/L (20 papers), the summary sensitivity was 89.5% (95% confidence interval 86.3% to 92.1%) and the summary specificity was 77.1% (68.7% to 83.7%).\n[10] At 3-5 ng/L (six papers), the summary sensitivity was 97.4% (94.9% to 98.7%) and the summary specificity was 42.4% (31.2% to 54.5%).\n[11] This means that if 21 of 100 consecutive patients have the target condition (21%, the median prevalence across the studies), 2 (95% confidence interval 2 to 3) of 21 patients with acute myocardial infarction will be missed (false negatives) if 14 ng/L is used as a cut-off value and 18 (13 to 25) of 79 patients without acute myocardial infarction will test positive (false positives).\n[12] If the 3-5 ng/L cut-off value is used, <1 (0 to 1) patient with acute myocardial infarction will be missed and 46 (36 to 54) patients without acute myocardial infarction will test positive.\n[13] CONCLUSIONS The results indicate that a single baseline measurement of the Elecsys Troponin T high-sensitive assay could be used to rule out acute myocardial infarction if lower cut-off values such as 3 ng/L or 5 ng/L are used.\n[14] However, this method should be part of a comprehensive triage strategy and may not be appropriate for patients who present less than three hours after symptom onset.\n[15] Care must also be exercised because of the higher imprecision of the evaluated assay and the greater effect of lot-to-lot reagent variation at low troponin concentrations.\n[16] SYSTEMATIC REVIEW REGISTRATION PROSPERO registration number CRD42013003926."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 494, "doc_id": 34873974, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [34873974], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Having a main partner improves HIV outcomes.\n\nDocument title: Stable partnership and progression to AIDS or death in HIV infected patients receiving highly active antiretroviral therapy: Swiss HIV cohort study.\n\nAbstract sentences:\n[0] OBJECTIVES To explore the association between a stable partnership and clinical outcome in HIV infected patients receiving highly active antiretroviral therapy (HAART).\n[1] DESIGN Prospective cohort study of adults with HIV (Swiss HIV cohort study).\n[2] SETTING Seven outpatient clinics throughout Switzerland.\n[3] PARTICIPANTS The 3736 patients in the cohort who started HAART before 2002 (median age 36 years, 29% female, median follow up 3.6 years).\n[4] MAIN OUTCOME MEASURES Time to AIDS or death (primary endpoint), death alone, increases in CD4 cell count of at least 50 and 100 above baseline, optimal viral suppression (a viral load below 400 copies/ml), and viral rebound.\n[5] RESULTS During follow up 2985 (80%) participants reported a stable partnership on at least one occasion.\n[6] When starting HAART, 52% (545/1042) of participants reported a stable partnership; after five years of follow up 46% (190/412) of participants reported a stable partnership.\n[7] In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without.\n[8] Adjusted hazards ratios for other endpoints were 0.59 (0.44 to 0.79) for progression to death, 1.15 (1.06 to 1.24) for an increase in CD4 cells of 100 counts/microl or more, and 1.06 (0.98 to 1.14) for optimal viral suppression.\n[9] CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 495, "doc_id": 17077004, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [17077004], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Having a main partner improves HIV outcomes.\n\nDocument title: Stable partnership and progression to AIDS or death in HIV infected patients receiving highly active antiretroviral therapy: Swiss HIV cohort study.\n\nAbstract sentences:\n[0] OBJECTIVES To explore the association between a stable partnership and clinical outcome in HIV infected patients receiving highly active antiretroviral therapy (HAART).\n[1] DESIGN Prospective cohort study of adults with HIV (Swiss HIV cohort study).\n[2] SETTING Seven outpatient clinics throughout Switzerland.\n[3] PARTICIPANTS The 3736 patients in the cohort who started HAART before 2002 (median age 36 years, 29% female, median follow up 3.6 years).\n[4] MAIN OUTCOME MEASURES Time to AIDS or death (primary endpoint), death alone, increases in CD4 cell count of at least 50 and 100 above baseline, optimal viral suppression (a viral load below 400 copies/ml), and viral rebound.\n[5] RESULTS During follow up 2985 (80%) participants reported a stable partnership on at least one occasion.\n[6] When starting HAART, 52% (545/1042) of participants reported a stable partnership; after five years of follow up 46% (190/412) of participants reported a stable partnership.\n[7] In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without.\n[8] Adjusted hazards ratios for other endpoints were 0.59 (0.44 to 0.79) for progression to death, 1.15 (1.06 to 1.24) for an increase in CD4 cells of 100 counts/microl or more, and 1.06 (0.98 to 1.14) for optimal viral suppression.\n[9] CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 495, "doc_id": 17077004, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [17077004], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Having a main partner worsens HIV outcomes.\n\nDocument title: Stable partnership and progression to AIDS or death in HIV infected patients receiving highly active antiretroviral therapy: Swiss HIV cohort study.\n\nAbstract sentences:\n[0] OBJECTIVES To explore the association between a stable partnership and clinical outcome in HIV infected patients receiving highly active antiretroviral therapy (HAART).\n[1] DESIGN Prospective cohort study of adults with HIV (Swiss HIV cohort study).\n[2] SETTING Seven outpatient clinics throughout Switzerland.\n[3] PARTICIPANTS The 3736 patients in the cohort who started HAART before 2002 (median age 36 years, 29% female, median follow up 3.6 years).\n[4] MAIN OUTCOME MEASURES Time to AIDS or death (primary endpoint), death alone, increases in CD4 cell count of at least 50 and 100 above baseline, optimal viral suppression (a viral load below 400 copies/ml), and viral rebound.\n[5] RESULTS During follow up 2985 (80%) participants reported a stable partnership on at least one occasion.\n[6] When starting HAART, 52% (545/1042) of participants reported a stable partnership; after five years of follow up 46% (190/412) of participants reported a stable partnership.\n[7] In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without.\n[8] Adjusted hazards ratios for other endpoints were 0.59 (0.44 to 0.79) for progression to death, 1.15 (1.06 to 1.24) for an increase in CD4 cells of 100 counts/microl or more, and 1.06 (0.98 to 1.14) for optimal viral suppression.\n[9] CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 498, "doc_id": 17077004, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [17077004], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Having a main partner worsens HIV outcomes.\n\nDocument title: Stable partnership and progression to AIDS or death in HIV infected patients receiving highly active antiretroviral therapy: Swiss HIV cohort study.\n\nAbstract sentences:\n[0] OBJECTIVES To explore the association between a stable partnership and clinical outcome in HIV infected patients receiving highly active antiretroviral therapy (HAART).\n[1] DESIGN Prospective cohort study of adults with HIV (Swiss HIV cohort study).\n[2] SETTING Seven outpatient clinics throughout Switzerland.\n[3] PARTICIPANTS The 3736 patients in the cohort who started HAART before 2002 (median age 36 years, 29% female, median follow up 3.6 years).\n[4] MAIN OUTCOME MEASURES Time to AIDS or death (primary endpoint), death alone, increases in CD4 cell count of at least 50 and 100 above baseline, optimal viral suppression (a viral load below 400 copies/ml), and viral rebound.\n[5] RESULTS During follow up 2985 (80%) participants reported a stable partnership on at least one occasion.\n[6] When starting HAART, 52% (545/1042) of participants reported a stable partnership; after five years of follow up 46% (190/412) of participants reported a stable partnership.\n[7] In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without.\n[8] Adjusted hazards ratios for other endpoints were 0.59 (0.44 to 0.79) for progression to death, 1.15 (1.06 to 1.24) for an increase in CD4 cells of 100 counts/microl or more, and 1.06 (0.98 to 1.14) for optimal viral suppression.\n[9] CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 498, "doc_id": 17077004, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [17077004], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: HbA1c consistently overestimates glycemic control in black individuals with Sickle cell trait (SCT).\n\nDocument title: Association of Sickle Cell Trait With Hemoglobin A1c in African Americans\n\nAbstract sentences:\n[0] Importance Hemoglobin A1c (HbA1c) reflects past glucose concentrations, but this relationship may differ between those with sickle cell trait (SCT) and those without it.\n[1] Objective To evaluate the association between SCT and HbA1c for given levels of fasting or 2-hour glucose levels among African Americans.\n[2] Design, Setting, and Participants Retrospective cohort study using data collected from 7938 participants in 2 community-based cohorts, the Coronary Artery Risk Development in Young Adults (CARDIA) study and the Jackson Heart Study (JHS).\n[3] From the CARDIA study, 2637 patients contributed a maximum of 2 visits (2005-2011); from the JHS, 5301 participants contributed a maximum of 3 visits (2000-2013).\n[4] All visits were scheduled at approximately 5-year intervals.\n[5] Participants without SCT data, those without any concurrent HbA1c and glucose measurements, and those with hemoglobin variants HbSS, HbCC, or HbAC were excluded.\n[6] Analysis of the primary outcome was conducted using generalized estimating equations (GEE) to examine the association of SCT with HbA1c levels, controlling for fasting or 2-hour glucose measures.\n[7] Exposures Presence of SCT.\n[8] Main Outcomes and Measures Hemoglobin A1c stratified by the presence or absence of SCT was the primary outcome measure.\n[9] Results The analytic sample included 4620 participants (mean age, 52.3 [SD, 11.8] years; 2835 women [61.3%]; 367 [7.9%] with SCT) with 9062 concurrent measures of fasting glucose and HbA1c levels.\n[10] In unadjusted GEE analyses, for a given fasting glucose, HbA1c values were statistically significantly lower in those with (5.72%) vs those without (6.01%) SCT (mean HbA1c difference, −0.29%; 95% CI, −0.35% to −0.23%).\n[11] Findings were similar in models adjusted for key risk factors and in analyses using 2001 concurrent measures of 2-hour glucose and HbA1c concentration for those with SCT (mean, 5.35%) vs those without SCT (mean, 5.65%) for a mean HbA1c difference of −0.30% (95% CI, −0.39% to −0.21%).\n[12] The HbA1c difference by SCT was greater at higher fasting (P = .02 for interaction) and 2-hour (P = .03) glucose concentrations.\n[13] The prevalence of prediabetes and diabetes was statistically significantly lower among participants with SCT when defined using HbA1c values (29.2% vs 48.6% for prediabetes and 3.8% vs 7.3% for diabetes in 572 observations from participants with SCT and 6877 observations from participants without SCT; P<.001 for both comparisons).\n[14] Conclusions and Relevance Among African Americans from 2 large, well-established cohorts, participants with SCT had lower levels of HbA1c at any given concentration of fasting or 2-hour glucose compared with participants without SCT.\n[15] These findings suggest that HbA1c may systematically underestimate past glycemia in black patients with SCT and may require further evaluation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"In unadjusted GEE analyses, for a given fasting glucose, HbA1c values were statistically significantly lower in those with (5.72%) vs those without (6.01%) SCT (mean HbA1c difference, −0.29%; 95% CI, −0.35% to −0.23%).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 499, "doc_id": 26064662, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [26064662], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: HbA1c consistently overestimates glycemic control in black individuals with Sickle cell trait (SCT).\n\nDocument title: Association of Sickle Cell Trait With Hemoglobin A1c in African Americans\n\nAbstract sentences:\n[0] Importance Hemoglobin A1c (HbA1c) reflects past glucose concentrations, but this relationship may differ between those with sickle cell trait (SCT) and those without it.\n[1] Objective To evaluate the association between SCT and HbA1c for given levels of fasting or 2-hour glucose levels among African Americans.\n[2] Design, Setting, and Participants Retrospective cohort study using data collected from 7938 participants in 2 community-based cohorts, the Coronary Artery Risk Development in Young Adults (CARDIA) study and the Jackson Heart Study (JHS).\n[3] From the CARDIA study, 2637 patients contributed a maximum of 2 visits (2005-2011); from the JHS, 5301 participants contributed a maximum of 3 visits (2000-2013).\n[4] All visits were scheduled at approximately 5-year intervals.\n[5] Participants without SCT data, those without any concurrent HbA1c and glucose measurements, and those with hemoglobin variants HbSS, HbCC, or HbAC were excluded.\n[6] Analysis of the primary outcome was conducted using generalized estimating equations (GEE) to examine the association of SCT with HbA1c levels, controlling for fasting or 2-hour glucose measures.\n[7] Exposures Presence of SCT.\n[8] Main Outcomes and Measures Hemoglobin A1c stratified by the presence or absence of SCT was the primary outcome measure.\n[9] Results The analytic sample included 4620 participants (mean age, 52.3 [SD, 11.8] years; 2835 women [61.3%]; 367 [7.9%] with SCT) with 9062 concurrent measures of fasting glucose and HbA1c levels.\n[10] In unadjusted GEE analyses, for a given fasting glucose, HbA1c values were statistically significantly lower in those with (5.72%) vs those without (6.01%) SCT (mean HbA1c difference, −0.29%; 95% CI, −0.35% to −0.23%).\n[11] Findings were similar in models adjusted for key risk factors and in analyses using 2001 concurrent measures of 2-hour glucose and HbA1c concentration for those with SCT (mean, 5.35%) vs those without SCT (mean, 5.65%) for a mean HbA1c difference of −0.30% (95% CI, −0.39% to −0.21%).\n[12] The HbA1c difference by SCT was greater at higher fasting (P = .02 for interaction) and 2-hour (P = .03) glucose concentrations.\n[13] The prevalence of prediabetes and diabetes was statistically significantly lower among participants with SCT when defined using HbA1c values (29.2% vs 48.6% for prediabetes and 3.8% vs 7.3% for diabetes in 572 observations from participants with SCT and 6877 observations from participants without SCT; P<.001 for both comparisons).\n[14] Conclusions and Relevance Among African Americans from 2 large, well-established cohorts, participants with SCT had lower levels of HbA1c at any given concentration of fasting or 2-hour glucose compared with participants without SCT.\n[15] These findings suggest that HbA1c may systematically underestimate past glycemia in black patients with SCT and may require further evaluation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"Findings were similar in models adjusted for key risk factors and in analyses using 2001 concurrent measures of 2-hour glucose and HbA1c concentration for those with SCT (mean, 5.35%) vs those without SCT (mean, 5.65%) for a mean HbA1c difference of −0.30% (95% CI, −0.39% to −0.21%).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 499, "doc_id": 26064662, "label": "CONTRADICTS", "evidence_sentence_ids": [11], "cited_doc_ids": [26064662], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: HbA1c consistently overestimates glycemic control in black individuals with Sickle cell trait (SCT).\n\nDocument title: Association of Sickle Cell Trait With Hemoglobin A1c in African Americans\n\nAbstract sentences:\n[0] Importance Hemoglobin A1c (HbA1c) reflects past glucose concentrations, but this relationship may differ between those with sickle cell trait (SCT) and those without it.\n[1] Objective To evaluate the association between SCT and HbA1c for given levels of fasting or 2-hour glucose levels among African Americans.\n[2] Design, Setting, and Participants Retrospective cohort study using data collected from 7938 participants in 2 community-based cohorts, the Coronary Artery Risk Development in Young Adults (CARDIA) study and the Jackson Heart Study (JHS).\n[3] From the CARDIA study, 2637 patients contributed a maximum of 2 visits (2005-2011); from the JHS, 5301 participants contributed a maximum of 3 visits (2000-2013).\n[4] All visits were scheduled at approximately 5-year intervals.\n[5] Participants without SCT data, those without any concurrent HbA1c and glucose measurements, and those with hemoglobin variants HbSS, HbCC, or HbAC were excluded.\n[6] Analysis of the primary outcome was conducted using generalized estimating equations (GEE) to examine the association of SCT with HbA1c levels, controlling for fasting or 2-hour glucose measures.\n[7] Exposures Presence of SCT.\n[8] Main Outcomes and Measures Hemoglobin A1c stratified by the presence or absence of SCT was the primary outcome measure.\n[9] Results The analytic sample included 4620 participants (mean age, 52.3 [SD, 11.8] years; 2835 women [61.3%]; 367 [7.9%] with SCT) with 9062 concurrent measures of fasting glucose and HbA1c levels.\n[10] In unadjusted GEE analyses, for a given fasting glucose, HbA1c values were statistically significantly lower in those with (5.72%) vs those without (6.01%) SCT (mean HbA1c difference, −0.29%; 95% CI, −0.35% to −0.23%).\n[11] Findings were similar in models adjusted for key risk factors and in analyses using 2001 concurrent measures of 2-hour glucose and HbA1c concentration for those with SCT (mean, 5.35%) vs those without SCT (mean, 5.65%) for a mean HbA1c difference of −0.30% (95% CI, −0.39% to −0.21%).\n[12] The HbA1c difference by SCT was greater at higher fasting (P = .02 for interaction) and 2-hour (P = .03) glucose concentrations.\n[13] The prevalence of prediabetes and diabetes was statistically significantly lower among participants with SCT when defined using HbA1c values (29.2% vs 48.6% for prediabetes and 3.8% vs 7.3% for diabetes in 572 observations from participants with SCT and 6877 observations from participants without SCT; P<.001 for both comparisons).\n[14] Conclusions and Relevance Among African Americans from 2 large, well-established cohorts, participants with SCT had lower levels of HbA1c at any given concentration of fasting or 2-hour glucose compared with participants without SCT.\n[15] These findings suggest that HbA1c may systematically underestimate past glycemia in black patients with SCT and may require further evaluation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"The prevalence of prediabetes and diabetes was statistically significantly lower among participants with SCT when defined using HbA1c values (29.2% vs 48.6% for prediabetes and 3.8% vs 7.3% for diabetes in 572 observations from participants with SCT and 6877 observations from participants without SCT; P<.001 for both comparisons).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 499, "doc_id": 26064662, "label": "CONTRADICTS", "evidence_sentence_ids": [13], "cited_doc_ids": [26064662], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: HbA1c consistently overestimates glycemic control in black individuals with Sickle cell trait (SCT).\n\nDocument title: Association of Sickle Cell Trait With Hemoglobin A1c in African Americans\n\nAbstract sentences:\n[0] Importance Hemoglobin A1c (HbA1c) reflects past glucose concentrations, but this relationship may differ between those with sickle cell trait (SCT) and those without it.\n[1] Objective To evaluate the association between SCT and HbA1c for given levels of fasting or 2-hour glucose levels among African Americans.\n[2] Design, Setting, and Participants Retrospective cohort study using data collected from 7938 participants in 2 community-based cohorts, the Coronary Artery Risk Development in Young Adults (CARDIA) study and the Jackson Heart Study (JHS).\n[3] From the CARDIA study, 2637 patients contributed a maximum of 2 visits (2005-2011); from the JHS, 5301 participants contributed a maximum of 3 visits (2000-2013).\n[4] All visits were scheduled at approximately 5-year intervals.\n[5] Participants without SCT data, those without any concurrent HbA1c and glucose measurements, and those with hemoglobin variants HbSS, HbCC, or HbAC were excluded.\n[6] Analysis of the primary outcome was conducted using generalized estimating equations (GEE) to examine the association of SCT with HbA1c levels, controlling for fasting or 2-hour glucose measures.\n[7] Exposures Presence of SCT.\n[8] Main Outcomes and Measures Hemoglobin A1c stratified by the presence or absence of SCT was the primary outcome measure.\n[9] Results The analytic sample included 4620 participants (mean age, 52.3 [SD, 11.8] years; 2835 women [61.3%]; 367 [7.9%] with SCT) with 9062 concurrent measures of fasting glucose and HbA1c levels.\n[10] In unadjusted GEE analyses, for a given fasting glucose, HbA1c values were statistically significantly lower in those with (5.72%) vs those without (6.01%) SCT (mean HbA1c difference, −0.29%; 95% CI, −0.35% to −0.23%).\n[11] Findings were similar in models adjusted for key risk factors and in analyses using 2001 concurrent measures of 2-hour glucose and HbA1c concentration for those with SCT (mean, 5.35%) vs those without SCT (mean, 5.65%) for a mean HbA1c difference of −0.30% (95% CI, −0.39% to −0.21%).\n[12] The HbA1c difference by SCT was greater at higher fasting (P = .02 for interaction) and 2-hour (P = .03) glucose concentrations.\n[13] The prevalence of prediabetes and diabetes was statistically significantly lower among participants with SCT when defined using HbA1c values (29.2% vs 48.6% for prediabetes and 3.8% vs 7.3% for diabetes in 572 observations from participants with SCT and 6877 observations from participants without SCT; P<.001 for both comparisons).\n[14] Conclusions and Relevance Among African Americans from 2 large, well-established cohorts, participants with SCT had lower levels of HbA1c at any given concentration of fasting or 2-hour glucose compared with participants without SCT.\n[15] These findings suggest that HbA1c may systematically underestimate past glycemia in black patients with SCT and may require further evaluation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [14]\nExplanation: Evidence states: \"Conclusions and Relevance Among African Americans from 2 large, well-established cohorts, participants with SCT had lower levels of HbA1c at any given concentration of fasting or 2-hour glucose compared with participants without SCT.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 499, "doc_id": 26064662, "label": "CONTRADICTS", "evidence_sentence_ids": [14], "cited_doc_ids": [26064662], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: HbA1c consistently overestimates glycemic control in black individuals with Sickle cell trait (SCT).\n\nDocument title: Association of Sickle Cell Trait With Hemoglobin A1c in African Americans\n\nAbstract sentences:\n[0] Importance Hemoglobin A1c (HbA1c) reflects past glucose concentrations, but this relationship may differ between those with sickle cell trait (SCT) and those without it.\n[1] Objective To evaluate the association between SCT and HbA1c for given levels of fasting or 2-hour glucose levels among African Americans.\n[2] Design, Setting, and Participants Retrospective cohort study using data collected from 7938 participants in 2 community-based cohorts, the Coronary Artery Risk Development in Young Adults (CARDIA) study and the Jackson Heart Study (JHS).\n[3] From the CARDIA study, 2637 patients contributed a maximum of 2 visits (2005-2011); from the JHS, 5301 participants contributed a maximum of 3 visits (2000-2013).\n[4] All visits were scheduled at approximately 5-year intervals.\n[5] Participants without SCT data, those without any concurrent HbA1c and glucose measurements, and those with hemoglobin variants HbSS, HbCC, or HbAC were excluded.\n[6] Analysis of the primary outcome was conducted using generalized estimating equations (GEE) to examine the association of SCT with HbA1c levels, controlling for fasting or 2-hour glucose measures.\n[7] Exposures Presence of SCT.\n[8] Main Outcomes and Measures Hemoglobin A1c stratified by the presence or absence of SCT was the primary outcome measure.\n[9] Results The analytic sample included 4620 participants (mean age, 52.3 [SD, 11.8] years; 2835 women [61.3%]; 367 [7.9%] with SCT) with 9062 concurrent measures of fasting glucose and HbA1c levels.\n[10] In unadjusted GEE analyses, for a given fasting glucose, HbA1c values were statistically significantly lower in those with (5.72%) vs those without (6.01%) SCT (mean HbA1c difference, −0.29%; 95% CI, −0.35% to −0.23%).\n[11] Findings were similar in models adjusted for key risk factors and in analyses using 2001 concurrent measures of 2-hour glucose and HbA1c concentration for those with SCT (mean, 5.35%) vs those without SCT (mean, 5.65%) for a mean HbA1c difference of −0.30% (95% CI, −0.39% to −0.21%).\n[12] The HbA1c difference by SCT was greater at higher fasting (P = .02 for interaction) and 2-hour (P = .03) glucose concentrations.\n[13] The prevalence of prediabetes and diabetes was statistically significantly lower among participants with SCT when defined using HbA1c values (29.2% vs 48.6% for prediabetes and 3.8% vs 7.3% for diabetes in 572 observations from participants with SCT and 6877 observations from participants without SCT; P<.001 for both comparisons).\n[14] Conclusions and Relevance Among African Americans from 2 large, well-established cohorts, participants with SCT had lower levels of HbA1c at any given concentration of fasting or 2-hour glucose compared with participants without SCT.\n[15] These findings suggest that HbA1c may systematically underestimate past glycemia in black patients with SCT and may require further evaluation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [15]\nExplanation: Evidence states: \"These findings suggest that HbA1c may systematically underestimate past glycemia in black patients with SCT and may require further evaluation.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 499, "doc_id": 26064662, "label": "CONTRADICTS", "evidence_sentence_ids": [15], "cited_doc_ids": [26064662], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Headaches are correlated with cognitive impairment.\n\nDocument title: Headache, migraine, and structural brain lesions and function: population based Epidemiology of Vascular Ageing-MRI study\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate the association of overall and specific headaches with volume of white matter hyperintensities, brain infarcts, and cognition.\n[1] DESIGN Population based, cross sectional study.\n[2] SETTING Epidemiology of Vascular Ageing study, Nantes, France.\n[3] PARTICIPANTS 780 participants (mean age 69, 58.5% women) with detailed headache assessment.\n[4] MAIN OUTCOME MEASURES Brain scans were evaluated for volume of white matter hyperintensities (by fully automated imaging processing) and for classification of infarcts (by visual reading with a standardised assessment grid).\n[5] Cognitive function was assessed by a battery of tests including the mini-mental state examination.\n[6] RESULTS 163 (20.9%) participants reported a history of severe headache and 116 had migraine, of whom 17 (14.7%) reported aura symptoms.\n[7] An association was found between any history of severe headache and increasing volume of white matter hyperintensities.\n[8] The adjusted odds ratio of being in the highest third for total volume of white matter hyperintensities was 2.0 (95% confidence interval 1.3 to 3.1, P for trend 0.002) for participants with any history of severe headache when compared with participants without severe headache being in the lowest third.\n[9] The association pattern was similar for all headache types.\n[10] Migraine with aura was the only headache type strongly associated with volume of deep white matter hyperintensities (highest third odds ratio 12.4, 1.6 to 99.4, P for trend 0.005) and with brain infarcts (3.4, 1.2 to 9.3).\n[11] The location of infarcts was predominantly outside the cerebellum and brain stem.\n[12] Evidence was lacking for cognitive impairment for any headache type with or without brain lesions.\n[13] CONCLUSIONS In this population based study, any history of severe headache was associated with an increased volume of white matter hyperintensities.\n[14] Migraine with aura was the only headache type associated with brain infarcts.\n[15] Evidence that headache of any type by itself or in combination with brain lesions was associated with cognitive impairment was lacking."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"Evidence was lacking for cognitive impairment for any headache type with or without brain lesions.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 500, "doc_id": 17930286, "label": "CONTRADICTS", "evidence_sentence_ids": [12], "cited_doc_ids": [17930286], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Healthy volunteers exhibit rapid and transient increase of cellular ATP after being bolus-injected with fructose.\n\nDocument title: Alterations in liver ATP homeostasis in human nonalcoholic steatohepatitis: a pilot study.\n\nAbstract sentences:\n[0] CONTEXT The mechanisms that drive progression from fatty liver to steatohepatitis and cirrhosis are unknown.\n[1] In animal models, obese mice with fatty livers are vulnerable to liver adenosine triphosphate (ATP) depletion and necrosis, suggesting that altered hepatic energy homeostasis may be involved.\n[2] OBJECTIVE To determine if patients with fatty liver disease exhibit impaired recovery from hepatic ATP depletion.\n[3] DESIGN Laboratory analysis of liver ATP stores monitored by nuclear magnetic resonance spectroscopy before and after transient hepatic ATP depletion was induced by fructose injection.\n[4] The study was conducted between July 15 and August 30, 1998.\n[5] SETTING University hospital.\n[6] PATIENTS Eight consecutive adults with biopsy-proven nonalcoholic steatohepatitis and 7 healthy age- and sex-matched controls.\n[7] MAIN OUTCOME MEASURE Level of ATP 1 hour after fructose infusion in patients vs controls.\n[8] RESULTS In patients, serum aminotransferase levels were increased (P = .02 vs controls); albumin and bilirubin values were normal and clinical evidence of portal hypertension was absent in both groups.\n[9] However, 2 patients had moderate fibrosis and 1 had cirrhosis on liver biopsy.\n[10] Mean serum glucose, cholesterol, and triglyceride levels were similar between groups but patients weighed significantly more than controls (P = .02).\n[11] Liver ATP levels were similar in the 2 groups before fructose infusion and decreased similarly in both after fructose infusion (P = .01 vs initial ATP levels).\n[12] However, controls replenished their hepatic ATP stores during the 1-hour follow-up period (P<.02 vs minimum ATP) but patients did not.\n[13] Hence, patients' hepatic ATP levels were lower than those of controls at the end of the study (P = .04).\n[14] Body mass index (BMI) correlated inversely with ATP recovery, even in controls (R = -0.768; P = .07).\n[15] Although BMI was greater in patients than controls (P = .02) and correlated strongly with fatty liver and serum aminotransferase elevations, neither of the latter 2 parameters nor the histologic severity of fibrosis strongly predicted hepatic ATP recovery.\n[16] CONCLUSIONS These data suggest that recovery from hepatic ATP depletion becomes progressively less efficient as body mass increases in healthy controls and is severely impaired in patients with obesity-related nonalcoholic steatohepatitis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"Liver ATP levels were similar in the 2 groups before fructose infusion and decreased similarly in both after fructose infusion (P = .01 vs initial ATP levels).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 504, "doc_id": 10883736, "label": "CONTRADICTS", "evidence_sentence_ids": [11], "cited_doc_ids": [10883736], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Helicobacter pylori-induced aberrant NF-kB-dependent expression of activation-induced cytidine deaminase contributes to the mutagenesis of host DNA.\n\nDocument title: Helicobacter pylori infection triggers aberrant expression of activation-induced cytidine deaminase in gastric epithelium\n\nAbstract sentences:\n[0] Infection with Helicobacter pylori (H. pylori) is a risk factor for the development of gastric cancer.\n[1] Here we show that infection of gastric epithelial cells with 'cag' pathogenicity island (cagPAI)-positive H. pylori induced aberrant expression of activation-induced cytidine deaminase (AID), a member of the cytidine-deaminase family that acts as a DNA- and RNA-editing enzyme, via the IκB kinase–dependent nuclear factor-κB activation pathway.\n[2] H. pylori–mediated upregulation of AID resulted in the accumulation of nucleotide alterations in the TP53 tumor suppressor gene in gastric cells in vitro.\n[3] Our findings provide evidence that aberrant AID expression caused by H. pylori infection might be a mechanism of mutation accumulation in the gastric mucosa during H. pylori–associated gastric carcinogenesis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Here we show that infection of gastric epithelial cells with 'cag' pathogenicity island (cagPAI)-positive H. pylori induced aberrant expression of activation-induced cytidine deaminase (AID), a member of the cytidine-deaminase family that acts as a DNA- and RNA-editing enzyme, via the IκB kinase–dependent nuclear factor-κB activation pathway.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 505, "doc_id": 22703082, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [22703082], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Helicobacter pylori-induced aberrant NF-kB-dependent expression of activation-induced cytidine deaminase contributes to the mutagenesis of host DNA.\n\nDocument title: Helicobacter pylori infection triggers aberrant expression of activation-induced cytidine deaminase in gastric epithelium\n\nAbstract sentences:\n[0] Infection with Helicobacter pylori (H. pylori) is a risk factor for the development of gastric cancer.\n[1] Here we show that infection of gastric epithelial cells with 'cag' pathogenicity island (cagPAI)-positive H. pylori induced aberrant expression of activation-induced cytidine deaminase (AID), a member of the cytidine-deaminase family that acts as a DNA- and RNA-editing enzyme, via the IκB kinase–dependent nuclear factor-κB activation pathway.\n[2] H. pylori–mediated upregulation of AID resulted in the accumulation of nucleotide alterations in the TP53 tumor suppressor gene in gastric cells in vitro.\n[3] Our findings provide evidence that aberrant AID expression caused by H. pylori infection might be a mechanism of mutation accumulation in the gastric mucosa during H. pylori–associated gastric carcinogenesis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Our findings provide evidence that aberrant AID expression caused by H. pylori infection might be a mechanism of mutation accumulation in the gastric mucosa during H. pylori–associated gastric carcinogenesis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 505, "doc_id": 22703082, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [22703082], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Helminths interfere with immune system control of coinfections by microbial pathogens 16.\n\nDocument title: Preexisting helminth infection induces inhibition of innate pulmonary anti-tuberculosis defense by engaging the IL-4 receptor pathway\n\nAbstract sentences:\n[0] Tuberculosis and helminthic infections coexist in many parts of the world, yet the impact of helminth-elicited Th2 responses on the ability of the host to control Mycobacterium tuberculosis (Mtb) infection has not been fully explored.\n[1] We show that mice infected with the intestinal helminth Nippostrongylus brasiliensis (Nb) exhibit a transitory impairment of resistance to airborne Mtb infection.\n[2] Furthermore, a second dose of Nb infection substantially increases the bacterial burden in the lungs of co-infected mice.\n[3] Interestingly, the Th2 response in the co-infected animals did not impair the onset and development of the protective Mtb-specific Th1 cellular immune responses.\n[4] However, the helminth-induced Th2 environment resulted in the accumulation of alternatively activated macrophages (AAMs) in the lung.\n[5] Co-infected mice lacking interleukin (IL) 4Rα exhibited improved ability to control Mtb infection, which was accompanied by significantly reduced accumulation of AAMs.\n[6] Moreover, IL-4Rα(-/-) mice adoptively transferred with wild-type macrophages had a significantly higher Mtb load in their lungs compared with those that received IL-4Rα(-/-) macrophages, suggesting a direct contribution for the IL-4R pathway to the heightened susceptibility of co-infected animals.\n[7] The Th2 response can thus enhance the intracellular persistence of Mtb, in part by mediating the alternative activation of macrophages via the IL-4Rα signaling pathway."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"We show that mice infected with the intestinal helminth Nippostrongylus brasiliensis (Nb) exhibit a transitory impairment of resistance to airborne Mtb infection.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 506, "doc_id": 7433668, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [7433668], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Helminths interfere with immune system control of coinfections by microbial pathogens 16.\n\nDocument title: Preexisting helminth infection induces inhibition of innate pulmonary anti-tuberculosis defense by engaging the IL-4 receptor pathway\n\nAbstract sentences:\n[0] Tuberculosis and helminthic infections coexist in many parts of the world, yet the impact of helminth-elicited Th2 responses on the ability of the host to control Mycobacterium tuberculosis (Mtb) infection has not been fully explored.\n[1] We show that mice infected with the intestinal helminth Nippostrongylus brasiliensis (Nb) exhibit a transitory impairment of resistance to airborne Mtb infection.\n[2] Furthermore, a second dose of Nb infection substantially increases the bacterial burden in the lungs of co-infected mice.\n[3] Interestingly, the Th2 response in the co-infected animals did not impair the onset and development of the protective Mtb-specific Th1 cellular immune responses.\n[4] However, the helminth-induced Th2 environment resulted in the accumulation of alternatively activated macrophages (AAMs) in the lung.\n[5] Co-infected mice lacking interleukin (IL) 4Rα exhibited improved ability to control Mtb infection, which was accompanied by significantly reduced accumulation of AAMs.\n[6] Moreover, IL-4Rα(-/-) mice adoptively transferred with wild-type macrophages had a significantly higher Mtb load in their lungs compared with those that received IL-4Rα(-/-) macrophages, suggesting a direct contribution for the IL-4R pathway to the heightened susceptibility of co-infected animals.\n[7] The Th2 response can thus enhance the intracellular persistence of Mtb, in part by mediating the alternative activation of macrophages via the IL-4Rα signaling pathway."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Furthermore, a second dose of Nb infection substantially increases the bacterial burden in the lungs of co-infected mice.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 506, "doc_id": 7433668, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [7433668], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Helminths interfere with immune system control of coinfections by microbial pathogens 16.\n\nDocument title: Preexisting helminth infection induces inhibition of innate pulmonary anti-tuberculosis defense by engaging the IL-4 receptor pathway\n\nAbstract sentences:\n[0] Tuberculosis and helminthic infections coexist in many parts of the world, yet the impact of helminth-elicited Th2 responses on the ability of the host to control Mycobacterium tuberculosis (Mtb) infection has not been fully explored.\n[1] We show that mice infected with the intestinal helminth Nippostrongylus brasiliensis (Nb) exhibit a transitory impairment of resistance to airborne Mtb infection.\n[2] Furthermore, a second dose of Nb infection substantially increases the bacterial burden in the lungs of co-infected mice.\n[3] Interestingly, the Th2 response in the co-infected animals did not impair the onset and development of the protective Mtb-specific Th1 cellular immune responses.\n[4] However, the helminth-induced Th2 environment resulted in the accumulation of alternatively activated macrophages (AAMs) in the lung.\n[5] Co-infected mice lacking interleukin (IL) 4Rα exhibited improved ability to control Mtb infection, which was accompanied by significantly reduced accumulation of AAMs.\n[6] Moreover, IL-4Rα(-/-) mice adoptively transferred with wild-type macrophages had a significantly higher Mtb load in their lungs compared with those that received IL-4Rα(-/-) macrophages, suggesting a direct contribution for the IL-4R pathway to the heightened susceptibility of co-infected animals.\n[7] The Th2 response can thus enhance the intracellular persistence of Mtb, in part by mediating the alternative activation of macrophages via the IL-4Rα signaling pathway."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"The Th2 response can thus enhance the intracellular persistence of Mtb, in part by mediating the alternative activation of macrophages via the IL-4Rα signaling pathway.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 506, "doc_id": 7433668, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [7433668], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Hematopoietic Stem Cell purification reaches purity rates above 90%.\n\nDocument title: Combined Single-Cell Functional and Gene Expression Analysis Resolves Heterogeneity within Stem Cell Populations\n\nAbstract sentences:\n[0] Heterogeneity within the self-renewal durability of adult hematopoietic stem cells (HSCs) challenges our understanding of the molecular framework underlying HSC function.\n[1] Gene expression studies have been hampered by the presence of multiple HSC subtypes and contaminating non-HSCs in bulk HSC populations.\n[2] To gain deeper insight into the gene expression program of murine HSCs, we combined single-cell functional assays with flow cytometric index sorting and single-cell gene expression assays.\n[3] Through bioinformatic integration of these datasets, we designed an unbiased sorting strategy that separates non-HSCs away from HSCs, and single-cell transplantation experiments using the enriched population were combined with RNA-seq data to identify key molecules that associate with long-term durable self-renewal, producing a single-cell molecular dataset that is linked to functional stem cell activity.\n[4] Finally, we demonstrated the broader applicability of this approach for linking key molecules with defined cellular functions in another stem cell system."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 509, "doc_id": 13980338, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [13980338], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: High levels of CRP lead to a higher risk of exacerbations in chronic obstructive pulmonary disease (COPD).\n\nDocument title: Inflammatory biomarkers and exacerbations in chronic obstructive pulmonary disease.\n\nAbstract sentences:\n[0] IMPORTANCE Exacerbations of respiratory symptoms in chronic obstructive pulmonary disease (COPD) have profound and long-lasting adverse effects on patients.\n[1] OBJECTIVE To test the hypothesis that elevated levels of inflammatory biomarkers in individuals with stable COPD are associated with an increased risk of having exacerbations.\n[2] DESIGN, SETTING, AND PARTICIPANTS Prospective cohort study examining 61,650 participants with spirometry measurements from the Copenhagen City Heart Study (2001-2003) and the Copenhagen General Population Study (2003-2008).\n[3] Of these, 6574 had COPD, defined as a ratio between forced expiratory volume in 1 second (FEV1) and forced vital capacity below 0.7.\n[4] MAIN OUTCOMES AND MEASURES Baseline levels of C-reactive protein (CRP) and fibrinogen and leukocyte count were measured in participants at a time when they were not experiencing symptoms of exacerbations.\n[5] Exacerbations were recorded and defined as short-course treatment with oral corticosteroids alone or in combination with an antibiotic or as a hospital admission due to COPD.\n[6] Levels of CRP and fibrinogen and leukocyte count were defined as high or low according to cut points of 3 mg/L, 14 μmol/L, and 9 ×10(9)/L, respectively.\n[7] RESULTS During follow-up, 3083 exacerbations were recorded (mean, 0.5/participant).\n[8] In the first year of follow-up, multivariable-adjusted odds ratios for having frequent exacerbations were 1.2 (95% CI, 0.7-2.2; 17 events/1000 person-years) for individuals with 1 high biomarker, 1.7 (95% CI, 0.9-3.2; 32 events/1000 person-years) for individuals with 2 high biomarkers, and 3.7 (95% CI, 1.9-7.4; 81 events/1000 person-years) for individuals with 3 high biomarkers compared with individuals who had no elevated biomarkers (9 events/1000 person-years; trend: P = 2 × 10(-5)).\n[9] Corresponding hazard ratios using maximum follow-up time were 1.4 (95% CI, 1.1-1.8), 1.6 (95% CI, 1.3-2.2), and 2.5 (95% CI, 1.8-3.4), respectively (trend: P = 1 × 10(-8)).\n[10] The addition of inflammatory biomarkers to a basic model including age, sex, FEV1 percent predicted, smoking, use of any inhaled medication, body mass index, history of previous exacerbations, and time since most recent prior exacerbation improved the C statistics from 0.71 to 0.73 (comparison: P = 9 × 10(-5)).\n[11] Relative risks were consistent in those with milder COPD, in those with no history of frequent exacerbations, and in the 2 studies separately.\n[12] The highest 5-year absolute risks of having frequent exacerbations in those with 3 high biomarkers (vs no high biomarkers) were 62% (vs 24%) for those with Global Initiative for Chronic Obstructive Lung Disease (GOLD) grades C-D (n = 558), 98% (vs 64%) in those with a history of frequent exacerbations (n = 127), and 52% (vs 15%) for those with GOLD grades 3-4 (n = 465).\n[13] CONCLUSIONS AND RELEVANCE Simultaneously elevated levels of CRP and fibrinogen and leukocyte count in individuals with COPD were associated with increased risk of having exacerbations, even in those with milder COPD and in those without previous exacerbations.\n[14] Further investigation is needed to determine the clinical value of these biomarkers for risk stratification."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"In the first year of follow-up, multivariable-adjusted odds ratios for having frequent exacerbations were 1.2 (95% CI, 0.7-2.2; 17 events/1000 person-years) for individuals with 1 high biomarker, 1.7 (95% CI, 0.9-3.2; 32 events/1000 person-years) for individuals with 2 high biomarkers, and 3.7 (95% CI, 1.9-7.4; 81 events/1000 person-years) for individuals with 3 high biomarkers compared with individuals who had no elevated biomarkers (9 events/1000 person-years; trend: P = 2 × 10(-5)).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 515, "doc_id": 29564505, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [29564505], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: High levels of CRP lead to a higher risk of exacerbations in chronic obstructive pulmonary disease (COPD).\n\nDocument title: Inflammatory biomarkers and exacerbations in chronic obstructive pulmonary disease.\n\nAbstract sentences:\n[0] IMPORTANCE Exacerbations of respiratory symptoms in chronic obstructive pulmonary disease (COPD) have profound and long-lasting adverse effects on patients.\n[1] OBJECTIVE To test the hypothesis that elevated levels of inflammatory biomarkers in individuals with stable COPD are associated with an increased risk of having exacerbations.\n[2] DESIGN, SETTING, AND PARTICIPANTS Prospective cohort study examining 61,650 participants with spirometry measurements from the Copenhagen City Heart Study (2001-2003) and the Copenhagen General Population Study (2003-2008).\n[3] Of these, 6574 had COPD, defined as a ratio between forced expiratory volume in 1 second (FEV1) and forced vital capacity below 0.7.\n[4] MAIN OUTCOMES AND MEASURES Baseline levels of C-reactive protein (CRP) and fibrinogen and leukocyte count were measured in participants at a time when they were not experiencing symptoms of exacerbations.\n[5] Exacerbations were recorded and defined as short-course treatment with oral corticosteroids alone or in combination with an antibiotic or as a hospital admission due to COPD.\n[6] Levels of CRP and fibrinogen and leukocyte count were defined as high or low according to cut points of 3 mg/L, 14 μmol/L, and 9 ×10(9)/L, respectively.\n[7] RESULTS During follow-up, 3083 exacerbations were recorded (mean, 0.5/participant).\n[8] In the first year of follow-up, multivariable-adjusted odds ratios for having frequent exacerbations were 1.2 (95% CI, 0.7-2.2; 17 events/1000 person-years) for individuals with 1 high biomarker, 1.7 (95% CI, 0.9-3.2; 32 events/1000 person-years) for individuals with 2 high biomarkers, and 3.7 (95% CI, 1.9-7.4; 81 events/1000 person-years) for individuals with 3 high biomarkers compared with individuals who had no elevated biomarkers (9 events/1000 person-years; trend: P = 2 × 10(-5)).\n[9] Corresponding hazard ratios using maximum follow-up time were 1.4 (95% CI, 1.1-1.8), 1.6 (95% CI, 1.3-2.2), and 2.5 (95% CI, 1.8-3.4), respectively (trend: P = 1 × 10(-8)).\n[10] The addition of inflammatory biomarkers to a basic model including age, sex, FEV1 percent predicted, smoking, use of any inhaled medication, body mass index, history of previous exacerbations, and time since most recent prior exacerbation improved the C statistics from 0.71 to 0.73 (comparison: P = 9 × 10(-5)).\n[11] Relative risks were consistent in those with milder COPD, in those with no history of frequent exacerbations, and in the 2 studies separately.\n[12] The highest 5-year absolute risks of having frequent exacerbations in those with 3 high biomarkers (vs no high biomarkers) were 62% (vs 24%) for those with Global Initiative for Chronic Obstructive Lung Disease (GOLD) grades C-D (n = 558), 98% (vs 64%) in those with a history of frequent exacerbations (n = 127), and 52% (vs 15%) for those with GOLD grades 3-4 (n = 465).\n[13] CONCLUSIONS AND RELEVANCE Simultaneously elevated levels of CRP and fibrinogen and leukocyte count in individuals with COPD were associated with increased risk of having exacerbations, even in those with milder COPD and in those without previous exacerbations.\n[14] Further investigation is needed to determine the clinical value of these biomarkers for risk stratification."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"CONCLUSIONS AND RELEVANCE Simultaneously elevated levels of CRP and fibrinogen and leukocyte count in individuals with COPD were associated with increased risk of having exacerbations, even in those with milder COPD and in those without previous exacerbations.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 515, "doc_id": 29564505, "label": "SUPPORTS", "evidence_sentence_ids": [13], "cited_doc_ids": [29564505], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Higher plasma levels of I-carnitine, when associated with trimethylamine N-oxide, are negatively correlated with cardiovascular events in humans.\n\nDocument title: Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis\n\nAbstract sentences:\n[0] Intestinal microbiota metabolism of choline and phosphatidylcholine produces trimethylamine (TMA), which is further metabolized to a proatherogenic species, trimethylamine-N-oxide (TMAO).\n[1] We demonstrate here that metabolism by intestinal microbiota of dietary L-carnitine, a trimethylamine abundant in red meat, also produces TMAO and accelerates atherosclerosis in mice.\n[2] Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine through a microbiota-dependent mechanism.\n[3] The presence of specific bacterial taxa in human feces was associated with both plasma TMAO concentration and dietary status.\n[4] Plasma L-carnitine levels in subjects undergoing cardiac evaluation (n = 2,595) predicted increased risks for both prevalent cardiovascular disease (CVD) and incident major adverse cardiac events (myocardial infarction, stroke or death), but only among subjects with concurrently high TMAO levels.\n[5] Chronic dietary L-carnitine supplementation in mice altered cecal microbial composition, markedly enhanced synthesis of TMA and TMAO, and increased atherosclerosis, but this did not occur if intestinal microbiota was concurrently suppressed.\n[6] In mice with an intact intestinal microbiota, dietary supplementation with TMAO or either carnitine or choline reduced in vivo reverse cholesterol transport.\n[7] Intestinal microbiota may thus contribute to the well-established link between high levels of red meat consumption and CVD risk."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"We demonstrate here that metabolism by intestinal microbiota of dietary L-carnitine, a trimethylamine abundant in red meat, also produces TMAO and accelerates atherosclerosis in mice.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 523, "doc_id": 14803797, "label": "CONTRADICTS", "evidence_sentence_ids": [1], "cited_doc_ids": [14803797], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Higher plasma levels of I-carnitine, when associated with trimethylamine N-oxide, are negatively correlated with cardiovascular events in humans.\n\nDocument title: Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis\n\nAbstract sentences:\n[0] Intestinal microbiota metabolism of choline and phosphatidylcholine produces trimethylamine (TMA), which is further metabolized to a proatherogenic species, trimethylamine-N-oxide (TMAO).\n[1] We demonstrate here that metabolism by intestinal microbiota of dietary L-carnitine, a trimethylamine abundant in red meat, also produces TMAO and accelerates atherosclerosis in mice.\n[2] Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine through a microbiota-dependent mechanism.\n[3] The presence of specific bacterial taxa in human feces was associated with both plasma TMAO concentration and dietary status.\n[4] Plasma L-carnitine levels in subjects undergoing cardiac evaluation (n = 2,595) predicted increased risks for both prevalent cardiovascular disease (CVD) and incident major adverse cardiac events (myocardial infarction, stroke or death), but only among subjects with concurrently high TMAO levels.\n[5] Chronic dietary L-carnitine supplementation in mice altered cecal microbial composition, markedly enhanced synthesis of TMA and TMAO, and increased atherosclerosis, but this did not occur if intestinal microbiota was concurrently suppressed.\n[6] In mice with an intact intestinal microbiota, dietary supplementation with TMAO or either carnitine or choline reduced in vivo reverse cholesterol transport.\n[7] Intestinal microbiota may thus contribute to the well-established link between high levels of red meat consumption and CVD risk."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Chronic dietary L-carnitine supplementation in mice altered cecal microbial composition, markedly enhanced synthesis of TMA and TMAO, and increased atherosclerosis, but this did not occur if intestinal microbiota was concurrently suppressed.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 523, "doc_id": 14803797, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [14803797], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Higher plasma levels of I-carnitine, when associated with trimethylamine N-oxide, are positively correlated with cardiovascular events in humans.\n\nDocument title: Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis\n\nAbstract sentences:\n[0] Intestinal microbiota metabolism of choline and phosphatidylcholine produces trimethylamine (TMA), which is further metabolized to a proatherogenic species, trimethylamine-N-oxide (TMAO).\n[1] We demonstrate here that metabolism by intestinal microbiota of dietary L-carnitine, a trimethylamine abundant in red meat, also produces TMAO and accelerates atherosclerosis in mice.\n[2] Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine through a microbiota-dependent mechanism.\n[3] The presence of specific bacterial taxa in human feces was associated with both plasma TMAO concentration and dietary status.\n[4] Plasma L-carnitine levels in subjects undergoing cardiac evaluation (n = 2,595) predicted increased risks for both prevalent cardiovascular disease (CVD) and incident major adverse cardiac events (myocardial infarction, stroke or death), but only among subjects with concurrently high TMAO levels.\n[5] Chronic dietary L-carnitine supplementation in mice altered cecal microbial composition, markedly enhanced synthesis of TMA and TMAO, and increased atherosclerosis, but this did not occur if intestinal microbiota was concurrently suppressed.\n[6] In mice with an intact intestinal microbiota, dietary supplementation with TMAO or either carnitine or choline reduced in vivo reverse cholesterol transport.\n[7] Intestinal microbiota may thus contribute to the well-established link between high levels of red meat consumption and CVD risk."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"We demonstrate here that metabolism by intestinal microbiota of dietary L-carnitine, a trimethylamine abundant in red meat, also produces TMAO and accelerates atherosclerosis in mice.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 524, "doc_id": 14803797, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [14803797], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Higher plasma levels of I-carnitine, when associated with trimethylamine N-oxide, are positively correlated with cardiovascular events in humans.\n\nDocument title: Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis\n\nAbstract sentences:\n[0] Intestinal microbiota metabolism of choline and phosphatidylcholine produces trimethylamine (TMA), which is further metabolized to a proatherogenic species, trimethylamine-N-oxide (TMAO).\n[1] We demonstrate here that metabolism by intestinal microbiota of dietary L-carnitine, a trimethylamine abundant in red meat, also produces TMAO and accelerates atherosclerosis in mice.\n[2] Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine through a microbiota-dependent mechanism.\n[3] The presence of specific bacterial taxa in human feces was associated with both plasma TMAO concentration and dietary status.\n[4] Plasma L-carnitine levels in subjects undergoing cardiac evaluation (n = 2,595) predicted increased risks for both prevalent cardiovascular disease (CVD) and incident major adverse cardiac events (myocardial infarction, stroke or death), but only among subjects with concurrently high TMAO levels.\n[5] Chronic dietary L-carnitine supplementation in mice altered cecal microbial composition, markedly enhanced synthesis of TMA and TMAO, and increased atherosclerosis, but this did not occur if intestinal microbiota was concurrently suppressed.\n[6] In mice with an intact intestinal microbiota, dietary supplementation with TMAO or either carnitine or choline reduced in vivo reverse cholesterol transport.\n[7] Intestinal microbiota may thus contribute to the well-established link between high levels of red meat consumption and CVD risk."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Chronic dietary L-carnitine supplementation in mice altered cecal microbial composition, markedly enhanced synthesis of TMA and TMAO, and increased atherosclerosis, but this did not occur if intestinal microbiota was concurrently suppressed.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 524, "doc_id": 14803797, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [14803797], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Homozygous deletion of murine Sbds gene from osterix-expressing mesenchymal stem and progenitor cells (MPCs) induces oxidative stress.\n\nDocument title: Mesenchymal Inflammation Drives Genotoxic Stress in Hematopoietic Stem Cells and Predicts Disease Evolution in Human Pre-leukemia.\n\nAbstract sentences:\n[0] Mesenchymal niche cells may drive tissue failure and malignant transformation in the hematopoietic system, but the underlying molecular mechanisms and relevance to human disease remain poorly defined.\n[1] Here, we show that perturbation of mesenchymal cells in a mouse model of the pre-leukemic disorder Shwachman-Diamond syndrome (SDS) induces mitochondrial dysfunction, oxidative stress, and activation of DNA damage responses in hematopoietic stem and progenitor cells.\n[2] Massive parallel RNA sequencing of highly purified mesenchymal cells in the SDS mouse model and a range of human pre-leukemic syndromes identified p53-S100A8/9-TLR inflammatory signaling as a common driving mechanism of genotoxic stress.\n[3] Transcriptional activation of this signaling axis in the mesenchymal niche predicted leukemic evolution and progression-free survival in myelodysplastic syndrome (MDS), the principal leukemia predisposition syndrome.\n[4] Collectively, our findings identify mesenchymal niche-induced genotoxic stress in heterotypic stem and progenitor cells through inflammatory signaling as a targetable determinant of disease outcome in human pre-leukemia."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 526, "doc_id": 3863543, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [3863543], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Human embryonic stem cells give rise to cell types from all three embryonic germ layers.\n\nDocument title: Evidence of a pluripotent human embryonic stem cell line derived from a cloned blastocyst.\n\nAbstract sentences:\n[0] Somatic cell nuclear transfer (SCNT) technology has recently been used to generate animals with a common genetic composition.\n[1] In this study, we report the derivation of a pluripotent embryonic stem (ES) cell line (SCNT-hES-1) from a cloned human blastocyst.\n[2] The SCNT-hES-1 cells displayed typical ES cell morphology and cell surface markers and were capable of differentiating into embryoid bodies in vitro and of forming teratomas in vivo containing cell derivatives from all three embryonic germ layers in severe combined immunodeficient mice.\n[3] After continuous proliferation for more than 70 passages, SCNT-hES-1 cells maintained normal karyotypes and were genetically identical to the somatic nuclear donor cells.\n[4] Although we cannot completely exclude the possibility that the cells had a parthenogenetic origin, imprinting analyses support a SCNT origin of the derived human ES cells."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"The SCNT-hES-1 cells displayed typical ES cell morphology and cell surface markers and were capable of differentiating into embryoid bodies in vitro and of forming teratomas in vivo containing cell derivatives from all three embryonic germ layers in severe combined immunodeficient mice.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 529, "doc_id": 10546779, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [10546779, 25413327, 36651210], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Human embryonic stem cells give rise to cell types from all three embryonic germ layers.\n\nDocument title: Clonally derived human embryonic stem cell lines maintain pluripotency and proliferative potential for prolonged periods of culture.\n\nAbstract sentences:\n[0] Embryonic stem (ES) cell lines derived from human blastocysts have the developmental potential to form derivatives of all three embryonic germ layers even after prolonged culture.\n[1] Here we describe the clonal derivation of two human ES cell lines, H9.1 and H9.2.\n[2] At the time of the clonal derivation of the H9.1 and H9.2 ES cell lines, the parental ES cell line, H9, had already been continuously cultured for 6 months.\n[3] After an additional 8 months of culture, H9.1 and H9.2 ES cell lines continued to: (1) actively proliferate, (2) express high levels of telomerase, and (3) retain normal karyotypes.\n[4] Telomere lengths, while somewhat variable, were maintained between 8 and 12 kb in high-passage H9.1 and H9.2 cells.\n[5] High-passage H9.1 and H9.2 cells both formed teratomas in SCID-beige mice that included differentiated derivatives of all three embryonic germ layers.\n[6] These results demonstrate the pluripotency of single human ES cells, the maintenance of pluripotency during an extended period of culture, and the long-term self-renewing properties of cultured human ES cells.\n[7] The remarkable developmental potential, proliferative capacity, and karyotypic stability of human ES cells distinguish them from adult cells."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Embryonic stem (ES) cell lines derived from human blastocysts have the developmental potential to form derivatives of all three embryonic germ layers even after prolonged culture.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 529, "doc_id": 25413327, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [10546779, 25413327, 36651210], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Human embryonic stem cells give rise to cell types from all three embryonic germ layers.\n\nDocument title: Clonally derived human embryonic stem cell lines maintain pluripotency and proliferative potential for prolonged periods of culture.\n\nAbstract sentences:\n[0] Embryonic stem (ES) cell lines derived from human blastocysts have the developmental potential to form derivatives of all three embryonic germ layers even after prolonged culture.\n[1] Here we describe the clonal derivation of two human ES cell lines, H9.1 and H9.2.\n[2] At the time of the clonal derivation of the H9.1 and H9.2 ES cell lines, the parental ES cell line, H9, had already been continuously cultured for 6 months.\n[3] After an additional 8 months of culture, H9.1 and H9.2 ES cell lines continued to: (1) actively proliferate, (2) express high levels of telomerase, and (3) retain normal karyotypes.\n[4] Telomere lengths, while somewhat variable, were maintained between 8 and 12 kb in high-passage H9.1 and H9.2 cells.\n[5] High-passage H9.1 and H9.2 cells both formed teratomas in SCID-beige mice that included differentiated derivatives of all three embryonic germ layers.\n[6] These results demonstrate the pluripotency of single human ES cells, the maintenance of pluripotency during an extended period of culture, and the long-term self-renewing properties of cultured human ES cells.\n[7] The remarkable developmental potential, proliferative capacity, and karyotypic stability of human ES cells distinguish them from adult cells."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"High-passage H9.1 and H9.2 cells both formed teratomas in SCID-beige mice that included differentiated derivatives of all three embryonic germ layers.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 529, "doc_id": 25413327, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [10546779, 25413327, 36651210], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Human embryonic stem cells give rise to cell types from all three embryonic germ layers.\n\nDocument title: Establishment and in vitro differentiation of a new embryonic stem cell line from human blastocyst.\n\nAbstract sentences:\n[0] Embryonic stem cells have the ability to remain undifferentiated and proliferate indefinitely in vitro while maintaining the potential to differentiate into derivatives of all three embryonic germ layers.\n[1] These cells have, therefore, potential for in vitro differentiation studies, gene function, and so on.\n[2] The aim of this study was to produce a human embryonic stem cell line.\n[3] An inner cell mass of a human blastocyst was separated and cultured on mouse embryonic fibroblasts in embryonic stem cell medium with related additives.\n[4] The established line was evaluated by morphology; passaging; freezing and thawing; alkaline phosphatase; Oct-4 expression; anti-surface markers including Tra-1-60 and Tra-1-81; and karyotype and spontaneous differentiation.\n[5] Differentiated cardiomyocytes and neurons were evaluated by transmission electron microscopy and immunocytochemistry.\n[6] Here, we report the derivation of a new embryonic stem cell line (Royan H1) from a human blastocyst that remains undifferentiated in morphology during continuous passaging for more than 30 passages, maintains a normal XX karyotype, is viable after freezing and thawing, and expresses alkaline phosphatase, Oct-4, Tra-1-60, and Tra-1-81.\n[7] These cells remain undifferentiated when grown on mouse embryonic fibroblast feeder layers in the presence or absence of recombinant human leukemia inhibitory factor.\n[8] Royan H1 cells can differentiate in vitro in the absence of feeder cells and can produce embryoid bodies that can further differentiate into beating cardiomyocytes as well as neurons.\n[9] These results define Royan H1 cells as a new human embryonic stem cell line."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Embryonic stem cells have the ability to remain undifferentiated and proliferate indefinitely in vitro while maintaining the potential to differentiate into derivatives of all three embryonic germ layers.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 529, "doc_id": 36651210, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [10546779, 25413327, 36651210], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Human embryonic stem cells give rise to cell types from the outer embryonic germ layer, but not the other two layers.\n\nDocument title: Evidence of a pluripotent human embryonic stem cell line derived from a cloned blastocyst.\n\nAbstract sentences:\n[0] Somatic cell nuclear transfer (SCNT) technology has recently been used to generate animals with a common genetic composition.\n[1] In this study, we report the derivation of a pluripotent embryonic stem (ES) cell line (SCNT-hES-1) from a cloned human blastocyst.\n[2] The SCNT-hES-1 cells displayed typical ES cell morphology and cell surface markers and were capable of differentiating into embryoid bodies in vitro and of forming teratomas in vivo containing cell derivatives from all three embryonic germ layers in severe combined immunodeficient mice.\n[3] After continuous proliferation for more than 70 passages, SCNT-hES-1 cells maintained normal karyotypes and were genetically identical to the somatic nuclear donor cells.\n[4] Although we cannot completely exclude the possibility that the cells had a parthenogenetic origin, imprinting analyses support a SCNT origin of the derived human ES cells."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"The SCNT-hES-1 cells displayed typical ES cell morphology and cell surface markers and were capable of differentiating into embryoid bodies in vitro and of forming teratomas in vivo containing cell derivatives from all three embryonic germ layers in severe combined immunodeficient mice.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 530, "doc_id": 10546779, "label": "CONTRADICTS", "evidence_sentence_ids": [2], "cited_doc_ids": [10546779, 25413327, 36651210, 87610599], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Human embryonic stem cells give rise to cell types from the outer embryonic germ layer, but not the other two layers.\n\nDocument title: Clonally derived human embryonic stem cell lines maintain pluripotency and proliferative potential for prolonged periods of culture.\n\nAbstract sentences:\n[0] Embryonic stem (ES) cell lines derived from human blastocysts have the developmental potential to form derivatives of all three embryonic germ layers even after prolonged culture.\n[1] Here we describe the clonal derivation of two human ES cell lines, H9.1 and H9.2.\n[2] At the time of the clonal derivation of the H9.1 and H9.2 ES cell lines, the parental ES cell line, H9, had already been continuously cultured for 6 months.\n[3] After an additional 8 months of culture, H9.1 and H9.2 ES cell lines continued to: (1) actively proliferate, (2) express high levels of telomerase, and (3) retain normal karyotypes.\n[4] Telomere lengths, while somewhat variable, were maintained between 8 and 12 kb in high-passage H9.1 and H9.2 cells.\n[5] High-passage H9.1 and H9.2 cells both formed teratomas in SCID-beige mice that included differentiated derivatives of all three embryonic germ layers.\n[6] These results demonstrate the pluripotency of single human ES cells, the maintenance of pluripotency during an extended period of culture, and the long-term self-renewing properties of cultured human ES cells.\n[7] The remarkable developmental potential, proliferative capacity, and karyotypic stability of human ES cells distinguish them from adult cells."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Embryonic stem (ES) cell lines derived from human blastocysts have the developmental potential to form derivatives of all three embryonic germ layers even after prolonged culture.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 530, "doc_id": 25413327, "label": "CONTRADICTS", "evidence_sentence_ids": [0], "cited_doc_ids": [10546779, 25413327, 36651210, 87610599], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Human embryonic stem cells give rise to cell types from the outer embryonic germ layer, but not the other two layers.\n\nDocument title: Clonally derived human embryonic stem cell lines maintain pluripotency and proliferative potential for prolonged periods of culture.\n\nAbstract sentences:\n[0] Embryonic stem (ES) cell lines derived from human blastocysts have the developmental potential to form derivatives of all three embryonic germ layers even after prolonged culture.\n[1] Here we describe the clonal derivation of two human ES cell lines, H9.1 and H9.2.\n[2] At the time of the clonal derivation of the H9.1 and H9.2 ES cell lines, the parental ES cell line, H9, had already been continuously cultured for 6 months.\n[3] After an additional 8 months of culture, H9.1 and H9.2 ES cell lines continued to: (1) actively proliferate, (2) express high levels of telomerase, and (3) retain normal karyotypes.\n[4] Telomere lengths, while somewhat variable, were maintained between 8 and 12 kb in high-passage H9.1 and H9.2 cells.\n[5] High-passage H9.1 and H9.2 cells both formed teratomas in SCID-beige mice that included differentiated derivatives of all three embryonic germ layers.\n[6] These results demonstrate the pluripotency of single human ES cells, the maintenance of pluripotency during an extended period of culture, and the long-term self-renewing properties of cultured human ES cells.\n[7] The remarkable developmental potential, proliferative capacity, and karyotypic stability of human ES cells distinguish them from adult cells."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"High-passage H9.1 and H9.2 cells both formed teratomas in SCID-beige mice that included differentiated derivatives of all three embryonic germ layers.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 530, "doc_id": 25413327, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [10546779, 25413327, 36651210, 87610599], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Human embryonic stem cells give rise to cell types from the outer embryonic germ layer, but not the other two layers.\n\nDocument title: Establishment and in vitro differentiation of a new embryonic stem cell line from human blastocyst.\n\nAbstract sentences:\n[0] Embryonic stem cells have the ability to remain undifferentiated and proliferate indefinitely in vitro while maintaining the potential to differentiate into derivatives of all three embryonic germ layers.\n[1] These cells have, therefore, potential for in vitro differentiation studies, gene function, and so on.\n[2] The aim of this study was to produce a human embryonic stem cell line.\n[3] An inner cell mass of a human blastocyst was separated and cultured on mouse embryonic fibroblasts in embryonic stem cell medium with related additives.\n[4] The established line was evaluated by morphology; passaging; freezing and thawing; alkaline phosphatase; Oct-4 expression; anti-surface markers including Tra-1-60 and Tra-1-81; and karyotype and spontaneous differentiation.\n[5] Differentiated cardiomyocytes and neurons were evaluated by transmission electron microscopy and immunocytochemistry.\n[6] Here, we report the derivation of a new embryonic stem cell line (Royan H1) from a human blastocyst that remains undifferentiated in morphology during continuous passaging for more than 30 passages, maintains a normal XX karyotype, is viable after freezing and thawing, and expresses alkaline phosphatase, Oct-4, Tra-1-60, and Tra-1-81.\n[7] These cells remain undifferentiated when grown on mouse embryonic fibroblast feeder layers in the presence or absence of recombinant human leukemia inhibitory factor.\n[8] Royan H1 cells can differentiate in vitro in the absence of feeder cells and can produce embryoid bodies that can further differentiate into beating cardiomyocytes as well as neurons.\n[9] These results define Royan H1 cells as a new human embryonic stem cell line."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Embryonic stem cells have the ability to remain undifferentiated and proliferate indefinitely in vitro while maintaining the potential to differentiate into derivatives of all three embryonic germ layers.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 530, "doc_id": 36651210, "label": "CONTRADICTS", "evidence_sentence_ids": [0], "cited_doc_ids": [10546779, 25413327, 36651210, 87610599], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Human embryonic stem cells have the capacity to give rise to differentiated progeny representative of all three embryonic germ layers.\n\nDocument title: Evidence of a pluripotent human embryonic stem cell line derived from a cloned blastocyst.\n\nAbstract sentences:\n[0] Somatic cell nuclear transfer (SCNT) technology has recently been used to generate animals with a common genetic composition.\n[1] In this study, we report the derivation of a pluripotent embryonic stem (ES) cell line (SCNT-hES-1) from a cloned human blastocyst.\n[2] The SCNT-hES-1 cells displayed typical ES cell morphology and cell surface markers and were capable of differentiating into embryoid bodies in vitro and of forming teratomas in vivo containing cell derivatives from all three embryonic germ layers in severe combined immunodeficient mice.\n[3] After continuous proliferation for more than 70 passages, SCNT-hES-1 cells maintained normal karyotypes and were genetically identical to the somatic nuclear donor cells.\n[4] Although we cannot completely exclude the possibility that the cells had a parthenogenetic origin, imprinting analyses support a SCNT origin of the derived human ES cells."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"The SCNT-hES-1 cells displayed typical ES cell morphology and cell surface markers and were capable of differentiating into embryoid bodies in vitro and of forming teratomas in vivo containing cell derivatives from all three embryonic germ layers in severe combined immunodeficient mice.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 531, "doc_id": 10546779, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [10546779, 25413327, 36651210], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Human embryonic stem cells have the capacity to give rise to differentiated progeny representative of all three embryonic germ layers.\n\nDocument title: Clonally derived human embryonic stem cell lines maintain pluripotency and proliferative potential for prolonged periods of culture.\n\nAbstract sentences:\n[0] Embryonic stem (ES) cell lines derived from human blastocysts have the developmental potential to form derivatives of all three embryonic germ layers even after prolonged culture.\n[1] Here we describe the clonal derivation of two human ES cell lines, H9.1 and H9.2.\n[2] At the time of the clonal derivation of the H9.1 and H9.2 ES cell lines, the parental ES cell line, H9, had already been continuously cultured for 6 months.\n[3] After an additional 8 months of culture, H9.1 and H9.2 ES cell lines continued to: (1) actively proliferate, (2) express high levels of telomerase, and (3) retain normal karyotypes.\n[4] Telomere lengths, while somewhat variable, were maintained between 8 and 12 kb in high-passage H9.1 and H9.2 cells.\n[5] High-passage H9.1 and H9.2 cells both formed teratomas in SCID-beige mice that included differentiated derivatives of all three embryonic germ layers.\n[6] These results demonstrate the pluripotency of single human ES cells, the maintenance of pluripotency during an extended period of culture, and the long-term self-renewing properties of cultured human ES cells.\n[7] The remarkable developmental potential, proliferative capacity, and karyotypic stability of human ES cells distinguish them from adult cells."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Embryonic stem (ES) cell lines derived from human blastocysts have the developmental potential to form derivatives of all three embryonic germ layers even after prolonged culture.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 531, "doc_id": 25413327, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [10546779, 25413327, 36651210], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Human embryonic stem cells have the capacity to give rise to differentiated progeny representative of all three embryonic germ layers.\n\nDocument title: Establishment and in vitro differentiation of a new embryonic stem cell line from human blastocyst.\n\nAbstract sentences:\n[0] Embryonic stem cells have the ability to remain undifferentiated and proliferate indefinitely in vitro while maintaining the potential to differentiate into derivatives of all three embryonic germ layers.\n[1] These cells have, therefore, potential for in vitro differentiation studies, gene function, and so on.\n[2] The aim of this study was to produce a human embryonic stem cell line.\n[3] An inner cell mass of a human blastocyst was separated and cultured on mouse embryonic fibroblasts in embryonic stem cell medium with related additives.\n[4] The established line was evaluated by morphology; passaging; freezing and thawing; alkaline phosphatase; Oct-4 expression; anti-surface markers including Tra-1-60 and Tra-1-81; and karyotype and spontaneous differentiation.\n[5] Differentiated cardiomyocytes and neurons were evaluated by transmission electron microscopy and immunocytochemistry.\n[6] Here, we report the derivation of a new embryonic stem cell line (Royan H1) from a human blastocyst that remains undifferentiated in morphology during continuous passaging for more than 30 passages, maintains a normal XX karyotype, is viable after freezing and thawing, and expresses alkaline phosphatase, Oct-4, Tra-1-60, and Tra-1-81.\n[7] These cells remain undifferentiated when grown on mouse embryonic fibroblast feeder layers in the presence or absence of recombinant human leukemia inhibitory factor.\n[8] Royan H1 cells can differentiate in vitro in the absence of feeder cells and can produce embryoid bodies that can further differentiate into beating cardiomyocytes as well as neurons.\n[9] These results define Royan H1 cells as a new human embryonic stem cell line."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Embryonic stem cells have the ability to remain undifferentiated and proliferate indefinitely in vitro while maintaining the potential to differentiate into derivatives of all three embryonic germ layers.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 531, "doc_id": 36651210, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [10546779, 25413327, 36651210], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Hypocretin neurones suppress panicprone state in rats.\n\nDocument title: A KEY ROLE FOR OREXIN IN PANIC ANXIETY\n\nAbstract sentences:\n[0] Panic disorder is a severe anxiety disorder with recurrent, debilitating panic attacks.\n[1] In individuals with panic disorder there is evidence of decreased central gamma-aminobutyric acid (GABA) activity as well as marked increases in autonomic and respiratory responses after intravenous infusions of hypertonic sodium lactate.\n[2] In a rat model of panic disorder, chronic inhibition of GABA synthesis in the dorsomedial-perifornical hypothalamus of rats produces anxiety-like states and a similar vulnerability to sodium lactate-induced cardioexcitatory responses.\n[3] The dorsomedial-perifornical hypothalamus is enriched in neurons containing orexin (ORX, also known as hypocretin), which have a crucial role in arousal, vigilance and central autonomic mobilization, all of which are key components of panic.\n[4] Here we show that activation of ORX-synthesizing neurons is necessary for developing a panic-prone state in the rat panic model, and either silencing of the hypothalamic gene encoding ORX (Hcrt) with RNAi or systemic ORX-1 receptor antagonists blocks the panic responses.\n[5] Moreover, we show that human subjects with panic anxiety have elevated levels of ORX in the cerebrospinal fluid compared to subjects without panic anxiety.\n[6] Taken together, our results suggest that the ORX system may be involved in the pathophysiology of panic anxiety and that ORX antagonists constitute a potential new treatment strategy for panic disorder."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Here we show that activation of ORX-synthesizing neurons is necessary for developing a panic-prone state in the rat panic model, and either silencing of the hypothalamic gene encoding ORX (Hcrt) with RNAi or systemic ORX-1 receptor antagonists blocks the panic responses.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 537, "doc_id": 16056514, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [16056514], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Hypothalamic glutamate neurotransmission is unrelated to energy balance.\n\nDocument title: Glutamate mediates the function of melanocortin receptor 4 on Sim1 neurons in body weight regulation.\n\nAbstract sentences:\n[0] The melanocortin receptor 4 (MC4R) is a well-established mediator of body weight homeostasis.\n[1] However, the neurotransmitter(s) that mediate MC4R function remain largely unknown; as a result, little is known about the second-order neurons of the MC4R neural pathway.\n[2] Single-minded 1 (Sim1)-expressing brain regions, which include the paraventricular nucleus of hypothalamus (PVH), represent key brain sites that mediate melanocortin action.\n[3] We conditionally restored MC4R expression in Sim1 neurons in the background of Mc4r-null mice.\n[4] The restoration dramatically reduced obesity in Mc4r-null mice.\n[5] The anti-obesity effect was completely reversed by selective disruption of glutamate release from those same Sim1 neurons.\n[6] The reversal was caused by lower energy expenditure and hyperphagia.\n[7] Corroboratively, selective disruption of glutamate release from adult PVH neurons led to rapid obesity development via reduced energy expenditure and hyperphagia.\n[8] Thus, this study establishes glutamate as the primary neurotransmitter that mediates MC4Rs on Sim1 neurons in body weight regulation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Corroboratively, selective disruption of glutamate release from adult PVH neurons led to rapid obesity development via reduced energy expenditure and hyperphagia.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 541, "doc_id": 45154987, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [45154987, 11886686, 25007443], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Hypothalamic glutamate neurotransmission is unrelated to energy balance.\n\nDocument title: Glutamate mediates the function of melanocortin receptor 4 on Sim1 neurons in body weight regulation.\n\nAbstract sentences:\n[0] The melanocortin receptor 4 (MC4R) is a well-established mediator of body weight homeostasis.\n[1] However, the neurotransmitter(s) that mediate MC4R function remain largely unknown; as a result, little is known about the second-order neurons of the MC4R neural pathway.\n[2] Single-minded 1 (Sim1)-expressing brain regions, which include the paraventricular nucleus of hypothalamus (PVH), represent key brain sites that mediate melanocortin action.\n[3] We conditionally restored MC4R expression in Sim1 neurons in the background of Mc4r-null mice.\n[4] The restoration dramatically reduced obesity in Mc4r-null mice.\n[5] The anti-obesity effect was completely reversed by selective disruption of glutamate release from those same Sim1 neurons.\n[6] The reversal was caused by lower energy expenditure and hyperphagia.\n[7] Corroboratively, selective disruption of glutamate release from adult PVH neurons led to rapid obesity development via reduced energy expenditure and hyperphagia.\n[8] Thus, this study establishes glutamate as the primary neurotransmitter that mediates MC4Rs on Sim1 neurons in body weight regulation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Thus, this study establishes glutamate as the primary neurotransmitter that mediates MC4Rs on Sim1 neurons in body weight regulation.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 541, "doc_id": 45154987, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [45154987, 11886686, 25007443], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Hypothalamic glutamate neurotransmission is unrelated to energy balance.\n\nDocument title: Synaptic glutamate release by ventromedial hypothalamic neurons is part of the neurocircuitry that prevents hypoglycemia.\n\nAbstract sentences:\n[0] The importance of neuropeptides in the hypothalamus has been experimentally established.\n[1] Due to difficulties in assessing function in vivo, the roles of the fast-acting neurotransmitters glutamate and GABA are largely unknown.\n[2] Synaptic vesicular transporters (VGLUTs for glutamate and VGAT for GABA) are required for vesicular uptake and, consequently, synaptic release of neurotransmitters.\n[3] Ventromedial hypothalamic (VMH) neurons are predominantly glutamatergic and express VGLUT2.\n[4] To evaluate the role of glutamate release from VMH neurons, we generated mice lacking VGLUT2 selectively in SF1 neurons (a major subset of VMH neurons).\n[5] These mice have hypoglycemia during fasting secondary to impaired fasting-induced increases in the glucose-raising pancreatic hormone glucagon and impaired induction in liver of mRNAs encoding PGC-1alpha and the gluconeogenic enzymes PEPCK and G6Pase.\n[6] Similarly, these mice have defective counterregulatory responses to insulin-induced hypoglycemia and 2-deoxyglucose (an antimetabolite).\n[7] Thus, glutamate release from VMH neurons is an important component of the neurocircuitry that functions to prevent hypoglycemia."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"These mice have hypoglycemia during fasting secondary to impaired fasting-induced increases in the glucose-raising pancreatic hormone glucagon and impaired induction in liver of mRNAs encoding PGC-1alpha and the gluconeogenic enzymes PEPCK and G6Pase.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 541, "doc_id": 11886686, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [45154987, 11886686, 25007443], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: IFI16 impedes STING phosphorylation and translocation, resulting in reduced activation of STING.\n\nDocument title: IFI16 and cGAS cooperate in the activation of STING during DNA sensing in human keratinocytes\n\nAbstract sentences:\n[0] Many human cells can sense the presence of exogenous DNA during infection though the cytosolic DNA receptor cyclic GMP-AMP synthase (cGAS), which produces the second messenger cyclic GMP-AMP (cGAMP).\n[1] Other putative DNA receptors have been described, but whether their functions are redundant, tissue-specific or integrated in the cGAS-cGAMP pathway is unclear.\n[2] Here we show that interferon-γ inducible protein 16 (IFI16) cooperates with cGAS during DNA sensing in human keratinocytes, as both cGAS and IFI16 are required for the full activation of an innate immune response to exogenous DNA and DNA viruses.\n[3] IFI16 is also required for the cGAMP-induced activation of STING, and interacts with STING to promote STING phosphorylation and translocation.\n[4] We propose that the two DNA sensors IFI16 and cGAS cooperate to prevent the spurious activation of the type I interferon response."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"IFI16 is also required for the cGAMP-induced activation of STING, and interacts with STING to promote STING phosphorylation and translocation.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 542, "doc_id": 19688024, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [19688024], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: IFIT1 speeds viral replication by allowing for the proliferation of mis-capped viral RNAs.\n\nDocument title: A Conserved Histidine in the RNA Sensor RIG-I Controls Immune Tolerance to N1-2'O-Methylated Self RNA.\n\nAbstract sentences:\n[0] The cytosolic helicase retinoic acid-inducible gene-I (RIG-I) initiates immune responses to most RNA viruses by detecting viral 5'-triphosphorylated RNA (pppRNA).\n[1] Although endogenous mRNA is also 5'-triphosphorylated, backbone modifications and the 5'-ppp-linked methylguanosine ((m7)G) cap prevent immunorecognition.\n[2] Here we show that the methylation status of endogenous capped mRNA at the 5'-terminal nucleotide (N1) was crucial to prevent RIG-I activation.\n[3] Moreover, we identified a single conserved amino acid (H830) in the RIG-I RNA binding pocket as the mediator of steric exclusion of N1-2'O-methylated RNA.\n[4] H830A alteration (RIG-I(H830A)) restored binding of N1-2'O-methylated pppRNA.\n[5] Consequently, endogenous mRNA activated the RIG-I(H830A) mutant but not wild-type RIG-I. Similarly, knockdown of the endogenous N1-2'O-methyltransferase led to considerable RIG-I stimulation in the absence of exogenous stimuli.\n[6] Studies involving yellow-fever-virus-encoded 2'O-methyltransferase and RIG-I(H830A) revealed that viruses exploit this mechanism to escape RIG-I. Our data reveal a new role for cap N1-2'O-methylation in RIG-I tolerance of self-RNA."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 545, "doc_id": 24221369, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [24221369], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: IL-10 production by monocytes inhibits CD4 + T cell response.\n\nDocument title: Programmed death-1–induced interleukin-10 production by monocytes impairs CD4+ T cell activation during HIV infection\n\nAbstract sentences:\n[0] Viral replication and microbial translocation from the gut to the blood during HIV infection lead to hyperimmune activation, which contributes to the decline in CD4+ T cell numbers during HIV infection.\n[1] Programmed death-1 (PD-1) and interleukin-10 (IL-10) are both upregulated during HIV infection.\n[2] Blocking interactions between PD-1 and programmed death ligand-1 (PD-L1) and between IL-10 and IL-10 receptor (IL-10R) results in viral clearance and improves T cell function in animal models of chronic viral infections.\n[3] Here we show that high amounts of microbial products and inflammatory cytokines in the plasma of HIV-infected subjects lead to upregulation of PD-1 expression on monocytes that correlates with high plasma concentrations of IL-10.\n[4] Triggering of PD-1 expressed on monocytes by PD-L1 expressed on various cell types induced IL-10 production and led to reversible CD4+ T cell dysfunction.\n[5] We describe a new function for PD-1 whereby microbial products inhibit T cell expansion and function by upregulating PD-1 levels and IL-10 production by monocytes after binding of PD-1 by PD-L1."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Triggering of PD-1 expressed on monocytes by PD-L1 expressed on various cell types induced IL-10 production and led to reversible CD4+ T cell dysfunction.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 547, "doc_id": 10648422, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [10648422], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: IL-10 production by monocytes inhibits CD4 + T cell response.\n\nDocument title: Programmed death-1–induced interleukin-10 production by monocytes impairs CD4+ T cell activation during HIV infection\n\nAbstract sentences:\n[0] Viral replication and microbial translocation from the gut to the blood during HIV infection lead to hyperimmune activation, which contributes to the decline in CD4+ T cell numbers during HIV infection.\n[1] Programmed death-1 (PD-1) and interleukin-10 (IL-10) are both upregulated during HIV infection.\n[2] Blocking interactions between PD-1 and programmed death ligand-1 (PD-L1) and between IL-10 and IL-10 receptor (IL-10R) results in viral clearance and improves T cell function in animal models of chronic viral infections.\n[3] Here we show that high amounts of microbial products and inflammatory cytokines in the plasma of HIV-infected subjects lead to upregulation of PD-1 expression on monocytes that correlates with high plasma concentrations of IL-10.\n[4] Triggering of PD-1 expressed on monocytes by PD-L1 expressed on various cell types induced IL-10 production and led to reversible CD4+ T cell dysfunction.\n[5] We describe a new function for PD-1 whereby microbial products inhibit T cell expansion and function by upregulating PD-1 levels and IL-10 production by monocytes after binding of PD-1 by PD-L1."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"We describe a new function for PD-1 whereby microbial products inhibit T cell expansion and function by upregulating PD-1 levels and IL-10 production by monocytes after binding of PD-1 by PD-L1.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 547, "doc_id": 10648422, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [10648422], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: IL-6 signaling plays a major role in atherosclerotic cardiovascular disease.\n\nDocument title: Interleukin-6 receptor pathways in coronary heart disease: a collaborative meta-analysis of 82 studies\n\nAbstract sentences:\n[0] BACKGROUND Persistent inflammation has been proposed to contribute to various stages in the pathogenesis of cardiovascular disease.\n[1] Interleukin-6 receptor (IL6R) signalling propagates downstream inflammation cascades.\n[2] To assess whether this pathway is causally relevant to coronary heart disease, we studied a functional genetic variant known to affect IL6R signalling.\n[3] METHODS In a collaborative meta-analysis, we studied Asp358Ala (rs2228145) in IL6R in relation to a panel of conventional risk factors and inflammation biomarkers in 125,222 participants.\n[4] We also compared the frequency of Asp358Ala in 51,441 patients with coronary heart disease and in 136,226 controls.\n[5] To gain insight into possible mechanisms, we assessed Asp358Ala in relation to localised gene expression and to postlipopolysaccharide stimulation of interleukin 6.\n[6] FINDINGS The minor allele frequency of Asp358Ala was 39%.\n[7] Asp358Ala was not associated with lipid concentrations, blood pressure, adiposity, dysglycaemia, or smoking (p value for association per minor allele ≥0·04 for each).\n[8] By contrast, for every copy of 358Ala inherited, mean concentration of IL6R increased by 34·3% (95% CI 30·4-38·2) and of interleukin 6 by 14·6% (10·7-18·4), and mean concentration of C-reactive protein was reduced by 7·5% (5·9-9·1) and of fibrinogen by 1·0% (0·7-1·3).\n[9] For every copy of 358Ala inherited, risk of coronary heart disease was reduced by 3·4% (1·8-5·0).\n[10] Asp358Ala was not related to IL6R mRNA levels or interleukin-6 production in monocytes.\n[11] INTERPRETATION Large-scale human genetic and biomarker data are consistent with a causal association between IL6R-related pathways and coronary heart disease.\n[12] FUNDING British Heart Foundation; UK Medical Research Council; UK National Institute of Health Research, Cambridge Biomedical Research Centre; BUPA Foundation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8, 9]\nExplanation: Evidence states: \"By contrast, for every copy of 358Ala inherited, mean concentration of IL6R increased by 34·3% (95% CI 30·4-38·2) and of interleukin 6 by 14·6% (10·7-18·4), and mean concentration of C-reactive protein was reduced by 7·5% (5·9-9·1) and of fibrinogen by 1·0% (0·7-1·3). For every copy of 358Ala inherited, risk of coronary heart disease was reduced by 3·4% (1·8-5·0).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 548, "doc_id": 18199839, "label": "SUPPORTS", "evidence_sentence_ids": [8, 9], "cited_doc_ids": [18199839], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: IL-6 signaling plays a major role in atherosclerotic cardiovascular disease.\n\nDocument title: Interleukin-6 receptor pathways in coronary heart disease: a collaborative meta-analysis of 82 studies\n\nAbstract sentences:\n[0] BACKGROUND Persistent inflammation has been proposed to contribute to various stages in the pathogenesis of cardiovascular disease.\n[1] Interleukin-6 receptor (IL6R) signalling propagates downstream inflammation cascades.\n[2] To assess whether this pathway is causally relevant to coronary heart disease, we studied a functional genetic variant known to affect IL6R signalling.\n[3] METHODS In a collaborative meta-analysis, we studied Asp358Ala (rs2228145) in IL6R in relation to a panel of conventional risk factors and inflammation biomarkers in 125,222 participants.\n[4] We also compared the frequency of Asp358Ala in 51,441 patients with coronary heart disease and in 136,226 controls.\n[5] To gain insight into possible mechanisms, we assessed Asp358Ala in relation to localised gene expression and to postlipopolysaccharide stimulation of interleukin 6.\n[6] FINDINGS The minor allele frequency of Asp358Ala was 39%.\n[7] Asp358Ala was not associated with lipid concentrations, blood pressure, adiposity, dysglycaemia, or smoking (p value for association per minor allele ≥0·04 for each).\n[8] By contrast, for every copy of 358Ala inherited, mean concentration of IL6R increased by 34·3% (95% CI 30·4-38·2) and of interleukin 6 by 14·6% (10·7-18·4), and mean concentration of C-reactive protein was reduced by 7·5% (5·9-9·1) and of fibrinogen by 1·0% (0·7-1·3).\n[9] For every copy of 358Ala inherited, risk of coronary heart disease was reduced by 3·4% (1·8-5·0).\n[10] Asp358Ala was not related to IL6R mRNA levels or interleukin-6 production in monocytes.\n[11] INTERPRETATION Large-scale human genetic and biomarker data are consistent with a causal association between IL6R-related pathways and coronary heart disease.\n[12] FUNDING British Heart Foundation; UK Medical Research Council; UK National Institute of Health Research, Cambridge Biomedical Research Centre; BUPA Foundation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"INTERPRETATION Large-scale human genetic and biomarker data are consistent with a causal association between IL6R-related pathways and coronary heart disease.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 548, "doc_id": 18199839, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [18199839], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: ITAM phosphorylation allows for the transfer of the T cell receptor (TCR) signal from the echo-domain to the cytoplasmic tail of the T cell receptor (TCR).\n\nDocument title: Full activation of the T cell receptor requires both clustering and conformational changes at CD3.\n\nAbstract sentences:\n[0] T cell receptor (TCR-CD3) triggering involves both receptor clustering and conformational changes at the cytoplasmic tails of the CD3 subunits.\n[1] The mechanism by which TCRalphabeta ligand binding confers conformational changes to CD3 is unknown.\n[2] By using well-defined ligands, we showed that induction of the conformational change requires both multivalent engagement and the mobility restriction of the TCR-CD3 imposed by the plasma membrane.\n[3] The conformational change is elicited by cooperative rearrangements of two TCR-CD3 complexes and does not require accompanying changes in the structure of the TCRalphabeta ectodomains.\n[4] This conformational change at CD3 reverts upon ligand dissociation and is required for T cell activation.\n[5] Thus, our permissive geometry model provides a molecular mechanism that rationalizes how the information of ligand binding to TCRalphabeta is transmitted to the CD3 subunits and to the intracellular signaling machinery."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 550, "doc_id": 33499189, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [33499189], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: IgA plasma cells that are specific for transglutaminase 2 are scarce in the duodenal mucosa of celiac disease patients when the disease is active.\n\nDocument title: High abundance of plasma cells secreting transglutaminase 2–specific IgA autoantibodies with limited somatic hypermutation in celiac disease intestinal lesions\n\nAbstract sentences:\n[0] Celiac disease is an immune-mediated disorder in which mucosal autoantibodies to the enzyme transglutaminase 2 (TG2) are generated in response to the exogenous antigen gluten in individuals who express human leukocyte antigen HLA-DQ2 or HLA-DQ8 (ref.\n[1] 3).\n[2] We assessed in a comprehensive and nonbiased manner the IgA anti-TG2 response by expression cloning of the antibody repertoire of ex vivo–isolated intestinal antibody-secreting cells (ASCs).\n[3] We found that TG2-specific plasma cells are markedly expanded within the duodenal mucosa in individuals with active celiac disease.\n[4] TG2-specific antibodies were of high affinity yet showed little adaptation by somatic mutations.\n[5] Unlike infection-induced peripheral blood plasmablasts, the TG2-specific ASCs had not recently proliferated and were not short-lived ex vivo.\n[6] Altogether, these observations demonstrate that there is a germline repertoire with high affinity for TG2 that may favor massive generation of autoreactive B cells.\n[7] TG2-specific antibodies did not block enzymatic activity and served as substrates for TG2-mediated crosslinking when expressed as IgD or IgM but not as IgA1 or IgG1.\n[8] This could result in preferential recruitment of plasma cells from naive IgD- and IgM-expressing B cells, thus possibly explaining why the antibody response to TG2 bears signs of a primary immune response despite the disease chronicity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"We found that TG2-specific plasma cells are markedly expanded within the duodenal mucosa in individuals with active celiac disease.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 553, "doc_id": 1471041, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [1471041], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Immune complex triggered cell death leads to extracellular release of nuclear DNA.\n\nDocument title: Neutrophil extracellular traps enriched in oxidized mitochondrial DNA are interferogenic and contribute to lupus-like disease\n\nAbstract sentences:\n[0] Neutrophil extracellular traps (NETs) are implicated in autoimmunity, but how they are generated and their roles in sterile inflammation remain unclear.\n[1] Ribonucleoprotein immune complexes (RNP ICs), inducers of NETosis, require mitochondrial reactive oxygen species (ROS) for maximal NET stimulation.\n[2] After RNP IC stimulation of neutrophils, mitochondria become hypopolarized and translocate to the cell surface.\n[3] Extracellular release of oxidized mitochondrial DNA is proinflammatory in vitro, and when this DNA is injected into mice, it stimulates type I interferon (IFN) signaling through a pathway dependent on the DNA sensor STING.\n[4] Mitochondrial ROS are also necessary for spontaneous NETosis of low-density granulocytes from individuals with systemic lupus erythematosus.\n[5] This was also observed in individuals with chronic granulomatous disease, who lack NADPH oxidase activity but still develop autoimmunity and type I IFN signatures.\n[6] Mitochondrial ROS inhibition in vivo reduces disease severity and type I IFN responses in a mouse model of lupus.\n[7] Together, these findings highlight a role for mitochondria in the generation not only of NETs but also of pro-inflammatory oxidized mitochondrial DNA in autoimmune diseases."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 555, "doc_id": 1049501, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [1049501], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Immune complex triggered cell death leads to sequestration of oxidized mitochondrial DNA.\n\nDocument title: Neutrophil extracellular traps enriched in oxidized mitochondrial DNA are interferogenic and contribute to lupus-like disease\n\nAbstract sentences:\n[0] Neutrophil extracellular traps (NETs) are implicated in autoimmunity, but how they are generated and their roles in sterile inflammation remain unclear.\n[1] Ribonucleoprotein immune complexes (RNP ICs), inducers of NETosis, require mitochondrial reactive oxygen species (ROS) for maximal NET stimulation.\n[2] After RNP IC stimulation of neutrophils, mitochondria become hypopolarized and translocate to the cell surface.\n[3] Extracellular release of oxidized mitochondrial DNA is proinflammatory in vitro, and when this DNA is injected into mice, it stimulates type I interferon (IFN) signaling through a pathway dependent on the DNA sensor STING.\n[4] Mitochondrial ROS are also necessary for spontaneous NETosis of low-density granulocytes from individuals with systemic lupus erythematosus.\n[5] This was also observed in individuals with chronic granulomatous disease, who lack NADPH oxidase activity but still develop autoimmunity and type I IFN signatures.\n[6] Mitochondrial ROS inhibition in vivo reduces disease severity and type I IFN responses in a mouse model of lupus.\n[7] Together, these findings highlight a role for mitochondria in the generation not only of NETs but also of pro-inflammatory oxidized mitochondrial DNA in autoimmune diseases."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 557, "doc_id": 1049501, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [1049501], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Immune responses in immune cells are geographically segregated.\n\nDocument title: Inflammatory signaling in human Tuberculosis granulomas is spatially organized\n\nAbstract sentences:\n[0] Granulomas are the pathological hallmark of tuberculosis (TB).\n[1] However, their function and mechanisms of formation remain poorly understood.\n[2] To understand the role of granulomas in TB, we analyzed the proteomes of granulomas from subjects with tuberculosis in an unbiased manner.\n[3] Using laser-capture microdissection, mass spectrometry and confocal microscopy, we generated detailed molecular maps of human granulomas.\n[4] We found that the centers of granulomas have a pro-inflammatory environment that is characterized by the presence of antimicrobial peptides, reactive oxygen species and pro-inflammatory eicosanoids.\n[5] Conversely, the tissue surrounding the caseum has a comparatively anti-inflammatory signature.\n[6] These findings are consistent across a set of six human subjects and in rabbits.\n[7] Although the balance between systemic pro- and anti-inflammatory signals is crucial to TB disease outcome, here we find that these signals are physically segregated within each granuloma.\n[8] From the protein and lipid snapshots of human and rabbit lesions analyzed here, we hypothesize that the pathologic response to TB is shaped by the precise anatomical localization of these inflammatory pathways during the development of the granuloma."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Although the balance between systemic pro- and anti-inflammatory signals is crucial to TB disease outcome, here we find that these signals are physically segregated within each granuloma.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 559, "doc_id": 3475317, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [3475317], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Improvements in OER catalysts show stable activity over several hundred hours.\n\nDocument title: Homogeneously dispersed multimetal oxygen-evolving catalysts\n\nAbstract sentences:\n[0] Earth-abundant first-row (3d) transition metal–based catalysts have been developed for the oxygen-evolution reaction (OER); however, they operate at overpotentials substantially above thermodynamic requirements.\n[1] Density functional theory suggested that non-3d high-valency metals such as tungsten can modulate 3d metal oxides, providing near-optimal adsorption energies for OER intermediates.\n[2] We developed a room-temperature synthesis to produce gelled oxyhydroxides materials with an atomically homogeneous metal distribution.\n[3] These gelled FeCoW oxyhydroxides exhibit the lowest overpotential (191 millivolts) reported at 10 milliamperes per square centimeter in alkaline electrolyte.\n[4] The catalyst shows no evidence of degradation after more than 500 hours of operation.\n[5] X-ray absorption and computational studies reveal a synergistic interplay between tungsten, iron, and cobalt in producing a favorable local coordination environment and electronic structure that enhance the energetics for OER."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"The catalyst shows no evidence of degradation after more than 500 hours of operation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 562, "doc_id": 20101846, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [20101846], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In British Men, haplogroup I decreases risk of cardiovascular disease.\n\nDocument title: Inheritance of coronary artery disease in men: an analysis of the role of the Y chromosome\n\nAbstract sentences:\n[0] BACKGROUND A sexual dimorphism exists in the incidence and prevalence of coronary artery disease--men are more commonly affected than are age-matched women.\n[1] We explored the role of the Y chromosome in coronary artery disease in the context of this sexual inequity.\n[2] METHODS We genotyped 11 markers of the male-specific region of the Y chromosome in 3233 biologically unrelated British men from three cohorts: the British Heart Foundation Family Heart Study (BHF-FHS), West of Scotland Coronary Prevention Study (WOSCOPS), and Cardiogenics Study.\n[3] On the basis of this information, each Y chromosome was tracked back into one of 13 ancient lineages defined as haplogroups.\n[4] We then examined associations between common Y chromosome haplogroups and the risk of coronary artery disease in cross-sectional BHF-FHS and prospective WOSCOPS.\n[5] Finally, we undertook functional analysis of Y chromosome effects on monocyte and macrophage transcriptome in British men from the Cardiogenics Study.\n[6] FINDINGS Of nine haplogroups identified, two (R1b1b2 and I) accounted for roughly 90% of the Y chromosome variants among British men.\n[7] Carriers of haplogroup I had about a 50% higher age-adjusted risk of coronary artery disease than did men with other Y chromosome lineages in BHF-FHS (odds ratio 1·75, 95% CI 1·20-2·54, p=0·004), WOSCOPS (1·45, 1·08-1·95, p=0·012), and joint analysis of both populations (1·56, 1·24-1·97, p=0·0002).\n[8] The association between haplogroup I and increased risk of coronary artery disease was independent of traditional cardiovascular and socioeconomic risk factors.\n[9] Analysis of macrophage transcriptome in the Cardiogenics Study revealed that 19 molecular pathways showing strong differential expression between men with haplogroup I and other lineages of the Y chromosome were interconnected by common genes related to inflammation and immunity, and that some of them have a strong relevance to atherosclerosis.\n[10] INTERPRETATION The human Y chromosome is associated with risk of coronary artery disease in men of European ancestry, possibly through interactions of immunity and inflammation.\n[11] FUNDING British Heart Foundation; UK National Institute for Health Research; LEW Carty Charitable Fund; National Health and Medical Research Council of Australia; European Union 6th Framework Programme; Wellcome Trust."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Carriers of haplogroup I had about a 50% higher age-adjusted risk of coronary artery disease than did men with other Y chromosome lineages in BHF-FHS (odds ratio 1·75, 95% CI 1·20-2·54, p=0·004), WOSCOPS (1·45, 1·08-1·95, p=0·012), and joint analysis of both populations (1·56, 1·24-1·97, p=0·0002).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 563, "doc_id": 2867345, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [2867345], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In British Men, haplogroup I increases risk of cardiovascular disease by 50%.\n\nDocument title: Inheritance of coronary artery disease in men: an analysis of the role of the Y chromosome\n\nAbstract sentences:\n[0] BACKGROUND A sexual dimorphism exists in the incidence and prevalence of coronary artery disease--men are more commonly affected than are age-matched women.\n[1] We explored the role of the Y chromosome in coronary artery disease in the context of this sexual inequity.\n[2] METHODS We genotyped 11 markers of the male-specific region of the Y chromosome in 3233 biologically unrelated British men from three cohorts: the British Heart Foundation Family Heart Study (BHF-FHS), West of Scotland Coronary Prevention Study (WOSCOPS), and Cardiogenics Study.\n[3] On the basis of this information, each Y chromosome was tracked back into one of 13 ancient lineages defined as haplogroups.\n[4] We then examined associations between common Y chromosome haplogroups and the risk of coronary artery disease in cross-sectional BHF-FHS and prospective WOSCOPS.\n[5] Finally, we undertook functional analysis of Y chromosome effects on monocyte and macrophage transcriptome in British men from the Cardiogenics Study.\n[6] FINDINGS Of nine haplogroups identified, two (R1b1b2 and I) accounted for roughly 90% of the Y chromosome variants among British men.\n[7] Carriers of haplogroup I had about a 50% higher age-adjusted risk of coronary artery disease than did men with other Y chromosome lineages in BHF-FHS (odds ratio 1·75, 95% CI 1·20-2·54, p=0·004), WOSCOPS (1·45, 1·08-1·95, p=0·012), and joint analysis of both populations (1·56, 1·24-1·97, p=0·0002).\n[8] The association between haplogroup I and increased risk of coronary artery disease was independent of traditional cardiovascular and socioeconomic risk factors.\n[9] Analysis of macrophage transcriptome in the Cardiogenics Study revealed that 19 molecular pathways showing strong differential expression between men with haplogroup I and other lineages of the Y chromosome were interconnected by common genes related to inflammation and immunity, and that some of them have a strong relevance to atherosclerosis.\n[10] INTERPRETATION The human Y chromosome is associated with risk of coronary artery disease in men of European ancestry, possibly through interactions of immunity and inflammation.\n[11] FUNDING British Heart Foundation; UK National Institute for Health Research; LEW Carty Charitable Fund; National Health and Medical Research Council of Australia; European Union 6th Framework Programme; Wellcome Trust."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Carriers of haplogroup I had about a 50% higher age-adjusted risk of coronary artery disease than did men with other Y chromosome lineages in BHF-FHS (odds ratio 1·75, 95% CI 1·20-2·54, p=0·004), WOSCOPS (1·45, 1·08-1·95, p=0·012), and joint analysis of both populations (1·56, 1·24-1·97, p=0·0002).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 564, "doc_id": 2867345, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [2867345], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In S. cerevisiae, the absence of RNA surveillance pathways causes sensitivity to high iron conditions.\n\nDocument title: Multiple RNA surveillance pathways limit aberrant expression of iron uptake mRNAs and prevent iron toxicity in S. cerevisiae.\n\nAbstract sentences:\n[0] Tight regulation of the expression of mRNAs encoding iron uptake proteins is essential to control iron homeostasis and avoid intracellular iron toxicity.\n[1] We show that many mRNAs encoding iron uptake or iron mobilization proteins are expressed in iron-replete conditions in the absence of the S. cerevisiae RNase III ortholog Rnt1p or of the nuclear exosome component Rrp6p.\n[2] Extended forms of these mRNAs accumulate in the absence of Rnt1p or of the 5'-->3' exonucleases Xrn1p and Rat1p, showing that multiple degradative pathways contribute to the surveillance of aberrant forms of these transcripts.\n[3] RNase III-deficient cells are hypersensitive to high iron concentrations, suggesting that Rnt1p-mediated RNA surveillance is required to prevent iron toxicity.\n[4] These results show that RNA surveillance through multiple ribonucleolytic pathways plays a role in iron homeostasis in yeast to avoid the potentially toxic effects of the expression of the iron starvation response in iron-replete conditions."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1, 2]\nExplanation: Evidence states: \"We show that many mRNAs encoding iron uptake or iron mobilization proteins are expressed in iron-replete conditions in the absence of the S. cerevisiae RNase III ortholog Rnt1p or of the nuclear exosome component Rrp6p. Extended forms of these mRNAs accumulate in the absence of Rnt1p or of the 5'-->3' exonucleases Xrn1p and Rat1p, showing that multiple degradative pathways contribute to the surveillance of aberrant forms of these transcripts.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 565, "doc_id": 16120395, "label": "SUPPORTS", "evidence_sentence_ids": [1, 2], "cited_doc_ids": [16120395], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In S. cerevisiae, the absence of RNA surveillance pathways causes sensitivity to high iron conditions.\n\nDocument title: Multiple RNA surveillance pathways limit aberrant expression of iron uptake mRNAs and prevent iron toxicity in S. cerevisiae.\n\nAbstract sentences:\n[0] Tight regulation of the expression of mRNAs encoding iron uptake proteins is essential to control iron homeostasis and avoid intracellular iron toxicity.\n[1] We show that many mRNAs encoding iron uptake or iron mobilization proteins are expressed in iron-replete conditions in the absence of the S. cerevisiae RNase III ortholog Rnt1p or of the nuclear exosome component Rrp6p.\n[2] Extended forms of these mRNAs accumulate in the absence of Rnt1p or of the 5'-->3' exonucleases Xrn1p and Rat1p, showing that multiple degradative pathways contribute to the surveillance of aberrant forms of these transcripts.\n[3] RNase III-deficient cells are hypersensitive to high iron concentrations, suggesting that Rnt1p-mediated RNA surveillance is required to prevent iron toxicity.\n[4] These results show that RNA surveillance through multiple ribonucleolytic pathways plays a role in iron homeostasis in yeast to avoid the potentially toxic effects of the expression of the iron starvation response in iron-replete conditions."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"RNase III-deficient cells are hypersensitive to high iron concentrations, suggesting that Rnt1p-mediated RNA surveillance is required to prevent iron toxicity.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 565, "doc_id": 16120395, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [16120395], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In S. cerevisiae, the absence of RNA surveillance pathways causes sensitivity to high iron conditions.\n\nDocument title: Multiple RNA surveillance pathways limit aberrant expression of iron uptake mRNAs and prevent iron toxicity in S. cerevisiae.\n\nAbstract sentences:\n[0] Tight regulation of the expression of mRNAs encoding iron uptake proteins is essential to control iron homeostasis and avoid intracellular iron toxicity.\n[1] We show that many mRNAs encoding iron uptake or iron mobilization proteins are expressed in iron-replete conditions in the absence of the S. cerevisiae RNase III ortholog Rnt1p or of the nuclear exosome component Rrp6p.\n[2] Extended forms of these mRNAs accumulate in the absence of Rnt1p or of the 5'-->3' exonucleases Xrn1p and Rat1p, showing that multiple degradative pathways contribute to the surveillance of aberrant forms of these transcripts.\n[3] RNase III-deficient cells are hypersensitive to high iron concentrations, suggesting that Rnt1p-mediated RNA surveillance is required to prevent iron toxicity.\n[4] These results show that RNA surveillance through multiple ribonucleolytic pathways plays a role in iron homeostasis in yeast to avoid the potentially toxic effects of the expression of the iron starvation response in iron-replete conditions."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"These results show that RNA surveillance through multiple ribonucleolytic pathways plays a role in iron homeostasis in yeast to avoid the potentially toxic effects of the expression of the iron starvation response in iron-replete conditions.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 565, "doc_id": 16120395, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [16120395], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In S. cerevisiae, the absence of RNA surveillance pathways reduces sensitivity to high iron conditions.\n\nDocument title: Multiple RNA surveillance pathways limit aberrant expression of iron uptake mRNAs and prevent iron toxicity in S. cerevisiae.\n\nAbstract sentences:\n[0] Tight regulation of the expression of mRNAs encoding iron uptake proteins is essential to control iron homeostasis and avoid intracellular iron toxicity.\n[1] We show that many mRNAs encoding iron uptake or iron mobilization proteins are expressed in iron-replete conditions in the absence of the S. cerevisiae RNase III ortholog Rnt1p or of the nuclear exosome component Rrp6p.\n[2] Extended forms of these mRNAs accumulate in the absence of Rnt1p or of the 5'-->3' exonucleases Xrn1p and Rat1p, showing that multiple degradative pathways contribute to the surveillance of aberrant forms of these transcripts.\n[3] RNase III-deficient cells are hypersensitive to high iron concentrations, suggesting that Rnt1p-mediated RNA surveillance is required to prevent iron toxicity.\n[4] These results show that RNA surveillance through multiple ribonucleolytic pathways plays a role in iron homeostasis in yeast to avoid the potentially toxic effects of the expression of the iron starvation response in iron-replete conditions."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [1, 2]\nExplanation: Evidence states: \"We show that many mRNAs encoding iron uptake or iron mobilization proteins are expressed in iron-replete conditions in the absence of the S. cerevisiae RNase III ortholog Rnt1p or of the nuclear exosome component Rrp6p. Extended forms of these mRNAs accumulate in the absence of Rnt1p or of the 5'-->3' exonucleases Xrn1p and Rat1p, showing that multiple degradative pathways contribute to the surveillance of aberrant forms of these transcripts.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 566, "doc_id": 16120395, "label": "CONTRADICTS", "evidence_sentence_ids": [1, 2], "cited_doc_ids": [16120395], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In S. cerevisiae, the absence of RNA surveillance pathways reduces sensitivity to high iron conditions.\n\nDocument title: Multiple RNA surveillance pathways limit aberrant expression of iron uptake mRNAs and prevent iron toxicity in S. cerevisiae.\n\nAbstract sentences:\n[0] Tight regulation of the expression of mRNAs encoding iron uptake proteins is essential to control iron homeostasis and avoid intracellular iron toxicity.\n[1] We show that many mRNAs encoding iron uptake or iron mobilization proteins are expressed in iron-replete conditions in the absence of the S. cerevisiae RNase III ortholog Rnt1p or of the nuclear exosome component Rrp6p.\n[2] Extended forms of these mRNAs accumulate in the absence of Rnt1p or of the 5'-->3' exonucleases Xrn1p and Rat1p, showing that multiple degradative pathways contribute to the surveillance of aberrant forms of these transcripts.\n[3] RNase III-deficient cells are hypersensitive to high iron concentrations, suggesting that Rnt1p-mediated RNA surveillance is required to prevent iron toxicity.\n[4] These results show that RNA surveillance through multiple ribonucleolytic pathways plays a role in iron homeostasis in yeast to avoid the potentially toxic effects of the expression of the iron starvation response in iron-replete conditions."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"RNase III-deficient cells are hypersensitive to high iron concentrations, suggesting that Rnt1p-mediated RNA surveillance is required to prevent iron toxicity.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 566, "doc_id": 16120395, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [16120395], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In S. cerevisiae, the absence of RNA surveillance pathways reduces sensitivity to high iron conditions.\n\nDocument title: Multiple RNA surveillance pathways limit aberrant expression of iron uptake mRNAs and prevent iron toxicity in S. cerevisiae.\n\nAbstract sentences:\n[0] Tight regulation of the expression of mRNAs encoding iron uptake proteins is essential to control iron homeostasis and avoid intracellular iron toxicity.\n[1] We show that many mRNAs encoding iron uptake or iron mobilization proteins are expressed in iron-replete conditions in the absence of the S. cerevisiae RNase III ortholog Rnt1p or of the nuclear exosome component Rrp6p.\n[2] Extended forms of these mRNAs accumulate in the absence of Rnt1p or of the 5'-->3' exonucleases Xrn1p and Rat1p, showing that multiple degradative pathways contribute to the surveillance of aberrant forms of these transcripts.\n[3] RNase III-deficient cells are hypersensitive to high iron concentrations, suggesting that Rnt1p-mediated RNA surveillance is required to prevent iron toxicity.\n[4] These results show that RNA surveillance through multiple ribonucleolytic pathways plays a role in iron homeostasis in yeast to avoid the potentially toxic effects of the expression of the iron starvation response in iron-replete conditions."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"These results show that RNA surveillance through multiple ribonucleolytic pathways plays a role in iron homeostasis in yeast to avoid the potentially toxic effects of the expression of the iron starvation response in iron-replete conditions.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 566, "doc_id": 16120395, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [16120395], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In a naive state, blocking Wingless-Int-1 secretion from mouse embryonic stem cells inhibits self-renewal of the mouse embryonic stem cells.\n\nDocument title: Embryonic stem cells require Wnt proteins to prevent differentiation to epiblast stem cells\n\nAbstract sentences:\n[0] Pluripotent stem cells exist in naive and primed states, epitomized by mouse embryonic stem cells (ESCs) and the developmentally more advanced epiblast stem cells (EpiSCs; ref. ).\n[1] In the naive state of ESCs, the genome has an unusual open conformation and possesses a minimum of repressive epigenetic marks.\n[2] In contrast, EpiSCs have activated the epigenetic machinery that supports differentiation towards the embryonic cell types.\n[3] The transition from naive to primed pluripotency therefore represents a pivotal event in cellular differentiation.\n[4] But the signals that control this fundamental differentiation step remain unclear.\n[5] We show here that paracrine and autocrine Wnt signals are essential self-renewal factors for ESCs, and are required to inhibit their differentiation into EpiSCs.\n[6] Moreover, we find that Wnt proteins in combination with the cytokine LIF are sufficient to support ESC self-renewal in the absence of any undefined factors, and support the derivation of new ESC lines, including ones from non-permissive mouse strains.\n[7] Our results not only demonstrate that Wnt signals regulate the naive-to-primed pluripotency transition, but also identify Wnt as an essential and limiting ESC self-renewal factor."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"We show here that paracrine and autocrine Wnt signals are essential self-renewal factors for ESCs, and are required to inhibit their differentiation into EpiSCs.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 568, "doc_id": 23418635, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [23418635], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In a naive state, blocking Wingless-Int-1 secretion from mouse embryonic stem cells inhibits self-renewal of the mouse embryonic stem cells.\n\nDocument title: Embryonic stem cells require Wnt proteins to prevent differentiation to epiblast stem cells\n\nAbstract sentences:\n[0] Pluripotent stem cells exist in naive and primed states, epitomized by mouse embryonic stem cells (ESCs) and the developmentally more advanced epiblast stem cells (EpiSCs; ref. ).\n[1] In the naive state of ESCs, the genome has an unusual open conformation and possesses a minimum of repressive epigenetic marks.\n[2] In contrast, EpiSCs have activated the epigenetic machinery that supports differentiation towards the embryonic cell types.\n[3] The transition from naive to primed pluripotency therefore represents a pivotal event in cellular differentiation.\n[4] But the signals that control this fundamental differentiation step remain unclear.\n[5] We show here that paracrine and autocrine Wnt signals are essential self-renewal factors for ESCs, and are required to inhibit their differentiation into EpiSCs.\n[6] Moreover, we find that Wnt proteins in combination with the cytokine LIF are sufficient to support ESC self-renewal in the absence of any undefined factors, and support the derivation of new ESC lines, including ones from non-permissive mouse strains.\n[7] Our results not only demonstrate that Wnt signals regulate the naive-to-primed pluripotency transition, but also identify Wnt as an essential and limiting ESC self-renewal factor."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Moreover, we find that Wnt proteins in combination with the cytokine LIF are sufficient to support ESC self-renewal in the absence of any undefined factors, and support the derivation of new ESC lines, including ones from non-permissive mouse strains.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 568, "doc_id": 23418635, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [23418635], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In a naive state, blocking Wingless-Int-1 secretion from mouse embryonic stem cells inhibits self-renewal of the mouse embryonic stem cells.\n\nDocument title: Embryonic stem cells require Wnt proteins to prevent differentiation to epiblast stem cells\n\nAbstract sentences:\n[0] Pluripotent stem cells exist in naive and primed states, epitomized by mouse embryonic stem cells (ESCs) and the developmentally more advanced epiblast stem cells (EpiSCs; ref. ).\n[1] In the naive state of ESCs, the genome has an unusual open conformation and possesses a minimum of repressive epigenetic marks.\n[2] In contrast, EpiSCs have activated the epigenetic machinery that supports differentiation towards the embryonic cell types.\n[3] The transition from naive to primed pluripotency therefore represents a pivotal event in cellular differentiation.\n[4] But the signals that control this fundamental differentiation step remain unclear.\n[5] We show here that paracrine and autocrine Wnt signals are essential self-renewal factors for ESCs, and are required to inhibit their differentiation into EpiSCs.\n[6] Moreover, we find that Wnt proteins in combination with the cytokine LIF are sufficient to support ESC self-renewal in the absence of any undefined factors, and support the derivation of new ESC lines, including ones from non-permissive mouse strains.\n[7] Our results not only demonstrate that Wnt signals regulate the naive-to-primed pluripotency transition, but also identify Wnt as an essential and limiting ESC self-renewal factor."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Our results not only demonstrate that Wnt signals regulate the naive-to-primed pluripotency transition, but also identify Wnt as an essential and limiting ESC self-renewal factor.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 568, "doc_id": 23418635, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [23418635], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In breast cancer, the loss of myoepithelial cells promotes the transition of ductal carcinoma in situ to invasive carcinoma.\n\nDocument title: Regulation of in situ to invasive breast carcinoma transition.\n\nAbstract sentences:\n[0] The transition of ductal carcinoma in situ (DCIS) to invasive carcinoma is a poorly understood key event in breast tumor progression.\n[1] Here, we analyzed the role of myoepithelial cells and fibroblasts in the progression of in situ carcinomas using a model of human DCIS and primary breast tumors.\n[2] Progression to invasion was promoted by fibroblasts and inhibited by normal myoepithelial cells.\n[3] Molecular profiles of isolated luminal epithelial and myoepithelial cells identified an intricate interaction network involving TGFbeta, Hedgehog, cell adhesion, and p63 required for myoepithelial cell differentiation, the elimination of which resulted in loss of myoepithelial cells and progression to invasion."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Progression to invasion was promoted by fibroblasts and inhibited by normal myoepithelial cells.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 570, "doc_id": 20333864, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [20333864], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In breast cancer, the loss of myoepithelial cells promotes the transition of ductal carcinoma in situ to invasive carcinoma.\n\nDocument title: Regulation of in situ to invasive breast carcinoma transition.\n\nAbstract sentences:\n[0] The transition of ductal carcinoma in situ (DCIS) to invasive carcinoma is a poorly understood key event in breast tumor progression.\n[1] Here, we analyzed the role of myoepithelial cells and fibroblasts in the progression of in situ carcinomas using a model of human DCIS and primary breast tumors.\n[2] Progression to invasion was promoted by fibroblasts and inhibited by normal myoepithelial cells.\n[3] Molecular profiles of isolated luminal epithelial and myoepithelial cells identified an intricate interaction network involving TGFbeta, Hedgehog, cell adhesion, and p63 required for myoepithelial cell differentiation, the elimination of which resulted in loss of myoepithelial cells and progression to invasion."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Molecular profiles of isolated luminal epithelial and myoepithelial cells identified an intricate interaction network involving TGFbeta, Hedgehog, cell adhesion, and p63 required for myoepithelial cell differentiation, the elimination of which resulted in loss of myoepithelial cells and progression to invasion.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 570, "doc_id": 20333864, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [20333864], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In breast cancer, the loss of myoepithelial cells slows the transition of ductal carcinoma in situ to invasive carcinoma.\n\nDocument title: Regulation of in situ to invasive breast carcinoma transition.\n\nAbstract sentences:\n[0] The transition of ductal carcinoma in situ (DCIS) to invasive carcinoma is a poorly understood key event in breast tumor progression.\n[1] Here, we analyzed the role of myoepithelial cells and fibroblasts in the progression of in situ carcinomas using a model of human DCIS and primary breast tumors.\n[2] Progression to invasion was promoted by fibroblasts and inhibited by normal myoepithelial cells.\n[3] Molecular profiles of isolated luminal epithelial and myoepithelial cells identified an intricate interaction network involving TGFbeta, Hedgehog, cell adhesion, and p63 required for myoepithelial cell differentiation, the elimination of which resulted in loss of myoepithelial cells and progression to invasion."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Progression to invasion was promoted by fibroblasts and inhibited by normal myoepithelial cells.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 571, "doc_id": 20333864, "label": "CONTRADICTS", "evidence_sentence_ids": [2], "cited_doc_ids": [20333864], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In breast cancer, the loss of myoepithelial cells slows the transition of ductal carcinoma in situ to invasive carcinoma.\n\nDocument title: Regulation of in situ to invasive breast carcinoma transition.\n\nAbstract sentences:\n[0] The transition of ductal carcinoma in situ (DCIS) to invasive carcinoma is a poorly understood key event in breast tumor progression.\n[1] Here, we analyzed the role of myoepithelial cells and fibroblasts in the progression of in situ carcinomas using a model of human DCIS and primary breast tumors.\n[2] Progression to invasion was promoted by fibroblasts and inhibited by normal myoepithelial cells.\n[3] Molecular profiles of isolated luminal epithelial and myoepithelial cells identified an intricate interaction network involving TGFbeta, Hedgehog, cell adhesion, and p63 required for myoepithelial cell differentiation, the elimination of which resulted in loss of myoepithelial cells and progression to invasion."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Molecular profiles of isolated luminal epithelial and myoepithelial cells identified an intricate interaction network involving TGFbeta, Hedgehog, cell adhesion, and p63 required for myoepithelial cell differentiation, the elimination of which resulted in loss of myoepithelial cells and progression to invasion.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 571, "doc_id": 20333864, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [20333864], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In chronic viral infections or tumors, peptides that selectively inhibit PTPRS can be utilized to boost insufficient activity of pDCs.\n\nDocument title: Modulation of the proteoglycan receptor PTPσ promotes recovery after spinal cord injury\n\nAbstract sentences:\n[0] Contusive spinal cord injury leads to a variety of disabilities owing to limited neuronal regeneration and functional plasticity.\n[1] It is well established that an upregulation of glial-derived chondroitin sulphate proteoglycans (CSPGs) within the glial scar and perineuronal net creates a barrier to axonal regrowth and sprouting.\n[2] Protein tyrosine phosphatase σ (PTPσ), along with its sister phosphatase leukocyte common antigen-related (LAR) and the nogo receptors 1 and 3 (NgR), have recently been identified as receptors for the inhibitory glycosylated side chains of CSPGs.\n[3] Here we find in rats that PTPσ has a critical role in converting growth cones into a dystrophic state by tightly stabilizing them within CSPG-rich substrates.\n[4] We generated a membrane-permeable peptide mimetic of the PTPσ wedge domain that binds to PTPσ and relieves CSPG-mediated inhibition.\n[5] Systemic delivery of this peptide over weeks restored substantial serotonergic innervation to the spinal cord below the level of injury and facilitated functional recovery of both locomotor and urinary systems.\n[6] Our results add a new layer of understanding to the critical role of PTPσ in mediating the growth-inhibited state of neurons due to CSPGs within the injured adult spinal cord."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 572, "doc_id": 4447055, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4447055], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In domesticated populations of Saccharomyces cerevisiae, segmental aneuploidy is very common.\n\nDocument title: Domestication and Divergence of Saccharomyces cerevisiae Beer Yeasts\n\nAbstract sentences:\n[0] Whereas domestication of livestock, pets, and crops is well documented, it is still unclear to what extent microbes associated with the production of food have also undergone human selection and where the plethora of industrial strains originates from.\n[1] Here, we present the genomes and phenomes of 157 industrial Saccharomyces cerevisiae yeasts.\n[2] Our analyses reveal that today's industrial yeasts can be divided into five sublineages that are genetically and phenotypically separated from wild strains and originate from only a few ancestors through complex patterns of domestication and local divergence.\n[3] Large-scale phenotyping and genome analysis further show strong industry-specific selection for stress tolerance, sugar utilization, and flavor production, while the sexual cycle and other phenotypes related to survival in nature show decay, particularly in beer yeasts.\n[4] Together, these results shed light on the origins, evolutionary history, and phenotypic diversity of industrial yeasts and provide a resource for further selection of superior strains.\n[5] PAPERCLIP."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 573, "doc_id": 10300888, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [10300888], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In domesticated populations of Saccharomyces cerevisiae, segmental aneuploidy occurs infrequently.\n\nDocument title: Domestication and Divergence of Saccharomyces cerevisiae Beer Yeasts\n\nAbstract sentences:\n[0] Whereas domestication of livestock, pets, and crops is well documented, it is still unclear to what extent microbes associated with the production of food have also undergone human selection and where the plethora of industrial strains originates from.\n[1] Here, we present the genomes and phenomes of 157 industrial Saccharomyces cerevisiae yeasts.\n[2] Our analyses reveal that today's industrial yeasts can be divided into five sublineages that are genetically and phenotypically separated from wild strains and originate from only a few ancestors through complex patterns of domestication and local divergence.\n[3] Large-scale phenotyping and genome analysis further show strong industry-specific selection for stress tolerance, sugar utilization, and flavor production, while the sexual cycle and other phenotypes related to survival in nature show decay, particularly in beer yeasts.\n[4] Together, these results shed light on the origins, evolutionary history, and phenotypic diversity of industrial yeasts and provide a resource for further selection of superior strains.\n[5] PAPERCLIP."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 574, "doc_id": 10300888, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [10300888], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In melanoma, anti-CTLA-4 treatment reinvigorates exhausted PD-1+Eomes+CD8 T cells.\n\nDocument title: Radiation and Dual Checkpoint Blockade Activates Non-Redundant Immune Mechanisms in Cancer\n\nAbstract sentences:\n[0] Immune checkpoint inhibitors result in impressive clinical responses, but optimal results will require combination with each other and other therapies.\n[1] This raises fundamental questions about mechanisms of non-redundancy and resistance.\n[2] Here we report major tumour regressions in a subset of patients with metastatic melanoma treated with an anti-CTLA4 antibody (anti-CTLA4) and radiation, and reproduced this effect in mouse models.\n[3] Although combined treatment improved responses in irradiated and unirradiated tumours, resistance was common.\n[4] Unbiased analyses of mice revealed that resistance was due to upregulation of PD-L1 on melanoma cells and associated with T-cell exhaustion.\n[5] Accordingly, optimal response in melanoma and other cancer types requires radiation, anti-CTLA4 and anti-PD-L1/PD-1.\n[6] Anti-CTLA4 predominantly inhibits T-regulatory cells (Treg cells), thereby increasing the CD8 T-cell to Treg (CD8/Treg) ratio.\n[7] Radiation enhances the diversity of the T-cell receptor (TCR) repertoire of intratumoral T cells.\n[8] Together, anti-CTLA4 promotes expansion of T cells, while radiation shapes the TCR repertoire of the expanded peripheral clones.\n[9] Addition of PD-L1 blockade reverses T-cell exhaustion to mitigate depression in the CD8/Treg ratio and further encourages oligoclonal T-cell expansion.\n[10] Similarly to results from mice, patients on our clinical trial with melanoma showing high PD-L1 did not respond to radiation plus anti-CTLA4, demonstrated persistent T-cell exhaustion, and rapidly progressed.\n[11] Thus, PD-L1 on melanoma cells allows tumours to escape anti-CTLA4-based therapy, and the combination of radiation, anti-CTLA4 and anti-PD-L1 promotes response and immunity through distinct mechanisms."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Unbiased analyses of mice revealed that resistance was due to upregulation of PD-L1 on melanoma cells and associated with T-cell exhaustion.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 576, "doc_id": 4468861, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [4468861], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In patients with congenital heart defects, β-blockers significantly improve clinical heart failure outcomes.\n\nDocument title: Carvedilol for children and adolescents with heart failure: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Although beta-blockers improve symptoms and survival in adults with heart failure, little is known about these medications in children and adolescents.\n[1] OBJECTIVE To prospectively evaluate the effects of carvedilol in children and adolescents with symptomatic systemic ventricular systolic dysfunction.\n[2] DESIGN, SETTING, AND PARTICIPANTS A multicenter, randomized, double-blind, placebo-controlled study of 161 children and adolescents with symptomatic systolic heart failure from 26 US centers.\n[3] In addition to treatment with conventional heart failure medications, patients were assigned to receive placebo or carvedilol.\n[4] Enrollment began in June 2000 and the last dose was given in May 2005 (each patient received medication for 8 months).\n[5] INTERVENTIONS Patients were randomized in a 1:1:1 ratio to twice-daily dosing with placebo, low-dose carvedilol (0.2 mg/kg per dose if weight <62.5 kg or 12.5 mg per dose if weight > or =62.5 kg), or high-dose carvedilol (0.4 mg/kg per dose if weight <62.5 kg or 25 mg per dose if weight > or =62.5 kg) and were stratified according to whether each patient's systemic ventricle was a left ventricle or not.\n[6] MAIN OUTCOME MEASURES The primary outcome was a composite measure of heart failure outcomes in patients receiving carvedilol (low- and high-dose combined) vs placebo.\n[7] Secondary efficacy variables included individual components of this composite, echocardiographic measures, and plasma b-type natriuretic peptide levels.\n[8] RESULTS There was no statistically significant difference between groups for the composite end point based on the percentage of patients who improved, worsened, or were unchanged.\n[9] Among 54 patients assigned to placebo, 30 improved (56%), 16 worsened (30%), and 8 were unchanged (15%); among 103 patients assigned to carvedilol, 58 improved (56%), 25 worsened (24%), and 20 were unchanged (19%).\n[10] The rates of worsening were lower than expected.\n[11] The odds ratio for worsened outcome for patients in the combined carvedilol group vs the placebo group was 0.79 (95% CI, 0.36-1.59; P = .47).\n[12] A prespecified subgroup analysis noted significant interaction between treatment and ventricular morphology (P = .02), indicating a possible differential effect of treatment between patients with a systemic left ventricle (beneficial trend) and those whose systemic ventricle was not a left ventricle (nonbeneficial trend).\n[13] CONCLUSIONS These preliminary results suggest that carvedilol does not significantly improve clinical heart failure outcomes in children and adolescents with symptomatic systolic heart failure.\n[14] However, given the lower than expected event rates, the trial may have been underpowered.\n[15] There may be a differential effect of carvedilol in children and adolescents based on ventricular morphology.\n[16] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00052026."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"CONCLUSIONS These preliminary results suggest that carvedilol does not significantly improve clinical heart failure outcomes in children and adolescents with symptomatic systolic heart failure.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 579, "doc_id": 34139429, "label": "CONTRADICTS", "evidence_sentence_ids": [13], "cited_doc_ids": [34139429], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In pediatric tissue, most T cells are naive T cell emigrants from the thymus.\n\nDocument title: Early life compartmentalization of human T cell differentiation and regulatory function in mucosal and lymphoid tissues\n\nAbstract sentences:\n[0] It is unclear how the immune response in early life becomes appropriately stimulated to provide protection while also avoiding excessive activation as a result of diverse new antigens.\n[1] T cells are integral to adaptive immunity; mouse studies indicate that tissue localization of T cell subsets is important for both protective immunity and immunoregulation.\n[2] In humans, however, the early development and function of T cells in tissues remain unexplored.\n[3] We present here an analysis of lymphoid and mucosal tissue T cells derived from pediatric organ donors in the first two years of life, as compared to adult organ donors, revealing early compartmentalization of T cell differentiation and regulation.\n[4] Whereas adult tissues contain a predominance of memory T cells, in pediatric blood and tissues the main subset consists of naive recent thymic emigrants, with effector memory T cells (T(EM)) found only in the lungs and small intestine.\n[5] Additionally, regulatory T (T(reg)) cells comprise a high proportion (30-40%) of CD4(+) T cells in pediatric tissues but are present at much lower frequencies (1-10%) in adult tissues.\n[6] Pediatric tissue T(reg) cells suppress endogenous T cell activation, and early T cell functionality is confined to the mucosal sites that have the lowest T(reg):T(EM) cell ratios, which suggests control in situ of immune responses in early life."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Whereas adult tissues contain a predominance of memory T cells, in pediatric blood and tissues the main subset consists of naive recent thymic emigrants, with effector memory T cells (T(EM)) found only in the lungs and small intestine.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 580, "doc_id": 23460562, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [23460562], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In rhesus macaques, daily subcutaneous injections of emtricitabine are ineffective at protecting against rectally transmitted simian-human immunodeficiency virus.\n\nDocument title: Prevention of Rectal SHIV Transmission in Macaques by Daily or Intermittent Prophylaxis with Emtricitabine and Tenofovir \n\nAbstract sentences:\n[0] BACKGROUND In the absence of an effective vaccine, HIV continues to spread globally, emphasizing the need for novel strategies to limit its transmission.\n[1] Pre-exposure prophylaxis (PrEP) with antiretroviral drugs could prove to be an effective intervention strategy if highly efficacious and cost-effective PrEP modalities are identified.\n[2] We evaluated daily and intermittent PrEP regimens of increasing antiviral activity in a macaque model that closely resembles human transmission.\n[3] METHODS AND FINDINGS We used a repeat-exposure macaque model with 14 weekly rectal virus challenges.\n[4] Three drug treatments were given once daily, each to a different group of six rhesus macaques.\n[5] Group 1 was treated subcutaneously with a human-equivalent dose of emtricitabine (FTC), group 2 received orally the human-equivalent dosing of both FTC and tenofovir-disoproxil fumarate (TDF), and group 3 received subcutaneously a similar dosing of FTC and a higher dose of tenofovir.\n[6] A fourth group of six rhesus macaques (group 4) received intermittently a PrEP regimen similar to group 3 only 2 h before and 24 h after each weekly virus challenge.\n[7] Results were compared to 18 control macaques that did not receive any drug treatment.\n[8] The risk of infection in macaques treated in groups 1 and 2 was 3.8- and 7.8-fold lower than in untreated macaques (p = 0.02 and p = 0.008, respectively).\n[9] All six macaques in group 3 were protected.\n[10] Breakthrough infections had blunted acute viremias; drug resistance was seen in two of six animals.\n[11] All six animals in group 4 that received intermittent PrEP were protected.\n[12] CONCLUSIONS This model suggests that single drugs for daily PrEP can be protective but a combination of antiretroviral drugs may be required to increase the level of protection.\n[13] Short but potent intermittent PrEP can provide protection comparable to that of daily PrEP in this SHIV/macaque model.\n[14] These findings support PrEP trials for HIV prevention in humans and identify promising PrEP modalities."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 582, "doc_id": 14260013, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14260013], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In rhesus macaques, daily subcutaneous injections of tenofovir protects against rectally transmitted simian-human immunodeficiency virus.\n\nDocument title: Prevention of Rectal SHIV Transmission in Macaques by Daily or Intermittent Prophylaxis with Emtricitabine and Tenofovir \n\nAbstract sentences:\n[0] BACKGROUND In the absence of an effective vaccine, HIV continues to spread globally, emphasizing the need for novel strategies to limit its transmission.\n[1] Pre-exposure prophylaxis (PrEP) with antiretroviral drugs could prove to be an effective intervention strategy if highly efficacious and cost-effective PrEP modalities are identified.\n[2] We evaluated daily and intermittent PrEP regimens of increasing antiviral activity in a macaque model that closely resembles human transmission.\n[3] METHODS AND FINDINGS We used a repeat-exposure macaque model with 14 weekly rectal virus challenges.\n[4] Three drug treatments were given once daily, each to a different group of six rhesus macaques.\n[5] Group 1 was treated subcutaneously with a human-equivalent dose of emtricitabine (FTC), group 2 received orally the human-equivalent dosing of both FTC and tenofovir-disoproxil fumarate (TDF), and group 3 received subcutaneously a similar dosing of FTC and a higher dose of tenofovir.\n[6] A fourth group of six rhesus macaques (group 4) received intermittently a PrEP regimen similar to group 3 only 2 h before and 24 h after each weekly virus challenge.\n[7] Results were compared to 18 control macaques that did not receive any drug treatment.\n[8] The risk of infection in macaques treated in groups 1 and 2 was 3.8- and 7.8-fold lower than in untreated macaques (p = 0.02 and p = 0.008, respectively).\n[9] All six macaques in group 3 were protected.\n[10] Breakthrough infections had blunted acute viremias; drug resistance was seen in two of six animals.\n[11] All six animals in group 4 that received intermittent PrEP were protected.\n[12] CONCLUSIONS This model suggests that single drugs for daily PrEP can be protective but a combination of antiretroviral drugs may be required to increase the level of protection.\n[13] Short but potent intermittent PrEP can provide protection comparable to that of daily PrEP in this SHIV/macaque model.\n[14] These findings support PrEP trials for HIV prevention in humans and identify promising PrEP modalities."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"All six macaques in group 3 were protected.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 584, "doc_id": 14260013, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [14260013], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In the UK, drowning affects boys and girls equally.\n\nDocument title: Preventing deaths by drowning in children in the United Kingdom: have we made progress in 10 years? Population based incidence study.\n\nAbstract sentences:\n[0] Detailed information on drowning in children is not routinely collected by offices of national statistics.\n[1] Few studies have been carried out in the United Kingdom, and none has been done on British children abroad.\n[2] In 1988-9, two of the authors (AMK and JRS) combined information from national statistical offices, police forces (Royal Life Saving Society), and from a press cutting service (Royal Society for Prevention of Accidents) for a detailed analysis of deaths by drowning in children.1, 2, 3 This analysis found that 149 children had drowned in the United Kingdom during 1998-9.\n[3] It also identified a safety agenda, which focused on young children in garden ponds and pools and on older children swimming without supervision.\n[4] Over the past 10 years there have been initiatives on children's safety in water, particularly swimming.\n[5] We obtained similar information for 1998-9 to identify changes that have …"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 585, "doc_id": 42291761, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [42291761], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In transgenic mice harboring green florescent protein under the control of the Sox2 promoter, more than 50 percent of the cells with green florescent colocalize with cell proliferation markers.\n\nDocument title: Cell Stem Cell Article In Vivo Fate Analysis Reveals the Multipotent and Self-Renewal Capacities of Sox2 + Neural Stem Cells in the Adult Hippocampus\n\nAbstract sentences:\n[0] To characterize the properties of adult neural stem cells (NSCs), we generated and analyzed Sox2-GFP transgenic mice.\n[1] Sox2-GFP cells in the subgranular zone (SGZ) express markers specific for progenitors, but they represent two morphologically distinct populations that differ in proliferation levels.\n[2] Lentivirus- and retrovirus-mediated fate-tracing studies showed that Sox2+ cells in the SGZ have potential to give rise to neurons and astrocytes, revealing their multipotency at the population as well as at a single-cell level.\n[3] A subpopulation of Sox2+ cells gives rise to cells that retain Sox2, highlighting Sox2+ cells as a primary source for adult NSCs.\n[4] In response to mitotic signals, increased proliferation of Sox2+ cells is coupled with the generation of Sox2+ NSCs as well as neuronal precursors.\n[5] An asymmetric contribution of Sox2+ NSCs may play an important role in maintaining the constant size of the NSC pool and producing newly born neurons during adult neurogenesis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 588, "doc_id": 16999023, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [16999023], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In young and middle-aged adults, current or remote uses of ADHD medications increase the risk of serious cardiovascular events.\n\nDocument title: ADHD medications and risk of serious cardiovascular events in young and middle-aged adults.\n\nAbstract sentences:\n[0] CONTEXT More than 1.5 million US adults use stimulants and other medications labeled for treatment of attention-deficit/hyperactivity disorder (ADHD).\n[1] These agents can increase heart rate and blood pressure, raising concerns about their cardiovascular safety.\n[2] OBJECTIVE To examine whether current use of medications prescribed primarily to treat ADHD is associated with increased risk of serious cardiovascular events in young and middle-aged adults.\n[3] DESIGN, SETTING, AND PARTICIPANTS Retrospective, population-based cohort study using electronic health care records from 4 study sites (OptumInsight Epidemiology, Tennessee Medicaid, Kaiser Permanente California, and the HMO Research Network), starting in 1986 at 1 site and ending in 2005 at all sites, with additional covariate assessment using 2007 survey data.\n[4] Participants were adults aged 25 through 64 years with dispensed prescriptions for methylphenidate, amphetamine, or atomoxetine at baseline.\n[5] Each medication user (n = 150,359) was matched to 2 nonusers on study site, birth year, sex, and calendar year (443,198 total users and nonusers).\n[6] MAIN OUTCOME MEASURES Serious cardiovascular events, including myocardial infarction (MI), sudden cardiac death (SCD), or stroke, with comparison between current or new users and remote users to account for potential healthy-user bias.\n[7] RESULTS During 806,182 person-years of follow-up (median, 1.3 years per person), 1357 cases of MI, 296 cases of SCD, and 575 cases of stroke occurred.\n[8] There were 107,322 person-years of current use (median, 0.33 years), with a crude incidence per 1000 person-years of 1.34 (95% CI, 1.14-1.57) for MI, 0.30 (95% CI, 0.20-0.42) for SCD, and 0.56 (95% CI, 0.43-0.72) for stroke.\n[9] The multivariable-adjusted rate ratio (RR) of serious cardiovascular events for current use vs nonuse of ADHD medications was 0.83 (95% CI, 0.72-0.96).\n[10] Among new users of ADHD medications, the adjusted RR was 0.77 (95% CI, 0.63-0.94).\n[11] The adjusted RR for current use vs remote use was 1.03 (95% CI, 0.86-1.24); for new use vs remote use, the adjusted RR was 1.02 (95% CI, 0.82-1.28); the upper limit of 1.28 corresponds to an additional 0.19 events per 1000 person-years at ages 25-44 years and 0.77 events per 1000 person-years at ages 45-64 years.\n[12] CONCLUSIONS Among young and middle-aged adults, current or new use of ADHD medications, compared with nonuse or remote use, was not associated with an increased risk of serious cardiovascular events.\n[13] Apparent protective associations likely represent healthy-user bias."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9, 10]\nExplanation: Evidence states: \"The multivariable-adjusted rate ratio (RR) of serious cardiovascular events for current use vs nonuse of ADHD medications was 0.83 (95% CI, 0.72-0.96). Among new users of ADHD medications, the adjusted RR was 0.77 (95% CI, 0.63-0.94).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 590, "doc_id": 10984005, "label": "CONTRADICTS", "evidence_sentence_ids": [9, 10], "cited_doc_ids": [10984005], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: In young and middle-aged adults, current or remote uses of ADHD medications increase the risk of serious cardiovascular events.\n\nDocument title: ADHD medications and risk of serious cardiovascular events in young and middle-aged adults.\n\nAbstract sentences:\n[0] CONTEXT More than 1.5 million US adults use stimulants and other medications labeled for treatment of attention-deficit/hyperactivity disorder (ADHD).\n[1] These agents can increase heart rate and blood pressure, raising concerns about their cardiovascular safety.\n[2] OBJECTIVE To examine whether current use of medications prescribed primarily to treat ADHD is associated with increased risk of serious cardiovascular events in young and middle-aged adults.\n[3] DESIGN, SETTING, AND PARTICIPANTS Retrospective, population-based cohort study using electronic health care records from 4 study sites (OptumInsight Epidemiology, Tennessee Medicaid, Kaiser Permanente California, and the HMO Research Network), starting in 1986 at 1 site and ending in 2005 at all sites, with additional covariate assessment using 2007 survey data.\n[4] Participants were adults aged 25 through 64 years with dispensed prescriptions for methylphenidate, amphetamine, or atomoxetine at baseline.\n[5] Each medication user (n = 150,359) was matched to 2 nonusers on study site, birth year, sex, and calendar year (443,198 total users and nonusers).\n[6] MAIN OUTCOME MEASURES Serious cardiovascular events, including myocardial infarction (MI), sudden cardiac death (SCD), or stroke, with comparison between current or new users and remote users to account for potential healthy-user bias.\n[7] RESULTS During 806,182 person-years of follow-up (median, 1.3 years per person), 1357 cases of MI, 296 cases of SCD, and 575 cases of stroke occurred.\n[8] There were 107,322 person-years of current use (median, 0.33 years), with a crude incidence per 1000 person-years of 1.34 (95% CI, 1.14-1.57) for MI, 0.30 (95% CI, 0.20-0.42) for SCD, and 0.56 (95% CI, 0.43-0.72) for stroke.\n[9] The multivariable-adjusted rate ratio (RR) of serious cardiovascular events for current use vs nonuse of ADHD medications was 0.83 (95% CI, 0.72-0.96).\n[10] Among new users of ADHD medications, the adjusted RR was 0.77 (95% CI, 0.63-0.94).\n[11] The adjusted RR for current use vs remote use was 1.03 (95% CI, 0.86-1.24); for new use vs remote use, the adjusted RR was 1.02 (95% CI, 0.82-1.28); the upper limit of 1.28 corresponds to an additional 0.19 events per 1000 person-years at ages 25-44 years and 0.77 events per 1000 person-years at ages 45-64 years.\n[12] CONCLUSIONS Among young and middle-aged adults, current or new use of ADHD medications, compared with nonuse or remote use, was not associated with an increased risk of serious cardiovascular events.\n[13] Apparent protective associations likely represent healthy-user bias."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"CONCLUSIONS Among young and middle-aged adults, current or new use of ADHD medications, compared with nonuse or remote use, was not associated with an increased risk of serious cardiovascular events.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 590, "doc_id": 10984005, "label": "CONTRADICTS", "evidence_sentence_ids": [12], "cited_doc_ids": [10984005], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Incidence of 10/66 dementia is higher than the incidence of DSM-IV dementia.\n\nDocument title: Dementia incidence and mortality in middle-income countries, and associations with indicators of cognitive reserve: a 10/66 Dementia Research Group population-based cohort study\n\nAbstract sentences:\n[0] BACKGROUND Results of the few cohort studies from countries with low incomes or middle incomes suggest a lower incidence of dementia than in high-income countries.\n[1] We assessed incidence of dementia according to criteria from the 10/66 Dementia Research Group and Diagnostic and Statistical Manual of Mental Disorders (DSM) IV, the effect of dementia at baseline on mortality, and the independent effects of age, sex, socioeconomic position, and indicators of cognitive reserve.\n[2] METHODS We did a population-based cohort study of all people aged 65 years and older living in urban sites in Cuba, the Dominican Republic, and Venezuela, and rural and urban sites in Peru, Mexico, and China, with ascertainment of incident 10/66 and DSM-IV dementia 3-5 years after cohort inception.\n[3] We used questionnaires to obtain information about age in years, sex, educational level, literacy, occupational attainment, and number of household assets.\n[4] We obtained information about mortality from all sites.\n[5] For participants who had died, we interviewed a friend or relative to ascertain the likelihood that they had dementia before death.\n[6] FINDINGS 12,887 participants were interviewed at baseline.\n[7] 11,718 were free of dementia, of whom 8137 (69%) were reinterviewed, contributing 34,718 person-years of follow-up.\n[8] Incidence for 10/66 dementia varied between 18·2 and 30·4 per 1000 person-years, and were 1·4-2·7 times higher than were those for DSM-IV dementia (9·9-15·7 per 1000 person-years).\n[9] Mortality hazards were 1·56-5·69 times higher in individuals with dementia at baseline than in those who were dementia-free.\n[10] Informant reports suggested a high incidence of dementia before death; overall incidence might be 4-19% higher if these data were included.\n[11] 10/66 dementia incidence was independently associated with increased age (HR 1·67; 95% CI 1·56-1·79), female sex (0·72; 0·61-0·84), and low education (0·89; 0·81-0·97), but not with occupational attainment (1·04; 0·95-1·13).\n[12] INTERPRETATION Our results provide supportive evidence for the cognitive reserve hypothesis, showing that in middle-income countries as in high-income countries, education, literacy, verbal fluency, and motor sequencing confer substantial protection against the onset of dementia.\n[13] FUNDING Wellcome Trust Health Consequences of Population Change Programme, WHO, US Alzheimer's Association, FONACIT/ CDCH/ UCV."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Incidence for 10/66 dementia varied between 18·2 and 30·4 per 1000 person-years, and were 1·4-2·7 times higher than were those for DSM-IV dementia (9·9-15·7 per 1000 person-years).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 591, "doc_id": 14682243, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [14682243], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Incidence of 10/66 dementia is lower than the incidence of DSM-IV dementia.\n\nDocument title: Dementia incidence and mortality in middle-income countries, and associations with indicators of cognitive reserve: a 10/66 Dementia Research Group population-based cohort study\n\nAbstract sentences:\n[0] BACKGROUND Results of the few cohort studies from countries with low incomes or middle incomes suggest a lower incidence of dementia than in high-income countries.\n[1] We assessed incidence of dementia according to criteria from the 10/66 Dementia Research Group and Diagnostic and Statistical Manual of Mental Disorders (DSM) IV, the effect of dementia at baseline on mortality, and the independent effects of age, sex, socioeconomic position, and indicators of cognitive reserve.\n[2] METHODS We did a population-based cohort study of all people aged 65 years and older living in urban sites in Cuba, the Dominican Republic, and Venezuela, and rural and urban sites in Peru, Mexico, and China, with ascertainment of incident 10/66 and DSM-IV dementia 3-5 years after cohort inception.\n[3] We used questionnaires to obtain information about age in years, sex, educational level, literacy, occupational attainment, and number of household assets.\n[4] We obtained information about mortality from all sites.\n[5] For participants who had died, we interviewed a friend or relative to ascertain the likelihood that they had dementia before death.\n[6] FINDINGS 12,887 participants were interviewed at baseline.\n[7] 11,718 were free of dementia, of whom 8137 (69%) were reinterviewed, contributing 34,718 person-years of follow-up.\n[8] Incidence for 10/66 dementia varied between 18·2 and 30·4 per 1000 person-years, and were 1·4-2·7 times higher than were those for DSM-IV dementia (9·9-15·7 per 1000 person-years).\n[9] Mortality hazards were 1·56-5·69 times higher in individuals with dementia at baseline than in those who were dementia-free.\n[10] Informant reports suggested a high incidence of dementia before death; overall incidence might be 4-19% higher if these data were included.\n[11] 10/66 dementia incidence was independently associated with increased age (HR 1·67; 95% CI 1·56-1·79), female sex (0·72; 0·61-0·84), and low education (0·89; 0·81-0·97), but not with occupational attainment (1·04; 0·95-1·13).\n[12] INTERPRETATION Our results provide supportive evidence for the cognitive reserve hypothesis, showing that in middle-income countries as in high-income countries, education, literacy, verbal fluency, and motor sequencing confer substantial protection against the onset of dementia.\n[13] FUNDING Wellcome Trust Health Consequences of Population Change Programme, WHO, US Alzheimer's Association, FONACIT/ CDCH/ UCV."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Incidence for 10/66 dementia varied between 18·2 and 30·4 per 1000 person-years, and were 1·4-2·7 times higher than were those for DSM-IV dementia (9·9-15·7 per 1000 person-years).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 592, "doc_id": 14682243, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [14682243], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Incidence of heart failure increased by 10% in women since 1979.\n\nDocument title: Trends in heart failure incidence and survival in a community-based population.\n\nAbstract sentences:\n[0] CONTEXT The epidemic of heart failure has yet to be fully investigated, and data on incidence, survival, and sex-specific temporal trends in community-based populations are limited.\n[1] OBJECTIVE To test the hypothesis that the incidence of heart failure has declined and survival after heart failure diagnosis has improved over time but that secular trends have diverged by sex.\n[2] DESIGN, SETTING, AND PARTICIPANTS Population-based cohort study using the resources of the Rochester Epidemiology Project conducted in Olmsted County, Minnesota.\n[3] Patients were 4537 Olmsted County residents (57% women; mean [SD] age, 74 [14] years) with a diagnosis of heart failure between 1979 and 2000.\n[4] Framingham criteria and clinical criteria were used to validate the diagnosis   MAIN OUTCOME MEASURES Incidence of heart failure and survival after heart failure diagnosis.\n[5] RESULTS The incidence of heart failure was higher among men (378/100 000 persons; 95% confidence interval [CI], 361-395 for men; 289/100 000 persons; 95% CI, 277-300 for women) and did not change over time among men or women.\n[6] After a mean follow-up of 4.2 years (range, 0-23.8 years), 3347 deaths occurred, including 1930 among women and 1417 among men.\n[7] Survival after heart failure diagnosis was worse among men than women (relative risk, 1.33; 95% CI, 1.24-1.43) but overall improved over time (5-year age-adjusted survival, 43% in 1979-1984 vs 52% in 1996-2000, P<.001).\n[8] However, men and younger persons experienced larger survival gains, contrasting with less or no improvement for women and elderly persons.\n[9] CONCLUSION In this community-based cohort, the incidence of heart failure has not declined during 2 decades, but survival after onset of heart failure has increased overall, with less improvement among women and elderly persons."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"RESULTS The incidence of heart failure was higher among men (378/100 000 persons; 95% confidence interval [CI], 361-395 for men; 289/100 000 persons; 95% CI, 277-300 for women) and did not change over time among men or women.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 594, "doc_id": 19675911, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [19675911], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Incidence of sepsis has fallen substantially from 2009 to 2014.\n\nDocument title: Incidence and Trends of Sepsis in US Hospitals Using Clinical vs Claims Data, 2009-2014\n\nAbstract sentences:\n[0] Importance Estimates from claims-based analyses suggest that the incidence of sepsis is increasing and mortality rates from sepsis are decreasing.\n[1] However, estimates from claims data may lack clinical fidelity and can be affected by changing diagnosis and coding practices over time.\n[2] Objective To estimate the US national incidence of sepsis and trends using detailed clinical data from the electronic health record (EHR) systems of diverse hospitals.\n[3] Design, Setting, and Population Retrospective cohort study of adult patients admitted to 409 academic, community, and federal hospitals from 2009-2014.\n[4] Exposures Sepsis was identified using clinical indicators of presumed infection and concurrent acute organ dysfunction, adapting Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) criteria for objective and consistent EHR-based surveillance.\n[5] Main Outcomes and Measures Sepsis incidence, outcomes, and trends from 2009-2014 were calculated using regression models and compared with claims-based estimates using International Classification of Diseases, Ninth Revision, Clinical Modification codes for severe sepsis or septic shock.\n[6] Case-finding criteria were validated against Sepsis-3 criteria using medical record reviews.\n[7] Results A total of 173 690 sepsis cases (mean age, 66.5 [SD, 15.5] y; 77 660 [42.4%] women) were identified using clinical criteria among 2 901 019 adults admitted to study hospitals in 2014 (6.0% incidence).\n[8] Of these, 26 061 (15.0%) died in the hospital and 10 731 (6.2%) were discharged to hospice.\n[9] From 2009-2014, sepsis incidence using clinical criteria was stable (+0.6% relative change/y [95% CI, −2.3% to 3.5%], P = .67) whereas incidence per claims increased (+10.3%/y [95% CI, 7.2% to 13.3%], P < .001).\n[10] In-hospital mortality using clinical criteria declined (−3.3%/y [95% CI, −5.6% to −1.0%], P = .004), but there was no significant change in the combined outcome of death or discharge to hospice (−1.3%/y [95% CI, −3.2% to 0.6%], P = .19).\n[11] In contrast, mortality using claims declined significantly (−7.0%/y [95% CI, −8.8% to −5.2%], P < .001), as did death or discharge to hospice (−4.5%/y [95% CI, −6.1% to −2.8%], P < .001).\n[12] Clinical criteria were more sensitive in identifying sepsis than claims (69.7% [95% CI, 52.9% to 92.0%] vs 32.3% [95% CI, 24.4% to 43.0%], P < .001), with comparable positive predictive value (70.4% [95% CI, 64.0% to 76.8%] vs 75.2% [95% CI, 69.8% to 80.6%], P = .23).\n[13] Conclusions and Relevance In clinical data from 409 hospitals, sepsis was present in 6% of adult hospitalizations, and in contrast to claims-based analyses, neither the incidence of sepsis nor the combined outcome of death or discharge to hospice changed significantly between 2009-2014.\n[14] The findings also suggest that EHR-based clinical data provide more objective estimates than claims-based data for sepsis surveillance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"From 2009-2014, sepsis incidence using clinical criteria was stable (+0.6% relative change/y [95% CI, −2.3% to 3.5%], P = .67) whereas incidence per claims increased (+10.3%/y [95% CI, 7.2% to 13.3%], P < .001).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 595, "doc_id": 4824840, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [4824840], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Incidence of sepsis has fallen substantially from 2009 to 2014.\n\nDocument title: Incidence and Trends of Sepsis in US Hospitals Using Clinical vs Claims Data, 2009-2014\n\nAbstract sentences:\n[0] Importance Estimates from claims-based analyses suggest that the incidence of sepsis is increasing and mortality rates from sepsis are decreasing.\n[1] However, estimates from claims data may lack clinical fidelity and can be affected by changing diagnosis and coding practices over time.\n[2] Objective To estimate the US national incidence of sepsis and trends using detailed clinical data from the electronic health record (EHR) systems of diverse hospitals.\n[3] Design, Setting, and Population Retrospective cohort study of adult patients admitted to 409 academic, community, and federal hospitals from 2009-2014.\n[4] Exposures Sepsis was identified using clinical indicators of presumed infection and concurrent acute organ dysfunction, adapting Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) criteria for objective and consistent EHR-based surveillance.\n[5] Main Outcomes and Measures Sepsis incidence, outcomes, and trends from 2009-2014 were calculated using regression models and compared with claims-based estimates using International Classification of Diseases, Ninth Revision, Clinical Modification codes for severe sepsis or septic shock.\n[6] Case-finding criteria were validated against Sepsis-3 criteria using medical record reviews.\n[7] Results A total of 173 690 sepsis cases (mean age, 66.5 [SD, 15.5] y; 77 660 [42.4%] women) were identified using clinical criteria among 2 901 019 adults admitted to study hospitals in 2014 (6.0% incidence).\n[8] Of these, 26 061 (15.0%) died in the hospital and 10 731 (6.2%) were discharged to hospice.\n[9] From 2009-2014, sepsis incidence using clinical criteria was stable (+0.6% relative change/y [95% CI, −2.3% to 3.5%], P = .67) whereas incidence per claims increased (+10.3%/y [95% CI, 7.2% to 13.3%], P < .001).\n[10] In-hospital mortality using clinical criteria declined (−3.3%/y [95% CI, −5.6% to −1.0%], P = .004), but there was no significant change in the combined outcome of death or discharge to hospice (−1.3%/y [95% CI, −3.2% to 0.6%], P = .19).\n[11] In contrast, mortality using claims declined significantly (−7.0%/y [95% CI, −8.8% to −5.2%], P < .001), as did death or discharge to hospice (−4.5%/y [95% CI, −6.1% to −2.8%], P < .001).\n[12] Clinical criteria were more sensitive in identifying sepsis than claims (69.7% [95% CI, 52.9% to 92.0%] vs 32.3% [95% CI, 24.4% to 43.0%], P < .001), with comparable positive predictive value (70.4% [95% CI, 64.0% to 76.8%] vs 75.2% [95% CI, 69.8% to 80.6%], P = .23).\n[13] Conclusions and Relevance In clinical data from 409 hospitals, sepsis was present in 6% of adult hospitalizations, and in contrast to claims-based analyses, neither the incidence of sepsis nor the combined outcome of death or discharge to hospice changed significantly between 2009-2014.\n[14] The findings also suggest that EHR-based clinical data provide more objective estimates than claims-based data for sepsis surveillance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"Conclusions and Relevance In clinical data from 409 hospitals, sepsis was present in 6% of adult hospitalizations, and in contrast to claims-based analyses, neither the incidence of sepsis nor the combined outcome of death or discharge to hospice changed significantly between 2009-2014.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 595, "doc_id": 4824840, "label": "CONTRADICTS", "evidence_sentence_ids": [13], "cited_doc_ids": [4824840], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Including pharmacists in rounding teams does not alter the incidence of adverse drug events (ADEs).\n\nDocument title: Pharmacist participation on physician rounds and adverse drug events in the intensive care unit.\n\nAbstract sentences:\n[0] CONTEXT Pharmacist review of medication orders in the intensive care unit (ICU) has been shown to prevent errors, and pharmacist consultation has reduced drug costs.\n[1] However, whether pharmacist participation in the ICU at the time of drug prescribing reduces adverse events has not been studied.\n[2] OBJECTIVE To measure the effect of pharmacist participation on medical rounds in the ICU on the rate of preventable adverse drug events (ADEs) caused by ordering errors.\n[3] DESIGN Before-after comparison between phase 1 (baseline) and phase 2 (after intervention implemented) and phase 2 comparison with a control unit that did not receive the intervention.\n[4] SETTING A medical ICU (study unit) and a coronary care unit (control unit) in a large urban teaching hospital.\n[5] PATIENTS Seventy-five patients randomly selected from each of 3 groups: all admissions to the study unit from February 1, 1993, through July 31, 1993 (baseline) and all admissions to the study unit (postintervention) and control unit from October 1, 1994, through July 7, 1995.\n[6] In addition, 50 patients were selected at random from the control unit during the baseline period.\n[7] INTERVENTION A senior pharmacist made rounds with the ICU team and remained in the ICU for consultation in the morning, and was available on call throughout the day.\n[8] MAIN OUTCOME MEASURES Preventable ADEs due to ordering (prescribing) errors and the number, type, and acceptance of interventions made by the pharmacist.\n[9] Preventable ADEs were identified by review of medical records of the randomly selected patients during both preintervention and postintervention phases.\n[10] Pharmacists recorded all recommendations, which were then analyzed by type and acceptance.\n[11] RESULTS The rate of preventable ordering ADEs decreased by 66% from 10.4 per 1000 patient-days (95% confidence interval [CI], 7-14) before the intervention to 3.5 (95% CI, 1-5; P<.001) after the intervention.\n[12] In the control unit, the rate was essentially unchanged during the same time periods: 10.9 (95% CI, 6-16) and 12.4 (95% CI, 8-17) per 1000 patient-days.\n[13] The pharmacist made 366 recommendations related to drug ordering, of which 362 (99%) were accepted by physicians.\n[14] CONCLUSIONS The presence of a pharmacist on rounds as a full member of the patient care team in a medical ICU was associated with a substantially lower rate of ADEs caused by prescribing errors.\n[15] Nearly all the changes were readily accepted by physicians."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"RESULTS The rate of preventable ordering ADEs decreased by 66% from 10.4 per 1000 patient-days (95% confidence interval [CI], 7-14) before the intervention to 3.5 (95% CI, 1-5; P<.001) after the intervention.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 600, "doc_id": 12258338, "label": "CONTRADICTS", "evidence_sentence_ids": [11], "cited_doc_ids": [12258338], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Including pharmacists in rounding teams does not alter the incidence of adverse drug events (ADEs).\n\nDocument title: Pharmacist participation on physician rounds and adverse drug events in the intensive care unit.\n\nAbstract sentences:\n[0] CONTEXT Pharmacist review of medication orders in the intensive care unit (ICU) has been shown to prevent errors, and pharmacist consultation has reduced drug costs.\n[1] However, whether pharmacist participation in the ICU at the time of drug prescribing reduces adverse events has not been studied.\n[2] OBJECTIVE To measure the effect of pharmacist participation on medical rounds in the ICU on the rate of preventable adverse drug events (ADEs) caused by ordering errors.\n[3] DESIGN Before-after comparison between phase 1 (baseline) and phase 2 (after intervention implemented) and phase 2 comparison with a control unit that did not receive the intervention.\n[4] SETTING A medical ICU (study unit) and a coronary care unit (control unit) in a large urban teaching hospital.\n[5] PATIENTS Seventy-five patients randomly selected from each of 3 groups: all admissions to the study unit from February 1, 1993, through July 31, 1993 (baseline) and all admissions to the study unit (postintervention) and control unit from October 1, 1994, through July 7, 1995.\n[6] In addition, 50 patients were selected at random from the control unit during the baseline period.\n[7] INTERVENTION A senior pharmacist made rounds with the ICU team and remained in the ICU for consultation in the morning, and was available on call throughout the day.\n[8] MAIN OUTCOME MEASURES Preventable ADEs due to ordering (prescribing) errors and the number, type, and acceptance of interventions made by the pharmacist.\n[9] Preventable ADEs were identified by review of medical records of the randomly selected patients during both preintervention and postintervention phases.\n[10] Pharmacists recorded all recommendations, which were then analyzed by type and acceptance.\n[11] RESULTS The rate of preventable ordering ADEs decreased by 66% from 10.4 per 1000 patient-days (95% confidence interval [CI], 7-14) before the intervention to 3.5 (95% CI, 1-5; P<.001) after the intervention.\n[12] In the control unit, the rate was essentially unchanged during the same time periods: 10.9 (95% CI, 6-16) and 12.4 (95% CI, 8-17) per 1000 patient-days.\n[13] The pharmacist made 366 recommendations related to drug ordering, of which 362 (99%) were accepted by physicians.\n[14] CONCLUSIONS The presence of a pharmacist on rounds as a full member of the patient care team in a medical ICU was associated with a substantially lower rate of ADEs caused by prescribing errors.\n[15] Nearly all the changes were readily accepted by physicians."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [14]\nExplanation: Evidence states: \"CONCLUSIONS The presence of a pharmacist on rounds as a full member of the patient care team in a medical ICU was associated with a substantially lower rate of ADEs caused by prescribing errors.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 600, "doc_id": 12258338, "label": "CONTRADICTS", "evidence_sentence_ids": [14], "cited_doc_ids": [12258338], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Including pharmacists in rounding teams reduces the incidence of adverse drug events (ADEs).\n\nDocument title: Pharmacist participation on physician rounds and adverse drug events in the intensive care unit.\n\nAbstract sentences:\n[0] CONTEXT Pharmacist review of medication orders in the intensive care unit (ICU) has been shown to prevent errors, and pharmacist consultation has reduced drug costs.\n[1] However, whether pharmacist participation in the ICU at the time of drug prescribing reduces adverse events has not been studied.\n[2] OBJECTIVE To measure the effect of pharmacist participation on medical rounds in the ICU on the rate of preventable adverse drug events (ADEs) caused by ordering errors.\n[3] DESIGN Before-after comparison between phase 1 (baseline) and phase 2 (after intervention implemented) and phase 2 comparison with a control unit that did not receive the intervention.\n[4] SETTING A medical ICU (study unit) and a coronary care unit (control unit) in a large urban teaching hospital.\n[5] PATIENTS Seventy-five patients randomly selected from each of 3 groups: all admissions to the study unit from February 1, 1993, through July 31, 1993 (baseline) and all admissions to the study unit (postintervention) and control unit from October 1, 1994, through July 7, 1995.\n[6] In addition, 50 patients were selected at random from the control unit during the baseline period.\n[7] INTERVENTION A senior pharmacist made rounds with the ICU team and remained in the ICU for consultation in the morning, and was available on call throughout the day.\n[8] MAIN OUTCOME MEASURES Preventable ADEs due to ordering (prescribing) errors and the number, type, and acceptance of interventions made by the pharmacist.\n[9] Preventable ADEs were identified by review of medical records of the randomly selected patients during both preintervention and postintervention phases.\n[10] Pharmacists recorded all recommendations, which were then analyzed by type and acceptance.\n[11] RESULTS The rate of preventable ordering ADEs decreased by 66% from 10.4 per 1000 patient-days (95% confidence interval [CI], 7-14) before the intervention to 3.5 (95% CI, 1-5; P<.001) after the intervention.\n[12] In the control unit, the rate was essentially unchanged during the same time periods: 10.9 (95% CI, 6-16) and 12.4 (95% CI, 8-17) per 1000 patient-days.\n[13] The pharmacist made 366 recommendations related to drug ordering, of which 362 (99%) were accepted by physicians.\n[14] CONCLUSIONS The presence of a pharmacist on rounds as a full member of the patient care team in a medical ICU was associated with a substantially lower rate of ADEs caused by prescribing errors.\n[15] Nearly all the changes were readily accepted by physicians."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"RESULTS The rate of preventable ordering ADEs decreased by 66% from 10.4 per 1000 patient-days (95% confidence interval [CI], 7-14) before the intervention to 3.5 (95% CI, 1-5; P<.001) after the intervention.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 601, "doc_id": 12258338, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [12258338], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Including pharmacists in rounding teams reduces the incidence of adverse drug events (ADEs).\n\nDocument title: Pharmacist participation on physician rounds and adverse drug events in the intensive care unit.\n\nAbstract sentences:\n[0] CONTEXT Pharmacist review of medication orders in the intensive care unit (ICU) has been shown to prevent errors, and pharmacist consultation has reduced drug costs.\n[1] However, whether pharmacist participation in the ICU at the time of drug prescribing reduces adverse events has not been studied.\n[2] OBJECTIVE To measure the effect of pharmacist participation on medical rounds in the ICU on the rate of preventable adverse drug events (ADEs) caused by ordering errors.\n[3] DESIGN Before-after comparison between phase 1 (baseline) and phase 2 (after intervention implemented) and phase 2 comparison with a control unit that did not receive the intervention.\n[4] SETTING A medical ICU (study unit) and a coronary care unit (control unit) in a large urban teaching hospital.\n[5] PATIENTS Seventy-five patients randomly selected from each of 3 groups: all admissions to the study unit from February 1, 1993, through July 31, 1993 (baseline) and all admissions to the study unit (postintervention) and control unit from October 1, 1994, through July 7, 1995.\n[6] In addition, 50 patients were selected at random from the control unit during the baseline period.\n[7] INTERVENTION A senior pharmacist made rounds with the ICU team and remained in the ICU for consultation in the morning, and was available on call throughout the day.\n[8] MAIN OUTCOME MEASURES Preventable ADEs due to ordering (prescribing) errors and the number, type, and acceptance of interventions made by the pharmacist.\n[9] Preventable ADEs were identified by review of medical records of the randomly selected patients during both preintervention and postintervention phases.\n[10] Pharmacists recorded all recommendations, which were then analyzed by type and acceptance.\n[11] RESULTS The rate of preventable ordering ADEs decreased by 66% from 10.4 per 1000 patient-days (95% confidence interval [CI], 7-14) before the intervention to 3.5 (95% CI, 1-5; P<.001) after the intervention.\n[12] In the control unit, the rate was essentially unchanged during the same time periods: 10.9 (95% CI, 6-16) and 12.4 (95% CI, 8-17) per 1000 patient-days.\n[13] The pharmacist made 366 recommendations related to drug ordering, of which 362 (99%) were accepted by physicians.\n[14] CONCLUSIONS The presence of a pharmacist on rounds as a full member of the patient care team in a medical ICU was associated with a substantially lower rate of ADEs caused by prescribing errors.\n[15] Nearly all the changes were readily accepted by physicians."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [14]\nExplanation: Evidence states: \"CONCLUSIONS The presence of a pharmacist on rounds as a full member of the patient care team in a medical ICU was associated with a substantially lower rate of ADEs caused by prescribing errors.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 601, "doc_id": 12258338, "label": "SUPPORTS", "evidence_sentence_ids": [14], "cited_doc_ids": [12258338], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Increase of p62 in prostate tumor stroma results in defective autophagy.\n\nDocument title: p62/SQSTM1 by Binding to Vitamin D Receptor Inhibits Hepatic Stellate Cell Activity, Fibrosis, and Liver Cancer.\n\nAbstract sentences:\n[0] Hepatic stellate cells (HSCs) play critical roles in liver fibrosis and hepatocellular carcinoma (HCC).\n[1] Vitamin D receptor (VDR) activation in HSCs inhibits liver inflammation and fibrosis.\n[2] We found that p62/SQSTM1, a protein upregulated in liver parenchymal cells but downregulated in HCC-associated HSCs, negatively controls HSC activation.\n[3] Total body or HSC-specific p62 ablation potentiates HSCs and enhances inflammation, fibrosis, and HCC progression.\n[4] p62 directly interacts with VDR and RXR promoting their heterodimerization, which is critical for VDR:RXR target gene recruitment.\n[5] Loss of p62 in HSCs impairs the repression of fibrosis and inflammation by VDR agonists.\n[6] This demonstrates that p62 is a negative regulator of liver inflammation and fibrosis through its ability to promote VDR signaling in HSCs, whose activation supports HCC."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 602, "doc_id": 3701541, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [3701541], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Increased LDL receptors plays a role in the reduction of plasma Lp(a).\n\nDocument title: Effects of PCSK9 Inhibition With Alirocumab on Lipoprotein Metabolism in Healthy Humans\n\nAbstract sentences:\n[0] BACKGROUND Alirocumab, a monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9), lowers plasma low-density lipoprotein (LDL) cholesterol and apolipoprotein B100 (apoB).\n[1] Although studies in mice and cells have identified increased hepatic LDL receptors as the basis for LDL lowering by PCSK9 inhibitors, there have been no human studies characterizing the effects of PCSK9 inhibitors on lipoprotein metabolism.\n[2] In particular, it is not known whether inhibition of PCSK9 has any effects on very low-density lipoprotein or intermediate-density lipoprotein (IDL) metabolism.\n[3] Inhibition of PCSK9 also results in reductions of plasma lipoprotein (a) levels.\n[4] The regulation of plasma Lp(a) levels, including the role of LDL receptors in the clearance of Lp(a), is poorly defined, and no mechanistic studies of the Lp(a) lowering by alirocumab in humans have been published to date.\n[5] METHODS Eighteen (10 F, 8 mol/L) participants completed a placebo-controlled, 2-period study.\n[6] They received 2 doses of placebo, 2 weeks apart, followed by 5 doses of 150 mg of alirocumab, 2 weeks apart.\n[7] At the end of each period, fractional clearance rates (FCRs) and production rates (PRs) of apoB and apo(a) were determined.\n[8] In 10 participants, postprandial triglycerides and apoB48 levels were measured.\n[9] RESULTS Alirocumab reduced ultracentrifugally isolated LDL-C by 55.1%, LDL-apoB by 56.3%, and plasma Lp(a) by 18.7%.\n[10] The fall in LDL-apoB was caused by an 80.4% increase in LDL-apoB FCR and a 23.9% reduction in LDL-apoB PR.\n[11] The latter was due to a 46.1% increase in IDL-apoB FCR coupled with a 27.2% decrease in conversion of IDL to LDL.\n[12] The FCR of apo(a) tended to increase (24.6%) without any change in apo(a) PR.\n[13] Alirocumab had no effects on FCRs or PRs of very low-density lipoproteins-apoB and very low-density lipoproteins triglycerides or on postprandial plasma triglycerides or apoB48 concentrations.\n[14] CONCLUSIONS Alirocumab decreased LDL-C and LDL-apoB by increasing IDL- and LDL-apoB FCRs and decreasing LDL-apoB PR.\n[15] These results are consistent with increases in LDL receptors available to clear IDL and LDL from blood during PCSK9 inhibition.\n[16] The increase in apo(a) FCR during alirocumab treatment suggests that increased LDL receptors may also play a role in the reduction of plasma Lp(a).\n[17] CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov.\n[18] Unique identifier: NCT01959971."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9, 10, 11]\nExplanation: Evidence states: \"RESULTS Alirocumab reduced ultracentrifugally isolated LDL-C by 55.1%, LDL-apoB by 56.3%, and plasma Lp(a) by 18.7%. The fall in LDL-apoB was caused by an 80.4% increase in LDL-apoB FCR and a 23.9% reduction in LDL-apoB PR. The latter was due to a 46.1% increase in IDL-apoB FCR coupled with a 27.2% decrease in conversion of IDL to LDL.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 603, "doc_id": 6540064, "label": "SUPPORTS", "evidence_sentence_ids": [9, 10, 11], "cited_doc_ids": [6540064], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Increased LDL receptors plays a role in the reduction of plasma Lp(a).\n\nDocument title: Effects of PCSK9 Inhibition With Alirocumab on Lipoprotein Metabolism in Healthy Humans\n\nAbstract sentences:\n[0] BACKGROUND Alirocumab, a monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9), lowers plasma low-density lipoprotein (LDL) cholesterol and apolipoprotein B100 (apoB).\n[1] Although studies in mice and cells have identified increased hepatic LDL receptors as the basis for LDL lowering by PCSK9 inhibitors, there have been no human studies characterizing the effects of PCSK9 inhibitors on lipoprotein metabolism.\n[2] In particular, it is not known whether inhibition of PCSK9 has any effects on very low-density lipoprotein or intermediate-density lipoprotein (IDL) metabolism.\n[3] Inhibition of PCSK9 also results in reductions of plasma lipoprotein (a) levels.\n[4] The regulation of plasma Lp(a) levels, including the role of LDL receptors in the clearance of Lp(a), is poorly defined, and no mechanistic studies of the Lp(a) lowering by alirocumab in humans have been published to date.\n[5] METHODS Eighteen (10 F, 8 mol/L) participants completed a placebo-controlled, 2-period study.\n[6] They received 2 doses of placebo, 2 weeks apart, followed by 5 doses of 150 mg of alirocumab, 2 weeks apart.\n[7] At the end of each period, fractional clearance rates (FCRs) and production rates (PRs) of apoB and apo(a) were determined.\n[8] In 10 participants, postprandial triglycerides and apoB48 levels were measured.\n[9] RESULTS Alirocumab reduced ultracentrifugally isolated LDL-C by 55.1%, LDL-apoB by 56.3%, and plasma Lp(a) by 18.7%.\n[10] The fall in LDL-apoB was caused by an 80.4% increase in LDL-apoB FCR and a 23.9% reduction in LDL-apoB PR.\n[11] The latter was due to a 46.1% increase in IDL-apoB FCR coupled with a 27.2% decrease in conversion of IDL to LDL.\n[12] The FCR of apo(a) tended to increase (24.6%) without any change in apo(a) PR.\n[13] Alirocumab had no effects on FCRs or PRs of very low-density lipoproteins-apoB and very low-density lipoproteins triglycerides or on postprandial plasma triglycerides or apoB48 concentrations.\n[14] CONCLUSIONS Alirocumab decreased LDL-C and LDL-apoB by increasing IDL- and LDL-apoB FCRs and decreasing LDL-apoB PR.\n[15] These results are consistent with increases in LDL receptors available to clear IDL and LDL from blood during PCSK9 inhibition.\n[16] The increase in apo(a) FCR during alirocumab treatment suggests that increased LDL receptors may also play a role in the reduction of plasma Lp(a).\n[17] CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov.\n[18] Unique identifier: NCT01959971."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [16]\nExplanation: Evidence states: \"The increase in apo(a) FCR during alirocumab treatment suggests that increased LDL receptors may also play a role in the reduction of plasma Lp(a).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 603, "doc_id": 6540064, "label": "SUPPORTS", "evidence_sentence_ids": [16], "cited_doc_ids": [6540064], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Increased conversion of PGE 2 to PPARy ligand 15-ket-PGE 2 causes accumulation of PGE.\n\nDocument title: Pharmacological correction of a defect in PPARγ signaling ameliorates disease severity in Cftr-deficient mice\n\nAbstract sentences:\n[0] Cystic fibrosis is caused by mutations in the cystic fibrosis transmembrane conductance regulator (encoded by Cftr) that impair its role as an apical chloride channel that supports bicarbonate transport.\n[1] Individuals with cystic fibrosis show retained, thickened mucus that plugs airways and obstructs luminal organs as well as numerous other abnormalities that include inflammation of affected organs, alterations in lipid metabolism and insulin resistance.\n[2] Here we show that colonic epithelial cells and whole lung tissue from Cftr-deficient mice show a defect in peroxisome proliferator-activated receptor-gamma (PPAR-gamma, encoded by Pparg) function that contributes to a pathological program of gene expression.\n[3] Lipidomic analysis of colonic epithelial cells suggests that this defect results in part from reduced amounts of the endogenous PPAR-gamma ligand 15-keto-prostaglandin E(2) (15-keto-PGE(2)).\n[4] Treatment of Cftr-deficient mice with the synthetic PPAR-gamma ligand rosiglitazone partially normalizes the altered gene expression pattern associated with Cftr deficiency and reduces disease severity.\n[5] Rosiglitazone has no effect on chloride secretion in the colon, but it increases expression of the genes encoding carbonic anhydrases 4 and 2 (Car4 and Car2), increases bicarbonate secretion and reduces mucus retention.\n[6] These studies reveal a reversible defect in PPAR-gamma signaling in Cftr-deficient cells that can be pharmacologically corrected to ameliorate the severity of the cystic fibrosis phenotype in mice."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 606, "doc_id": 712078, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [712078], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Increased diastolic blood pressure (DBP) is associated with abdominal aortic aneurysm.\n\nDocument title: Blood pressure and incidence of twelve cardiovascular diseases: lifetime risks, healthy life-years lost, and age-specific associations in 1·25 million people\n\nAbstract sentences:\n[0] BACKGROUND The associations of blood pressure with the different manifestations of incident cardiovascular disease in a contemporary population have not been compared.\n[1] In this study, we aimed to analyse the associations of blood pressure with 12 different presentations of cardiovascular disease.\n[2] METHODS We used linked electronic health records from 1997 to 2010 in the CALIBER (CArdiovascular research using LInked Bespoke studies and Electronic health Records) programme to assemble a cohort of 1·25 million patients, 30 years of age or older and initially free from cardiovascular disease, a fifth of whom received blood pressure-lowering treatments.\n[3] We studied the heterogeneity in the age-specific associations of clinically measured blood pressure with 12 acute and chronic cardiovascular diseases, and estimated the lifetime risks (up to 95 years of age) and cardiovascular disease-free life-years lost adjusted for other risk factors at index ages 30, 60, and 80 years.\n[4] This study is registered at ClinicalTrials.gov, number NCT01164371.\n[5] FINDINGS During 5·2 years median follow-up, we recorded 83,098 initial cardiovascular disease presentations.\n[6] In each age group, the lowest risk for cardiovascular disease was in people with systolic blood pressure of 90-114 mm Hg and diastolic blood pressure of 60-74 mm Hg, with no evidence of a J-shaped increased risk at lower blood pressures.\n[7] The effect of high blood pressure varied by cardiovascular disease endpoint, from strongly positive to no effect.\n[8] Associations with high systolic blood pressure were strongest for intracerebral haemorrhage (hazard ratio 1·44 [95% CI 1·32-1·58]), subarachnoid haemorrhage (1·43 [1·25-1·63]), and stable angina (1·41 [1·36-1·46]), and weakest for abdominal aortic aneurysm (1·08 [1·00-1·17]).\n[9] Compared with diastolic blood pressure, raised systolic blood pressure had a greater effect on angina, myocardial infarction, and peripheral arterial disease, whereas raised diastolic blood pressure had a greater effect on abdominal aortic aneurysm than did raised systolic pressure.\n[10] Pulse pressure associations were inverse for abdominal aortic aneurysm (HR per 10 mm Hg 0·91 [95% CI 0·86-0·98]) and strongest for peripheral arterial disease (1·23 [1·20-1·27]).\n[11] People with hypertension (blood pressure ≥140/90 mm Hg or those receiving blood pressure-lowering drugs) had a lifetime risk of overall cardiovascular disease at 30 years of age of 63·3% (95% CI 62·9-63·8) compared with 46·1% (45·5-46·8) for those with normal blood pressure, and developed cardiovascular disease 5·0 years earlier (95% CI 4·8-5·2).\n[12] Stable and unstable angina accounted for most (43%) of the cardiovascular disease-free years of life lost associated with hypertension from index age 30 years, whereas heart failure and stable angina accounted for the largest proportion (19% each) of years of life lost from index age 80 years.\n[13] INTERPRETATION The widely held assumptions that blood pressure has strong associations with the occurrence of all cardiovascular diseases across a wide age range, and that diastolic and systolic associations are concordant, are not supported by the findings of this high-resolution study.\n[14] Despite modern treatments, the lifetime burden of hypertension is substantial.\n[15] These findings emphasise the need for new blood pressure-lowering strategies, and will help to inform the design of randomised trials to assess them.\n[16] FUNDING Medical Research Council, National Institute for Health Research, and Wellcome Trust."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Compared with diastolic blood pressure, raised systolic blood pressure had a greater effect on angina, myocardial infarction, and peripheral arterial disease, whereas raised diastolic blood pressure had a greater effect on abdominal aortic aneurysm than did raised systolic pressure.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 607, "doc_id": 4506414, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [4506414], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Increased flux of microbial products provokes immune responses.\n\nDocument title: Compromised intestinal epithelial barrier induces adaptive immune compensation that protects from colitis.\n\nAbstract sentences:\n[0] Mice lacking junctional adhesion molecule A (JAM-A, encoded by F11r) exhibit enhanced intestinal epithelial permeability, bacterial translocation, and elevated colonic lymphocyte numbers, yet do not develop colitis.\n[1] To investigate the contribution of adaptive immune compensation in response to increased intestinal epithelial permeability, we examined the susceptibility of F11r(-/-)Rag1(-/-) mice to acute colitis.\n[2] Although negligible contributions of adaptive immunity in F11r(+/+)Rag1(-/-) mice were observed, F11r(-/-)Rag1(-/-) mice exhibited increased microflora-dependent colitis.\n[3] Elimination of T cell subsets and cytokine analyses revealed a protective role for TGF-β-producing CD4(+) T cells in F11r(-/-) mice.\n[4] Additionally, loss of JAM-A resulted in elevated mucosal and serum IgA that was dependent upon CD4(+) T cells and TGF-β.\n[5] Absence of IgA in F11r(+/+)Igha(-/-) mice did not affect disease, whereas F11r(-/-)Igha(-/-) mice displayed markedly increased susceptibility to acute injury-induced colitis.\n[6] These data establish a role for adaptive immune-mediated protection from acute colitis under conditions of intestinal epithelial barrier compromise."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 609, "doc_id": 40096222, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [40096222], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Increased flux of microbial products suppresses immune responses.\n\nDocument title: Compromised intestinal epithelial barrier induces adaptive immune compensation that protects from colitis.\n\nAbstract sentences:\n[0] Mice lacking junctional adhesion molecule A (JAM-A, encoded by F11r) exhibit enhanced intestinal epithelial permeability, bacterial translocation, and elevated colonic lymphocyte numbers, yet do not develop colitis.\n[1] To investigate the contribution of adaptive immune compensation in response to increased intestinal epithelial permeability, we examined the susceptibility of F11r(-/-)Rag1(-/-) mice to acute colitis.\n[2] Although negligible contributions of adaptive immunity in F11r(+/+)Rag1(-/-) mice were observed, F11r(-/-)Rag1(-/-) mice exhibited increased microflora-dependent colitis.\n[3] Elimination of T cell subsets and cytokine analyses revealed a protective role for TGF-β-producing CD4(+) T cells in F11r(-/-) mice.\n[4] Additionally, loss of JAM-A resulted in elevated mucosal and serum IgA that was dependent upon CD4(+) T cells and TGF-β.\n[5] Absence of IgA in F11r(+/+)Igha(-/-) mice did not affect disease, whereas F11r(-/-)Igha(-/-) mice displayed markedly increased susceptibility to acute injury-induced colitis.\n[6] These data establish a role for adaptive immune-mediated protection from acute colitis under conditions of intestinal epithelial barrier compromise."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 610, "doc_id": 40096222, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [40096222], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Increased lipolysis leads to higher P38 phosphorylation in adipose tissue.\n\nDocument title: Activation of AMPKα2 in adipocytes is essential for nicotine-induced insulin resistance in vivo\n\nAbstract sentences:\n[0] Cigarette smoking promotes body weight reduction in humans while paradoxically also promoting insulin resistance (IR) and hyperinsulinemia.\n[1] However, the mechanisms behind these effects are unclear.\n[2] Here we show that nicotine, a major constituent of cigarette smoke, selectively activates AMP-activated protein kinase α2 (AMPKα2) in adipocytes, which in turn phosphorylates MAP kinase phosphatase-1 (MKP1) at serine 334, initiating its proteasome-dependent degradation.\n[3] The nicotine-dependent reduction of MKP1 induces the aberrant activation of both p38 mitogen-activated protein kinase and c-Jun N-terminal kinase, leading to increased phosphorylation of insulin receptor substrate 1 (IRS1) at serine 307.\n[4] Phosphorylation of IRS1 leads to its degradation, protein kinase B inhibition, and the loss of insulin-mediated inhibition of lipolysis.\n[5] Consequently, nicotine increases lipolysis, which results in body weight reduction, but this increase also elevates the levels of circulating free fatty acids and thus causes IR in insulin-sensitive tissues.\n[6] These results establish AMPKα2 as an essential mediator of nicotine-induced whole-body IR in spite of reductions in adiposity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 611, "doc_id": 32408470, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [32408470], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Increased microtubule acetylation exacerbates LRRK2 Roc-COR domain mutation induced locomotor deficits.\n\nDocument title: Increasing microtubule acetylation rescues axonal transport and locomotor deficits caused by LRRK2 Roc-COR domain mutations\n\nAbstract sentences:\n[0] Leucine-rich repeat kinase 2 (LRRK2) mutations are the most common genetic cause of Parkinson's disease.\n[1] LRRK2 is a multifunctional protein affecting many cellular processes and has been described to bind microtubules.\n[2] Defective microtubule-based axonal transport is hypothesized to contribute to Parkinson's disease, but whether LRRK2 mutations affect this process to mediate pathogenesis is not known.\n[3] Here we find that LRRK2 containing pathogenic Roc-COR domain mutations (R1441C, Y1699C) preferentially associates with deacetylated microtubules, and inhibits axonal transport in primary neurons and in Drosophila, causing locomotor deficits in vivo.\n[4] In vitro, increasing microtubule acetylation using deacetylase inhibitors or the tubulin acetylase αTAT1 prevents association of mutant LRRK2 with microtubules, and the deacetylase inhibitor trichostatin A (TSA) restores axonal transport.\n[5] In vivo knockdown of the deacetylases HDAC6 and Sirt2, or administration of TSA rescues both axonal transport and locomotor behavior.\n[6] Thus, this study reveals a pathogenic mechanism and a potential intervention for Parkinson's disease."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"In vitro, increasing microtubule acetylation using deacetylase inhibitors or the tubulin acetylase αTAT1 prevents association of mutant LRRK2 with microtubules, and the deacetylase inhibitor trichostatin A (TSA) restores axonal transport.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 612, "doc_id": 9638032, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [9638032], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Increased microtubule acetylation repairs interference of axonal transport caused by LRRK2 Roc-COR domain mutations.\n\nDocument title: Increasing microtubule acetylation rescues axonal transport and locomotor deficits caused by LRRK2 Roc-COR domain mutations\n\nAbstract sentences:\n[0] Leucine-rich repeat kinase 2 (LRRK2) mutations are the most common genetic cause of Parkinson's disease.\n[1] LRRK2 is a multifunctional protein affecting many cellular processes and has been described to bind microtubules.\n[2] Defective microtubule-based axonal transport is hypothesized to contribute to Parkinson's disease, but whether LRRK2 mutations affect this process to mediate pathogenesis is not known.\n[3] Here we find that LRRK2 containing pathogenic Roc-COR domain mutations (R1441C, Y1699C) preferentially associates with deacetylated microtubules, and inhibits axonal transport in primary neurons and in Drosophila, causing locomotor deficits in vivo.\n[4] In vitro, increasing microtubule acetylation using deacetylase inhibitors or the tubulin acetylase αTAT1 prevents association of mutant LRRK2 with microtubules, and the deacetylase inhibitor trichostatin A (TSA) restores axonal transport.\n[5] In vivo knockdown of the deacetylases HDAC6 and Sirt2, or administration of TSA rescues both axonal transport and locomotor behavior.\n[6] Thus, this study reveals a pathogenic mechanism and a potential intervention for Parkinson's disease."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"In vitro, increasing microtubule acetylation using deacetylase inhibitors or the tubulin acetylase αTAT1 prevents association of mutant LRRK2 with microtubules, and the deacetylase inhibitor trichostatin A (TSA) restores axonal transport.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 614, "doc_id": 9638032, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [9638032], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Increased microtubule acetylation repairs interference of axonal transport caused by LRRK2 Roc-COR domain mutations.\n\nDocument title: Increasing microtubule acetylation rescues axonal transport and locomotor deficits caused by LRRK2 Roc-COR domain mutations\n\nAbstract sentences:\n[0] Leucine-rich repeat kinase 2 (LRRK2) mutations are the most common genetic cause of Parkinson's disease.\n[1] LRRK2 is a multifunctional protein affecting many cellular processes and has been described to bind microtubules.\n[2] Defective microtubule-based axonal transport is hypothesized to contribute to Parkinson's disease, but whether LRRK2 mutations affect this process to mediate pathogenesis is not known.\n[3] Here we find that LRRK2 containing pathogenic Roc-COR domain mutations (R1441C, Y1699C) preferentially associates with deacetylated microtubules, and inhibits axonal transport in primary neurons and in Drosophila, causing locomotor deficits in vivo.\n[4] In vitro, increasing microtubule acetylation using deacetylase inhibitors or the tubulin acetylase αTAT1 prevents association of mutant LRRK2 with microtubules, and the deacetylase inhibitor trichostatin A (TSA) restores axonal transport.\n[5] In vivo knockdown of the deacetylases HDAC6 and Sirt2, or administration of TSA rescues both axonal transport and locomotor behavior.\n[6] Thus, this study reveals a pathogenic mechanism and a potential intervention for Parkinson's disease."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"In vivo knockdown of the deacetylases HDAC6 and Sirt2, or administration of TSA rescues both axonal transport and locomotor behavior.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 614, "doc_id": 9638032, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [9638032], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Increased microtubule acetylation worsens interference of axonal transport caused by LRRK2 Roc-COR domain mutations.\n\nDocument title: Increasing microtubule acetylation rescues axonal transport and locomotor deficits caused by LRRK2 Roc-COR domain mutations\n\nAbstract sentences:\n[0] Leucine-rich repeat kinase 2 (LRRK2) mutations are the most common genetic cause of Parkinson's disease.\n[1] LRRK2 is a multifunctional protein affecting many cellular processes and has been described to bind microtubules.\n[2] Defective microtubule-based axonal transport is hypothesized to contribute to Parkinson's disease, but whether LRRK2 mutations affect this process to mediate pathogenesis is not known.\n[3] Here we find that LRRK2 containing pathogenic Roc-COR domain mutations (R1441C, Y1699C) preferentially associates with deacetylated microtubules, and inhibits axonal transport in primary neurons and in Drosophila, causing locomotor deficits in vivo.\n[4] In vitro, increasing microtubule acetylation using deacetylase inhibitors or the tubulin acetylase αTAT1 prevents association of mutant LRRK2 with microtubules, and the deacetylase inhibitor trichostatin A (TSA) restores axonal transport.\n[5] In vivo knockdown of the deacetylases HDAC6 and Sirt2, or administration of TSA rescues both axonal transport and locomotor behavior.\n[6] Thus, this study reveals a pathogenic mechanism and a potential intervention for Parkinson's disease."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"In vitro, increasing microtubule acetylation using deacetylase inhibitors or the tubulin acetylase αTAT1 prevents association of mutant LRRK2 with microtubules, and the deacetylase inhibitor trichostatin A (TSA) restores axonal transport.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 615, "doc_id": 9638032, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [9638032], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Increased microtubule acetylation worsens interference of axonal transport caused by LRRK2 Roc-COR domain mutations.\n\nDocument title: Increasing microtubule acetylation rescues axonal transport and locomotor deficits caused by LRRK2 Roc-COR domain mutations\n\nAbstract sentences:\n[0] Leucine-rich repeat kinase 2 (LRRK2) mutations are the most common genetic cause of Parkinson's disease.\n[1] LRRK2 is a multifunctional protein affecting many cellular processes and has been described to bind microtubules.\n[2] Defective microtubule-based axonal transport is hypothesized to contribute to Parkinson's disease, but whether LRRK2 mutations affect this process to mediate pathogenesis is not known.\n[3] Here we find that LRRK2 containing pathogenic Roc-COR domain mutations (R1441C, Y1699C) preferentially associates with deacetylated microtubules, and inhibits axonal transport in primary neurons and in Drosophila, causing locomotor deficits in vivo.\n[4] In vitro, increasing microtubule acetylation using deacetylase inhibitors or the tubulin acetylase αTAT1 prevents association of mutant LRRK2 with microtubules, and the deacetylase inhibitor trichostatin A (TSA) restores axonal transport.\n[5] In vivo knockdown of the deacetylases HDAC6 and Sirt2, or administration of TSA rescues both axonal transport and locomotor behavior.\n[6] Thus, this study reveals a pathogenic mechanism and a potential intervention for Parkinson's disease."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"In vivo knockdown of the deacetylases HDAC6 and Sirt2, or administration of TSA rescues both axonal transport and locomotor behavior.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 615, "doc_id": 9638032, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [9638032], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Increased mobility of retrotransposons does not lead to mutation and higher tumorigenesis rates.\n\nDocument title: The DNA Methylome of Human Peripheral Blood Mononuclear Cells\n\nAbstract sentences:\n[0] DNA methylation plays an important role in biological processes in human health and disease.\n[1] Recent technological advances allow unbiased whole-genome DNA methylation (methylome) analysis to be carried out on human cells.\n[2] Using whole-genome bisulfite sequencing at 24.7-fold coverage (12.3-fold per strand), we report a comprehensive (92.62%) methylome and analysis of the unique sequences in human peripheral blood mononuclear cells (PBMC) from the same Asian individual whose genome was deciphered in the YH project.\n[3] PBMC constitute an important source for clinical blood tests world-wide.\n[4] We found that 68.4% of CpG sites and <0.2% of non-CpG sites were methylated, demonstrating that non-CpG cytosine methylation is minor in human PBMC.\n[5] Analysis of the PBMC methylome revealed a rich epigenomic landscape for 20 distinct genomic features, including regulatory, protein-coding, non-coding, RNA-coding, and repeat sequences.\n[6] Integration of our methylome data with the YH genome sequence enabled a first comprehensive assessment of allele-specific methylation (ASM) between the two haploid methylomes of any individual and allowed the identification of 599 haploid differentially methylated regions (hDMRs) covering 287 genes.\n[7] Of these, 76 genes had hDMRs within 2 kb of their transcriptional start sites of which >80% displayed allele-specific expression (ASE).\n[8] These data demonstrate that ASM is a recurrent phenomenon and is highly correlated with ASE in human PBMCs.\n[9] Together with recently reported similar studies, our study provides a comprehensive resource for future epigenomic research and confirms new sequencing technology as a paradigm for large-scale epigenomics studies."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 616, "doc_id": 18670, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [18670], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Increased mobility of retrotransposons is assosciated with mutation and higher tumorigenesis rates.\n\nDocument title: The DNA Methylome of Human Peripheral Blood Mononuclear Cells\n\nAbstract sentences:\n[0] DNA methylation plays an important role in biological processes in human health and disease.\n[1] Recent technological advances allow unbiased whole-genome DNA methylation (methylome) analysis to be carried out on human cells.\n[2] Using whole-genome bisulfite sequencing at 24.7-fold coverage (12.3-fold per strand), we report a comprehensive (92.62%) methylome and analysis of the unique sequences in human peripheral blood mononuclear cells (PBMC) from the same Asian individual whose genome was deciphered in the YH project.\n[3] PBMC constitute an important source for clinical blood tests world-wide.\n[4] We found that 68.4% of CpG sites and <0.2% of non-CpG sites were methylated, demonstrating that non-CpG cytosine methylation is minor in human PBMC.\n[5] Analysis of the PBMC methylome revealed a rich epigenomic landscape for 20 distinct genomic features, including regulatory, protein-coding, non-coding, RNA-coding, and repeat sequences.\n[6] Integration of our methylome data with the YH genome sequence enabled a first comprehensive assessment of allele-specific methylation (ASM) between the two haploid methylomes of any individual and allowed the identification of 599 haploid differentially methylated regions (hDMRs) covering 287 genes.\n[7] Of these, 76 genes had hDMRs within 2 kb of their transcriptional start sites of which >80% displayed allele-specific expression (ASE).\n[8] These data demonstrate that ASM is a recurrent phenomenon and is highly correlated with ASE in human PBMCs.\n[9] Together with recently reported similar studies, our study provides a comprehensive resource for future epigenomic research and confirms new sequencing technology as a paradigm for large-scale epigenomics studies."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 617, "doc_id": 18670, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [18670], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Increased purity of cytoplasmic membranes isolated from overexpressors is indicated by stronger spots for OmpF in 2D BN-PAGE gels.\n\nDocument title: Identification of a Multicomponent Complex Required for Outer Membrane Biogenesis in Escherichia coli\n\nAbstract sentences:\n[0] Gram-negative bacteria have an outer membrane (OM) that functions as a barrier to protect the cell from toxic compounds such as antibiotics and detergents.\n[1] The OM is a highly asymmetric bilayer composed of phospholipids, glycolipids, and proteins.\n[2] Assembly of this essential organelle occurs outside the cytoplasm in an environment that lacks obvious energy sources such as ATP, and the mechanisms involved are poorly understood.\n[3] We describe the identification of a multiprotein complex required for the assembly of proteins in the OM of Escherichia coli.\n[4] We also demonstrate genetic interactions between genes encoding components of this protein assembly complex and imp, which encodes a protein involved in the assembly of lipopolysaccharides (LPS) in the OM.\n[5] These genetic interactions suggest a role for YfgL, one of the lipoprotein components of the protein assembly complex, in a homeostatic control mechanism that coordinates the overall OM assembly process."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 618, "doc_id": 6836086, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [6836086], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Increased vessel density along with a reduction in fibrosis improves the efficacy of chemotherapy treatments.\n\nDocument title: Hyaluronan impairs vascular function and drug delivery in a mouse model of pancreatic cancer\n\nAbstract sentences:\n[0] OBJECTIVE Pancreatic ductal adenocarcinoma (PDA) is characterised by stromal desmoplasia and vascular dysfunction, which critically impair drug delivery.\n[1] This study examines the role of an abundant extracellular matrix component, the megadalton glycosaminoglycan hyaluronan (HA), as a novel therapeutic target in PDA.\n[2] METHODS Using a genetically engineered mouse model of PDA, the authors enzymatically depleted HA by a clinically formulated PEGylated human recombinant PH20 hyaluronidase (PEGPH20) and examined tumour perfusion, vascular permeability and drug delivery.\n[3] The preclinical utility of PEGPH20 in combination with gemcitabine was assessed by short-term and survival studies.\n[4] RESULTS PEGPH20 rapidly and sustainably depleted HA, inducing the re-expansion of PDA blood vessels and increasing the intratumoral delivery of two chemotherapeutic agents, doxorubicin and gemcitabine.\n[5] Moreover, PEGPH20 triggered fenestrations and interendothelial junctional gaps in PDA tumour endothelia and promoted a tumour-specific increase in macromolecular permeability.\n[6] Finally, combination therapy with PEGPH20 and gemcitabine led to inhibition of PDA tumour growth and prolonged survival over gemcitabine monotherapy, suggesting immediate clinical utility.\n[7] CONCLUSIONS The authors demonstrate that HA impedes the intratumoral vasculature in PDA and propose that its enzymatic depletion be explored as a means to improve drug delivery and response in patients with pancreatic cancer."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 620, "doc_id": 2565138, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [2565138], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Individuals with Alzheimers who participate in six months of physical activity improve cognitive function for up to 18 months.\n\nDocument title: Effect of physical activity on cognitive function in older adults at risk for Alzheimer disease: a randomized trial.\n\nAbstract sentences:\n[0] CONTEXT Many observational studies have shown that physical activity reduces the risk of cognitive decline; however, evidence from randomized trials is lacking.\n[1] OBJECTIVE To determine whether physical activity reduces the rate of cognitive decline among older adults at risk.\n[2] DESIGN AND SETTING Randomized controlled trial of a 24-week physical activity intervention conducted between 2004 and 2007 in metropolitan Perth, Western Australia.\n[3] Assessors of cognitive function were blinded to group membership.\n[4] PARTICIPANTS We recruited volunteers who reported memory problems but did not meet criteria for dementia.\n[5] Three hundred eleven individuals aged 50 years or older were screened for eligibility, 89 were not eligible, and 52 refused to participate.\n[6] A total of 170 participants were randomized and 138 participants completed the 18-month assessment.\n[7] INTERVENTION Participants were randomly allocated to an education and usual care group or to a 24-week home-based program of physical activity.\n[8] MAIN OUTCOME MEASURE Change in Alzheimer Disease Assessment Scale-Cognitive Subscale (ADAS-Cog) scores (possible range, 0-70) over 18 months.\n[9] RESULTS In an intent-to-treat analysis, participants in the intervention group improved 0.26 points (95% confidence interval, -0.89 to 0.54) and those in the usual care group deteriorated 1.04 points (95% confidence interval, 0.32 to 1.82) on the ADAS-Cog at the end of the intervention.\n[10] The absolute difference of the outcome measure between the intervention and control groups was -1.3 points (95% confidence interval,-2.38 to -0.22) at the end of the intervention.\n[11] At 18 months, participants in the intervention group improved 0.73 points (95% confidence interval, -1.27 to 0.03) on the ADAS-Cog, and those in the usual care group improved 0.04 points (95% confidence interval, -0.46 to 0.88).\n[12] Word list delayed recall and Clinical Dementia Rating sum of boxes improved modestly as well, whereas word list total immediate recall, digit symbol coding, verbal fluency, Beck depression score, and Medical Outcomes 36-Item Short-Form physical and mental component summaries did not change significantly.\n[13] CONCLUSIONS In this study of adults with subjective memory impairment, a 6-month program of physical activity provided a modest improvement in cognition over an 18-month follow-up period.\n[14] TRIAL REGISTRATION anzctr.org.au Identifier: ACTRN12605000136606."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"RESULTS In an intent-to-treat analysis, participants in the intervention group improved 0.26 points (95% confidence interval, -0.89 to 0.54) and those in the usual care group deteriorated 1.04 points (95% confidence interval, 0.32 to 1.82) on the ADAS-Cog at the end of the intervention.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 621, "doc_id": 1642727, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [1642727], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Individuals with Alzheimers who participate in six months of physical activity improve cognitive function for up to 18 months.\n\nDocument title: Effect of physical activity on cognitive function in older adults at risk for Alzheimer disease: a randomized trial.\n\nAbstract sentences:\n[0] CONTEXT Many observational studies have shown that physical activity reduces the risk of cognitive decline; however, evidence from randomized trials is lacking.\n[1] OBJECTIVE To determine whether physical activity reduces the rate of cognitive decline among older adults at risk.\n[2] DESIGN AND SETTING Randomized controlled trial of a 24-week physical activity intervention conducted between 2004 and 2007 in metropolitan Perth, Western Australia.\n[3] Assessors of cognitive function were blinded to group membership.\n[4] PARTICIPANTS We recruited volunteers who reported memory problems but did not meet criteria for dementia.\n[5] Three hundred eleven individuals aged 50 years or older were screened for eligibility, 89 were not eligible, and 52 refused to participate.\n[6] A total of 170 participants were randomized and 138 participants completed the 18-month assessment.\n[7] INTERVENTION Participants were randomly allocated to an education and usual care group or to a 24-week home-based program of physical activity.\n[8] MAIN OUTCOME MEASURE Change in Alzheimer Disease Assessment Scale-Cognitive Subscale (ADAS-Cog) scores (possible range, 0-70) over 18 months.\n[9] RESULTS In an intent-to-treat analysis, participants in the intervention group improved 0.26 points (95% confidence interval, -0.89 to 0.54) and those in the usual care group deteriorated 1.04 points (95% confidence interval, 0.32 to 1.82) on the ADAS-Cog at the end of the intervention.\n[10] The absolute difference of the outcome measure between the intervention and control groups was -1.3 points (95% confidence interval,-2.38 to -0.22) at the end of the intervention.\n[11] At 18 months, participants in the intervention group improved 0.73 points (95% confidence interval, -1.27 to 0.03) on the ADAS-Cog, and those in the usual care group improved 0.04 points (95% confidence interval, -0.46 to 0.88).\n[12] Word list delayed recall and Clinical Dementia Rating sum of boxes improved modestly as well, whereas word list total immediate recall, digit symbol coding, verbal fluency, Beck depression score, and Medical Outcomes 36-Item Short-Form physical and mental component summaries did not change significantly.\n[13] CONCLUSIONS In this study of adults with subjective memory impairment, a 6-month program of physical activity provided a modest improvement in cognition over an 18-month follow-up period.\n[14] TRIAL REGISTRATION anzctr.org.au Identifier: ACTRN12605000136606."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"CONCLUSIONS In this study of adults with subjective memory impairment, a 6-month program of physical activity provided a modest improvement in cognition over an 18-month follow-up period.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 621, "doc_id": 1642727, "label": "SUPPORTS", "evidence_sentence_ids": [13], "cited_doc_ids": [1642727], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Individuals with low serum vitamin D concentrations have decreased risk of multiple sclerosis.\n\nDocument title: Past exposure to sun, skin phenotype, and risk of multiple sclerosis: case-control study.\n\nAbstract sentences:\n[0] OBJECTIVE To examine whether past high sun exposure is associated with a reduced risk of multiple sclerosis.\n[1] DESIGN Population based case-control study.\n[2] SETTING Tasmania, latitudes 41-3 degrees S.   PARTICIPANTS 136 cases with multiple sclerosis and 272 controls randomly drawn from the community and matched on sex and year of birth.\n[3] MAIN OUTCOME MEASURE Multiple sclerosis defined by both clinical and magnetic resonance imaging criteria.\n[4] RESULTS Higher sun exposure when aged 6-15 years (average 2-3 hours or more a day in summer during weekends and holidays) was associated with a decreased risk of multiple sclerosis (adjusted odds ratio 0.31, 95% confidence interval 0.16 to 0.59).\n[5] Higher exposure in winter seemed more important than higher exposure in summer.\n[6] Greater actinic damage was also independently associated with a decreased risk of multiple sclerosis (0.32, 0.11 to 0.88 for grades 4-6 disease).\n[7] A dose-response relation was observed between multiple sclerosis and decreasing sun exposure when aged 6-15 years and with actinic damage.\n[8] CONCLUSION Higher sun exposure during childhood and early adolescence is associated with a reduced risk of multiple sclerosis.\n[9] Insufficient ultraviolet radiation may therefore influence the development of multiple sclerosis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 622, "doc_id": 17000834, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [17000834], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Induced hepatic stem cells possess the potential to differentiate into cholangiocytic cells.\n\nDocument title: Reprogramming fibroblasts into bipotential hepatic stem cells by defined factors.\n\nAbstract sentences:\n[0] Recent studies have demonstrated direct reprogramming of fibroblasts into a range of somatic cell types, but to date stem or progenitor cells have only been reprogrammed for the blood and neuronal lineages.\n[1] We previously reported generation of induced hepatocyte-like (iHep) cells by transduction of Gata4, Hnf1α, and Foxa3 in p19 Arf null mouse embryonic fibroblasts (MEFs).\n[2] Here, we show that Hnf1β and Foxa3, liver organogenesis transcription factors, are sufficient to reprogram MEFs into induced hepatic stem cells (iHepSCs).\n[3] iHepSCs can be stably expanded in vitro and possess the potential of bidirectional differentiation into both hepatocytic and cholangiocytic lineages.\n[4] In the injured liver of fumarylacetoacetate hydrolase (Fah)-deficient mice, repopulating iHepSCs become hepatocyte-like cells.\n[5] They also engraft as cholangiocytes into bile ducts of mice with DDC-induced bile ductular injury.\n[6] Lineage conversion into bipotential expandable iHepSCs provides a strategy to enable efficient derivation of both hepatocytes and cholangiocytes for use in disease modeling and tissue engineering."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"iHepSCs can be stably expanded in vitro and possess the potential of bidirectional differentiation into both hepatocytic and cholangiocytic lineages.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 624, "doc_id": 20033112, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [20033112], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Induced hepatic stem cells possess the potential to differentiate into cholangiocytic cells.\n\nDocument title: Reprogramming fibroblasts into bipotential hepatic stem cells by defined factors.\n\nAbstract sentences:\n[0] Recent studies have demonstrated direct reprogramming of fibroblasts into a range of somatic cell types, but to date stem or progenitor cells have only been reprogrammed for the blood and neuronal lineages.\n[1] We previously reported generation of induced hepatocyte-like (iHep) cells by transduction of Gata4, Hnf1α, and Foxa3 in p19 Arf null mouse embryonic fibroblasts (MEFs).\n[2] Here, we show that Hnf1β and Foxa3, liver organogenesis transcription factors, are sufficient to reprogram MEFs into induced hepatic stem cells (iHepSCs).\n[3] iHepSCs can be stably expanded in vitro and possess the potential of bidirectional differentiation into both hepatocytic and cholangiocytic lineages.\n[4] In the injured liver of fumarylacetoacetate hydrolase (Fah)-deficient mice, repopulating iHepSCs become hepatocyte-like cells.\n[5] They also engraft as cholangiocytes into bile ducts of mice with DDC-induced bile ductular injury.\n[6] Lineage conversion into bipotential expandable iHepSCs provides a strategy to enable efficient derivation of both hepatocytes and cholangiocytes for use in disease modeling and tissue engineering."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Lineage conversion into bipotential expandable iHepSCs provides a strategy to enable efficient derivation of both hepatocytes and cholangiocytes for use in disease modeling and tissue engineering.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 624, "doc_id": 20033112, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [20033112], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Induced hepatic stem cells possess the potential to differentiate into hepatocytic cells.\n\nDocument title: Reprogramming fibroblasts into bipotential hepatic stem cells by defined factors.\n\nAbstract sentences:\n[0] Recent studies have demonstrated direct reprogramming of fibroblasts into a range of somatic cell types, but to date stem or progenitor cells have only been reprogrammed for the blood and neuronal lineages.\n[1] We previously reported generation of induced hepatocyte-like (iHep) cells by transduction of Gata4, Hnf1α, and Foxa3 in p19 Arf null mouse embryonic fibroblasts (MEFs).\n[2] Here, we show that Hnf1β and Foxa3, liver organogenesis transcription factors, are sufficient to reprogram MEFs into induced hepatic stem cells (iHepSCs).\n[3] iHepSCs can be stably expanded in vitro and possess the potential of bidirectional differentiation into both hepatocytic and cholangiocytic lineages.\n[4] In the injured liver of fumarylacetoacetate hydrolase (Fah)-deficient mice, repopulating iHepSCs become hepatocyte-like cells.\n[5] They also engraft as cholangiocytes into bile ducts of mice with DDC-induced bile ductular injury.\n[6] Lineage conversion into bipotential expandable iHepSCs provides a strategy to enable efficient derivation of both hepatocytes and cholangiocytes for use in disease modeling and tissue engineering."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"iHepSCs can be stably expanded in vitro and possess the potential of bidirectional differentiation into both hepatocytic and cholangiocytic lineages.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 625, "doc_id": 20033112, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [20033112], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Induction of urokinase receptor signaling in podocytes causes foot process effacement and proteinuria.\n\nDocument title: Modification of kidney barrier function by the urokinase receptor\n\nAbstract sentences:\n[0] Podocyte dysfunction, represented by foot process effacement and proteinuria, is often the starting point for progressive kidney disease.\n[1] Therapies aimed at the cellular level of the disease are currently not available.\n[2] Here we show that induction of urokinase receptor (uPAR) signaling in podocytes leads to foot process effacement and urinary protein loss via a mechanism that includes lipid-dependent activation of αvβ3 integrin.\n[3] Mice lacking uPAR (Plaur−/−) are protected from lipopolysaccharide (LPS)-mediated proteinuria but develop disease after expression of a constitutively active β3 integrin.\n[4] Gene transfer studies reveal a prerequisite for uPAR expression in podocytes, but not in endothelial cells, for the development of LPS-mediated proteinuria.\n[5] Mechanistically, uPAR is required to activate αvβ3 integrin in podocytes, promoting cell motility and activation of the small GTPases Cdc42 and Rac1.\n[6] Blockade of αvβ3 integrin reduces podocyte motility in vitro and lowers proteinuria in mice.\n[7] Our findings show a physiological role for uPAR signaling in the regulation of kidney permeability."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here we show that induction of urokinase receptor (uPAR) signaling in podocytes leads to foot process effacement and urinary protein loss via a mechanism that includes lipid-dependent activation of αvβ3 integrin.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 626, "doc_id": 16355392, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [16355392], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Inhibiting HDAC6 increases survival of mice with ARID1A mutated tumors.\n\nDocument title: ARID1A-mutated ovarian cancers depend on HDAC6 activity\n\nAbstract sentences:\n[0] ARID1A, encoding a subunit of the SWI/SNF chromatin-remodelling complex, is the most frequently mutated epigenetic regulator across all human cancers.\n[1] ARID1A and TP53 mutations are typically mutually exclusive.\n[2] Therapeutic approaches that correlate with this genetic characteristic remain to be explored.\n[3] Here, we show that HDAC6 activity is essential in ARID1A-mutated ovarian cancers.\n[4] Inhibition of HDAC6 activity using a clinically applicable small-molecule inhibitor significantly improved the survival of mice bearing ARID1A-mutated tumours.\n[5] This correlated with the suppression of growth and dissemination of ARID1A-mutated, but not wild-type, tumours.\n[6] The dependence on HDAC6 activity in ARID1A-mutated cells correlated with a direct transcriptional repression of HDAC6 by ARID1A.\n[7] HDAC6 inhibition selectively promoted apoptosis of ARID1A-mutated cells.\n[8] HDAC6 directly deacetylates Lys120 of p53, a pro-apoptotic post-translational modification.\n[9] Thus, ARID1A mutation inactivates the apoptosis-promoting function of p53 by upregulating HDAC6.\n[10] Together, these results indicate that pharmacological inhibition of HDAC6 is a therapeutic strategy for ARID1A-mutated cancers."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Inhibition of HDAC6 activity using a clinically applicable small-molecule inhibitor significantly improved the survival of mice bearing ARID1A-mutated tumours.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 631, "doc_id": 5468807, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [5468807], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Inhibiting focal adhesion formation enables cells to convert mechanical strain into eventual scarring.\n\nDocument title: Focal adhesion kinase links mechanical force to skin fibrosis via inflammatory signaling\n\nAbstract sentences:\n[0] Exuberant fibroproliferation is a common complication after injury for reasons that are not well understood.\n[1] One key component of wound repair that is often overlooked is mechanical force, which regulates cell-matrix interactions through intracellular focal adhesion components, including focal adhesion kinase (FAK).\n[2] Here we report that FAK is activated after cutaneous injury and that this process is potentiated by mechanical loading.\n[3] Fibroblast-specific FAK knockout mice have substantially less inflammation and fibrosis than control mice in a model of hypertrophic scar formation.\n[4] We show that FAK acts through extracellular-related kinase (ERK) to mechanically trigger the secretion of monocyte chemoattractant protein-1 (MCP-1, also known as CCL2), a potent chemokine that is linked to human fibrotic disorders.\n[5] Similarly, MCP-1 knockout mice form minimal scars, indicating that inflammatory chemokine pathways are a major mechanism by which FAK mechanotransduction induces fibrosis.\n[6] Small-molecule inhibition of FAK blocks these effects in human cells and reduces scar formation in vivo through attenuated MCP-1 signaling and inflammatory cell recruitment.\n[7] These findings collectively indicate that physical force regulates fibrosis through inflammatory FAK–ERK–MCP-1 pathways and that molecular strategies targeting FAK can effectively uncouple mechanical force from pathologic scar formation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Fibroblast-specific FAK knockout mice have substantially less inflammation and fibrosis than control mice in a model of hypertrophic scar formation.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 632, "doc_id": 5172048, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [5172048], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Inhibiting focal adhesion formation enables cells to convert mechanical strain into eventual scarring.\n\nDocument title: Focal adhesion kinase links mechanical force to skin fibrosis via inflammatory signaling\n\nAbstract sentences:\n[0] Exuberant fibroproliferation is a common complication after injury for reasons that are not well understood.\n[1] One key component of wound repair that is often overlooked is mechanical force, which regulates cell-matrix interactions through intracellular focal adhesion components, including focal adhesion kinase (FAK).\n[2] Here we report that FAK is activated after cutaneous injury and that this process is potentiated by mechanical loading.\n[3] Fibroblast-specific FAK knockout mice have substantially less inflammation and fibrosis than control mice in a model of hypertrophic scar formation.\n[4] We show that FAK acts through extracellular-related kinase (ERK) to mechanically trigger the secretion of monocyte chemoattractant protein-1 (MCP-1, also known as CCL2), a potent chemokine that is linked to human fibrotic disorders.\n[5] Similarly, MCP-1 knockout mice form minimal scars, indicating that inflammatory chemokine pathways are a major mechanism by which FAK mechanotransduction induces fibrosis.\n[6] Small-molecule inhibition of FAK blocks these effects in human cells and reduces scar formation in vivo through attenuated MCP-1 signaling and inflammatory cell recruitment.\n[7] These findings collectively indicate that physical force regulates fibrosis through inflammatory FAK–ERK–MCP-1 pathways and that molecular strategies targeting FAK can effectively uncouple mechanical force from pathologic scar formation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Similarly, MCP-1 knockout mice form minimal scars, indicating that inflammatory chemokine pathways are a major mechanism by which FAK mechanotransduction induces fibrosis.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 632, "doc_id": 5172048, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [5172048], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Inhibiting focal adhesion formation enables cells to convert mechanical strain into eventual scarring.\n\nDocument title: Focal adhesion kinase links mechanical force to skin fibrosis via inflammatory signaling\n\nAbstract sentences:\n[0] Exuberant fibroproliferation is a common complication after injury for reasons that are not well understood.\n[1] One key component of wound repair that is often overlooked is mechanical force, which regulates cell-matrix interactions through intracellular focal adhesion components, including focal adhesion kinase (FAK).\n[2] Here we report that FAK is activated after cutaneous injury and that this process is potentiated by mechanical loading.\n[3] Fibroblast-specific FAK knockout mice have substantially less inflammation and fibrosis than control mice in a model of hypertrophic scar formation.\n[4] We show that FAK acts through extracellular-related kinase (ERK) to mechanically trigger the secretion of monocyte chemoattractant protein-1 (MCP-1, also known as CCL2), a potent chemokine that is linked to human fibrotic disorders.\n[5] Similarly, MCP-1 knockout mice form minimal scars, indicating that inflammatory chemokine pathways are a major mechanism by which FAK mechanotransduction induces fibrosis.\n[6] Small-molecule inhibition of FAK blocks these effects in human cells and reduces scar formation in vivo through attenuated MCP-1 signaling and inflammatory cell recruitment.\n[7] These findings collectively indicate that physical force regulates fibrosis through inflammatory FAK–ERK–MCP-1 pathways and that molecular strategies targeting FAK can effectively uncouple mechanical force from pathologic scar formation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Small-molecule inhibition of FAK blocks these effects in human cells and reduces scar formation in vivo through attenuated MCP-1 signaling and inflammatory cell recruitment.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 632, "doc_id": 5172048, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [5172048], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Inhibiting focal adhesion formation enables cells to convert mechanical strain into eventual scarring.\n\nDocument title: Focal adhesion kinase links mechanical force to skin fibrosis via inflammatory signaling\n\nAbstract sentences:\n[0] Exuberant fibroproliferation is a common complication after injury for reasons that are not well understood.\n[1] One key component of wound repair that is often overlooked is mechanical force, which regulates cell-matrix interactions through intracellular focal adhesion components, including focal adhesion kinase (FAK).\n[2] Here we report that FAK is activated after cutaneous injury and that this process is potentiated by mechanical loading.\n[3] Fibroblast-specific FAK knockout mice have substantially less inflammation and fibrosis than control mice in a model of hypertrophic scar formation.\n[4] We show that FAK acts through extracellular-related kinase (ERK) to mechanically trigger the secretion of monocyte chemoattractant protein-1 (MCP-1, also known as CCL2), a potent chemokine that is linked to human fibrotic disorders.\n[5] Similarly, MCP-1 knockout mice form minimal scars, indicating that inflammatory chemokine pathways are a major mechanism by which FAK mechanotransduction induces fibrosis.\n[6] Small-molecule inhibition of FAK blocks these effects in human cells and reduces scar formation in vivo through attenuated MCP-1 signaling and inflammatory cell recruitment.\n[7] These findings collectively indicate that physical force regulates fibrosis through inflammatory FAK–ERK–MCP-1 pathways and that molecular strategies targeting FAK can effectively uncouple mechanical force from pathologic scar formation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"These findings collectively indicate that physical force regulates fibrosis through inflammatory FAK–ERK–MCP-1 pathways and that molecular strategies targeting FAK can effectively uncouple mechanical force from pathologic scar formation.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 632, "doc_id": 5172048, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [5172048], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Inhibiting focal adhesion formation increases the rate at which cells convert mechanical strain into inflammation and fibrosis.\n\nDocument title: Focal adhesion kinase links mechanical force to skin fibrosis via inflammatory signaling\n\nAbstract sentences:\n[0] Exuberant fibroproliferation is a common complication after injury for reasons that are not well understood.\n[1] One key component of wound repair that is often overlooked is mechanical force, which regulates cell-matrix interactions through intracellular focal adhesion components, including focal adhesion kinase (FAK).\n[2] Here we report that FAK is activated after cutaneous injury and that this process is potentiated by mechanical loading.\n[3] Fibroblast-specific FAK knockout mice have substantially less inflammation and fibrosis than control mice in a model of hypertrophic scar formation.\n[4] We show that FAK acts through extracellular-related kinase (ERK) to mechanically trigger the secretion of monocyte chemoattractant protein-1 (MCP-1, also known as CCL2), a potent chemokine that is linked to human fibrotic disorders.\n[5] Similarly, MCP-1 knockout mice form minimal scars, indicating that inflammatory chemokine pathways are a major mechanism by which FAK mechanotransduction induces fibrosis.\n[6] Small-molecule inhibition of FAK blocks these effects in human cells and reduces scar formation in vivo through attenuated MCP-1 signaling and inflammatory cell recruitment.\n[7] These findings collectively indicate that physical force regulates fibrosis through inflammatory FAK–ERK–MCP-1 pathways and that molecular strategies targeting FAK can effectively uncouple mechanical force from pathologic scar formation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Fibroblast-specific FAK knockout mice have substantially less inflammation and fibrosis than control mice in a model of hypertrophic scar formation.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 633, "doc_id": 5172048, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [5172048], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Inhibiting focal adhesion formation increases the rate at which cells convert mechanical strain into inflammation and fibrosis.\n\nDocument title: Focal adhesion kinase links mechanical force to skin fibrosis via inflammatory signaling\n\nAbstract sentences:\n[0] Exuberant fibroproliferation is a common complication after injury for reasons that are not well understood.\n[1] One key component of wound repair that is often overlooked is mechanical force, which regulates cell-matrix interactions through intracellular focal adhesion components, including focal adhesion kinase (FAK).\n[2] Here we report that FAK is activated after cutaneous injury and that this process is potentiated by mechanical loading.\n[3] Fibroblast-specific FAK knockout mice have substantially less inflammation and fibrosis than control mice in a model of hypertrophic scar formation.\n[4] We show that FAK acts through extracellular-related kinase (ERK) to mechanically trigger the secretion of monocyte chemoattractant protein-1 (MCP-1, also known as CCL2), a potent chemokine that is linked to human fibrotic disorders.\n[5] Similarly, MCP-1 knockout mice form minimal scars, indicating that inflammatory chemokine pathways are a major mechanism by which FAK mechanotransduction induces fibrosis.\n[6] Small-molecule inhibition of FAK blocks these effects in human cells and reduces scar formation in vivo through attenuated MCP-1 signaling and inflammatory cell recruitment.\n[7] These findings collectively indicate that physical force regulates fibrosis through inflammatory FAK–ERK–MCP-1 pathways and that molecular strategies targeting FAK can effectively uncouple mechanical force from pathologic scar formation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"These findings collectively indicate that physical force regulates fibrosis through inflammatory FAK–ERK–MCP-1 pathways and that molecular strategies targeting FAK can effectively uncouple mechanical force from pathologic scar formation.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 633, "doc_id": 5172048, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [5172048], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Inhibiting glucose-6-phospate dehydrogenase improves lipogenesis by deactivating LKB1-AMPK signaling.\n\nDocument title: 6-phosphogluconate dehydrogenase links oxidative PPP, lipogenesis and tumor growth by inhibiting LKB1-AMPK signaling\n\nAbstract sentences:\n[0] The oxidative pentose phosphate pathway (PPP) contributes to tumour growth, but the precise contribution of 6-phosphogluconate dehydrogenase (6PGD), the third enzyme in this pathway, to tumorigenesis remains unclear.\n[1] We found that suppression of 6PGD decreased lipogenesis and RNA biosynthesis and elevated ROS levels in cancer cells, attenuating cell proliferation and tumour growth.\n[2] 6PGD-mediated production of ribulose-5-phosphate (Ru-5-P) inhibits AMPK activation by disrupting the active LKB1 complex, thereby activating acetyl-CoA carboxylase 1 and lipogenesis.\n[3] Ru-5-P and NADPH are thought to be precursors in RNA biosynthesis and lipogenesis, respectively; thus, our findings provide an additional link between the oxidative PPP and lipogenesis through Ru-5-P-dependent inhibition of LKB1-AMPK signalling.\n[4] Moreover, we identified and developed 6PGD inhibitors, physcion and its derivative S3, that effectively inhibited 6PGD, cancer cell proliferation and tumour growth in nude mice xenografts without obvious toxicity, suggesting that 6PGD could be an anticancer target."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [1, 2]\nExplanation: Evidence states: \"We found that suppression of 6PGD decreased lipogenesis and RNA biosynthesis and elevated ROS levels in cancer cells, attenuating cell proliferation and tumour growth. 6PGD-mediated production of ribulose-5-phosphate (Ru-5-P) inhibits AMPK activation by disrupting the active LKB1 complex, thereby activating acetyl-CoA carboxylase 1 and lipogenesis.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 635, "doc_id": 1686997, "label": "CONTRADICTS", "evidence_sentence_ids": [1, 2], "cited_doc_ids": [1686997], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Input from  mental and physical health care professionals is not effective at decreasing homelessness.\n\nDocument title: Mental health problems of homeless children and families: longitudinal study.\n\nAbstract sentences:\n[0] OBJECTIVE To establish the mental health needs of homeless children and families before and after rehousing.\n[1] DESIGN Cross sectional, longitudinal study.\n[2] SETTING City of Birmingham.\n[3] SUBJECTS 58 rehoused families with 103 children aged 2-16 years and 21 comparison families of low socioeconomic status in stable housing, with 54 children.\n[4] MAIN OUTCOME MEASURES Children's mental health problems and level of communication; mothers' mental health problems and social support one year after rehousing.\n[5] RESULTS Mental health problems remained significantly higher in rehoused mothers and their children than in the comparison group (mothers 26% v 5%, P = 0.04; children 39% v 11%, P = 0.0003).\n[6] Homeless mothers continued to have significantly less social support at follow up.\n[7] Mothers with a history of abuse and poor social integration were more likely to have children with persistent mental health problems.\n[8] CONCLUSIONS Homeless families have a high level of complex needs that cannot be met by conventional health services and arrangements.\n[9] Local strategies for rapid rehousing into permanent accommodation, effective social support and health care for parents and children, and protection from violence and intimidation should be developed and implemented."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 638, "doc_id": 25649714, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [25649714], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Inside the body, falciparum parasites reproduce asexually.\n\nDocument title: Malaria biology and disease pathogenesis: insights for new treatments\n\nAbstract sentences:\n[0] Plasmodium falciparum malaria, an infectious disease caused by a parasitic protozoan, claims the lives of nearly a million children each year in Africa alone and is a top public health concern.\n[1] Evidence is accumulating that resistance to artemisinin derivatives, the frontline therapy for the asexual blood stage of the infection, is developing in southeast Asia.\n[2] Renewed initiatives to eliminate malaria will benefit from an expanded repertoire of antimalarials, including new drugs that kill circulating P. falciparum gametocytes, thereby preventing transmission.\n[3] Our current understanding of the biology of asexual blood-stage parasites and gametocytes and the ability to culture them in vitro lends optimism that high-throughput screenings of large chemical libraries will produce a new generation of antimalarial drugs.\n[4] There is also a need for new therapies to reduce the high mortality of severe malaria.\n[5] An understanding of the pathophysiology of severe disease may identify rational targets for drugs that improve survival."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Evidence is accumulating that resistance to artemisinin derivatives, the frontline therapy for the asexual blood stage of the infection, is developing in southeast Asia.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 640, "doc_id": 6503185, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [6503185], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Inside the body, falciparum parasites reproduce asexually.\n\nDocument title: Malaria biology and disease pathogenesis: insights for new treatments\n\nAbstract sentences:\n[0] Plasmodium falciparum malaria, an infectious disease caused by a parasitic protozoan, claims the lives of nearly a million children each year in Africa alone and is a top public health concern.\n[1] Evidence is accumulating that resistance to artemisinin derivatives, the frontline therapy for the asexual blood stage of the infection, is developing in southeast Asia.\n[2] Renewed initiatives to eliminate malaria will benefit from an expanded repertoire of antimalarials, including new drugs that kill circulating P. falciparum gametocytes, thereby preventing transmission.\n[3] Our current understanding of the biology of asexual blood-stage parasites and gametocytes and the ability to culture them in vitro lends optimism that high-throughput screenings of large chemical libraries will produce a new generation of antimalarial drugs.\n[4] There is also a need for new therapies to reduce the high mortality of severe malaria.\n[5] An understanding of the pathophysiology of severe disease may identify rational targets for drugs that improve survival."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Our current understanding of the biology of asexual blood-stage parasites and gametocytes and the ability to culture them in vitro lends optimism that high-throughput screenings of large chemical libraries will produce a new generation of antimalarial drugs.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 640, "doc_id": 6503185, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [6503185], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Insulin decreases risk of severe kidney failure.\n\nDocument title: Diabetes treatments and risk of amputation, blindness, severe kidney failure, hyperglycaemia, and hypoglycaemia: open cohort study in primary care\n\nAbstract sentences:\n[0] OBJECTIVE To assess the risks of amputation, blindness, severe kidney failure, hyperglycaemia, and hypoglycaemia in patients with type 2 diabetes associated with prescribed diabetes drugs, particularly newer agents including gliptins or glitazones (thiazolidinediones).\n[1] DESIGN Open cohort study in primary care.\n[2] SETTING 1243 practices contributing data to the QResearch database in England.\n[3] PARTICIPANTS 469,688 patients with type 2 diabetes aged 25-84 years between 1 April 2007 and 31 January 2015.\n[4] EXPOSURES Hypoglycaemic agents (glitazones, gliptins, metformin, sulphonylureas, insulin, and other) alone and in combination.\n[5] MAIN OUTCOME MEASURES First recorded diagnoses of amputation, blindness, severe kidney failure, hyperglycaemia, and hypoglycaemia recorded on patients' primary care, mortality, or hospital records.\n[6] Cox models estimated hazard ratios for diabetes treatments adjusting for potential confounders.\n[7] RESULTS 21,308 (4.5%) and 32,533 (6.9%) patients received prescriptions for glitazones and gliptins during follow-up, respectively.\n[8] Compared with non-use, glitazones were associated with a decreased risk of blindness (adjusted hazard ratio 0.71, 95% confidence interval 0.57 to 0.89; rate 14.4 per 10,000 person years of exposure) and an increased risk of hypoglycaemia (1.22, 1.10 to 1.37; 65.1); gliptins were associated with a decreased risk of hypoglycaemia (0.86, 0.77 to 0.96; 45.8).\n[9] Although the numbers of patients prescribed gliptin monotherapy or glitazones monotherapy were relatively low, there were significantly increased risks of severe kidney failure compared with metformin monotherapy (adjusted hazard ratio 2.55, 95% confidence interval 1.13 to 5.74).\n[10] We found significantly lower risks of hyperglycaemia among patients prescribed dual therapy involving metformin with either gliptins (0.78, 0.62 to 0.97) or glitazones (0.60, 0.45 to 0.80) compared with metformin monotherapy.\n[11] Patients prescribed triple therapy with metformin, sulphonylureas, and either gliptins (adjusted hazard ratio 5.07, 95% confidence interval 4.28 to 6.00) or glitazones (6.32, 5.35 to 7.45) had significantly higher risks of hypoglycaemia than those prescribed metformin monotherapy, but these risks were similar to those involving dual therapy with metformin and sulphonylureas (6.03, 5.47 to 6.63).\n[12] Patients prescribed triple therapy with metformin, sulphonylureas, and glitazones had a significantly reduced risk of blindness compared with metformin monotherapy (0.67, 0.48 to 0.94).\n[13] CONCLUSIONS We have found lower risks of hyperglycaemia among patients prescribed dual therapy involving metformin with either gliptins or glitazones compared with metformin alone.\n[14] Compared with metformin monotherapy, triple therapy with metformin, sulphonylureas, and either gliptins or glitazones was associated with an increased risk of hypoglycaemia, which was similar to the risk for dual therapy with metformin and sulphonylureas.\n[15] Compared with metformin monotherapy, triple therapy with metformin, sulphonylureas, and glitazones was associated with a reduced risk of blindness.\n[16] These results, while subject to residual confounding, could have implications for the prescribing of hypoglycaemic drugs."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 642, "doc_id": 13619127, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [13619127], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Insulin effects appetite via ventral tegmental neurons.\n\nDocument title: Role for insulin signaling in catecholaminergic neurons in control of energy homeostasis.\n\nAbstract sentences:\n[0] Dopaminergic midbrain neurons integrate signals on food palatability and food-associated reward into the complex control of energy homeostasis.\n[1] To define the role of insulin receptor (IR) signaling in this circuitry, we inactivated IR signaling in tyrosine hydroxylase (Th)-expressing cells of mice (IR(ΔTh)).\n[2] IR inactivation in Th-expressing cells of mice resulted in increased body weight, increased fat mass, and hyperphagia.\n[3] While insulin acutely stimulated firing frequency in 50% of dopaminergic VTA/SN neurons, this response was abolished in IR(ΔTh) mice.\n[4] Moreover, these mice exhibited an altered response to cocaine under food-restricted conditions.\n[5] Taken together, these data provide in vivo evidence for a critical role of insulin signaling in catecholaminergic neurons to control food intake and energy homeostasis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3, 5]\nExplanation: Evidence states: \"While insulin acutely stimulated firing frequency in 50% of dopaminergic VTA/SN neurons, this response was abolished in IR(ΔTh) mice. Taken together, these data provide in vivo evidence for a critical role of insulin signaling in catecholaminergic neurons to control food intake and energy homeostasis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 643, "doc_id": 15535511, "label": "SUPPORTS", "evidence_sentence_ids": [3, 5], "cited_doc_ids": [15535511], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Intake of folic acid (FA) and vitamin B6 (VB6) increases levels of homocysteine.\n\nDocument title: Folate and vitamin B6 from diet and supplements in relation to risk of coronary heart disease among women.\n\nAbstract sentences:\n[0] CONTEXT Hyperhomocysteinemia is caused by genetic and lifestyle influences, including low intakes of folate and vitamin B6.\n[1] However, prospective data relating intake of these vitamins to risk of coronary heart disease (CHD) are not available.\n[2] OBJECTIVE To examine intakes of folate and vitamin B6 in relation to the incidence of nonfatal myocardial infarction (MI) and fatal CHD.\n[3] DESIGN Prospective cohort study.\n[4] SETTING AND PATIENTS In 1980, a total of 80082 women from the Nurses' Health Study with no previous history of cardiovascular disease, cancer, hypercholesterolemia, or diabetes completed a detailed food frequency questionnaire from which we derived usual intake of folate and vitamin B6.\n[5] MAIN OUTCOME MEASURE Nonfatal MI and fatal CHD confirmed by World Health Organization criteria.\n[6] RESULTS During 14 years of follow-up, we documented 658 incident cases of nonfatal MI and 281 cases of fatal CHD.\n[7] After controlling for cardiovascular risk factors, including smoking and hypertension and intake of alcohol, fiber, vitamin E, and saturated, polyunsaturated, and trans fat, the relative risks (RRs) of CHD between extreme quintiles were 0.69 (95% confidence interval [CI], 0.55-0.87) for folate (median intake, 696 microg/d vs 158 microg/d) and 0.67 (95% CI, 0.53-0.85) for vitamin B6 (median intake, 4.6 mg/d vs 1.1 mg/d).\n[8] Controlling for the same variables, the RR was 0.55 (95% CI, 0.41-0.74) among women in the highest quintile of both folate and vitamin B6 intake compared with the opposite extreme.\n[9] Risk of CHD was reduced among women who regularly used multiple vitamins (RR=0.76; 95% CI, 0.65-0.90), the major source of folate and vitamin B6, and after excluding multiple vitamin users, among those with higher dietary intakes of folate and vitamin B6.\n[10] In a subgroup analysis, compared with nondrinkers, the inverse association between a high-folate diet and CHD was strongest among women who consumed up to 1 alcoholic beverage per day (RR =0.69; 95% CI, 0.49-0.97) or more than 1 drink per day (RR=0.27; 95% CI, 0.13-0.58).\n[11] CONCLUSION These results suggest that intake of folate and vitamin B6 above the current recommended dietary allowance may be important in the primary prevention of CHD among women."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"CONTEXT Hyperhomocysteinemia is caused by genetic and lifestyle influences, including low intakes of folate and vitamin B6.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 645, "doc_id": 12810152, "label": "CONTRADICTS", "evidence_sentence_ids": [0], "cited_doc_ids": [12810152], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Intake of folic acid (FA) and vitamin B6 (VB6) reduces levels of homocysteine.\n\nDocument title: Folate and vitamin B6 from diet and supplements in relation to risk of coronary heart disease among women.\n\nAbstract sentences:\n[0] CONTEXT Hyperhomocysteinemia is caused by genetic and lifestyle influences, including low intakes of folate and vitamin B6.\n[1] However, prospective data relating intake of these vitamins to risk of coronary heart disease (CHD) are not available.\n[2] OBJECTIVE To examine intakes of folate and vitamin B6 in relation to the incidence of nonfatal myocardial infarction (MI) and fatal CHD.\n[3] DESIGN Prospective cohort study.\n[4] SETTING AND PATIENTS In 1980, a total of 80082 women from the Nurses' Health Study with no previous history of cardiovascular disease, cancer, hypercholesterolemia, or diabetes completed a detailed food frequency questionnaire from which we derived usual intake of folate and vitamin B6.\n[5] MAIN OUTCOME MEASURE Nonfatal MI and fatal CHD confirmed by World Health Organization criteria.\n[6] RESULTS During 14 years of follow-up, we documented 658 incident cases of nonfatal MI and 281 cases of fatal CHD.\n[7] After controlling for cardiovascular risk factors, including smoking and hypertension and intake of alcohol, fiber, vitamin E, and saturated, polyunsaturated, and trans fat, the relative risks (RRs) of CHD between extreme quintiles were 0.69 (95% confidence interval [CI], 0.55-0.87) for folate (median intake, 696 microg/d vs 158 microg/d) and 0.67 (95% CI, 0.53-0.85) for vitamin B6 (median intake, 4.6 mg/d vs 1.1 mg/d).\n[8] Controlling for the same variables, the RR was 0.55 (95% CI, 0.41-0.74) among women in the highest quintile of both folate and vitamin B6 intake compared with the opposite extreme.\n[9] Risk of CHD was reduced among women who regularly used multiple vitamins (RR=0.76; 95% CI, 0.65-0.90), the major source of folate and vitamin B6, and after excluding multiple vitamin users, among those with higher dietary intakes of folate and vitamin B6.\n[10] In a subgroup analysis, compared with nondrinkers, the inverse association between a high-folate diet and CHD was strongest among women who consumed up to 1 alcoholic beverage per day (RR =0.69; 95% CI, 0.49-0.97) or more than 1 drink per day (RR=0.27; 95% CI, 0.13-0.58).\n[11] CONCLUSION These results suggest that intake of folate and vitamin B6 above the current recommended dietary allowance may be important in the primary prevention of CHD among women."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"CONTEXT Hyperhomocysteinemia is caused by genetic and lifestyle influences, including low intakes of folate and vitamin B6.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 646, "doc_id": 12810152, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [12810152], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Integrated care is ineffective at tackling multiple comorbidities.\n\nDocument title: Functional outcomes of multi-condition collaborative care and successful ageing: results of randomised trial\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate the effectiveness of integrated care for chronic physical diseases and depression in reducing disability and improving quality of life.\n[1] DESIGN A randomised controlled trial of multi-condition collaborative care for depression and poorly controlled diabetes and/or risk factors for coronary heart disease compared with usual care among middle aged and elderly people   SETTING Fourteen primary care clinics in Seattle, Washington.   PARTICIPANTS Patients with diabetes or coronary heart disease, or both, and blood pressure above 140/90 mm Hg, low density lipoprotein concentration >3.37 mmol/L, or glycated haemoglobin 8.5% or higher, and PHQ-9 depression scores of ≥ 10.\n[2] INTERVENTION A 12 month intervention to improve depression, glycaemic control, blood pressure, and lipid control by integrating a \"treat to target\" programme for diabetes and risk factors for coronary heart disease with collaborative care for depression.\n[3] The intervention combined self management support, monitoring of disease control, and pharmacotherapy to control depression, hyperglycaemia, hypertension, and hyperlipidaemia.\n[4] MAIN OUTCOME MEASURES Social role disability (Sheehan disability scale), global quality of life rating, and World Health Organization disability assessment schedule (WHODAS-2) scales to measure disabilities in activities of daily living (mobility, self care, household maintenance).\n[5] RESULTS Of 214 patients enrolled (106 intervention and 108 usual care), disability and quality of life measures were obtained for 97 intervention patients at six months (92%) and 92 at 12 months (87%), and for 96 usual care patients at six months (89%) and 92 at 12 months (85%).\n[6] Improvements from baseline on the Sheehan disability scale (-0.9, 95% confidence interval -1.5 to -0.2; P = 0.006) and global quality of life rating (0.7, 0.2 to 1.2; P = 0.005) were significantly greater at six and 12 months in patients in the intervention group.\n[7] There was a trend toward greater improvement in disabilities in activities of daily living (-1.5, -3.3 to 0.4; P = 0.10).\n[8] CONCLUSIONS Integrated care that covers chronic physical disease and comorbid depression can reduce social role disability and enhance global quality of life.\n[9] Trial registration Clinical Trials NCT00468676."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Improvements from baseline on the Sheehan disability scale (-0.9, 95% confidence interval -1.5 to -0.2; P = 0.006) and global quality of life rating (0.7, 0.2 to 1.2; P = 0.005) were significantly greater at six and 12 months in patients in the intervention group.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 647, "doc_id": 15041758, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [15041758], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Integrated care is ineffective at tackling multiple comorbidities.\n\nDocument title: Functional outcomes of multi-condition collaborative care and successful ageing: results of randomised trial\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate the effectiveness of integrated care for chronic physical diseases and depression in reducing disability and improving quality of life.\n[1] DESIGN A randomised controlled trial of multi-condition collaborative care for depression and poorly controlled diabetes and/or risk factors for coronary heart disease compared with usual care among middle aged and elderly people   SETTING Fourteen primary care clinics in Seattle, Washington.   PARTICIPANTS Patients with diabetes or coronary heart disease, or both, and blood pressure above 140/90 mm Hg, low density lipoprotein concentration >3.37 mmol/L, or glycated haemoglobin 8.5% or higher, and PHQ-9 depression scores of ≥ 10.\n[2] INTERVENTION A 12 month intervention to improve depression, glycaemic control, blood pressure, and lipid control by integrating a \"treat to target\" programme for diabetes and risk factors for coronary heart disease with collaborative care for depression.\n[3] The intervention combined self management support, monitoring of disease control, and pharmacotherapy to control depression, hyperglycaemia, hypertension, and hyperlipidaemia.\n[4] MAIN OUTCOME MEASURES Social role disability (Sheehan disability scale), global quality of life rating, and World Health Organization disability assessment schedule (WHODAS-2) scales to measure disabilities in activities of daily living (mobility, self care, household maintenance).\n[5] RESULTS Of 214 patients enrolled (106 intervention and 108 usual care), disability and quality of life measures were obtained for 97 intervention patients at six months (92%) and 92 at 12 months (87%), and for 96 usual care patients at six months (89%) and 92 at 12 months (85%).\n[6] Improvements from baseline on the Sheehan disability scale (-0.9, 95% confidence interval -1.5 to -0.2; P = 0.006) and global quality of life rating (0.7, 0.2 to 1.2; P = 0.005) were significantly greater at six and 12 months in patients in the intervention group.\n[7] There was a trend toward greater improvement in disabilities in activities of daily living (-1.5, -3.3 to 0.4; P = 0.10).\n[8] CONCLUSIONS Integrated care that covers chronic physical disease and comorbid depression can reduce social role disability and enhance global quality of life.\n[9] Trial registration Clinical Trials NCT00468676."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"There was a trend toward greater improvement in disabilities in activities of daily living (-1.5, -3.3 to 0.4; P = 0.10).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 647, "doc_id": 15041758, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [15041758], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Integrated care is ineffective at tackling multiple comorbidities.\n\nDocument title: Functional outcomes of multi-condition collaborative care and successful ageing: results of randomised trial\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate the effectiveness of integrated care for chronic physical diseases and depression in reducing disability and improving quality of life.\n[1] DESIGN A randomised controlled trial of multi-condition collaborative care for depression and poorly controlled diabetes and/or risk factors for coronary heart disease compared with usual care among middle aged and elderly people   SETTING Fourteen primary care clinics in Seattle, Washington.   PARTICIPANTS Patients with diabetes or coronary heart disease, or both, and blood pressure above 140/90 mm Hg, low density lipoprotein concentration >3.37 mmol/L, or glycated haemoglobin 8.5% or higher, and PHQ-9 depression scores of ≥ 10.\n[2] INTERVENTION A 12 month intervention to improve depression, glycaemic control, blood pressure, and lipid control by integrating a \"treat to target\" programme for diabetes and risk factors for coronary heart disease with collaborative care for depression.\n[3] The intervention combined self management support, monitoring of disease control, and pharmacotherapy to control depression, hyperglycaemia, hypertension, and hyperlipidaemia.\n[4] MAIN OUTCOME MEASURES Social role disability (Sheehan disability scale), global quality of life rating, and World Health Organization disability assessment schedule (WHODAS-2) scales to measure disabilities in activities of daily living (mobility, self care, household maintenance).\n[5] RESULTS Of 214 patients enrolled (106 intervention and 108 usual care), disability and quality of life measures were obtained for 97 intervention patients at six months (92%) and 92 at 12 months (87%), and for 96 usual care patients at six months (89%) and 92 at 12 months (85%).\n[6] Improvements from baseline on the Sheehan disability scale (-0.9, 95% confidence interval -1.5 to -0.2; P = 0.006) and global quality of life rating (0.7, 0.2 to 1.2; P = 0.005) were significantly greater at six and 12 months in patients in the intervention group.\n[7] There was a trend toward greater improvement in disabilities in activities of daily living (-1.5, -3.3 to 0.4; P = 0.10).\n[8] CONCLUSIONS Integrated care that covers chronic physical disease and comorbid depression can reduce social role disability and enhance global quality of life.\n[9] Trial registration Clinical Trials NCT00468676."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"CONCLUSIONS Integrated care that covers chronic physical disease and comorbid depression can reduce social role disability and enhance global quality of life.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 647, "doc_id": 15041758, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [15041758], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Integrated care is successful at tackling multiple comorbidities.\n\nDocument title: Functional outcomes of multi-condition collaborative care and successful ageing: results of randomised trial\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate the effectiveness of integrated care for chronic physical diseases and depression in reducing disability and improving quality of life.\n[1] DESIGN A randomised controlled trial of multi-condition collaborative care for depression and poorly controlled diabetes and/or risk factors for coronary heart disease compared with usual care among middle aged and elderly people   SETTING Fourteen primary care clinics in Seattle, Washington.   PARTICIPANTS Patients with diabetes or coronary heart disease, or both, and blood pressure above 140/90 mm Hg, low density lipoprotein concentration >3.37 mmol/L, or glycated haemoglobin 8.5% or higher, and PHQ-9 depression scores of ≥ 10.\n[2] INTERVENTION A 12 month intervention to improve depression, glycaemic control, blood pressure, and lipid control by integrating a \"treat to target\" programme for diabetes and risk factors for coronary heart disease with collaborative care for depression.\n[3] The intervention combined self management support, monitoring of disease control, and pharmacotherapy to control depression, hyperglycaemia, hypertension, and hyperlipidaemia.\n[4] MAIN OUTCOME MEASURES Social role disability (Sheehan disability scale), global quality of life rating, and World Health Organization disability assessment schedule (WHODAS-2) scales to measure disabilities in activities of daily living (mobility, self care, household maintenance).\n[5] RESULTS Of 214 patients enrolled (106 intervention and 108 usual care), disability and quality of life measures were obtained for 97 intervention patients at six months (92%) and 92 at 12 months (87%), and for 96 usual care patients at six months (89%) and 92 at 12 months (85%).\n[6] Improvements from baseline on the Sheehan disability scale (-0.9, 95% confidence interval -1.5 to -0.2; P = 0.006) and global quality of life rating (0.7, 0.2 to 1.2; P = 0.005) were significantly greater at six and 12 months in patients in the intervention group.\n[7] There was a trend toward greater improvement in disabilities in activities of daily living (-1.5, -3.3 to 0.4; P = 0.10).\n[8] CONCLUSIONS Integrated care that covers chronic physical disease and comorbid depression can reduce social role disability and enhance global quality of life.\n[9] Trial registration Clinical Trials NCT00468676."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Improvements from baseline on the Sheehan disability scale (-0.9, 95% confidence interval -1.5 to -0.2; P = 0.006) and global quality of life rating (0.7, 0.2 to 1.2; P = 0.005) were significantly greater at six and 12 months in patients in the intervention group.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 648, "doc_id": 15041758, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [15041758], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Integrated care is successful at tackling multiple comorbidities.\n\nDocument title: Functional outcomes of multi-condition collaborative care and successful ageing: results of randomised trial\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate the effectiveness of integrated care for chronic physical diseases and depression in reducing disability and improving quality of life.\n[1] DESIGN A randomised controlled trial of multi-condition collaborative care for depression and poorly controlled diabetes and/or risk factors for coronary heart disease compared with usual care among middle aged and elderly people   SETTING Fourteen primary care clinics in Seattle, Washington.   PARTICIPANTS Patients with diabetes or coronary heart disease, or both, and blood pressure above 140/90 mm Hg, low density lipoprotein concentration >3.37 mmol/L, or glycated haemoglobin 8.5% or higher, and PHQ-9 depression scores of ≥ 10.\n[2] INTERVENTION A 12 month intervention to improve depression, glycaemic control, blood pressure, and lipid control by integrating a \"treat to target\" programme for diabetes and risk factors for coronary heart disease with collaborative care for depression.\n[3] The intervention combined self management support, monitoring of disease control, and pharmacotherapy to control depression, hyperglycaemia, hypertension, and hyperlipidaemia.\n[4] MAIN OUTCOME MEASURES Social role disability (Sheehan disability scale), global quality of life rating, and World Health Organization disability assessment schedule (WHODAS-2) scales to measure disabilities in activities of daily living (mobility, self care, household maintenance).\n[5] RESULTS Of 214 patients enrolled (106 intervention and 108 usual care), disability and quality of life measures were obtained for 97 intervention patients at six months (92%) and 92 at 12 months (87%), and for 96 usual care patients at six months (89%) and 92 at 12 months (85%).\n[6] Improvements from baseline on the Sheehan disability scale (-0.9, 95% confidence interval -1.5 to -0.2; P = 0.006) and global quality of life rating (0.7, 0.2 to 1.2; P = 0.005) were significantly greater at six and 12 months in patients in the intervention group.\n[7] There was a trend toward greater improvement in disabilities in activities of daily living (-1.5, -3.3 to 0.4; P = 0.10).\n[8] CONCLUSIONS Integrated care that covers chronic physical disease and comorbid depression can reduce social role disability and enhance global quality of life.\n[9] Trial registration Clinical Trials NCT00468676."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"There was a trend toward greater improvement in disabilities in activities of daily living (-1.5, -3.3 to 0.4; P = 0.10).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 648, "doc_id": 15041758, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [15041758], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Integrated care is successful at tackling multiple comorbidities.\n\nDocument title: Functional outcomes of multi-condition collaborative care and successful ageing: results of randomised trial\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate the effectiveness of integrated care for chronic physical diseases and depression in reducing disability and improving quality of life.\n[1] DESIGN A randomised controlled trial of multi-condition collaborative care for depression and poorly controlled diabetes and/or risk factors for coronary heart disease compared with usual care among middle aged and elderly people   SETTING Fourteen primary care clinics in Seattle, Washington.   PARTICIPANTS Patients with diabetes or coronary heart disease, or both, and blood pressure above 140/90 mm Hg, low density lipoprotein concentration >3.37 mmol/L, or glycated haemoglobin 8.5% or higher, and PHQ-9 depression scores of ≥ 10.\n[2] INTERVENTION A 12 month intervention to improve depression, glycaemic control, blood pressure, and lipid control by integrating a \"treat to target\" programme for diabetes and risk factors for coronary heart disease with collaborative care for depression.\n[3] The intervention combined self management support, monitoring of disease control, and pharmacotherapy to control depression, hyperglycaemia, hypertension, and hyperlipidaemia.\n[4] MAIN OUTCOME MEASURES Social role disability (Sheehan disability scale), global quality of life rating, and World Health Organization disability assessment schedule (WHODAS-2) scales to measure disabilities in activities of daily living (mobility, self care, household maintenance).\n[5] RESULTS Of 214 patients enrolled (106 intervention and 108 usual care), disability and quality of life measures were obtained for 97 intervention patients at six months (92%) and 92 at 12 months (87%), and for 96 usual care patients at six months (89%) and 92 at 12 months (85%).\n[6] Improvements from baseline on the Sheehan disability scale (-0.9, 95% confidence interval -1.5 to -0.2; P = 0.006) and global quality of life rating (0.7, 0.2 to 1.2; P = 0.005) were significantly greater at six and 12 months in patients in the intervention group.\n[7] There was a trend toward greater improvement in disabilities in activities of daily living (-1.5, -3.3 to 0.4; P = 0.10).\n[8] CONCLUSIONS Integrated care that covers chronic physical disease and comorbid depression can reduce social role disability and enhance global quality of life.\n[9] Trial registration Clinical Trials NCT00468676."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"CONCLUSIONS Integrated care that covers chronic physical disease and comorbid depression can reduce social role disability and enhance global quality of life.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 648, "doc_id": 15041758, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [15041758], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Integrating classroom-based collaborative learning with Web-based collaborative learning offers the best class performance.\n\nDocument title: Computer assisted learning in undergraduate medical education.\n\nAbstract sentences:\n[0] It is becoming “a truth universally acknowledged” that the education of undergraduate medical students will be enhanced through the use of computer assisted learning.\n[1] Access to the wide range of online options illustrated in the figure must surely make learning more exciting, effective, and likely to be retained.\n[2] This assumption is potentially but by no means inevitably correct.\n[3] ### Box 1: Why fund computer assisted learning?\n[4] Computer assisted learning is inevitable —Individual lecturers and departments are already beginning to introduce a wide range of computer based applications, sometimes in a haphazard way.\n[5] Planned and coordinated development is better than indiscriminate expansion  It is convenient and flexible —Courses supported by computer assisted learning applications may require fewer face to face lectures and seminars and place fewer geographical and temporal constraints on staff and students.\n[6] Students at peripheral hospitals or primary care centres may benefit in particular  Unique presentational benefits —Computer presentation is particularly suited to subjects that are visually intensive, detail oriented, and difficult to conceptualise, such as complex biochemical processes or microscopic images.1 Furthermore, “virtual” cases may reduce the need to use animal or human tissue in learning  Personalised learning —Each learner can progress at his or her preferred pace.\n[7] They can repeat, interrupt, and resume at will, which may have particular advantages for weaker students  Economies of scale —Once an application has been set up, the incremental cost of offering it to additional students is relatively small  Competitive advantage —Potential applicants may use the quality of information technology to discriminate between medical schools.\n[8] A “leading edge” virtual campus is likely to attract good students  Achieves the ultimate goal of higher education —The goal is to link people into learning communities.\n[9] Computer applications, especially the internet and world wide web, are an extremely efficient way of doing this2  Expands pedagogical horizons —The most controversial argument for … RETURN TO TEXT"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 650, "doc_id": 12789595, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [12789595], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Interferon stimulated genes (ISGs) Irf1, Irg1, Ifi27, and Rsad2 encourage West Nile virus replication in cortical neurons.\n\nDocument title: Differential innate immune response programs in neuronal subtypes determine susceptibility to infection in the brain by positive stranded RNA viruses\n\nAbstract sentences:\n[0] Although susceptibility of neurons in the brain to microbial infection is a major determinant of clinical outcome, little is known about the molecular factors governing this vulnerability.\n[1] Here we show that two types of neurons from distinct brain regions showed differential permissivity to replication of several positive-stranded RNA viruses.\n[2] Granule cell neurons of the cerebellum and cortical neurons from the cerebral cortex have unique innate immune programs that confer differential susceptibility to viral infection ex vivo and in vivo.\n[3] By transducing cortical neurons with genes that were expressed more highly in granule cell neurons, we identified three interferon-stimulated genes (ISGs; Ifi27, Irg1 and Rsad2 (also known as Viperin)) that mediated the antiviral effects against different neurotropic viruses.\n[4] Moreover, we found that the epigenetic state and microRNA (miRNA)-mediated regulation of ISGs correlates with enhanced antiviral response in granule cell neurons.\n[5] Thus, neurons from evolutionarily distinct brain regions have unique innate immune signatures, which probably contribute to their relative permissiveness to infection."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 651, "doc_id": 9433958, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [9433958], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Interferon stimulated genes (ISGs) Irf1, Irg1, Ifi27, and Rsad2 inhibit West Nile virus replication in cortical neurons.\n\nDocument title: Differential innate immune response programs in neuronal subtypes determine susceptibility to infection in the brain by positive stranded RNA viruses\n\nAbstract sentences:\n[0] Although susceptibility of neurons in the brain to microbial infection is a major determinant of clinical outcome, little is known about the molecular factors governing this vulnerability.\n[1] Here we show that two types of neurons from distinct brain regions showed differential permissivity to replication of several positive-stranded RNA viruses.\n[2] Granule cell neurons of the cerebellum and cortical neurons from the cerebral cortex have unique innate immune programs that confer differential susceptibility to viral infection ex vivo and in vivo.\n[3] By transducing cortical neurons with genes that were expressed more highly in granule cell neurons, we identified three interferon-stimulated genes (ISGs; Ifi27, Irg1 and Rsad2 (also known as Viperin)) that mediated the antiviral effects against different neurotropic viruses.\n[4] Moreover, we found that the epigenetic state and microRNA (miRNA)-mediated regulation of ISGs correlates with enhanced antiviral response in granule cell neurons.\n[5] Thus, neurons from evolutionarily distinct brain regions have unique innate immune signatures, which probably contribute to their relative permissiveness to infection."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 652, "doc_id": 9433958, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [9433958], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Interleukin-18 plays an important role in the pathogenesis of atherosclerosis.\n\nDocument title: Interleukin 18 function in atherosclerosis is mediated by the interleukin 18 receptor and the Na-Cl co-transporter\n\nAbstract sentences:\n[0] Interleukin-18 (IL18) participates in atherogenesis through several putative mechanisms.\n[1] Interruption of IL18 action reduces atherosclerosis in mice.\n[2] Here, we show that absence of the IL18 receptor (IL18r) does not affect atherosclerosis in apolipoprotein E–deficient (Apoe−/−) mice, nor does it affect IL18 cell surface binding to or signaling in endothelial cells.\n[3] As identified initially by co-immunoprecipitation with IL18, we found that IL18 interacts with the Na-Cl co-transporter (NCC; also known as SLC12A3), a 12-transmembrane-domain ion transporter protein preferentially expressed in the kidney.\n[4] NCC is expressed in atherosclerotic lesions, where it colocalizes with IL18r.\n[5] In Apoe−/− mice, combined deficiency of IL18r and NCC, but not single deficiency of either protein, protects mice from atherosclerosis.\n[6] Peritoneal macrophages from Apoe−/− mice or from Apoe−/− mice lacking IL18r or NCC show IL18 binding and induction of cell signaling and cytokine and chemokine expression, but macrophages from Apoe−/− mice with combined deficiency of IL18r and NCC have a blunted response.\n[7] An interaction between NCC and IL18r on macrophages was detected by co-immunoprecipitation.\n[8] IL18 binds to the cell surface of NCC-transfected COS-7 cells, which do not express IL18r, and induces cell signaling and cytokine expression.\n[9] This study identifies NCC as an IL18-binding protein that collaborates with IL18r in cell signaling, inflammatory molecule expression, and experimental atherogenesis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Interleukin-18 (IL18) participates in atherogenesis through several putative mechanisms.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 653, "doc_id": 24384587, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [24384587], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Interleukin-18 plays an important role in the pathogenesis of atherosclerosis.\n\nDocument title: Interleukin 18 function in atherosclerosis is mediated by the interleukin 18 receptor and the Na-Cl co-transporter\n\nAbstract sentences:\n[0] Interleukin-18 (IL18) participates in atherogenesis through several putative mechanisms.\n[1] Interruption of IL18 action reduces atherosclerosis in mice.\n[2] Here, we show that absence of the IL18 receptor (IL18r) does not affect atherosclerosis in apolipoprotein E–deficient (Apoe−/−) mice, nor does it affect IL18 cell surface binding to or signaling in endothelial cells.\n[3] As identified initially by co-immunoprecipitation with IL18, we found that IL18 interacts with the Na-Cl co-transporter (NCC; also known as SLC12A3), a 12-transmembrane-domain ion transporter protein preferentially expressed in the kidney.\n[4] NCC is expressed in atherosclerotic lesions, where it colocalizes with IL18r.\n[5] In Apoe−/− mice, combined deficiency of IL18r and NCC, but not single deficiency of either protein, protects mice from atherosclerosis.\n[6] Peritoneal macrophages from Apoe−/− mice or from Apoe−/− mice lacking IL18r or NCC show IL18 binding and induction of cell signaling and cytokine and chemokine expression, but macrophages from Apoe−/− mice with combined deficiency of IL18r and NCC have a blunted response.\n[7] An interaction between NCC and IL18r on macrophages was detected by co-immunoprecipitation.\n[8] IL18 binds to the cell surface of NCC-transfected COS-7 cells, which do not express IL18r, and induces cell signaling and cytokine expression.\n[9] This study identifies NCC as an IL18-binding protein that collaborates with IL18r in cell signaling, inflammatory molecule expression, and experimental atherogenesis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Interruption of IL18 action reduces atherosclerosis in mice.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 653, "doc_id": 24384587, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [24384587], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Interleukin-18 plays an important role in the pathogenesis of atherosclerosis.\n\nDocument title: Interleukin 18 function in atherosclerosis is mediated by the interleukin 18 receptor and the Na-Cl co-transporter\n\nAbstract sentences:\n[0] Interleukin-18 (IL18) participates in atherogenesis through several putative mechanisms.\n[1] Interruption of IL18 action reduces atherosclerosis in mice.\n[2] Here, we show that absence of the IL18 receptor (IL18r) does not affect atherosclerosis in apolipoprotein E–deficient (Apoe−/−) mice, nor does it affect IL18 cell surface binding to or signaling in endothelial cells.\n[3] As identified initially by co-immunoprecipitation with IL18, we found that IL18 interacts with the Na-Cl co-transporter (NCC; also known as SLC12A3), a 12-transmembrane-domain ion transporter protein preferentially expressed in the kidney.\n[4] NCC is expressed in atherosclerotic lesions, where it colocalizes with IL18r.\n[5] In Apoe−/− mice, combined deficiency of IL18r and NCC, but not single deficiency of either protein, protects mice from atherosclerosis.\n[6] Peritoneal macrophages from Apoe−/− mice or from Apoe−/− mice lacking IL18r or NCC show IL18 binding and induction of cell signaling and cytokine and chemokine expression, but macrophages from Apoe−/− mice with combined deficiency of IL18r and NCC have a blunted response.\n[7] An interaction between NCC and IL18r on macrophages was detected by co-immunoprecipitation.\n[8] IL18 binds to the cell surface of NCC-transfected COS-7 cells, which do not express IL18r, and induces cell signaling and cytokine expression.\n[9] This study identifies NCC as an IL18-binding protein that collaborates with IL18r in cell signaling, inflammatory molecule expression, and experimental atherogenesis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"In Apoe−/− mice, combined deficiency of IL18r and NCC, but not single deficiency of either protein, protects mice from atherosclerosis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 653, "doc_id": 24384587, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [24384587], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Intra-cerebroventricular infusion of amyloid-β oligomers increases expression of fibronectin type-III domain-containing protein 5 mRNA in mice hippocampi.\n\nDocument title: Exercise-linked FNDC5/irisin rescues synaptic plasticity and memory defects in Alzheimer’s models\n\nAbstract sentences:\n[0] Defective brain hormonal signaling has been associated with Alzheimer's disease (AD), a disorder characterized by synapse and memory failure.\n[1] Irisin is an exercise-induced myokine released on cleavage of the membrane-bound precursor protein fibronectin type III domain-containing protein 5 (FNDC5), also expressed in the hippocampus.\n[2] Here we show that FNDC5/irisin levels are reduced in AD hippocampi and cerebrospinal fluid, and in experimental AD models.\n[3] Knockdown of brain FNDC5/irisin impairs long-term potentiation and novel object recognition memory in mice.\n[4] Conversely, boosting brain levels of FNDC5/irisin rescues synaptic plasticity and memory in AD mouse models.\n[5] Peripheral overexpression of FNDC5/irisin rescues memory impairment, whereas blockade of either peripheral or brain FNDC5/irisin attenuates the neuroprotective actions of physical exercise on synaptic plasticity and memory in AD mice.\n[6] By showing that FNDC5/irisin is an important mediator of the beneficial effects of exercise in AD models, our findings place FNDC5/irisin as a novel agent capable of opposing synapse failure and memory impairment in AD."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 654, "doc_id": 57574395, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [57574395], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Intra-cerebroventricular infusion of amyloid-β oligomers reduces expression of fibronectin type-III domain-containing protein 5 mRNA in mice hippocampi.\n\nDocument title: Exercise-linked FNDC5/irisin rescues synaptic plasticity and memory defects in Alzheimer’s models\n\nAbstract sentences:\n[0] Defective brain hormonal signaling has been associated with Alzheimer's disease (AD), a disorder characterized by synapse and memory failure.\n[1] Irisin is an exercise-induced myokine released on cleavage of the membrane-bound precursor protein fibronectin type III domain-containing protein 5 (FNDC5), also expressed in the hippocampus.\n[2] Here we show that FNDC5/irisin levels are reduced in AD hippocampi and cerebrospinal fluid, and in experimental AD models.\n[3] Knockdown of brain FNDC5/irisin impairs long-term potentiation and novel object recognition memory in mice.\n[4] Conversely, boosting brain levels of FNDC5/irisin rescues synaptic plasticity and memory in AD mouse models.\n[5] Peripheral overexpression of FNDC5/irisin rescues memory impairment, whereas blockade of either peripheral or brain FNDC5/irisin attenuates the neuroprotective actions of physical exercise on synaptic plasticity and memory in AD mice.\n[6] By showing that FNDC5/irisin is an important mediator of the beneficial effects of exercise in AD models, our findings place FNDC5/irisin as a novel agent capable of opposing synapse failure and memory impairment in AD."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 655, "doc_id": 57574395, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [57574395], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Intramembrane cleavage by signal peptide peptidase aids in the degradation of proteins with a complex membrane orientation.\n\nDocument title: Ubiquitin-dependent intramembrane rhomboid protease promotes ERAD of membrane proteins.\n\nAbstract sentences:\n[0] The ER-associated degradation (ERAD) pathway serves as an important cellular safeguard by directing incorrectly folded and unassembled proteins from the ER to the proteasome.\n[1] Still, however, little is known about the components mediating ERAD of membrane proteins.\n[2] Here we show that the evolutionary conserved rhomboid family protein RHBDL4 is a ubiquitin-dependent ER-resident intramembrane protease that is upregulated upon ER stress.\n[3] RHBDL4 cleaves single-spanning and polytopic membrane proteins with unstable transmembrane helices, leading to their degradation by the canonical ERAD machinery.\n[4] RHBDL4 specifically binds the AAA+-ATPase p97, suggesting that proteolytic processing and dislocation into the cytosol are functionally linked.\n[5] The phylogenetic relationship between rhomboids and the ERAD factor derlin suggests that substrates for intramembrane proteolysis and protein dislocation are recruited by a shared mechanism."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2, 3]\nExplanation: Evidence states: \"Here we show that the evolutionary conserved rhomboid family protein RHBDL4 is a ubiquitin-dependent ER-resident intramembrane protease that is upregulated upon ER stress. RHBDL4 cleaves single-spanning and polytopic membrane proteins with unstable transmembrane helices, leading to their degradation by the canonical ERAD machinery.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 657, "doc_id": 8533245, "label": "SUPPORTS", "evidence_sentence_ids": [2, 3], "cited_doc_ids": [8533245], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: It is not proven that moderate consumption of candy and chocolate reduces the risk of cardiovascular disease (CVD) specifically.\n\nDocument title: Life is sweet: candy consumption and longevity.\n\nAbstract sentences:\n[0] Our attitude towards candy—“if it tastes that good, it can't be healthy”—betrays society's puritanical stance towards pleasure.\n[1] Candy has been blamed for various ills, including hyperactivity in children; however, clinical trials have not supported this.1  Candy—sugar confectionery and chocolate—is not a recent invention: the ancient Arabs, Chinese, and Egyptians candied fruits and nuts in honey, and the Aztecs made a chocolate drink from the bean of the cacao tree.\n[2] Today, Americans gratify themselves with, on average, 5.4 kg of sugar candy and 6.5 kg of chocolate per person annually.2  Since candy has existed for centuries, we surmised that it cannot be totally unhealthy.\n[3] We decided to investigate whether candy consumption was associated with longevity.\n[4] Subjects were from the Harvard alumni health study, an ongoing study of men entering Harvard University as undergraduates between 1916 and 1950.\n[5] We included 7841 men, free of cardiovascular disease and cancer, who responded to a health survey …"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 658, "doc_id": 5293024, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [5293024], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: JMJD6 catalyzes the hydroxylation of C-terminal lysine and supresses transcriptional activity.\n\nDocument title: JMJD6 Promotes Colon Carcinogenesis through Negative Regulation of p53 by Hydroxylation\n\nAbstract sentences:\n[0] Jumonji domain-containing 6 (JMJD6) is a member of the Jumonji C domain-containing family of proteins.\n[1] Compared to other members of the family, the cellular activity of JMJD6 is still not clearly defined and its biological function is still largely unexplored.\n[2] Here we report that JMJD6 is physically associated with the tumor suppressor p53.\n[3] We demonstrated that JMJD6 acts as an α-ketoglutarate- and Fe(II)-dependent lysyl hydroxylase to catalyze p53 hydroxylation.\n[4] We found that p53 indeed exists as a hydroxylated protein in vivo and that the hydroxylation occurs mainly on lysine 382 of p53.\n[5] We showed that JMJD6 antagonizes p53 acetylation, promotes the association of p53 with its negative regulator MDMX, and represses transcriptional activity of p53.\n[6] Depletion of JMJD6 enhances p53 transcriptional activity, arrests cells in the G1 phase, promotes cell apoptosis, and sensitizes cells to DNA damaging agent-induced cell death.\n[7] Importantly, knockdown of JMJD6 represses p53-dependent colon cell proliferation and tumorigenesis in vivo, and significantly, the expression of JMJD6 is markedly up-regulated in various types of human cancer especially in colon cancer, and high nuclear JMJD6 protein is strongly correlated with aggressive clinical behaviors of colon adenocarcinomas.\n[8] Our results reveal a novel posttranslational modification for p53 and support the pursuit of JMJD6 as a potential biomarker for colon cancer aggressiveness and a potential target for colon cancer intervention."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3, 4, 6]\nExplanation: Evidence states: \"We demonstrated that JMJD6 acts as an α-ketoglutarate- and Fe(II)-dependent lysyl hydroxylase to catalyze p53 hydroxylation. We found that p53 indeed exists as a hydroxylated protein in vivo and that the hydroxylation occurs mainly on lysine 382 of p53. Depletion of JMJD6 enhances p53 transcriptional activity, arrests cells in the G1 phase, promotes cell apoptosis, and sensitizes cells to DNA damaging agent-induced cell death.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 661, "doc_id": 37204802, "label": "SUPPORTS", "evidence_sentence_ids": [3, 4, 6], "cited_doc_ids": [37204802], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: JMJD6 slows the hydroxylation of C-terminal lysine\n\nDocument title: JMJD6 Promotes Colon Carcinogenesis through Negative Regulation of p53 by Hydroxylation\n\nAbstract sentences:\n[0] Jumonji domain-containing 6 (JMJD6) is a member of the Jumonji C domain-containing family of proteins.\n[1] Compared to other members of the family, the cellular activity of JMJD6 is still not clearly defined and its biological function is still largely unexplored.\n[2] Here we report that JMJD6 is physically associated with the tumor suppressor p53.\n[3] We demonstrated that JMJD6 acts as an α-ketoglutarate- and Fe(II)-dependent lysyl hydroxylase to catalyze p53 hydroxylation.\n[4] We found that p53 indeed exists as a hydroxylated protein in vivo and that the hydroxylation occurs mainly on lysine 382 of p53.\n[5] We showed that JMJD6 antagonizes p53 acetylation, promotes the association of p53 with its negative regulator MDMX, and represses transcriptional activity of p53.\n[6] Depletion of JMJD6 enhances p53 transcriptional activity, arrests cells in the G1 phase, promotes cell apoptosis, and sensitizes cells to DNA damaging agent-induced cell death.\n[7] Importantly, knockdown of JMJD6 represses p53-dependent colon cell proliferation and tumorigenesis in vivo, and significantly, the expression of JMJD6 is markedly up-regulated in various types of human cancer especially in colon cancer, and high nuclear JMJD6 protein is strongly correlated with aggressive clinical behaviors of colon adenocarcinomas.\n[8] Our results reveal a novel posttranslational modification for p53 and support the pursuit of JMJD6 as a potential biomarker for colon cancer aggressiveness and a potential target for colon cancer intervention."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3, 4, 6]\nExplanation: Evidence states: \"We demonstrated that JMJD6 acts as an α-ketoglutarate- and Fe(II)-dependent lysyl hydroxylase to catalyze p53 hydroxylation. We found that p53 indeed exists as a hydroxylated protein in vivo and that the hydroxylation occurs mainly on lysine 382 of p53. Depletion of JMJD6 enhances p53 transcriptional activity, arrests cells in the G1 phase, promotes cell apoptosis, and sensitizes cells to DNA damaging agent-induced cell death.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 662, "doc_id": 37204802, "label": "CONTRADICTS", "evidence_sentence_ids": [3, 4, 6], "cited_doc_ids": [37204802], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: KLF4 is necessary for VSMCs to gain genetic characteristics of other cell types within atherosclerotic lesions.\n\nDocument title: KLF4-dependent phenotypic modulation of smooth muscle cells has a key role in atherosclerotic plaque pathogenesis\n\nAbstract sentences:\n[0] Previous studies investigating the role of smooth muscle cells (SMCs) and macrophages in the pathogenesis of atherosclerosis have provided controversial results owing to the use of unreliable methods for clearly identifying each of these cell types.\n[1] Here, using Myh11-CreERT2 ROSA floxed STOP eYFP Apoe−/− mice to perform SMC lineage tracing, we find that traditional methods for detecting SMCs based on immunostaining for SMC markers fail to detect >80% of SMC-derived cells within advanced atherosclerotic lesions.\n[2] These unidentified SMC-derived cells exhibit phenotypes of other cell lineages, including macrophages and mesenchymal stem cells (MSCs).\n[3] SMC-specific conditional knockout of Krüppel-like factor 4 (Klf4) resulted in reduced numbers of SMC-derived MSC- and macrophage-like cells, a marked reduction in lesion size, and increases in multiple indices of plaque stability, including an increase in fibrous cap thickness as compared to wild-type controls.\n[4] On the basis of in vivo KLF4 chromatin immunoprecipitation–sequencing (ChIP-seq) analyses and studies of cholesterol-treated cultured SMCs, we identified >800 KLF4 target genes, including many that regulate pro-inflammatory responses of SMCs.\n[5] Our findings indicate that the contribution of SMCs to atherosclerotic plaques has been greatly underestimated, and that KLF4-dependent transitions in SMC phenotype are critical in lesion pathogenesis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Our findings indicate that the contribution of SMCs to atherosclerotic plaques has been greatly underestimated, and that KLF4-dependent transitions in SMC phenotype are critical in lesion pathogenesis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 663, "doc_id": 22080671, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [22080671], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: KRT17 modulates the expression of the transcriptional regulator AIRE in diseased epithelia.\n\nDocument title: Keratin-dependent regulation of Aire and gene expression in skin tumor keratinocytes\n\nAbstract sentences:\n[0] Expression of the intermediate filament protein keratin 17 (K17) is robustly upregulated in inflammatory skin diseases and in many tumors originating in stratified and pseudostratified epithelia.\n[1] We report that autoimmune regulator (Aire), a transcriptional regulator, is inducibly expressed in human and mouse tumor keratinocytes in a K17-dependent manner and is required for timely onset of Gli2-induced skin tumorigenesis in mice.\n[2] The induction of Aire mRNA in keratinocytes depends on a functional interaction between K17 and the heterogeneous nuclear ribonucleoprotein hnRNP K. Further, K17 colocalizes with Aire protein in the nucleus of tumor-prone keratinocytes, and each factor is bound to a specific promoter region featuring an NF-κB consensus sequence in a relevant subset of K17- and Aire-dependent proinflammatory genes.\n[3] These findings provide radically new insight into keratin intermediate filament and Aire function, along with a molecular basis for the K17-dependent amplification of inflammatory and immune responses in diseased epithelia."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"We report that autoimmune regulator (Aire), a transcriptional regulator, is inducibly expressed in human and mouse tumor keratinocytes in a K17-dependent manner and is required for timely onset of Gli2-induced skin tumorigenesis in mice.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 665, "doc_id": 12580014, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [12580014], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: KRT17 modulates the expression of the transcriptional regulator AIRE in diseased epithelia.\n\nDocument title: Keratin-dependent regulation of Aire and gene expression in skin tumor keratinocytes\n\nAbstract sentences:\n[0] Expression of the intermediate filament protein keratin 17 (K17) is robustly upregulated in inflammatory skin diseases and in many tumors originating in stratified and pseudostratified epithelia.\n[1] We report that autoimmune regulator (Aire), a transcriptional regulator, is inducibly expressed in human and mouse tumor keratinocytes in a K17-dependent manner and is required for timely onset of Gli2-induced skin tumorigenesis in mice.\n[2] The induction of Aire mRNA in keratinocytes depends on a functional interaction between K17 and the heterogeneous nuclear ribonucleoprotein hnRNP K. Further, K17 colocalizes with Aire protein in the nucleus of tumor-prone keratinocytes, and each factor is bound to a specific promoter region featuring an NF-κB consensus sequence in a relevant subset of K17- and Aire-dependent proinflammatory genes.\n[3] These findings provide radically new insight into keratin intermediate filament and Aire function, along with a molecular basis for the K17-dependent amplification of inflammatory and immune responses in diseased epithelia."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"The induction of Aire mRNA in keratinocytes depends on a functional interaction between K17 and the heterogeneous nuclear ribonucleoprotein hnRNP K. Further, K17 colocalizes with Aire protein in the nucleus of tumor-prone keratinocytes, and each factor is bound to a specific promoter region featuring an NF-κB consensus sequence in a relevant subset of K17- and Aire-dependent proinflammatory genes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 665, "doc_id": 12580014, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [12580014], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Kir7.1 modulates channel activity by the G protein-coupled melanocortin-4 receptor (MC4R) in the paraventricular nucleus of the hypothalamus.\n\nDocument title: G-protein-independent coupling of MC4R to Kir7.1 in hypothalamic neurons\n\nAbstract sentences:\n[0] The regulated release of anorexigenic α-melanocyte stimulating hormone (α-MSH) and orexigenic Agouti-related protein (AgRP) from discrete hypothalamic arcuate neurons onto common target sites in the central nervous system has a fundamental role in the regulation of energy homeostasis.\n[1] Both peptides bind with high affinity to the melanocortin-4 receptor (MC4R); existing data show that α-MSH is an agonist that couples the receptor to the Gαs signalling pathway, while AgRP binds competitively to block α-MSH binding and blocks the constitutive activity mediated by the ligand-mimetic amino-terminal domain of the receptor.\n[2] Here we show that, in mice, regulation of firing activity of neurons from the paraventricular nucleus of the hypothalamus (PVN) by α-MSH and AgRP can be mediated independently of Gαs signalling by ligand-induced coupling of MC4R to closure of inwardly rectifying potassium channel, Kir7.1.\n[3] Furthermore, AgRP is a biased agonist that hyperpolarizes neurons by binding to MC4R and opening Kir7.1, independently of its inhibition of α-MSH binding.\n[4] Consequently, Kir7.1 signalling appears to be central to melanocortin-mediated regulation of energy homeostasis within the PVN.\n[5] Coupling of MC4R to Kir7.1 may explain unusual aspects of the control of energy homeostasis by melanocortin signalling, including the gene dosage effect of MC4R and the sustained effects of AgRP on food intake."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here we show that, in mice, regulation of firing activity of neurons from the paraventricular nucleus of the hypothalamus (PVN) by α-MSH and AgRP can be mediated independently of Gαs signalling by ligand-induced coupling of MC4R to closure of inwardly rectifying potassium channel, Kir7.1.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 666, "doc_id": 4469125, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [4469125], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Klf2 is important for proper myeloid cell function.\n\nDocument title: The myeloid transcription factor KLF2 regulates the host response to polymicrobial infection and endotoxic shock.\n\nAbstract sentences:\n[0] Precise control of myeloid cell activation is required for optimal host defense.\n[1] However, this activation process must be under exquisite control to prevent uncontrolled inflammation.\n[2] Herein, we identify the Kruppel-like transcription factor 2 (KLF2) as a potent regulator of myeloid cell activation in vivo.\n[3] Exposure of myeloid cells to hypoxia and/or bacterial products reduced KLF2 expression while inducing hypoxia inducible factor-1α (HIF-1α), findings that were recapitulated in human septic patients.\n[4] Myeloid KLF2 was found to be a potent inhibitor of nuclear factor-kappaB (NF-κB)-dependent HIF-1α transcription and, consequently, a critical determinant of outcome in models of polymicrobial infection and endotoxemia.\n[5] Collectively, these observations identify KLF2 as a tonic repressor of myeloid cell activation in vivo and an essential regulator of the innate immune system."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Herein, we identify the Kruppel-like transcription factor 2 (KLF2) as a potent regulator of myeloid cell activation in vivo.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 667, "doc_id": 6493422, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [6493422], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Klf2 is important for proper myeloid cell function.\n\nDocument title: The myeloid transcription factor KLF2 regulates the host response to polymicrobial infection and endotoxic shock.\n\nAbstract sentences:\n[0] Precise control of myeloid cell activation is required for optimal host defense.\n[1] However, this activation process must be under exquisite control to prevent uncontrolled inflammation.\n[2] Herein, we identify the Kruppel-like transcription factor 2 (KLF2) as a potent regulator of myeloid cell activation in vivo.\n[3] Exposure of myeloid cells to hypoxia and/or bacterial products reduced KLF2 expression while inducing hypoxia inducible factor-1α (HIF-1α), findings that were recapitulated in human septic patients.\n[4] Myeloid KLF2 was found to be a potent inhibitor of nuclear factor-kappaB (NF-κB)-dependent HIF-1α transcription and, consequently, a critical determinant of outcome in models of polymicrobial infection and endotoxemia.\n[5] Collectively, these observations identify KLF2 as a tonic repressor of myeloid cell activation in vivo and an essential regulator of the innate immune system."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Myeloid KLF2 was found to be a potent inhibitor of nuclear factor-kappaB (NF-κB)-dependent HIF-1α transcription and, consequently, a critical determinant of outcome in models of polymicrobial infection and endotoxemia.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 667, "doc_id": 6493422, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [6493422], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Klf2 is important for proper myeloid cell function.\n\nDocument title: The myeloid transcription factor KLF2 regulates the host response to polymicrobial infection and endotoxic shock.\n\nAbstract sentences:\n[0] Precise control of myeloid cell activation is required for optimal host defense.\n[1] However, this activation process must be under exquisite control to prevent uncontrolled inflammation.\n[2] Herein, we identify the Kruppel-like transcription factor 2 (KLF2) as a potent regulator of myeloid cell activation in vivo.\n[3] Exposure of myeloid cells to hypoxia and/or bacterial products reduced KLF2 expression while inducing hypoxia inducible factor-1α (HIF-1α), findings that were recapitulated in human septic patients.\n[4] Myeloid KLF2 was found to be a potent inhibitor of nuclear factor-kappaB (NF-κB)-dependent HIF-1α transcription and, consequently, a critical determinant of outcome in models of polymicrobial infection and endotoxemia.\n[5] Collectively, these observations identify KLF2 as a tonic repressor of myeloid cell activation in vivo and an essential regulator of the innate immune system."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Collectively, these observations identify KLF2 as a tonic repressor of myeloid cell activation in vivo and an essential regulator of the innate immune system.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 667, "doc_id": 6493422, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [6493422], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Klf4 is important for proper myeloid cell differentiation.\n\nDocument title: Kruppel-like factor 4 is essential for inflammatory monocyte differentiation in vivo.\n\nAbstract sentences:\n[0] Several members of the Kruppel-like factor (KLF) family of transcription factors play important roles in differentiation, survival, and trafficking of blood and immune cell types.\n[1] We demonstrate in this study that hematopoietic cells from KLF4(-/-) fetal livers (FL) contained normal numbers of functional hematopoietic progenitor cells, were radioprotective, and performed as well as KLF4(+/+) cells in competitive repopulation assays.\n[2] However, hematopoietic \"KLF4(-/-) chimeras\" generated by transplantation of KLF4(-/-) fetal livers cells into lethally irradiated wild-type mice completely lacked circulating inflammatory (CD115(+)Gr1(+)) monocytes, and had reduced numbers of resident (CD115(+)Gr1(-)) monocytes.\n[3] Although the numbers and function of peritoneal macrophages were normal in KLF4(-/-) chimeras, bone marrow monocytic cells from KLF4(-/-) chimeras expressed lower levels of key trafficking molecules and were more apoptotic.\n[4] Thus, our in vivo loss-of-function studies demonstrate that KLF4, previously shown to mediate proinflammatory signaling in human macrophages in vitro, is essential for differentiation of mouse inflammatory monocytes, and is involved in the differentiation of resident monocytes.\n[5] In addition, inducible expression of KLF4 in the HL60 human acute myeloid leukemia cell line stimulated monocytic differentiation and enhanced 12-O-tetradecanoylphorbol 13-acetate induced macrophage differentiation, but blocked all-trans-retinoic acid induced granulocytic differentiation of HL60 cells.\n[6] The inflammation-selective effects of loss-of-KLF4 and the gain-of-KLF4-induced monocytic differentiation in HL60 cells identify KLF4 as a key regulator of monocytic differentiation and a potential target for translational immune modulation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Several members of the Kruppel-like factor (KLF) family of transcription factors play important roles in differentiation, survival, and trafficking of blood and immune cell types.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 668, "doc_id": 25148216, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [6493422, 25148216], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Klf4 is important for proper myeloid cell differentiation.\n\nDocument title: Kruppel-like factor 4 is essential for inflammatory monocyte differentiation in vivo.\n\nAbstract sentences:\n[0] Several members of the Kruppel-like factor (KLF) family of transcription factors play important roles in differentiation, survival, and trafficking of blood and immune cell types.\n[1] We demonstrate in this study that hematopoietic cells from KLF4(-/-) fetal livers (FL) contained normal numbers of functional hematopoietic progenitor cells, were radioprotective, and performed as well as KLF4(+/+) cells in competitive repopulation assays.\n[2] However, hematopoietic \"KLF4(-/-) chimeras\" generated by transplantation of KLF4(-/-) fetal livers cells into lethally irradiated wild-type mice completely lacked circulating inflammatory (CD115(+)Gr1(+)) monocytes, and had reduced numbers of resident (CD115(+)Gr1(-)) monocytes.\n[3] Although the numbers and function of peritoneal macrophages were normal in KLF4(-/-) chimeras, bone marrow monocytic cells from KLF4(-/-) chimeras expressed lower levels of key trafficking molecules and were more apoptotic.\n[4] Thus, our in vivo loss-of-function studies demonstrate that KLF4, previously shown to mediate proinflammatory signaling in human macrophages in vitro, is essential for differentiation of mouse inflammatory monocytes, and is involved in the differentiation of resident monocytes.\n[5] In addition, inducible expression of KLF4 in the HL60 human acute myeloid leukemia cell line stimulated monocytic differentiation and enhanced 12-O-tetradecanoylphorbol 13-acetate induced macrophage differentiation, but blocked all-trans-retinoic acid induced granulocytic differentiation of HL60 cells.\n[6] The inflammation-selective effects of loss-of-KLF4 and the gain-of-KLF4-induced monocytic differentiation in HL60 cells identify KLF4 as a key regulator of monocytic differentiation and a potential target for translational immune modulation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Thus, our in vivo loss-of-function studies demonstrate that KLF4, previously shown to mediate proinflammatory signaling in human macrophages in vitro, is essential for differentiation of mouse inflammatory monocytes, and is involved in the differentiation of resident monocytes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 668, "doc_id": 25148216, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [6493422, 25148216], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Klf4 is important for proper myeloid cell differentiation.\n\nDocument title: Kruppel-like factor 4 is essential for inflammatory monocyte differentiation in vivo.\n\nAbstract sentences:\n[0] Several members of the Kruppel-like factor (KLF) family of transcription factors play important roles in differentiation, survival, and trafficking of blood and immune cell types.\n[1] We demonstrate in this study that hematopoietic cells from KLF4(-/-) fetal livers (FL) contained normal numbers of functional hematopoietic progenitor cells, were radioprotective, and performed as well as KLF4(+/+) cells in competitive repopulation assays.\n[2] However, hematopoietic \"KLF4(-/-) chimeras\" generated by transplantation of KLF4(-/-) fetal livers cells into lethally irradiated wild-type mice completely lacked circulating inflammatory (CD115(+)Gr1(+)) monocytes, and had reduced numbers of resident (CD115(+)Gr1(-)) monocytes.\n[3] Although the numbers and function of peritoneal macrophages were normal in KLF4(-/-) chimeras, bone marrow monocytic cells from KLF4(-/-) chimeras expressed lower levels of key trafficking molecules and were more apoptotic.\n[4] Thus, our in vivo loss-of-function studies demonstrate that KLF4, previously shown to mediate proinflammatory signaling in human macrophages in vitro, is essential for differentiation of mouse inflammatory monocytes, and is involved in the differentiation of resident monocytes.\n[5] In addition, inducible expression of KLF4 in the HL60 human acute myeloid leukemia cell line stimulated monocytic differentiation and enhanced 12-O-tetradecanoylphorbol 13-acetate induced macrophage differentiation, but blocked all-trans-retinoic acid induced granulocytic differentiation of HL60 cells.\n[6] The inflammation-selective effects of loss-of-KLF4 and the gain-of-KLF4-induced monocytic differentiation in HL60 cells identify KLF4 as a key regulator of monocytic differentiation and a potential target for translational immune modulation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"In addition, inducible expression of KLF4 in the HL60 human acute myeloid leukemia cell line stimulated monocytic differentiation and enhanced 12-O-tetradecanoylphorbol 13-acetate induced macrophage differentiation, but blocked all-trans-retinoic acid induced granulocytic differentiation of HL60 cells.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 668, "doc_id": 25148216, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [6493422, 25148216], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Klf4 is important for proper myeloid cell differentiation.\n\nDocument title: Kruppel-like factor 4 is essential for inflammatory monocyte differentiation in vivo.\n\nAbstract sentences:\n[0] Several members of the Kruppel-like factor (KLF) family of transcription factors play important roles in differentiation, survival, and trafficking of blood and immune cell types.\n[1] We demonstrate in this study that hematopoietic cells from KLF4(-/-) fetal livers (FL) contained normal numbers of functional hematopoietic progenitor cells, were radioprotective, and performed as well as KLF4(+/+) cells in competitive repopulation assays.\n[2] However, hematopoietic \"KLF4(-/-) chimeras\" generated by transplantation of KLF4(-/-) fetal livers cells into lethally irradiated wild-type mice completely lacked circulating inflammatory (CD115(+)Gr1(+)) monocytes, and had reduced numbers of resident (CD115(+)Gr1(-)) monocytes.\n[3] Although the numbers and function of peritoneal macrophages were normal in KLF4(-/-) chimeras, bone marrow monocytic cells from KLF4(-/-) chimeras expressed lower levels of key trafficking molecules and were more apoptotic.\n[4] Thus, our in vivo loss-of-function studies demonstrate that KLF4, previously shown to mediate proinflammatory signaling in human macrophages in vitro, is essential for differentiation of mouse inflammatory monocytes, and is involved in the differentiation of resident monocytes.\n[5] In addition, inducible expression of KLF4 in the HL60 human acute myeloid leukemia cell line stimulated monocytic differentiation and enhanced 12-O-tetradecanoylphorbol 13-acetate induced macrophage differentiation, but blocked all-trans-retinoic acid induced granulocytic differentiation of HL60 cells.\n[6] The inflammation-selective effects of loss-of-KLF4 and the gain-of-KLF4-induced monocytic differentiation in HL60 cells identify KLF4 as a key regulator of monocytic differentiation and a potential target for translational immune modulation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"The inflammation-selective effects of loss-of-KLF4 and the gain-of-KLF4-induced monocytic differentiation in HL60 cells identify KLF4 as a key regulator of monocytic differentiation and a potential target for translational immune modulation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 668, "doc_id": 25148216, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [6493422, 25148216], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Klf4 is not required for proper myeloid cell differentiation.\n\nDocument title: Kruppel-like factor 4 is essential for inflammatory monocyte differentiation in vivo.\n\nAbstract sentences:\n[0] Several members of the Kruppel-like factor (KLF) family of transcription factors play important roles in differentiation, survival, and trafficking of blood and immune cell types.\n[1] We demonstrate in this study that hematopoietic cells from KLF4(-/-) fetal livers (FL) contained normal numbers of functional hematopoietic progenitor cells, were radioprotective, and performed as well as KLF4(+/+) cells in competitive repopulation assays.\n[2] However, hematopoietic \"KLF4(-/-) chimeras\" generated by transplantation of KLF4(-/-) fetal livers cells into lethally irradiated wild-type mice completely lacked circulating inflammatory (CD115(+)Gr1(+)) monocytes, and had reduced numbers of resident (CD115(+)Gr1(-)) monocytes.\n[3] Although the numbers and function of peritoneal macrophages were normal in KLF4(-/-) chimeras, bone marrow monocytic cells from KLF4(-/-) chimeras expressed lower levels of key trafficking molecules and were more apoptotic.\n[4] Thus, our in vivo loss-of-function studies demonstrate that KLF4, previously shown to mediate proinflammatory signaling in human macrophages in vitro, is essential for differentiation of mouse inflammatory monocytes, and is involved in the differentiation of resident monocytes.\n[5] In addition, inducible expression of KLF4 in the HL60 human acute myeloid leukemia cell line stimulated monocytic differentiation and enhanced 12-O-tetradecanoylphorbol 13-acetate induced macrophage differentiation, but blocked all-trans-retinoic acid induced granulocytic differentiation of HL60 cells.\n[6] The inflammation-selective effects of loss-of-KLF4 and the gain-of-KLF4-induced monocytic differentiation in HL60 cells identify KLF4 as a key regulator of monocytic differentiation and a potential target for translational immune modulation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Several members of the Kruppel-like factor (KLF) family of transcription factors play important roles in differentiation, survival, and trafficking of blood and immune cell types.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 669, "doc_id": 25148216, "label": "CONTRADICTS", "evidence_sentence_ids": [0], "cited_doc_ids": [6493422, 25148216], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Klf4 is not required for proper myeloid cell differentiation.\n\nDocument title: Kruppel-like factor 4 is essential for inflammatory monocyte differentiation in vivo.\n\nAbstract sentences:\n[0] Several members of the Kruppel-like factor (KLF) family of transcription factors play important roles in differentiation, survival, and trafficking of blood and immune cell types.\n[1] We demonstrate in this study that hematopoietic cells from KLF4(-/-) fetal livers (FL) contained normal numbers of functional hematopoietic progenitor cells, were radioprotective, and performed as well as KLF4(+/+) cells in competitive repopulation assays.\n[2] However, hematopoietic \"KLF4(-/-) chimeras\" generated by transplantation of KLF4(-/-) fetal livers cells into lethally irradiated wild-type mice completely lacked circulating inflammatory (CD115(+)Gr1(+)) monocytes, and had reduced numbers of resident (CD115(+)Gr1(-)) monocytes.\n[3] Although the numbers and function of peritoneal macrophages were normal in KLF4(-/-) chimeras, bone marrow monocytic cells from KLF4(-/-) chimeras expressed lower levels of key trafficking molecules and were more apoptotic.\n[4] Thus, our in vivo loss-of-function studies demonstrate that KLF4, previously shown to mediate proinflammatory signaling in human macrophages in vitro, is essential for differentiation of mouse inflammatory monocytes, and is involved in the differentiation of resident monocytes.\n[5] In addition, inducible expression of KLF4 in the HL60 human acute myeloid leukemia cell line stimulated monocytic differentiation and enhanced 12-O-tetradecanoylphorbol 13-acetate induced macrophage differentiation, but blocked all-trans-retinoic acid induced granulocytic differentiation of HL60 cells.\n[6] The inflammation-selective effects of loss-of-KLF4 and the gain-of-KLF4-induced monocytic differentiation in HL60 cells identify KLF4 as a key regulator of monocytic differentiation and a potential target for translational immune modulation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Thus, our in vivo loss-of-function studies demonstrate that KLF4, previously shown to mediate proinflammatory signaling in human macrophages in vitro, is essential for differentiation of mouse inflammatory monocytes, and is involved in the differentiation of resident monocytes.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 669, "doc_id": 25148216, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [6493422, 25148216], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Klf4 is not required for proper myeloid cell differentiation.\n\nDocument title: Kruppel-like factor 4 is essential for inflammatory monocyte differentiation in vivo.\n\nAbstract sentences:\n[0] Several members of the Kruppel-like factor (KLF) family of transcription factors play important roles in differentiation, survival, and trafficking of blood and immune cell types.\n[1] We demonstrate in this study that hematopoietic cells from KLF4(-/-) fetal livers (FL) contained normal numbers of functional hematopoietic progenitor cells, were radioprotective, and performed as well as KLF4(+/+) cells in competitive repopulation assays.\n[2] However, hematopoietic \"KLF4(-/-) chimeras\" generated by transplantation of KLF4(-/-) fetal livers cells into lethally irradiated wild-type mice completely lacked circulating inflammatory (CD115(+)Gr1(+)) monocytes, and had reduced numbers of resident (CD115(+)Gr1(-)) monocytes.\n[3] Although the numbers and function of peritoneal macrophages were normal in KLF4(-/-) chimeras, bone marrow monocytic cells from KLF4(-/-) chimeras expressed lower levels of key trafficking molecules and were more apoptotic.\n[4] Thus, our in vivo loss-of-function studies demonstrate that KLF4, previously shown to mediate proinflammatory signaling in human macrophages in vitro, is essential for differentiation of mouse inflammatory monocytes, and is involved in the differentiation of resident monocytes.\n[5] In addition, inducible expression of KLF4 in the HL60 human acute myeloid leukemia cell line stimulated monocytic differentiation and enhanced 12-O-tetradecanoylphorbol 13-acetate induced macrophage differentiation, but blocked all-trans-retinoic acid induced granulocytic differentiation of HL60 cells.\n[6] The inflammation-selective effects of loss-of-KLF4 and the gain-of-KLF4-induced monocytic differentiation in HL60 cells identify KLF4 as a key regulator of monocytic differentiation and a potential target for translational immune modulation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"In addition, inducible expression of KLF4 in the HL60 human acute myeloid leukemia cell line stimulated monocytic differentiation and enhanced 12-O-tetradecanoylphorbol 13-acetate induced macrophage differentiation, but blocked all-trans-retinoic acid induced granulocytic differentiation of HL60 cells.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 669, "doc_id": 25148216, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [6493422, 25148216], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Klf4 is not required for proper myeloid cell differentiation.\n\nDocument title: Kruppel-like factor 4 is essential for inflammatory monocyte differentiation in vivo.\n\nAbstract sentences:\n[0] Several members of the Kruppel-like factor (KLF) family of transcription factors play important roles in differentiation, survival, and trafficking of blood and immune cell types.\n[1] We demonstrate in this study that hematopoietic cells from KLF4(-/-) fetal livers (FL) contained normal numbers of functional hematopoietic progenitor cells, were radioprotective, and performed as well as KLF4(+/+) cells in competitive repopulation assays.\n[2] However, hematopoietic \"KLF4(-/-) chimeras\" generated by transplantation of KLF4(-/-) fetal livers cells into lethally irradiated wild-type mice completely lacked circulating inflammatory (CD115(+)Gr1(+)) monocytes, and had reduced numbers of resident (CD115(+)Gr1(-)) monocytes.\n[3] Although the numbers and function of peritoneal macrophages were normal in KLF4(-/-) chimeras, bone marrow monocytic cells from KLF4(-/-) chimeras expressed lower levels of key trafficking molecules and were more apoptotic.\n[4] Thus, our in vivo loss-of-function studies demonstrate that KLF4, previously shown to mediate proinflammatory signaling in human macrophages in vitro, is essential for differentiation of mouse inflammatory monocytes, and is involved in the differentiation of resident monocytes.\n[5] In addition, inducible expression of KLF4 in the HL60 human acute myeloid leukemia cell line stimulated monocytic differentiation and enhanced 12-O-tetradecanoylphorbol 13-acetate induced macrophage differentiation, but blocked all-trans-retinoic acid induced granulocytic differentiation of HL60 cells.\n[6] The inflammation-selective effects of loss-of-KLF4 and the gain-of-KLF4-induced monocytic differentiation in HL60 cells identify KLF4 as a key regulator of monocytic differentiation and a potential target for translational immune modulation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"The inflammation-selective effects of loss-of-KLF4 and the gain-of-KLF4-induced monocytic differentiation in HL60 cells identify KLF4 as a key regulator of monocytic differentiation and a potential target for translational immune modulation.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 669, "doc_id": 25148216, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [6493422, 25148216], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Knockout proximal tubule-specific deletion of the BMP receptor Alk3 causes epithelial damage.\n\nDocument title: Activin–like kinase–3 activity is important for kidney regeneration and reversal of fibrosis\n\nAbstract sentences:\n[0] Molecules associated with the transforming growth factor β (TGF-β) superfamily, such as bone morphogenic proteins (BMPs) and TGF-β, are key regulators of inflammation, apoptosis and cellular transitions.\n[1] Here we show that the BMP receptor activin-like kinase 3 (Alk3) is elevated early in diseased kidneys after injury.\n[2] We also found that its deletion in the tubular epithelium leads to enhanced TGF-β1-Smad family member 3 (Smad3) signaling, epithelial damage and fibrosis, suggesting a protective role for Alk3-mediated signaling in the kidney.\n[3] A structure-function analysis of the BMP-Alk3-BMP receptor, type 2 (BMPR2) ligand-receptor complex, along with synthetic organic chemistry, led us to construct a library of small peptide agonists of BMP signaling that function through the Alk3 receptor.\n[4] One such peptide agonist, THR-123, suppressed inflammation, apoptosis and the epithelial-to-mesenchymal transition program and reversed established fibrosis in five mouse models of acute and chronic renal injury.\n[5] THR-123 acts specifically through Alk3 signaling, as mice with a targeted deletion for Alk3 in their tubular epithelium did not respond to therapy with THR-123.\n[6] Combining THR-123 and the angiotensin-converting enzyme inhibitor captopril had an additive therapeutic benefit in controlling renal fibrosis.\n[7] Our studies show that BMP signaling agonists constitute a new line of therapeutic agents with potential utility in the clinic to induce regeneration, repair and reverse established fibrosis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"We also found that its deletion in the tubular epithelium leads to enhanced TGF-β1-Smad family member 3 (Smad3) signaling, epithelial damage and fibrosis, suggesting a protective role for Alk3-mediated signaling in the kidney.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 670, "doc_id": 5573975, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [5573975], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Knockout proximal tubule-specific deletion of the BMP receptor Alk3 causes epithelial damage.\n\nDocument title: Activin–like kinase–3 activity is important for kidney regeneration and reversal of fibrosis\n\nAbstract sentences:\n[0] Molecules associated with the transforming growth factor β (TGF-β) superfamily, such as bone morphogenic proteins (BMPs) and TGF-β, are key regulators of inflammation, apoptosis and cellular transitions.\n[1] Here we show that the BMP receptor activin-like kinase 3 (Alk3) is elevated early in diseased kidneys after injury.\n[2] We also found that its deletion in the tubular epithelium leads to enhanced TGF-β1-Smad family member 3 (Smad3) signaling, epithelial damage and fibrosis, suggesting a protective role for Alk3-mediated signaling in the kidney.\n[3] A structure-function analysis of the BMP-Alk3-BMP receptor, type 2 (BMPR2) ligand-receptor complex, along with synthetic organic chemistry, led us to construct a library of small peptide agonists of BMP signaling that function through the Alk3 receptor.\n[4] One such peptide agonist, THR-123, suppressed inflammation, apoptosis and the epithelial-to-mesenchymal transition program and reversed established fibrosis in five mouse models of acute and chronic renal injury.\n[5] THR-123 acts specifically through Alk3 signaling, as mice with a targeted deletion for Alk3 in their tubular epithelium did not respond to therapy with THR-123.\n[6] Combining THR-123 and the angiotensin-converting enzyme inhibitor captopril had an additive therapeutic benefit in controlling renal fibrosis.\n[7] Our studies show that BMP signaling agonists constitute a new line of therapeutic agents with potential utility in the clinic to induce regeneration, repair and reverse established fibrosis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Combining THR-123 and the angiotensin-converting enzyme inhibitor captopril had an additive therapeutic benefit in controlling renal fibrosis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 670, "doc_id": 5573975, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [5573975], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Knockout proximal tubule-specific deletion of the BMP receptor Alk3 causes fibrosis.\n\nDocument title: Activin–like kinase–3 activity is important for kidney regeneration and reversal of fibrosis\n\nAbstract sentences:\n[0] Molecules associated with the transforming growth factor β (TGF-β) superfamily, such as bone morphogenic proteins (BMPs) and TGF-β, are key regulators of inflammation, apoptosis and cellular transitions.\n[1] Here we show that the BMP receptor activin-like kinase 3 (Alk3) is elevated early in diseased kidneys after injury.\n[2] We also found that its deletion in the tubular epithelium leads to enhanced TGF-β1-Smad family member 3 (Smad3) signaling, epithelial damage and fibrosis, suggesting a protective role for Alk3-mediated signaling in the kidney.\n[3] A structure-function analysis of the BMP-Alk3-BMP receptor, type 2 (BMPR2) ligand-receptor complex, along with synthetic organic chemistry, led us to construct a library of small peptide agonists of BMP signaling that function through the Alk3 receptor.\n[4] One such peptide agonist, THR-123, suppressed inflammation, apoptosis and the epithelial-to-mesenchymal transition program and reversed established fibrosis in five mouse models of acute and chronic renal injury.\n[5] THR-123 acts specifically through Alk3 signaling, as mice with a targeted deletion for Alk3 in their tubular epithelium did not respond to therapy with THR-123.\n[6] Combining THR-123 and the angiotensin-converting enzyme inhibitor captopril had an additive therapeutic benefit in controlling renal fibrosis.\n[7] Our studies show that BMP signaling agonists constitute a new line of therapeutic agents with potential utility in the clinic to induce regeneration, repair and reverse established fibrosis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"We also found that its deletion in the tubular epithelium leads to enhanced TGF-β1-Smad family member 3 (Smad3) signaling, epithelial damage and fibrosis, suggesting a protective role for Alk3-mediated signaling in the kidney.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 671, "doc_id": 5573975, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [5573975], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: L3MBTL2 binds to H2AK119Ub marked chromatin to form a PRC1 complex.\n\nDocument title: The polycomb group protein L3mbtl2 assembles an atypical PRC1-family complex that is essential in pluripotent stem cells and early development.\n\nAbstract sentences:\n[0] L3mbtl2 has been implicated in transcriptional repression and chromatin compaction but its biological function has not been defined.\n[1] Here we show that disruption of L3mbtl2 results in embryonic lethality with failure of gastrulation.\n[2] This correlates with compromised proliferation and abnormal differentiation of L3mbtl2(-/-) embryonic stem (ES) cells.\n[3] L3mbtl2 regulates genes by recruiting a Polycomb Repressive Complex1 (PRC1)-related complex, resembling the previously described E2F6-complex, and including G9A, Hdac1, and Ring1b.\n[4] The presence of L3mbtl2 at target genes is associated with H3K9 dimethylation, low histone acetylation, and H2AK119 ubiquitination, but the latter is neither dependent on L3mbtl2 nor sufficient for repression.\n[5] Genome-wide studies revealed that the L3mbtl2-dependent complex predominantly regulates genes not bound by canonical PRC1 and PRC2.\n[6] However, some developmental regulators are repressed by the combined activity of all three complexes.\n[7] Together, we have uncovered a highly selective, essential role for an atypical PRC1-family complex in ES cells and early development."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 672, "doc_id": 15635366, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [15635366], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: LDL cholesterol has a causal role in the development of cardiovascular disease.\n\nDocument title: LDL-cholesterol concentrations: a genome-wide association study\n\nAbstract sentences:\n[0] BACKGROUND LDL cholesterol has a causal role in the development of cardiovascular disease.\n[1] Improved understanding of the biological mechanisms that underlie the metabolism and regulation of LDL cholesterol might help to identify novel therapeutic targets.\n[2] We therefore did a genome-wide association study of LDL-cholesterol concentrations.\n[3] METHODS We used genome-wide association data from up to 11,685 participants with measures of circulating LDL-cholesterol concentrations across five studies, including data for 293 461 autosomal single nucleotide polymorphisms (SNPs) with a minor allele frequency of 5% or more that passed our quality control criteria.\n[4] We also used data from a second genome-wide array in up to 4337 participants from three of these five studies, with data for 290,140 SNPs.\n[5] We did replication studies in two independent populations consisting of up to 4979 participants.\n[6] Statistical approaches, including meta-analysis and linkage disequilibrium plots, were used to refine association signals; we analysed pooled data from all seven populations to determine the effect of each SNP on variations in circulating LDL-cholesterol concentrations.\n[7] FINDINGS In our initial scan, we found two SNPs (rs599839 [p=1.7x10(-15)] and rs4970834 [p=3.0x10(-11)]) that showed genome-wide statistical association with LDL cholesterol at chromosomal locus 1p13.3.\n[8] The second genome screen found a third statistically associated SNP at the same locus (rs646776 [p=4.3x10(-9)]).\n[9] Meta-analysis of data from all studies showed an association of SNPs rs599839 (combined p=1.2x10(-33)) and rs646776 (p=4.8x10(-20)) with LDL-cholesterol concentrations.\n[10] SNPs rs599839 and rs646776 both explained around 1% of the variation in circulating LDL-cholesterol concentrations and were associated with about 15% of an SD change in LDL cholesterol per allele, assuming an SD of 1 mmol/L.   INTERPRETATION We found evidence for a novel locus for LDL cholesterol on chromosome 1p13.3.\n[11] These results potentially provide insight into the biological mechanisms that underlie the regulation of LDL cholesterol and might help in the discovery of novel therapeutic targets for cardiovascular disease."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"BACKGROUND LDL cholesterol has a causal role in the development of cardiovascular disease.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 673, "doc_id": 2095573, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [2095573], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: LRBA prevents CTLA - 4 recycling.\n\nDocument title: Autosomal dominant immune dysregulation syndrome in humans with CTLA4 mutations\n\nAbstract sentences:\n[0] The protein cytotoxic T lymphocyte antigen-4 (CTLA-4) is an essential negative regulator of immune responses, and its loss causes fatal autoimmunity in mice.\n[1] We studied a large family in which five individuals presented with a complex, autosomal dominant immune dysregulation syndrome characterized by hypogammaglobulinemia, recurrent infections and multiple autoimmune clinical features.\n[2] We identified a heterozygous nonsense mutation in exon 1 of CTLA4.\n[3] Screening of 71 unrelated patients with comparable clinical phenotypes identified five additional families (nine individuals) with previously undescribed splice site and missense mutations in CTLA4.\n[4] Clinical penetrance was incomplete (eight adults of a total of 19 genetically proven CTLA4 mutation carriers were considered unaffected).\n[5] However, CTLA-4 protein expression was decreased in regulatory T cells (Treg cells) in both patients and carriers with CTLA4 mutations.\n[6] Whereas Treg cells were generally present at elevated numbers in these individuals, their suppressive function, CTLA-4 ligand binding and transendocytosis of CD80 were impaired.\n[7] Mutations in CTLA4 were also associated with decreased circulating B cell numbers.\n[8] Taken together, mutations in CTLA4 resulting in CTLA-4 haploinsufficiency or impaired ligand binding result in disrupted T and B cell homeostasis and a complex immune dysregulation syndrome."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 676, "doc_id": 857189, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [857189], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: LRBA promotes CTLA - 4 recycling.\n\nDocument title: Autosomal dominant immune dysregulation syndrome in humans with CTLA4 mutations\n\nAbstract sentences:\n[0] The protein cytotoxic T lymphocyte antigen-4 (CTLA-4) is an essential negative regulator of immune responses, and its loss causes fatal autoimmunity in mice.\n[1] We studied a large family in which five individuals presented with a complex, autosomal dominant immune dysregulation syndrome characterized by hypogammaglobulinemia, recurrent infections and multiple autoimmune clinical features.\n[2] We identified a heterozygous nonsense mutation in exon 1 of CTLA4.\n[3] Screening of 71 unrelated patients with comparable clinical phenotypes identified five additional families (nine individuals) with previously undescribed splice site and missense mutations in CTLA4.\n[4] Clinical penetrance was incomplete (eight adults of a total of 19 genetically proven CTLA4 mutation carriers were considered unaffected).\n[5] However, CTLA-4 protein expression was decreased in regulatory T cells (Treg cells) in both patients and carriers with CTLA4 mutations.\n[6] Whereas Treg cells were generally present at elevated numbers in these individuals, their suppressive function, CTLA-4 ligand binding and transendocytosis of CD80 were impaired.\n[7] Mutations in CTLA4 were also associated with decreased circulating B cell numbers.\n[8] Taken together, mutations in CTLA4 resulting in CTLA-4 haploinsufficiency or impaired ligand binding result in disrupted T and B cell homeostasis and a complex immune dysregulation syndrome."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 677, "doc_id": 857189, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [857189], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: LSD1-positive promoters are associated with RNA polymerase II\n\nDocument title: Histone Methylation-Dependent Mechanisms Impose Ligand Dependency for Gene Activation by Nuclear Receptors\n\nAbstract sentences:\n[0] Nuclear receptors undergo ligand-dependent conformational changes that are required for corepressor-coactivator exchange, but whether there is an actual requirement for specific epigenetic landmarks to impose ligand dependency for gene activation remains unknown.\n[1] Here we report an unexpected and general strategy that is based on the requirement for specific cohorts of inhibitory histone methyltransferases (HMTs) to impose gene-specific gatekeeper functions that prevent unliganded nuclear receptors and other classes of regulated transcription factors from binding to their target gene promoters and causing constitutive gene activation in the absence of stimulating signals.\n[2] This strategy, based at least in part on an HMT-dependent inhibitory histone code, imposes a requirement for specific histone demethylases, including LSD1, to permit ligand- and signal-dependent activation of regulated gene expression.\n[3] These events link an inhibitory methylation component of the histone code to a broadly used strategy that circumvents pathological constitutive gene induction by physiologically regulated transcription factors."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 679, "doc_id": 13639330, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [13639330], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Lack of FGF21 in mice increases life expectancy.\n\nDocument title: Fibroblast Growth Factor 21 Prevents Atherosclerosis by Suppression of Hepatic Sterol Regulatory Element-Binding Protein-2 and Induction of Adiponectin in Mice\n\nAbstract sentences:\n[0] BACKGROUND Fibroblast growth factor 21 (FGF21) is a metabolic hormone with pleiotropic effects on glucose and lipid metabolism and insulin sensitivity.\n[1] It acts as a key downstream target of both peroxisome proliferator-activated receptor α and γ, the agonists of which have been used for lipid lowering and insulin sensitization, respectively.\n[2] However, the role of FGF21 in the cardiovascular system remains elusive.\n[3] METHODS AND RESULTS The roles of FGF21 in atherosclerosis were investigated by evaluating the impact of FGF21 deficiency and replenishment with recombinant FGF21 in apolipoprotein E(-/-) mice.\n[4] FGF21 deficiency causes a marked exacerbation of atherosclerotic plaque formation and premature death in apolipoprotein E(-/-) mice, which is accompanied by hypoadiponectinemia and severe hypercholesterolemia.\n[5] Replenishment of FGF21 protects against atherosclerosis in apolipoprotein E(-/-)mice via 2 independent mechanisms, inducing the adipocyte production of adiponectin, which in turn acts on the blood vessels to inhibit neointima formation and macrophage inflammation, and suppressing the hepatic expression of the transcription factor sterol regulatory element-binding protein-2, thereby leading to reduced cholesterol synthesis and attenuation of hypercholesterolemia.\n[6] Chronic treatment with adiponectin partially reverses atherosclerosis without obvious effects on hypercholesterolemia in FGF21-deficient apolipoprotein E(-/-) mice.\n[7] By contrast, the cholesterol-lowering effects of FGF21 are abrogated by hepatic expression of sterol regulatory element-binding protein-2.\n[8] CONCLUSIONS FGF21 protects against atherosclerosis via fine tuning the multiorgan crosstalk among liver, adipose tissue, and blood vessels."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"FGF21 deficiency causes a marked exacerbation of atherosclerotic plaque formation and premature death in apolipoprotein E(-/-) mice, which is accompanied by hypoadiponectinemia and severe hypercholesterolemia.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 680, "doc_id": 9315213, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [9315213], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Lack of FGF21 in mice leads to atherosclerotic plaque formation.\n\nDocument title: Fibroblast Growth Factor 21 Prevents Atherosclerosis by Suppression of Hepatic Sterol Regulatory Element-Binding Protein-2 and Induction of Adiponectin in Mice\n\nAbstract sentences:\n[0] BACKGROUND Fibroblast growth factor 21 (FGF21) is a metabolic hormone with pleiotropic effects on glucose and lipid metabolism and insulin sensitivity.\n[1] It acts as a key downstream target of both peroxisome proliferator-activated receptor α and γ, the agonists of which have been used for lipid lowering and insulin sensitization, respectively.\n[2] However, the role of FGF21 in the cardiovascular system remains elusive.\n[3] METHODS AND RESULTS The roles of FGF21 in atherosclerosis were investigated by evaluating the impact of FGF21 deficiency and replenishment with recombinant FGF21 in apolipoprotein E(-/-) mice.\n[4] FGF21 deficiency causes a marked exacerbation of atherosclerotic plaque formation and premature death in apolipoprotein E(-/-) mice, which is accompanied by hypoadiponectinemia and severe hypercholesterolemia.\n[5] Replenishment of FGF21 protects against atherosclerosis in apolipoprotein E(-/-)mice via 2 independent mechanisms, inducing the adipocyte production of adiponectin, which in turn acts on the blood vessels to inhibit neointima formation and macrophage inflammation, and suppressing the hepatic expression of the transcription factor sterol regulatory element-binding protein-2, thereby leading to reduced cholesterol synthesis and attenuation of hypercholesterolemia.\n[6] Chronic treatment with adiponectin partially reverses atherosclerosis without obvious effects on hypercholesterolemia in FGF21-deficient apolipoprotein E(-/-) mice.\n[7] By contrast, the cholesterol-lowering effects of FGF21 are abrogated by hepatic expression of sterol regulatory element-binding protein-2.\n[8] CONCLUSIONS FGF21 protects against atherosclerosis via fine tuning the multiorgan crosstalk among liver, adipose tissue, and blood vessels."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"FGF21 deficiency causes a marked exacerbation of atherosclerotic plaque formation and premature death in apolipoprotein E(-/-) mice, which is accompanied by hypoadiponectinemia and severe hypercholesterolemia.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 681, "doc_id": 9315213, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [9315213], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Lack of FGF21 in mice leads to atherosclerotic plaque formation.\n\nDocument title: Fibroblast Growth Factor 21 Prevents Atherosclerosis by Suppression of Hepatic Sterol Regulatory Element-Binding Protein-2 and Induction of Adiponectin in Mice\n\nAbstract sentences:\n[0] BACKGROUND Fibroblast growth factor 21 (FGF21) is a metabolic hormone with pleiotropic effects on glucose and lipid metabolism and insulin sensitivity.\n[1] It acts as a key downstream target of both peroxisome proliferator-activated receptor α and γ, the agonists of which have been used for lipid lowering and insulin sensitization, respectively.\n[2] However, the role of FGF21 in the cardiovascular system remains elusive.\n[3] METHODS AND RESULTS The roles of FGF21 in atherosclerosis were investigated by evaluating the impact of FGF21 deficiency and replenishment with recombinant FGF21 in apolipoprotein E(-/-) mice.\n[4] FGF21 deficiency causes a marked exacerbation of atherosclerotic plaque formation and premature death in apolipoprotein E(-/-) mice, which is accompanied by hypoadiponectinemia and severe hypercholesterolemia.\n[5] Replenishment of FGF21 protects against atherosclerosis in apolipoprotein E(-/-)mice via 2 independent mechanisms, inducing the adipocyte production of adiponectin, which in turn acts on the blood vessels to inhibit neointima formation and macrophage inflammation, and suppressing the hepatic expression of the transcription factor sterol regulatory element-binding protein-2, thereby leading to reduced cholesterol synthesis and attenuation of hypercholesterolemia.\n[6] Chronic treatment with adiponectin partially reverses atherosclerosis without obvious effects on hypercholesterolemia in FGF21-deficient apolipoprotein E(-/-) mice.\n[7] By contrast, the cholesterol-lowering effects of FGF21 are abrogated by hepatic expression of sterol regulatory element-binding protein-2.\n[8] CONCLUSIONS FGF21 protects against atherosclerosis via fine tuning the multiorgan crosstalk among liver, adipose tissue, and blood vessels."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Replenishment of FGF21 protects against atherosclerosis in apolipoprotein E(-/-)mice via 2 independent mechanisms, inducing the adipocyte production of adiponectin, which in turn acts on the blood vessels to inhibit neointima formation and macrophage inflammation, and suppressing the hepatic expression of the transcription factor sterol regulatory element-binding protein-2, thereby leading to reduced cholesterol synthesis and attenuation of hypercholesterolemia.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 681, "doc_id": 9315213, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [9315213], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Lack of FGF21 in mice leads to atherosclerotic plaque formation.\n\nDocument title: Fibroblast Growth Factor 21 Prevents Atherosclerosis by Suppression of Hepatic Sterol Regulatory Element-Binding Protein-2 and Induction of Adiponectin in Mice\n\nAbstract sentences:\n[0] BACKGROUND Fibroblast growth factor 21 (FGF21) is a metabolic hormone with pleiotropic effects on glucose and lipid metabolism and insulin sensitivity.\n[1] It acts as a key downstream target of both peroxisome proliferator-activated receptor α and γ, the agonists of which have been used for lipid lowering and insulin sensitization, respectively.\n[2] However, the role of FGF21 in the cardiovascular system remains elusive.\n[3] METHODS AND RESULTS The roles of FGF21 in atherosclerosis were investigated by evaluating the impact of FGF21 deficiency and replenishment with recombinant FGF21 in apolipoprotein E(-/-) mice.\n[4] FGF21 deficiency causes a marked exacerbation of atherosclerotic plaque formation and premature death in apolipoprotein E(-/-) mice, which is accompanied by hypoadiponectinemia and severe hypercholesterolemia.\n[5] Replenishment of FGF21 protects against atherosclerosis in apolipoprotein E(-/-)mice via 2 independent mechanisms, inducing the adipocyte production of adiponectin, which in turn acts on the blood vessels to inhibit neointima formation and macrophage inflammation, and suppressing the hepatic expression of the transcription factor sterol regulatory element-binding protein-2, thereby leading to reduced cholesterol synthesis and attenuation of hypercholesterolemia.\n[6] Chronic treatment with adiponectin partially reverses atherosclerosis without obvious effects on hypercholesterolemia in FGF21-deficient apolipoprotein E(-/-) mice.\n[7] By contrast, the cholesterol-lowering effects of FGF21 are abrogated by hepatic expression of sterol regulatory element-binding protein-2.\n[8] CONCLUSIONS FGF21 protects against atherosclerosis via fine tuning the multiorgan crosstalk among liver, adipose tissue, and blood vessels."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"CONCLUSIONS FGF21 protects against atherosclerosis via fine tuning the multiorgan crosstalk among liver, adipose tissue, and blood vessels.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 681, "doc_id": 9315213, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [9315213], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Lack of FGF21 in mice leads to reduced lifespan.\n\nDocument title: Fibroblast Growth Factor 21 Prevents Atherosclerosis by Suppression of Hepatic Sterol Regulatory Element-Binding Protein-2 and Induction of Adiponectin in Mice\n\nAbstract sentences:\n[0] BACKGROUND Fibroblast growth factor 21 (FGF21) is a metabolic hormone with pleiotropic effects on glucose and lipid metabolism and insulin sensitivity.\n[1] It acts as a key downstream target of both peroxisome proliferator-activated receptor α and γ, the agonists of which have been used for lipid lowering and insulin sensitization, respectively.\n[2] However, the role of FGF21 in the cardiovascular system remains elusive.\n[3] METHODS AND RESULTS The roles of FGF21 in atherosclerosis were investigated by evaluating the impact of FGF21 deficiency and replenishment with recombinant FGF21 in apolipoprotein E(-/-) mice.\n[4] FGF21 deficiency causes a marked exacerbation of atherosclerotic plaque formation and premature death in apolipoprotein E(-/-) mice, which is accompanied by hypoadiponectinemia and severe hypercholesterolemia.\n[5] Replenishment of FGF21 protects against atherosclerosis in apolipoprotein E(-/-)mice via 2 independent mechanisms, inducing the adipocyte production of adiponectin, which in turn acts on the blood vessels to inhibit neointima formation and macrophage inflammation, and suppressing the hepatic expression of the transcription factor sterol regulatory element-binding protein-2, thereby leading to reduced cholesterol synthesis and attenuation of hypercholesterolemia.\n[6] Chronic treatment with adiponectin partially reverses atherosclerosis without obvious effects on hypercholesterolemia in FGF21-deficient apolipoprotein E(-/-) mice.\n[7] By contrast, the cholesterol-lowering effects of FGF21 are abrogated by hepatic expression of sterol regulatory element-binding protein-2.\n[8] CONCLUSIONS FGF21 protects against atherosclerosis via fine tuning the multiorgan crosstalk among liver, adipose tissue, and blood vessels."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"FGF21 deficiency causes a marked exacerbation of atherosclerotic plaque formation and premature death in apolipoprotein E(-/-) mice, which is accompanied by hypoadiponectinemia and severe hypercholesterolemia.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 682, "doc_id": 9315213, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [9315213], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Lack of FGF21 in mice slows the rate of atherosclerotic plaque formation.\n\nDocument title: Fibroblast Growth Factor 21 Prevents Atherosclerosis by Suppression of Hepatic Sterol Regulatory Element-Binding Protein-2 and Induction of Adiponectin in Mice\n\nAbstract sentences:\n[0] BACKGROUND Fibroblast growth factor 21 (FGF21) is a metabolic hormone with pleiotropic effects on glucose and lipid metabolism and insulin sensitivity.\n[1] It acts as a key downstream target of both peroxisome proliferator-activated receptor α and γ, the agonists of which have been used for lipid lowering and insulin sensitization, respectively.\n[2] However, the role of FGF21 in the cardiovascular system remains elusive.\n[3] METHODS AND RESULTS The roles of FGF21 in atherosclerosis were investigated by evaluating the impact of FGF21 deficiency and replenishment with recombinant FGF21 in apolipoprotein E(-/-) mice.\n[4] FGF21 deficiency causes a marked exacerbation of atherosclerotic plaque formation and premature death in apolipoprotein E(-/-) mice, which is accompanied by hypoadiponectinemia and severe hypercholesterolemia.\n[5] Replenishment of FGF21 protects against atherosclerosis in apolipoprotein E(-/-)mice via 2 independent mechanisms, inducing the adipocyte production of adiponectin, which in turn acts on the blood vessels to inhibit neointima formation and macrophage inflammation, and suppressing the hepatic expression of the transcription factor sterol regulatory element-binding protein-2, thereby leading to reduced cholesterol synthesis and attenuation of hypercholesterolemia.\n[6] Chronic treatment with adiponectin partially reverses atherosclerosis without obvious effects on hypercholesterolemia in FGF21-deficient apolipoprotein E(-/-) mice.\n[7] By contrast, the cholesterol-lowering effects of FGF21 are abrogated by hepatic expression of sterol regulatory element-binding protein-2.\n[8] CONCLUSIONS FGF21 protects against atherosclerosis via fine tuning the multiorgan crosstalk among liver, adipose tissue, and blood vessels."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"FGF21 deficiency causes a marked exacerbation of atherosclerotic plaque formation and premature death in apolipoprotein E(-/-) mice, which is accompanied by hypoadiponectinemia and severe hypercholesterolemia.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 683, "doc_id": 9315213, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [9315213], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Lack of FGF21 in mice slows the rate of atherosclerotic plaque formation.\n\nDocument title: Fibroblast Growth Factor 21 Prevents Atherosclerosis by Suppression of Hepatic Sterol Regulatory Element-Binding Protein-2 and Induction of Adiponectin in Mice\n\nAbstract sentences:\n[0] BACKGROUND Fibroblast growth factor 21 (FGF21) is a metabolic hormone with pleiotropic effects on glucose and lipid metabolism and insulin sensitivity.\n[1] It acts as a key downstream target of both peroxisome proliferator-activated receptor α and γ, the agonists of which have been used for lipid lowering and insulin sensitization, respectively.\n[2] However, the role of FGF21 in the cardiovascular system remains elusive.\n[3] METHODS AND RESULTS The roles of FGF21 in atherosclerosis were investigated by evaluating the impact of FGF21 deficiency and replenishment with recombinant FGF21 in apolipoprotein E(-/-) mice.\n[4] FGF21 deficiency causes a marked exacerbation of atherosclerotic plaque formation and premature death in apolipoprotein E(-/-) mice, which is accompanied by hypoadiponectinemia and severe hypercholesterolemia.\n[5] Replenishment of FGF21 protects against atherosclerosis in apolipoprotein E(-/-)mice via 2 independent mechanisms, inducing the adipocyte production of adiponectin, which in turn acts on the blood vessels to inhibit neointima formation and macrophage inflammation, and suppressing the hepatic expression of the transcription factor sterol regulatory element-binding protein-2, thereby leading to reduced cholesterol synthesis and attenuation of hypercholesterolemia.\n[6] Chronic treatment with adiponectin partially reverses atherosclerosis without obvious effects on hypercholesterolemia in FGF21-deficient apolipoprotein E(-/-) mice.\n[7] By contrast, the cholesterol-lowering effects of FGF21 are abrogated by hepatic expression of sterol regulatory element-binding protein-2.\n[8] CONCLUSIONS FGF21 protects against atherosclerosis via fine tuning the multiorgan crosstalk among liver, adipose tissue, and blood vessels."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Replenishment of FGF21 protects against atherosclerosis in apolipoprotein E(-/-)mice via 2 independent mechanisms, inducing the adipocyte production of adiponectin, which in turn acts on the blood vessels to inhibit neointima formation and macrophage inflammation, and suppressing the hepatic expression of the transcription factor sterol regulatory element-binding protein-2, thereby leading to reduced cholesterol synthesis and attenuation of hypercholesterolemia.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 683, "doc_id": 9315213, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [9315213], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Lack of FGF21 in mice slows the rate of atherosclerotic plaque formation.\n\nDocument title: Fibroblast Growth Factor 21 Prevents Atherosclerosis by Suppression of Hepatic Sterol Regulatory Element-Binding Protein-2 and Induction of Adiponectin in Mice\n\nAbstract sentences:\n[0] BACKGROUND Fibroblast growth factor 21 (FGF21) is a metabolic hormone with pleiotropic effects on glucose and lipid metabolism and insulin sensitivity.\n[1] It acts as a key downstream target of both peroxisome proliferator-activated receptor α and γ, the agonists of which have been used for lipid lowering and insulin sensitization, respectively.\n[2] However, the role of FGF21 in the cardiovascular system remains elusive.\n[3] METHODS AND RESULTS The roles of FGF21 in atherosclerosis were investigated by evaluating the impact of FGF21 deficiency and replenishment with recombinant FGF21 in apolipoprotein E(-/-) mice.\n[4] FGF21 deficiency causes a marked exacerbation of atherosclerotic plaque formation and premature death in apolipoprotein E(-/-) mice, which is accompanied by hypoadiponectinemia and severe hypercholesterolemia.\n[5] Replenishment of FGF21 protects against atherosclerosis in apolipoprotein E(-/-)mice via 2 independent mechanisms, inducing the adipocyte production of adiponectin, which in turn acts on the blood vessels to inhibit neointima formation and macrophage inflammation, and suppressing the hepatic expression of the transcription factor sterol regulatory element-binding protein-2, thereby leading to reduced cholesterol synthesis and attenuation of hypercholesterolemia.\n[6] Chronic treatment with adiponectin partially reverses atherosclerosis without obvious effects on hypercholesterolemia in FGF21-deficient apolipoprotein E(-/-) mice.\n[7] By contrast, the cholesterol-lowering effects of FGF21 are abrogated by hepatic expression of sterol regulatory element-binding protein-2.\n[8] CONCLUSIONS FGF21 protects against atherosclerosis via fine tuning the multiorgan crosstalk among liver, adipose tissue, and blood vessels."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"CONCLUSIONS FGF21 protects against atherosclerosis via fine tuning the multiorgan crosstalk among liver, adipose tissue, and blood vessels.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 683, "doc_id": 9315213, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [9315213], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Lamins are associated with nuclear membrane structure maintenance.\n\nDocument title: Autophagy mediates degradation of nuclear lamina\n\nAbstract sentences:\n[0] Macroautophagy (hereafter referred to as autophagy) is a catabolic membrane trafficking process that degrades a variety of cellular constituents and is associated with human diseases.\n[1] Although extensive studies have focused on autophagic turnover of cytoplasmic materials, little is known about the role of autophagy in degrading nuclear components.\n[2] Here we report that the autophagy machinery mediates degradation of nuclear lamina components in mammals.\n[3] The autophagy protein LC3/Atg8, which is involved in autophagy membrane trafficking and substrate delivery, is present in the nucleus and directly interacts with the nuclear lamina protein lamin B1, and binds to lamin-associated domains on chromatin.\n[4] This LC3-lamin B1 interaction does not downregulate lamin B1 during starvation, but mediates its degradation upon oncogenic insults, such as by activated RAS.\n[5] Lamin B1 degradation is achieved by nucleus-to-cytoplasm transport that delivers lamin B1 to the lysosome.\n[6] Inhibiting autophagy or the LC3-lamin B1 interaction prevents activated RAS-induced lamin B1 loss and attenuates oncogene-induced senescence in primary human cells.\n[7] Our study suggests that this new function of autophagy acts as a guarding mechanism protecting cells from tumorigenesis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 685, "doc_id": 4452659, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4452659], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Lamins are found within the inner layer of the mitochondrial membrane of all cells.\n\nDocument title: Autophagy mediates degradation of nuclear lamina\n\nAbstract sentences:\n[0] Macroautophagy (hereafter referred to as autophagy) is a catabolic membrane trafficking process that degrades a variety of cellular constituents and is associated with human diseases.\n[1] Although extensive studies have focused on autophagic turnover of cytoplasmic materials, little is known about the role of autophagy in degrading nuclear components.\n[2] Here we report that the autophagy machinery mediates degradation of nuclear lamina components in mammals.\n[3] The autophagy protein LC3/Atg8, which is involved in autophagy membrane trafficking and substrate delivery, is present in the nucleus and directly interacts with the nuclear lamina protein lamin B1, and binds to lamin-associated domains on chromatin.\n[4] This LC3-lamin B1 interaction does not downregulate lamin B1 during starvation, but mediates its degradation upon oncogenic insults, such as by activated RAS.\n[5] Lamin B1 degradation is achieved by nucleus-to-cytoplasm transport that delivers lamin B1 to the lysosome.\n[6] Inhibiting autophagy or the LC3-lamin B1 interaction prevents activated RAS-induced lamin B1 loss and attenuates oncogene-induced senescence in primary human cells.\n[7] Our study suggests that this new function of autophagy acts as a guarding mechanism protecting cells from tumorigenesis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 686, "doc_id": 4452659, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4452659], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Lamins are found within the inner layer of the nuclear membrane of all cells.\n\nDocument title: Autophagy mediates degradation of nuclear lamina\n\nAbstract sentences:\n[0] Macroautophagy (hereafter referred to as autophagy) is a catabolic membrane trafficking process that degrades a variety of cellular constituents and is associated with human diseases.\n[1] Although extensive studies have focused on autophagic turnover of cytoplasmic materials, little is known about the role of autophagy in degrading nuclear components.\n[2] Here we report that the autophagy machinery mediates degradation of nuclear lamina components in mammals.\n[3] The autophagy protein LC3/Atg8, which is involved in autophagy membrane trafficking and substrate delivery, is present in the nucleus and directly interacts with the nuclear lamina protein lamin B1, and binds to lamin-associated domains on chromatin.\n[4] This LC3-lamin B1 interaction does not downregulate lamin B1 during starvation, but mediates its degradation upon oncogenic insults, such as by activated RAS.\n[5] Lamin B1 degradation is achieved by nucleus-to-cytoplasm transport that delivers lamin B1 to the lysosome.\n[6] Inhibiting autophagy or the LC3-lamin B1 interaction prevents activated RAS-induced lamin B1 loss and attenuates oncogene-induced senescence in primary human cells.\n[7] Our study suggests that this new function of autophagy acts as a guarding mechanism protecting cells from tumorigenesis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 687, "doc_id": 4452659, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4452659], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Lamins have no effect on nuclear membrane structure maintenance.\n\nDocument title: Autophagy mediates degradation of nuclear lamina\n\nAbstract sentences:\n[0] Macroautophagy (hereafter referred to as autophagy) is a catabolic membrane trafficking process that degrades a variety of cellular constituents and is associated with human diseases.\n[1] Although extensive studies have focused on autophagic turnover of cytoplasmic materials, little is known about the role of autophagy in degrading nuclear components.\n[2] Here we report that the autophagy machinery mediates degradation of nuclear lamina components in mammals.\n[3] The autophagy protein LC3/Atg8, which is involved in autophagy membrane trafficking and substrate delivery, is present in the nucleus and directly interacts with the nuclear lamina protein lamin B1, and binds to lamin-associated domains on chromatin.\n[4] This LC3-lamin B1 interaction does not downregulate lamin B1 during starvation, but mediates its degradation upon oncogenic insults, such as by activated RAS.\n[5] Lamin B1 degradation is achieved by nucleus-to-cytoplasm transport that delivers lamin B1 to the lysosome.\n[6] Inhibiting autophagy or the LC3-lamin B1 interaction prevents activated RAS-induced lamin B1 loss and attenuates oncogene-induced senescence in primary human cells.\n[7] Our study suggests that this new function of autophagy acts as a guarding mechanism protecting cells from tumorigenesis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 688, "doc_id": 4452659, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4452659], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Less than 10% of patients exposed to radiation have activated markers of mesenchymal stem cells.\n\nDocument title: KLF4-dependent phenotypic modulation of smooth muscle cells has a key role in atherosclerotic plaque pathogenesis\n\nAbstract sentences:\n[0] Previous studies investigating the role of smooth muscle cells (SMCs) and macrophages in the pathogenesis of atherosclerosis have provided controversial results owing to the use of unreliable methods for clearly identifying each of these cell types.\n[1] Here, using Myh11-CreERT2 ROSA floxed STOP eYFP Apoe−/− mice to perform SMC lineage tracing, we find that traditional methods for detecting SMCs based on immunostaining for SMC markers fail to detect >80% of SMC-derived cells within advanced atherosclerotic lesions.\n[2] These unidentified SMC-derived cells exhibit phenotypes of other cell lineages, including macrophages and mesenchymal stem cells (MSCs).\n[3] SMC-specific conditional knockout of Krüppel-like factor 4 (Klf4) resulted in reduced numbers of SMC-derived MSC- and macrophage-like cells, a marked reduction in lesion size, and increases in multiple indices of plaque stability, including an increase in fibrous cap thickness as compared to wild-type controls.\n[4] On the basis of in vivo KLF4 chromatin immunoprecipitation–sequencing (ChIP-seq) analyses and studies of cholesterol-treated cultured SMCs, we identified >800 KLF4 target genes, including many that regulate pro-inflammatory responses of SMCs.\n[5] Our findings indicate that the contribution of SMCs to atherosclerotic plaques has been greatly underestimated, and that KLF4-dependent transitions in SMC phenotype are critical in lesion pathogenesis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 689, "doc_id": 22080671, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [22080671], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Lice attenuated SIV vaccines induce a stronger antigen-specific T cell response in lymph node cells.\n\nDocument title: Lymph node T cell responses predict the efficacy of live attenuated SIV vaccines\n\nAbstract sentences:\n[0] Live attenuated simian immunodeficiency virus (SIV) vaccines (LAVs) remain the most efficacious of all vaccines in nonhuman primate models of HIV and AIDS, yet the basis of their robust protection remains poorly understood.\n[1] Here we show that the degree of LAV-mediated protection against intravenous wild-type SIVmac239 challenge strongly correlates with the magnitude and function of SIV-specific, effector-differentiated T cells in the lymph node but not with the responses of such T cells in the blood or with other cellular, humoral and innate immune parameters.\n[2] We found that maintenance of protective T cell responses is associated with persistent LAV replication in the lymph node, which occurs almost exclusively in follicular helper T cells.\n[3] Thus, effective LAVs maintain lymphoid tissue-based, effector-differentiated, SIV-specific T cells that intercept and suppress early wild-type SIV amplification and, if present in sufficient frequencies, can completely control and perhaps clear infection, an observation that provides a rationale for the development of safe, persistent vectors that can elicit and maintain such responses."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Here we show that the degree of LAV-mediated protection against intravenous wild-type SIVmac239 challenge strongly correlates with the magnitude and function of SIV-specific, effector-differentiated T cells in the lymph node but not with the responses of such T cells in the blood or with other cellular, humoral and innate immune parameters.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 694, "doc_id": 1071991, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [1071991], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Lipopolysaccharides have an inflammation independent effect on kidney barrier function.\n\nDocument title: Modification of kidney barrier function by the urokinase receptor\n\nAbstract sentences:\n[0] Podocyte dysfunction, represented by foot process effacement and proteinuria, is often the starting point for progressive kidney disease.\n[1] Therapies aimed at the cellular level of the disease are currently not available.\n[2] Here we show that induction of urokinase receptor (uPAR) signaling in podocytes leads to foot process effacement and urinary protein loss via a mechanism that includes lipid-dependent activation of αvβ3 integrin.\n[3] Mice lacking uPAR (Plaur−/−) are protected from lipopolysaccharide (LPS)-mediated proteinuria but develop disease after expression of a constitutively active β3 integrin.\n[4] Gene transfer studies reveal a prerequisite for uPAR expression in podocytes, but not in endothelial cells, for the development of LPS-mediated proteinuria.\n[5] Mechanistically, uPAR is required to activate αvβ3 integrin in podocytes, promoting cell motility and activation of the small GTPases Cdc42 and Rac1.\n[6] Blockade of αvβ3 integrin reduces podocyte motility in vitro and lowers proteinuria in mice.\n[7] Our findings show a physiological role for uPAR signaling in the regulation of kidney permeability."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 696, "doc_id": 16355392, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [16355392], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Lmna knock-in models are appropriate for testing therapeutic approaches against Hutchinson-Gilford progeria syndrome (HGPS).\n\nDocument title: Reversal of the cellular phenotype in the premature aging disease Hutchinson-Gilford progeria syndrome\n\nAbstract sentences:\n[0] Hutchinson-Gilford progeria syndrome (HGPS) is a childhood premature aging disease caused by a spontaneous point mutation in lamin A (encoded by LMNA), one of the major architectural elements of the mammalian cell nucleus.\n[1] The HGPS mutation activates an aberrant cryptic splice site in LMNA pre-mRNA, leading to synthesis of a truncated lamin A protein and concomitant reduction in wild-type lamin A. Fibroblasts from individuals with HGPS have severe morphological abnormalities in nuclear envelope structure.\n[2] Here we show that the cellular disease phenotype is reversible in cells from individuals with HGPS.\n[3] Introduction of wild-type lamin A protein does not rescue the cellular disease symptoms.\n[4] The mutant LMNA mRNA and lamin A protein can be efficiently eliminated by correction of the aberrant splicing event using a modified oligonucleotide targeted to the activated cryptic splice site.\n[5] Upon splicing correction, HGPS fibroblasts assume normal nuclear morphology, the aberrant nuclear distribution and cellular levels of lamina-associated proteins are rescued, defects in heterochromatin-specific histone modifications are corrected and proper expression of several misregulated genes is reestablished.\n[6] Our results establish proof of principle for the correction of the premature aging phenotype in individuals with HGPS."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 698, "doc_id": 22544171, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [22544171], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Localization of PIN1 in the roots of Arabidopsis requires VPS9a\n\nDocument title: Generation of cell polarity in plants links endocytosis, auxin distribution and cell fate decisions\n\nAbstract sentences:\n[0] Dynamically polarized membrane proteins define different cell boundaries and have an important role in intercellular communication—a vital feature of multicellular development.\n[1] Efflux carriers for the signalling molecule auxin from the PIN family are landmarks of cell polarity in plants and have a crucial involvement in auxin distribution-dependent development including embryo patterning, organogenesis and tropisms.\n[2] Polar PIN localization determines the direction of intercellular auxin flow, yet the mechanisms generating PIN polarity remain unclear.\n[3] Here we identify an endocytosis-dependent mechanism of PIN polarity generation and analyse its developmental implications.\n[4] Real-time PIN tracking showed that after synthesis, PINs are initially delivered to the plasma membrane in a non-polar manner and their polarity is established by subsequent endocytic recycling.\n[5] Interference with PIN endocytosis either by auxin or by manipulation of the Arabidopsis Rab5 GTPase pathway prevents PIN polarization.\n[6] Failure of PIN polarization transiently alters asymmetric auxin distribution during embryogenesis and increases the local auxin response in apical embryo regions.\n[7] This results in ectopic expression of auxin pathway-associated root-forming master regulators in embryonic leaves and promotes homeotic transformation of leaves to roots.\n[8] Our results indicate a two-step mechanism for the generation of PIN polar localization and the essential role of endocytosis in this process.\n[9] It also highlights the link between endocytosis-dependent polarity of individual cells and auxin distribution-dependent cell fate establishment for multicellular patterning."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 703, "doc_id": 4350400, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4350400], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Long - range chromatin interactions regulate transcription.\n\nDocument title: Enhancer Evolution across 20 Mammalian Species\n\nAbstract sentences:\n[0] The mammalian radiation has corresponded with rapid changes in noncoding regions of the genome, but we lack a comprehensive understanding of regulatory evolution in mammals.\n[1] Here, we track the evolution of promoters and enhancers active in liver across 20 mammalian species from six diverse orders by profiling genomic enrichment of H3K27 acetylation and H3K4 trimethylation.\n[2] We report that rapid evolution of enhancers is a universal feature of mammalian genomes.\n[3] Most of the recently evolved enhancers arise from ancestral DNA exaptation, rather than lineage-specific expansions of repeat elements.\n[4] In contrast, almost all liver promoters are partially or fully conserved across these species.\n[5] Our data further reveal that recently evolved enhancers can be associated with genes under positive selection, demonstrating the power of this approach for annotating regulatory adaptations in genomic sequences.\n[6] These results provide important insight into the functional genetics underpinning mammalian regulatory evolution."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 704, "doc_id": 14658685, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14658685], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Long chain polyunsaturated fatty acids supplementation has no significant effects on wheezing or asthma at 3 and 6 years.\n\nDocument title: Effect of n-3 long chain polyunsaturated fatty acid supplementation in pregnancy on infants’ allergies in first year of life: randomised controlled trial\n\nAbstract sentences:\n[0] OBJECTIVE To determine whether dietary n-3 long chain polyunsaturated fatty acid (LCPUFA) supplementation of pregnant women with a fetus at high risk of allergic disease reduces immunoglobulin E associated eczema or food allergy at 1 year of age.\n[1] DESIGN Follow-up of infants at high hereditary risk of allergic disease in the Docosahexaenoic Acid to Optimise Mother Infant Outcome (DOMInO) randomised controlled trial.\n[2] SETTING Adelaide, South Australia.\n[3] PARTICIPANTS 706 infants at high hereditary risk of developing allergic disease whose mothers were participating in the DOMInO trial.\n[4] INTERVENTIONS The intervention group (n=368) was randomly allocated to receive fish oil capsules (providing 900 mg of n-3 LCPUFA daily) from 21 weeks' gestation until birth; the control group (n=338) received matched vegetable oil capsules without n-3 LCPUFA.\n[5] MAIN OUTCOME MEASURE Immunoglobulin E associated allergic disease (eczema or food allergy with sensitisation) at 1 year of age.\n[6] RESULTS No differences were seen in the overall percentage of infants with immunoglobulin E associated allergic disease between the n-3 LCPUFA and control groups (32/368 (9%) v 43/338 (13%); unadjusted relative risk 0.68, 95% confidence interval 0.43 to 1.05, P=0.08; adjusted relative risk 0.70, 0.45 to 1.09, P=0.12), although the percentage of infants diagnosed as having atopic eczema (that is, eczema with associated sensitisation) was lower in the n-3 LCPUFA group (26/368 (7%) v 39/338 (12%); unadjusted relative risk 0.61, 0.38 to 0.98, P=0.04; adjusted relative risk 0.64, 0.40 to 1.02, P=0.06).\n[7] Fewer infants were sensitised to egg in the n-3 LCPUFA group (34/368 (9%) v 52/338 (15%); unadjusted relative risk 0.61, 0.40 to 0.91, P=0.02; adjusted relative risk 0.62, 0.41 to 0.93, P=0.02), but no difference between groups in immunoglobulin E associated food allergy was seen.\n[8] CONCLUSION n-3 LCPUFA supplementation in pregnancy did not reduce the overall incidence of immunoglobulin E associated allergies in the first year of life, although atopic eczema and egg sensitisation were lower.\n[9] Longer term follow-up is needed to determine if supplementation has an effect on respiratory allergic diseases and aeroallergen sensitisation in childhood.\n[10] TRIAL REGISTRATION Australian New Zealand Clinical Trials Registry ACTRN12610000735055 (DOMInO trial: ACTRN12605000569606)."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 705, "doc_id": 22442133, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [22442133], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Long chain polyunsaturated fatty acids supplementation is associated with lower rates of atopic eczema at 1 year.\n\nDocument title: Effect of n-3 long chain polyunsaturated fatty acid supplementation in pregnancy on infants’ allergies in first year of life: randomised controlled trial\n\nAbstract sentences:\n[0] OBJECTIVE To determine whether dietary n-3 long chain polyunsaturated fatty acid (LCPUFA) supplementation of pregnant women with a fetus at high risk of allergic disease reduces immunoglobulin E associated eczema or food allergy at 1 year of age.\n[1] DESIGN Follow-up of infants at high hereditary risk of allergic disease in the Docosahexaenoic Acid to Optimise Mother Infant Outcome (DOMInO) randomised controlled trial.\n[2] SETTING Adelaide, South Australia.\n[3] PARTICIPANTS 706 infants at high hereditary risk of developing allergic disease whose mothers were participating in the DOMInO trial.\n[4] INTERVENTIONS The intervention group (n=368) was randomly allocated to receive fish oil capsules (providing 900 mg of n-3 LCPUFA daily) from 21 weeks' gestation until birth; the control group (n=338) received matched vegetable oil capsules without n-3 LCPUFA.\n[5] MAIN OUTCOME MEASURE Immunoglobulin E associated allergic disease (eczema or food allergy with sensitisation) at 1 year of age.\n[6] RESULTS No differences were seen in the overall percentage of infants with immunoglobulin E associated allergic disease between the n-3 LCPUFA and control groups (32/368 (9%) v 43/338 (13%); unadjusted relative risk 0.68, 95% confidence interval 0.43 to 1.05, P=0.08; adjusted relative risk 0.70, 0.45 to 1.09, P=0.12), although the percentage of infants diagnosed as having atopic eczema (that is, eczema with associated sensitisation) was lower in the n-3 LCPUFA group (26/368 (7%) v 39/338 (12%); unadjusted relative risk 0.61, 0.38 to 0.98, P=0.04; adjusted relative risk 0.64, 0.40 to 1.02, P=0.06).\n[7] Fewer infants were sensitised to egg in the n-3 LCPUFA group (34/368 (9%) v 52/338 (15%); unadjusted relative risk 0.61, 0.40 to 0.91, P=0.02; adjusted relative risk 0.62, 0.41 to 0.93, P=0.02), but no difference between groups in immunoglobulin E associated food allergy was seen.\n[8] CONCLUSION n-3 LCPUFA supplementation in pregnancy did not reduce the overall incidence of immunoglobulin E associated allergies in the first year of life, although atopic eczema and egg sensitisation were lower.\n[9] Longer term follow-up is needed to determine if supplementation has an effect on respiratory allergic diseases and aeroallergen sensitisation in childhood.\n[10] TRIAL REGISTRATION Australian New Zealand Clinical Trials Registry ACTRN12610000735055 (DOMInO trial: ACTRN12605000569606)."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"RESULTS No differences were seen in the overall percentage of infants with immunoglobulin E associated allergic disease between the n-3 LCPUFA and control groups (32/368 (9%) v 43/338 (13%); unadjusted relative risk 0.68, 95% confidence interval 0.43 to 1.05, P=0.08; adjusted relative risk 0.70, 0.45 to 1.09, P=0.12), although the percentage of infants diagnosed as having atopic eczema (that is, eczema with associated sensitisation) was lower in the n-3 LCPUFA group (26/368 (7%) v 39/338 (12%); unadjusted relative risk 0.61, 0.38 to 0.98, P=0.04; adjusted relative risk 0.64, 0.40 to 1.02, P=0.06).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 709, "doc_id": 22442133, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [22442133], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Long chain polyunsaturated fatty acids supplementation is associated with lower rates of atopic eczema at 1 year.\n\nDocument title: Effect of n-3 long chain polyunsaturated fatty acid supplementation in pregnancy on infants’ allergies in first year of life: randomised controlled trial\n\nAbstract sentences:\n[0] OBJECTIVE To determine whether dietary n-3 long chain polyunsaturated fatty acid (LCPUFA) supplementation of pregnant women with a fetus at high risk of allergic disease reduces immunoglobulin E associated eczema or food allergy at 1 year of age.\n[1] DESIGN Follow-up of infants at high hereditary risk of allergic disease in the Docosahexaenoic Acid to Optimise Mother Infant Outcome (DOMInO) randomised controlled trial.\n[2] SETTING Adelaide, South Australia.\n[3] PARTICIPANTS 706 infants at high hereditary risk of developing allergic disease whose mothers were participating in the DOMInO trial.\n[4] INTERVENTIONS The intervention group (n=368) was randomly allocated to receive fish oil capsules (providing 900 mg of n-3 LCPUFA daily) from 21 weeks' gestation until birth; the control group (n=338) received matched vegetable oil capsules without n-3 LCPUFA.\n[5] MAIN OUTCOME MEASURE Immunoglobulin E associated allergic disease (eczema or food allergy with sensitisation) at 1 year of age.\n[6] RESULTS No differences were seen in the overall percentage of infants with immunoglobulin E associated allergic disease between the n-3 LCPUFA and control groups (32/368 (9%) v 43/338 (13%); unadjusted relative risk 0.68, 95% confidence interval 0.43 to 1.05, P=0.08; adjusted relative risk 0.70, 0.45 to 1.09, P=0.12), although the percentage of infants diagnosed as having atopic eczema (that is, eczema with associated sensitisation) was lower in the n-3 LCPUFA group (26/368 (7%) v 39/338 (12%); unadjusted relative risk 0.61, 0.38 to 0.98, P=0.04; adjusted relative risk 0.64, 0.40 to 1.02, P=0.06).\n[7] Fewer infants were sensitised to egg in the n-3 LCPUFA group (34/368 (9%) v 52/338 (15%); unadjusted relative risk 0.61, 0.40 to 0.91, P=0.02; adjusted relative risk 0.62, 0.41 to 0.93, P=0.02), but no difference between groups in immunoglobulin E associated food allergy was seen.\n[8] CONCLUSION n-3 LCPUFA supplementation in pregnancy did not reduce the overall incidence of immunoglobulin E associated allergies in the first year of life, although atopic eczema and egg sensitisation were lower.\n[9] Longer term follow-up is needed to determine if supplementation has an effect on respiratory allergic diseases and aeroallergen sensitisation in childhood.\n[10] TRIAL REGISTRATION Australian New Zealand Clinical Trials Registry ACTRN12610000735055 (DOMInO trial: ACTRN12605000569606)."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"CONCLUSION n-3 LCPUFA supplementation in pregnancy did not reduce the overall incidence of immunoglobulin E associated allergies in the first year of life, although atopic eczema and egg sensitisation were lower.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 709, "doc_id": 22442133, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [22442133], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Long chain polyunsaturated fatty acids supplementation reduces wheezing and asthma.\n\nDocument title: Effect of n-3 long chain polyunsaturated fatty acid supplementation in pregnancy on infants’ allergies in first year of life: randomised controlled trial\n\nAbstract sentences:\n[0] OBJECTIVE To determine whether dietary n-3 long chain polyunsaturated fatty acid (LCPUFA) supplementation of pregnant women with a fetus at high risk of allergic disease reduces immunoglobulin E associated eczema or food allergy at 1 year of age.\n[1] DESIGN Follow-up of infants at high hereditary risk of allergic disease in the Docosahexaenoic Acid to Optimise Mother Infant Outcome (DOMInO) randomised controlled trial.\n[2] SETTING Adelaide, South Australia.\n[3] PARTICIPANTS 706 infants at high hereditary risk of developing allergic disease whose mothers were participating in the DOMInO trial.\n[4] INTERVENTIONS The intervention group (n=368) was randomly allocated to receive fish oil capsules (providing 900 mg of n-3 LCPUFA daily) from 21 weeks' gestation until birth; the control group (n=338) received matched vegetable oil capsules without n-3 LCPUFA.\n[5] MAIN OUTCOME MEASURE Immunoglobulin E associated allergic disease (eczema or food allergy with sensitisation) at 1 year of age.\n[6] RESULTS No differences were seen in the overall percentage of infants with immunoglobulin E associated allergic disease between the n-3 LCPUFA and control groups (32/368 (9%) v 43/338 (13%); unadjusted relative risk 0.68, 95% confidence interval 0.43 to 1.05, P=0.08; adjusted relative risk 0.70, 0.45 to 1.09, P=0.12), although the percentage of infants diagnosed as having atopic eczema (that is, eczema with associated sensitisation) was lower in the n-3 LCPUFA group (26/368 (7%) v 39/338 (12%); unadjusted relative risk 0.61, 0.38 to 0.98, P=0.04; adjusted relative risk 0.64, 0.40 to 1.02, P=0.06).\n[7] Fewer infants were sensitised to egg in the n-3 LCPUFA group (34/368 (9%) v 52/338 (15%); unadjusted relative risk 0.61, 0.40 to 0.91, P=0.02; adjusted relative risk 0.62, 0.41 to 0.93, P=0.02), but no difference between groups in immunoglobulin E associated food allergy was seen.\n[8] CONCLUSION n-3 LCPUFA supplementation in pregnancy did not reduce the overall incidence of immunoglobulin E associated allergies in the first year of life, although atopic eczema and egg sensitisation were lower.\n[9] Longer term follow-up is needed to determine if supplementation has an effect on respiratory allergic diseases and aeroallergen sensitisation in childhood.\n[10] TRIAL REGISTRATION Australian New Zealand Clinical Trials Registry ACTRN12610000735055 (DOMInO trial: ACTRN12605000569606)."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 710, "doc_id": 22442133, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [22442133], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Low expression of miR7a does not repress target genes or exert a biological function in ovaries.\n\nDocument title: Assessing the ceRNA hypothesis with quantitative measurements of miRNA and target abundance.\n\nAbstract sentences:\n[0] Recent studies have reported that competitive endogenous RNAs (ceRNAs) can act as sponges for a microRNA (miRNA) through their binding sites and that changes in ceRNA abundances from individual genes can modulate the activity of miRNAs.\n[1] Consideration of this hypothesis would benefit from knowing the quantitative relationship between a miRNA and its endogenous target sites.\n[2] Here, we altered intracellular target site abundance through expression of an miR-122 target in hepatocytes and livers and analyzed the effects on miR-122 target genes.\n[3] Target repression was released in a threshold-like manner at high target site abundance (≥1.5 × 10(5) added target sites per cell), and this threshold was insensitive to the effective levels of the miRNA.\n[4] Furthermore, in response to extreme metabolic liver disease models, global target site abundance of hepatocytes did not change sufficiently to affect miRNA-mediated repression.\n[5] Thus, modulation of miRNA target abundance is unlikely to cause significant effects on gene expression and metabolism through a ceRNA effect."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 713, "doc_id": 18421962, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [18421962], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Low expression of miR7a does not repress target genes or exert a biological function in testis.\n\nDocument title: Assessing the ceRNA hypothesis with quantitative measurements of miRNA and target abundance.\n\nAbstract sentences:\n[0] Recent studies have reported that competitive endogenous RNAs (ceRNAs) can act as sponges for a microRNA (miRNA) through their binding sites and that changes in ceRNA abundances from individual genes can modulate the activity of miRNAs.\n[1] Consideration of this hypothesis would benefit from knowing the quantitative relationship between a miRNA and its endogenous target sites.\n[2] Here, we altered intracellular target site abundance through expression of an miR-122 target in hepatocytes and livers and analyzed the effects on miR-122 target genes.\n[3] Target repression was released in a threshold-like manner at high target site abundance (≥1.5 × 10(5) added target sites per cell), and this threshold was insensitive to the effective levels of the miRNA.\n[4] Furthermore, in response to extreme metabolic liver disease models, global target site abundance of hepatocytes did not change sufficiently to affect miRNA-mediated repression.\n[5] Thus, modulation of miRNA target abundance is unlikely to cause significant effects on gene expression and metabolism through a ceRNA effect."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 714, "doc_id": 18421962, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [18421962], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Low nucleosome occupancy correlates with high methylation levels across species.\n\nDocument title: Dnmt1-Independent CG Methylation Contributes to Nucleosome Positioning in Diverse Eukaryotes\n\nAbstract sentences:\n[0] Dnmt1 epigenetically propagates symmetrical CG methylation in many eukaryotes.\n[1] Their genomes are typically depleted of CG dinucleotides because of imperfect repair of deaminated methylcytosines.\n[2] Here, we extensively survey diverse species lacking Dnmt1 and show that, surprisingly, symmetrical CG methylation is nonetheless frequently present and catalyzed by a different DNA methyltransferase family, Dnmt5.\n[3] Numerous Dnmt5-containing organisms that diverged more than a billion years ago exhibit clustered methylation, specifically in nucleosome linkers.\n[4] Clustered methylation occurs at unprecedented densities and directly disfavors nucleosomes, contributing to nucleosome positioning between clusters.\n[5] Dense methylation is enabled by a regime of genomic sequence evolution that enriches CG dinucleotides and drives the highest CG frequencies known.\n[6] Species with linker methylation have small, transcriptionally active nuclei that approach the physical limits of chromatin compaction.\n[7] These features constitute a previously unappreciated genome architecture, in which dense methylation influences nucleosome positions, likely facilitating nuclear processes under extreme spatial constraints."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Clustered methylation occurs at unprecedented densities and directly disfavors nucleosomes, contributing to nucleosome positioning between clusters.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 717, "doc_id": 17587795, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [17587795], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ly49Q directs the organization of neutrophil polarization by regulating membrane raft functions.\n\nDocument title: The Ly49Q receptor plays a crucial role in neutrophil polarization and migration by regulating raft trafficking.\n\nAbstract sentences:\n[0] Neutrophils rapidly undergo polarization and directional movement to infiltrate the sites of infection and inflammation.\n[1] Here, we show that an inhibitory MHC I receptor, Ly49Q, was crucial for the swift polarization of and tissue infiltration by neutrophils.\n[2] During the steady state, Ly49Q inhibited neutrophil adhesion by preventing focal-complex formation, likely by inhibiting Src and PI3 kinases.\n[3] However, in the presence of inflammatory stimuli, Ly49Q mediated rapid neutrophil polarization and tissue infiltration in an ITIM-domain-dependent manner.\n[4] These opposite functions appeared to be mediated by distinct use of effector phosphatase SHP-1 and SHP-2.\n[5] Ly49Q-dependent polarization and migration were affected by Ly49Q regulation of membrane raft functions.\n[6] We propose that Ly49Q is pivotal in switching neutrophils to their polarized morphology and rapid migration upon inflammation, through its spatiotemporal regulation of membrane rafts and raft-associated signaling molecules."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Ly49Q-dependent polarization and migration were affected by Ly49Q regulation of membrane raft functions.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 724, "doc_id": 5531479, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [5531479], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ly49Q directs the organization of neutrophil polarization by regulating membrane raft functions.\n\nDocument title: The Ly49Q receptor plays a crucial role in neutrophil polarization and migration by regulating raft trafficking.\n\nAbstract sentences:\n[0] Neutrophils rapidly undergo polarization and directional movement to infiltrate the sites of infection and inflammation.\n[1] Here, we show that an inhibitory MHC I receptor, Ly49Q, was crucial for the swift polarization of and tissue infiltration by neutrophils.\n[2] During the steady state, Ly49Q inhibited neutrophil adhesion by preventing focal-complex formation, likely by inhibiting Src and PI3 kinases.\n[3] However, in the presence of inflammatory stimuli, Ly49Q mediated rapid neutrophil polarization and tissue infiltration in an ITIM-domain-dependent manner.\n[4] These opposite functions appeared to be mediated by distinct use of effector phosphatase SHP-1 and SHP-2.\n[5] Ly49Q-dependent polarization and migration were affected by Ly49Q regulation of membrane raft functions.\n[6] We propose that Ly49Q is pivotal in switching neutrophils to their polarized morphology and rapid migration upon inflammation, through its spatiotemporal regulation of membrane rafts and raft-associated signaling molecules."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"We propose that Ly49Q is pivotal in switching neutrophils to their polarized morphology and rapid migration upon inflammation, through its spatiotemporal regulation of membrane rafts and raft-associated signaling molecules.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 724, "doc_id": 5531479, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [5531479], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ly6C hi monocytes have a higher inflammatory capacity than Ly6C lo monocytes.\n\nDocument title: Subpopulations of mouse blood monocytes differ in maturation stage and inflammatory response.\n\nAbstract sentences:\n[0] Blood monocytes are well-characterized precursors for macrophages and dendritic cells.\n[1] Subsets of human monocytes with differential representation in various disease states are well known.\n[2] In contrast, mouse monocyte subsets have been characterized minimally.\n[3] In this study we identify three subpopulations of mouse monocytes that can be distinguished by differential expression of Ly-6C, CD43, CD11c, MBR, and CD62L.\n[4] The subsets share the characteristics of extensive phagocytosis, similar expression of M-CSF receptor (CD115), and development into macrophages upon M-CSF stimulation.\n[5] By eliminating blood monocytes with dichloromethylene-bisphosphonate-loaded liposomes and monitoring their repopulation, we showed a developmental relationship between the subsets.\n[6] Monocytes were maximally depleted 18 h after liposome application and subsequently reappeared in the circulation.\n[7] These cells were exclusively of the Ly-6C(high) subset, resembling bone marrow monocytes.\n[8] Serial flow cytometric analyses of newly released Ly-6C(high) monocytes showed that Ly-6C expression on these cells was down-regulated while in circulation.\n[9] Under inflammatory conditions elicited either by acute infection with Listeria monocytogenes or chronic infection with Leishmania major, there was a significant increase in immature Ly-6C(high) monocytes, resembling the inflammatory left shift of granulocytes.\n[10] In addition, acute peritoneal inflammation recruited preferentially Ly-6C(med-high) monocytes.\n[11] Taken together, these data identify distinct subpopulations of mouse blood monocytes that differ in maturation stage and capacity to become recruited to inflammatory sites."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Under inflammatory conditions elicited either by acute infection with Listeria monocytogenes or chronic infection with Leishmania major, there was a significant increase in immature Ly-6C(high) monocytes, resembling the inflammatory left shift of granulocytes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 726, "doc_id": 36444198, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [7521113, 36444198], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ly6C hi monocytes have a higher inflammatory capacity than Ly6C lo monocytes.\n\nDocument title: Subpopulations of mouse blood monocytes differ in maturation stage and inflammatory response.\n\nAbstract sentences:\n[0] Blood monocytes are well-characterized precursors for macrophages and dendritic cells.\n[1] Subsets of human monocytes with differential representation in various disease states are well known.\n[2] In contrast, mouse monocyte subsets have been characterized minimally.\n[3] In this study we identify three subpopulations of mouse monocytes that can be distinguished by differential expression of Ly-6C, CD43, CD11c, MBR, and CD62L.\n[4] The subsets share the characteristics of extensive phagocytosis, similar expression of M-CSF receptor (CD115), and development into macrophages upon M-CSF stimulation.\n[5] By eliminating blood monocytes with dichloromethylene-bisphosphonate-loaded liposomes and monitoring their repopulation, we showed a developmental relationship between the subsets.\n[6] Monocytes were maximally depleted 18 h after liposome application and subsequently reappeared in the circulation.\n[7] These cells were exclusively of the Ly-6C(high) subset, resembling bone marrow monocytes.\n[8] Serial flow cytometric analyses of newly released Ly-6C(high) monocytes showed that Ly-6C expression on these cells was down-regulated while in circulation.\n[9] Under inflammatory conditions elicited either by acute infection with Listeria monocytogenes or chronic infection with Leishmania major, there was a significant increase in immature Ly-6C(high) monocytes, resembling the inflammatory left shift of granulocytes.\n[10] In addition, acute peritoneal inflammation recruited preferentially Ly-6C(med-high) monocytes.\n[11] Taken together, these data identify distinct subpopulations of mouse blood monocytes that differ in maturation stage and capacity to become recruited to inflammatory sites."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"In addition, acute peritoneal inflammation recruited preferentially Ly-6C(med-high) monocytes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 726, "doc_id": 36444198, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [7521113, 36444198], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Lysine histone demethylase inhibitor JIB 04 is inactive against KDM5A.\n\nDocument title: A small molecule modulates Jumonji histone demethylase activity and selectively inhibits cancer growth\n\nAbstract sentences:\n[0] The pharmacological inhibition of general transcriptional regulators has the potential to block growth through targeting multiple tumorigenic signalling pathways simultaneously.\n[1] Here, using an innovative cell-based screen, we identify a structurally unique small molecule (named JIB-04) that specifically inhibits the activity of the Jumonji family of histone demethylases in vitro, in cancer cells, and in tumours in vivo.\n[2] Unlike known inhibitors, JIB-04 is not a competitive inhibitor of α-ketoglutarate.\n[3] In cancer, but not in patient-matched normal cells, JIB-04 alters a subset of transcriptional pathways and blocks viability.\n[4] In mice, JIB-04 reduces tumour burden and prolongs survival.\n[5] Importantly, we find that patients with breast tumours that overexpress Jumonji demethylases have significantly lower survival.\n[6] Thus, JIB-04, a novel inhibitor of Jumonji demethylases in vitro and in vivo, constitutes a unique potential therapeutic and research tool against cancer, and validates the use of unbiased cellular screens to discover chemical modulators with disease relevance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 730, "doc_id": 13400643, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [13400643], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: M. stadtmanae does not induce ASC speck formation in BlaER1 monocytes.\n\nDocument title: Human Monocytes Engage an Alternative Inflammasome Pathway.\n\nAbstract sentences:\n[0] Interleukin-1β (IL-1β) is a cytokine whose bioactivity is controlled by activation of the inflammasome.\n[1] However, in response to lipopolysaccharide, human monocytes secrete IL-1β independently of classical inflammasome stimuli.\n[2] Here, we report that this constituted a species-specific response that is not observed in the murine system.\n[3] Indeed, in human monocytes, lipopolysaccharide triggered an \"alternative inflammasome\" that relied on NLRP3-ASC-caspase-1 signaling, yet was devoid of any classical inflammasome characteristics including pyroptosome formation, pyroptosis induction, and K(+) efflux dependency.\n[4] Genetic dissection of the underlying signaling pathway in a monocyte transdifferentiation system revealed that alternative inflammasome activation was propagated by TLR4-TRIF-RIPK1-FADD-CASP8 signaling upstream of NLRP3.\n[5] Importantly, involvement of this signaling cascade was limited to alternative inflammasome activation and did not extend to classical NLRP3 activation.\n[6] Because alternative inflammasome activation embraces both sensitivity and promiscuity of TLR4, we propose a pivotal role for this signaling cascade in TLR4-driven, IL-1β-mediated immune responses and immunopathology in humans."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 732, "doc_id": 34469966, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [34469966], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: M. stadtmanae induces ASC speck formation in BlaER1 monocytes.\n\nDocument title: Human Monocytes Engage an Alternative Inflammasome Pathway.\n\nAbstract sentences:\n[0] Interleukin-1β (IL-1β) is a cytokine whose bioactivity is controlled by activation of the inflammasome.\n[1] However, in response to lipopolysaccharide, human monocytes secrete IL-1β independently of classical inflammasome stimuli.\n[2] Here, we report that this constituted a species-specific response that is not observed in the murine system.\n[3] Indeed, in human monocytes, lipopolysaccharide triggered an \"alternative inflammasome\" that relied on NLRP3-ASC-caspase-1 signaling, yet was devoid of any classical inflammasome characteristics including pyroptosome formation, pyroptosis induction, and K(+) efflux dependency.\n[4] Genetic dissection of the underlying signaling pathway in a monocyte transdifferentiation system revealed that alternative inflammasome activation was propagated by TLR4-TRIF-RIPK1-FADD-CASP8 signaling upstream of NLRP3.\n[5] Importantly, involvement of this signaling cascade was limited to alternative inflammasome activation and did not extend to classical NLRP3 activation.\n[6] Because alternative inflammasome activation embraces both sensitivity and promiscuity of TLR4, we propose a pivotal role for this signaling cascade in TLR4-driven, IL-1β-mediated immune responses and immunopathology in humans."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 733, "doc_id": 34469966, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [34469966], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: MEK inhibitors are effective treatments in RAS-driven mouse models of cancer.\n\nDocument title: Effective Use of PI3K and MEK Inhibitors to Treat Mutant K-Ras G12D and PIK3CA H1047R Murine Lung Cancers\n\nAbstract sentences:\n[0] Somatic mutations that activate phosphoinositide 3-kinase (PI3K) have been identified in the p110-alpha catalytic subunit (encoded by PIK3CA).\n[1] They are most frequently observed in two hotspots: the helical domain (E545K and E542K) and the kinase domain (H1047R).\n[2] Although the p110-alpha mutants are transforming in vitro, their oncogenic potential has not been assessed in genetically engineered mouse models.\n[3] Furthermore, clinical trials with PI3K inhibitors have recently been initiated, and it is unknown if their efficacy will be restricted to specific, genetically defined malignancies.\n[4] In this study, we engineered a mouse model of lung adenocarcinomas initiated and maintained by expression of p110-alpha H1047R.\n[5] Treatment of these tumors with NVP-BEZ235, a dual pan-PI3K and mammalian target of rapamycin (mTOR) inhibitor in clinical development, led to marked tumor regression as shown by positron emission tomography-computed tomography, magnetic resonance imaging and microscopic examination.\n[6] In contrast, mouse lung cancers driven by mutant Kras did not substantially respond to single-agent NVP-BEZ235.\n[7] However, when NVP-BEZ235 was combined with a mitogen-activated protein kinase kinase (MEK) inhibitor, ARRY-142886, there was marked synergy in shrinking these Kras-mutant cancers.\n[8] These in vivo studies suggest that inhibitors of the PI3K-mTOR pathway may be active in cancers with PIK3CA mutations and, when combined with MEK inhibitors, may effectively treat KRAS mutated lung cancers."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"However, when NVP-BEZ235 was combined with a mitogen-activated protein kinase kinase (MEK) inhibitor, ARRY-142886, there was marked synergy in shrinking these Kras-mutant cancers.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 734, "doc_id": 4961038, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [4961038], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: MFGE8 regulates fat absorption by binding to av-Beta3 and av-Beta5 integrins.\n\nDocument title: Mfge8 promotes obesity by mediating the uptake of dietary fats and serum fatty acids\n\nAbstract sentences:\n[0] Fatty acids are integral mediators of energy storage, membrane formation and cell signaling.\n[1] The pathways that orchestrate uptake of fatty acids remain incompletely understood.\n[2] Expression of the integrin ligand Mfge8 is increased in human obesity and in mice on a high-fat diet, but its role in obesity is unknown.\n[3] We show here that Mfge8 promotes the absorption of dietary triglycerides and the cellular uptake of fatty acid and that Mfge8-deficient (Mfge8−/−) mice are protected from diet-induced obesity, steatohepatitis and insulin resistance.\n[4] Mechanistically, we found that Mfge8 coordinates fatty acid uptake through αvβ3 integrin– and αvβ5 integrin–dependent phosphorylation of Akt by phosphatidylinositide-3 kinase and mTOR complex 2, leading to translocation of Cd36 and Fatp1 from cytoplasmic vesicles to the cell surface.\n[5] Collectively, our results imply a role for Mfge8 in regulating the absorption and storage of dietary fats, as well as in the development of obesity and its complications."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Mechanistically, we found that Mfge8 coordinates fatty acid uptake through αvβ3 integrin– and αvβ5 integrin–dependent phosphorylation of Akt by phosphatidylinositide-3 kinase and mTOR complex 2, leading to translocation of Cd36 and Fatp1 from cytoplasmic vesicles to the cell surface.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 736, "doc_id": 5389095, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [5389095], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: MICAL redox enzymes regulate actin dynamics in many cell types.\n\nDocument title: Drosophila MICAL regulates myofilament organization and synaptic structure\n\nAbstract sentences:\n[0] The overall size and structure of a synaptic terminal is an important determinant of its function.\n[1] In a large-scale mutagenesis screen, designed to identify Drosophila mutants with abnormally structured neuromuscular junctions (NMJs), we discovered mutations in Drosophila mical, a conserved gene encoding a multi-domain protein with a N-terminal monooxygenase domain.\n[2] In mical mutants, synaptic boutons do not sprout normally over the muscle surface and tend to form clusters along synaptic branches and at nerve entry sites.\n[3] Consistent with high expression of MICAL in somatic muscles, immunohistochemical stainings reveal that the subcellular localization and architecture of contractile muscle filaments are dramatically disturbed in mical mutants.\n[4] Instead of being integrated into a regular sarcomeric pattern, actin and myosin filaments are disorganized and accumulate beneath the plasmamembrane.\n[5] Whereas contractile elements are strongly deranged, the proposed organizer of sarcomeric structure, D-Titin, is much less affected.\n[6] Transgenic expression of interfering RNA molecules demonstrates that MICAL is required in muscles for the higher order arrangement of myofilaments.\n[7] Ultrastructural analysis confirms that myosin-rich thick filaments enter submembranous regions and interfere with synaptic development, indicating that the disorganized myofilaments may cause the synaptic growth phenotype.\n[8] As a model, we suggest that the filamentous network around synaptic boutons restrains the spreading of synaptic branches."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Instead of being integrated into a regular sarcomeric pattern, actin and myosin filaments are disorganized and accumulate beneath the plasmamembrane.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 737, "doc_id": 16562534, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [16562534, 6609935], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: MICAL redox enzymes regulate actin dynamics in many cell types.\n\nDocument title: Drosophila MICAL regulates myofilament organization and synaptic structure\n\nAbstract sentences:\n[0] The overall size and structure of a synaptic terminal is an important determinant of its function.\n[1] In a large-scale mutagenesis screen, designed to identify Drosophila mutants with abnormally structured neuromuscular junctions (NMJs), we discovered mutations in Drosophila mical, a conserved gene encoding a multi-domain protein with a N-terminal monooxygenase domain.\n[2] In mical mutants, synaptic boutons do not sprout normally over the muscle surface and tend to form clusters along synaptic branches and at nerve entry sites.\n[3] Consistent with high expression of MICAL in somatic muscles, immunohistochemical stainings reveal that the subcellular localization and architecture of contractile muscle filaments are dramatically disturbed in mical mutants.\n[4] Instead of being integrated into a regular sarcomeric pattern, actin and myosin filaments are disorganized and accumulate beneath the plasmamembrane.\n[5] Whereas contractile elements are strongly deranged, the proposed organizer of sarcomeric structure, D-Titin, is much less affected.\n[6] Transgenic expression of interfering RNA molecules demonstrates that MICAL is required in muscles for the higher order arrangement of myofilaments.\n[7] Ultrastructural analysis confirms that myosin-rich thick filaments enter submembranous regions and interfere with synaptic development, indicating that the disorganized myofilaments may cause the synaptic growth phenotype.\n[8] As a model, we suggest that the filamentous network around synaptic boutons restrains the spreading of synaptic branches."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Transgenic expression of interfering RNA molecules demonstrates that MICAL is required in muscles for the higher order arrangement of myofilaments.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 737, "doc_id": 16562534, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [16562534, 6609935], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: MICAL redox enzymes regulate actin dynamics in many cell types.\n\nDocument title: Differential regulation of actin microfilaments by human MICAL proteins.\n\nAbstract sentences:\n[0] The Drosophila melanogaster MICAL protein is essential for the neuronal growth cone machinery that functions through plexin- and semaphorin-mediated axonal signaling.\n[1] Drosophila MICAL is also involved in regulating myofilament organization and synaptic structures, and serves as an actin disassembly factor downstream of plexin-mediated axonal repulsion.\n[2] In mammalian cells there are three known isoforms, MICAL1, MICAL2 and MICAL3, as well as the MICAL-like proteins MICAL-L1 and MICAL-L2, but little is known of their function, and information comes almost exclusively from neural cells.\n[3] In this study we show that in non-neural cells human MICALs are required for normal actin organization, and all three MICALs regulate actin stress fibers.\n[4] Moreover, we provide evidence that the generation of reactive oxygen species by MICAL proteins is crucial for their actin-regulatory function.\n[5] However, although MICAL1 is auto-inhibited by its C-terminal coiled-coil region, MICAL2 remains constitutively active and affects stress fibers.\n[6] These data suggest differential but complementary roles for MICAL1 and MICAL2 in actin microfilament regulation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"In this study we show that in non-neural cells human MICALs are required for normal actin organization, and all three MICALs regulate actin stress fibers.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 737, "doc_id": 6609935, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [16562534, 6609935], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: MICAL redox enzymes regulate actin dynamics.\n\nDocument title: Drosophila MICAL regulates myofilament organization and synaptic structure\n\nAbstract sentences:\n[0] The overall size and structure of a synaptic terminal is an important determinant of its function.\n[1] In a large-scale mutagenesis screen, designed to identify Drosophila mutants with abnormally structured neuromuscular junctions (NMJs), we discovered mutations in Drosophila mical, a conserved gene encoding a multi-domain protein with a N-terminal monooxygenase domain.\n[2] In mical mutants, synaptic boutons do not sprout normally over the muscle surface and tend to form clusters along synaptic branches and at nerve entry sites.\n[3] Consistent with high expression of MICAL in somatic muscles, immunohistochemical stainings reveal that the subcellular localization and architecture of contractile muscle filaments are dramatically disturbed in mical mutants.\n[4] Instead of being integrated into a regular sarcomeric pattern, actin and myosin filaments are disorganized and accumulate beneath the plasmamembrane.\n[5] Whereas contractile elements are strongly deranged, the proposed organizer of sarcomeric structure, D-Titin, is much less affected.\n[6] Transgenic expression of interfering RNA molecules demonstrates that MICAL is required in muscles for the higher order arrangement of myofilaments.\n[7] Ultrastructural analysis confirms that myosin-rich thick filaments enter submembranous regions and interfere with synaptic development, indicating that the disorganized myofilaments may cause the synaptic growth phenotype.\n[8] As a model, we suggest that the filamentous network around synaptic boutons restrains the spreading of synaptic branches."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Consistent with high expression of MICAL in somatic muscles, immunohistochemical stainings reveal that the subcellular localization and architecture of contractile muscle filaments are dramatically disturbed in mical mutants.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 738, "doc_id": 16562534, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [16562534, 6609935, 33912020], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: MICAL redox enzymes regulate actin dynamics.\n\nDocument title: Drosophila MICAL regulates myofilament organization and synaptic structure\n\nAbstract sentences:\n[0] The overall size and structure of a synaptic terminal is an important determinant of its function.\n[1] In a large-scale mutagenesis screen, designed to identify Drosophila mutants with abnormally structured neuromuscular junctions (NMJs), we discovered mutations in Drosophila mical, a conserved gene encoding a multi-domain protein with a N-terminal monooxygenase domain.\n[2] In mical mutants, synaptic boutons do not sprout normally over the muscle surface and tend to form clusters along synaptic branches and at nerve entry sites.\n[3] Consistent with high expression of MICAL in somatic muscles, immunohistochemical stainings reveal that the subcellular localization and architecture of contractile muscle filaments are dramatically disturbed in mical mutants.\n[4] Instead of being integrated into a regular sarcomeric pattern, actin and myosin filaments are disorganized and accumulate beneath the plasmamembrane.\n[5] Whereas contractile elements are strongly deranged, the proposed organizer of sarcomeric structure, D-Titin, is much less affected.\n[6] Transgenic expression of interfering RNA molecules demonstrates that MICAL is required in muscles for the higher order arrangement of myofilaments.\n[7] Ultrastructural analysis confirms that myosin-rich thick filaments enter submembranous regions and interfere with synaptic development, indicating that the disorganized myofilaments may cause the synaptic growth phenotype.\n[8] As a model, we suggest that the filamentous network around synaptic boutons restrains the spreading of synaptic branches."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Transgenic expression of interfering RNA molecules demonstrates that MICAL is required in muscles for the higher order arrangement of myofilaments.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 738, "doc_id": 16562534, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [16562534, 6609935, 33912020], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: MICAL redox enzymes regulate actin dynamics.\n\nDocument title: Differential regulation of actin microfilaments by human MICAL proteins.\n\nAbstract sentences:\n[0] The Drosophila melanogaster MICAL protein is essential for the neuronal growth cone machinery that functions through plexin- and semaphorin-mediated axonal signaling.\n[1] Drosophila MICAL is also involved in regulating myofilament organization and synaptic structures, and serves as an actin disassembly factor downstream of plexin-mediated axonal repulsion.\n[2] In mammalian cells there are three known isoforms, MICAL1, MICAL2 and MICAL3, as well as the MICAL-like proteins MICAL-L1 and MICAL-L2, but little is known of their function, and information comes almost exclusively from neural cells.\n[3] In this study we show that in non-neural cells human MICALs are required for normal actin organization, and all three MICALs regulate actin stress fibers.\n[4] Moreover, we provide evidence that the generation of reactive oxygen species by MICAL proteins is crucial for their actin-regulatory function.\n[5] However, although MICAL1 is auto-inhibited by its C-terminal coiled-coil region, MICAL2 remains constitutively active and affects stress fibers.\n[6] These data suggest differential but complementary roles for MICAL1 and MICAL2 in actin microfilament regulation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"In this study we show that in non-neural cells human MICALs are required for normal actin organization, and all three MICALs regulate actin stress fibers.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 738, "doc_id": 6609935, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [16562534, 6609935, 33912020], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: MICAL redox enzymes regulate actin dynamics.\n\nDocument title: Differential regulation of actin microfilaments by human MICAL proteins.\n\nAbstract sentences:\n[0] The Drosophila melanogaster MICAL protein is essential for the neuronal growth cone machinery that functions through plexin- and semaphorin-mediated axonal signaling.\n[1] Drosophila MICAL is also involved in regulating myofilament organization and synaptic structures, and serves as an actin disassembly factor downstream of plexin-mediated axonal repulsion.\n[2] In mammalian cells there are three known isoforms, MICAL1, MICAL2 and MICAL3, as well as the MICAL-like proteins MICAL-L1 and MICAL-L2, but little is known of their function, and information comes almost exclusively from neural cells.\n[3] In this study we show that in non-neural cells human MICALs are required for normal actin organization, and all three MICALs regulate actin stress fibers.\n[4] Moreover, we provide evidence that the generation of reactive oxygen species by MICAL proteins is crucial for their actin-regulatory function.\n[5] However, although MICAL1 is auto-inhibited by its C-terminal coiled-coil region, MICAL2 remains constitutively active and affects stress fibers.\n[6] These data suggest differential but complementary roles for MICAL1 and MICAL2 in actin microfilament regulation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Moreover, we provide evidence that the generation of reactive oxygen species by MICAL proteins is crucial for their actin-regulatory function.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 738, "doc_id": 6609935, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [16562534, 6609935, 33912020], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: MICAL redox enzymes regulate actin dynamics.\n\nDocument title: Differential regulation of actin microfilaments by human MICAL proteins.\n\nAbstract sentences:\n[0] The Drosophila melanogaster MICAL protein is essential for the neuronal growth cone machinery that functions through plexin- and semaphorin-mediated axonal signaling.\n[1] Drosophila MICAL is also involved in regulating myofilament organization and synaptic structures, and serves as an actin disassembly factor downstream of plexin-mediated axonal repulsion.\n[2] In mammalian cells there are three known isoforms, MICAL1, MICAL2 and MICAL3, as well as the MICAL-like proteins MICAL-L1 and MICAL-L2, but little is known of their function, and information comes almost exclusively from neural cells.\n[3] In this study we show that in non-neural cells human MICALs are required for normal actin organization, and all three MICALs regulate actin stress fibers.\n[4] Moreover, we provide evidence that the generation of reactive oxygen species by MICAL proteins is crucial for their actin-regulatory function.\n[5] However, although MICAL1 is auto-inhibited by its C-terminal coiled-coil region, MICAL2 remains constitutively active and affects stress fibers.\n[6] These data suggest differential but complementary roles for MICAL1 and MICAL2 in actin microfilament regulation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"These data suggest differential but complementary roles for MICAL1 and MICAL2 in actin microfilament regulation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 738, "doc_id": 6609935, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [16562534, 6609935, 33912020], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: MICAL redox enzymes regulate actin dynamics.\n\nDocument title: Thioredoxin mediates oxidation-dependent phosphorylation of CRMP2 and growth cone collapse.\n\nAbstract sentences:\n[0] Semaphorin3A (Sema3A) is a repulsive guidance molecule for axons, which acts by inducing growth cone collapse through phosphorylation of CRMP2 (collapsin response mediator protein 2).\n[1] Here, we show a role for CRMP2 oxidation and thioredoxin (TRX) in the regulation of CRMP2 phosphorylation and growth cone collapse.\n[2] Sema3A stimulation generated hydrogen peroxide (H2O2) through MICAL (molecule interacting with CasL) and oxidized CRMP2, enabling it to form a disulfide-linked homodimer through cysteine-504.\n[3] Oxidized CRMP2 then formed a transient disulfide-linked complex with TRX, which stimulated CRMP2 phosphorylation by glycogen synthase kinase-3, leading to growth cone collapse.\n[4] We also reconstituted oxidation-dependent phosphorylation of CRMP2 in vitro, using a limited set of purified proteins.\n[5] Our results not only clarify the importance of H2O2 and CRMP2 oxidation in Sema3A-induced growth cone collapse but also indicate an unappreciated role for TRX in linking CRMP2 oxidation to phosphorylation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2, 3, 5]\nExplanation: Evidence states: \"Sema3A stimulation generated hydrogen peroxide (H2O2) through MICAL (molecule interacting with CasL) and oxidized CRMP2, enabling it to form a disulfide-linked homodimer through cysteine-504. Oxidized CRMP2 then formed a transient disulfide-linked complex with TRX, which stimulated CRMP2 phosphorylation by glycogen synthase kinase-3, leading to growth cone collapse. Our results not only clarify the importance of H2O2 and CRMP2 oxidation in Sema3A-induced growth cone collapse but also indicate an unappreciated role for TRX in linking CRMP2 oxidation to phosphorylation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 738, "doc_id": 33912020, "label": "SUPPORTS", "evidence_sentence_ids": [2, 3, 5], "cited_doc_ids": [16562534, 6609935, 33912020], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: MT binding domain drives amyloid structure formation.\n\nDocument title: Cryo-EM structures of Tau filaments from Alzheimer’s disease brain\n\nAbstract sentences:\n[0] Alzheimer's disease is the most common neurodegenerative disease, and there are no mechanism-based therapies.\n[1] The disease is defined by the presence of abundant neurofibrillary lesions and neuritic plaques in the cerebral cortex.\n[2] Neurofibrillary lesions comprise paired helical and straight tau filaments, whereas tau filaments with different morphologies characterize other neurodegenerative diseases.\n[3] No high-resolution structures of tau filaments are available.\n[4] Here we present cryo-electron microscopy (cryo-EM) maps at 3.4-3.5 Å resolution and corresponding atomic models of paired helical and straight filaments from the brain of an individual with Alzheimer's disease.\n[5] Filament cores are made of two identical protofilaments comprising residues 306-378 of tau protein, which adopt a combined cross-β/β-helix structure and define the seed for tau aggregation.\n[6] Paired helical and straight filaments differ in their inter-protofilament packing, showing that they are ultrastructural polymorphs.\n[7] These findings demonstrate that cryo-EM allows atomic characterization of amyloid filaments from patient-derived material, and pave the way for investigation of a range of neurodegenerative diseases."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 739, "doc_id": 4446814, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4446814], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: MUC1-C activates the NF-κB p65 signaling pathway by interacting with IκB kinase ß.\n\nDocument title: MUC1 oncoprotein activates the IκB kinase β complex and constitutive NF-κB signalling\n\nAbstract sentences:\n[0] Nuclear factor-κB (NF-κB) is constitutively activated in diverse human malignancies by mechanisms that are not understood.\n[1] The MUC1 oncoprotein is aberrantly overexpressed by most human carcinomas and, similarly to NF-κB, blocks apoptosis and induces transformation.\n[2] This study demonstrates that overexpression of MUC1 in human carcinoma cells is associated with constitutive activation of NF-κB p65.\n[3] We show that MUC1 interacts with the high-molecular-weight IκB kinase (IKK) complex in vivo and that the MUC1 cytoplasmic domain binds directly to IKKβ and IKKγ.\n[4] Interaction of MUC1 with both IKKβ and IKKγ is necessary for IKKβ activation, resulting in phosphorylation and degradation of IκBα.\n[5] Studies in non-malignant epithelial cells show that MUC1 is recruited to the TNF-R1 complex and interacts with IKKβ–IKKγ in response to TNFα stimulation.\n[6] TNFα-induced recruitment of MUC1 is dependent on TRADD and TRAF2, but not the death-domain kinase RIP1.\n[7] In addition, MUC1-mediated activation of IKKβ is dependent on TAK1 and TAB2.\n[8] These findings indicate that MUC1 is important for physiological activation of IKKβ and that overexpression of MUC1, as found in human cancers, confers sustained induction of the IKKβ–NF-κB p65 pathway."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"These findings indicate that MUC1 is important for physiological activation of IKKβ and that overexpression of MUC1, as found in human cancers, confers sustained induction of the IKKβ–NF-κB p65 pathway.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 740, "doc_id": 23078022, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [23078022], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: MafA phosphorylation decreases its ubiquitination.\n\nDocument title: GSK-3-mediated phosphorylation enhances Maf-transforming activity.\n\nAbstract sentences:\n[0] The Maf oncoproteins are b-Zip transcription factors of the AP-1 superfamily.\n[1] They are involved in developmental, metabolic, and tumorigenic processes.\n[2] Maf proteins are overexpressed in about 50% of human multiple myelomas.\n[3] Here, we show that Maf-transforming activity is controlled by GSK-3-dependent phosphorylation and that phosphorylation by GSK-3 can increase the oncogenic activity of a protein.\n[4] Using microarray analysis, we identify a gene-expression subprogram regulated by GSK-3-mediated Maf phosphorylation involved in extracellular matrix remodeling and relevant to cancer progression.\n[5] We also demonstrate that GSK-3 triggers MafA sequential phosphorylation on residues S61, T57, T53, and S49, inducing its ubiquitination and degradation.\n[6] Paradoxically, this phosphorylation increases MafA-transcriptional activity through the recruitment of the coactivator P/CAF.\n[7] We further demonstrate that P/CAF protects MafA from ubiquitination and degradation, suggesting that, upon the release of the coactivator complex, MafA becomes polyubiquitinated and degraded to allow the response to terminate."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"We also demonstrate that GSK-3 triggers MafA sequential phosphorylation on residues S61, T57, T53, and S49, inducing its ubiquitination and degradation.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 745, "doc_id": 11291348, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [11291348], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: MafA phosphorylation enhances its ubiquitination.\n\nDocument title: GSK-3-mediated phosphorylation enhances Maf-transforming activity.\n\nAbstract sentences:\n[0] The Maf oncoproteins are b-Zip transcription factors of the AP-1 superfamily.\n[1] They are involved in developmental, metabolic, and tumorigenic processes.\n[2] Maf proteins are overexpressed in about 50% of human multiple myelomas.\n[3] Here, we show that Maf-transforming activity is controlled by GSK-3-dependent phosphorylation and that phosphorylation by GSK-3 can increase the oncogenic activity of a protein.\n[4] Using microarray analysis, we identify a gene-expression subprogram regulated by GSK-3-mediated Maf phosphorylation involved in extracellular matrix remodeling and relevant to cancer progression.\n[5] We also demonstrate that GSK-3 triggers MafA sequential phosphorylation on residues S61, T57, T53, and S49, inducing its ubiquitination and degradation.\n[6] Paradoxically, this phosphorylation increases MafA-transcriptional activity through the recruitment of the coactivator P/CAF.\n[7] We further demonstrate that P/CAF protects MafA from ubiquitination and degradation, suggesting that, upon the release of the coactivator complex, MafA becomes polyubiquitinated and degraded to allow the response to terminate."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"We also demonstrate that GSK-3 triggers MafA sequential phosphorylation on residues S61, T57, T53, and S49, inducing its ubiquitination and degradation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 746, "doc_id": 11291348, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [11291348], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: MafA ubiquitination decreases the recruitment of coavtivator P/CAF by MafA.\n\nDocument title: GSK-3-mediated phosphorylation enhances Maf-transforming activity.\n\nAbstract sentences:\n[0] The Maf oncoproteins are b-Zip transcription factors of the AP-1 superfamily.\n[1] They are involved in developmental, metabolic, and tumorigenic processes.\n[2] Maf proteins are overexpressed in about 50% of human multiple myelomas.\n[3] Here, we show that Maf-transforming activity is controlled by GSK-3-dependent phosphorylation and that phosphorylation by GSK-3 can increase the oncogenic activity of a protein.\n[4] Using microarray analysis, we identify a gene-expression subprogram regulated by GSK-3-mediated Maf phosphorylation involved in extracellular matrix remodeling and relevant to cancer progression.\n[5] We also demonstrate that GSK-3 triggers MafA sequential phosphorylation on residues S61, T57, T53, and S49, inducing its ubiquitination and degradation.\n[6] Paradoxically, this phosphorylation increases MafA-transcriptional activity through the recruitment of the coactivator P/CAF.\n[7] We further demonstrate that P/CAF protects MafA from ubiquitination and degradation, suggesting that, upon the release of the coactivator complex, MafA becomes polyubiquitinated and degraded to allow the response to terminate."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Paradoxically, this phosphorylation increases MafA-transcriptional activity through the recruitment of the coactivator P/CAF.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 747, "doc_id": 11291348, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [11291348], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: MafA ubiquitination increases the recruitment of coavtivator P/CAF by MafA.\n\nDocument title: GSK-3-mediated phosphorylation enhances Maf-transforming activity.\n\nAbstract sentences:\n[0] The Maf oncoproteins are b-Zip transcription factors of the AP-1 superfamily.\n[1] They are involved in developmental, metabolic, and tumorigenic processes.\n[2] Maf proteins are overexpressed in about 50% of human multiple myelomas.\n[3] Here, we show that Maf-transforming activity is controlled by GSK-3-dependent phosphorylation and that phosphorylation by GSK-3 can increase the oncogenic activity of a protein.\n[4] Using microarray analysis, we identify a gene-expression subprogram regulated by GSK-3-mediated Maf phosphorylation involved in extracellular matrix remodeling and relevant to cancer progression.\n[5] We also demonstrate that GSK-3 triggers MafA sequential phosphorylation on residues S61, T57, T53, and S49, inducing its ubiquitination and degradation.\n[6] Paradoxically, this phosphorylation increases MafA-transcriptional activity through the recruitment of the coactivator P/CAF.\n[7] We further demonstrate that P/CAF protects MafA from ubiquitination and degradation, suggesting that, upon the release of the coactivator complex, MafA becomes polyubiquitinated and degraded to allow the response to terminate."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Paradoxically, this phosphorylation increases MafA-transcriptional activity through the recruitment of the coactivator P/CAF.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 748, "doc_id": 11291348, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [11291348], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Major antigen-induced signals from the T cell receptor and secondary signals from costimulatory receptors are required for T cell activation.\n\nDocument title: CD28 Costimulation: From Mechanism to Therapy.\n\nAbstract sentences:\n[0] Ligation of the CD28 receptor on T cells provides a critical second signal alongside T cell receptor (TCR) ligation for naive T cell activation.\n[1] Here, we discuss the expression, structure, and biochemistry of CD28 and its ligands.\n[2] CD28 signals play a key role in many T cell processes, including cytoskeletal remodeling, production of cytokines, survival, and differentiation.\n[3] CD28 ligation leads to unique epigenetic, transcriptional, and post-translational changes in T cells that cannot be recapitulated by TCR ligation alone.\n[4] We discuss the function of CD28 and its ligands in both effector and regulatory T cells.\n[5] CD28 is critical for regulatory T cell survival and the maintenance of immune homeostasis.\n[6] We outline the roles that CD28 and its family members play in human disease and we review the clinical efficacy of drugs that block CD28 ligands.\n[7] Despite the centrality of CD28 and its family members and ligands to immune function, many aspects of CD28 biology remain unclear.\n[8] Translation of a basic understanding of CD28 function into immunomodulatory therapeutics has been uneven, with both successes and failures.\n[9] Such real-world results might stem from multiple factors, including complex receptor-ligand interactions among CD28 family members, differences between the mouse and human CD28 families, and cell-type specific roles of CD28 family members."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Ligation of the CD28 receptor on T cells provides a critical second signal alongside T cell receptor (TCR) ligation for naive T cell activation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 749, "doc_id": 13868795, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [13868795], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Major vault protein (MVP) leads to more aggressive tumors by regulating the sorting of tumor suppressive miR-193a into extracellular vesicles (EVs).\n\nDocument title: MVP-mediated exosomal sorting of miR-193a promotes colon cancer progression\n\nAbstract sentences:\n[0] Exosomes are emerging mediators of intercellular communication; whether the release of exosomes has an effect on the exosome donor cells in addition to the recipient cells has not been investigated to any extent.\n[1] Here, we examine different exosomal miRNA expression profiles in primary mouse colon tumour, liver metastasis of colon cancer and naive colon tissues.\n[2] In more advanced disease, higher levels of tumour suppressor miRNAs are encapsulated in the exosomes.\n[3] miR-193a interacts with major vault protein (MVP).\n[4] Knockout of MVP leads to miR-193a accumulation in the exosomal donor cells instead of exosomes, inhibiting tumour progression.\n[5] Furthermore, miR-193a causes cell cycle G1 arrest and cell proliferation repression through targeting of Caprin1, which upregulates Ccnd2 and c-Myc.\n[6] Human colon cancer patients with more advanced disease show higher levels of circulating exosomal miR-193a.\n[7] In summary, our data demonstrate that MVP-mediated selective sorting of tumour suppressor miRNA into exosomes promotes tumour progression."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Knockout of MVP leads to miR-193a accumulation in the exosomal donor cells instead of exosomes, inhibiting tumour progression.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 751, "doc_id": 19800147, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [19800147], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Major vault protein (MVP) leads to more aggressive tumors by regulating the sorting of tumor suppressive miR-193a into extracellular vesicles (EVs).\n\nDocument title: MVP-mediated exosomal sorting of miR-193a promotes colon cancer progression\n\nAbstract sentences:\n[0] Exosomes are emerging mediators of intercellular communication; whether the release of exosomes has an effect on the exosome donor cells in addition to the recipient cells has not been investigated to any extent.\n[1] Here, we examine different exosomal miRNA expression profiles in primary mouse colon tumour, liver metastasis of colon cancer and naive colon tissues.\n[2] In more advanced disease, higher levels of tumour suppressor miRNAs are encapsulated in the exosomes.\n[3] miR-193a interacts with major vault protein (MVP).\n[4] Knockout of MVP leads to miR-193a accumulation in the exosomal donor cells instead of exosomes, inhibiting tumour progression.\n[5] Furthermore, miR-193a causes cell cycle G1 arrest and cell proliferation repression through targeting of Caprin1, which upregulates Ccnd2 and c-Myc.\n[6] Human colon cancer patients with more advanced disease show higher levels of circulating exosomal miR-193a.\n[7] In summary, our data demonstrate that MVP-mediated selective sorting of tumour suppressor miRNA into exosomes promotes tumour progression."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"In summary, our data demonstrate that MVP-mediated selective sorting of tumour suppressor miRNA into exosomes promotes tumour progression.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 751, "doc_id": 19800147, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [19800147], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Major vault protein regulates sorting of tumor suppressive miR-193a into EVs.\n\nDocument title: MVP-mediated exosomal sorting of miR-193a promotes colon cancer progression\n\nAbstract sentences:\n[0] Exosomes are emerging mediators of intercellular communication; whether the release of exosomes has an effect on the exosome donor cells in addition to the recipient cells has not been investigated to any extent.\n[1] Here, we examine different exosomal miRNA expression profiles in primary mouse colon tumour, liver metastasis of colon cancer and naive colon tissues.\n[2] In more advanced disease, higher levels of tumour suppressor miRNAs are encapsulated in the exosomes.\n[3] miR-193a interacts with major vault protein (MVP).\n[4] Knockout of MVP leads to miR-193a accumulation in the exosomal donor cells instead of exosomes, inhibiting tumour progression.\n[5] Furthermore, miR-193a causes cell cycle G1 arrest and cell proliferation repression through targeting of Caprin1, which upregulates Ccnd2 and c-Myc.\n[6] Human colon cancer patients with more advanced disease show higher levels of circulating exosomal miR-193a.\n[7] In summary, our data demonstrate that MVP-mediated selective sorting of tumour suppressor miRNA into exosomes promotes tumour progression."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Knockout of MVP leads to miR-193a accumulation in the exosomal donor cells instead of exosomes, inhibiting tumour progression.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 752, "doc_id": 19800147, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [19800147], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Malaria has a high vectorial capacity.\n\nDocument title: Ranking of elimination feasibility between malaria-endemic countries\n\nAbstract sentences:\n[0] Experience gained from the Global Malaria Eradication Program (1955-72) identified a set of shared technical and operational factors that enabled some countries to successfully eliminate malaria.\n[1] Spatial data for these factors were assembled for all malaria-endemic countries and combined to provide an objective, relative ranking of countries by technical, operational, and combined elimination feasibility.\n[2] The analysis was done separately for Plasmodium falciparum and Plasmodium vivax, and the limitations of the approach were discussed.\n[3] The relative rankings suggested that malaria elimination would be most feasible in countries in the Americas and Asia, and least feasible in countries in central and west Africa.\n[4] The results differed when feasibility was measured by technical or operational factors, highlighting the different types of challenge faced by each country.\n[5] The results are not intended to be prescriptive, predictive, or to provide absolute assessments of feasibility, but they do show that spatial information is available to facilitate evidence-based assessments of the relative feasibility of malaria elimination by country that can be rapidly updated."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 753, "doc_id": 1173667, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [1173667], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Many cytokines that are produced by cancer cells also contribute to carcinogenesis.\n\nDocument title: Autocrine VEGF Signaling Synergizes with EGFR in Tumor Cells to Promote Epithelial Cancer Development\n\nAbstract sentences:\n[0] It is established that tumor cell-derived VEGF acts on endothelial cells to promote angiogenesis and tumor growth.\n[1] Here, we demonstrate that in K5-SOS-dependent mouse skin tumors, autocrine VEGF is required for tumor cell proliferation in a cell-autonomous and angiogenesis-independent manner.\n[2] VEGF is upregulated in SOS-expressing tumors, and its deletion in epidermal cells delays tumorigenesis by suppressing angiogenesis and tumor cell proliferation.\n[3] Epidermis-specific Flt1 deletion also impairs tumorigenesis and proliferation.\n[4] Surprisingly, complete tumor inhibition occurs in the absence of VEGF in EGFR mutant mice, demonstrating that VEGFR and EGFR synergize in neoplastic cells to promote tumor growth.\n[5] Mechanistically, K5-SOS upregulates VEGF, Flt1, and Neuropilin-1 in an Erk-dependent manner, thereby activating an autocrine proliferation loop, whereas EGFR prevents tumor cells from apoptosis.\n[6] Moreover, Flt1 is upregulated in human SCC, and its inhibition in SCC cells impairs proliferation.\n[7] Thus, in addition to regulating angiogenesis, VEGF has to be considered as a potent growth factor for epidermal tumors."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 755, "doc_id": 17844478, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [17844478], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Many transmembrane receptors transmit signals by long-range conformational changes in the association of alpha-helices across the plasma membrane.\n\nDocument title: Dynamic Helix Interactions in Transmembrane Signaling\n\nAbstract sentences:\n[0] Studying how protein transmembrane domains transmit signals across membranes is beset by unique challenges.\n[1] Here, we discuss the circumstances that have led to success and reflect on what has been learned from these examples.\n[2] Such efforts suggest that some of the most interesting properties of transmembrane helix interactions may be the least amenable to study by current techniques."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 757, "doc_id": 17123657, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [17123657], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Marmosets have a brain region homologous to Broca's area.\n\nDocument title: Responses of primate frontal cortex neurons during natural vocal communication.\n\nAbstract sentences:\n[0] The role of primate frontal cortex in vocal communication and its significance in language evolution have a controversial history.\n[1] While evidence indicates that vocalization processing occurs in ventrolateral prefrontal cortex neurons, vocal-motor activity has been conjectured to be primarily subcortical and suggestive of a distinctly different neural architecture from humans.\n[2] Direct evidence of neural activity during natural vocal communication is limited, as previous studies were performed in chair-restrained animals.\n[3] Here we recorded the activity of single neurons across multiple regions of prefrontal and premotor cortex while freely moving marmosets engaged in a natural vocal behavior known as antiphonal calling.\n[4] Our aim was to test whether neurons in marmoset frontal cortex exhibited responses during vocal-signal processing and/or vocal-motor production in the context of active, natural communication.\n[5] We observed motor-related changes in single neuron activity during vocal production, but relatively weak sensory responses for vocalization processing during this natural behavior.\n[6] Vocal-motor responses occurred both prior to and during call production and were typically coupled to the timing of each vocalization pulse.\n[7] Despite the relatively weak sensory responses a population classifier was able to distinguish between neural activity that occurred during presentations of vocalization stimuli that elicited an antiphonal response and those that did not.\n[8] These findings are suggestive of the role that nonhuman primate frontal cortex neurons play in natural communication and provide an important foundation for more explicit tests of the functional contributions of these neocortical areas during vocal behaviors."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 758, "doc_id": 14195528, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14195528], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mathematical models predict that using Artemisinin-based combination therapy over nongametocytocidal drugs have only a modest impact in reducing malaria transmission.\n\nDocument title: Modelling the Impact of Artemisinin Combination Therapy and Long-Acting Treatments on Malaria Transmission Intensity\n\nAbstract sentences:\n[0] BACKGROUND Artemisinin derivatives used in recently introduced combination therapies (ACTs) for Plasmodium falciparum malaria significantly lower patient infectiousness and have the potential to reduce population-level transmission of the parasite.\n[1] With the increased interest in malaria elimination, understanding the impact on transmission of ACT and other antimalarial drugs with different pharmacodynamics becomes a key issue.\n[2] This study estimates the reduction in transmission that may be achieved by introducing different types of treatment for symptomatic P. falciparum malaria in endemic areas.\n[3] METHODS AND FINDINGS We developed a mathematical model to predict the potential impact on transmission outcomes of introducing ACT as first-line treatment for uncomplicated malaria in six areas of varying transmission intensity in Tanzania.\n[4] We also estimated the impact that could be achieved by antimalarials with different efficacy, prophylactic time, and gametocytocidal effects.\n[5] Rates of treatment, asymptomatic infection, and symptomatic infection in the six study areas were estimated using the model together with data from a cross-sectional survey of 5,667 individuals conducted prior to policy change from sulfadoxine-pyrimethamine to ACT.\n[6] The effects of ACT and other drug types on gametocytaemia and infectiousness to mosquitoes were independently estimated from clinical trial data.\n[7] Predicted percentage reductions in prevalence of infection and incidence of clinical episodes achieved by ACT were highest in the areas with low initial transmission.\n[8] A 53% reduction in prevalence of infection was seen if 100% of current treatment was switched to ACT in the area where baseline slide-prevalence of parasitaemia was lowest (3.7%), compared to an 11% reduction in the highest-transmission setting (baseline slide prevalence = 57.1%).\n[9] Estimated percentage reductions in incidence of clinical episodes were similar.\n[10] The absolute size of the public health impact, however, was greater in the highest-transmission area, with 54 clinical episodes per 100 persons per year averted compared to five per 100 persons per year in the lowest-transmission area.\n[11] High coverage was important.\n[12] Reducing presumptive treatment through improved diagnosis substantially reduced the number of treatment courses required per clinical episode averted in the lower-transmission settings although there was some loss of overall impact on transmission.\n[13] An efficacious antimalarial regimen with no specific gametocytocidal properties but a long prophylactic time was estimated to be more effective at reducing transmission than a short-acting ACT in the highest-transmission setting.\n[14] CONCLUSIONS Our results suggest that ACTs have the potential for transmission reductions approaching those achieved by insecticide-treated nets in lower-transmission settings.\n[15] ACT partner drugs and nonartemisinin regimens with longer prophylactic times could result in a larger impact in higher-transmission settings, although their long term benefit must be evaluated in relation to the risk of development of parasite resistance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"An efficacious antimalarial regimen with no specific gametocytocidal properties but a long prophylactic time was estimated to be more effective at reducing transmission than a short-acting ACT in the highest-transmission setting.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 760, "doc_id": 1805641, "label": "SUPPORTS", "evidence_sentence_ids": [13], "cited_doc_ids": [1805641], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: MeCP2 influences the synaptic maturation of neurons.\n\nDocument title: Structural Homeostasis: Compensatory Adjustments of Dendritic Arbor Geometry in Response to Variations of Synaptic Input \n\nAbstract sentences:\n[0] As the nervous system develops, there is an inherent variability in the connections formed between differentiating neurons.\n[1] Despite this variability, neural circuits form that are functional and remarkably robust.\n[2] One way in which neurons deal with variability in their inputs is through compensatory, homeostatic changes in their electrical properties.\n[3] Here, we show that neurons also make compensatory adjustments to their structure.\n[4] We analysed the development of dendrites on an identified central neuron (aCC) in the late Drosophila embryo at the stage when it receives its first connections and first becomes electrically active.\n[5] At the same time, we charted the distribution of presynaptic sites on the developing postsynaptic arbor.\n[6] Genetic manipulations of the presynaptic partners demonstrate that the postsynaptic dendritic arbor adjusts its growth to compensate for changes in the activity and density of synaptic sites.\n[7] Blocking the synthesis or evoked release of presynaptic neurotransmitter results in greater dendritic extension.\n[8] Conversely, an increase in the density of presynaptic release sites induces a reduction in the extent of the dendritic arbor.\n[9] These growth adjustments occur locally in the arbor and are the result of the promotion or inhibition of growth of neurites in the proximity of presynaptic sites.\n[10] We provide evidence that suggest a role for the postsynaptic activity state of protein kinase A in mediating this structural adjustment, which modifies dendritic growth in response to synaptic activity.\n[11] These findings suggest that the dendritic arbor, at least during early stages of connectivity, behaves as a homeostatic device that adjusts its size and geometry to the level and the distribution of input received.\n[12] The growing arbor thus counterbalances naturally occurring variations in synaptic density and activity so as to ensure that an appropriate level of input is achieved."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 761, "doc_id": 10009203, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [10009203], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Measuring routine outcomes is more beneficial to clinical practice than assessing treatment adherence.\n\nDocument title: Anxiety\n\nAbstract sentences:\n[0] OBJECTIVES To examine the effect of routinely administered psychiatric questionnaires on the recognition, management, and outcome of psychiatric disorders in non-psychiatric settings.\n[1] DATA SOURCES Embase, Medline, PsycLIT, Cinahl, Cochrane Controlled Trials Register, and hand searches of key journals.\n[2] METHODS A systematic review of randomised controlled trials of the administration and routine feedback of psychiatric screening and outcome questionnaires to clinicians in non-psychiatric settings.\n[3] Narrative overview of key design features and end points, together with a random effects quantitative synthesis of comparable studies.\n[4] MAIN OUTCOME MEASURES Recognition of psychiatric disorders after feedback of questionnaire results; interventions for psychiatric disorders; and outcome of psychiatric disorders.\n[5] RESULTS Nine randomised studies were identified that examined the use of common psychiatric instruments in primary care and general hospital settings.\n[6] Studies compared the effect of the administration of these instruments followed by the feedback of the results to clinicians, with administration with no feedback.\n[7] Meta-analytic pooling was possible for four of these studies (2457 participants), which measured the effect of feedback on the recognition of depressive disorders.\n[8] Routine administration and feedback of scores for all patients (irrespective of score) did not increase the overall rate of recognition of mental disorders such as anxiety and depression (relative risk of detection of depression by clinician after feedback 0.95, 95% confidence interval 0.83 to 1.09).\n[9] Two studies showed that routine administration followed by selective feedback for only high scorers increased the rate of recognition of depression (relative risk of detection of depression after feedback 2.64, 1.62 to 4.31).\n[10] This increased recognition, however, did not translate into an increased rate of intervention.\n[11] Overall, studies of routine administration of psychiatric measures did not show an effect on patient outcome.\n[12] CONCLUSIONS The routine measurement of outcome is a costly exercise.\n[13] Little evidence shows that it is of benefit in improving psychosocial outcomes of those with psychiatric disorder managed in non-psychiatric settings."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 762, "doc_id": 4695046, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4695046], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Medications to treat obesity are highly effective.\n\nDocument title: Long term pharmacotherapy for obesity and overweight: updated meta-analysis.\n\nAbstract sentences:\n[0] OBJECTIVE To summarise the long term efficacy of anti-obesity drugs in reducing weight and improving health status.\n[1] DESIGN Updated meta-analysis of randomised trials.\n[2] DATA SOURCES Medline, Embase, the Cochrane controlled trials register, the Current Science meta-register of controlled trials, and reference lists of identified articles.\n[3] All data sources were searched from December 2002 (end date of last search) to December 2006.\n[4] STUDIES REVIEWED Double blind randomised placebo controlled trials of approved anti-obesity drugs used in adults (age over 18) for one year or longer.\n[5] RESULTS 30 trials of one to four years' duration met the inclusion criteria: 16 orlistat (n=10 631 participants), 10 sibutramine (n=2623), and four rimonabant (n=6365).\n[6] Of these, 14 trials were new and 16 had previously been identified.\n[7] Attrition rates averaged 30-40%.\n[8] Compared with placebo, orlistat reduced weight by 2.9 kg (95% confidence interval 2.5 kg to 3.2 kg), sibutramine by 4.2 kg (3.6 kg to 4.7 kg), and rimonabant by 4.7 kg (4.1 kg to 5.3 kg).\n[9] Patients receiving active drug treatment were significantly more likely to achieve 5% and 10% weight loss thresholds.\n[10] Orlistat reduced the incidence of diabetes and improved concentrations of total cholesterol and low density lipoprotein cholesterol, blood pressure, and glycaemic control in patients with diabetes but increased rates of gastrointestinal side effects and slightly lowered concentrations of high density lipoprotein.\n[11] Sibutramine improved [corrected] concentrations of high density lipoprotein cholesterol and triglycerides [corrected] Rimonabant improved concentrations of high density lipoprotein cholesterol and triglycerides, blood pressure, and glycaemic control in patients with diabetes but increased the risk of mood disorders.\n[12] CONCLUSIONS Orlistat, sibutramine, and rimonabant modestly reduce weight, have differing effects on cardiovascular risk profiles, and have specific adverse effects."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Compared with placebo, orlistat reduced weight by 2.9 kg (95% confidence interval 2.5 kg to 3.2 kg), sibutramine by 4.2 kg (3.6 kg to 4.7 kg), and rimonabant by 4.7 kg (4.1 kg to 5.3 kg).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 764, "doc_id": 7552215, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [7552215], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Medications to treat obesity are highly effective.\n\nDocument title: Long term pharmacotherapy for obesity and overweight: updated meta-analysis.\n\nAbstract sentences:\n[0] OBJECTIVE To summarise the long term efficacy of anti-obesity drugs in reducing weight and improving health status.\n[1] DESIGN Updated meta-analysis of randomised trials.\n[2] DATA SOURCES Medline, Embase, the Cochrane controlled trials register, the Current Science meta-register of controlled trials, and reference lists of identified articles.\n[3] All data sources were searched from December 2002 (end date of last search) to December 2006.\n[4] STUDIES REVIEWED Double blind randomised placebo controlled trials of approved anti-obesity drugs used in adults (age over 18) for one year or longer.\n[5] RESULTS 30 trials of one to four years' duration met the inclusion criteria: 16 orlistat (n=10 631 participants), 10 sibutramine (n=2623), and four rimonabant (n=6365).\n[6] Of these, 14 trials were new and 16 had previously been identified.\n[7] Attrition rates averaged 30-40%.\n[8] Compared with placebo, orlistat reduced weight by 2.9 kg (95% confidence interval 2.5 kg to 3.2 kg), sibutramine by 4.2 kg (3.6 kg to 4.7 kg), and rimonabant by 4.7 kg (4.1 kg to 5.3 kg).\n[9] Patients receiving active drug treatment were significantly more likely to achieve 5% and 10% weight loss thresholds.\n[10] Orlistat reduced the incidence of diabetes and improved concentrations of total cholesterol and low density lipoprotein cholesterol, blood pressure, and glycaemic control in patients with diabetes but increased rates of gastrointestinal side effects and slightly lowered concentrations of high density lipoprotein.\n[11] Sibutramine improved [corrected] concentrations of high density lipoprotein cholesterol and triglycerides [corrected] Rimonabant improved concentrations of high density lipoprotein cholesterol and triglycerides, blood pressure, and glycaemic control in patients with diabetes but increased the risk of mood disorders.\n[12] CONCLUSIONS Orlistat, sibutramine, and rimonabant modestly reduce weight, have differing effects on cardiovascular risk profiles, and have specific adverse effects."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"CONCLUSIONS Orlistat, sibutramine, and rimonabant modestly reduce weight, have differing effects on cardiovascular risk profiles, and have specific adverse effects.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 764, "doc_id": 7552215, "label": "CONTRADICTS", "evidence_sentence_ids": [12], "cited_doc_ids": [7552215], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Medications to treat obesity do not have side effects.\n\nDocument title: Long term pharmacotherapy for obesity and overweight: updated meta-analysis.\n\nAbstract sentences:\n[0] OBJECTIVE To summarise the long term efficacy of anti-obesity drugs in reducing weight and improving health status.\n[1] DESIGN Updated meta-analysis of randomised trials.\n[2] DATA SOURCES Medline, Embase, the Cochrane controlled trials register, the Current Science meta-register of controlled trials, and reference lists of identified articles.\n[3] All data sources were searched from December 2002 (end date of last search) to December 2006.\n[4] STUDIES REVIEWED Double blind randomised placebo controlled trials of approved anti-obesity drugs used in adults (age over 18) for one year or longer.\n[5] RESULTS 30 trials of one to four years' duration met the inclusion criteria: 16 orlistat (n=10 631 participants), 10 sibutramine (n=2623), and four rimonabant (n=6365).\n[6] Of these, 14 trials were new and 16 had previously been identified.\n[7] Attrition rates averaged 30-40%.\n[8] Compared with placebo, orlistat reduced weight by 2.9 kg (95% confidence interval 2.5 kg to 3.2 kg), sibutramine by 4.2 kg (3.6 kg to 4.7 kg), and rimonabant by 4.7 kg (4.1 kg to 5.3 kg).\n[9] Patients receiving active drug treatment were significantly more likely to achieve 5% and 10% weight loss thresholds.\n[10] Orlistat reduced the incidence of diabetes and improved concentrations of total cholesterol and low density lipoprotein cholesterol, blood pressure, and glycaemic control in patients with diabetes but increased rates of gastrointestinal side effects and slightly lowered concentrations of high density lipoprotein.\n[11] Sibutramine improved [corrected] concentrations of high density lipoprotein cholesterol and triglycerides [corrected] Rimonabant improved concentrations of high density lipoprotein cholesterol and triglycerides, blood pressure, and glycaemic control in patients with diabetes but increased the risk of mood disorders.\n[12] CONCLUSIONS Orlistat, sibutramine, and rimonabant modestly reduce weight, have differing effects on cardiovascular risk profiles, and have specific adverse effects."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Orlistat reduced the incidence of diabetes and improved concentrations of total cholesterol and low density lipoprotein cholesterol, blood pressure, and glycaemic control in patients with diabetes but increased rates of gastrointestinal side effects and slightly lowered concentrations of high density lipoprotein.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 765, "doc_id": 7552215, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [7552215], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Medications to treat obesity do not have side effects.\n\nDocument title: Long term pharmacotherapy for obesity and overweight: updated meta-analysis.\n\nAbstract sentences:\n[0] OBJECTIVE To summarise the long term efficacy of anti-obesity drugs in reducing weight and improving health status.\n[1] DESIGN Updated meta-analysis of randomised trials.\n[2] DATA SOURCES Medline, Embase, the Cochrane controlled trials register, the Current Science meta-register of controlled trials, and reference lists of identified articles.\n[3] All data sources were searched from December 2002 (end date of last search) to December 2006.\n[4] STUDIES REVIEWED Double blind randomised placebo controlled trials of approved anti-obesity drugs used in adults (age over 18) for one year or longer.\n[5] RESULTS 30 trials of one to four years' duration met the inclusion criteria: 16 orlistat (n=10 631 participants), 10 sibutramine (n=2623), and four rimonabant (n=6365).\n[6] Of these, 14 trials were new and 16 had previously been identified.\n[7] Attrition rates averaged 30-40%.\n[8] Compared with placebo, orlistat reduced weight by 2.9 kg (95% confidence interval 2.5 kg to 3.2 kg), sibutramine by 4.2 kg (3.6 kg to 4.7 kg), and rimonabant by 4.7 kg (4.1 kg to 5.3 kg).\n[9] Patients receiving active drug treatment were significantly more likely to achieve 5% and 10% weight loss thresholds.\n[10] Orlistat reduced the incidence of diabetes and improved concentrations of total cholesterol and low density lipoprotein cholesterol, blood pressure, and glycaemic control in patients with diabetes but increased rates of gastrointestinal side effects and slightly lowered concentrations of high density lipoprotein.\n[11] Sibutramine improved [corrected] concentrations of high density lipoprotein cholesterol and triglycerides [corrected] Rimonabant improved concentrations of high density lipoprotein cholesterol and triglycerides, blood pressure, and glycaemic control in patients with diabetes but increased the risk of mood disorders.\n[12] CONCLUSIONS Orlistat, sibutramine, and rimonabant modestly reduce weight, have differing effects on cardiovascular risk profiles, and have specific adverse effects."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"Sibutramine improved [corrected] concentrations of high density lipoprotein cholesterol and triglycerides [corrected] Rimonabant improved concentrations of high density lipoprotein cholesterol and triglycerides, blood pressure, and glycaemic control in patients with diabetes but increased the risk of mood disorders.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 765, "doc_id": 7552215, "label": "CONTRADICTS", "evidence_sentence_ids": [11], "cited_doc_ids": [7552215], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Medications to treat obesity do not have side effects.\n\nDocument title: Long term pharmacotherapy for obesity and overweight: updated meta-analysis.\n\nAbstract sentences:\n[0] OBJECTIVE To summarise the long term efficacy of anti-obesity drugs in reducing weight and improving health status.\n[1] DESIGN Updated meta-analysis of randomised trials.\n[2] DATA SOURCES Medline, Embase, the Cochrane controlled trials register, the Current Science meta-register of controlled trials, and reference lists of identified articles.\n[3] All data sources were searched from December 2002 (end date of last search) to December 2006.\n[4] STUDIES REVIEWED Double blind randomised placebo controlled trials of approved anti-obesity drugs used in adults (age over 18) for one year or longer.\n[5] RESULTS 30 trials of one to four years' duration met the inclusion criteria: 16 orlistat (n=10 631 participants), 10 sibutramine (n=2623), and four rimonabant (n=6365).\n[6] Of these, 14 trials were new and 16 had previously been identified.\n[7] Attrition rates averaged 30-40%.\n[8] Compared with placebo, orlistat reduced weight by 2.9 kg (95% confidence interval 2.5 kg to 3.2 kg), sibutramine by 4.2 kg (3.6 kg to 4.7 kg), and rimonabant by 4.7 kg (4.1 kg to 5.3 kg).\n[9] Patients receiving active drug treatment were significantly more likely to achieve 5% and 10% weight loss thresholds.\n[10] Orlistat reduced the incidence of diabetes and improved concentrations of total cholesterol and low density lipoprotein cholesterol, blood pressure, and glycaemic control in patients with diabetes but increased rates of gastrointestinal side effects and slightly lowered concentrations of high density lipoprotein.\n[11] Sibutramine improved [corrected] concentrations of high density lipoprotein cholesterol and triglycerides [corrected] Rimonabant improved concentrations of high density lipoprotein cholesterol and triglycerides, blood pressure, and glycaemic control in patients with diabetes but increased the risk of mood disorders.\n[12] CONCLUSIONS Orlistat, sibutramine, and rimonabant modestly reduce weight, have differing effects on cardiovascular risk profiles, and have specific adverse effects."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"CONCLUSIONS Orlistat, sibutramine, and rimonabant modestly reduce weight, have differing effects on cardiovascular risk profiles, and have specific adverse effects.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 765, "doc_id": 7552215, "label": "CONTRADICTS", "evidence_sentence_ids": [12], "cited_doc_ids": [7552215], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Medications to treat obesity have unwanted side effects.\n\nDocument title: Long term pharmacotherapy for obesity and overweight: updated meta-analysis.\n\nAbstract sentences:\n[0] OBJECTIVE To summarise the long term efficacy of anti-obesity drugs in reducing weight and improving health status.\n[1] DESIGN Updated meta-analysis of randomised trials.\n[2] DATA SOURCES Medline, Embase, the Cochrane controlled trials register, the Current Science meta-register of controlled trials, and reference lists of identified articles.\n[3] All data sources were searched from December 2002 (end date of last search) to December 2006.\n[4] STUDIES REVIEWED Double blind randomised placebo controlled trials of approved anti-obesity drugs used in adults (age over 18) for one year or longer.\n[5] RESULTS 30 trials of one to four years' duration met the inclusion criteria: 16 orlistat (n=10 631 participants), 10 sibutramine (n=2623), and four rimonabant (n=6365).\n[6] Of these, 14 trials were new and 16 had previously been identified.\n[7] Attrition rates averaged 30-40%.\n[8] Compared with placebo, orlistat reduced weight by 2.9 kg (95% confidence interval 2.5 kg to 3.2 kg), sibutramine by 4.2 kg (3.6 kg to 4.7 kg), and rimonabant by 4.7 kg (4.1 kg to 5.3 kg).\n[9] Patients receiving active drug treatment were significantly more likely to achieve 5% and 10% weight loss thresholds.\n[10] Orlistat reduced the incidence of diabetes and improved concentrations of total cholesterol and low density lipoprotein cholesterol, blood pressure, and glycaemic control in patients with diabetes but increased rates of gastrointestinal side effects and slightly lowered concentrations of high density lipoprotein.\n[11] Sibutramine improved [corrected] concentrations of high density lipoprotein cholesterol and triglycerides [corrected] Rimonabant improved concentrations of high density lipoprotein cholesterol and triglycerides, blood pressure, and glycaemic control in patients with diabetes but increased the risk of mood disorders.\n[12] CONCLUSIONS Orlistat, sibutramine, and rimonabant modestly reduce weight, have differing effects on cardiovascular risk profiles, and have specific adverse effects."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Orlistat reduced the incidence of diabetes and improved concentrations of total cholesterol and low density lipoprotein cholesterol, blood pressure, and glycaemic control in patients with diabetes but increased rates of gastrointestinal side effects and slightly lowered concentrations of high density lipoprotein.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 766, "doc_id": 7552215, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [7552215], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Medications to treat obesity have unwanted side effects.\n\nDocument title: Long term pharmacotherapy for obesity and overweight: updated meta-analysis.\n\nAbstract sentences:\n[0] OBJECTIVE To summarise the long term efficacy of anti-obesity drugs in reducing weight and improving health status.\n[1] DESIGN Updated meta-analysis of randomised trials.\n[2] DATA SOURCES Medline, Embase, the Cochrane controlled trials register, the Current Science meta-register of controlled trials, and reference lists of identified articles.\n[3] All data sources were searched from December 2002 (end date of last search) to December 2006.\n[4] STUDIES REVIEWED Double blind randomised placebo controlled trials of approved anti-obesity drugs used in adults (age over 18) for one year or longer.\n[5] RESULTS 30 trials of one to four years' duration met the inclusion criteria: 16 orlistat (n=10 631 participants), 10 sibutramine (n=2623), and four rimonabant (n=6365).\n[6] Of these, 14 trials were new and 16 had previously been identified.\n[7] Attrition rates averaged 30-40%.\n[8] Compared with placebo, orlistat reduced weight by 2.9 kg (95% confidence interval 2.5 kg to 3.2 kg), sibutramine by 4.2 kg (3.6 kg to 4.7 kg), and rimonabant by 4.7 kg (4.1 kg to 5.3 kg).\n[9] Patients receiving active drug treatment were significantly more likely to achieve 5% and 10% weight loss thresholds.\n[10] Orlistat reduced the incidence of diabetes and improved concentrations of total cholesterol and low density lipoprotein cholesterol, blood pressure, and glycaemic control in patients with diabetes but increased rates of gastrointestinal side effects and slightly lowered concentrations of high density lipoprotein.\n[11] Sibutramine improved [corrected] concentrations of high density lipoprotein cholesterol and triglycerides [corrected] Rimonabant improved concentrations of high density lipoprotein cholesterol and triglycerides, blood pressure, and glycaemic control in patients with diabetes but increased the risk of mood disorders.\n[12] CONCLUSIONS Orlistat, sibutramine, and rimonabant modestly reduce weight, have differing effects on cardiovascular risk profiles, and have specific adverse effects."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"Sibutramine improved [corrected] concentrations of high density lipoprotein cholesterol and triglycerides [corrected] Rimonabant improved concentrations of high density lipoprotein cholesterol and triglycerides, blood pressure, and glycaemic control in patients with diabetes but increased the risk of mood disorders.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 766, "doc_id": 7552215, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [7552215], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Medications to treat obesity have unwanted side effects.\n\nDocument title: Long term pharmacotherapy for obesity and overweight: updated meta-analysis.\n\nAbstract sentences:\n[0] OBJECTIVE To summarise the long term efficacy of anti-obesity drugs in reducing weight and improving health status.\n[1] DESIGN Updated meta-analysis of randomised trials.\n[2] DATA SOURCES Medline, Embase, the Cochrane controlled trials register, the Current Science meta-register of controlled trials, and reference lists of identified articles.\n[3] All data sources were searched from December 2002 (end date of last search) to December 2006.\n[4] STUDIES REVIEWED Double blind randomised placebo controlled trials of approved anti-obesity drugs used in adults (age over 18) for one year or longer.\n[5] RESULTS 30 trials of one to four years' duration met the inclusion criteria: 16 orlistat (n=10 631 participants), 10 sibutramine (n=2623), and four rimonabant (n=6365).\n[6] Of these, 14 trials were new and 16 had previously been identified.\n[7] Attrition rates averaged 30-40%.\n[8] Compared with placebo, orlistat reduced weight by 2.9 kg (95% confidence interval 2.5 kg to 3.2 kg), sibutramine by 4.2 kg (3.6 kg to 4.7 kg), and rimonabant by 4.7 kg (4.1 kg to 5.3 kg).\n[9] Patients receiving active drug treatment were significantly more likely to achieve 5% and 10% weight loss thresholds.\n[10] Orlistat reduced the incidence of diabetes and improved concentrations of total cholesterol and low density lipoprotein cholesterol, blood pressure, and glycaemic control in patients with diabetes but increased rates of gastrointestinal side effects and slightly lowered concentrations of high density lipoprotein.\n[11] Sibutramine improved [corrected] concentrations of high density lipoprotein cholesterol and triglycerides [corrected] Rimonabant improved concentrations of high density lipoprotein cholesterol and triglycerides, blood pressure, and glycaemic control in patients with diabetes but increased the risk of mood disorders.\n[12] CONCLUSIONS Orlistat, sibutramine, and rimonabant modestly reduce weight, have differing effects on cardiovascular risk profiles, and have specific adverse effects."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"CONCLUSIONS Orlistat, sibutramine, and rimonabant modestly reduce weight, have differing effects on cardiovascular risk profiles, and have specific adverse effects.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 766, "doc_id": 7552215, "label": "SUPPORTS", "evidence_sentence_ids": [12], "cited_doc_ids": [7552215], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Men are more susceptible to death due to pneumonia when compared to women.\n\nDocument title: Gender-dependent differences in outcome after the treatment of infection in hospitalized patients.\n\nAbstract sentences:\n[0] CONTEXT While it is established that management strategies and outcomes differ by gender for many diseases, its effect on infection has not been adequately studied.\n[1] OBJECTIVE To investigate the role of gender among hospitalized patients treated for infection.\n[2] DESIGN Observational cohort study conducted during a 26-month period from December 1996 through January 1999.\n[3] SETTING University-affiliated hospital.\n[4] PARTICIPANTS A total of 892 patients in the surgical units of the hospital with 1470 consecutive infectious episodes (782 in men and 688 in women).\n[5] MAIN OUTCOME MEASURES Mortality during hospitalization by gender for infection episodes overall and for specific infectious sites, including lung, peritoneum, bloodstream, catheter, urine, surgical site, and skin/soft tissue.\n[6] RESULTS Among all infections, there was no significant difference in mortality based on gender (men, 11.1% vs women, 14.2%; P = .07).\n[7] After logistic regression analysis, factors independently associated with mortality included higher APACHE (Acute Physiology and Chronic Health Evaluation) II score, older age, malignancy, blood transfusion, and diagnosis of infection more than 7 days after admission, but not gender (female odds ratio [OR] for death, 1.32; 95% confidence interval [CI], 0.90-1.94; P = .16).\n[8] Mortality was higher in women for lung (men, 18% vs women, 34%; P = .002) and soft tissue (men, 2% vs women, 10%; P < or = .05) infection; for other infectious sites, mortality did not differ by gender.\n[9] Factors associated with mortality due to pneumonia by logistic regression included higher APACHE II score, malignancy, diabetes mellitus, diagnosis of infection more than 7 days after admission, older age, transplantation, and female gender (OR for death, 2.25; 95% CI, 1.17-4.32; P = .02).\n[10] CONCLUSIONS Although gender may not be predictive of mortality among all infections, women appear to be at increased risk for death from hospital-acquired pneumonia, even after controlling for other comorbidities."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"CONCLUSIONS Although gender may not be predictive of mortality among all infections, women appear to be at increased risk for death from hospital-acquired pneumonia, even after controlling for other comorbidities.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 767, "doc_id": 2488880, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [2488880], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Metastatic colorectal cancer treated with a single agent fluoropyrimidines resulted in similar efficacy and better quality of life when compared with oxaliplatin-based chemotherapy in elderly patients.\n\nDocument title: Chemotherapy options in elderly and frail patients with metastatic colorectal cancer (MRC FOCUS2): an open-label, randomised factorial trial\n\nAbstract sentences:\n[0] BACKGROUND Elderly and frail patients with cancer, although often treated with chemotherapy, are under-represented in clinical trials.\n[1] We designed FOCUS2 to investigate reduced-dose chemotherapy options and to seek objective predictors of outcome in frail patients with advanced colorectal cancer.\n[2] METHODS We undertook an open, 2 × 2 factorial trial in 61 UK centres for patients with previously untreated advanced colorectal cancer who were considered unfit for full-dose chemotherapy.\n[3] After comprehensive health assessment (CHA), patients were randomly assigned by minimisation to: 48-h intravenous fluorouracil with levofolinate (group A); oxaliplatin and fluorouracil (group B); capecitabine (group C); or oxaliplatin and capecitabine (group D).\n[4] Treatment allocation was not masked.\n[5] Starting doses were 80% of standard doses, with discretionary escalation to full dose after 6 weeks.\n[6] The two primary outcome measures were: addition of oxaliplatin ([A vs B] + [C vs D]), assessed with progression-free survival (PFS); and substitution of fluorouracil with capecitabine ([A vs C] + [B vs D]), assessed by change from baseline to 12 weeks in global quality of life (QoL).\n[7] Analysis was by intention to treat.\n[8] Baseline clinical and CHA data were modelled against outcomes with a novel composite measure, overall treatment utility (OTU).\n[9] This study is registered, number ISRCTN21221452.\n[10] FINDINGS 459 patients were randomly assigned (115 to each of groups A-C, 114 to group D).\n[11] Factorial comparison of addition of oxaliplatin versus no addition suggested some improvement in PFS, but the finding was not significant (median 5·8 months [IQR 3·3-7·5] vs 4·5 months [2·8-6·4]; hazard ratio 0·84, 95% CI 0·69-1·01, p=0·07).\n[12] Replacement of fluorouracil with capecitabine did not improve global QoL: 69 of 124 (56%) patients receiving fluorouracil reported improvement in global QoL compared with 69 of 123 (56%) receiving capecitabine.\n[13] The risk of having any grade 3 or worse toxic effect was not significantly increased with oxaliplatin (83/219 [38%] vs 70/221 [32%]; p=0·17), but was higher with capecitabine than with fluorouracil (88/222 [40%] vs 65/218 [30%]; p=0·03).\n[14] In multivariable analysis, fewer baseline symptoms (odds ratio 1·32, 95% CI 1·14-1·52), less widespread disease (1·51, 1·05-2·19), and use of oxaliplatin (0·57, 0·39-0·82) were predictive of better OTU.\n[15] INTERPRETATION FOCUS2 shows that with an appropriate design, including reduced starting doses of chemotherapy, frail and elderly patients can participate in a randomised controlled trial.\n[16] On balance, a combination including oxaliplatin was preferable to single-agent fluoropyrimidines, although the primary endpoint of PFS was not met.\n[17] Capecitabine did not improve QoL compared with fluorouracil.\n[18] Comprehensive baseline assessment holds promise as an objective predictor of treatment benefit.\n[19] FUNDING Cancer Research UK and the Medical Research Council."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [16]\nExplanation: Evidence states: \"On balance, a combination including oxaliplatin was preferable to single-agent fluoropyrimidines, although the primary endpoint of PFS was not met.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 771, "doc_id": 15476777, "label": "CONTRADICTS", "evidence_sentence_ids": [16], "cited_doc_ids": [15476777], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mice are incapable of producing neutralizing antibodies in reponse to the Chikungunya virus (CHIKV) produced in mosquitos.\n\nDocument title: A chikungunya fever vaccine utilizing an insect-specific virus platform\n\nAbstract sentences:\n[0] Traditionally, vaccine development involves tradeoffs between immunogenicity and safety.\n[1] Live-attenuated vaccines typically offer rapid and durable immunity but have reduced safety when compared to inactivated vaccines.\n[2] In contrast, the inability of inactivated vaccines to replicate enhances safety at the expense of immunogenicity, often necessitating multiple doses and boosters.\n[3] To overcome these tradeoffs, we developed the insect-specific alphavirus, Eilat virus (EILV), as a vaccine platform.\n[4] To address the chikungunya fever (CHIKF) pandemic, we used an EILV cDNA clone to design a chimeric virus containing the chikungunya virus (CHIKV) structural proteins.\n[5] The recombinant EILV/CHIKV was structurally identical at 10 Å to wild-type CHIKV, as determined by single-particle cryo-electron microscopy, and it mimicked the early stages of CHIKV replication in vertebrate cells from attachment and entry to viral RNA delivery.\n[6] Yet the recombinant virus remained completely defective for productive replication, providing a high degree of safety.\n[7] A single dose of EILV/CHIKV produced in mosquito cells elicited rapid (within 4 d) and long-lasting (>290 d) neutralizing antibodies that provided complete protection in two different mouse models.\n[8] In nonhuman primates, EILV/CHIKV elicited rapid and robust immunity that protected against viremia and telemetrically monitored fever.\n[9] Our EILV platform represents the first structurally native application of an insect-specific virus in preclinical vaccine development and highlights the potential application of such viruses in vaccinology."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"A single dose of EILV/CHIKV produced in mosquito cells elicited rapid (within 4 d) and long-lasting (>290 d) neutralizing antibodies that provided complete protection in two different mouse models.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 772, "doc_id": 24922825, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [24922825], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mice defective for deoxyribonucleic acid (DNA) polymerase I (polI) fail to reveal increased sensitivity to ionizing radiation (IR).\n\nDocument title: Nonoverlapping functions of DNA polymerases mu, lambda, and terminal deoxynucleotidyltransferase during immunoglobulin V(D)J recombination in vivo.\n\nAbstract sentences:\n[0] DNA polymerases mu (pol mu), lambda (pol lambda), and terminal deoxynucleotidyltransferase (TdT) are enzymes of the pol X family that share homology in sequence and functional domain organization.\n[1] We showed previously that pol mu participates in light chain but surprisingly not heavy chain gene rearrangement.\n[2] We show here that immunoglobulin heavy chain junctions from pol lambda-deficient animals have shorter length with normal N-additions, thus indicating that pol lambda is recruited during heavy chain rearrangement at a step that precedes the action of TdT. In contrast to previous in vitro studies, analysis of animals with combined inactivation of these enzymes revealed no overlapping or compensatory activities for V(D)J recombination between pol mu, pol lambda, and TdT. This complex usage of polymerases with distinct catalytic specificities may correspond to the specific function that the third hypervariable region assumes for each immunoglobulin chain, with pol lambda maintaining a large heavy chain junctional heterogeneity and pol mu ensuring a restricted light chain junctional variability."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 774, "doc_id": 32275758, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [32275758], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mice defective for deoxyribonucleic acid (DNA) polymerase m (polm) fail to reveal increased sensitivity to ionizing radiation (IR).\n\nDocument title: Nonoverlapping functions of DNA polymerases mu, lambda, and terminal deoxynucleotidyltransferase during immunoglobulin V(D)J recombination in vivo.\n\nAbstract sentences:\n[0] DNA polymerases mu (pol mu), lambda (pol lambda), and terminal deoxynucleotidyltransferase (TdT) are enzymes of the pol X family that share homology in sequence and functional domain organization.\n[1] We showed previously that pol mu participates in light chain but surprisingly not heavy chain gene rearrangement.\n[2] We show here that immunoglobulin heavy chain junctions from pol lambda-deficient animals have shorter length with normal N-additions, thus indicating that pol lambda is recruited during heavy chain rearrangement at a step that precedes the action of TdT. In contrast to previous in vitro studies, analysis of animals with combined inactivation of these enzymes revealed no overlapping or compensatory activities for V(D)J recombination between pol mu, pol lambda, and TdT. This complex usage of polymerases with distinct catalytic specificities may correspond to the specific function that the third hypervariable region assumes for each immunoglobulin chain, with pol lambda maintaining a large heavy chain junctional heterogeneity and pol mu ensuring a restricted light chain junctional variability."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 776, "doc_id": 32275758, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [32275758], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mice defective for deoxyribonucleic acid (DNA) polymerase m (polm) reveal increased sensitivity to ionizing radiation (IR).\n\nDocument title: Nonoverlapping functions of DNA polymerases mu, lambda, and terminal deoxynucleotidyltransferase during immunoglobulin V(D)J recombination in vivo.\n\nAbstract sentences:\n[0] DNA polymerases mu (pol mu), lambda (pol lambda), and terminal deoxynucleotidyltransferase (TdT) are enzymes of the pol X family that share homology in sequence and functional domain organization.\n[1] We showed previously that pol mu participates in light chain but surprisingly not heavy chain gene rearrangement.\n[2] We show here that immunoglobulin heavy chain junctions from pol lambda-deficient animals have shorter length with normal N-additions, thus indicating that pol lambda is recruited during heavy chain rearrangement at a step that precedes the action of TdT. In contrast to previous in vitro studies, analysis of animals with combined inactivation of these enzymes revealed no overlapping or compensatory activities for V(D)J recombination between pol mu, pol lambda, and TdT. This complex usage of polymerases with distinct catalytic specificities may correspond to the specific function that the third hypervariable region assumes for each immunoglobulin chain, with pol lambda maintaining a large heavy chain junctional heterogeneity and pol mu ensuring a restricted light chain junctional variability."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 777, "doc_id": 32275758, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [32275758], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mice lacking Sirt1 in Sf1-expressing neurons are immune to diet-induced obesity and insulin resistance.\n\nDocument title: SIRT1 deacetylase in SF1 neurons protects against metabolic imbalance.\n\nAbstract sentences:\n[0] Chronic feeding on high-calorie diets causes obesity and type 2 diabetes mellitus (T2DM), illnesses that affect hundreds of millions.\n[1] Thus, understanding the pathways protecting against diet-induced metabolic imbalance is of paramount medical importance.\n[2] Here, we show that mice lacking SIRT1 in steroidogenic factor 1 (SF1) neurons are hypersensitive to dietary obesity owing to maladaptive energy expenditure.\n[3] Also, mutant mice have increased susceptibility to developing dietary T2DM due to insulin resistance in skeletal muscle.\n[4] Mechanistically, these aberrations arise, in part, from impaired metabolic actions of the neuropeptide orexin-A and the hormone leptin.\n[5] Conversely, mice overexpressing SIRT1 in SF1 neurons are more resistant to diet-induced obesity and insulin resistance due to increased energy expenditure and enhanced skeletal muscle insulin sensitivity.\n[6] Our results unveil important protective roles of SIRT1 in SF1 neurons against dietary metabolic imbalance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [2, 3]\nExplanation: Evidence states: \"Here, we show that mice lacking SIRT1 in steroidogenic factor 1 (SF1) neurons are hypersensitive to dietary obesity owing to maladaptive energy expenditure. Also, mutant mice have increased susceptibility to developing dietary T2DM due to insulin resistance in skeletal muscle.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 778, "doc_id": 13001323, "label": "CONTRADICTS", "evidence_sentence_ids": [2, 3], "cited_doc_ids": [13001323], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mice lacking Sirt1 in Sf1-expressing neurons are immune to diet-induced obesity and insulin resistance.\n\nDocument title: SIRT1 deacetylase in SF1 neurons protects against metabolic imbalance.\n\nAbstract sentences:\n[0] Chronic feeding on high-calorie diets causes obesity and type 2 diabetes mellitus (T2DM), illnesses that affect hundreds of millions.\n[1] Thus, understanding the pathways protecting against diet-induced metabolic imbalance is of paramount medical importance.\n[2] Here, we show that mice lacking SIRT1 in steroidogenic factor 1 (SF1) neurons are hypersensitive to dietary obesity owing to maladaptive energy expenditure.\n[3] Also, mutant mice have increased susceptibility to developing dietary T2DM due to insulin resistance in skeletal muscle.\n[4] Mechanistically, these aberrations arise, in part, from impaired metabolic actions of the neuropeptide orexin-A and the hormone leptin.\n[5] Conversely, mice overexpressing SIRT1 in SF1 neurons are more resistant to diet-induced obesity and insulin resistance due to increased energy expenditure and enhanced skeletal muscle insulin sensitivity.\n[6] Our results unveil important protective roles of SIRT1 in SF1 neurons against dietary metabolic imbalance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Conversely, mice overexpressing SIRT1 in SF1 neurons are more resistant to diet-induced obesity and insulin resistance due to increased energy expenditure and enhanced skeletal muscle insulin sensitivity.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 778, "doc_id": 13001323, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [13001323], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mice lacking Sirt1 in Sf1-expressing neurons have increased susceptibility to diet-induced obesity and insulin resistance.\n\nDocument title: SIRT1 deacetylase in SF1 neurons protects against metabolic imbalance.\n\nAbstract sentences:\n[0] Chronic feeding on high-calorie diets causes obesity and type 2 diabetes mellitus (T2DM), illnesses that affect hundreds of millions.\n[1] Thus, understanding the pathways protecting against diet-induced metabolic imbalance is of paramount medical importance.\n[2] Here, we show that mice lacking SIRT1 in steroidogenic factor 1 (SF1) neurons are hypersensitive to dietary obesity owing to maladaptive energy expenditure.\n[3] Also, mutant mice have increased susceptibility to developing dietary T2DM due to insulin resistance in skeletal muscle.\n[4] Mechanistically, these aberrations arise, in part, from impaired metabolic actions of the neuropeptide orexin-A and the hormone leptin.\n[5] Conversely, mice overexpressing SIRT1 in SF1 neurons are more resistant to diet-induced obesity and insulin resistance due to increased energy expenditure and enhanced skeletal muscle insulin sensitivity.\n[6] Our results unveil important protective roles of SIRT1 in SF1 neurons against dietary metabolic imbalance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2, 3]\nExplanation: Evidence states: \"Here, we show that mice lacking SIRT1 in steroidogenic factor 1 (SF1) neurons are hypersensitive to dietary obesity owing to maladaptive energy expenditure. Also, mutant mice have increased susceptibility to developing dietary T2DM due to insulin resistance in skeletal muscle.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 779, "doc_id": 13001323, "label": "SUPPORTS", "evidence_sentence_ids": [2, 3], "cited_doc_ids": [13001323], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mice lacking Sirt1 in Sf1-expressing neurons have increased susceptibility to diet-induced obesity and insulin resistance.\n\nDocument title: SIRT1 deacetylase in SF1 neurons protects against metabolic imbalance.\n\nAbstract sentences:\n[0] Chronic feeding on high-calorie diets causes obesity and type 2 diabetes mellitus (T2DM), illnesses that affect hundreds of millions.\n[1] Thus, understanding the pathways protecting against diet-induced metabolic imbalance is of paramount medical importance.\n[2] Here, we show that mice lacking SIRT1 in steroidogenic factor 1 (SF1) neurons are hypersensitive to dietary obesity owing to maladaptive energy expenditure.\n[3] Also, mutant mice have increased susceptibility to developing dietary T2DM due to insulin resistance in skeletal muscle.\n[4] Mechanistically, these aberrations arise, in part, from impaired metabolic actions of the neuropeptide orexin-A and the hormone leptin.\n[5] Conversely, mice overexpressing SIRT1 in SF1 neurons are more resistant to diet-induced obesity and insulin resistance due to increased energy expenditure and enhanced skeletal muscle insulin sensitivity.\n[6] Our results unveil important protective roles of SIRT1 in SF1 neurons against dietary metabolic imbalance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Conversely, mice overexpressing SIRT1 in SF1 neurons are more resistant to diet-induced obesity and insulin resistance due to increased energy expenditure and enhanced skeletal muscle insulin sensitivity.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 779, "doc_id": 13001323, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [13001323], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mice that lack Interferon-γ or its receptor are highly susceptible to experimental autoimmune myocarditis.\n\nDocument title: the Development of Autoimmune Myocarditis in Mice by an\n\nAbstract sentences:\n[0] BACKGROUND Interleukin (IL)-12 exerts a potent proinflammatory effect by stimulating T-helper (Th) 1 responses.\n[1] This effect is believed to be mediated primarily through the activation of STAT4 and subsequent production of interferon (IFN)-gamma.\n[2] Methods and Results- We examined the role of IL-12 receptor (IL-12R) signaling in the development of murine experimental autoimmune myocarditis (EAM) induced by cardiac myosin immunization.\n[3] Both IL-12Rbeta1-deficient mice and STAT4-deficient mice were resistant to the induction of myocarditis.\n[4] Treatment with exogenous IL-12 exacerbated disease.\n[5] We questioned whether IFN-gamma is required for the disease-promoting activity of IL-12.\n[6] On the contrary, we found that IFN-gamma suppresses EAM.\n[7] Lack of IFN-gamma due to either depletion with an antibody or a genetic deficiency exacerbated myocarditis.\n[8] Spleens from IFN-gamma-deficient mice immunized with cardiac myosin showed increased cellularity; greater numbers of CD3+, CD4+, CD8+, and IL-2-producing cells; and heightened ability to produce cytokines on stimulation in vitro.\n[9] Treatment of mice with recombinant IFN-gamma suppressed the development of myocarditis.\n[10] CONCLUSIONS IL-12/IL-12R/STAT4 signaling promotes the development of EAM.\n[11] In contrast, IFN-gamma plays a protective role.\n[12] The disease-limiting effects of IFN-gamma might be explained by its ability to control the expansion of activated T lymphocytes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Lack of IFN-gamma due to either depletion with an antibody or a genetic deficiency exacerbated myocarditis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 780, "doc_id": 8246922, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [8246922, 24338780], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mice that lack Interferon-γ or its receptor are highly susceptible to experimental autoimmune myocarditis.\n\nDocument title: the Development of Autoimmune Myocarditis in Mice by an\n\nAbstract sentences:\n[0] BACKGROUND Interleukin (IL)-12 exerts a potent proinflammatory effect by stimulating T-helper (Th) 1 responses.\n[1] This effect is believed to be mediated primarily through the activation of STAT4 and subsequent production of interferon (IFN)-gamma.\n[2] Methods and Results- We examined the role of IL-12 receptor (IL-12R) signaling in the development of murine experimental autoimmune myocarditis (EAM) induced by cardiac myosin immunization.\n[3] Both IL-12Rbeta1-deficient mice and STAT4-deficient mice were resistant to the induction of myocarditis.\n[4] Treatment with exogenous IL-12 exacerbated disease.\n[5] We questioned whether IFN-gamma is required for the disease-promoting activity of IL-12.\n[6] On the contrary, we found that IFN-gamma suppresses EAM.\n[7] Lack of IFN-gamma due to either depletion with an antibody or a genetic deficiency exacerbated myocarditis.\n[8] Spleens from IFN-gamma-deficient mice immunized with cardiac myosin showed increased cellularity; greater numbers of CD3+, CD4+, CD8+, and IL-2-producing cells; and heightened ability to produce cytokines on stimulation in vitro.\n[9] Treatment of mice with recombinant IFN-gamma suppressed the development of myocarditis.\n[10] CONCLUSIONS IL-12/IL-12R/STAT4 signaling promotes the development of EAM.\n[11] In contrast, IFN-gamma plays a protective role.\n[12] The disease-limiting effects of IFN-gamma might be explained by its ability to control the expansion of activated T lymphocytes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"In contrast, IFN-gamma plays a protective role.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 780, "doc_id": 8246922, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [8246922, 24338780], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mice that lack Interferon-γ or its receptor are highly susceptible to experimental autoimmune myocarditis.\n\nDocument title: Lethal autoimmune myocarditis in interferon-gamma receptor-deficient mice: enhanced disease severity by impaired inducible nitric oxide synthase induction.\n\nAbstract sentences:\n[0] BACKGROUND Interferon-gamma (IFN-gamma) is an essential cytokine in the regulation of inflammatory responses in autoimmune diseases.\n[1] Little is known about its role in inflammatory heart disease.\n[2] METHODS AND RESULTS We showed that IFN-gamma receptor-deficient mice (IFN-gammaR(-/-)) on a BALB/c background immunized with a peptide derived from cardiac alpha-myosin heavy chain develop severe myocarditis with high mortality.\n[3] Although myocarditis subsided in wild-type mice after 3 weeks, IFN-gammaR(-/-) mice showed persistent disease.\n[4] The persistent inflammation was accompanied by vigorous in vitro CD4 T-cell responses and impaired inducible nitric oxide synthase expression, together with evidence of impaired nitric oxide production in IFN-gammaR(-/-) hearts.\n[5] Treatment of wild-type mice with the nitric oxide synthetase inhibitor N:-nitro-l-arginine-methyl-ester enhanced in vitro CD4 T-cell proliferation and prevented healing of myocarditis.\n[6] CONCLUSIONS Our data provide evidence that IFN-gamma protects mice from lethal autoimmune myocarditis by inducing the expression of inducible nitric oxide synthase followed by the downregulation of T-cell responses."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"METHODS AND RESULTS We showed that IFN-gamma receptor-deficient mice (IFN-gammaR(-/-)) on a BALB/c background immunized with a peptide derived from cardiac alpha-myosin heavy chain develop severe myocarditis with high mortality.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 780, "doc_id": 24338780, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [8246922, 24338780], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mice that lack Interferon-γ or its receptor are highly susceptible to experimental autoimmune myocarditis.\n\nDocument title: Lethal autoimmune myocarditis in interferon-gamma receptor-deficient mice: enhanced disease severity by impaired inducible nitric oxide synthase induction.\n\nAbstract sentences:\n[0] BACKGROUND Interferon-gamma (IFN-gamma) is an essential cytokine in the regulation of inflammatory responses in autoimmune diseases.\n[1] Little is known about its role in inflammatory heart disease.\n[2] METHODS AND RESULTS We showed that IFN-gamma receptor-deficient mice (IFN-gammaR(-/-)) on a BALB/c background immunized with a peptide derived from cardiac alpha-myosin heavy chain develop severe myocarditis with high mortality.\n[3] Although myocarditis subsided in wild-type mice after 3 weeks, IFN-gammaR(-/-) mice showed persistent disease.\n[4] The persistent inflammation was accompanied by vigorous in vitro CD4 T-cell responses and impaired inducible nitric oxide synthase expression, together with evidence of impaired nitric oxide production in IFN-gammaR(-/-) hearts.\n[5] Treatment of wild-type mice with the nitric oxide synthetase inhibitor N:-nitro-l-arginine-methyl-ester enhanced in vitro CD4 T-cell proliferation and prevented healing of myocarditis.\n[6] CONCLUSIONS Our data provide evidence that IFN-gamma protects mice from lethal autoimmune myocarditis by inducing the expression of inducible nitric oxide synthase followed by the downregulation of T-cell responses."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Although myocarditis subsided in wild-type mice after 3 weeks, IFN-gammaR(-/-) mice showed persistent disease.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 780, "doc_id": 24338780, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [8246922, 24338780], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mice that lack Interferon-γ or its receptor are highly susceptible to experimental autoimmune myocarditis.\n\nDocument title: Lethal autoimmune myocarditis in interferon-gamma receptor-deficient mice: enhanced disease severity by impaired inducible nitric oxide synthase induction.\n\nAbstract sentences:\n[0] BACKGROUND Interferon-gamma (IFN-gamma) is an essential cytokine in the regulation of inflammatory responses in autoimmune diseases.\n[1] Little is known about its role in inflammatory heart disease.\n[2] METHODS AND RESULTS We showed that IFN-gamma receptor-deficient mice (IFN-gammaR(-/-)) on a BALB/c background immunized with a peptide derived from cardiac alpha-myosin heavy chain develop severe myocarditis with high mortality.\n[3] Although myocarditis subsided in wild-type mice after 3 weeks, IFN-gammaR(-/-) mice showed persistent disease.\n[4] The persistent inflammation was accompanied by vigorous in vitro CD4 T-cell responses and impaired inducible nitric oxide synthase expression, together with evidence of impaired nitric oxide production in IFN-gammaR(-/-) hearts.\n[5] Treatment of wild-type mice with the nitric oxide synthetase inhibitor N:-nitro-l-arginine-methyl-ester enhanced in vitro CD4 T-cell proliferation and prevented healing of myocarditis.\n[6] CONCLUSIONS Our data provide evidence that IFN-gamma protects mice from lethal autoimmune myocarditis by inducing the expression of inducible nitric oxide synthase followed by the downregulation of T-cell responses."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"CONCLUSIONS Our data provide evidence that IFN-gamma protects mice from lethal autoimmune myocarditis by inducing the expression of inducible nitric oxide synthase followed by the downregulation of T-cell responses.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 780, "doc_id": 24338780, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [8246922, 24338780], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mice without IFN-γ or its receptor are highly susceptible to EAM induced with α-MyHC/CFA.\n\nDocument title: the Development of Autoimmune Myocarditis in Mice by an\n\nAbstract sentences:\n[0] BACKGROUND Interleukin (IL)-12 exerts a potent proinflammatory effect by stimulating T-helper (Th) 1 responses.\n[1] This effect is believed to be mediated primarily through the activation of STAT4 and subsequent production of interferon (IFN)-gamma.\n[2] Methods and Results- We examined the role of IL-12 receptor (IL-12R) signaling in the development of murine experimental autoimmune myocarditis (EAM) induced by cardiac myosin immunization.\n[3] Both IL-12Rbeta1-deficient mice and STAT4-deficient mice were resistant to the induction of myocarditis.\n[4] Treatment with exogenous IL-12 exacerbated disease.\n[5] We questioned whether IFN-gamma is required for the disease-promoting activity of IL-12.\n[6] On the contrary, we found that IFN-gamma suppresses EAM.\n[7] Lack of IFN-gamma due to either depletion with an antibody or a genetic deficiency exacerbated myocarditis.\n[8] Spleens from IFN-gamma-deficient mice immunized with cardiac myosin showed increased cellularity; greater numbers of CD3+, CD4+, CD8+, and IL-2-producing cells; and heightened ability to produce cytokines on stimulation in vitro.\n[9] Treatment of mice with recombinant IFN-gamma suppressed the development of myocarditis.\n[10] CONCLUSIONS IL-12/IL-12R/STAT4 signaling promotes the development of EAM.\n[11] In contrast, IFN-gamma plays a protective role.\n[12] The disease-limiting effects of IFN-gamma might be explained by its ability to control the expansion of activated T lymphocytes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Lack of IFN-gamma due to either depletion with an antibody or a genetic deficiency exacerbated myocarditis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 782, "doc_id": 8246922, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [8246922], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mice without IFN-γ or its receptor are highly susceptible to EAM induced with α-MyHC/CFA.\n\nDocument title: the Development of Autoimmune Myocarditis in Mice by an\n\nAbstract sentences:\n[0] BACKGROUND Interleukin (IL)-12 exerts a potent proinflammatory effect by stimulating T-helper (Th) 1 responses.\n[1] This effect is believed to be mediated primarily through the activation of STAT4 and subsequent production of interferon (IFN)-gamma.\n[2] Methods and Results- We examined the role of IL-12 receptor (IL-12R) signaling in the development of murine experimental autoimmune myocarditis (EAM) induced by cardiac myosin immunization.\n[3] Both IL-12Rbeta1-deficient mice and STAT4-deficient mice were resistant to the induction of myocarditis.\n[4] Treatment with exogenous IL-12 exacerbated disease.\n[5] We questioned whether IFN-gamma is required for the disease-promoting activity of IL-12.\n[6] On the contrary, we found that IFN-gamma suppresses EAM.\n[7] Lack of IFN-gamma due to either depletion with an antibody or a genetic deficiency exacerbated myocarditis.\n[8] Spleens from IFN-gamma-deficient mice immunized with cardiac myosin showed increased cellularity; greater numbers of CD3+, CD4+, CD8+, and IL-2-producing cells; and heightened ability to produce cytokines on stimulation in vitro.\n[9] Treatment of mice with recombinant IFN-gamma suppressed the development of myocarditis.\n[10] CONCLUSIONS IL-12/IL-12R/STAT4 signaling promotes the development of EAM.\n[11] In contrast, IFN-gamma plays a protective role.\n[12] The disease-limiting effects of IFN-gamma might be explained by its ability to control the expansion of activated T lymphocytes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"In contrast, IFN-gamma plays a protective role.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 782, "doc_id": 8246922, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [8246922], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Microcin J25 encourages nucleoside triphosphate (NTP) binding.\n\nDocument title: Antibacterial peptide microcin J25 inhibits transcription by binding within and obstructing the RNA polymerase secondary channel.\n\nAbstract sentences:\n[0] The antibacterial peptide microcin J25 (MccJ25) inhibits transcription by bacterial RNA polymerase (RNAP).\n[1] Biochemical results indicate that inhibition of transcription occurs at the level of NTP uptake or NTP binding by RNAP.\n[2] Genetic results indicate that inhibition of transcription requires an extensive determinant, comprising more than 50 amino acid residues, within the RNAP secondary channel (also known as the \"NTP-uptake channel\" or \"pore\").\n[3] Biophysical results indicate that inhibition of transcription involves binding of MccJ25 within the RNAP secondary channel.\n[4] Molecular modeling indicates that binding of MccJ25 within the RNAP secondary channel obstructs the RNAP secondary channel.\n[5] We conclude that MccJ25 inhibits transcription by binding within and obstructing the RNAP secondary channel--acting essentially as a \"cork in a bottle.\n[6] \"\n[7] Obstruction of the RNAP secondary channel represents an attractive target for drug discovery."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Biochemical results indicate that inhibition of transcription occurs at the level of NTP uptake or NTP binding by RNAP.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 787, "doc_id": 4740447, "label": "CONTRADICTS", "evidence_sentence_ids": [1], "cited_doc_ids": [4740447], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Microcin J25 inhibits nucleoside triphosphate (NTP) binding.\n\nDocument title: Antibacterial peptide microcin J25 inhibits transcription by binding within and obstructing the RNA polymerase secondary channel.\n\nAbstract sentences:\n[0] The antibacterial peptide microcin J25 (MccJ25) inhibits transcription by bacterial RNA polymerase (RNAP).\n[1] Biochemical results indicate that inhibition of transcription occurs at the level of NTP uptake or NTP binding by RNAP.\n[2] Genetic results indicate that inhibition of transcription requires an extensive determinant, comprising more than 50 amino acid residues, within the RNAP secondary channel (also known as the \"NTP-uptake channel\" or \"pore\").\n[3] Biophysical results indicate that inhibition of transcription involves binding of MccJ25 within the RNAP secondary channel.\n[4] Molecular modeling indicates that binding of MccJ25 within the RNAP secondary channel obstructs the RNAP secondary channel.\n[5] We conclude that MccJ25 inhibits transcription by binding within and obstructing the RNAP secondary channel--acting essentially as a \"cork in a bottle.\n[6] \"\n[7] Obstruction of the RNAP secondary channel represents an attractive target for drug discovery."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Biochemical results indicate that inhibition of transcription occurs at the level of NTP uptake or NTP binding by RNAP.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 788, "doc_id": 4740447, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [4740447], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Microglia are an innate immune cell type of the central nervous system.\n\nDocument title: Sublime Microglia: Expanding Roles for the Guardians of the CNS\n\nAbstract sentences:\n[0] Recent findings challenge the concept that microglia solely function in disease states in the central nervous system (CNS).\n[1] Rather than simply reacting to CNS injury, infection, or pathology, emerging lines of evidence indicate that microglia sculpt the structure of the CNS, refine neuronal circuitry and network connectivity, and contribute to plasticity.\n[2] These physiological functions of microglia in the normal CNS begin during development and persist into maturity.\n[3] Here, we develop a conceptual framework for functions of microglia beyond neuroinflammation and discuss the rich repertoire of signaling and communication motifs in microglia that are critical both in pathology and for the normal physiology of the CNS."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"These physiological functions of microglia in the normal CNS begin during development and persist into maturity.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 789, "doc_id": 15493354, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [15493354], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Microglia are an innate immune cell type of the central nervous system.\n\nDocument title: Sublime Microglia: Expanding Roles for the Guardians of the CNS\n\nAbstract sentences:\n[0] Recent findings challenge the concept that microglia solely function in disease states in the central nervous system (CNS).\n[1] Rather than simply reacting to CNS injury, infection, or pathology, emerging lines of evidence indicate that microglia sculpt the structure of the CNS, refine neuronal circuitry and network connectivity, and contribute to plasticity.\n[2] These physiological functions of microglia in the normal CNS begin during development and persist into maturity.\n[3] Here, we develop a conceptual framework for functions of microglia beyond neuroinflammation and discuss the rich repertoire of signaling and communication motifs in microglia that are critical both in pathology and for the normal physiology of the CNS."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Here, we develop a conceptual framework for functions of microglia beyond neuroinflammation and discuss the rich repertoire of signaling and communication motifs in microglia that are critical both in pathology and for the normal physiology of the CNS.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 789, "doc_id": 15493354, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [15493354], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Microglia are an innate immune cell type of the peripheral nervous system.\n\nDocument title: Sublime Microglia: Expanding Roles for the Guardians of the CNS\n\nAbstract sentences:\n[0] Recent findings challenge the concept that microglia solely function in disease states in the central nervous system (CNS).\n[1] Rather than simply reacting to CNS injury, infection, or pathology, emerging lines of evidence indicate that microglia sculpt the structure of the CNS, refine neuronal circuitry and network connectivity, and contribute to plasticity.\n[2] These physiological functions of microglia in the normal CNS begin during development and persist into maturity.\n[3] Here, we develop a conceptual framework for functions of microglia beyond neuroinflammation and discuss the rich repertoire of signaling and communication motifs in microglia that are critical both in pathology and for the normal physiology of the CNS."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"These physiological functions of microglia in the normal CNS begin during development and persist into maturity.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 790, "doc_id": 15493354, "label": "CONTRADICTS", "evidence_sentence_ids": [2], "cited_doc_ids": [15493354], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Microglia are an innate immune cell type of the peripheral nervous system.\n\nDocument title: Sublime Microglia: Expanding Roles for the Guardians of the CNS\n\nAbstract sentences:\n[0] Recent findings challenge the concept that microglia solely function in disease states in the central nervous system (CNS).\n[1] Rather than simply reacting to CNS injury, infection, or pathology, emerging lines of evidence indicate that microglia sculpt the structure of the CNS, refine neuronal circuitry and network connectivity, and contribute to plasticity.\n[2] These physiological functions of microglia in the normal CNS begin during development and persist into maturity.\n[3] Here, we develop a conceptual framework for functions of microglia beyond neuroinflammation and discuss the rich repertoire of signaling and communication motifs in microglia that are critical both in pathology and for the normal physiology of the CNS."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Here, we develop a conceptual framework for functions of microglia beyond neuroinflammation and discuss the rich repertoire of signaling and communication motifs in microglia that are critical both in pathology and for the normal physiology of the CNS.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 790, "doc_id": 15493354, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [15493354], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Migraine with aura is associated with ischemic stroke.\n\nDocument title: Migraine and cardiovascular disease: systematic review and meta-analysis.\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate the association between migraine and cardiovascular disease, including stroke, myocardial infarction, and death due to cardiovascular disease.\n[1] DESIGN Systematic review and meta-analysis.\n[2] DATA SOURCES Electronic databases (PubMed, Embase, Cochrane Library) and reference lists of included studies and reviews published until January 2009.\n[3] Selection criteria Case-control and cohort studies investigating the association between any migraine or specific migraine subtypes and cardiovascular disease.\n[4] Review methods Two investigators independently assessed eligibility of identified studies in a two step approach.\n[5] Disagreements were resolved by consensus.\n[6] Studies were grouped according to a priori categories on migraine and cardiovascular disease.\n[7] DATA EXTRACTION Two investigators extracted data.\n[8] Pooled relative risks and 95% confidence intervals were calculated.\n[9] RESULTS Studies were heterogeneous for participant characteristics and definition of cardiovascular disease.\n[10] Nine studies investigated the association between any migraine and ischaemic stroke (pooled relative risk 1.73, 95% confidence interval 1.31 to 2.29).\n[11] Additional analyses indicated a significantly higher risk among people who had migraine with aura (2.16, 1.53 to 3.03) compared with people who had migraine without aura (1.23, 0.90 to 1.69; meta-regression for aura status P=0.02).\n[12] Furthermore, results suggested a greater risk among women (2.08, 1.13 to 3.84) compared with men (1.37, 0.89 to 2.11).\n[13] Age less than 45 years, smoking, and oral contraceptive use further increased the risk.\n[14] Eight studies investigated the association between migraine and myocardial infarction (1.12, 0.95 to 1.32) and five between migraine and death due to cardiovascular disease (1.03, 0.79 to 1.34).\n[15] Only one study investigated the association between women who had migraine with aura and myocardial infarction and death due to cardiovascular disease, showing a twofold increased risk.\n[16] CONCLUSION Migraine is associated with a twofold increased risk of ischaemic stroke, which is only apparent among people who have migraine with aura.\n[17] Our results also suggest a higher risk among women and risk was further magnified for people with migraine who were aged less than 45, smokers, and women who used oral contraceptives.\n[18] We did not find an overall association between any migraine and myocardial infarction or death due to cardiovascular disease.\n[19] Too few studies are available to reliably evaluate the impact of modifying factors, such as migraine aura, on these associations."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"Additional analyses indicated a significantly higher risk among people who had migraine with aura (2.16, 1.53 to 3.03) compared with people who had migraine without aura (1.23, 0.90 to 1.69; meta-regression for aura status P=0.02).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 791, "doc_id": 15984735, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [15984735], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Migraine with aura is associated with ischemic stroke.\n\nDocument title: Migraine and cardiovascular disease: systematic review and meta-analysis.\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate the association between migraine and cardiovascular disease, including stroke, myocardial infarction, and death due to cardiovascular disease.\n[1] DESIGN Systematic review and meta-analysis.\n[2] DATA SOURCES Electronic databases (PubMed, Embase, Cochrane Library) and reference lists of included studies and reviews published until January 2009.\n[3] Selection criteria Case-control and cohort studies investigating the association between any migraine or specific migraine subtypes and cardiovascular disease.\n[4] Review methods Two investigators independently assessed eligibility of identified studies in a two step approach.\n[5] Disagreements were resolved by consensus.\n[6] Studies were grouped according to a priori categories on migraine and cardiovascular disease.\n[7] DATA EXTRACTION Two investigators extracted data.\n[8] Pooled relative risks and 95% confidence intervals were calculated.\n[9] RESULTS Studies were heterogeneous for participant characteristics and definition of cardiovascular disease.\n[10] Nine studies investigated the association between any migraine and ischaemic stroke (pooled relative risk 1.73, 95% confidence interval 1.31 to 2.29).\n[11] Additional analyses indicated a significantly higher risk among people who had migraine with aura (2.16, 1.53 to 3.03) compared with people who had migraine without aura (1.23, 0.90 to 1.69; meta-regression for aura status P=0.02).\n[12] Furthermore, results suggested a greater risk among women (2.08, 1.13 to 3.84) compared with men (1.37, 0.89 to 2.11).\n[13] Age less than 45 years, smoking, and oral contraceptive use further increased the risk.\n[14] Eight studies investigated the association between migraine and myocardial infarction (1.12, 0.95 to 1.32) and five between migraine and death due to cardiovascular disease (1.03, 0.79 to 1.34).\n[15] Only one study investigated the association between women who had migraine with aura and myocardial infarction and death due to cardiovascular disease, showing a twofold increased risk.\n[16] CONCLUSION Migraine is associated with a twofold increased risk of ischaemic stroke, which is only apparent among people who have migraine with aura.\n[17] Our results also suggest a higher risk among women and risk was further magnified for people with migraine who were aged less than 45, smokers, and women who used oral contraceptives.\n[18] We did not find an overall association between any migraine and myocardial infarction or death due to cardiovascular disease.\n[19] Too few studies are available to reliably evaluate the impact of modifying factors, such as migraine aura, on these associations."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [16]\nExplanation: Evidence states: \"CONCLUSION Migraine is associated with a twofold increased risk of ischaemic stroke, which is only apparent among people who have migraine with aura.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 791, "doc_id": 15984735, "label": "SUPPORTS", "evidence_sentence_ids": [16], "cited_doc_ids": [15984735], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Misunderstandings between doctors and patients can lead to non-adherence.\n\nDocument title: Misunderstandings in prescribing decisions in general practice: qualitative study.\n\nAbstract sentences:\n[0] OBJECTIVES To identify and describe misunderstandings between patients and doctors associated with prescribing decisions in general practice.\n[1] DESIGN Qualitative study.\n[2] SETTING 20 general practices in the West Midlands and south east England.\n[3] PARTICIPANTS 20 general practitioners and 35 consulting patients.\n[4] MAIN OUTCOME MEASURES Misunderstandings between patients and doctors that have potential or actual adverse consequences for taking medicine.\n[5] RESULTS 14 categories of misunderstanding were identified relating to patient information unknown to the doctor, doctor information unknown to the patient, conflicting information, disagreement about attribution of side effects, failure of communication about doctor's decision, and relationship factors.\n[6] All the misunderstandings were associated with lack of patients' participation in the consultation in terms of the voicing of expectations and preferences or the voicing of responses to doctors' decisions and actions.\n[7] They were all associated with potential or actual adverse outcomes such as non-adherence to treatment.\n[8] Many were based on inaccurate guesses and assumptions.\n[9] In particular doctors seemed unaware of the relevance of patients' ideas about medicines for successful prescribing.\n[10] CONCLUSIONS Patients' participation in the consultation and the adverse consequences of lack of participation are important.\n[11] The authors are developing an educational intervention that builds on these findings."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6, 7]\nExplanation: Evidence states: \"All the misunderstandings were associated with lack of patients' participation in the consultation in terms of the voicing of expectations and preferences or the voicing of responses to doctors' decisions and actions. They were all associated with potential or actual adverse outcomes such as non-adherence to treatment.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 792, "doc_id": 3610080, "label": "SUPPORTS", "evidence_sentence_ids": [6, 7], "cited_doc_ids": [3610080], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mitochondria play a major role in apoptosis.\n\nDocument title: Mitochondria: Dynamic Organelles in Disease, Aging, and Development\n\nAbstract sentences:\n[0] Mitochondria are the primary energy-generating system in most eukaryotic cells.\n[1] Additionally, they participate in intermediary metabolism, calcium signaling, and apoptosis.\n[2] Given these well-established functions, it might be expected that mitochondrial dysfunction would give rise to a simple and predictable set of defects in all tissues.\n[3] However, mitochondrial dysfunction has pleiotropic effects in multicellular organisms.\n[4] Clearly, much about the basic biology of mitochondria remains to be understood.\n[5] Here we discuss recent work that suggests that the dynamics (fusion and fission) of these organelles is important in development and disease."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Additionally, they participate in intermediary metabolism, calcium signaling, and apoptosis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 795, "doc_id": 8551160, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [8551160], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mitochondria play a major role in energy production.\n\nDocument title: Mitochondria: Dynamic Organelles in Disease, Aging, and Development\n\nAbstract sentences:\n[0] Mitochondria are the primary energy-generating system in most eukaryotic cells.\n[1] Additionally, they participate in intermediary metabolism, calcium signaling, and apoptosis.\n[2] Given these well-established functions, it might be expected that mitochondrial dysfunction would give rise to a simple and predictable set of defects in all tissues.\n[3] However, mitochondrial dysfunction has pleiotropic effects in multicellular organisms.\n[4] Clearly, much about the basic biology of mitochondria remains to be understood.\n[5] Here we discuss recent work that suggests that the dynamics (fusion and fission) of these organelles is important in development and disease."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Mitochondria are the primary energy-generating system in most eukaryotic cells.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 797, "doc_id": 8551160, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [8551160], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mitochondria play a trivial role in calcium homeostasis.\n\nDocument title: Mitochondria: Dynamic Organelles in Disease, Aging, and Development\n\nAbstract sentences:\n[0] Mitochondria are the primary energy-generating system in most eukaryotic cells.\n[1] Additionally, they participate in intermediary metabolism, calcium signaling, and apoptosis.\n[2] Given these well-established functions, it might be expected that mitochondrial dysfunction would give rise to a simple and predictable set of defects in all tissues.\n[3] However, mitochondrial dysfunction has pleiotropic effects in multicellular organisms.\n[4] Clearly, much about the basic biology of mitochondria remains to be understood.\n[5] Here we discuss recent work that suggests that the dynamics (fusion and fission) of these organelles is important in development and disease."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Additionally, they participate in intermediary metabolism, calcium signaling, and apoptosis.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 798, "doc_id": 8551160, "label": "CONTRADICTS", "evidence_sentence_ids": [1], "cited_doc_ids": [8551160], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Moderate consumption of candy and chocolate reduces the risk of cardiovascular disease (CVD).\n\nDocument title: Life is sweet: candy consumption and longevity.\n\nAbstract sentences:\n[0] Our attitude towards candy—“if it tastes that good, it can't be healthy”—betrays society's puritanical stance towards pleasure.\n[1] Candy has been blamed for various ills, including hyperactivity in children; however, clinical trials have not supported this.1  Candy—sugar confectionery and chocolate—is not a recent invention: the ancient Arabs, Chinese, and Egyptians candied fruits and nuts in honey, and the Aztecs made a chocolate drink from the bean of the cacao tree.\n[2] Today, Americans gratify themselves with, on average, 5.4 kg of sugar candy and 6.5 kg of chocolate per person annually.2  Since candy has existed for centuries, we surmised that it cannot be totally unhealthy.\n[3] We decided to investigate whether candy consumption was associated with longevity.\n[4] Subjects were from the Harvard alumni health study, an ongoing study of men entering Harvard University as undergraduates between 1916 and 1950.\n[5] We included 7841 men, free of cardiovascular disease and cancer, who responded to a health survey …"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 799, "doc_id": 5293024, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [5293024], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Monoclonal antibody targeting of N-cadherin encourages castration resistance.\n\nDocument title: Monoclonal antibody targeting of N-cadherin inhibits prostate cancer growth, metastasis and castration resistance\n\nAbstract sentences:\n[0] The transition from androgen-dependent to castration-resistant prostate cancer (CRPC) is a lethal event of uncertain molecular etiology.\n[1] Comparing gene expression in isogenic androgen-dependent and CRPC xenografts, we found a reproducible increase in N-cadherin expression, which was also elevated in primary and metastatic tumors of individuals with CRPC.\n[2] Ectopic expression of N-cadherin in nonmetastatic, androgen-dependent prostate cancer models caused castration resistance, invasion and metastasis.\n[3] Monoclonal antibodies against the ectodomain of N-cadherin reduced proliferation, adhesion and invasion of prostate cancer cells in vitro.\n[4] In vivo, these antibodies slowed the growth of multiple established CRPC xenografts, blocked local invasion and metastasis and, at higher doses, led to complete regression.\n[5] N-cadherin–specific antibodies markedly delayed the time to emergence of castration resistance, markedly affected tumor histology and angiogenesis, and reduced both AKT serine-threonine kinase activity and serum interleukin-8 (IL-8) secretion.\n[6] These data indicate that N-cadherin is a major cause of both prostate cancer metastasis and castration resistance.\n[7] Therapeutic targeting of this factor with monoclonal antibodies may have considerable clinical benefit."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"N-cadherin–specific antibodies markedly delayed the time to emergence of castration resistance, markedly affected tumor histology and angiogenesis, and reduced both AKT serine-threonine kinase activity and serum interleukin-8 (IL-8) secretion.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 801, "doc_id": 22180793, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [22180793], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Monoclonal antibody targeting of N-cadherin encourages metastasis.\n\nDocument title: Monoclonal antibody targeting of N-cadherin inhibits prostate cancer growth, metastasis and castration resistance\n\nAbstract sentences:\n[0] The transition from androgen-dependent to castration-resistant prostate cancer (CRPC) is a lethal event of uncertain molecular etiology.\n[1] Comparing gene expression in isogenic androgen-dependent and CRPC xenografts, we found a reproducible increase in N-cadherin expression, which was also elevated in primary and metastatic tumors of individuals with CRPC.\n[2] Ectopic expression of N-cadherin in nonmetastatic, androgen-dependent prostate cancer models caused castration resistance, invasion and metastasis.\n[3] Monoclonal antibodies against the ectodomain of N-cadherin reduced proliferation, adhesion and invasion of prostate cancer cells in vitro.\n[4] In vivo, these antibodies slowed the growth of multiple established CRPC xenografts, blocked local invasion and metastasis and, at higher doses, led to complete regression.\n[5] N-cadherin–specific antibodies markedly delayed the time to emergence of castration resistance, markedly affected tumor histology and angiogenesis, and reduced both AKT serine-threonine kinase activity and serum interleukin-8 (IL-8) secretion.\n[6] These data indicate that N-cadherin is a major cause of both prostate cancer metastasis and castration resistance.\n[7] Therapeutic targeting of this factor with monoclonal antibodies may have considerable clinical benefit."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"In vivo, these antibodies slowed the growth of multiple established CRPC xenografts, blocked local invasion and metastasis and, at higher doses, led to complete regression.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 802, "doc_id": 22180793, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [22180793], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Monoclonal antibody targeting of N-cadherin encourages metastasis.\n\nDocument title: Monoclonal antibody targeting of N-cadherin inhibits prostate cancer growth, metastasis and castration resistance\n\nAbstract sentences:\n[0] The transition from androgen-dependent to castration-resistant prostate cancer (CRPC) is a lethal event of uncertain molecular etiology.\n[1] Comparing gene expression in isogenic androgen-dependent and CRPC xenografts, we found a reproducible increase in N-cadherin expression, which was also elevated in primary and metastatic tumors of individuals with CRPC.\n[2] Ectopic expression of N-cadherin in nonmetastatic, androgen-dependent prostate cancer models caused castration resistance, invasion and metastasis.\n[3] Monoclonal antibodies against the ectodomain of N-cadherin reduced proliferation, adhesion and invasion of prostate cancer cells in vitro.\n[4] In vivo, these antibodies slowed the growth of multiple established CRPC xenografts, blocked local invasion and metastasis and, at higher doses, led to complete regression.\n[5] N-cadherin–specific antibodies markedly delayed the time to emergence of castration resistance, markedly affected tumor histology and angiogenesis, and reduced both AKT serine-threonine kinase activity and serum interleukin-8 (IL-8) secretion.\n[6] These data indicate that N-cadherin is a major cause of both prostate cancer metastasis and castration resistance.\n[7] Therapeutic targeting of this factor with monoclonal antibodies may have considerable clinical benefit."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Therapeutic targeting of this factor with monoclonal antibodies may have considerable clinical benefit.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 802, "doc_id": 22180793, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [22180793], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Monoclonal antibody targeting of N-cadherin inhibits castration resistance.\n\nDocument title: Monoclonal antibody targeting of N-cadherin inhibits prostate cancer growth, metastasis and castration resistance\n\nAbstract sentences:\n[0] The transition from androgen-dependent to castration-resistant prostate cancer (CRPC) is a lethal event of uncertain molecular etiology.\n[1] Comparing gene expression in isogenic androgen-dependent and CRPC xenografts, we found a reproducible increase in N-cadherin expression, which was also elevated in primary and metastatic tumors of individuals with CRPC.\n[2] Ectopic expression of N-cadherin in nonmetastatic, androgen-dependent prostate cancer models caused castration resistance, invasion and metastasis.\n[3] Monoclonal antibodies against the ectodomain of N-cadherin reduced proliferation, adhesion and invasion of prostate cancer cells in vitro.\n[4] In vivo, these antibodies slowed the growth of multiple established CRPC xenografts, blocked local invasion and metastasis and, at higher doses, led to complete regression.\n[5] N-cadherin–specific antibodies markedly delayed the time to emergence of castration resistance, markedly affected tumor histology and angiogenesis, and reduced both AKT serine-threonine kinase activity and serum interleukin-8 (IL-8) secretion.\n[6] These data indicate that N-cadherin is a major cause of both prostate cancer metastasis and castration resistance.\n[7] Therapeutic targeting of this factor with monoclonal antibodies may have considerable clinical benefit."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"N-cadherin–specific antibodies markedly delayed the time to emergence of castration resistance, markedly affected tumor histology and angiogenesis, and reduced both AKT serine-threonine kinase activity and serum interleukin-8 (IL-8) secretion.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 803, "doc_id": 22180793, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [22180793], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Monoclonal antibody targeting of N-cadherin inhibits growth.\n\nDocument title: Monoclonal antibody targeting of N-cadherin inhibits prostate cancer growth, metastasis and castration resistance\n\nAbstract sentences:\n[0] The transition from androgen-dependent to castration-resistant prostate cancer (CRPC) is a lethal event of uncertain molecular etiology.\n[1] Comparing gene expression in isogenic androgen-dependent and CRPC xenografts, we found a reproducible increase in N-cadherin expression, which was also elevated in primary and metastatic tumors of individuals with CRPC.\n[2] Ectopic expression of N-cadherin in nonmetastatic, androgen-dependent prostate cancer models caused castration resistance, invasion and metastasis.\n[3] Monoclonal antibodies against the ectodomain of N-cadherin reduced proliferation, adhesion and invasion of prostate cancer cells in vitro.\n[4] In vivo, these antibodies slowed the growth of multiple established CRPC xenografts, blocked local invasion and metastasis and, at higher doses, led to complete regression.\n[5] N-cadherin–specific antibodies markedly delayed the time to emergence of castration resistance, markedly affected tumor histology and angiogenesis, and reduced both AKT serine-threonine kinase activity and serum interleukin-8 (IL-8) secretion.\n[6] These data indicate that N-cadherin is a major cause of both prostate cancer metastasis and castration resistance.\n[7] Therapeutic targeting of this factor with monoclonal antibodies may have considerable clinical benefit."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Monoclonal antibodies against the ectodomain of N-cadherin reduced proliferation, adhesion and invasion of prostate cancer cells in vitro.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 804, "doc_id": 22180793, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [22180793], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Most termination events in Okazaki fragments are dictated by initiation patterns.\n\nDocument title: Quantitative, genome-wide analysis of eukaryotic replication initiation and termination.\n\nAbstract sentences:\n[0] Many fundamental aspects of DNA replication, such as the exact locations where DNA synthesis is initiated and terminated, how frequently origins are used, and how fork progression is influenced by transcription, are poorly understood.\n[1] Via the deep sequencing of Okazaki fragments, we comprehensively document replication fork directionality throughout the S. cerevisiae genome, which permits the systematic analysis of initiation, origin efficiency, fork progression, and termination.\n[2] We show that leading-strand initiation preferentially occurs within a nucleosome-free region at replication origins.\n[3] Using a strain in which late origins can be induced to fire early, we show that replication termination is a largely passive phenomenon that does not rely on cis-acting sequences or replication fork pausing.\n[4] The replication profile is predominantly determined by the kinetics of origin firing, allowing us to reconstruct chromosome-wide timing profiles from an asynchronous culture."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"The replication profile is predominantly determined by the kinetics of origin firing, allowing us to reconstruct chromosome-wide timing profiles from an asynchronous culture.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 807, "doc_id": 36606083, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [36606083], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mouse models can be generated using \"artificial spermatids.\"\n\nDocument title: Generation of Genetically Modified Mice by Oocyte Injection of Androgenetic Haploid Embryonic Stem Cells\n\nAbstract sentences:\n[0] Haploid cells are amenable for genetic analysis.\n[1] Recent success in the derivation of mouse haploid embryonic stem cells (haESCs) via parthenogenesis has enabled genetic screening in mammalian cells.\n[2] However, successful generation of live animals from these haESCs, which is needed to extend the genetic analysis to the organism level, has not been achieved.\n[3] Here, we report the derivation of haESCs from androgenetic blastocysts.\n[4] These cells, designated as AG-haESCs, partially maintain paternal imprints, express classical ESC pluripotency markers, and contribute to various tissues, including the germline, upon injection into diploid blastocysts.\n[5] Strikingly, live mice can be obtained upon injection of AG-haESCs into MII oocytes, and these mice bear haESC-carried genetic traits and develop into fertile adults.\n[6] Furthermore, gene targeting via homologous recombination is feasible in the AG-haESCs.\n[7] Our results demonstrate that AG-haESCs can be used as a genetically tractable fertilization agent for the production of live animals via injection into oocytes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Strikingly, live mice can be obtained upon injection of AG-haESCs into MII oocytes, and these mice bear haESC-carried genetic traits and develop into fertile adults.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 810, "doc_id": 13513790, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [13513790], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mutant mice lacking SVCT2 have severely reduced ascorbic acid levels in both brain and adrenals.\n\nDocument title: Ascorbic-acid transporter Slc23a1 is essential for vitamin C transport into the brain and for perinatal survival\n\nAbstract sentences:\n[0] The only proven requirement for ascorbic acid (vitamin C) is in preventing scurvy, presumably because it is a cofactor for hydroxylases required for post-translational modifications that stabilize collagen.\n[1] We have created mice deficient in the mouse ortholog (solute carrier family 23 member 1 or Slc23a1) of a rat ascorbic-acid transporter, Svct2 (ref.\n[2] 4).\n[3] Cultured embryonic fibroblasts from homozygous Slc23a1−/− mice had less than 5% of normal ascorbic-acid uptake.\n[4] Ascorbic-acid levels were undetectable or markedly reduced in the blood and tissues of Slc23a1−/− mice.\n[5] Prenatal supplementation of pregnant females did not elevate blood ascorbic acid in Slc23a1−/− fetuses, suggesting Slc23a1 is important in placental ascorbic-acid transport.\n[6] Slc23a1−/− mice died within a few minutes of birth with respiratory failure and intraparenchymal brain hemorrhage.\n[7] Lungs showed no postnatal expansion but had normal surfactant protein B levels.\n[8] Brain hemorrhage was unlikely to be simply a form of scurvy since Slc23a1−/− mice showed no hemorrhage in any other tissues and their skin had normal skin 4-hydroxyproline levels despite low ascorbic-acid content.\n[9] We conclude that Slc23a1 is required for transport of ascorbic acid into many tissues and across the placenta.\n[10] Deficiency of the transporter is lethal in newborn mice, thereby revealing a previously unrecognized requirement for ascorbic acid in the perinatal period."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4, 6]\nExplanation: Evidence states: \"Ascorbic-acid levels were undetectable or markedly reduced in the blood and tissues of Slc23a1−/− mice. Slc23a1−/− mice died within a few minutes of birth with respiratory failure and intraparenchymal brain hemorrhage.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 812, "doc_id": 19799455, "label": "SUPPORTS", "evidence_sentence_ids": [4, 6], "cited_doc_ids": [19799455], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mutant mice lacking SVCT2 have severely reduced ascorbic acid levels in both brain and adrenals.\n\nDocument title: Ascorbic-acid transporter Slc23a1 is essential for vitamin C transport into the brain and for perinatal survival\n\nAbstract sentences:\n[0] The only proven requirement for ascorbic acid (vitamin C) is in preventing scurvy, presumably because it is a cofactor for hydroxylases required for post-translational modifications that stabilize collagen.\n[1] We have created mice deficient in the mouse ortholog (solute carrier family 23 member 1 or Slc23a1) of a rat ascorbic-acid transporter, Svct2 (ref.\n[2] 4).\n[3] Cultured embryonic fibroblasts from homozygous Slc23a1−/− mice had less than 5% of normal ascorbic-acid uptake.\n[4] Ascorbic-acid levels were undetectable or markedly reduced in the blood and tissues of Slc23a1−/− mice.\n[5] Prenatal supplementation of pregnant females did not elevate blood ascorbic acid in Slc23a1−/− fetuses, suggesting Slc23a1 is important in placental ascorbic-acid transport.\n[6] Slc23a1−/− mice died within a few minutes of birth with respiratory failure and intraparenchymal brain hemorrhage.\n[7] Lungs showed no postnatal expansion but had normal surfactant protein B levels.\n[8] Brain hemorrhage was unlikely to be simply a form of scurvy since Slc23a1−/− mice showed no hemorrhage in any other tissues and their skin had normal skin 4-hydroxyproline levels despite low ascorbic-acid content.\n[9] We conclude that Slc23a1 is required for transport of ascorbic acid into many tissues and across the placenta.\n[10] Deficiency of the transporter is lethal in newborn mice, thereby revealing a previously unrecognized requirement for ascorbic acid in the perinatal period."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Brain hemorrhage was unlikely to be simply a form of scurvy since Slc23a1−/− mice showed no hemorrhage in any other tissues and their skin had normal skin 4-hydroxyproline levels despite low ascorbic-acid content.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 812, "doc_id": 19799455, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [19799455], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mutations in G-Beta protein GNB1 are present in many cancers, resulting in loss of interaction with G-alpha subunits and concomitant activation of AKT pathway.\n\nDocument title: Mutations in G protein beta subunits promote transformation and kinase inhibitor resistance\n\nAbstract sentences:\n[0] Activating mutations in genes encoding G protein α (Gα) subunits occur in 4-5% of all human cancers, but oncogenic alterations in Gβ subunits have not been defined.\n[1] Here we demonstrate that recurrent mutations in the Gβ proteins GNB1 and GNB2 confer cytokine-independent growth and activate canonical G protein signaling.\n[2] Multiple mutations in GNB1 affect the protein interface that binds Gα subunits as well as downstream effectors and disrupt Gα interactions with the Gβγ dimer.\n[3] Different mutations in Gβ proteins clustered partly on the basis of lineage; for example, all 11 GNB1 K57 mutations were in myeloid neoplasms, and seven of eight GNB1 I80 mutations were in B cell neoplasms.\n[4] Expression of patient-derived GNB1 variants in Cdkn2a-deficient mouse bone marrow followed by transplantation resulted in either myeloid or B cell malignancies.\n[5] In vivo treatment with the dual PI3K-mTOR inhibitor BEZ235 suppressed GNB1-induced signaling and markedly increased survival.\n[6] In several human tumors, mutations in the gene encoding GNB1 co-occurred with oncogenic kinase alterations, including the BCR-ABL fusion protein, the V617F substitution in JAK2 and the V600K substitution in BRAF.\n[7] Coexpression of patient-derived GNB1 variants with these mutant kinases resulted in inhibitor resistance in each context.\n[8] Thus, GNB1 and GNB2 alterations confer transformed and resistance phenotypes across a range of human tumors and may be targetable with inhibitors of G protein signaling."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 813, "doc_id": 33387953, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [33387953], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mutations in RIM1 decrease levels of IME1 RNA.\n\nDocument title: Molecular characterization of the yeast meiotic regulatory gene RIM1.\n\nAbstract sentences:\n[0] In the yeast Saccharomyces cerevisiae, genetic studies suggest that the RIM1 gene encodes a positive regulator of meiosis.\n[1] rim1 mutations cause reduced expression of IME1, which is required for expression of many meiotic genes, and thus lead to a partial defect in meiosis and spore formation.\n[2] We report the sequence of RIM1 and functional analysis of its coding region.\n[3] The RIM1 gene product (RIM1) contains three regions similar to C2H2 zinc fingers.\n[4] Serine substitutions for cysteine in each of the putative zinc fingers abolish RIM1 function.\n[5] The carboxyl-terminus of RIM1 is enriched in acidic amino acids and is required for full RIM1 activity.\n[6] RIM1 also contains two putative cAMP-dependent protein kinase (cAPK) phosphorylation sites.\n[7] At one site, substitution of alanine for serine does not affect RIM1 activity; at the other site, this substitution impairs activity.\n[8] This analysis of RIM1 suggests that the protein may function as a transcriptional activator.\n[9] We have used the cloned RIM1 gene to create a complete rim1 deletion.\n[10] This null allele, like previously isolated rim1 mutations, causes a partial meiotic defect.\n[11] In addition to RIM1, maximum IME1 expression requires the MCK1 and IME4 gene products.\n[12] Defects associated with rim1, mck1, and ime4 mutations in expression of a meiotic reporter gene (ime2-lacZ) and in sporulation are additive.\n[13] These findings suggest that RIM1 acts independently of MCK1 and IME4 to stimulate IME1 expression."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"rim1 mutations cause reduced expression of IME1, which is required for expression of many meiotic genes, and thus lead to a partial defect in meiosis and spore formation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 815, "doc_id": 8148304, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [8148304], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mutations in RIM1 decrease levels of IME1 RNA.\n\nDocument title: Molecular characterization of the yeast meiotic regulatory gene RIM1.\n\nAbstract sentences:\n[0] In the yeast Saccharomyces cerevisiae, genetic studies suggest that the RIM1 gene encodes a positive regulator of meiosis.\n[1] rim1 mutations cause reduced expression of IME1, which is required for expression of many meiotic genes, and thus lead to a partial defect in meiosis and spore formation.\n[2] We report the sequence of RIM1 and functional analysis of its coding region.\n[3] The RIM1 gene product (RIM1) contains three regions similar to C2H2 zinc fingers.\n[4] Serine substitutions for cysteine in each of the putative zinc fingers abolish RIM1 function.\n[5] The carboxyl-terminus of RIM1 is enriched in acidic amino acids and is required for full RIM1 activity.\n[6] RIM1 also contains two putative cAMP-dependent protein kinase (cAPK) phosphorylation sites.\n[7] At one site, substitution of alanine for serine does not affect RIM1 activity; at the other site, this substitution impairs activity.\n[8] This analysis of RIM1 suggests that the protein may function as a transcriptional activator.\n[9] We have used the cloned RIM1 gene to create a complete rim1 deletion.\n[10] This null allele, like previously isolated rim1 mutations, causes a partial meiotic defect.\n[11] In addition to RIM1, maximum IME1 expression requires the MCK1 and IME4 gene products.\n[12] Defects associated with rim1, mck1, and ime4 mutations in expression of a meiotic reporter gene (ime2-lacZ) and in sporulation are additive.\n[13] These findings suggest that RIM1 acts independently of MCK1 and IME4 to stimulate IME1 expression."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"These findings suggest that RIM1 acts independently of MCK1 and IME4 to stimulate IME1 expression.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 815, "doc_id": 8148304, "label": "SUPPORTS", "evidence_sentence_ids": [13], "cited_doc_ids": [8148304], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mutations in RIM1 raise levels of IME1 RNA.\n\nDocument title: Molecular characterization of the yeast meiotic regulatory gene RIM1.\n\nAbstract sentences:\n[0] In the yeast Saccharomyces cerevisiae, genetic studies suggest that the RIM1 gene encodes a positive regulator of meiosis.\n[1] rim1 mutations cause reduced expression of IME1, which is required for expression of many meiotic genes, and thus lead to a partial defect in meiosis and spore formation.\n[2] We report the sequence of RIM1 and functional analysis of its coding region.\n[3] The RIM1 gene product (RIM1) contains three regions similar to C2H2 zinc fingers.\n[4] Serine substitutions for cysteine in each of the putative zinc fingers abolish RIM1 function.\n[5] The carboxyl-terminus of RIM1 is enriched in acidic amino acids and is required for full RIM1 activity.\n[6] RIM1 also contains two putative cAMP-dependent protein kinase (cAPK) phosphorylation sites.\n[7] At one site, substitution of alanine for serine does not affect RIM1 activity; at the other site, this substitution impairs activity.\n[8] This analysis of RIM1 suggests that the protein may function as a transcriptional activator.\n[9] We have used the cloned RIM1 gene to create a complete rim1 deletion.\n[10] This null allele, like previously isolated rim1 mutations, causes a partial meiotic defect.\n[11] In addition to RIM1, maximum IME1 expression requires the MCK1 and IME4 gene products.\n[12] Defects associated with rim1, mck1, and ime4 mutations in expression of a meiotic reporter gene (ime2-lacZ) and in sporulation are additive.\n[13] These findings suggest that RIM1 acts independently of MCK1 and IME4 to stimulate IME1 expression."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"rim1 mutations cause reduced expression of IME1, which is required for expression of many meiotic genes, and thus lead to a partial defect in meiosis and spore formation.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 816, "doc_id": 8148304, "label": "CONTRADICTS", "evidence_sentence_ids": [1], "cited_doc_ids": [8148304], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Mutations in RIM1 raise levels of IME1 RNA.\n\nDocument title: Molecular characterization of the yeast meiotic regulatory gene RIM1.\n\nAbstract sentences:\n[0] In the yeast Saccharomyces cerevisiae, genetic studies suggest that the RIM1 gene encodes a positive regulator of meiosis.\n[1] rim1 mutations cause reduced expression of IME1, which is required for expression of many meiotic genes, and thus lead to a partial defect in meiosis and spore formation.\n[2] We report the sequence of RIM1 and functional analysis of its coding region.\n[3] The RIM1 gene product (RIM1) contains three regions similar to C2H2 zinc fingers.\n[4] Serine substitutions for cysteine in each of the putative zinc fingers abolish RIM1 function.\n[5] The carboxyl-terminus of RIM1 is enriched in acidic amino acids and is required for full RIM1 activity.\n[6] RIM1 also contains two putative cAMP-dependent protein kinase (cAPK) phosphorylation sites.\n[7] At one site, substitution of alanine for serine does not affect RIM1 activity; at the other site, this substitution impairs activity.\n[8] This analysis of RIM1 suggests that the protein may function as a transcriptional activator.\n[9] We have used the cloned RIM1 gene to create a complete rim1 deletion.\n[10] This null allele, like previously isolated rim1 mutations, causes a partial meiotic defect.\n[11] In addition to RIM1, maximum IME1 expression requires the MCK1 and IME4 gene products.\n[12] Defects associated with rim1, mck1, and ime4 mutations in expression of a meiotic reporter gene (ime2-lacZ) and in sporulation are additive.\n[13] These findings suggest that RIM1 acts independently of MCK1 and IME4 to stimulate IME1 expression."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"These findings suggest that RIM1 acts independently of MCK1 and IME4 to stimulate IME1 expression.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 816, "doc_id": 8148304, "label": "CONTRADICTS", "evidence_sentence_ids": [13], "cited_doc_ids": [8148304], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Myelin sheaths are lipid-rich cellular structures.\n\nDocument title: Label-free in vivo imaging of myelinated axons in health and disease with spectral confocal reflectance microscopy\n\nAbstract sentences:\n[0] We report a newly developed technique for high-resolution in vivo imaging of myelinated axons in the brain, spinal cord and peripheral nerve that requires no fluorescent labeling.\n[1] This method, based on spectral confocal reflectance microscopy (SCoRe), uses a conventional laser-scanning confocal system to generate images by merging the simultaneously reflected signals from multiple lasers of different wavelengths.\n[2] Striking color patterns unique to individual myelinated fibers are generated that facilitate their tracing in dense axonal areas.\n[3] These patterns highlight nodes of Ranvier and Schmidt-Lanterman incisures and can be used to detect various myelin pathologies.\n[4] Using SCoRe we carried out chronic brain imaging up to 400 μm deep, capturing de novo myelination of mouse cortical axons in vivo.\n[5] We also established the feasibility of imaging myelinated axons in the human cerebral cortex.\n[6] SCoRe adds a powerful component to the evolving toolbox for imaging myelination in living animals and potentially in humans."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 817, "doc_id": 17814815, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [17814815], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Myelin sheaths play a role in action potential propagation.\n\nDocument title: Label-free in vivo imaging of myelinated axons in health and disease with spectral confocal reflectance microscopy\n\nAbstract sentences:\n[0] We report a newly developed technique for high-resolution in vivo imaging of myelinated axons in the brain, spinal cord and peripheral nerve that requires no fluorescent labeling.\n[1] This method, based on spectral confocal reflectance microscopy (SCoRe), uses a conventional laser-scanning confocal system to generate images by merging the simultaneously reflected signals from multiple lasers of different wavelengths.\n[2] Striking color patterns unique to individual myelinated fibers are generated that facilitate their tracing in dense axonal areas.\n[3] These patterns highlight nodes of Ranvier and Schmidt-Lanterman incisures and can be used to detect various myelin pathologies.\n[4] Using SCoRe we carried out chronic brain imaging up to 400 μm deep, capturing de novo myelination of mouse cortical axons in vivo.\n[5] We also established the feasibility of imaging myelinated axons in the human cerebral cortex.\n[6] SCoRe adds a powerful component to the evolving toolbox for imaging myelination in living animals and potentially in humans."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"We report a newly developed technique for high-resolution in vivo imaging of myelinated axons in the brain, spinal cord and peripheral nerve that requires no fluorescent labeling.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 818, "doc_id": 17814815, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [17814815], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Myelin sheaths play a role in action potential propagation.\n\nDocument title: Label-free in vivo imaging of myelinated axons in health and disease with spectral confocal reflectance microscopy\n\nAbstract sentences:\n[0] We report a newly developed technique for high-resolution in vivo imaging of myelinated axons in the brain, spinal cord and peripheral nerve that requires no fluorescent labeling.\n[1] This method, based on spectral confocal reflectance microscopy (SCoRe), uses a conventional laser-scanning confocal system to generate images by merging the simultaneously reflected signals from multiple lasers of different wavelengths.\n[2] Striking color patterns unique to individual myelinated fibers are generated that facilitate their tracing in dense axonal areas.\n[3] These patterns highlight nodes of Ranvier and Schmidt-Lanterman incisures and can be used to detect various myelin pathologies.\n[4] Using SCoRe we carried out chronic brain imaging up to 400 μm deep, capturing de novo myelination of mouse cortical axons in vivo.\n[5] We also established the feasibility of imaging myelinated axons in the human cerebral cortex.\n[6] SCoRe adds a powerful component to the evolving toolbox for imaging myelination in living animals and potentially in humans."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Striking color patterns unique to individual myelinated fibers are generated that facilitate their tracing in dense axonal areas.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 818, "doc_id": 17814815, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [17814815], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: N348I mutations cause resistance to nevirapine.\n\nDocument title: N348I in the Connection Domain of HIV-1 Reverse Transcriptase Confers Zidovudine and Nevirapine Resistance\n\nAbstract sentences:\n[0] Background The catalytically active 66-kDa subunit of the human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) consists of DNA polymerase, connection, and ribonuclease H (RNase H) domains.\n[1] Almost all known RT inhibitor resistance mutations identified to date map to the polymerase domain of the enzyme.\n[2] However, the connection and RNase H domains are not routinely analysed in clinical samples and none of the genotyping assays available for patient management sequence the entire RT coding region.\n[3] The British Columbia Centre for Excellence in HIV/AIDS (the Centre) genotypes clinical isolates up to codon 400 in RT, and our retrospective statistical analyses of the Centre’s database have identified an N348I mutation in the RT connection domain in treatment-experienced individuals.\n[4] The objective of this multidisciplinary study was to establish the in vivo relevance of this mutation and its role in drug resistance.\n[5] Methods and Findings The prevalence of N348I in clinical isolates, the time taken for it to emerge under selective drug pressure, and its association with changes in viral load, specific drug treatment, and known drug resistance mutations was analysed from genotypes, viral loads, and treatment histories from the Centre’s database.\n[6] N348I increased in prevalence from below 1% in 368 treatmentnao ¨ve individuals to 12.1% in 1,009 treatment-experienced patients (p ¼ 7.7 3 10 � 12 ).\n[7] N348I appeared early in therapy and was highly associated with thymidine analogue mutations (TAMs) M41L and T215Y/F (p , 0.001), the lamivudine resistance mutations M184V/I (p , 0.001), and non-nucleoside RTI (NNRTI) resistance mutations K103N and Y181C/I (p , 0.001).\n[8] The association with TAMs and NNRTI resistance mutations was consistent with the selection of N348I in patients treated with regimens that included both zidovudine and nevirapine (odds ratio 2.62, 95% confidence interval 1.43–4.81).\n[9] The appearance of N348I was associated with a significant increase in viral load (p , 0.001), which was as large as the viral load increases observed for any of the TAMs.\n[10] However, this analysis did not account for the simultaneous selection of other RT or protease inhibitor resistance mutations on viral load.\n[11] To delineate the role of this mutation in RT inhibitor resistance, N348I was introduced into HIV-1 molecular clones containing different genetic backbones.\n[12] N348I decreased zidovudine susceptibility 2- to 4-fold in the context of wildtype HIV-1 or when combined with TAMs.\n[13] N348I also decreased susceptibility to nevirapine (7.4fold) and efavirenz (2.5-fold) and significantly potentiated resistance to these drugs when combined with K103N.\n[14] Biochemical analyses of recombinant RT containing N348I provide supporting evidence for the role of this mutation in zidovudine and NNRTI resistance and give some insight into the molecular mechanism of resistance.\n[15] Conclusions"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"N348I also decreased susceptibility to nevirapine (7.4fold) and efavirenz (2.5-fold) and significantly potentiated resistance to these drugs when combined with K103N.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 822, "doc_id": 15319019, "label": "SUPPORTS", "evidence_sentence_ids": [13], "cited_doc_ids": [15319019], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: N348I mutations reduce resistance to nevirapine.\n\nDocument title: N348I in the Connection Domain of HIV-1 Reverse Transcriptase Confers Zidovudine and Nevirapine Resistance\n\nAbstract sentences:\n[0] Background The catalytically active 66-kDa subunit of the human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) consists of DNA polymerase, connection, and ribonuclease H (RNase H) domains.\n[1] Almost all known RT inhibitor resistance mutations identified to date map to the polymerase domain of the enzyme.\n[2] However, the connection and RNase H domains are not routinely analysed in clinical samples and none of the genotyping assays available for patient management sequence the entire RT coding region.\n[3] The British Columbia Centre for Excellence in HIV/AIDS (the Centre) genotypes clinical isolates up to codon 400 in RT, and our retrospective statistical analyses of the Centre’s database have identified an N348I mutation in the RT connection domain in treatment-experienced individuals.\n[4] The objective of this multidisciplinary study was to establish the in vivo relevance of this mutation and its role in drug resistance.\n[5] Methods and Findings The prevalence of N348I in clinical isolates, the time taken for it to emerge under selective drug pressure, and its association with changes in viral load, specific drug treatment, and known drug resistance mutations was analysed from genotypes, viral loads, and treatment histories from the Centre’s database.\n[6] N348I increased in prevalence from below 1% in 368 treatmentnao ¨ve individuals to 12.1% in 1,009 treatment-experienced patients (p ¼ 7.7 3 10 � 12 ).\n[7] N348I appeared early in therapy and was highly associated with thymidine analogue mutations (TAMs) M41L and T215Y/F (p , 0.001), the lamivudine resistance mutations M184V/I (p , 0.001), and non-nucleoside RTI (NNRTI) resistance mutations K103N and Y181C/I (p , 0.001).\n[8] The association with TAMs and NNRTI resistance mutations was consistent with the selection of N348I in patients treated with regimens that included both zidovudine and nevirapine (odds ratio 2.62, 95% confidence interval 1.43–4.81).\n[9] The appearance of N348I was associated with a significant increase in viral load (p , 0.001), which was as large as the viral load increases observed for any of the TAMs.\n[10] However, this analysis did not account for the simultaneous selection of other RT or protease inhibitor resistance mutations on viral load.\n[11] To delineate the role of this mutation in RT inhibitor resistance, N348I was introduced into HIV-1 molecular clones containing different genetic backbones.\n[12] N348I decreased zidovudine susceptibility 2- to 4-fold in the context of wildtype HIV-1 or when combined with TAMs.\n[13] N348I also decreased susceptibility to nevirapine (7.4fold) and efavirenz (2.5-fold) and significantly potentiated resistance to these drugs when combined with K103N.\n[14] Biochemical analyses of recombinant RT containing N348I provide supporting evidence for the role of this mutation in zidovudine and NNRTI resistance and give some insight into the molecular mechanism of resistance.\n[15] Conclusions"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"N348I also decreased susceptibility to nevirapine (7.4fold) and efavirenz (2.5-fold) and significantly potentiated resistance to these drugs when combined with K103N.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 825, "doc_id": 15319019, "label": "CONTRADICTS", "evidence_sentence_ids": [13], "cited_doc_ids": [15319019], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: NAC destabilizes NO to increase the effect of contrast agents on renal functions.\n\nDocument title: Acetylcysteine for prevention of acute deterioration of renal function following elective coronary angiography and intervention: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT The antioxidant acetylcysteine prevents acute contrast nephrotoxicity in patients with impaired renal function who undergo computed tomography scanning.\n[1] However, its role in coronary angiography is unclear.\n[2] OBJECTIVE To determine whether oral acetylcysteine prevents acute deterioration in renal function in patients with moderate renal insufficiency who undergo elective coronary angiography.\n[3] DESIGN AND SETTING Prospective, randomized, double-blind, placebo-controlled trial conducted from May 2000 to December 2001 at the Grantham Hospital at the University of Hong Kong.\n[4] PARTICIPANTS Two hundred Chinese patients aged mean (SD) 68 (6.5) years with stable moderate renal insufficiency (creatinine clearance <60 mL/min [1.00 mL/s]) who were undergoing elective coronary angiography with or without intervention.\n[5] INTERVENTION Participants were randomly assigned to receive oral acetylcysteine(600 mg twice per day; n = 102) or matching placebo tablets (n = 98) on the day before and the day of angiography.\n[6] All patients received low-osmolality contrast agent.\n[7] MAIN OUTCOME MEASURES Occurrence of more than a 25% increase in serum creatinine level within 48 hours after contrast administration; change in creatinine clearance and serum creatinine level.\n[8] RESULTS Twelve control patients (12%) and 4 acetylcysteine patients (4%) developed a more than 25% increase in serum creatinine level within 48 hours after contrast administration (relative risk, 0.32; 95% confidence interval [CI], 0.10-0.96; P =.03).\n[9] Serum creatinine was lower in the acetylcysteine group (1.22 mg/dL [107.8 micromol/L]; 95% CI, 1.11-1.33 mg/dL vs 1.38 mg/dL [122.9 micromol/L]; 95% CI, 1.27-1.49 mg/dL; P =.006) during the first 48 hours after angiography.\n[10] Acetylcysteine treatment significantly increased creatinine clearance from 44.8 mL/min (0.75 mL/s) (95% CI, 42.7-47.6 mL/min) to 58.9 mL/min (0.98 mL/s) (95% CI, 55.6-62.3 mL/min) 2 days after the contrast administration (P<.001).\n[11] The increase was not significant in the control group (from 42.1 to 44.1 mL/min [0.70 to 0.74 mL/s]; P =.15).\n[12] The benefit of acetylcysteine was consistent among various patient subgroups and persistent for at least 7 days.\n[13] There were no major treatment-related adverse events.\n[14] CONCLUSION Acetylcysteine protects patients with moderate chronic renal insufficiency from contrast-induced deterioration in renal function after coronary angiographic procedures, with minimal adverse effects and at a low cost."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 826, "doc_id": 4678846, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4678846], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: NAC inhibits the generation of angiotensin-converting enzyme.\n\nDocument title: Acetylcysteine for prevention of acute deterioration of renal function following elective coronary angiography and intervention: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT The antioxidant acetylcysteine prevents acute contrast nephrotoxicity in patients with impaired renal function who undergo computed tomography scanning.\n[1] However, its role in coronary angiography is unclear.\n[2] OBJECTIVE To determine whether oral acetylcysteine prevents acute deterioration in renal function in patients with moderate renal insufficiency who undergo elective coronary angiography.\n[3] DESIGN AND SETTING Prospective, randomized, double-blind, placebo-controlled trial conducted from May 2000 to December 2001 at the Grantham Hospital at the University of Hong Kong.\n[4] PARTICIPANTS Two hundred Chinese patients aged mean (SD) 68 (6.5) years with stable moderate renal insufficiency (creatinine clearance <60 mL/min [1.00 mL/s]) who were undergoing elective coronary angiography with or without intervention.\n[5] INTERVENTION Participants were randomly assigned to receive oral acetylcysteine(600 mg twice per day; n = 102) or matching placebo tablets (n = 98) on the day before and the day of angiography.\n[6] All patients received low-osmolality contrast agent.\n[7] MAIN OUTCOME MEASURES Occurrence of more than a 25% increase in serum creatinine level within 48 hours after contrast administration; change in creatinine clearance and serum creatinine level.\n[8] RESULTS Twelve control patients (12%) and 4 acetylcysteine patients (4%) developed a more than 25% increase in serum creatinine level within 48 hours after contrast administration (relative risk, 0.32; 95% confidence interval [CI], 0.10-0.96; P =.03).\n[9] Serum creatinine was lower in the acetylcysteine group (1.22 mg/dL [107.8 micromol/L]; 95% CI, 1.11-1.33 mg/dL vs 1.38 mg/dL [122.9 micromol/L]; 95% CI, 1.27-1.49 mg/dL; P =.006) during the first 48 hours after angiography.\n[10] Acetylcysteine treatment significantly increased creatinine clearance from 44.8 mL/min (0.75 mL/s) (95% CI, 42.7-47.6 mL/min) to 58.9 mL/min (0.98 mL/s) (95% CI, 55.6-62.3 mL/min) 2 days after the contrast administration (P<.001).\n[11] The increase was not significant in the control group (from 42.1 to 44.1 mL/min [0.70 to 0.74 mL/s]; P =.15).\n[12] The benefit of acetylcysteine was consistent among various patient subgroups and persistent for at least 7 days.\n[13] There were no major treatment-related adverse events.\n[14] CONCLUSION Acetylcysteine protects patients with moderate chronic renal insufficiency from contrast-induced deterioration in renal function after coronary angiographic procedures, with minimal adverse effects and at a low cost."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 828, "doc_id": 4678846, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4678846], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: NR5A2 does not play a role in development of endometrial tissues.\n\nDocument title: Liver receptor homolog-1 is essential for pregnancy\n\nAbstract sentences:\n[0] Successful pregnancy requires coordination of an array of signals and factors from multiple tissues.\n[1] One such element, liver receptor homolog-1 (Lrh-1), is an orphan nuclear receptor that regulates metabolism and hormone synthesis.\n[2] It is strongly expressed in granulosa cells of ovarian follicles and in the corpus luteum of rodents and humans.\n[3] Germline ablation of Nr5a2 (also called Lrh-1), the gene coding for Lrh-1, in mice is embryonically lethal at gastrulation.\n[4] Depletion of Lrh-1 in the ovarian follicle shows that it regulates genes required for both steroid synthesis and ovulation.\n[5] To study the effects of Lrh-1 on mouse gestation, we genetically disrupted its expression in the corpus luteum, resulting in luteal insufficiency.\n[6] Hormone replacement permitted embryo implantation but was followed by gestational failure with impaired endometrial decidualization, compromised placental formation, fetal growth retardation and fetal death.\n[7] Lrh-1 is also expressed in the mouse and human endometrium, and in a primary culture of human endometrial stromal cells, reduction of NR5A2 transcript abundance by RNA interference abrogated decidualization.\n[8] These findings show that Lrh-1 is necessary for maintenance of the corpus luteum, for promotion of decidualization and for formation of the placenta.\n[9] It therefore has multiple, indispensible roles in establishing and sustaining pregnancy."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5, 6]\nExplanation: Evidence states: \"To study the effects of Lrh-1 on mouse gestation, we genetically disrupted its expression in the corpus luteum, resulting in luteal insufficiency. Hormone replacement permitted embryo implantation but was followed by gestational failure with impaired endometrial decidualization, compromised placental formation, fetal growth retardation and fetal death.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 835, "doc_id": 15928989, "label": "CONTRADICTS", "evidence_sentence_ids": [5, 6], "cited_doc_ids": [15928989], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: NR5A2 does not play a role in development of endometrial tissues.\n\nDocument title: Liver receptor homolog-1 is essential for pregnancy\n\nAbstract sentences:\n[0] Successful pregnancy requires coordination of an array of signals and factors from multiple tissues.\n[1] One such element, liver receptor homolog-1 (Lrh-1), is an orphan nuclear receptor that regulates metabolism and hormone synthesis.\n[2] It is strongly expressed in granulosa cells of ovarian follicles and in the corpus luteum of rodents and humans.\n[3] Germline ablation of Nr5a2 (also called Lrh-1), the gene coding for Lrh-1, in mice is embryonically lethal at gastrulation.\n[4] Depletion of Lrh-1 in the ovarian follicle shows that it regulates genes required for both steroid synthesis and ovulation.\n[5] To study the effects of Lrh-1 on mouse gestation, we genetically disrupted its expression in the corpus luteum, resulting in luteal insufficiency.\n[6] Hormone replacement permitted embryo implantation but was followed by gestational failure with impaired endometrial decidualization, compromised placental formation, fetal growth retardation and fetal death.\n[7] Lrh-1 is also expressed in the mouse and human endometrium, and in a primary culture of human endometrial stromal cells, reduction of NR5A2 transcript abundance by RNA interference abrogated decidualization.\n[8] These findings show that Lrh-1 is necessary for maintenance of the corpus luteum, for promotion of decidualization and for formation of the placenta.\n[9] It therefore has multiple, indispensible roles in establishing and sustaining pregnancy."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Lrh-1 is also expressed in the mouse and human endometrium, and in a primary culture of human endometrial stromal cells, reduction of NR5A2 transcript abundance by RNA interference abrogated decidualization.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 835, "doc_id": 15928989, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [15928989], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: NR5A2 is important in reverse cholesterol transport in humans.\n\nDocument title: Liver receptor homolog-1 is essential for pregnancy\n\nAbstract sentences:\n[0] Successful pregnancy requires coordination of an array of signals and factors from multiple tissues.\n[1] One such element, liver receptor homolog-1 (Lrh-1), is an orphan nuclear receptor that regulates metabolism and hormone synthesis.\n[2] It is strongly expressed in granulosa cells of ovarian follicles and in the corpus luteum of rodents and humans.\n[3] Germline ablation of Nr5a2 (also called Lrh-1), the gene coding for Lrh-1, in mice is embryonically lethal at gastrulation.\n[4] Depletion of Lrh-1 in the ovarian follicle shows that it regulates genes required for both steroid synthesis and ovulation.\n[5] To study the effects of Lrh-1 on mouse gestation, we genetically disrupted its expression in the corpus luteum, resulting in luteal insufficiency.\n[6] Hormone replacement permitted embryo implantation but was followed by gestational failure with impaired endometrial decidualization, compromised placental formation, fetal growth retardation and fetal death.\n[7] Lrh-1 is also expressed in the mouse and human endometrium, and in a primary culture of human endometrial stromal cells, reduction of NR5A2 transcript abundance by RNA interference abrogated decidualization.\n[8] These findings show that Lrh-1 is necessary for maintenance of the corpus luteum, for promotion of decidualization and for formation of the placenta.\n[9] It therefore has multiple, indispensible roles in establishing and sustaining pregnancy."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 838, "doc_id": 15928989, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [15928989], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Natriuretic peptides increase susceptibility to diabetes.\n\nDocument title: Mendelian Randomization Study of B-Type Natriuretic Peptide and Type 2 Diabetes: Evidence of Causal Association from Population Studies\n\nAbstract sentences:\n[0] BACKGROUND Genetic and epidemiological evidence suggests an inverse association between B-type natriuretic peptide (BNP) levels in blood and risk of type 2 diabetes (T2D), but the prospective association of BNP with T2D is uncertain, and it is unclear whether the association is confounded.\n[1] METHODS AND FINDINGS We analysed the association between levels of the N-terminal fragment of pro-BNP (NT-pro-BNP) in blood and risk of incident T2D in a prospective case-cohort study and genotyped the variant rs198389 within the BNP locus in three T2D case-control studies.\n[2] We combined our results with existing data in a meta-analysis of 11 case-control studies.\n[3] Using a Mendelian randomization approach, we compared the observed association between rs198389 and T2D to that expected from the NT-pro-BNP level to T2D association and the NT-pro-BNP difference per C allele of rs198389.\n[4] In participants of our case-cohort study who were free of T2D and cardiovascular disease at baseline, we observed a 21% (95% CI 3%-36%) decreased risk of incident T2D per one standard deviation (SD) higher log-transformed NT-pro-BNP levels in analysis adjusted for age, sex, body mass index, systolic blood pressure, smoking, family history of T2D, history of hypertension, and levels of triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol.\n[5] The association between rs198389 and T2D observed in case-control studies (odds ratio = 0.94 per C allele, 95% CI 0.91-0.97) was similar to that expected (0.96, 0.93-0.98) based on the pooled estimate for the log-NT-pro-BNP level to T2D association derived from a meta-analysis of our study and published data (hazard ratio = 0.82 per SD, 0.74-0.90) and the difference in NT-pro-BNP levels (0.22 SD, 0.15-0.29) per C allele of rs198389.\n[6] No significant associations were observed between the rs198389 genotype and potential confounders.\n[7] CONCLUSIONS Our results provide evidence for a potential causal role of the BNP system in the aetiology of T2D.\n[8] Further studies are needed to investigate the mechanisms underlying this association and possibilities for preventive interventions.\n[9] Please see later in the article for the Editors' Summary."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4, 7]\nExplanation: Evidence states: \"In participants of our case-cohort study who were free of T2D and cardiovascular disease at baseline, we observed a 21% (95% CI 3%-36%) decreased risk of incident T2D per one standard deviation (SD) higher log-transformed NT-pro-BNP levels in analysis adjusted for age, sex, body mass index, systolic blood pressure, smoking, family history of T2D, history of hypertension, and levels of triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol. CONCLUSIONS Our results provide evidence for a potential causal role of the BNP system in the aetiology of T2D.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 840, "doc_id": 15663829, "label": "CONTRADICTS", "evidence_sentence_ids": [4, 7], "cited_doc_ids": [15663829], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Natriuretic peptides protect against diabetes.\n\nDocument title: Mendelian Randomization Study of B-Type Natriuretic Peptide and Type 2 Diabetes: Evidence of Causal Association from Population Studies\n\nAbstract sentences:\n[0] BACKGROUND Genetic and epidemiological evidence suggests an inverse association between B-type natriuretic peptide (BNP) levels in blood and risk of type 2 diabetes (T2D), but the prospective association of BNP with T2D is uncertain, and it is unclear whether the association is confounded.\n[1] METHODS AND FINDINGS We analysed the association between levels of the N-terminal fragment of pro-BNP (NT-pro-BNP) in blood and risk of incident T2D in a prospective case-cohort study and genotyped the variant rs198389 within the BNP locus in three T2D case-control studies.\n[2] We combined our results with existing data in a meta-analysis of 11 case-control studies.\n[3] Using a Mendelian randomization approach, we compared the observed association between rs198389 and T2D to that expected from the NT-pro-BNP level to T2D association and the NT-pro-BNP difference per C allele of rs198389.\n[4] In participants of our case-cohort study who were free of T2D and cardiovascular disease at baseline, we observed a 21% (95% CI 3%-36%) decreased risk of incident T2D per one standard deviation (SD) higher log-transformed NT-pro-BNP levels in analysis adjusted for age, sex, body mass index, systolic blood pressure, smoking, family history of T2D, history of hypertension, and levels of triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol.\n[5] The association between rs198389 and T2D observed in case-control studies (odds ratio = 0.94 per C allele, 95% CI 0.91-0.97) was similar to that expected (0.96, 0.93-0.98) based on the pooled estimate for the log-NT-pro-BNP level to T2D association derived from a meta-analysis of our study and published data (hazard ratio = 0.82 per SD, 0.74-0.90) and the difference in NT-pro-BNP levels (0.22 SD, 0.15-0.29) per C allele of rs198389.\n[6] No significant associations were observed between the rs198389 genotype and potential confounders.\n[7] CONCLUSIONS Our results provide evidence for a potential causal role of the BNP system in the aetiology of T2D.\n[8] Further studies are needed to investigate the mechanisms underlying this association and possibilities for preventive interventions.\n[9] Please see later in the article for the Editors' Summary."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"In participants of our case-cohort study who were free of T2D and cardiovascular disease at baseline, we observed a 21% (95% CI 3%-36%) decreased risk of incident T2D per one standard deviation (SD) higher log-transformed NT-pro-BNP levels in analysis adjusted for age, sex, body mass index, systolic blood pressure, smoking, family history of T2D, history of hypertension, and levels of triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 841, "doc_id": 15663829, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [15663829], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Natriuretic peptides protect against diabetes.\n\nDocument title: Mendelian Randomization Study of B-Type Natriuretic Peptide and Type 2 Diabetes: Evidence of Causal Association from Population Studies\n\nAbstract sentences:\n[0] BACKGROUND Genetic and epidemiological evidence suggests an inverse association between B-type natriuretic peptide (BNP) levels in blood and risk of type 2 diabetes (T2D), but the prospective association of BNP with T2D is uncertain, and it is unclear whether the association is confounded.\n[1] METHODS AND FINDINGS We analysed the association between levels of the N-terminal fragment of pro-BNP (NT-pro-BNP) in blood and risk of incident T2D in a prospective case-cohort study and genotyped the variant rs198389 within the BNP locus in three T2D case-control studies.\n[2] We combined our results with existing data in a meta-analysis of 11 case-control studies.\n[3] Using a Mendelian randomization approach, we compared the observed association between rs198389 and T2D to that expected from the NT-pro-BNP level to T2D association and the NT-pro-BNP difference per C allele of rs198389.\n[4] In participants of our case-cohort study who were free of T2D and cardiovascular disease at baseline, we observed a 21% (95% CI 3%-36%) decreased risk of incident T2D per one standard deviation (SD) higher log-transformed NT-pro-BNP levels in analysis adjusted for age, sex, body mass index, systolic blood pressure, smoking, family history of T2D, history of hypertension, and levels of triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol.\n[5] The association between rs198389 and T2D observed in case-control studies (odds ratio = 0.94 per C allele, 95% CI 0.91-0.97) was similar to that expected (0.96, 0.93-0.98) based on the pooled estimate for the log-NT-pro-BNP level to T2D association derived from a meta-analysis of our study and published data (hazard ratio = 0.82 per SD, 0.74-0.90) and the difference in NT-pro-BNP levels (0.22 SD, 0.15-0.29) per C allele of rs198389.\n[6] No significant associations were observed between the rs198389 genotype and potential confounders.\n[7] CONCLUSIONS Our results provide evidence for a potential causal role of the BNP system in the aetiology of T2D.\n[8] Further studies are needed to investigate the mechanisms underlying this association and possibilities for preventive interventions.\n[9] Please see later in the article for the Editors' Summary."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"CONCLUSIONS Our results provide evidence for a potential causal role of the BNP system in the aetiology of T2D.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 841, "doc_id": 15663829, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [15663829], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Neutrophil extracellular trap (NET) antigens may contain the targeted autoantigens PR3 and MPO.\n\nDocument title: Netting neutrophils in autoimmune small-vessel vasculitis\n\nAbstract sentences:\n[0] Small-vessel vasculitis (SVV) is a chronic autoinflammatory condition linked to antineutrophil cytoplasm autoantibodies (ANCAs).\n[1] Here we show that chromatin fibers, so-called neutrophil extracellular traps (NETs), are released by ANCA-stimulated neutrophils and contain the targeted autoantigens proteinase-3 (PR3) and myeloperoxidase (MPO).\n[2] Deposition of NETs in inflamed kidneys and circulating MPO-DNA complexes suggest that NET formation triggers vasculitis and promotes the autoimmune response against neutrophil components in individuals with SVV."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Here we show that chromatin fibers, so-called neutrophil extracellular traps (NETs), are released by ANCA-stimulated neutrophils and contain the targeted autoantigens proteinase-3 (PR3) and myeloperoxidase (MPO).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 844, "doc_id": 17741440, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [17741440], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Neutrophils produce IL-1β in response to large particles.\n\nDocument title: Reactive Oxygen Species Localization Programs Inflammation to Clear Microbes of Different Size\n\nAbstract sentences:\n[0] How the number of immune cells recruited to sites of infection is determined and adjusted to differences in the cellular stoichiometry between host and pathogen is unknown.\n[1] Here, we have uncovered a role for reactive oxygen species (ROS) as sensors of microbe size.\n[2] By sensing the differential localization of ROS generated in response to microbes of different size, neutrophils tuned their interleukin (IL)-1β expression via the selective oxidation of NF-κB, in order to implement distinct inflammatory programs.\n[3] Small microbes triggered ROS intracellularly, suppressing IL-1β expression to limit neutrophil recruitment as each phagocyte eliminated numerous pathogens.\n[4] In contrast, large microbes triggered ROS extracellularly, amplifying IL-1β expression to recruit numerous neutrophils forming cooperative clusters.\n[5] Defects in ROS-mediated microbe size sensing resulted in large neutrophil infiltrates and clusters in response to small microbes that contribute to inflammatory disease.\n[6] These findings highlight the impact of ROS localization on signal transduction."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"In contrast, large microbes triggered ROS extracellularly, amplifying IL-1β expression to recruit numerous neutrophils forming cooperative clusters.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 846, "doc_id": 22696649, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [22696649], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Nigerian physicians constitue the largest component of sub-Saharan Africa-trained physicians in the United States.\n\nDocument title: Physician Emigration from Sub-Saharan Africa to the United States: Analysis of the 2011 AMA Physician Masterfile\n\nAbstract sentences:\n[0] BACKGROUND The large-scale emigration of physicians from sub-Saharan Africa (SSA) to high-income nations is a serious development concern.\n[1] Our objective was to determine current emigration trends of SSA physicians found in the physician workforce of the United States.\n[2] METHODS AND FINDINGS We analyzed physician data from the World Health Organization (WHO) Global Health Workforce Statistics along with graduation and residency data from the 2011 American Medical Association Physician Masterfile (AMA-PM) on physicians trained or born in SSA countries who currently practice in the US.\n[3] We estimated emigration proportions, year of US entry, years of practice before emigration, and length of time in the US.\n[4] According to the 2011 AMA-PM, 10,819 physicians were born or trained in 28 SSA countries.\n[5] Sixty-eight percent (n = 7,370) were SSA-trained, 20% (n = 2,126) were US-trained, and 12% (n = 1,323) were trained outside both SSA and the US.\n[6] We estimated active physicians (age ≤ 70 years) to represent 96% (n = 10,377) of the total.\n[7] Migration trends among SSA-trained physicians increased from 2002 to 2011 for all but one principal source country; the exception was South Africa whose physician migration to the US decreased by 8% (-156).\n[8] The increase in last-decade migration was >50% in Nigeria (+1,113) and Ghana (+243), >100% in Ethiopia (+274), and >200% (+244) in Sudan.\n[9] Liberia was the most affected by migration to the US with 77% (n = 175) of its estimated physicians in the 2011 AMA-PM.\n[10] On average, SSA-trained physicians have been in the US for 18 years.\n[11] They practiced for 6.5 years before US entry, and nearly half emigrated during the implementation years (1984-1999) of the structural adjustment programs.\n[12] CONCLUSION Physician emigration from SSA to the US is increasing for most SSA source countries.\n[13] Unless far-reaching policies are implemented by the US and SSA countries, the current emigration trends will persist, and the US will remain a leading destination for SSA physicians emigrating from the continent of greatest need.\n[14] Please see later in the article for the Editors' Summary."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 848, "doc_id": 14500725, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14500725], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Nonhuman primates are incapable of producing neutralizing antibodies in reponse to the Eilat virus (EILV) produced in mosquitos.\n\nDocument title: A chikungunya fever vaccine utilizing an insect-specific virus platform\n\nAbstract sentences:\n[0] Traditionally, vaccine development involves tradeoffs between immunogenicity and safety.\n[1] Live-attenuated vaccines typically offer rapid and durable immunity but have reduced safety when compared to inactivated vaccines.\n[2] In contrast, the inability of inactivated vaccines to replicate enhances safety at the expense of immunogenicity, often necessitating multiple doses and boosters.\n[3] To overcome these tradeoffs, we developed the insect-specific alphavirus, Eilat virus (EILV), as a vaccine platform.\n[4] To address the chikungunya fever (CHIKF) pandemic, we used an EILV cDNA clone to design a chimeric virus containing the chikungunya virus (CHIKV) structural proteins.\n[5] The recombinant EILV/CHIKV was structurally identical at 10 Å to wild-type CHIKV, as determined by single-particle cryo-electron microscopy, and it mimicked the early stages of CHIKV replication in vertebrate cells from attachment and entry to viral RNA delivery.\n[6] Yet the recombinant virus remained completely defective for productive replication, providing a high degree of safety.\n[7] A single dose of EILV/CHIKV produced in mosquito cells elicited rapid (within 4 d) and long-lasting (>290 d) neutralizing antibodies that provided complete protection in two different mouse models.\n[8] In nonhuman primates, EILV/CHIKV elicited rapid and robust immunity that protected against viremia and telemetrically monitored fever.\n[9] Our EILV platform represents the first structurally native application of an insect-specific virus in preclinical vaccine development and highlights the potential application of such viruses in vaccinology."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7, 8]\nExplanation: Evidence states: \"A single dose of EILV/CHIKV produced in mosquito cells elicited rapid (within 4 d) and long-lasting (>290 d) neutralizing antibodies that provided complete protection in two different mouse models. In nonhuman primates, EILV/CHIKV elicited rapid and robust immunity that protected against viremia and telemetrically monitored fever.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 853, "doc_id": 24922825, "label": "CONTRADICTS", "evidence_sentence_ids": [7, 8], "cited_doc_ids": [24922825], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Nonhypertensive people who are 55 years old have a 90% chance of developing hypertension during their lifetime.\n\nDocument title: Residual lifetime risk for developing hypertension in middle-aged women and men: The Framingham Heart Study.\n\nAbstract sentences:\n[0] CONTEXT The long-term risk for developing hypertension is best described by the lifetime risk statistic.\n[1] The lifetime risk for hypertension and trends in this risk over time are unknown.\n[2] OBJECTIVES To estimate the residual lifetime risk for hypertension in older US adults and to evaluate temporal trends in this risk.\n[3] DESIGN, SETTING, AND PARTICIPANTS Community-based prospective cohort study of 1298 participants from the Framingham Heart Study who were aged 55 to 65 years and free of hypertension at baseline (1976-1998).\n[4] MAIN OUTCOME MEASURES Residual lifetime risk (lifetime cumulative incidence not adjusted for competing causes of mortality) for hypertension, defined as blood pressure of 140/90 mm Hg or greater or use of antihypertensive medications.\n[5] RESULTS The residual lifetime risks for developing hypertension and stage 1 high blood pressure or higher (greater-than-or-equal to 140/90 mm Hg regardless of treatment) were 90% in both 55- and 65-year-old participants.\n[6] The lifetime probability of receiving antihypertensive medication was 60%.\n[7] The risk for hypertension remained unchanged for women, but it was approximately 60% higher for men in the contemporary 1976-1998 period compared with an earlier 1952-1975 period.\n[8] In contrast, the residual lifetime risk for stage 2 high blood pressure or higher (greater-than-or-equal to 160/100 mm Hg regardless of treatment) was considerably lower in both sexes in the recent period (35%-57% in 1952-1975 vs 35%-44% in 1976-1998), likely due to a marked increase in treatment of individuals with substantially elevated blood pressure.\n[9] CONCLUSION The residual lifetime risk for hypertension for middle-aged and elderly individuals is 90%, indicating a huge public health burden.\n[10] Although the decline in lifetime risk for stage 2 high blood pressure or higher represents a major achievement, efforts should be directed at the primary prevention of hypertension."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"RESULTS The residual lifetime risks for developing hypertension and stage 1 high blood pressure or higher (greater-than-or-equal to 140/90 mm Hg regardless of treatment) were 90% in both 55- and 65-year-old participants.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 854, "doc_id": 12206390, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [12206390], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Nonhypertensive people who are 55 years old have a 90% chance of developing hypertension during their lifetime.\n\nDocument title: Residual lifetime risk for developing hypertension in middle-aged women and men: The Framingham Heart Study.\n\nAbstract sentences:\n[0] CONTEXT The long-term risk for developing hypertension is best described by the lifetime risk statistic.\n[1] The lifetime risk for hypertension and trends in this risk over time are unknown.\n[2] OBJECTIVES To estimate the residual lifetime risk for hypertension in older US adults and to evaluate temporal trends in this risk.\n[3] DESIGN, SETTING, AND PARTICIPANTS Community-based prospective cohort study of 1298 participants from the Framingham Heart Study who were aged 55 to 65 years and free of hypertension at baseline (1976-1998).\n[4] MAIN OUTCOME MEASURES Residual lifetime risk (lifetime cumulative incidence not adjusted for competing causes of mortality) for hypertension, defined as blood pressure of 140/90 mm Hg or greater or use of antihypertensive medications.\n[5] RESULTS The residual lifetime risks for developing hypertension and stage 1 high blood pressure or higher (greater-than-or-equal to 140/90 mm Hg regardless of treatment) were 90% in both 55- and 65-year-old participants.\n[6] The lifetime probability of receiving antihypertensive medication was 60%.\n[7] The risk for hypertension remained unchanged for women, but it was approximately 60% higher for men in the contemporary 1976-1998 period compared with an earlier 1952-1975 period.\n[8] In contrast, the residual lifetime risk for stage 2 high blood pressure or higher (greater-than-or-equal to 160/100 mm Hg regardless of treatment) was considerably lower in both sexes in the recent period (35%-57% in 1952-1975 vs 35%-44% in 1976-1998), likely due to a marked increase in treatment of individuals with substantially elevated blood pressure.\n[9] CONCLUSION The residual lifetime risk for hypertension for middle-aged and elderly individuals is 90%, indicating a huge public health burden.\n[10] Although the decline in lifetime risk for stage 2 high blood pressure or higher represents a major achievement, efforts should be directed at the primary prevention of hypertension."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"CONCLUSION The residual lifetime risk for hypertension for middle-aged and elderly individuals is 90%, indicating a huge public health burden.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 854, "doc_id": 12206390, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [12206390], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Noninvasive positive pressure ventilation is not predictive of acute respiratory failure after solid organ transplantation.\n\nDocument title: Noninvasive ventilation for treatment of acute respiratory failure in patients undergoing solid organ transplantation: a randomized trial.\n\nAbstract sentences:\n[0] CONTEXT Noninvasive ventilation (NIV) has been associated with lower rates of endotracheal intubation in populations of patients with acute respiratory failure.\n[1] OBJECTIVE To compare NIV with standard treatment using supplemental oxygen administration to avoid endotracheal intubation in recipients of solid organ transplantation with acute hypoxemic respiratory failure.\n[2] DESIGN AND SETTING Prospective randomized study conducted at a 14-bed, general intensive care unit of a university hospital.\n[3] PATIENTS Of 238 patients who underwent solid organ transplantation from December 1995 to October 1997, 51 were treated for acute respiratory failure.\n[4] Of these, 40 were eligible and 20 were randomized to each group.\n[5] INTERVENTION Noninvasive ventilation vs standard treatment with supplemental oxygen administration.\n[6] MAIN OUTCOME MEASURES The need for endotracheal intubation and mechanical ventilation at any time during the study, complications not present on admission, duration of ventilatory assistance, length of hospital stay, and intensive care unit mortality.\n[7] RESULTS The 2 groups were similar at study entry.\n[8] Within the first hour of treatment, 14 patients (70%) in the NIV group, and 5 patients (25%) in the standard treatment group improved their ratio of the PaO2 to the fraction of inspired oxygen (FIO2).\n[9] Over time, a sustained improvement in PaO2 to FIO2 was noted in 12 patients (60%) in the NIV group, and in 5 patients (25%) randomized to standard treatment (P = .03).\n[10] The use of NIV was associated with a significant reduction in the rate of endotracheal intubation (20% vs 70%; P = .002), rate of fatal complications (20% vs 50%; P = .05), length of stay in the intensive care unit by survivors (mean [SD] days, 5.5 [3] vs 9 [4]; P = .03), and intensive care unit mortality (20% vs 50%; P = .05).\n[11] Hospital mortality did not differ.\n[12] CONCLUSIONS These results indicate that transplantation programs should consider NIV in the treatment of selected recipients of transplantation with acute respiratory failure."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Within the first hour of treatment, 14 patients (70%) in the NIV group, and 5 patients (25%) in the standard treatment group improved their ratio of the PaO2 to the fraction of inspired oxygen (FIO2).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 855, "doc_id": 8190282, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [8190282], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Noninvasive positive pressure ventilation is not predictive of acute respiratory failure after solid organ transplantation.\n\nDocument title: Noninvasive ventilation for treatment of acute respiratory failure in patients undergoing solid organ transplantation: a randomized trial.\n\nAbstract sentences:\n[0] CONTEXT Noninvasive ventilation (NIV) has been associated with lower rates of endotracheal intubation in populations of patients with acute respiratory failure.\n[1] OBJECTIVE To compare NIV with standard treatment using supplemental oxygen administration to avoid endotracheal intubation in recipients of solid organ transplantation with acute hypoxemic respiratory failure.\n[2] DESIGN AND SETTING Prospective randomized study conducted at a 14-bed, general intensive care unit of a university hospital.\n[3] PATIENTS Of 238 patients who underwent solid organ transplantation from December 1995 to October 1997, 51 were treated for acute respiratory failure.\n[4] Of these, 40 were eligible and 20 were randomized to each group.\n[5] INTERVENTION Noninvasive ventilation vs standard treatment with supplemental oxygen administration.\n[6] MAIN OUTCOME MEASURES The need for endotracheal intubation and mechanical ventilation at any time during the study, complications not present on admission, duration of ventilatory assistance, length of hospital stay, and intensive care unit mortality.\n[7] RESULTS The 2 groups were similar at study entry.\n[8] Within the first hour of treatment, 14 patients (70%) in the NIV group, and 5 patients (25%) in the standard treatment group improved their ratio of the PaO2 to the fraction of inspired oxygen (FIO2).\n[9] Over time, a sustained improvement in PaO2 to FIO2 was noted in 12 patients (60%) in the NIV group, and in 5 patients (25%) randomized to standard treatment (P = .03).\n[10] The use of NIV was associated with a significant reduction in the rate of endotracheal intubation (20% vs 70%; P = .002), rate of fatal complications (20% vs 50%; P = .05), length of stay in the intensive care unit by survivors (mean [SD] days, 5.5 [3] vs 9 [4]; P = .03), and intensive care unit mortality (20% vs 50%; P = .05).\n[11] Hospital mortality did not differ.\n[12] CONCLUSIONS These results indicate that transplantation programs should consider NIV in the treatment of selected recipients of transplantation with acute respiratory failure."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Over time, a sustained improvement in PaO2 to FIO2 was noted in 12 patients (60%) in the NIV group, and in 5 patients (25%) randomized to standard treatment (P = .03).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 855, "doc_id": 8190282, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [8190282], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Noninvasive positive pressure ventilation is not predictive of acute respiratory failure after solid organ transplantation.\n\nDocument title: Noninvasive ventilation for treatment of acute respiratory failure in patients undergoing solid organ transplantation: a randomized trial.\n\nAbstract sentences:\n[0] CONTEXT Noninvasive ventilation (NIV) has been associated with lower rates of endotracheal intubation in populations of patients with acute respiratory failure.\n[1] OBJECTIVE To compare NIV with standard treatment using supplemental oxygen administration to avoid endotracheal intubation in recipients of solid organ transplantation with acute hypoxemic respiratory failure.\n[2] DESIGN AND SETTING Prospective randomized study conducted at a 14-bed, general intensive care unit of a university hospital.\n[3] PATIENTS Of 238 patients who underwent solid organ transplantation from December 1995 to October 1997, 51 were treated for acute respiratory failure.\n[4] Of these, 40 were eligible and 20 were randomized to each group.\n[5] INTERVENTION Noninvasive ventilation vs standard treatment with supplemental oxygen administration.\n[6] MAIN OUTCOME MEASURES The need for endotracheal intubation and mechanical ventilation at any time during the study, complications not present on admission, duration of ventilatory assistance, length of hospital stay, and intensive care unit mortality.\n[7] RESULTS The 2 groups were similar at study entry.\n[8] Within the first hour of treatment, 14 patients (70%) in the NIV group, and 5 patients (25%) in the standard treatment group improved their ratio of the PaO2 to the fraction of inspired oxygen (FIO2).\n[9] Over time, a sustained improvement in PaO2 to FIO2 was noted in 12 patients (60%) in the NIV group, and in 5 patients (25%) randomized to standard treatment (P = .03).\n[10] The use of NIV was associated with a significant reduction in the rate of endotracheal intubation (20% vs 70%; P = .002), rate of fatal complications (20% vs 50%; P = .05), length of stay in the intensive care unit by survivors (mean [SD] days, 5.5 [3] vs 9 [4]; P = .03), and intensive care unit mortality (20% vs 50%; P = .05).\n[11] Hospital mortality did not differ.\n[12] CONCLUSIONS These results indicate that transplantation programs should consider NIV in the treatment of selected recipients of transplantation with acute respiratory failure."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"The use of NIV was associated with a significant reduction in the rate of endotracheal intubation (20% vs 70%; P = .002), rate of fatal complications (20% vs 50%; P = .05), length of stay in the intensive care unit by survivors (mean [SD] days, 5.5 [3] vs 9 [4]; P = .03), and intensive care unit mortality (20% vs 50%; P = .05).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 855, "doc_id": 8190282, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [8190282], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Noninvasive positive pressure ventilation is not predictive of acute respiratory failure after solid organ transplantation.\n\nDocument title: Noninvasive ventilation for treatment of acute respiratory failure in patients undergoing solid organ transplantation: a randomized trial.\n\nAbstract sentences:\n[0] CONTEXT Noninvasive ventilation (NIV) has been associated with lower rates of endotracheal intubation in populations of patients with acute respiratory failure.\n[1] OBJECTIVE To compare NIV with standard treatment using supplemental oxygen administration to avoid endotracheal intubation in recipients of solid organ transplantation with acute hypoxemic respiratory failure.\n[2] DESIGN AND SETTING Prospective randomized study conducted at a 14-bed, general intensive care unit of a university hospital.\n[3] PATIENTS Of 238 patients who underwent solid organ transplantation from December 1995 to October 1997, 51 were treated for acute respiratory failure.\n[4] Of these, 40 were eligible and 20 were randomized to each group.\n[5] INTERVENTION Noninvasive ventilation vs standard treatment with supplemental oxygen administration.\n[6] MAIN OUTCOME MEASURES The need for endotracheal intubation and mechanical ventilation at any time during the study, complications not present on admission, duration of ventilatory assistance, length of hospital stay, and intensive care unit mortality.\n[7] RESULTS The 2 groups were similar at study entry.\n[8] Within the first hour of treatment, 14 patients (70%) in the NIV group, and 5 patients (25%) in the standard treatment group improved their ratio of the PaO2 to the fraction of inspired oxygen (FIO2).\n[9] Over time, a sustained improvement in PaO2 to FIO2 was noted in 12 patients (60%) in the NIV group, and in 5 patients (25%) randomized to standard treatment (P = .03).\n[10] The use of NIV was associated with a significant reduction in the rate of endotracheal intubation (20% vs 70%; P = .002), rate of fatal complications (20% vs 50%; P = .05), length of stay in the intensive care unit by survivors (mean [SD] days, 5.5 [3] vs 9 [4]; P = .03), and intensive care unit mortality (20% vs 50%; P = .05).\n[11] Hospital mortality did not differ.\n[12] CONCLUSIONS These results indicate that transplantation programs should consider NIV in the treatment of selected recipients of transplantation with acute respiratory failure."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"CONCLUSIONS These results indicate that transplantation programs should consider NIV in the treatment of selected recipients of transplantation with acute respiratory failure.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 855, "doc_id": 8190282, "label": "CONTRADICTS", "evidence_sentence_ids": [12], "cited_doc_ids": [8190282], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Nonsteroidal antinflammatory drugs are ineffective as cancer treatments.\n\nDocument title: Association of aspirin and NSAID use with risk of colorectal cancer according to genetic variants.\n\nAbstract sentences:\n[0] IMPORTANCE Use of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with lower risk of colorectal cancer.\n[1] OBJECTIVE To identify common genetic markers that may confer differential benefit from aspirin or NSAID chemoprevention, we tested gene × environment interactions between regular use of aspirin and/or NSAIDs and single-nucleotide polymorphisms (SNPs) in relation to risk of colorectal cancer.\n[2] DESIGN, SETTING, AND PARTICIPANTS Case-control study using data from 5 case-control and 5 cohort studies initiated between 1976 and 2003 across the United States, Canada, Australia, and Germany and including colorectal cancer cases (n=8634) and matched controls (n=8553) ascertained between 1976 and 2011.\n[3] Participants were all of European descent.\n[4] EXPOSURES Genome-wide SNP data and information on regular use of aspirin and/or NSAIDs and other risk factors.\n[5] MAIN OUTCOMES AND MEASURES Colorectal cancer.\n[6] RESULTS Regular use of aspirin and/or NSAIDs was associated with lower risk of colorectal cancer (prevalence, 28% vs 38%; odds ratio [OR], 0.69 [95% CI, 0.64-0.74]; P = 6.2 × 10(-28)) compared with nonregular use.\n[7] In the conventional logistic regression analysis, the SNP rs2965667 at chromosome 12p12.3 near the MGST1 gene showed a genome-wide significant interaction with aspirin and/or NSAID use (P = 4.6 × 10(-9) for interaction).\n[8] Aspirin and/or NSAID use was associated with a lower risk of colorectal cancer among individuals with rs2965667-TT genotype (prevalence, 28% vs 38%; OR, 0.66 [95% CI, 0.61-0.70]; P = 7.7 × 10(-33)) but with a higher risk among those with rare (4%) TA or AA genotypes (prevalence, 35% vs 29%; OR, 1.89 [95% CI, 1.27-2.81]; P = .002).\n[9] In case-only interaction analysis, the SNP rs16973225 at chromosome 15q25.2 near the IL16 gene showed a genome-wide significant interaction with use of aspirin and/or NSAIDs (P = 8.2 × 10(-9) for interaction).\n[10] Regular use was associated with a lower risk of colorectal cancer among individuals with rs16973225-AA genotype (prevalence, 28% vs 38%; OR, 0.66 [95% CI, 0.62-0.71]; P = 1.9 × 10(-30)) but was not associated with risk of colorectal cancer among those with less common (9%) AC or CC genotypes (prevalence, 36% vs 39%; OR, 0.97 [95% CI, 0.78-1.20]; P = .76).\n[11] CONCLUSIONS AND RELEVANCE In this genome-wide investigation of gene × environment interactions, use of aspirin and/or NSAIDs was associated with lower risk of colorectal cancer, and this association differed according to genetic variation at 2 SNPs at chromosomes 12 and 15.\n[12] Validation of these findings in additional populations may facilitate targeted colorectal cancer prevention strategies."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"RESULTS Regular use of aspirin and/or NSAIDs was associated with lower risk of colorectal cancer (prevalence, 28% vs 38%; odds ratio [OR], 0.69 [95% CI, 0.64-0.74]; P = 6.2 × 10(-28)) compared with nonregular use.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 856, "doc_id": 43334921, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [43334921], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Nonsteroidal antinflammatory drugs are ineffective as cancer treatments.\n\nDocument title: Association of aspirin and NSAID use with risk of colorectal cancer according to genetic variants.\n\nAbstract sentences:\n[0] IMPORTANCE Use of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with lower risk of colorectal cancer.\n[1] OBJECTIVE To identify common genetic markers that may confer differential benefit from aspirin or NSAID chemoprevention, we tested gene × environment interactions between regular use of aspirin and/or NSAIDs and single-nucleotide polymorphisms (SNPs) in relation to risk of colorectal cancer.\n[2] DESIGN, SETTING, AND PARTICIPANTS Case-control study using data from 5 case-control and 5 cohort studies initiated between 1976 and 2003 across the United States, Canada, Australia, and Germany and including colorectal cancer cases (n=8634) and matched controls (n=8553) ascertained between 1976 and 2011.\n[3] Participants were all of European descent.\n[4] EXPOSURES Genome-wide SNP data and information on regular use of aspirin and/or NSAIDs and other risk factors.\n[5] MAIN OUTCOMES AND MEASURES Colorectal cancer.\n[6] RESULTS Regular use of aspirin and/or NSAIDs was associated with lower risk of colorectal cancer (prevalence, 28% vs 38%; odds ratio [OR], 0.69 [95% CI, 0.64-0.74]; P = 6.2 × 10(-28)) compared with nonregular use.\n[7] In the conventional logistic regression analysis, the SNP rs2965667 at chromosome 12p12.3 near the MGST1 gene showed a genome-wide significant interaction with aspirin and/or NSAID use (P = 4.6 × 10(-9) for interaction).\n[8] Aspirin and/or NSAID use was associated with a lower risk of colorectal cancer among individuals with rs2965667-TT genotype (prevalence, 28% vs 38%; OR, 0.66 [95% CI, 0.61-0.70]; P = 7.7 × 10(-33)) but with a higher risk among those with rare (4%) TA or AA genotypes (prevalence, 35% vs 29%; OR, 1.89 [95% CI, 1.27-2.81]; P = .002).\n[9] In case-only interaction analysis, the SNP rs16973225 at chromosome 15q25.2 near the IL16 gene showed a genome-wide significant interaction with use of aspirin and/or NSAIDs (P = 8.2 × 10(-9) for interaction).\n[10] Regular use was associated with a lower risk of colorectal cancer among individuals with rs16973225-AA genotype (prevalence, 28% vs 38%; OR, 0.66 [95% CI, 0.62-0.71]; P = 1.9 × 10(-30)) but was not associated with risk of colorectal cancer among those with less common (9%) AC or CC genotypes (prevalence, 36% vs 39%; OR, 0.97 [95% CI, 0.78-1.20]; P = .76).\n[11] CONCLUSIONS AND RELEVANCE In this genome-wide investigation of gene × environment interactions, use of aspirin and/or NSAIDs was associated with lower risk of colorectal cancer, and this association differed according to genetic variation at 2 SNPs at chromosomes 12 and 15.\n[12] Validation of these findings in additional populations may facilitate targeted colorectal cancer prevention strategies."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Aspirin and/or NSAID use was associated with a lower risk of colorectal cancer among individuals with rs2965667-TT genotype (prevalence, 28% vs 38%; OR, 0.66 [95% CI, 0.61-0.70]; P = 7.7 × 10(-33)) but with a higher risk among those with rare (4%) TA or AA genotypes (prevalence, 35% vs 29%; OR, 1.89 [95% CI, 1.27-2.81]; P = .002).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 856, "doc_id": 43334921, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [43334921], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Nonsteroidal antinflammatory drugs are ineffective as cancer treatments.\n\nDocument title: Association of aspirin and NSAID use with risk of colorectal cancer according to genetic variants.\n\nAbstract sentences:\n[0] IMPORTANCE Use of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with lower risk of colorectal cancer.\n[1] OBJECTIVE To identify common genetic markers that may confer differential benefit from aspirin or NSAID chemoprevention, we tested gene × environment interactions between regular use of aspirin and/or NSAIDs and single-nucleotide polymorphisms (SNPs) in relation to risk of colorectal cancer.\n[2] DESIGN, SETTING, AND PARTICIPANTS Case-control study using data from 5 case-control and 5 cohort studies initiated between 1976 and 2003 across the United States, Canada, Australia, and Germany and including colorectal cancer cases (n=8634) and matched controls (n=8553) ascertained between 1976 and 2011.\n[3] Participants were all of European descent.\n[4] EXPOSURES Genome-wide SNP data and information on regular use of aspirin and/or NSAIDs and other risk factors.\n[5] MAIN OUTCOMES AND MEASURES Colorectal cancer.\n[6] RESULTS Regular use of aspirin and/or NSAIDs was associated with lower risk of colorectal cancer (prevalence, 28% vs 38%; odds ratio [OR], 0.69 [95% CI, 0.64-0.74]; P = 6.2 × 10(-28)) compared with nonregular use.\n[7] In the conventional logistic regression analysis, the SNP rs2965667 at chromosome 12p12.3 near the MGST1 gene showed a genome-wide significant interaction with aspirin and/or NSAID use (P = 4.6 × 10(-9) for interaction).\n[8] Aspirin and/or NSAID use was associated with a lower risk of colorectal cancer among individuals with rs2965667-TT genotype (prevalence, 28% vs 38%; OR, 0.66 [95% CI, 0.61-0.70]; P = 7.7 × 10(-33)) but with a higher risk among those with rare (4%) TA or AA genotypes (prevalence, 35% vs 29%; OR, 1.89 [95% CI, 1.27-2.81]; P = .002).\n[9] In case-only interaction analysis, the SNP rs16973225 at chromosome 15q25.2 near the IL16 gene showed a genome-wide significant interaction with use of aspirin and/or NSAIDs (P = 8.2 × 10(-9) for interaction).\n[10] Regular use was associated with a lower risk of colorectal cancer among individuals with rs16973225-AA genotype (prevalence, 28% vs 38%; OR, 0.66 [95% CI, 0.62-0.71]; P = 1.9 × 10(-30)) but was not associated with risk of colorectal cancer among those with less common (9%) AC or CC genotypes (prevalence, 36% vs 39%; OR, 0.97 [95% CI, 0.78-1.20]; P = .76).\n[11] CONCLUSIONS AND RELEVANCE In this genome-wide investigation of gene × environment interactions, use of aspirin and/or NSAIDs was associated with lower risk of colorectal cancer, and this association differed according to genetic variation at 2 SNPs at chromosomes 12 and 15.\n[12] Validation of these findings in additional populations may facilitate targeted colorectal cancer prevention strategies."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Regular use was associated with a lower risk of colorectal cancer among individuals with rs16973225-AA genotype (prevalence, 28% vs 38%; OR, 0.66 [95% CI, 0.62-0.71]; P = 1.9 × 10(-30)) but was not associated with risk of colorectal cancer among those with less common (9%) AC or CC genotypes (prevalence, 36% vs 39%; OR, 0.97 [95% CI, 0.78-1.20]; P = .76).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 856, "doc_id": 43334921, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [43334921], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Nonsteroidal antinflammatory drugs show potential anticancer indications.\n\nDocument title: Association of aspirin and NSAID use with risk of colorectal cancer according to genetic variants.\n\nAbstract sentences:\n[0] IMPORTANCE Use of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with lower risk of colorectal cancer.\n[1] OBJECTIVE To identify common genetic markers that may confer differential benefit from aspirin or NSAID chemoprevention, we tested gene × environment interactions between regular use of aspirin and/or NSAIDs and single-nucleotide polymorphisms (SNPs) in relation to risk of colorectal cancer.\n[2] DESIGN, SETTING, AND PARTICIPANTS Case-control study using data from 5 case-control and 5 cohort studies initiated between 1976 and 2003 across the United States, Canada, Australia, and Germany and including colorectal cancer cases (n=8634) and matched controls (n=8553) ascertained between 1976 and 2011.\n[3] Participants were all of European descent.\n[4] EXPOSURES Genome-wide SNP data and information on regular use of aspirin and/or NSAIDs and other risk factors.\n[5] MAIN OUTCOMES AND MEASURES Colorectal cancer.\n[6] RESULTS Regular use of aspirin and/or NSAIDs was associated with lower risk of colorectal cancer (prevalence, 28% vs 38%; odds ratio [OR], 0.69 [95% CI, 0.64-0.74]; P = 6.2 × 10(-28)) compared with nonregular use.\n[7] In the conventional logistic regression analysis, the SNP rs2965667 at chromosome 12p12.3 near the MGST1 gene showed a genome-wide significant interaction with aspirin and/or NSAID use (P = 4.6 × 10(-9) for interaction).\n[8] Aspirin and/or NSAID use was associated with a lower risk of colorectal cancer among individuals with rs2965667-TT genotype (prevalence, 28% vs 38%; OR, 0.66 [95% CI, 0.61-0.70]; P = 7.7 × 10(-33)) but with a higher risk among those with rare (4%) TA or AA genotypes (prevalence, 35% vs 29%; OR, 1.89 [95% CI, 1.27-2.81]; P = .002).\n[9] In case-only interaction analysis, the SNP rs16973225 at chromosome 15q25.2 near the IL16 gene showed a genome-wide significant interaction with use of aspirin and/or NSAIDs (P = 8.2 × 10(-9) for interaction).\n[10] Regular use was associated with a lower risk of colorectal cancer among individuals with rs16973225-AA genotype (prevalence, 28% vs 38%; OR, 0.66 [95% CI, 0.62-0.71]; P = 1.9 × 10(-30)) but was not associated with risk of colorectal cancer among those with less common (9%) AC or CC genotypes (prevalence, 36% vs 39%; OR, 0.97 [95% CI, 0.78-1.20]; P = .76).\n[11] CONCLUSIONS AND RELEVANCE In this genome-wide investigation of gene × environment interactions, use of aspirin and/or NSAIDs was associated with lower risk of colorectal cancer, and this association differed according to genetic variation at 2 SNPs at chromosomes 12 and 15.\n[12] Validation of these findings in additional populations may facilitate targeted colorectal cancer prevention strategies."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"RESULTS Regular use of aspirin and/or NSAIDs was associated with lower risk of colorectal cancer (prevalence, 28% vs 38%; odds ratio [OR], 0.69 [95% CI, 0.64-0.74]; P = 6.2 × 10(-28)) compared with nonregular use.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 857, "doc_id": 43334921, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [43334921], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Nonsteroidal antinflammatory drugs show potential anticancer indications.\n\nDocument title: Association of aspirin and NSAID use with risk of colorectal cancer according to genetic variants.\n\nAbstract sentences:\n[0] IMPORTANCE Use of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with lower risk of colorectal cancer.\n[1] OBJECTIVE To identify common genetic markers that may confer differential benefit from aspirin or NSAID chemoprevention, we tested gene × environment interactions between regular use of aspirin and/or NSAIDs and single-nucleotide polymorphisms (SNPs) in relation to risk of colorectal cancer.\n[2] DESIGN, SETTING, AND PARTICIPANTS Case-control study using data from 5 case-control and 5 cohort studies initiated between 1976 and 2003 across the United States, Canada, Australia, and Germany and including colorectal cancer cases (n=8634) and matched controls (n=8553) ascertained between 1976 and 2011.\n[3] Participants were all of European descent.\n[4] EXPOSURES Genome-wide SNP data and information on regular use of aspirin and/or NSAIDs and other risk factors.\n[5] MAIN OUTCOMES AND MEASURES Colorectal cancer.\n[6] RESULTS Regular use of aspirin and/or NSAIDs was associated with lower risk of colorectal cancer (prevalence, 28% vs 38%; odds ratio [OR], 0.69 [95% CI, 0.64-0.74]; P = 6.2 × 10(-28)) compared with nonregular use.\n[7] In the conventional logistic regression analysis, the SNP rs2965667 at chromosome 12p12.3 near the MGST1 gene showed a genome-wide significant interaction with aspirin and/or NSAID use (P = 4.6 × 10(-9) for interaction).\n[8] Aspirin and/or NSAID use was associated with a lower risk of colorectal cancer among individuals with rs2965667-TT genotype (prevalence, 28% vs 38%; OR, 0.66 [95% CI, 0.61-0.70]; P = 7.7 × 10(-33)) but with a higher risk among those with rare (4%) TA or AA genotypes (prevalence, 35% vs 29%; OR, 1.89 [95% CI, 1.27-2.81]; P = .002).\n[9] In case-only interaction analysis, the SNP rs16973225 at chromosome 15q25.2 near the IL16 gene showed a genome-wide significant interaction with use of aspirin and/or NSAIDs (P = 8.2 × 10(-9) for interaction).\n[10] Regular use was associated with a lower risk of colorectal cancer among individuals with rs16973225-AA genotype (prevalence, 28% vs 38%; OR, 0.66 [95% CI, 0.62-0.71]; P = 1.9 × 10(-30)) but was not associated with risk of colorectal cancer among those with less common (9%) AC or CC genotypes (prevalence, 36% vs 39%; OR, 0.97 [95% CI, 0.78-1.20]; P = .76).\n[11] CONCLUSIONS AND RELEVANCE In this genome-wide investigation of gene × environment interactions, use of aspirin and/or NSAIDs was associated with lower risk of colorectal cancer, and this association differed according to genetic variation at 2 SNPs at chromosomes 12 and 15.\n[12] Validation of these findings in additional populations may facilitate targeted colorectal cancer prevention strategies."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Aspirin and/or NSAID use was associated with a lower risk of colorectal cancer among individuals with rs2965667-TT genotype (prevalence, 28% vs 38%; OR, 0.66 [95% CI, 0.61-0.70]; P = 7.7 × 10(-33)) but with a higher risk among those with rare (4%) TA or AA genotypes (prevalence, 35% vs 29%; OR, 1.89 [95% CI, 1.27-2.81]; P = .002).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 857, "doc_id": 43334921, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [43334921], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Nonsteroidal antinflammatory drugs show potential anticancer indications.\n\nDocument title: Association of aspirin and NSAID use with risk of colorectal cancer according to genetic variants.\n\nAbstract sentences:\n[0] IMPORTANCE Use of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with lower risk of colorectal cancer.\n[1] OBJECTIVE To identify common genetic markers that may confer differential benefit from aspirin or NSAID chemoprevention, we tested gene × environment interactions between regular use of aspirin and/or NSAIDs and single-nucleotide polymorphisms (SNPs) in relation to risk of colorectal cancer.\n[2] DESIGN, SETTING, AND PARTICIPANTS Case-control study using data from 5 case-control and 5 cohort studies initiated between 1976 and 2003 across the United States, Canada, Australia, and Germany and including colorectal cancer cases (n=8634) and matched controls (n=8553) ascertained between 1976 and 2011.\n[3] Participants were all of European descent.\n[4] EXPOSURES Genome-wide SNP data and information on regular use of aspirin and/or NSAIDs and other risk factors.\n[5] MAIN OUTCOMES AND MEASURES Colorectal cancer.\n[6] RESULTS Regular use of aspirin and/or NSAIDs was associated with lower risk of colorectal cancer (prevalence, 28% vs 38%; odds ratio [OR], 0.69 [95% CI, 0.64-0.74]; P = 6.2 × 10(-28)) compared with nonregular use.\n[7] In the conventional logistic regression analysis, the SNP rs2965667 at chromosome 12p12.3 near the MGST1 gene showed a genome-wide significant interaction with aspirin and/or NSAID use (P = 4.6 × 10(-9) for interaction).\n[8] Aspirin and/or NSAID use was associated with a lower risk of colorectal cancer among individuals with rs2965667-TT genotype (prevalence, 28% vs 38%; OR, 0.66 [95% CI, 0.61-0.70]; P = 7.7 × 10(-33)) but with a higher risk among those with rare (4%) TA or AA genotypes (prevalence, 35% vs 29%; OR, 1.89 [95% CI, 1.27-2.81]; P = .002).\n[9] In case-only interaction analysis, the SNP rs16973225 at chromosome 15q25.2 near the IL16 gene showed a genome-wide significant interaction with use of aspirin and/or NSAIDs (P = 8.2 × 10(-9) for interaction).\n[10] Regular use was associated with a lower risk of colorectal cancer among individuals with rs16973225-AA genotype (prevalence, 28% vs 38%; OR, 0.66 [95% CI, 0.62-0.71]; P = 1.9 × 10(-30)) but was not associated with risk of colorectal cancer among those with less common (9%) AC or CC genotypes (prevalence, 36% vs 39%; OR, 0.97 [95% CI, 0.78-1.20]; P = .76).\n[11] CONCLUSIONS AND RELEVANCE In this genome-wide investigation of gene × environment interactions, use of aspirin and/or NSAIDs was associated with lower risk of colorectal cancer, and this association differed according to genetic variation at 2 SNPs at chromosomes 12 and 15.\n[12] Validation of these findings in additional populations may facilitate targeted colorectal cancer prevention strategies."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Regular use was associated with a lower risk of colorectal cancer among individuals with rs16973225-AA genotype (prevalence, 28% vs 38%; OR, 0.66 [95% CI, 0.62-0.71]; P = 1.9 × 10(-30)) but was not associated with risk of colorectal cancer among those with less common (9%) AC or CC genotypes (prevalence, 36% vs 39%; OR, 0.97 [95% CI, 0.78-1.20]; P = .76).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 857, "doc_id": 43334921, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [43334921], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Normal expression of RUNX1 causes tumorsupressing effects.\n\nDocument title: Reverse engineering of TLX oncogenic transcriptional networks identifies RUNX1 as tumor suppressor in T-ALL\n\nAbstract sentences:\n[0] The TLX1 and TLX3 transcription factor oncogenes have a key role in the pathogenesis of T cell acute lymphoblastic leukemia (T-ALL).\n[1] Here we used reverse engineering of global transcriptional networks to decipher the oncogenic regulatory circuit controlled by TLX1 and TLX3.\n[2] This systems biology analysis defined T cell leukemia homeobox 1 (TLX1) and TLX3 as master regulators of an oncogenic transcriptional circuit governing T-ALL.\n[3] Notably, a network structure analysis of this hierarchical network identified RUNX1 as a key mediator of the T-ALL induced by TLX1 and TLX3 and predicted a tumor-suppressor role for RUNX1 in T cell transformation.\n[4] Consistent with these results, we identified recurrent somatic loss-of-function mutations in RUNX1 in human T-ALL.\n[5] Overall, these results place TLX1 and TLX3 at the top of an oncogenic transcriptional network controlling leukemia development, show the power of network analyses to identify key elements in the regulatory circuits governing human cancer and identify RUNX1 as a tumor-suppressor gene in T-ALL."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Notably, a network structure analysis of this hierarchical network identified RUNX1 as a key mediator of the T-ALL induced by TLX1 and TLX3 and predicted a tumor-suppressor role for RUNX1 in T cell transformation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 858, "doc_id": 1982286, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [1982286], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Normal granulomas form in the absence of TNF in Zebrafish.\n\nDocument title: Tumor necrosis factor signaling mediates resistance to mycobacteria by inhibiting bacterial growth and macrophage death.\n\nAbstract sentences:\n[0] Tumor necrosis factor (TNF), a key effector in controlling tuberculosis, is thought to exert protection by directing formation of granulomas, organized aggregates of macrophages and other immune cells.\n[1] Loss of TNF signaling causes progression of tuberculosis in humans, and the increased mortality of Mycobacterium tuberculosis-infected mice is associated with disorganized necrotic granulomas, although the precise roles of TNF signaling preceding this endpoint remain undefined.\n[2] We monitored transparent Mycobacterium marinum-infected zebrafish live to conduct a stepwise dissection of how TNF signaling operates in mycobacterial pathogenesis.\n[3] We found that loss of TNF signaling caused increased mortality even when only innate immunity was operant.\n[4] In the absence of TNF, intracellular bacterial growth and granuloma formation were accelerated and was followed by necrotic death of overladen macrophages and granuloma breakdown.\n[5] Thus, TNF is not required for tuberculous granuloma formation, but maintains granuloma integrity indirectly by restricting mycobacterial growth within macrophages and preventing their necrosis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"In the absence of TNF, intracellular bacterial growth and granuloma formation were accelerated and was followed by necrotic death of overladen macrophages and granuloma breakdown.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 860, "doc_id": 16066726, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [16066726], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Normal granulomas form in the absence of TNF in Zebrafish.\n\nDocument title: Tumor necrosis factor signaling mediates resistance to mycobacteria by inhibiting bacterial growth and macrophage death.\n\nAbstract sentences:\n[0] Tumor necrosis factor (TNF), a key effector in controlling tuberculosis, is thought to exert protection by directing formation of granulomas, organized aggregates of macrophages and other immune cells.\n[1] Loss of TNF signaling causes progression of tuberculosis in humans, and the increased mortality of Mycobacterium tuberculosis-infected mice is associated with disorganized necrotic granulomas, although the precise roles of TNF signaling preceding this endpoint remain undefined.\n[2] We monitored transparent Mycobacterium marinum-infected zebrafish live to conduct a stepwise dissection of how TNF signaling operates in mycobacterial pathogenesis.\n[3] We found that loss of TNF signaling caused increased mortality even when only innate immunity was operant.\n[4] In the absence of TNF, intracellular bacterial growth and granuloma formation were accelerated and was followed by necrotic death of overladen macrophages and granuloma breakdown.\n[5] Thus, TNF is not required for tuberculous granuloma formation, but maintains granuloma integrity indirectly by restricting mycobacterial growth within macrophages and preventing their necrosis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Thus, TNF is not required for tuberculous granuloma formation, but maintains granuloma integrity indirectly by restricting mycobacterial growth within macrophages and preventing their necrosis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 860, "doc_id": 16066726, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [16066726], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Normal granulomas form in the presence of TNF in Zebrafish.\n\nDocument title: Tumor necrosis factor signaling mediates resistance to mycobacteria by inhibiting bacterial growth and macrophage death.\n\nAbstract sentences:\n[0] Tumor necrosis factor (TNF), a key effector in controlling tuberculosis, is thought to exert protection by directing formation of granulomas, organized aggregates of macrophages and other immune cells.\n[1] Loss of TNF signaling causes progression of tuberculosis in humans, and the increased mortality of Mycobacterium tuberculosis-infected mice is associated with disorganized necrotic granulomas, although the precise roles of TNF signaling preceding this endpoint remain undefined.\n[2] We monitored transparent Mycobacterium marinum-infected zebrafish live to conduct a stepwise dissection of how TNF signaling operates in mycobacterial pathogenesis.\n[3] We found that loss of TNF signaling caused increased mortality even when only innate immunity was operant.\n[4] In the absence of TNF, intracellular bacterial growth and granuloma formation were accelerated and was followed by necrotic death of overladen macrophages and granuloma breakdown.\n[5] Thus, TNF is not required for tuberculous granuloma formation, but maintains granuloma integrity indirectly by restricting mycobacterial growth within macrophages and preventing their necrosis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"In the absence of TNF, intracellular bacterial growth and granuloma formation were accelerated and was followed by necrotic death of overladen macrophages and granuloma breakdown.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 861, "doc_id": 16066726, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [16066726], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Normal granulomas form in the presence of TNF in Zebrafish.\n\nDocument title: Tumor necrosis factor signaling mediates resistance to mycobacteria by inhibiting bacterial growth and macrophage death.\n\nAbstract sentences:\n[0] Tumor necrosis factor (TNF), a key effector in controlling tuberculosis, is thought to exert protection by directing formation of granulomas, organized aggregates of macrophages and other immune cells.\n[1] Loss of TNF signaling causes progression of tuberculosis in humans, and the increased mortality of Mycobacterium tuberculosis-infected mice is associated with disorganized necrotic granulomas, although the precise roles of TNF signaling preceding this endpoint remain undefined.\n[2] We monitored transparent Mycobacterium marinum-infected zebrafish live to conduct a stepwise dissection of how TNF signaling operates in mycobacterial pathogenesis.\n[3] We found that loss of TNF signaling caused increased mortality even when only innate immunity was operant.\n[4] In the absence of TNF, intracellular bacterial growth and granuloma formation were accelerated and was followed by necrotic death of overladen macrophages and granuloma breakdown.\n[5] Thus, TNF is not required for tuberculous granuloma formation, but maintains granuloma integrity indirectly by restricting mycobacterial growth within macrophages and preventing their necrosis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Thus, TNF is not required for tuberculous granuloma formation, but maintains granuloma integrity indirectly by restricting mycobacterial growth within macrophages and preventing their necrosis.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 861, "doc_id": 16066726, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [16066726], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Notch signaling occurs between tumor cells and stromal cells.\n\nDocument title: Crosstalk between tumor and endothelial cells promotes tumor angiogenesis by MAPK activation of Notch signaling.\n\nAbstract sentences:\n[0] While significant progress has been made in understanding the induction of tumor vasculature by secreted angiogenic factors, little is known regarding contact-dependent signals that promote tumor angiogenesis.\n[1] Here, we report that the Notch ligand Jagged1 induced by growth factors via mitogen-activating protein kinase (MAPK) in head and neck squamous cell carcinoma (HNSCC) cells triggered Notch activation in neighboring endothelial cells (ECs) and promoted capillary-like sprout formation.\n[2] Jagged1-expressing HNSCC cells significantly enhanced neovascularization and tumor growth in vivo.\n[3] Moreover, the level of Jagged1 was significantly correlated with tumor blood vessel content and associated with HNSCC development.\n[4] Our results elucidate a novel mechanism by which the direct interplay between tumor cells and ECs promotes angiogenesis through MAPK and Notch signaling pathways."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Here, we report that the Notch ligand Jagged1 induced by growth factors via mitogen-activating protein kinase (MAPK) in head and neck squamous cell carcinoma (HNSCC) cells triggered Notch activation in neighboring endothelial cells (ECs) and promoted capillary-like sprout formation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 863, "doc_id": 20568364, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [20568364, 16361581], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Notch signaling occurs between tumor cells and stromal cells.\n\nDocument title: Crosstalk between tumor and endothelial cells promotes tumor angiogenesis by MAPK activation of Notch signaling.\n\nAbstract sentences:\n[0] While significant progress has been made in understanding the induction of tumor vasculature by secreted angiogenic factors, little is known regarding contact-dependent signals that promote tumor angiogenesis.\n[1] Here, we report that the Notch ligand Jagged1 induced by growth factors via mitogen-activating protein kinase (MAPK) in head and neck squamous cell carcinoma (HNSCC) cells triggered Notch activation in neighboring endothelial cells (ECs) and promoted capillary-like sprout formation.\n[2] Jagged1-expressing HNSCC cells significantly enhanced neovascularization and tumor growth in vivo.\n[3] Moreover, the level of Jagged1 was significantly correlated with tumor blood vessel content and associated with HNSCC development.\n[4] Our results elucidate a novel mechanism by which the direct interplay between tumor cells and ECs promotes angiogenesis through MAPK and Notch signaling pathways."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Our results elucidate a novel mechanism by which the direct interplay between tumor cells and ECs promotes angiogenesis through MAPK and Notch signaling pathways.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 863, "doc_id": 20568364, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [20568364, 16361581], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Notch signaling occurs between tumor cells and stromal cells.\n\nDocument title: Jagged1-induced Notch signaling drives proliferation of multiple myeloma cells.\n\nAbstract sentences:\n[0] Notch receptors expressed on hematopoietic stem cells interact with their ligands on bone marrow stromal cells and thereby control cell fate decisions and survival.\n[1] We recently demonstrated that Notch signaling is involved in proliferation and survival of B cell-derived tumor cells of classic Hodgkin disease and described a novel mechanism for the oncogenic capacity of Notch.\n[2] In this study we investigated whether Notch signaling is involved in the tight interactions between neoplastic plasma cells and their bone marrow microenvironment, which are essential for tumor cell growth in multiple myeloma (MM).\n[3] Here we demonstrate that Notch receptors and their ligand Jagged1 are highly expressed in cultured and primary MM cells, whereas nonneoplastic counterparts show low to undetectable levels of Notch.\n[4] Functional data indicate that ligand-induced Notch signaling is a growth factor for MM cells and suggest that these interactions contribute to myelomagenesis in vivo."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"We recently demonstrated that Notch signaling is involved in proliferation and survival of B cell-derived tumor cells of classic Hodgkin disease and described a novel mechanism for the oncogenic capacity of Notch.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 863, "doc_id": 16361581, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [20568364, 16361581], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Nuclear transfer from adult human fibroblasts to human oocytes can give rise to blastocysts containing expandable pluripotent cells.\n\nDocument title: Human somatic cell nuclear transfer using adult cells.\n\nAbstract sentences:\n[0] Derivation of patient-specific human pluripotent stem cells via somatic cell nuclear transfer (SCNT) has the potential for applications in a range of therapeutic contexts.\n[1] However, successful SCNT with human cells has proved challenging to achieve, and thus far has only been reported with fetal or infant somatic cells.\n[2] In this study, we describe the application of a recently developed methodology for the generation of human ESCs via SCNT using dermal fibroblasts from 35- and 75-year-old males.\n[3] Our study therefore demonstrates the applicability of SCNT for adult human cells and supports further investigation of SCNT as a strategy for regenerative medicine."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 866, "doc_id": 37822406, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [37822406], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Oat tolerant coeliac patients may have oat specific inflammatory cells in their small bowel mucosa.\n\nDocument title: The Molecular Basis for Oat Intolerance in Patients with Celiac Disease\n\nAbstract sentences:\n[0] Background  Celiac disease is a small intestinal inflammatory disorder characterized by malabsorption, nutrient deficiency, and a range of clinical manifestations.\n[1] It is caused by an inappropriate immune response to dietary gluten and is treated with a gluten-free diet.\n[2] Recent feeding studies have indicated oats to be safe for celiac disease patients, and oats are now often included in the celiac disease diet.\n[3] This study aimed to investigate whether oat intolerance exists in celiac disease and to characterize the cells and processes underlying this intolerance.\n[4] Methods and Findings  We selected for study nine adults with celiac disease who had a history of oats exposure.\n[5] Four of the patients had clinical symptoms on an oats-containing diet, and three of these four patients had intestinal inflammation typical of celiac disease at the time of oats exposure.\n[6] We established oats-avenin-specific and -reactive intestinal T-cell lines from these three patients, as well as from two other patients who appeared to tolerate oats.\n[7] The avenin-reactive T-cell lines recognized avenin peptides in the context of HLA-DQ2.\n[8] These peptides have sequences rich in proline and glutamine residues closely resembling wheat gluten epitopes.\n[9] Deamidation (glutamine→glutamic acid conversion) by tissue transglutaminase was involved in the avenin epitope formation.\n[10] Conclusions  We conclude that some celiac disease patients have avenin-reactive mucosal T-cells that can cause mucosal inflammation.\n[11] Oat intolerance may be a reason for villous atrophy and inflammation in patients with celiac disease who are eating oats but otherwise are adhering to a strict gluten-free diet.\n[12] Clinical follow-up of celiac disease patients eating oats is advisable."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"We established oats-avenin-specific and -reactive intestinal T-cell lines from these three patients, as well as from two other patients who appeared to tolerate oats.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 867, "doc_id": 14340571, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [14340571], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Obesity decreases life quality.\n\nDocument title: Body-mass index and cause-specific mortality in 900 000 adults: collaborative analyses of 57 prospective studies.\n\nAbstract sentences:\n[0] BACKGROUND The main associations of body-mass index (BMI) with overall and cause-specific mortality can best be assessed by long-term prospective follow-up of large numbers of people.\n[1] The Prospective Studies Collaboration aimed to investigate these associations by sharing data from many studies.\n[2] METHODS Collaborative analyses were undertaken of baseline BMI versus mortality in 57 prospective studies with 894 576 participants, mostly in western Europe and North America (61% [n=541 452] male, mean recruitment age 46 [SD 11] years, median recruitment year 1979 [IQR 1975-85], mean BMI 25 [SD 4] kg/m(2)).\n[3] The analyses were adjusted for age, sex, smoking status, and study.\n[4] To limit reverse causality, the first 5 years of follow-up were excluded, leaving 66 552 deaths of known cause during a mean of 8 (SD 6) further years of follow-up (mean age at death 67 [SD 10] years): 30 416 vascular; 2070 diabetic, renal or hepatic; 22 592 neoplastic; 3770 respiratory; 7704 other.\n[5] FINDINGS In both sexes, mortality was lowest at about 22.5-25 kg/m(2).\n[6] Above this range, positive associations were recorded for several specific causes and inverse associations for none, the absolute excess risks for higher BMI and smoking were roughly additive, and each 5 kg/m(2) higher BMI was on average associated with about 30% higher overall mortality (hazard ratio per 5 kg/m(2) [HR] 1.29 [95% CI 1.27-1.32]): 40% for vascular mortality (HR 1.41 [1.37-1.45]); 60-120% for diabetic, renal, and hepatic mortality (HRs 2.16 [1.89-2.46], 1.59 [1.27-1.99], and 1.82 [1.59-2.09], respectively); 10% for neoplastic mortality (HR 1.10 [1.06-1.15]); and 20% for respiratory and for all other mortality (HRs 1.20 [1.07-1.34] and 1.20 [1.16-1.25], respectively).\n[7] Below the range 22.5-25 kg/m(2), BMI was associated inversely with overall mortality, mainly because of strong inverse associations with respiratory disease and lung cancer.\n[8] These inverse associations were much stronger for smokers than for non-smokers, despite cigarette consumption per smoker varying little with BMI.\n[9] INTERPRETATION Although other anthropometric measures (eg, waist circumference, waist-to-hip ratio) could well add extra information to BMI, and BMI to them, BMI is in itself a strong predictor of overall mortality both above and below the apparent optimum of about 22.5-25 kg/m(2).\n[10] The progressive excess mortality above this range is due mainly to vascular disease and is probably largely causal.\n[11] At 30-35 kg/m(2), median survival is reduced by 2-4 years; at 40-45 kg/m(2), it is reduced by 8-10 years (which is comparable with the effects of smoking).\n[12] The definite excess mortality below 22.5 kg/m(2) is due mainly to smoking-related diseases, and is not fully explained."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 871, "doc_id": 195689316, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [195689316], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Obesity raises life quality.\n\nDocument title: Body-mass index and cause-specific mortality in 900 000 adults: collaborative analyses of 57 prospective studies.\n\nAbstract sentences:\n[0] BACKGROUND The main associations of body-mass index (BMI) with overall and cause-specific mortality can best be assessed by long-term prospective follow-up of large numbers of people.\n[1] The Prospective Studies Collaboration aimed to investigate these associations by sharing data from many studies.\n[2] METHODS Collaborative analyses were undertaken of baseline BMI versus mortality in 57 prospective studies with 894 576 participants, mostly in western Europe and North America (61% [n=541 452] male, mean recruitment age 46 [SD 11] years, median recruitment year 1979 [IQR 1975-85], mean BMI 25 [SD 4] kg/m(2)).\n[3] The analyses were adjusted for age, sex, smoking status, and study.\n[4] To limit reverse causality, the first 5 years of follow-up were excluded, leaving 66 552 deaths of known cause during a mean of 8 (SD 6) further years of follow-up (mean age at death 67 [SD 10] years): 30 416 vascular; 2070 diabetic, renal or hepatic; 22 592 neoplastic; 3770 respiratory; 7704 other.\n[5] FINDINGS In both sexes, mortality was lowest at about 22.5-25 kg/m(2).\n[6] Above this range, positive associations were recorded for several specific causes and inverse associations for none, the absolute excess risks for higher BMI and smoking were roughly additive, and each 5 kg/m(2) higher BMI was on average associated with about 30% higher overall mortality (hazard ratio per 5 kg/m(2) [HR] 1.29 [95% CI 1.27-1.32]): 40% for vascular mortality (HR 1.41 [1.37-1.45]); 60-120% for diabetic, renal, and hepatic mortality (HRs 2.16 [1.89-2.46], 1.59 [1.27-1.99], and 1.82 [1.59-2.09], respectively); 10% for neoplastic mortality (HR 1.10 [1.06-1.15]); and 20% for respiratory and for all other mortality (HRs 1.20 [1.07-1.34] and 1.20 [1.16-1.25], respectively).\n[7] Below the range 22.5-25 kg/m(2), BMI was associated inversely with overall mortality, mainly because of strong inverse associations with respiratory disease and lung cancer.\n[8] These inverse associations were much stronger for smokers than for non-smokers, despite cigarette consumption per smoker varying little with BMI.\n[9] INTERPRETATION Although other anthropometric measures (eg, waist circumference, waist-to-hip ratio) could well add extra information to BMI, and BMI to them, BMI is in itself a strong predictor of overall mortality both above and below the apparent optimum of about 22.5-25 kg/m(2).\n[10] The progressive excess mortality above this range is due mainly to vascular disease and is probably largely causal.\n[11] At 30-35 kg/m(2), median survival is reduced by 2-4 years; at 40-45 kg/m(2), it is reduced by 8-10 years (which is comparable with the effects of smoking).\n[12] The definite excess mortality below 22.5 kg/m(2) is due mainly to smoking-related diseases, and is not fully explained."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 876, "doc_id": 195689316, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [195689316], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Occipital activation levels are associated with auditory spatial performance in parietal regions of the brain.\n\nDocument title: A Functional Neuroimaging Study of Sound Localization: Visual Cortex Activity Predicts Performance in Early-Blind Individuals\n\nAbstract sentences:\n[0] Blind individuals often demonstrate enhanced nonvisual perceptual abilities.\n[1] However, the neural substrate that underlies this improved performance remains to be fully understood.\n[2] An earlier behavioral study demonstrated that some early-blind people localize sounds more accurately than sighted controls using monaural cues.\n[3] In order to investigate the neural basis of these behavioral differences in humans, we carried out functional imaging studies using positron emission tomography and a speaker array that permitted pseudo-free-field presentations within the scanner.\n[4] During binaural sound localization, a sighted control group showed decreased cerebral blood flow in the occipital lobe, which was not seen in early-blind individuals.\n[5] During monaural sound localization (one ear plugged), the subgroup of early-blind subjects who were behaviorally superior at sound localization displayed two activation foci in the occipital cortex.\n[6] This effect was not seen in blind persons who did not have superior monaural sound localization abilities, nor in sighted individuals.\n[7] The degree of activation of one of these foci was strongly correlated with sound localization accuracy across the entire group of blind subjects.\n[8] The results show that those blind persons who perform better than sighted persons recruit occipital areas to carry out auditory localization under monaural conditions.\n[9] We therefore conclude that computations carried out in the occipital cortex specifically underlie the enhanced capacity to use monaural cues.\n[10] Our findings shed light not only on intermodal compensatory mechanisms, but also on individual differences in these mechanisms and on inhibitory patterns that differ between sighted individuals and those deprived of vision early in life."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 877, "doc_id": 313394, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [313394], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Omnivores produce less trimethylamine N-oxide from dietary I-carnitine than vegans.\n\nDocument title: Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis\n\nAbstract sentences:\n[0] Intestinal microbiota metabolism of choline and phosphatidylcholine produces trimethylamine (TMA), which is further metabolized to a proatherogenic species, trimethylamine-N-oxide (TMAO).\n[1] We demonstrate here that metabolism by intestinal microbiota of dietary L-carnitine, a trimethylamine abundant in red meat, also produces TMAO and accelerates atherosclerosis in mice.\n[2] Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine through a microbiota-dependent mechanism.\n[3] The presence of specific bacterial taxa in human feces was associated with both plasma TMAO concentration and dietary status.\n[4] Plasma L-carnitine levels in subjects undergoing cardiac evaluation (n = 2,595) predicted increased risks for both prevalent cardiovascular disease (CVD) and incident major adverse cardiac events (myocardial infarction, stroke or death), but only among subjects with concurrently high TMAO levels.\n[5] Chronic dietary L-carnitine supplementation in mice altered cecal microbial composition, markedly enhanced synthesis of TMA and TMAO, and increased atherosclerosis, but this did not occur if intestinal microbiota was concurrently suppressed.\n[6] In mice with an intact intestinal microbiota, dietary supplementation with TMAO or either carnitine or choline reduced in vivo reverse cholesterol transport.\n[7] Intestinal microbiota may thus contribute to the well-established link between high levels of red meat consumption and CVD risk."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine through a microbiota-dependent mechanism.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 881, "doc_id": 14803797, "label": "CONTRADICTS", "evidence_sentence_ids": [2], "cited_doc_ids": [14803797], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Omnivores produce more trimethylamine N-oxide from dietary I-carnitine than vegans.\n\nDocument title: Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis\n\nAbstract sentences:\n[0] Intestinal microbiota metabolism of choline and phosphatidylcholine produces trimethylamine (TMA), which is further metabolized to a proatherogenic species, trimethylamine-N-oxide (TMAO).\n[1] We demonstrate here that metabolism by intestinal microbiota of dietary L-carnitine, a trimethylamine abundant in red meat, also produces TMAO and accelerates atherosclerosis in mice.\n[2] Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine through a microbiota-dependent mechanism.\n[3] The presence of specific bacterial taxa in human feces was associated with both plasma TMAO concentration and dietary status.\n[4] Plasma L-carnitine levels in subjects undergoing cardiac evaluation (n = 2,595) predicted increased risks for both prevalent cardiovascular disease (CVD) and incident major adverse cardiac events (myocardial infarction, stroke or death), but only among subjects with concurrently high TMAO levels.\n[5] Chronic dietary L-carnitine supplementation in mice altered cecal microbial composition, markedly enhanced synthesis of TMA and TMAO, and increased atherosclerosis, but this did not occur if intestinal microbiota was concurrently suppressed.\n[6] In mice with an intact intestinal microbiota, dietary supplementation with TMAO or either carnitine or choline reduced in vivo reverse cholesterol transport.\n[7] Intestinal microbiota may thus contribute to the well-established link between high levels of red meat consumption and CVD risk."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine through a microbiota-dependent mechanism.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 883, "doc_id": 14803797, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [14803797], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Omnivores produce more trimethylamine N-oxide from dietary I-carnitine than vegetarians.\n\nDocument title: Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis\n\nAbstract sentences:\n[0] Intestinal microbiota metabolism of choline and phosphatidylcholine produces trimethylamine (TMA), which is further metabolized to a proatherogenic species, trimethylamine-N-oxide (TMAO).\n[1] We demonstrate here that metabolism by intestinal microbiota of dietary L-carnitine, a trimethylamine abundant in red meat, also produces TMAO and accelerates atherosclerosis in mice.\n[2] Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine through a microbiota-dependent mechanism.\n[3] The presence of specific bacterial taxa in human feces was associated with both plasma TMAO concentration and dietary status.\n[4] Plasma L-carnitine levels in subjects undergoing cardiac evaluation (n = 2,595) predicted increased risks for both prevalent cardiovascular disease (CVD) and incident major adverse cardiac events (myocardial infarction, stroke or death), but only among subjects with concurrently high TMAO levels.\n[5] Chronic dietary L-carnitine supplementation in mice altered cecal microbial composition, markedly enhanced synthesis of TMA and TMAO, and increased atherosclerosis, but this did not occur if intestinal microbiota was concurrently suppressed.\n[6] In mice with an intact intestinal microbiota, dietary supplementation with TMAO or either carnitine or choline reduced in vivo reverse cholesterol transport.\n[7] Intestinal microbiota may thus contribute to the well-established link between high levels of red meat consumption and CVD risk."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine through a microbiota-dependent mechanism.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 884, "doc_id": 14803797, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [14803797], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: One in five surgical randomized controlled trials are discontinued early.\n\nDocument title: Discontinuation and non-publication of surgical randomised controlled trials: observational study\n\nAbstract sentences:\n[0] OBJECTIVE To determine the rate of early discontinuation and non-publication of randomised controlled trials involving patients undergoing surgery.\n[1] DESIGN Cross sectional observational study of registered and published trials.\n[2] SETTING Randomised controlled trials of interventions in patients undergoing a surgical procedure.\n[3] DATA SOURCES The ClinicalTrials.gov database was searched for interventional trials registered between January 2008 and December 2009 using the keyword \"surgery\".\n[4] Recruitment status was extracted from the ClinicalTrials.gov database.\n[5] A systematic search for studies published in peer reviewed journals was performed; if they were not found, results posted on the ClinicalTrials.gov results database were sought.\n[6] Email queries were sent to trial investigators of discontinued and unpublished completed trials if no reason for the respective status was disclosed.\n[7] MAIN OUTCOME MEASURES Trial discontinuation before completion and non-publication after completion.\n[8] Logistic regression was used to determine the effect of funding source on publication status, with adjustment for intervention type and trial size.\n[9] RESULTS Of 818 registered trials found using the keyword \"surgery\", 395 met the inclusion criteria.\n[10] Of these, 21% (81/395) were discontinued early, most commonly owing to poor recruitment (44%, 36/81).\n[11] The remaining 314 (79%) trials proceeded to completion, with a publication rate of 66% (208/314) at a median time of 4.9 (interquartile range 4.0-6.0) years from study completion to publication search.\n[12] A further 6% (20/314) of studies presented results on ClinicalTrials.gov without a corresponding peer reviewed publication.\n[13] Industry funding did not affect the rate of discontinuation (adjusted odds ratio 0.91, 95% confidence interval 0.54 to 1.55) but was associated with a lower odds of publication for completed trials (0.43, 0.26 to 0.72).\n[14] Investigators' email addresses for trials with an uncertain fate were identified for 71.4% (10/14) of discontinued trials and 83% (101/122) of unpublished studies.\n[15] Only 43% (6/14) and 20% (25/122) replies were received.\n[16] Email responses for completed trials indicated 11 trials in press, five published studies (four in non-indexed peer reviewed journals), and nine trials remaining unpublished.\n[17] CONCLUSIONS One in five surgical randomised controlled trials are discontinued early, one in three completed trials remain unpublished, and investigators of unpublished studies are frequently not contactable.\n[18] This represents a waste of research resources and raises ethical concerns regarding hidden clinical data and futile participation by patients with its attendant risks.\n[19] To promote future efficiency and transparency, changes are proposed to research governance frameworks to overcome these concerns."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Of these, 21% (81/395) were discontinued early, most commonly owing to poor recruitment (44%, 36/81).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 885, "doc_id": 6477536, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [6477536], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: One in five surgical randomized controlled trials are discontinued early.\n\nDocument title: Discontinuation and non-publication of surgical randomised controlled trials: observational study\n\nAbstract sentences:\n[0] OBJECTIVE To determine the rate of early discontinuation and non-publication of randomised controlled trials involving patients undergoing surgery.\n[1] DESIGN Cross sectional observational study of registered and published trials.\n[2] SETTING Randomised controlled trials of interventions in patients undergoing a surgical procedure.\n[3] DATA SOURCES The ClinicalTrials.gov database was searched for interventional trials registered between January 2008 and December 2009 using the keyword \"surgery\".\n[4] Recruitment status was extracted from the ClinicalTrials.gov database.\n[5] A systematic search for studies published in peer reviewed journals was performed; if they were not found, results posted on the ClinicalTrials.gov results database were sought.\n[6] Email queries were sent to trial investigators of discontinued and unpublished completed trials if no reason for the respective status was disclosed.\n[7] MAIN OUTCOME MEASURES Trial discontinuation before completion and non-publication after completion.\n[8] Logistic regression was used to determine the effect of funding source on publication status, with adjustment for intervention type and trial size.\n[9] RESULTS Of 818 registered trials found using the keyword \"surgery\", 395 met the inclusion criteria.\n[10] Of these, 21% (81/395) were discontinued early, most commonly owing to poor recruitment (44%, 36/81).\n[11] The remaining 314 (79%) trials proceeded to completion, with a publication rate of 66% (208/314) at a median time of 4.9 (interquartile range 4.0-6.0) years from study completion to publication search.\n[12] A further 6% (20/314) of studies presented results on ClinicalTrials.gov without a corresponding peer reviewed publication.\n[13] Industry funding did not affect the rate of discontinuation (adjusted odds ratio 0.91, 95% confidence interval 0.54 to 1.55) but was associated with a lower odds of publication for completed trials (0.43, 0.26 to 0.72).\n[14] Investigators' email addresses for trials with an uncertain fate were identified for 71.4% (10/14) of discontinued trials and 83% (101/122) of unpublished studies.\n[15] Only 43% (6/14) and 20% (25/122) replies were received.\n[16] Email responses for completed trials indicated 11 trials in press, five published studies (four in non-indexed peer reviewed journals), and nine trials remaining unpublished.\n[17] CONCLUSIONS One in five surgical randomised controlled trials are discontinued early, one in three completed trials remain unpublished, and investigators of unpublished studies are frequently not contactable.\n[18] This represents a waste of research resources and raises ethical concerns regarding hidden clinical data and futile participation by patients with its attendant risks.\n[19] To promote future efficiency and transparency, changes are proposed to research governance frameworks to overcome these concerns."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [17]\nExplanation: Evidence states: \"CONCLUSIONS One in five surgical randomised controlled trials are discontinued early, one in three completed trials remain unpublished, and investigators of unpublished studies are frequently not contactable.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 885, "doc_id": 6477536, "label": "SUPPORTS", "evidence_sentence_ids": [17], "cited_doc_ids": [6477536], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: One in two surgical randomized controlled trials are discontinued early.\n\nDocument title: Discontinuation and non-publication of surgical randomised controlled trials: observational study\n\nAbstract sentences:\n[0] OBJECTIVE To determine the rate of early discontinuation and non-publication of randomised controlled trials involving patients undergoing surgery.\n[1] DESIGN Cross sectional observational study of registered and published trials.\n[2] SETTING Randomised controlled trials of interventions in patients undergoing a surgical procedure.\n[3] DATA SOURCES The ClinicalTrials.gov database was searched for interventional trials registered between January 2008 and December 2009 using the keyword \"surgery\".\n[4] Recruitment status was extracted from the ClinicalTrials.gov database.\n[5] A systematic search for studies published in peer reviewed journals was performed; if they were not found, results posted on the ClinicalTrials.gov results database were sought.\n[6] Email queries were sent to trial investigators of discontinued and unpublished completed trials if no reason for the respective status was disclosed.\n[7] MAIN OUTCOME MEASURES Trial discontinuation before completion and non-publication after completion.\n[8] Logistic regression was used to determine the effect of funding source on publication status, with adjustment for intervention type and trial size.\n[9] RESULTS Of 818 registered trials found using the keyword \"surgery\", 395 met the inclusion criteria.\n[10] Of these, 21% (81/395) were discontinued early, most commonly owing to poor recruitment (44%, 36/81).\n[11] The remaining 314 (79%) trials proceeded to completion, with a publication rate of 66% (208/314) at a median time of 4.9 (interquartile range 4.0-6.0) years from study completion to publication search.\n[12] A further 6% (20/314) of studies presented results on ClinicalTrials.gov without a corresponding peer reviewed publication.\n[13] Industry funding did not affect the rate of discontinuation (adjusted odds ratio 0.91, 95% confidence interval 0.54 to 1.55) but was associated with a lower odds of publication for completed trials (0.43, 0.26 to 0.72).\n[14] Investigators' email addresses for trials with an uncertain fate were identified for 71.4% (10/14) of discontinued trials and 83% (101/122) of unpublished studies.\n[15] Only 43% (6/14) and 20% (25/122) replies were received.\n[16] Email responses for completed trials indicated 11 trials in press, five published studies (four in non-indexed peer reviewed journals), and nine trials remaining unpublished.\n[17] CONCLUSIONS One in five surgical randomised controlled trials are discontinued early, one in three completed trials remain unpublished, and investigators of unpublished studies are frequently not contactable.\n[18] This represents a waste of research resources and raises ethical concerns regarding hidden clinical data and futile participation by patients with its attendant risks.\n[19] To promote future efficiency and transparency, changes are proposed to research governance frameworks to overcome these concerns."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Of these, 21% (81/395) were discontinued early, most commonly owing to poor recruitment (44%, 36/81).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 886, "doc_id": 6477536, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [6477536], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: One in two surgical randomized controlled trials are discontinued early.\n\nDocument title: Discontinuation and non-publication of surgical randomised controlled trials: observational study\n\nAbstract sentences:\n[0] OBJECTIVE To determine the rate of early discontinuation and non-publication of randomised controlled trials involving patients undergoing surgery.\n[1] DESIGN Cross sectional observational study of registered and published trials.\n[2] SETTING Randomised controlled trials of interventions in patients undergoing a surgical procedure.\n[3] DATA SOURCES The ClinicalTrials.gov database was searched for interventional trials registered between January 2008 and December 2009 using the keyword \"surgery\".\n[4] Recruitment status was extracted from the ClinicalTrials.gov database.\n[5] A systematic search for studies published in peer reviewed journals was performed; if they were not found, results posted on the ClinicalTrials.gov results database were sought.\n[6] Email queries were sent to trial investigators of discontinued and unpublished completed trials if no reason for the respective status was disclosed.\n[7] MAIN OUTCOME MEASURES Trial discontinuation before completion and non-publication after completion.\n[8] Logistic regression was used to determine the effect of funding source on publication status, with adjustment for intervention type and trial size.\n[9] RESULTS Of 818 registered trials found using the keyword \"surgery\", 395 met the inclusion criteria.\n[10] Of these, 21% (81/395) were discontinued early, most commonly owing to poor recruitment (44%, 36/81).\n[11] The remaining 314 (79%) trials proceeded to completion, with a publication rate of 66% (208/314) at a median time of 4.9 (interquartile range 4.0-6.0) years from study completion to publication search.\n[12] A further 6% (20/314) of studies presented results on ClinicalTrials.gov without a corresponding peer reviewed publication.\n[13] Industry funding did not affect the rate of discontinuation (adjusted odds ratio 0.91, 95% confidence interval 0.54 to 1.55) but was associated with a lower odds of publication for completed trials (0.43, 0.26 to 0.72).\n[14] Investigators' email addresses for trials with an uncertain fate were identified for 71.4% (10/14) of discontinued trials and 83% (101/122) of unpublished studies.\n[15] Only 43% (6/14) and 20% (25/122) replies were received.\n[16] Email responses for completed trials indicated 11 trials in press, five published studies (four in non-indexed peer reviewed journals), and nine trials remaining unpublished.\n[17] CONCLUSIONS One in five surgical randomised controlled trials are discontinued early, one in three completed trials remain unpublished, and investigators of unpublished studies are frequently not contactable.\n[18] This represents a waste of research resources and raises ethical concerns regarding hidden clinical data and futile participation by patients with its attendant risks.\n[19] To promote future efficiency and transparency, changes are proposed to research governance frameworks to overcome these concerns."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [17]\nExplanation: Evidence states: \"CONCLUSIONS One in five surgical randomised controlled trials are discontinued early, one in three completed trials remain unpublished, and investigators of unpublished studies are frequently not contactable.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 886, "doc_id": 6477536, "label": "CONTRADICTS", "evidence_sentence_ids": [17], "cited_doc_ids": [6477536], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Origin gross domestic product(GDP) is negatively related to dengue virus (DENV-1) diffusion in air traffic shipments.\n\nDocument title: Population Density, Water Supply, and the Risk of Dengue Fever in Vietnam: Cohort Study and Spatial Analysis\n\nAbstract sentences:\n[0] BACKGROUND Aedes aegypti, the major vector of dengue viruses, often breeds in water storage containers used by households without tap water supply, and occurs in high numbers even in dense urban areas.\n[1] We analysed the interaction between human population density and lack of tap water as a cause of dengue fever outbreaks with the aim of identifying geographic areas at highest risk.\n[2] METHODS AND FINDINGS We conducted an individual-level cohort study in a population of 75,000 geo-referenced households in Vietnam over the course of two epidemics, on the basis of dengue hospital admissions (n = 3,013).\n[3] We applied space-time scan statistics and mathematical models to confirm the findings.\n[4] We identified a surprisingly narrow range of critical human population densities between around 3,000 to 7,000 people/km² prone to dengue outbreaks.\n[5] In the study area, this population density was typical of villages and some peri-urban areas.\n[6] Scan statistics showed that areas with a high population density or adequate water supply did not experience severe outbreaks.\n[7] The risk of dengue was higher in rural than in urban areas, largely explained by lack of piped water supply, and in human population densities more often falling within the critical range.\n[8] Mathematical modeling suggests that simple assumptions regarding area-level vector/host ratios may explain the occurrence of outbreaks.\n[9] CONCLUSIONS Rural areas may contribute at least as much to the dissemination of dengue fever as cities.\n[10] Improving water supply and vector control in areas with a human population density critical for dengue transmission could increase the efficiency of control efforts.\n[11] Please see later in the article for the Editors' Summary."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 890, "doc_id": 2097256, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [2097256], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Origin gross domestic product(GDP) is positively related to dengue virus (DENV-1) diffusion in air traffic shipments.\n\nDocument title: Population Density, Water Supply, and the Risk of Dengue Fever in Vietnam: Cohort Study and Spatial Analysis\n\nAbstract sentences:\n[0] BACKGROUND Aedes aegypti, the major vector of dengue viruses, often breeds in water storage containers used by households without tap water supply, and occurs in high numbers even in dense urban areas.\n[1] We analysed the interaction between human population density and lack of tap water as a cause of dengue fever outbreaks with the aim of identifying geographic areas at highest risk.\n[2] METHODS AND FINDINGS We conducted an individual-level cohort study in a population of 75,000 geo-referenced households in Vietnam over the course of two epidemics, on the basis of dengue hospital admissions (n = 3,013).\n[3] We applied space-time scan statistics and mathematical models to confirm the findings.\n[4] We identified a surprisingly narrow range of critical human population densities between around 3,000 to 7,000 people/km² prone to dengue outbreaks.\n[5] In the study area, this population density was typical of villages and some peri-urban areas.\n[6] Scan statistics showed that areas with a high population density or adequate water supply did not experience severe outbreaks.\n[7] The risk of dengue was higher in rural than in urban areas, largely explained by lack of piped water supply, and in human population densities more often falling within the critical range.\n[8] Mathematical modeling suggests that simple assumptions regarding area-level vector/host ratios may explain the occurrence of outbreaks.\n[9] CONCLUSIONS Rural areas may contribute at least as much to the dissemination of dengue fever as cities.\n[10] Improving water supply and vector control in areas with a human population density critical for dengue transmission could increase the efficiency of control efforts.\n[11] Please see later in the article for the Editors' Summary."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 891, "doc_id": 2097256, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [2097256], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Osteocytes have an essential role in G-CSF induced HSPC mobilization.\n\nDocument title: Matrix-embedded osteocytes regulate mobilization of hematopoietic stem/progenitor cells.\n\nAbstract sentences:\n[0] The bone marrow (BM) niche comprises multiple cell types that regulate hematopoietic stem/progenitor cell (HSPC) migration out of the niche and into the circulation.\n[1] Here, we demonstrate that osteocytes, the major cellular component of mature bone, are regulators of HSPC egress.\n[2] Granulocyte colony-stimulating factor (G-CSF), used clinically to mobilize HSPCs, induces changes in the morphology and gene expression of the osteocytic network that precedes changes in osteoblasts.\n[3] This rapid response is likely under control of the sympathetic nervous system, since osteocytes express the β2-adrenergic receptor and surgical sympathectomy prevents it.\n[4] Mice with targeted ablation of osteocytes or a disrupted osteocyte network have comparable numbers of HSPCs in the BM but fail to mobilize HSPCs in response to G-CSF.\n[5] Taken together, these results indicate that the BM/bone niche interface is critically controlled from inside of the bone matrix and establish an important physiological role for skeletal tissues in hematopoietic function."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Granulocyte colony-stimulating factor (G-CSF), used clinically to mobilize HSPCs, induces changes in the morphology and gene expression of the osteocytic network that precedes changes in osteoblasts.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 893, "doc_id": 13509809, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [13509809], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Osteocytes have an essential role in G-CSF induced HSPC mobilization.\n\nDocument title: Matrix-embedded osteocytes regulate mobilization of hematopoietic stem/progenitor cells.\n\nAbstract sentences:\n[0] The bone marrow (BM) niche comprises multiple cell types that regulate hematopoietic stem/progenitor cell (HSPC) migration out of the niche and into the circulation.\n[1] Here, we demonstrate that osteocytes, the major cellular component of mature bone, are regulators of HSPC egress.\n[2] Granulocyte colony-stimulating factor (G-CSF), used clinically to mobilize HSPCs, induces changes in the morphology and gene expression of the osteocytic network that precedes changes in osteoblasts.\n[3] This rapid response is likely under control of the sympathetic nervous system, since osteocytes express the β2-adrenergic receptor and surgical sympathectomy prevents it.\n[4] Mice with targeted ablation of osteocytes or a disrupted osteocyte network have comparable numbers of HSPCs in the BM but fail to mobilize HSPCs in response to G-CSF.\n[5] Taken together, these results indicate that the BM/bone niche interface is critically controlled from inside of the bone matrix and establish an important physiological role for skeletal tissues in hematopoietic function."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Mice with targeted ablation of osteocytes or a disrupted osteocyte network have comparable numbers of HSPCs in the BM but fail to mobilize HSPCs in response to G-CSF.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 893, "doc_id": 13509809, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [13509809], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Osteoparthritis (OA) is characterized by degeneration of articular cartilage, joint edge, and subchondral bone hyperplasia.\n\nDocument title: Effect of glucosamine on pain-related disability in patients with chronic low back pain and degenerative lumbar osteoarthritis: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Chronic low back pain (LBP) with degenerative lumbar osteoarthritis (OA) is widespread in the adult population.\n[1] Although glucosamine is increasingly used by patients with chronic LBP, little is known about its effect in this setting.\n[2] OBJECTIVE To investigate the effect of glucosamine in patients with chronic LBP and degenerative lumbar OA.\n[3] DESIGN, SETTING, AND PARTICIPANTS A double-blind, randomized, placebo-controlled trial conducted at Oslo University Hospital Outpatient Clinic, Oslo, Norway, with 250 patients older than 25 years of age with chronic LBP (>6 months) and degenerative lumbar OA.\n[4] INTERVENTIONS Daily intake of 1500 mg of oral glucosamine (n = 125) or placebo (n = 125) for 6 months, with assessment of effect after the 6-month intervention period and at 1 year (6 months postintervention).\n[5] MAIN OUTCOME MEASURES The primary outcome was pain-related disability measured with the Roland Morris Disability Questionnaire (RMDQ).\n[6] Secondary outcomes were numerical scores from pain-rating scales of patients at rest and during activity, and the quality-of-life EuroQol-5 Dimensions (EQ-5D) instrument.\n[7] Data collection occurred during the intervention period at baseline, 6 weeks, 3 and 6 months, and again 6 months following the intervention at 1 year.\n[8] Group differences were analyzed using linear mixed models analysis.\n[9] RESULTS At baseline, mean RMDQ scores were 9.2 (95% confidence interval [CI], 8.4-10.0) for glucosamine and 9.7 (95% CI, 8.9-10.5) for the placebo group (P = .37).\n[10] At 6 months, the mean RMDQ score was the same for the glucosamine and placebo groups (5.0; 95% CI, 4.2-5.8).\n[11] At 1 year, the mean RMDQ scores were 4.8 (95% CI, 3.9-5.6) for glucosamine and 5.5 (95% CI, 4.7-6.4) for the placebo group.\n[12] No statistically significant difference in change between groups was found when assessed after the 6-month intervention period and at 1 year: RMDQ (P = .72), LBP at rest (P = .91), LBP during activity (P = .97), and quality-of-life EQ-5D (P = .20).\n[13] Mild adverse events were reported in 40 patients in the glucosamine group and 46 in the placebo group (P = .48).\n[14] CONCLUSIONS Among patients with chronic LBP and degenerative lumbar OA, 6-month treatment with oral glucosamine compared with placebo did not result in reduced pain-related disability after the 6-month intervention and after 1-year follow-up.\n[15] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00404079."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 894, "doc_id": 14724693, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14724693], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Over half of the gabonese children with Schimmelpenning-Feuerstein-Mims syndrome (SFM) had a plasma lactate of more than 5mmol/L.\n\nDocument title: Assessment of Volume Depletion in Children with Malaria\n\nAbstract sentences:\n[0] Background The degree of volume depletion in severe malaria is currently unknown, although knowledge of fluid compartment volumes can guide therapy.\n[1] To assist management of severely ill children, and to test the hypothesis that volume changes in fluid compartments reflect disease severity, we measured body compartment volumes in Gabonese children with malaria.\n[2] Methods and Findings Total body water volume (TBW) and extracellular water volume (ECW) were estimated in children with severe or moderate malaria and in convalescence by tracer dilution with heavy water and bromide, respectively.\n[3] Intracellular water volume (ICW) was derived from these parameters.\n[4] Bioelectrical impedance analysis estimates of TBW and ECW were calibrated against dilution methods, and bioelectrical impedance analysis measurements were taken daily until discharge.\n[5] Sixteen children had severe and 19 moderate malaria.\n[6] Severe childhood malaria was associated with depletion of TBW (mean [SD] of 37 [33] ml/kg, or 6.7% [6.0%]) relative to measurement at discharge.\n[7] This is defined as mild dehydration in other conditions.\n[8] ECW measurements were normal on admission in children with severe malaria and did not rise in the first few days of admission.\n[9] Volumes in different compartments (TBW, ECW, and ICW) were not related to hyperlactataemia or other clinical and laboratory markers of disease severity.\n[10] Moderate malaria was not associated with a depletion of TBW."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 895, "doc_id": 18750453, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [18750453], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Overexpressing Cnp1 N-tail variants exacerbates the temperature-sensitive growth defect of scm3-139.\n\nDocument title: Fission Yeast Scm3: A CENP-A Receptor Required for Integrity of Subkinetochore Chromatin\n\nAbstract sentences:\n[0] The mechanisms ensuring specific incorporation of CENP-A at centromeres are poorly understood.\n[1] Mis16 and Mis18 are required for CENP-A localization at centromeres and form a complex that is conserved from fission yeast to human.\n[2] Fission yeast sim1 mutants that alleviate kinetochore domain silencing are defective in Scm3(Sp), the ortholog of budding yeast Scm3(Sc).\n[3] Scm3(Sp) depends on Mis16/18 for its centromere localization and like them is recruited to centromeres in late anaphase.\n[4] Importantly, Scm3(Sp) coaffinity purifies with CENP-A(Cnp1) and associates with CENP-A(Cnp1) in vitro, yet localizes independently of intact CENP-A(Cnp1) chromatin and is differentially released from chromatin.\n[5] While Scm3(Sc) has been proposed to form a unique hexameric nucleosome with CENP-A(Cse4) and histone H4 at budding yeast point centromeres, we favor a model in which Scm3(Sp) acts as a CENP-A(Cnp1) receptor/assembly factor, cooperating with Mis16 and Mis18 to receive CENP-A(Cnp1) from the Sim3 escort and mediate assembly of CENP-A(Cnp1) into subkinetochore chromatin."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 896, "doc_id": 14338915, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14338915], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Overexpressing Cnp1 N-tail variants rescues the temperature-sensitive growth defect of scm3-139.\n\nDocument title: Fission Yeast Scm3: A CENP-A Receptor Required for Integrity of Subkinetochore Chromatin\n\nAbstract sentences:\n[0] The mechanisms ensuring specific incorporation of CENP-A at centromeres are poorly understood.\n[1] Mis16 and Mis18 are required for CENP-A localization at centromeres and form a complex that is conserved from fission yeast to human.\n[2] Fission yeast sim1 mutants that alleviate kinetochore domain silencing are defective in Scm3(Sp), the ortholog of budding yeast Scm3(Sc).\n[3] Scm3(Sp) depends on Mis16/18 for its centromere localization and like them is recruited to centromeres in late anaphase.\n[4] Importantly, Scm3(Sp) coaffinity purifies with CENP-A(Cnp1) and associates with CENP-A(Cnp1) in vitro, yet localizes independently of intact CENP-A(Cnp1) chromatin and is differentially released from chromatin.\n[5] While Scm3(Sc) has been proposed to form a unique hexameric nucleosome with CENP-A(Cse4) and histone H4 at budding yeast point centromeres, we favor a model in which Scm3(Sp) acts as a CENP-A(Cnp1) receptor/assembly factor, cooperating with Mis16 and Mis18 to receive CENP-A(Cnp1) from the Sim3 escort and mediate assembly of CENP-A(Cnp1) into subkinetochore chromatin."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 897, "doc_id": 14338915, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14338915], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Oxidative DNA damage activates STING signalling.\n\nDocument title: Oxidative damage of DNA confers resistance to cytosolic nuclease TREX1 degradation and potentiates STING-dependent immune sensing.\n\nAbstract sentences:\n[0] Immune sensing of DNA is critical for antiviral immunity but can also trigger autoimmune diseases such as lupus erythematosus (LE).\n[1] Here we have provided evidence for the involvement of a damage-associated DNA modification in the detection of cytosolic DNA.\n[2] The oxidized base 8-hydroxyguanosine (8-OHG), a marker of oxidative damage in DNA, potentiated cytosolic immune recognition by decreasing its susceptibility to 3' repair exonuclease 1 (TREX1)-mediated degradation.\n[3] Oxidizative modifications arose physiologically in pathogen DNA during lysosomal reactive oxygen species (ROS) exposure, as well as in neutrophil extracellular trap (NET) DNA during the oxidative burst.\n[4] 8-OHG was also abundant in UV-exposed skin lesions of LE patients and colocalized with type I interferon (IFN).\n[5] Injection of oxidized DNA in the skin of lupus-prone mice induced lesions that closely matched respective lesions in patients.\n[6] Thus, oxidized DNA represents a prototypic damage-associated molecular pattern (DAMP) with important implications for infection, sterile inflammation, and autoimmunity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 898, "doc_id": 13106686, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [13106686, 5572127], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Oxidative DNA damage inhibits STING signalling.\n\nDocument title: Oxidative damage of DNA confers resistance to cytosolic nuclease TREX1 degradation and potentiates STING-dependent immune sensing.\n\nAbstract sentences:\n[0] Immune sensing of DNA is critical for antiviral immunity but can also trigger autoimmune diseases such as lupus erythematosus (LE).\n[1] Here we have provided evidence for the involvement of a damage-associated DNA modification in the detection of cytosolic DNA.\n[2] The oxidized base 8-hydroxyguanosine (8-OHG), a marker of oxidative damage in DNA, potentiated cytosolic immune recognition by decreasing its susceptibility to 3' repair exonuclease 1 (TREX1)-mediated degradation.\n[3] Oxidizative modifications arose physiologically in pathogen DNA during lysosomal reactive oxygen species (ROS) exposure, as well as in neutrophil extracellular trap (NET) DNA during the oxidative burst.\n[4] 8-OHG was also abundant in UV-exposed skin lesions of LE patients and colocalized with type I interferon (IFN).\n[5] Injection of oxidized DNA in the skin of lupus-prone mice induced lesions that closely matched respective lesions in patients.\n[6] Thus, oxidized DNA represents a prototypic damage-associated molecular pattern (DAMP) with important implications for infection, sterile inflammation, and autoimmunity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 899, "doc_id": 13106686, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [13106686, 5572127], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Oxidative phosphorylation is one of the primary glycometabolic pathways in cells.\n\nDocument title: Vesicular Glycolysis Provides On-Board Energy for Fast Axonal Transport\n\nAbstract sentences:\n[0] Fast axonal transport (FAT) requires consistent energy over long distances to fuel the molecular motors that transport vesicles.\n[1] We demonstrate that glycolysis provides ATP for the FAT of vesicles.\n[2] Although inhibiting ATP production from mitochondria did not affect vesicles motility, pharmacological or genetic inhibition of the glycolytic enzyme GAPDH reduced transport in cultured neurons and in Drosophila larvae.\n[3] GAPDH localizes on vesicles via a huntingtin-dependent mechanism and is transported on fast-moving vesicles within axons.\n[4] Purified motile vesicles showed GAPDH enzymatic activity and produced ATP.\n[5] Finally, we show that vesicular GAPDH is necessary and sufficient to provide on-board energy for fast vesicular transport.\n[6] Although detaching GAPDH from vesicles reduced transport, targeting GAPDH to vesicles was sufficient to promote FAT in GAPDH deficient neurons.\n[7] This specifically localized glycolytic machinery may supply constant energy, independent of mitochondria, for the processive movement of vesicles over long distances in axons."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 900, "doc_id": 18678095, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [18678095], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: PCSK9 inhibitors decrease plasma Lp(a) levels.\n\nDocument title: Effects of PCSK9 Inhibition With Alirocumab on Lipoprotein Metabolism in Healthy Humans\n\nAbstract sentences:\n[0] BACKGROUND Alirocumab, a monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9), lowers plasma low-density lipoprotein (LDL) cholesterol and apolipoprotein B100 (apoB).\n[1] Although studies in mice and cells have identified increased hepatic LDL receptors as the basis for LDL lowering by PCSK9 inhibitors, there have been no human studies characterizing the effects of PCSK9 inhibitors on lipoprotein metabolism.\n[2] In particular, it is not known whether inhibition of PCSK9 has any effects on very low-density lipoprotein or intermediate-density lipoprotein (IDL) metabolism.\n[3] Inhibition of PCSK9 also results in reductions of plasma lipoprotein (a) levels.\n[4] The regulation of plasma Lp(a) levels, including the role of LDL receptors in the clearance of Lp(a), is poorly defined, and no mechanistic studies of the Lp(a) lowering by alirocumab in humans have been published to date.\n[5] METHODS Eighteen (10 F, 8 mol/L) participants completed a placebo-controlled, 2-period study.\n[6] They received 2 doses of placebo, 2 weeks apart, followed by 5 doses of 150 mg of alirocumab, 2 weeks apart.\n[7] At the end of each period, fractional clearance rates (FCRs) and production rates (PRs) of apoB and apo(a) were determined.\n[8] In 10 participants, postprandial triglycerides and apoB48 levels were measured.\n[9] RESULTS Alirocumab reduced ultracentrifugally isolated LDL-C by 55.1%, LDL-apoB by 56.3%, and plasma Lp(a) by 18.7%.\n[10] The fall in LDL-apoB was caused by an 80.4% increase in LDL-apoB FCR and a 23.9% reduction in LDL-apoB PR.\n[11] The latter was due to a 46.1% increase in IDL-apoB FCR coupled with a 27.2% decrease in conversion of IDL to LDL.\n[12] The FCR of apo(a) tended to increase (24.6%) without any change in apo(a) PR.\n[13] Alirocumab had no effects on FCRs or PRs of very low-density lipoproteins-apoB and very low-density lipoproteins triglycerides or on postprandial plasma triglycerides or apoB48 concentrations.\n[14] CONCLUSIONS Alirocumab decreased LDL-C and LDL-apoB by increasing IDL- and LDL-apoB FCRs and decreasing LDL-apoB PR.\n[15] These results are consistent with increases in LDL receptors available to clear IDL and LDL from blood during PCSK9 inhibition.\n[16] The increase in apo(a) FCR during alirocumab treatment suggests that increased LDL receptors may also play a role in the reduction of plasma Lp(a).\n[17] CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov.\n[18] Unique identifier: NCT01959971."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Inhibition of PCSK9 also results in reductions of plasma lipoprotein (a) levels.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 901, "doc_id": 6540064, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [6540064], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: PCSK9 inhibitors decrease plasma Lp(a) levels.\n\nDocument title: Effects of PCSK9 Inhibition With Alirocumab on Lipoprotein Metabolism in Healthy Humans\n\nAbstract sentences:\n[0] BACKGROUND Alirocumab, a monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9), lowers plasma low-density lipoprotein (LDL) cholesterol and apolipoprotein B100 (apoB).\n[1] Although studies in mice and cells have identified increased hepatic LDL receptors as the basis for LDL lowering by PCSK9 inhibitors, there have been no human studies characterizing the effects of PCSK9 inhibitors on lipoprotein metabolism.\n[2] In particular, it is not known whether inhibition of PCSK9 has any effects on very low-density lipoprotein or intermediate-density lipoprotein (IDL) metabolism.\n[3] Inhibition of PCSK9 also results in reductions of plasma lipoprotein (a) levels.\n[4] The regulation of plasma Lp(a) levels, including the role of LDL receptors in the clearance of Lp(a), is poorly defined, and no mechanistic studies of the Lp(a) lowering by alirocumab in humans have been published to date.\n[5] METHODS Eighteen (10 F, 8 mol/L) participants completed a placebo-controlled, 2-period study.\n[6] They received 2 doses of placebo, 2 weeks apart, followed by 5 doses of 150 mg of alirocumab, 2 weeks apart.\n[7] At the end of each period, fractional clearance rates (FCRs) and production rates (PRs) of apoB and apo(a) were determined.\n[8] In 10 participants, postprandial triglycerides and apoB48 levels were measured.\n[9] RESULTS Alirocumab reduced ultracentrifugally isolated LDL-C by 55.1%, LDL-apoB by 56.3%, and plasma Lp(a) by 18.7%.\n[10] The fall in LDL-apoB was caused by an 80.4% increase in LDL-apoB FCR and a 23.9% reduction in LDL-apoB PR.\n[11] The latter was due to a 46.1% increase in IDL-apoB FCR coupled with a 27.2% decrease in conversion of IDL to LDL.\n[12] The FCR of apo(a) tended to increase (24.6%) without any change in apo(a) PR.\n[13] Alirocumab had no effects on FCRs or PRs of very low-density lipoproteins-apoB and very low-density lipoproteins triglycerides or on postprandial plasma triglycerides or apoB48 concentrations.\n[14] CONCLUSIONS Alirocumab decreased LDL-C and LDL-apoB by increasing IDL- and LDL-apoB FCRs and decreasing LDL-apoB PR.\n[15] These results are consistent with increases in LDL receptors available to clear IDL and LDL from blood during PCSK9 inhibition.\n[16] The increase in apo(a) FCR during alirocumab treatment suggests that increased LDL receptors may also play a role in the reduction of plasma Lp(a).\n[17] CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov.\n[18] Unique identifier: NCT01959971."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [16]\nExplanation: Evidence states: \"The increase in apo(a) FCR during alirocumab treatment suggests that increased LDL receptors may also play a role in the reduction of plasma Lp(a).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 901, "doc_id": 6540064, "label": "SUPPORTS", "evidence_sentence_ids": [16], "cited_doc_ids": [6540064], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: PD-1 triggering on monocytes enhances IL-10 production by monocytes.\n\nDocument title: Programmed death-1–induced interleukin-10 production by monocytes impairs CD4+ T cell activation during HIV infection\n\nAbstract sentences:\n[0] Viral replication and microbial translocation from the gut to the blood during HIV infection lead to hyperimmune activation, which contributes to the decline in CD4+ T cell numbers during HIV infection.\n[1] Programmed death-1 (PD-1) and interleukin-10 (IL-10) are both upregulated during HIV infection.\n[2] Blocking interactions between PD-1 and programmed death ligand-1 (PD-L1) and between IL-10 and IL-10 receptor (IL-10R) results in viral clearance and improves T cell function in animal models of chronic viral infections.\n[3] Here we show that high amounts of microbial products and inflammatory cytokines in the plasma of HIV-infected subjects lead to upregulation of PD-1 expression on monocytes that correlates with high plasma concentrations of IL-10.\n[4] Triggering of PD-1 expressed on monocytes by PD-L1 expressed on various cell types induced IL-10 production and led to reversible CD4+ T cell dysfunction.\n[5] We describe a new function for PD-1 whereby microbial products inhibit T cell expansion and function by upregulating PD-1 levels and IL-10 production by monocytes after binding of PD-1 by PD-L1."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Triggering of PD-1 expressed on monocytes by PD-L1 expressed on various cell types induced IL-10 production and led to reversible CD4+ T cell dysfunction.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 902, "doc_id": 10648422, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [10648422], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: PD-1 triggering on monocytes enhances IL-10 production by monocytes.\n\nDocument title: Programmed death-1–induced interleukin-10 production by monocytes impairs CD4+ T cell activation during HIV infection\n\nAbstract sentences:\n[0] Viral replication and microbial translocation from the gut to the blood during HIV infection lead to hyperimmune activation, which contributes to the decline in CD4+ T cell numbers during HIV infection.\n[1] Programmed death-1 (PD-1) and interleukin-10 (IL-10) are both upregulated during HIV infection.\n[2] Blocking interactions between PD-1 and programmed death ligand-1 (PD-L1) and between IL-10 and IL-10 receptor (IL-10R) results in viral clearance and improves T cell function in animal models of chronic viral infections.\n[3] Here we show that high amounts of microbial products and inflammatory cytokines in the plasma of HIV-infected subjects lead to upregulation of PD-1 expression on monocytes that correlates with high plasma concentrations of IL-10.\n[4] Triggering of PD-1 expressed on monocytes by PD-L1 expressed on various cell types induced IL-10 production and led to reversible CD4+ T cell dysfunction.\n[5] We describe a new function for PD-1 whereby microbial products inhibit T cell expansion and function by upregulating PD-1 levels and IL-10 production by monocytes after binding of PD-1 by PD-L1."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"We describe a new function for PD-1 whereby microbial products inhibit T cell expansion and function by upregulating PD-1 levels and IL-10 production by monocytes after binding of PD-1 by PD-L1.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 902, "doc_id": 10648422, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [10648422], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: PGE 2 suppresss intestinal tumor growth by altering the expression of tumor suppressing and DNA repair genes.\n\nDocument title: Prostaglandin E2 promotes intestinal tumor growth via DNA methylation\n\nAbstract sentences:\n[0] Although aberrant DNA methylation is considered to be one of the key ways by which tumor-suppressor and DNA-repair genes are silenced during tumor initiation and progression, the mechanisms underlying DNA methylation alterations in cancer remain unclear.\n[1] Here we show that prostaglandin E(2) (PGE(2)) silences certain tumor-suppressor and DNA-repair genes through DNA methylation to promote tumor growth.\n[2] These findings uncover a previously unrecognized role for PGE(2) in the promotion of tumor progression."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 908, "doc_id": 6923961, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [6923961], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: PKG-la does not have a large impact on expression of pain hypersensitivity in PGK-la knockout mice.\n\nDocument title: Presynaptically Localized Cyclic GMP-Dependent Protein Kinase 1 Is a Key Determinant of Spinal Synaptic Potentiation and Pain Hypersensitivity\n\nAbstract sentences:\n[0] Synaptic long-term potentiation (LTP) at spinal neurons directly communicating pain-specific inputs from the periphery to the brain has been proposed to serve as a trigger for pain hypersensitivity in pathological states.\n[1] Previous studies have functionally implicated the NMDA receptor-NO pathway and the downstream second messenger, cGMP, in these processes.\n[2] Because cGMP can broadly influence diverse ion-channels, kinases, and phosphodiesterases, pre- as well as post-synaptically, the precise identity of cGMP targets mediating spinal LTP, their mechanisms of action, and their locus in the spinal circuitry are still unclear.\n[3] Here, we found that Protein Kinase G1 (PKG-I) localized presynaptically in nociceptor terminals plays an essential role in the expression of spinal LTP.\n[4] Using the Cre-lox P system, we generated nociceptor-specific knockout mice lacking PKG-I specifically in presynaptic terminals of nociceptors in the spinal cord, but not in post-synaptic neurons or elsewhere (SNS-PKG-I(-/-) mice).\n[5] Patch clamp recordings showed that activity-induced LTP at identified synapses between nociceptors and spinal neurons projecting to the periaqueductal grey (PAG) was completely abolished in SNS-PKG-I(-/-) mice, although basal synaptic transmission was not affected.\n[6] Analyses of synaptic failure rates and paired-pulse ratios indicated a role for presynaptic PKG-I in regulating the probability of neurotransmitter release.\n[7] Inositol 1,4,5-triphosphate receptor 1 and myosin light chain kinase were recruited as key phosphorylation targets of presynaptic PKG-I in nociceptive neurons.\n[8] Finally, behavioural analyses in vivo showed marked defects in SNS-PKG-I(-/-) mice in several models of activity-induced nociceptive hypersensitivity, and pharmacological studies identified a clear contribution of PKG-I expressed in spinal terminals of nociceptors.\n[9] Our results thus indicate that presynaptic mechanisms involving an increase in release probability from nociceptors are operational in the expression of synaptic LTP on spinal-PAG projection neurons and that PKG-I localized in presynaptic nociceptor terminals plays an essential role in this process to regulate pain sensitivity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Here, we found that Protein Kinase G1 (PKG-I) localized presynaptically in nociceptor terminals plays an essential role in the expression of spinal LTP.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 909, "doc_id": 11254556, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [11254556], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: PKG-la does not have a large impact on expression of pain hypersensitivity in PGK-la knockout mice.\n\nDocument title: Presynaptically Localized Cyclic GMP-Dependent Protein Kinase 1 Is a Key Determinant of Spinal Synaptic Potentiation and Pain Hypersensitivity\n\nAbstract sentences:\n[0] Synaptic long-term potentiation (LTP) at spinal neurons directly communicating pain-specific inputs from the periphery to the brain has been proposed to serve as a trigger for pain hypersensitivity in pathological states.\n[1] Previous studies have functionally implicated the NMDA receptor-NO pathway and the downstream second messenger, cGMP, in these processes.\n[2] Because cGMP can broadly influence diverse ion-channels, kinases, and phosphodiesterases, pre- as well as post-synaptically, the precise identity of cGMP targets mediating spinal LTP, their mechanisms of action, and their locus in the spinal circuitry are still unclear.\n[3] Here, we found that Protein Kinase G1 (PKG-I) localized presynaptically in nociceptor terminals plays an essential role in the expression of spinal LTP.\n[4] Using the Cre-lox P system, we generated nociceptor-specific knockout mice lacking PKG-I specifically in presynaptic terminals of nociceptors in the spinal cord, but not in post-synaptic neurons or elsewhere (SNS-PKG-I(-/-) mice).\n[5] Patch clamp recordings showed that activity-induced LTP at identified synapses between nociceptors and spinal neurons projecting to the periaqueductal grey (PAG) was completely abolished in SNS-PKG-I(-/-) mice, although basal synaptic transmission was not affected.\n[6] Analyses of synaptic failure rates and paired-pulse ratios indicated a role for presynaptic PKG-I in regulating the probability of neurotransmitter release.\n[7] Inositol 1,4,5-triphosphate receptor 1 and myosin light chain kinase were recruited as key phosphorylation targets of presynaptic PKG-I in nociceptive neurons.\n[8] Finally, behavioural analyses in vivo showed marked defects in SNS-PKG-I(-/-) mice in several models of activity-induced nociceptive hypersensitivity, and pharmacological studies identified a clear contribution of PKG-I expressed in spinal terminals of nociceptors.\n[9] Our results thus indicate that presynaptic mechanisms involving an increase in release probability from nociceptors are operational in the expression of synaptic LTP on spinal-PAG projection neurons and that PKG-I localized in presynaptic nociceptor terminals plays an essential role in this process to regulate pain sensitivity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Our results thus indicate that presynaptic mechanisms involving an increase in release probability from nociceptors are operational in the expression of synaptic LTP on spinal-PAG projection neurons and that PKG-I localized in presynaptic nociceptor terminals plays an essential role in this process to regulate pain sensitivity.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 909, "doc_id": 11254556, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [11254556], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: PKG-la does not have a large impact on expression of spinal long term potentiation in PGK-la knockout mice.\n\nDocument title: Presynaptically Localized Cyclic GMP-Dependent Protein Kinase 1 Is a Key Determinant of Spinal Synaptic Potentiation and Pain Hypersensitivity\n\nAbstract sentences:\n[0] Synaptic long-term potentiation (LTP) at spinal neurons directly communicating pain-specific inputs from the periphery to the brain has been proposed to serve as a trigger for pain hypersensitivity in pathological states.\n[1] Previous studies have functionally implicated the NMDA receptor-NO pathway and the downstream second messenger, cGMP, in these processes.\n[2] Because cGMP can broadly influence diverse ion-channels, kinases, and phosphodiesterases, pre- as well as post-synaptically, the precise identity of cGMP targets mediating spinal LTP, their mechanisms of action, and their locus in the spinal circuitry are still unclear.\n[3] Here, we found that Protein Kinase G1 (PKG-I) localized presynaptically in nociceptor terminals plays an essential role in the expression of spinal LTP.\n[4] Using the Cre-lox P system, we generated nociceptor-specific knockout mice lacking PKG-I specifically in presynaptic terminals of nociceptors in the spinal cord, but not in post-synaptic neurons or elsewhere (SNS-PKG-I(-/-) mice).\n[5] Patch clamp recordings showed that activity-induced LTP at identified synapses between nociceptors and spinal neurons projecting to the periaqueductal grey (PAG) was completely abolished in SNS-PKG-I(-/-) mice, although basal synaptic transmission was not affected.\n[6] Analyses of synaptic failure rates and paired-pulse ratios indicated a role for presynaptic PKG-I in regulating the probability of neurotransmitter release.\n[7] Inositol 1,4,5-triphosphate receptor 1 and myosin light chain kinase were recruited as key phosphorylation targets of presynaptic PKG-I in nociceptive neurons.\n[8] Finally, behavioural analyses in vivo showed marked defects in SNS-PKG-I(-/-) mice in several models of activity-induced nociceptive hypersensitivity, and pharmacological studies identified a clear contribution of PKG-I expressed in spinal terminals of nociceptors.\n[9] Our results thus indicate that presynaptic mechanisms involving an increase in release probability from nociceptors are operational in the expression of synaptic LTP on spinal-PAG projection neurons and that PKG-I localized in presynaptic nociceptor terminals plays an essential role in this process to regulate pain sensitivity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Patch clamp recordings showed that activity-induced LTP at identified synapses between nociceptors and spinal neurons projecting to the periaqueductal grey (PAG) was completely abolished in SNS-PKG-I(-/-) mice, although basal synaptic transmission was not affected.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 910, "doc_id": 11254556, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [11254556], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: PKG-la plays an essential role in expression of spinal long term potentiation in PGK-la knockout mice.\n\nDocument title: Presynaptically Localized Cyclic GMP-Dependent Protein Kinase 1 Is a Key Determinant of Spinal Synaptic Potentiation and Pain Hypersensitivity\n\nAbstract sentences:\n[0] Synaptic long-term potentiation (LTP) at spinal neurons directly communicating pain-specific inputs from the periphery to the brain has been proposed to serve as a trigger for pain hypersensitivity in pathological states.\n[1] Previous studies have functionally implicated the NMDA receptor-NO pathway and the downstream second messenger, cGMP, in these processes.\n[2] Because cGMP can broadly influence diverse ion-channels, kinases, and phosphodiesterases, pre- as well as post-synaptically, the precise identity of cGMP targets mediating spinal LTP, their mechanisms of action, and their locus in the spinal circuitry are still unclear.\n[3] Here, we found that Protein Kinase G1 (PKG-I) localized presynaptically in nociceptor terminals plays an essential role in the expression of spinal LTP.\n[4] Using the Cre-lox P system, we generated nociceptor-specific knockout mice lacking PKG-I specifically in presynaptic terminals of nociceptors in the spinal cord, but not in post-synaptic neurons or elsewhere (SNS-PKG-I(-/-) mice).\n[5] Patch clamp recordings showed that activity-induced LTP at identified synapses between nociceptors and spinal neurons projecting to the periaqueductal grey (PAG) was completely abolished in SNS-PKG-I(-/-) mice, although basal synaptic transmission was not affected.\n[6] Analyses of synaptic failure rates and paired-pulse ratios indicated a role for presynaptic PKG-I in regulating the probability of neurotransmitter release.\n[7] Inositol 1,4,5-triphosphate receptor 1 and myosin light chain kinase were recruited as key phosphorylation targets of presynaptic PKG-I in nociceptive neurons.\n[8] Finally, behavioural analyses in vivo showed marked defects in SNS-PKG-I(-/-) mice in several models of activity-induced nociceptive hypersensitivity, and pharmacological studies identified a clear contribution of PKG-I expressed in spinal terminals of nociceptors.\n[9] Our results thus indicate that presynaptic mechanisms involving an increase in release probability from nociceptors are operational in the expression of synaptic LTP on spinal-PAG projection neurons and that PKG-I localized in presynaptic nociceptor terminals plays an essential role in this process to regulate pain sensitivity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Patch clamp recordings showed that activity-induced LTP at identified synapses between nociceptors and spinal neurons projecting to the periaqueductal grey (PAG) was completely abolished in SNS-PKG-I(-/-) mice, although basal synaptic transmission was not affected.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 912, "doc_id": 11254556, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [11254556], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: PRC1-bound plasmids sediment at a slower rate in unbound plasmids than in sucrose gradients.\n\nDocument title: Polycomb Proteins Remain Bound to Chromatin and DNA during DNA Replication In Vitro\n\nAbstract sentences:\n[0] The transcriptional status of a gene can be maintained through multiple rounds of cell division during development.\n[1] This epigenetic effect is believed to reflect heritable changes in chromatin folding and histone modifications or variants at target genes, but little is known about how these chromatin features are inherited through cell division.\n[2] A particular challenge for maintaining transcription states is DNA replication, which disrupts or dilutes chromatin-associated proteins and histone modifications.\n[3] PRC1-class Polycomb group protein complexes are essential for development and are thought to heritably silence transcription by altering chromatin folding and histone modifications.\n[4] It is not known whether these complexes and their effects are maintained during DNA replication or subsequently re-established.\n[5] We find that when PRC1-class Polycomb complex-bound chromatin or DNA is replicated in vitro, Polycomb complexes remain bound to replicated templates.\n[6] Retention of Polycomb proteins through DNA replication may contribute to maintenance of transcriptional silencing through cell division."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 916, "doc_id": 18037805, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [18037805], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: PTEN is a regulator for the transcriptional activity of SRF\n\nDocument title: Nuclear PTEN functions as an essential regulator of SRF-dependent transcription to control smooth muscle differentiation\n\nAbstract sentences:\n[0] Vascular disease progression is associated with marked changes in vascular smooth muscle cell (SMC) phenotype and function.\n[1] SMC contractile gene expression and, thus differentiation, is under direct transcriptional control by the transcription factor, serum response factor (SRF); however, the mechanisms dynamically regulating SMC phenotype are not fully defined.\n[2] Here we report that the lipid and protein phosphatase, PTEN, has a novel role in the nucleus by functioning as an indispensible regulator with SRF to maintain the differentiated SM phenotype.\n[3] PTEN interacts with the N-terminal domain of SRF and PTEN-SRF interaction promotes SRF binding to essential promoter elements in SM-specific genes.\n[4] Factors inducing phenotypic switching promote loss of nuclear PTEN through nucleo-cytoplasmic translocation resulting in reduced myogenically active SRF, but enhanced SRF activity on target genes involved in proliferation.\n[5] Overall decreased expression of PTEN was observed in intimal SMCs of human atherosclerotic lesions underlying the potential clinical importance of these findings."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here we report that the lipid and protein phosphatase, PTEN, has a novel role in the nucleus by functioning as an indispensible regulator with SRF to maintain the differentiated SM phenotype.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 917, "doc_id": 34071621, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [34071621], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: PTEN is a regulator for the transcriptional activity of SRF\n\nDocument title: Nuclear PTEN functions as an essential regulator of SRF-dependent transcription to control smooth muscle differentiation\n\nAbstract sentences:\n[0] Vascular disease progression is associated with marked changes in vascular smooth muscle cell (SMC) phenotype and function.\n[1] SMC contractile gene expression and, thus differentiation, is under direct transcriptional control by the transcription factor, serum response factor (SRF); however, the mechanisms dynamically regulating SMC phenotype are not fully defined.\n[2] Here we report that the lipid and protein phosphatase, PTEN, has a novel role in the nucleus by functioning as an indispensible regulator with SRF to maintain the differentiated SM phenotype.\n[3] PTEN interacts with the N-terminal domain of SRF and PTEN-SRF interaction promotes SRF binding to essential promoter elements in SM-specific genes.\n[4] Factors inducing phenotypic switching promote loss of nuclear PTEN through nucleo-cytoplasmic translocation resulting in reduced myogenically active SRF, but enhanced SRF activity on target genes involved in proliferation.\n[5] Overall decreased expression of PTEN was observed in intimal SMCs of human atherosclerotic lesions underlying the potential clinical importance of these findings."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"PTEN interacts with the N-terminal domain of SRF and PTEN-SRF interaction promotes SRF binding to essential promoter elements in SM-specific genes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 917, "doc_id": 34071621, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [34071621], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: PTEN is a regulator for the transcriptional activity of SRF\n\nDocument title: Nuclear PTEN functions as an essential regulator of SRF-dependent transcription to control smooth muscle differentiation\n\nAbstract sentences:\n[0] Vascular disease progression is associated with marked changes in vascular smooth muscle cell (SMC) phenotype and function.\n[1] SMC contractile gene expression and, thus differentiation, is under direct transcriptional control by the transcription factor, serum response factor (SRF); however, the mechanisms dynamically regulating SMC phenotype are not fully defined.\n[2] Here we report that the lipid and protein phosphatase, PTEN, has a novel role in the nucleus by functioning as an indispensible regulator with SRF to maintain the differentiated SM phenotype.\n[3] PTEN interacts with the N-terminal domain of SRF and PTEN-SRF interaction promotes SRF binding to essential promoter elements in SM-specific genes.\n[4] Factors inducing phenotypic switching promote loss of nuclear PTEN through nucleo-cytoplasmic translocation resulting in reduced myogenically active SRF, but enhanced SRF activity on target genes involved in proliferation.\n[5] Overall decreased expression of PTEN was observed in intimal SMCs of human atherosclerotic lesions underlying the potential clinical importance of these findings."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Factors inducing phenotypic switching promote loss of nuclear PTEN through nucleo-cytoplasmic translocation resulting in reduced myogenically active SRF, but enhanced SRF activity on target genes involved in proliferation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 917, "doc_id": 34071621, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [34071621], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Participants who quit smoking reduce lung cancer risk by approximately 50%.\n\nDocument title: Effect of smoking reduction on lung cancer risk.\n\nAbstract sentences:\n[0] CONTEXT Many smokers are unable or unwilling to completely quit smoking.\n[1] A proposed means of harm reduction is to reduce the number of cigarettes smoked per day.\n[2] However, it is not clear whether this strategy decreases the risk for tobacco-related diseases.\n[3] OBJECTIVE To assess the effects of smoking reduction on lung cancer incidence.\n[4] DESIGN, SETTING, AND PARTICIPANTS Observational population-based cohort study with up to 31 years of follow-up from the Copenhagen Centre for Prospective Population Studies, which administrates data from 3 longitudinal studies conducted in Copenhagen and suburbs, the Copenhagen City Heart Study, the Copenhagen Male Study, and the Glostrup Population Studies, Denmark.\n[5] Participants were 11,151 men and 8563 women (N = 19,714) aged 20 to 93 years, who attended 2 consecutive examinations with a 5- to 10-year interval between 1964 and 1988.\n[6] Participants underwent a physical examination and completed self-filled questionnaires about lifestyle habits.\n[7] The study population was divided into 6 groups according to smoking habits: continued heavy smokers (> or =15 cigarettes/d), reducers (reduced from > or =15 cigarettes/d by minimum of 50% without quitting), continued light smokers (1-14 cigarettes/d), quitters (stopped between first and second examination), stable ex-smokers, and never smokers.\n[8] MAIN OUTCOME MEASURE Incident primary lung cancer cases assessed by record linkage with the National Cancer Registry until December 31, 2003.\n[9] RESULTS There were 864 incident lung cancers during follow-up.\n[10] Using Cox regression, the adjusted hazard ratio (HR) for lung cancer in reducers was 0.73 (95% confidence interval [CI], 0.54-0.98) compared with persistent heavy smokers.\n[11] The HR for light smokers was 0.44 (95% CI, 0.35-0.56); for quitters, HR 0.50 (95% CI, 0.36-0.69), for stable ex-smokers, HR 0.17 (95% CI, 0.13-0.23), and for never smokers, HR 0.09 (95% CI, 0.06-0.13).\n[12] CONCLUSION Among individuals who smoke 15 or more cigarettes per day, smoking reduction by 50% significantly reduces the risk of lung cancer."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"The HR for light smokers was 0.44 (95% CI, 0.35-0.56); for quitters, HR 0.50 (95% CI, 0.36-0.69), for stable ex-smokers, HR 0.17 (95% CI, 0.13-0.23), and for never smokers, HR 0.09 (95% CI, 0.06-0.13).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 919, "doc_id": 16422880, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [16422880], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Patients in stable partnerships have a slower progression from HIV to AIDS.\n\nDocument title: Stable partnership and progression to AIDS or death in HIV infected patients receiving highly active antiretroviral therapy: Swiss HIV cohort study.\n\nAbstract sentences:\n[0] OBJECTIVES To explore the association between a stable partnership and clinical outcome in HIV infected patients receiving highly active antiretroviral therapy (HAART).\n[1] DESIGN Prospective cohort study of adults with HIV (Swiss HIV cohort study).\n[2] SETTING Seven outpatient clinics throughout Switzerland.\n[3] PARTICIPANTS The 3736 patients in the cohort who started HAART before 2002 (median age 36 years, 29% female, median follow up 3.6 years).\n[4] MAIN OUTCOME MEASURES Time to AIDS or death (primary endpoint), death alone, increases in CD4 cell count of at least 50 and 100 above baseline, optimal viral suppression (a viral load below 400 copies/ml), and viral rebound.\n[5] RESULTS During follow up 2985 (80%) participants reported a stable partnership on at least one occasion.\n[6] When starting HAART, 52% (545/1042) of participants reported a stable partnership; after five years of follow up 46% (190/412) of participants reported a stable partnership.\n[7] In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without.\n[8] Adjusted hazards ratios for other endpoints were 0.59 (0.44 to 0.79) for progression to death, 1.15 (1.06 to 1.24) for an increase in CD4 cells of 100 counts/microl or more, and 1.06 (0.98 to 1.14) for optimal viral suppression.\n[9] CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 923, "doc_id": 17077004, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [17077004], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Patients in stable partnerships have a slower progression from HIV to AIDS.\n\nDocument title: Stable partnership and progression to AIDS or death in HIV infected patients receiving highly active antiretroviral therapy: Swiss HIV cohort study.\n\nAbstract sentences:\n[0] OBJECTIVES To explore the association between a stable partnership and clinical outcome in HIV infected patients receiving highly active antiretroviral therapy (HAART).\n[1] DESIGN Prospective cohort study of adults with HIV (Swiss HIV cohort study).\n[2] SETTING Seven outpatient clinics throughout Switzerland.\n[3] PARTICIPANTS The 3736 patients in the cohort who started HAART before 2002 (median age 36 years, 29% female, median follow up 3.6 years).\n[4] MAIN OUTCOME MEASURES Time to AIDS or death (primary endpoint), death alone, increases in CD4 cell count of at least 50 and 100 above baseline, optimal viral suppression (a viral load below 400 copies/ml), and viral rebound.\n[5] RESULTS During follow up 2985 (80%) participants reported a stable partnership on at least one occasion.\n[6] When starting HAART, 52% (545/1042) of participants reported a stable partnership; after five years of follow up 46% (190/412) of participants reported a stable partnership.\n[7] In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without.\n[8] Adjusted hazards ratios for other endpoints were 0.59 (0.44 to 0.79) for progression to death, 1.15 (1.06 to 1.24) for an increase in CD4 cells of 100 counts/microl or more, and 1.06 (0.98 to 1.14) for optimal viral suppression.\n[9] CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 923, "doc_id": 17077004, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [17077004], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Patients in stable partnerships progress from HIV to death at the same rate as patients not in partnerships.\n\nDocument title: Stable partnership and progression to AIDS or death in HIV infected patients receiving highly active antiretroviral therapy: Swiss HIV cohort study.\n\nAbstract sentences:\n[0] OBJECTIVES To explore the association between a stable partnership and clinical outcome in HIV infected patients receiving highly active antiretroviral therapy (HAART).\n[1] DESIGN Prospective cohort study of adults with HIV (Swiss HIV cohort study).\n[2] SETTING Seven outpatient clinics throughout Switzerland.\n[3] PARTICIPANTS The 3736 patients in the cohort who started HAART before 2002 (median age 36 years, 29% female, median follow up 3.6 years).\n[4] MAIN OUTCOME MEASURES Time to AIDS or death (primary endpoint), death alone, increases in CD4 cell count of at least 50 and 100 above baseline, optimal viral suppression (a viral load below 400 copies/ml), and viral rebound.\n[5] RESULTS During follow up 2985 (80%) participants reported a stable partnership on at least one occasion.\n[6] When starting HAART, 52% (545/1042) of participants reported a stable partnership; after five years of follow up 46% (190/412) of participants reported a stable partnership.\n[7] In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without.\n[8] Adjusted hazards ratios for other endpoints were 0.59 (0.44 to 0.79) for progression to death, 1.15 (1.06 to 1.24) for an increase in CD4 cells of 100 counts/microl or more, and 1.06 (0.98 to 1.14) for optimal viral suppression.\n[9] CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 925, "doc_id": 17077004, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [17077004], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Patients in stable partnerships progress from HIV to death at the same rate as patients not in partnerships.\n\nDocument title: Stable partnership and progression to AIDS or death in HIV infected patients receiving highly active antiretroviral therapy: Swiss HIV cohort study.\n\nAbstract sentences:\n[0] OBJECTIVES To explore the association between a stable partnership and clinical outcome in HIV infected patients receiving highly active antiretroviral therapy (HAART).\n[1] DESIGN Prospective cohort study of adults with HIV (Swiss HIV cohort study).\n[2] SETTING Seven outpatient clinics throughout Switzerland.\n[3] PARTICIPANTS The 3736 patients in the cohort who started HAART before 2002 (median age 36 years, 29% female, median follow up 3.6 years).\n[4] MAIN OUTCOME MEASURES Time to AIDS or death (primary endpoint), death alone, increases in CD4 cell count of at least 50 and 100 above baseline, optimal viral suppression (a viral load below 400 copies/ml), and viral rebound.\n[5] RESULTS During follow up 2985 (80%) participants reported a stable partnership on at least one occasion.\n[6] When starting HAART, 52% (545/1042) of participants reported a stable partnership; after five years of follow up 46% (190/412) of participants reported a stable partnership.\n[7] In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without.\n[8] Adjusted hazards ratios for other endpoints were 0.59 (0.44 to 0.79) for progression to death, 1.15 (1.06 to 1.24) for an increase in CD4 cells of 100 counts/microl or more, and 1.06 (0.98 to 1.14) for optimal viral suppression.\n[9] CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 925, "doc_id": 17077004, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [17077004], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Patients with common epithelial cancers  are more likely to have an emergency event as their first hospital admission if they live in resource-deprived areas.\n\nDocument title: Social variations in access to hospital care for patients with colorectal, breast, and lung cancer between 1999 and 2006: retrospective analysis of hospital episode statistics\n\nAbstract sentences:\n[0] OBJECTIVES To determine the extent to which type of hospital admission (emergency compared with elective) and surgical procedure varied by socioeconomic circumstances, age, sex, and year of admission for colorectal, breast, and lung cancer.\n[1] DESIGN Repeated cross sectional study with data from individual patients, 1 April 1999 to 31 March 2006.\n[2] SETTING Hospital episode statistics (HES) dataset.\n[3] PARTICIPANTS 564 821 patients aged 50 and over admitted with a diagnosis of colorectal, breast, or lung cancer.\n[4] MAIN OUTCOME MEASURES Proportion of patients admitted as emergencies, and the proportion receiving the recommended surgical treatment.\n[5] RESULTS Patients from deprived areas, older people, and women were more likely to be admitted as emergencies.\n[6] For example, the adjusted odds ratio for patients with breast cancer in the least compared with most deprived fifth of deprivation was 0.63 (95% confidence interval 0.60 to 0.66) and the adjusted odds ratio for patients with lung cancer aged 80-89 compared with those aged 50-59 was 3.13 (2.93 to 3.34).\n[7] There were some improvements in disparities between age groups but not for patients living in deprived areas over time.\n[8] Patients from deprived areas were less likely to receive preferred procedures for rectal, breast, and lung cancer.\n[9] These findings did not improve with time.\n[10] For example, 67.4% (3529/5237) of patients in the most deprived fifth of deprivation had anterior resection for rectal cancer compared with 75.5% (4497/5959) of patients in the least deprived fifth (1.34, 1.22 to 1.47).\n[11] Over half (54.0%, 11 256/20 849) of patients in the most deprived fifth of deprivation had breast conserving surgery compared with 63.7% (18 445/28 960) of patients in the least deprived fifth (1.21, 1.16 to 1.26).\n[12] Men were less likely than women to undergo anterior resection and lung cancer resection and older people were less likely to receive breast conserving surgery and lung cancer resection.\n[13] For example, the adjusted odds ratio for lung cancer patients aged 80-89 compared with those aged 50-59 was 0.52 (0.46 to 0.59).\n[14] Conclusions Despite the implementation of the NHS Cancer Plan, social factors still strongly influence access to and the provision of care."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6, 7]\nExplanation: Evidence states: \"For example, the adjusted odds ratio for patients with breast cancer in the least compared with most deprived fifth of deprivation was 0.63 (95% confidence interval 0.60 to 0.66) and the adjusted odds ratio for patients with lung cancer aged 80-89 compared with those aged 50-59 was 3.13 (2.93 to 3.34). There were some improvements in disparities between age groups but not for patients living in deprived areas over time.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 926, "doc_id": 16390264, "label": "SUPPORTS", "evidence_sentence_ids": [6, 7], "cited_doc_ids": [16390264], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Patients with common epithelial cancers  are more likely to have an emergency event as their first hospital admission if they live in resource-deprived areas.\n\nDocument title: Social variations in access to hospital care for patients with colorectal, breast, and lung cancer between 1999 and 2006: retrospective analysis of hospital episode statistics\n\nAbstract sentences:\n[0] OBJECTIVES To determine the extent to which type of hospital admission (emergency compared with elective) and surgical procedure varied by socioeconomic circumstances, age, sex, and year of admission for colorectal, breast, and lung cancer.\n[1] DESIGN Repeated cross sectional study with data from individual patients, 1 April 1999 to 31 March 2006.\n[2] SETTING Hospital episode statistics (HES) dataset.\n[3] PARTICIPANTS 564 821 patients aged 50 and over admitted with a diagnosis of colorectal, breast, or lung cancer.\n[4] MAIN OUTCOME MEASURES Proportion of patients admitted as emergencies, and the proportion receiving the recommended surgical treatment.\n[5] RESULTS Patients from deprived areas, older people, and women were more likely to be admitted as emergencies.\n[6] For example, the adjusted odds ratio for patients with breast cancer in the least compared with most deprived fifth of deprivation was 0.63 (95% confidence interval 0.60 to 0.66) and the adjusted odds ratio for patients with lung cancer aged 80-89 compared with those aged 50-59 was 3.13 (2.93 to 3.34).\n[7] There were some improvements in disparities between age groups but not for patients living in deprived areas over time.\n[8] Patients from deprived areas were less likely to receive preferred procedures for rectal, breast, and lung cancer.\n[9] These findings did not improve with time.\n[10] For example, 67.4% (3529/5237) of patients in the most deprived fifth of deprivation had anterior resection for rectal cancer compared with 75.5% (4497/5959) of patients in the least deprived fifth (1.34, 1.22 to 1.47).\n[11] Over half (54.0%, 11 256/20 849) of patients in the most deprived fifth of deprivation had breast conserving surgery compared with 63.7% (18 445/28 960) of patients in the least deprived fifth (1.21, 1.16 to 1.26).\n[12] Men were less likely than women to undergo anterior resection and lung cancer resection and older people were less likely to receive breast conserving surgery and lung cancer resection.\n[13] For example, the adjusted odds ratio for lung cancer patients aged 80-89 compared with those aged 50-59 was 0.52 (0.46 to 0.59).\n[14] Conclusions Despite the implementation of the NHS Cancer Plan, social factors still strongly influence access to and the provision of care."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"For example, 67.4% (3529/5237) of patients in the most deprived fifth of deprivation had anterior resection for rectal cancer compared with 75.5% (4497/5959) of patients in the least deprived fifth (1.34, 1.22 to 1.47).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 926, "doc_id": 16390264, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [16390264], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Patients with common epithelial cancers are less likely to have an emergency event as their first hospital admission if they live in resource-deprived areas.\n\nDocument title: Social variations in access to hospital care for patients with colorectal, breast, and lung cancer between 1999 and 2006: retrospective analysis of hospital episode statistics\n\nAbstract sentences:\n[0] OBJECTIVES To determine the extent to which type of hospital admission (emergency compared with elective) and surgical procedure varied by socioeconomic circumstances, age, sex, and year of admission for colorectal, breast, and lung cancer.\n[1] DESIGN Repeated cross sectional study with data from individual patients, 1 April 1999 to 31 March 2006.\n[2] SETTING Hospital episode statistics (HES) dataset.\n[3] PARTICIPANTS 564 821 patients aged 50 and over admitted with a diagnosis of colorectal, breast, or lung cancer.\n[4] MAIN OUTCOME MEASURES Proportion of patients admitted as emergencies, and the proportion receiving the recommended surgical treatment.\n[5] RESULTS Patients from deprived areas, older people, and women were more likely to be admitted as emergencies.\n[6] For example, the adjusted odds ratio for patients with breast cancer in the least compared with most deprived fifth of deprivation was 0.63 (95% confidence interval 0.60 to 0.66) and the adjusted odds ratio for patients with lung cancer aged 80-89 compared with those aged 50-59 was 3.13 (2.93 to 3.34).\n[7] There were some improvements in disparities between age groups but not for patients living in deprived areas over time.\n[8] Patients from deprived areas were less likely to receive preferred procedures for rectal, breast, and lung cancer.\n[9] These findings did not improve with time.\n[10] For example, 67.4% (3529/5237) of patients in the most deprived fifth of deprivation had anterior resection for rectal cancer compared with 75.5% (4497/5959) of patients in the least deprived fifth (1.34, 1.22 to 1.47).\n[11] Over half (54.0%, 11 256/20 849) of patients in the most deprived fifth of deprivation had breast conserving surgery compared with 63.7% (18 445/28 960) of patients in the least deprived fifth (1.21, 1.16 to 1.26).\n[12] Men were less likely than women to undergo anterior resection and lung cancer resection and older people were less likely to receive breast conserving surgery and lung cancer resection.\n[13] For example, the adjusted odds ratio for lung cancer patients aged 80-89 compared with those aged 50-59 was 0.52 (0.46 to 0.59).\n[14] Conclusions Despite the implementation of the NHS Cancer Plan, social factors still strongly influence access to and the provision of care."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6, 7]\nExplanation: Evidence states: \"For example, the adjusted odds ratio for patients with breast cancer in the least compared with most deprived fifth of deprivation was 0.63 (95% confidence interval 0.60 to 0.66) and the adjusted odds ratio for patients with lung cancer aged 80-89 compared with those aged 50-59 was 3.13 (2.93 to 3.34). There were some improvements in disparities between age groups but not for patients living in deprived areas over time.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 927, "doc_id": 16390264, "label": "CONTRADICTS", "evidence_sentence_ids": [6, 7], "cited_doc_ids": [16390264], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Patients with common epithelial cancers are less likely to have an emergency event as their first hospital admission if they live in resource-deprived areas.\n\nDocument title: Social variations in access to hospital care for patients with colorectal, breast, and lung cancer between 1999 and 2006: retrospective analysis of hospital episode statistics\n\nAbstract sentences:\n[0] OBJECTIVES To determine the extent to which type of hospital admission (emergency compared with elective) and surgical procedure varied by socioeconomic circumstances, age, sex, and year of admission for colorectal, breast, and lung cancer.\n[1] DESIGN Repeated cross sectional study with data from individual patients, 1 April 1999 to 31 March 2006.\n[2] SETTING Hospital episode statistics (HES) dataset.\n[3] PARTICIPANTS 564 821 patients aged 50 and over admitted with a diagnosis of colorectal, breast, or lung cancer.\n[4] MAIN OUTCOME MEASURES Proportion of patients admitted as emergencies, and the proportion receiving the recommended surgical treatment.\n[5] RESULTS Patients from deprived areas, older people, and women were more likely to be admitted as emergencies.\n[6] For example, the adjusted odds ratio for patients with breast cancer in the least compared with most deprived fifth of deprivation was 0.63 (95% confidence interval 0.60 to 0.66) and the adjusted odds ratio for patients with lung cancer aged 80-89 compared with those aged 50-59 was 3.13 (2.93 to 3.34).\n[7] There were some improvements in disparities between age groups but not for patients living in deprived areas over time.\n[8] Patients from deprived areas were less likely to receive preferred procedures for rectal, breast, and lung cancer.\n[9] These findings did not improve with time.\n[10] For example, 67.4% (3529/5237) of patients in the most deprived fifth of deprivation had anterior resection for rectal cancer compared with 75.5% (4497/5959) of patients in the least deprived fifth (1.34, 1.22 to 1.47).\n[11] Over half (54.0%, 11 256/20 849) of patients in the most deprived fifth of deprivation had breast conserving surgery compared with 63.7% (18 445/28 960) of patients in the least deprived fifth (1.21, 1.16 to 1.26).\n[12] Men were less likely than women to undergo anterior resection and lung cancer resection and older people were less likely to receive breast conserving surgery and lung cancer resection.\n[13] For example, the adjusted odds ratio for lung cancer patients aged 80-89 compared with those aged 50-59 was 0.52 (0.46 to 0.59).\n[14] Conclusions Despite the implementation of the NHS Cancer Plan, social factors still strongly influence access to and the provision of care."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"For example, 67.4% (3529/5237) of patients in the most deprived fifth of deprivation had anterior resection for rectal cancer compared with 75.5% (4497/5959) of patients in the least deprived fifth (1.34, 1.22 to 1.47).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 927, "doc_id": 16390264, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [16390264], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Patients with microcytosis and higher erythrocyte count are more vulnerable to severe malarial anaemia when infected with Plasmodium falciparum.\n\nDocument title: Increased Microerythrocyte Count in Homozygous α+-Thalassaemia Contributes to Protection against Severe Malarial Anaemia\n\nAbstract sentences:\n[0] BACKGROUND The heritable haemoglobinopathy alpha(+)-thalassaemia is caused by the reduced synthesis of alpha-globin chains that form part of normal adult haemoglobin (Hb).\n[1] Individuals homozygous for alpha(+)-thalassaemia have microcytosis and an increased erythrocyte count.\n[2] Alpha(+)-thalassaemia homozygosity confers considerable protection against severe malaria, including severe malarial anaemia (SMA) (Hb concentration < 50 g/l), but does not influence parasite count.\n[3] We tested the hypothesis that the erythrocyte indices associated with alpha(+)-thalassaemia homozygosity provide a haematological benefit during acute malaria.\n[4] METHODS AND FINDINGS Data from children living on the north coast of Papua New Guinea who had participated in a case-control study of the protection afforded by alpha(+)-thalassaemia against severe malaria were reanalysed to assess the genotype-specific reduction in erythrocyte count and Hb levels associated with acute malarial disease.\n[5] We observed a reduction in median erythrocyte count of approximately 1.5 x 10(12)/l in all children with acute falciparum malaria relative to values in community children (p < 0.001).\n[6] We developed a simple mathematical model of the linear relationship between Hb concentration and erythrocyte count.\n[7] This model predicted that children homozygous for alpha(+)-thalassaemia lose less Hb than children of normal genotype for a reduction in erythrocyte count of >1.1 x 10(12)/l as a result of the reduced mean cell Hb in homozygous alpha(+)-thalassaemia.\n[8] In addition, children homozygous for alpha(+)-thalassaemia require a 10% greater reduction in erythrocyte count than children of normal genotype (p = 0.02) for Hb concentration to fall to 50 g/l, the cutoff for SMA.\n[9] We estimated that the haematological profile in children homozygous for alpha(+)-thalassaemia reduces the risk of SMA during acute malaria compared to children of normal genotype (relative risk 0.52; 95% confidence interval [CI] 0.24-1.12, p = 0.09).\n[10] CONCLUSIONS The increased erythrocyte count and microcytosis in children homozygous for alpha(+)-thalassaemia may contribute substantially to their protection against SMA.\n[11] A lower concentration of Hb per erythrocyte and a larger population of erythrocytes may be a biologically advantageous strategy against the significant reduction in erythrocyte count that occurs during acute infection with the malaria parasite Plasmodium falciparum.\n[12] This haematological profile may reduce the risk of anaemia by other Plasmodium species, as well as other causes of anaemia.\n[13] Other host polymorphisms that induce an increased erythrocyte count and microcytosis may confer a similar advantage."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Alpha(+)-thalassaemia homozygosity confers considerable protection against severe malaria, including severe malarial anaemia (SMA) (Hb concentration < 50 g/l), but does not influence parasite count.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 928, "doc_id": 18174210, "label": "CONTRADICTS", "evidence_sentence_ids": [2], "cited_doc_ids": [18174210], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Patients with microcytosis and higher erythrocyte count are more vulnerable to severe malarial anaemia when infected with Plasmodium falciparum.\n\nDocument title: Increased Microerythrocyte Count in Homozygous α+-Thalassaemia Contributes to Protection against Severe Malarial Anaemia\n\nAbstract sentences:\n[0] BACKGROUND The heritable haemoglobinopathy alpha(+)-thalassaemia is caused by the reduced synthesis of alpha-globin chains that form part of normal adult haemoglobin (Hb).\n[1] Individuals homozygous for alpha(+)-thalassaemia have microcytosis and an increased erythrocyte count.\n[2] Alpha(+)-thalassaemia homozygosity confers considerable protection against severe malaria, including severe malarial anaemia (SMA) (Hb concentration < 50 g/l), but does not influence parasite count.\n[3] We tested the hypothesis that the erythrocyte indices associated with alpha(+)-thalassaemia homozygosity provide a haematological benefit during acute malaria.\n[4] METHODS AND FINDINGS Data from children living on the north coast of Papua New Guinea who had participated in a case-control study of the protection afforded by alpha(+)-thalassaemia against severe malaria were reanalysed to assess the genotype-specific reduction in erythrocyte count and Hb levels associated with acute malarial disease.\n[5] We observed a reduction in median erythrocyte count of approximately 1.5 x 10(12)/l in all children with acute falciparum malaria relative to values in community children (p < 0.001).\n[6] We developed a simple mathematical model of the linear relationship between Hb concentration and erythrocyte count.\n[7] This model predicted that children homozygous for alpha(+)-thalassaemia lose less Hb than children of normal genotype for a reduction in erythrocyte count of >1.1 x 10(12)/l as a result of the reduced mean cell Hb in homozygous alpha(+)-thalassaemia.\n[8] In addition, children homozygous for alpha(+)-thalassaemia require a 10% greater reduction in erythrocyte count than children of normal genotype (p = 0.02) for Hb concentration to fall to 50 g/l, the cutoff for SMA.\n[9] We estimated that the haematological profile in children homozygous for alpha(+)-thalassaemia reduces the risk of SMA during acute malaria compared to children of normal genotype (relative risk 0.52; 95% confidence interval [CI] 0.24-1.12, p = 0.09).\n[10] CONCLUSIONS The increased erythrocyte count and microcytosis in children homozygous for alpha(+)-thalassaemia may contribute substantially to their protection against SMA.\n[11] A lower concentration of Hb per erythrocyte and a larger population of erythrocytes may be a biologically advantageous strategy against the significant reduction in erythrocyte count that occurs during acute infection with the malaria parasite Plasmodium falciparum.\n[12] This haematological profile may reduce the risk of anaemia by other Plasmodium species, as well as other causes of anaemia.\n[13] Other host polymorphisms that induce an increased erythrocyte count and microcytosis may confer a similar advantage."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"We estimated that the haematological profile in children homozygous for alpha(+)-thalassaemia reduces the risk of SMA during acute malaria compared to children of normal genotype (relative risk 0.52; 95% confidence interval [CI] 0.24-1.12, p = 0.09).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 928, "doc_id": 18174210, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [18174210], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Patients with microcytosis and higher erythrocyte count are more vulnerable to severe malarial anaemia when infected with Plasmodium falciparum.\n\nDocument title: Increased Microerythrocyte Count in Homozygous α+-Thalassaemia Contributes to Protection against Severe Malarial Anaemia\n\nAbstract sentences:\n[0] BACKGROUND The heritable haemoglobinopathy alpha(+)-thalassaemia is caused by the reduced synthesis of alpha-globin chains that form part of normal adult haemoglobin (Hb).\n[1] Individuals homozygous for alpha(+)-thalassaemia have microcytosis and an increased erythrocyte count.\n[2] Alpha(+)-thalassaemia homozygosity confers considerable protection against severe malaria, including severe malarial anaemia (SMA) (Hb concentration < 50 g/l), but does not influence parasite count.\n[3] We tested the hypothesis that the erythrocyte indices associated with alpha(+)-thalassaemia homozygosity provide a haematological benefit during acute malaria.\n[4] METHODS AND FINDINGS Data from children living on the north coast of Papua New Guinea who had participated in a case-control study of the protection afforded by alpha(+)-thalassaemia against severe malaria were reanalysed to assess the genotype-specific reduction in erythrocyte count and Hb levels associated with acute malarial disease.\n[5] We observed a reduction in median erythrocyte count of approximately 1.5 x 10(12)/l in all children with acute falciparum malaria relative to values in community children (p < 0.001).\n[6] We developed a simple mathematical model of the linear relationship between Hb concentration and erythrocyte count.\n[7] This model predicted that children homozygous for alpha(+)-thalassaemia lose less Hb than children of normal genotype for a reduction in erythrocyte count of >1.1 x 10(12)/l as a result of the reduced mean cell Hb in homozygous alpha(+)-thalassaemia.\n[8] In addition, children homozygous for alpha(+)-thalassaemia require a 10% greater reduction in erythrocyte count than children of normal genotype (p = 0.02) for Hb concentration to fall to 50 g/l, the cutoff for SMA.\n[9] We estimated that the haematological profile in children homozygous for alpha(+)-thalassaemia reduces the risk of SMA during acute malaria compared to children of normal genotype (relative risk 0.52; 95% confidence interval [CI] 0.24-1.12, p = 0.09).\n[10] CONCLUSIONS The increased erythrocyte count and microcytosis in children homozygous for alpha(+)-thalassaemia may contribute substantially to their protection against SMA.\n[11] A lower concentration of Hb per erythrocyte and a larger population of erythrocytes may be a biologically advantageous strategy against the significant reduction in erythrocyte count that occurs during acute infection with the malaria parasite Plasmodium falciparum.\n[12] This haematological profile may reduce the risk of anaemia by other Plasmodium species, as well as other causes of anaemia.\n[13] Other host polymorphisms that induce an increased erythrocyte count and microcytosis may confer a similar advantage."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"CONCLUSIONS The increased erythrocyte count and microcytosis in children homozygous for alpha(+)-thalassaemia may contribute substantially to their protection against SMA.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 928, "doc_id": 18174210, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [18174210], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Patients with microcytosis and higher erythrocyte count were more resistant to severe malarial anaemia when infected with Plasmodium falciparum.\n\nDocument title: Increased Microerythrocyte Count in Homozygous α+-Thalassaemia Contributes to Protection against Severe Malarial Anaemia\n\nAbstract sentences:\n[0] BACKGROUND The heritable haemoglobinopathy alpha(+)-thalassaemia is caused by the reduced synthesis of alpha-globin chains that form part of normal adult haemoglobin (Hb).\n[1] Individuals homozygous for alpha(+)-thalassaemia have microcytosis and an increased erythrocyte count.\n[2] Alpha(+)-thalassaemia homozygosity confers considerable protection against severe malaria, including severe malarial anaemia (SMA) (Hb concentration < 50 g/l), but does not influence parasite count.\n[3] We tested the hypothesis that the erythrocyte indices associated with alpha(+)-thalassaemia homozygosity provide a haematological benefit during acute malaria.\n[4] METHODS AND FINDINGS Data from children living on the north coast of Papua New Guinea who had participated in a case-control study of the protection afforded by alpha(+)-thalassaemia against severe malaria were reanalysed to assess the genotype-specific reduction in erythrocyte count and Hb levels associated with acute malarial disease.\n[5] We observed a reduction in median erythrocyte count of approximately 1.5 x 10(12)/l in all children with acute falciparum malaria relative to values in community children (p < 0.001).\n[6] We developed a simple mathematical model of the linear relationship between Hb concentration and erythrocyte count.\n[7] This model predicted that children homozygous for alpha(+)-thalassaemia lose less Hb than children of normal genotype for a reduction in erythrocyte count of >1.1 x 10(12)/l as a result of the reduced mean cell Hb in homozygous alpha(+)-thalassaemia.\n[8] In addition, children homozygous for alpha(+)-thalassaemia require a 10% greater reduction in erythrocyte count than children of normal genotype (p = 0.02) for Hb concentration to fall to 50 g/l, the cutoff for SMA.\n[9] We estimated that the haematological profile in children homozygous for alpha(+)-thalassaemia reduces the risk of SMA during acute malaria compared to children of normal genotype (relative risk 0.52; 95% confidence interval [CI] 0.24-1.12, p = 0.09).\n[10] CONCLUSIONS The increased erythrocyte count and microcytosis in children homozygous for alpha(+)-thalassaemia may contribute substantially to their protection against SMA.\n[11] A lower concentration of Hb per erythrocyte and a larger population of erythrocytes may be a biologically advantageous strategy against the significant reduction in erythrocyte count that occurs during acute infection with the malaria parasite Plasmodium falciparum.\n[12] This haematological profile may reduce the risk of anaemia by other Plasmodium species, as well as other causes of anaemia.\n[13] Other host polymorphisms that induce an increased erythrocyte count and microcytosis may confer a similar advantage."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Alpha(+)-thalassaemia homozygosity confers considerable protection against severe malaria, including severe malarial anaemia (SMA) (Hb concentration < 50 g/l), but does not influence parasite count.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 929, "doc_id": 18174210, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [18174210], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Patients with microcytosis and higher erythrocyte count were more resistant to severe malarial anaemia when infected with Plasmodium falciparum.\n\nDocument title: Increased Microerythrocyte Count in Homozygous α+-Thalassaemia Contributes to Protection against Severe Malarial Anaemia\n\nAbstract sentences:\n[0] BACKGROUND The heritable haemoglobinopathy alpha(+)-thalassaemia is caused by the reduced synthesis of alpha-globin chains that form part of normal adult haemoglobin (Hb).\n[1] Individuals homozygous for alpha(+)-thalassaemia have microcytosis and an increased erythrocyte count.\n[2] Alpha(+)-thalassaemia homozygosity confers considerable protection against severe malaria, including severe malarial anaemia (SMA) (Hb concentration < 50 g/l), but does not influence parasite count.\n[3] We tested the hypothesis that the erythrocyte indices associated with alpha(+)-thalassaemia homozygosity provide a haematological benefit during acute malaria.\n[4] METHODS AND FINDINGS Data from children living on the north coast of Papua New Guinea who had participated in a case-control study of the protection afforded by alpha(+)-thalassaemia against severe malaria were reanalysed to assess the genotype-specific reduction in erythrocyte count and Hb levels associated with acute malarial disease.\n[5] We observed a reduction in median erythrocyte count of approximately 1.5 x 10(12)/l in all children with acute falciparum malaria relative to values in community children (p < 0.001).\n[6] We developed a simple mathematical model of the linear relationship between Hb concentration and erythrocyte count.\n[7] This model predicted that children homozygous for alpha(+)-thalassaemia lose less Hb than children of normal genotype for a reduction in erythrocyte count of >1.1 x 10(12)/l as a result of the reduced mean cell Hb in homozygous alpha(+)-thalassaemia.\n[8] In addition, children homozygous for alpha(+)-thalassaemia require a 10% greater reduction in erythrocyte count than children of normal genotype (p = 0.02) for Hb concentration to fall to 50 g/l, the cutoff for SMA.\n[9] We estimated that the haematological profile in children homozygous for alpha(+)-thalassaemia reduces the risk of SMA during acute malaria compared to children of normal genotype (relative risk 0.52; 95% confidence interval [CI] 0.24-1.12, p = 0.09).\n[10] CONCLUSIONS The increased erythrocyte count and microcytosis in children homozygous for alpha(+)-thalassaemia may contribute substantially to their protection against SMA.\n[11] A lower concentration of Hb per erythrocyte and a larger population of erythrocytes may be a biologically advantageous strategy against the significant reduction in erythrocyte count that occurs during acute infection with the malaria parasite Plasmodium falciparum.\n[12] This haematological profile may reduce the risk of anaemia by other Plasmodium species, as well as other causes of anaemia.\n[13] Other host polymorphisms that induce an increased erythrocyte count and microcytosis may confer a similar advantage."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"We estimated that the haematological profile in children homozygous for alpha(+)-thalassaemia reduces the risk of SMA during acute malaria compared to children of normal genotype (relative risk 0.52; 95% confidence interval [CI] 0.24-1.12, p = 0.09).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 929, "doc_id": 18174210, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [18174210], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Patients with microcytosis and higher erythrocyte count were more resistant to severe malarial anaemia when infected with Plasmodium falciparum.\n\nDocument title: Increased Microerythrocyte Count in Homozygous α+-Thalassaemia Contributes to Protection against Severe Malarial Anaemia\n\nAbstract sentences:\n[0] BACKGROUND The heritable haemoglobinopathy alpha(+)-thalassaemia is caused by the reduced synthesis of alpha-globin chains that form part of normal adult haemoglobin (Hb).\n[1] Individuals homozygous for alpha(+)-thalassaemia have microcytosis and an increased erythrocyte count.\n[2] Alpha(+)-thalassaemia homozygosity confers considerable protection against severe malaria, including severe malarial anaemia (SMA) (Hb concentration < 50 g/l), but does not influence parasite count.\n[3] We tested the hypothesis that the erythrocyte indices associated with alpha(+)-thalassaemia homozygosity provide a haematological benefit during acute malaria.\n[4] METHODS AND FINDINGS Data from children living on the north coast of Papua New Guinea who had participated in a case-control study of the protection afforded by alpha(+)-thalassaemia against severe malaria were reanalysed to assess the genotype-specific reduction in erythrocyte count and Hb levels associated with acute malarial disease.\n[5] We observed a reduction in median erythrocyte count of approximately 1.5 x 10(12)/l in all children with acute falciparum malaria relative to values in community children (p < 0.001).\n[6] We developed a simple mathematical model of the linear relationship between Hb concentration and erythrocyte count.\n[7] This model predicted that children homozygous for alpha(+)-thalassaemia lose less Hb than children of normal genotype for a reduction in erythrocyte count of >1.1 x 10(12)/l as a result of the reduced mean cell Hb in homozygous alpha(+)-thalassaemia.\n[8] In addition, children homozygous for alpha(+)-thalassaemia require a 10% greater reduction in erythrocyte count than children of normal genotype (p = 0.02) for Hb concentration to fall to 50 g/l, the cutoff for SMA.\n[9] We estimated that the haematological profile in children homozygous for alpha(+)-thalassaemia reduces the risk of SMA during acute malaria compared to children of normal genotype (relative risk 0.52; 95% confidence interval [CI] 0.24-1.12, p = 0.09).\n[10] CONCLUSIONS The increased erythrocyte count and microcytosis in children homozygous for alpha(+)-thalassaemia may contribute substantially to their protection against SMA.\n[11] A lower concentration of Hb per erythrocyte and a larger population of erythrocytes may be a biologically advantageous strategy against the significant reduction in erythrocyte count that occurs during acute infection with the malaria parasite Plasmodium falciparum.\n[12] This haematological profile may reduce the risk of anaemia by other Plasmodium species, as well as other causes of anaemia.\n[13] Other host polymorphisms that induce an increased erythrocyte count and microcytosis may confer a similar advantage."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"CONCLUSIONS The increased erythrocyte count and microcytosis in children homozygous for alpha(+)-thalassaemia may contribute substantially to their protection against SMA.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 929, "doc_id": 18174210, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [18174210], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Patients with panic anxiety show decreased CSF levels of hypocretin.\n\nDocument title: A KEY ROLE FOR OREXIN IN PANIC ANXIETY\n\nAbstract sentences:\n[0] Panic disorder is a severe anxiety disorder with recurrent, debilitating panic attacks.\n[1] In individuals with panic disorder there is evidence of decreased central gamma-aminobutyric acid (GABA) activity as well as marked increases in autonomic and respiratory responses after intravenous infusions of hypertonic sodium lactate.\n[2] In a rat model of panic disorder, chronic inhibition of GABA synthesis in the dorsomedial-perifornical hypothalamus of rats produces anxiety-like states and a similar vulnerability to sodium lactate-induced cardioexcitatory responses.\n[3] The dorsomedial-perifornical hypothalamus is enriched in neurons containing orexin (ORX, also known as hypocretin), which have a crucial role in arousal, vigilance and central autonomic mobilization, all of which are key components of panic.\n[4] Here we show that activation of ORX-synthesizing neurons is necessary for developing a panic-prone state in the rat panic model, and either silencing of the hypothalamic gene encoding ORX (Hcrt) with RNAi or systemic ORX-1 receptor antagonists blocks the panic responses.\n[5] Moreover, we show that human subjects with panic anxiety have elevated levels of ORX in the cerebrospinal fluid compared to subjects without panic anxiety.\n[6] Taken together, our results suggest that the ORX system may be involved in the pathophysiology of panic anxiety and that ORX antagonists constitute a potential new treatment strategy for panic disorder."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Moreover, we show that human subjects with panic anxiety have elevated levels of ORX in the cerebrospinal fluid compared to subjects without panic anxiety.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 930, "doc_id": 16056514, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [16056514], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pediatric SCD patients with vaso-occlusive crisis show increased morphine use after breathing 80 ppm iNO for 4 hours.\n\nDocument title: Preliminary assessment of inhaled nitric oxide for acute vaso-occlusive crisis in pediatric patients with sickle cell disease.\n\nAbstract sentences:\n[0] CONTEXT Vaso-occlusion is central to the painful crises and acute and chronic organ damage in sickle cell disease.\n[1] Abnormal nitric oxide-dependent regulation of vascular tone, adhesion, platelet activation, and inflammation contributes to the pathophysiology of vaso-occlusion.\n[2] Nitric oxide may have promise as a mechanism-of-disease-based therapy for treatment of vaso-occlusion.\n[3] OBJECTIVE To explore the efficacy and safety of inhaled nitric oxide (INO) for treatment of vaso-occlusive crisis in pediatric patients.\n[4] DESIGN Prospective, double-blind, placebo-controlled, randomized clinical trial with enrollment between September 1999 and October 2001.\n[5] SETTING Urban, tertiary care children's hospital in the United States.\n[6] PARTICIPANTS Twenty patients aged 10 to 21 years with sickle cell disease and severe acute vaso-occlusive crisis.\n[7] INTERVENTION Patients were randomly assigned to receive INO (80 ppm with 21% final concentration of inspired oxygen; n = 10), or placebo (21% inspired oxygen; n = 10) for 4 hours.\n[8] MAIN OUTCOME MEASURES Change in pain at 4 hours of inhalation compared with preinhalation pain, measured on a 10-cm visual analog scale (VAS); secondary outcome measures were pain over 6 hours, parenteral narcotic use over 24 hours, duration of hospitalization, blood pressure, oxygen saturation, and methemoglobin concentration.\n[9] RESULTS Preinhalation VAS pain scores were similar in the INO and placebo groups (P =.80).\n[10] The decrease in VAS pain scores at 4 hours was 2.0 cm in the INO group and 1.2 cm in the placebo group (P =.37).\n[11] Repeated-measures analysis of variance for hourly pain scores showed a 1-cm/h greater reduction in the INO group than the placebo group (P =.02).\n[12] Morphine use over 6 hours was significantly less in the INO group (mean cumulative use, 0.29 vs 0.44 mg/kg; P =.03) but was not different over 4 hours (0.26 vs 0.32 mg/kg; P =.21) or 24 hours (0.63 vs 0.91 mg/kg; P =.15).\n[13] Duration of hospitalization was 78 and 100 hours in the INO and placebo groups, respectively (P =.19).\n[14] No INO toxicity was observed.\n[15] CONCLUSIONS Results of this exploratory study suggest that INO may be beneficial for acute vaso-occlusive crisis.\n[16] These preliminary results warrant further investigation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"Morphine use over 6 hours was significantly less in the INO group (mean cumulative use, 0.29 vs 0.44 mg/kg; P =.03) but was not different over 4 hours (0.26 vs 0.32 mg/kg; P =.21) or 24 hours (0.63 vs 0.91 mg/kg; P =.15).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 933, "doc_id": 14711483, "label": "SUPPORTS", "evidence_sentence_ids": [12], "cited_doc_ids": [14711483], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Perigenital skin is not the primary site of HIV acquisition.\n\nDocument title: Persistence of HIV-1 Receptor-Positive Cells after HSV-2 Reactivation: A Potential Mechanism for Increased HIV-1 Acquisition\n\nAbstract sentences:\n[0] To explore the mechanism by which herpes simplex virus (HSV)-2 infection is related to HIV-1 acquisition, we conducted in situ analysis of the cellular infiltrate from sequential biopsies of HSV-2 lesions from patients on and off antiviral therapy.\n[1] CD4(+) and CD8(+) T cells and a mixed population of plasmacytoid and myeloid dendritic cells (DCs), including cells expressing the C-type lectin receptor DC-SIGN, persisted at sites of HSV-2 reactivation for months after healing, even with daily antiviral therapy.\n[2] The CD4(+) T cells that persisted reacted to HSV-2 antigen, were enriched for expression of the chemokine receptor CCR5, and were contiguous to DCs expressing the interleukin-3 receptor CD123 or DC-SIGN.\n[3] Ex vivo infection with a CCR5-tropic strain of HIV-1 revealed greater concentrations of integrated HIV-1 DNA in cells derived from healed genital lesion biopsies than in cells from control skin biopsies.\n[4] The persistence and enrichment of HIV receptor-positive inflammatory cells in the genitalia help explain the inability of anti-HSV-2 therapy to reduce HIV acquisition."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 934, "doc_id": 8563659, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [8563659], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Peroxynitrite is required for induction of T cell tolerance.\n\nDocument title: Altered recognition of antigen is a mechanism of CD8+ T cell tolerance in cancer\n\nAbstract sentences:\n[0] Antigen-specific CD8+ T-cell tolerance, induced by myeloid-derived suppressor cells (MDSCs), is one of the main mechanisms of tumor escape.\n[1] Using in vivo models, we show here that MDSCs directly disrupt the binding of specific peptide–major histocompatibility complex (pMHC) dimers to CD8-expressing T cells through nitration of tyrosines in a T-cell receptor (TCR)-CD8 complex.\n[2] This process makes CD8-expressing T cells unable to bind pMHC and to respond to the specific peptide, although they retain their ability to respond to nonspecific stimulation.\n[3] Nitration of TCR-CD8 is induced by MDSCs through hyperproduction of reactive oxygen species and peroxynitrite during direct cell-cell contact.\n[4] Molecular modeling suggests specific sites of nitration that might affect the conformational flexibility of TCR-CD8 and its interaction with pMHC.\n[5] These data identify a previously unknown mechanism of T-cell tolerance in cancer that is also pertinent to many pathological conditions associated with accumulation of MDSCs."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3, 5]\nExplanation: Evidence states: \"Nitration of TCR-CD8 is induced by MDSCs through hyperproduction of reactive oxygen species and peroxynitrite during direct cell-cell contact. These data identify a previously unknown mechanism of T-cell tolerance in cancer that is also pertinent to many pathological conditions associated with accumulation of MDSCs.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 935, "doc_id": 5483793, "label": "SUPPORTS", "evidence_sentence_ids": [3, 5], "cited_doc_ids": [5483793], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Persister cells provide relapse resistance in cancer patients.\n\nDocument title: A framework for understanding and targeting residual disease in oncogene-driven solid cancers\n\nAbstract sentences:\n[0] Molecular targeted therapy has the potential to dramatically improve survival in patients with cancer.\n[1] However, complete and durable responses to targeted therapy are rare in individuals with advanced-stage solid cancers.\n[2] Even the most effective targeted therapies generally do not induce a complete tumor response, resulting in residual disease and tumor progression that limits patient survival.\n[3] We discuss the emerging need to more fully understand the molecular basis of residual disease as a prelude to designing therapeutic strategies to minimize or eliminate residual disease so that we can move from temporary to chronic control of disease, or a cure, for patients with advanced-stage solid cancers.\n[4] Ultimately, we propose a shift from the current reactive paradigm of analyzing and treating acquired drug resistance to a pre-emptive paradigm of defining the mechanisms that result in residual disease, to target and limit this disease reservoir."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 938, "doc_id": 26231129, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [26231129], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Persistor cells are one reason for incomplete responses to Tyrosine kinase inhibitor (TKI) therapy in cancer patients.\n\nDocument title: A framework for understanding and targeting residual disease in oncogene-driven solid cancers\n\nAbstract sentences:\n[0] Molecular targeted therapy has the potential to dramatically improve survival in patients with cancer.\n[1] However, complete and durable responses to targeted therapy are rare in individuals with advanced-stage solid cancers.\n[2] Even the most effective targeted therapies generally do not induce a complete tumor response, resulting in residual disease and tumor progression that limits patient survival.\n[3] We discuss the emerging need to more fully understand the molecular basis of residual disease as a prelude to designing therapeutic strategies to minimize or eliminate residual disease so that we can move from temporary to chronic control of disease, or a cure, for patients with advanced-stage solid cancers.\n[4] Ultimately, we propose a shift from the current reactive paradigm of analyzing and treating acquired drug resistance to a pre-emptive paradigm of defining the mechanisms that result in residual disease, to target and limit this disease reservoir."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 939, "doc_id": 26231129, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [26231129], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pharmacist attendance at ward rounds increases adverse events in wards.\n\nDocument title: Pharmacist participation on physician rounds and adverse drug events in the intensive care unit.\n\nAbstract sentences:\n[0] CONTEXT Pharmacist review of medication orders in the intensive care unit (ICU) has been shown to prevent errors, and pharmacist consultation has reduced drug costs.\n[1] However, whether pharmacist participation in the ICU at the time of drug prescribing reduces adverse events has not been studied.\n[2] OBJECTIVE To measure the effect of pharmacist participation on medical rounds in the ICU on the rate of preventable adverse drug events (ADEs) caused by ordering errors.\n[3] DESIGN Before-after comparison between phase 1 (baseline) and phase 2 (after intervention implemented) and phase 2 comparison with a control unit that did not receive the intervention.\n[4] SETTING A medical ICU (study unit) and a coronary care unit (control unit) in a large urban teaching hospital.\n[5] PATIENTS Seventy-five patients randomly selected from each of 3 groups: all admissions to the study unit from February 1, 1993, through July 31, 1993 (baseline) and all admissions to the study unit (postintervention) and control unit from October 1, 1994, through July 7, 1995.\n[6] In addition, 50 patients were selected at random from the control unit during the baseline period.\n[7] INTERVENTION A senior pharmacist made rounds with the ICU team and remained in the ICU for consultation in the morning, and was available on call throughout the day.\n[8] MAIN OUTCOME MEASURES Preventable ADEs due to ordering (prescribing) errors and the number, type, and acceptance of interventions made by the pharmacist.\n[9] Preventable ADEs were identified by review of medical records of the randomly selected patients during both preintervention and postintervention phases.\n[10] Pharmacists recorded all recommendations, which were then analyzed by type and acceptance.\n[11] RESULTS The rate of preventable ordering ADEs decreased by 66% from 10.4 per 1000 patient-days (95% confidence interval [CI], 7-14) before the intervention to 3.5 (95% CI, 1-5; P<.001) after the intervention.\n[12] In the control unit, the rate was essentially unchanged during the same time periods: 10.9 (95% CI, 6-16) and 12.4 (95% CI, 8-17) per 1000 patient-days.\n[13] The pharmacist made 366 recommendations related to drug ordering, of which 362 (99%) were accepted by physicians.\n[14] CONCLUSIONS The presence of a pharmacist on rounds as a full member of the patient care team in a medical ICU was associated with a substantially lower rate of ADEs caused by prescribing errors.\n[15] Nearly all the changes were readily accepted by physicians."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"RESULTS The rate of preventable ordering ADEs decreased by 66% from 10.4 per 1000 patient-days (95% confidence interval [CI], 7-14) before the intervention to 3.5 (95% CI, 1-5; P<.001) after the intervention.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 940, "doc_id": 12258338, "label": "CONTRADICTS", "evidence_sentence_ids": [11], "cited_doc_ids": [12258338], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pharmacist attendance at ward rounds increases adverse events in wards.\n\nDocument title: Pharmacist participation on physician rounds and adverse drug events in the intensive care unit.\n\nAbstract sentences:\n[0] CONTEXT Pharmacist review of medication orders in the intensive care unit (ICU) has been shown to prevent errors, and pharmacist consultation has reduced drug costs.\n[1] However, whether pharmacist participation in the ICU at the time of drug prescribing reduces adverse events has not been studied.\n[2] OBJECTIVE To measure the effect of pharmacist participation on medical rounds in the ICU on the rate of preventable adverse drug events (ADEs) caused by ordering errors.\n[3] DESIGN Before-after comparison between phase 1 (baseline) and phase 2 (after intervention implemented) and phase 2 comparison with a control unit that did not receive the intervention.\n[4] SETTING A medical ICU (study unit) and a coronary care unit (control unit) in a large urban teaching hospital.\n[5] PATIENTS Seventy-five patients randomly selected from each of 3 groups: all admissions to the study unit from February 1, 1993, through July 31, 1993 (baseline) and all admissions to the study unit (postintervention) and control unit from October 1, 1994, through July 7, 1995.\n[6] In addition, 50 patients were selected at random from the control unit during the baseline period.\n[7] INTERVENTION A senior pharmacist made rounds with the ICU team and remained in the ICU for consultation in the morning, and was available on call throughout the day.\n[8] MAIN OUTCOME MEASURES Preventable ADEs due to ordering (prescribing) errors and the number, type, and acceptance of interventions made by the pharmacist.\n[9] Preventable ADEs were identified by review of medical records of the randomly selected patients during both preintervention and postintervention phases.\n[10] Pharmacists recorded all recommendations, which were then analyzed by type and acceptance.\n[11] RESULTS The rate of preventable ordering ADEs decreased by 66% from 10.4 per 1000 patient-days (95% confidence interval [CI], 7-14) before the intervention to 3.5 (95% CI, 1-5; P<.001) after the intervention.\n[12] In the control unit, the rate was essentially unchanged during the same time periods: 10.9 (95% CI, 6-16) and 12.4 (95% CI, 8-17) per 1000 patient-days.\n[13] The pharmacist made 366 recommendations related to drug ordering, of which 362 (99%) were accepted by physicians.\n[14] CONCLUSIONS The presence of a pharmacist on rounds as a full member of the patient care team in a medical ICU was associated with a substantially lower rate of ADEs caused by prescribing errors.\n[15] Nearly all the changes were readily accepted by physicians."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [14]\nExplanation: Evidence states: \"CONCLUSIONS The presence of a pharmacist on rounds as a full member of the patient care team in a medical ICU was associated with a substantially lower rate of ADEs caused by prescribing errors.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 940, "doc_id": 12258338, "label": "CONTRADICTS", "evidence_sentence_ids": [14], "cited_doc_ids": [12258338], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pharmacist attendance at ward rounds reduces adverse events in wards.\n\nDocument title: Pharmacist participation on physician rounds and adverse drug events in the intensive care unit.\n\nAbstract sentences:\n[0] CONTEXT Pharmacist review of medication orders in the intensive care unit (ICU) has been shown to prevent errors, and pharmacist consultation has reduced drug costs.\n[1] However, whether pharmacist participation in the ICU at the time of drug prescribing reduces adverse events has not been studied.\n[2] OBJECTIVE To measure the effect of pharmacist participation on medical rounds in the ICU on the rate of preventable adverse drug events (ADEs) caused by ordering errors.\n[3] DESIGN Before-after comparison between phase 1 (baseline) and phase 2 (after intervention implemented) and phase 2 comparison with a control unit that did not receive the intervention.\n[4] SETTING A medical ICU (study unit) and a coronary care unit (control unit) in a large urban teaching hospital.\n[5] PATIENTS Seventy-five patients randomly selected from each of 3 groups: all admissions to the study unit from February 1, 1993, through July 31, 1993 (baseline) and all admissions to the study unit (postintervention) and control unit from October 1, 1994, through July 7, 1995.\n[6] In addition, 50 patients were selected at random from the control unit during the baseline period.\n[7] INTERVENTION A senior pharmacist made rounds with the ICU team and remained in the ICU for consultation in the morning, and was available on call throughout the day.\n[8] MAIN OUTCOME MEASURES Preventable ADEs due to ordering (prescribing) errors and the number, type, and acceptance of interventions made by the pharmacist.\n[9] Preventable ADEs were identified by review of medical records of the randomly selected patients during both preintervention and postintervention phases.\n[10] Pharmacists recorded all recommendations, which were then analyzed by type and acceptance.\n[11] RESULTS The rate of preventable ordering ADEs decreased by 66% from 10.4 per 1000 patient-days (95% confidence interval [CI], 7-14) before the intervention to 3.5 (95% CI, 1-5; P<.001) after the intervention.\n[12] In the control unit, the rate was essentially unchanged during the same time periods: 10.9 (95% CI, 6-16) and 12.4 (95% CI, 8-17) per 1000 patient-days.\n[13] The pharmacist made 366 recommendations related to drug ordering, of which 362 (99%) were accepted by physicians.\n[14] CONCLUSIONS The presence of a pharmacist on rounds as a full member of the patient care team in a medical ICU was associated with a substantially lower rate of ADEs caused by prescribing errors.\n[15] Nearly all the changes were readily accepted by physicians."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"RESULTS The rate of preventable ordering ADEs decreased by 66% from 10.4 per 1000 patient-days (95% confidence interval [CI], 7-14) before the intervention to 3.5 (95% CI, 1-5; P<.001) after the intervention.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 941, "doc_id": 12258338, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [12258338], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pharmacist attendance at ward rounds reduces adverse events in wards.\n\nDocument title: Pharmacist participation on physician rounds and adverse drug events in the intensive care unit.\n\nAbstract sentences:\n[0] CONTEXT Pharmacist review of medication orders in the intensive care unit (ICU) has been shown to prevent errors, and pharmacist consultation has reduced drug costs.\n[1] However, whether pharmacist participation in the ICU at the time of drug prescribing reduces adverse events has not been studied.\n[2] OBJECTIVE To measure the effect of pharmacist participation on medical rounds in the ICU on the rate of preventable adverse drug events (ADEs) caused by ordering errors.\n[3] DESIGN Before-after comparison between phase 1 (baseline) and phase 2 (after intervention implemented) and phase 2 comparison with a control unit that did not receive the intervention.\n[4] SETTING A medical ICU (study unit) and a coronary care unit (control unit) in a large urban teaching hospital.\n[5] PATIENTS Seventy-five patients randomly selected from each of 3 groups: all admissions to the study unit from February 1, 1993, through July 31, 1993 (baseline) and all admissions to the study unit (postintervention) and control unit from October 1, 1994, through July 7, 1995.\n[6] In addition, 50 patients were selected at random from the control unit during the baseline period.\n[7] INTERVENTION A senior pharmacist made rounds with the ICU team and remained in the ICU for consultation in the morning, and was available on call throughout the day.\n[8] MAIN OUTCOME MEASURES Preventable ADEs due to ordering (prescribing) errors and the number, type, and acceptance of interventions made by the pharmacist.\n[9] Preventable ADEs were identified by review of medical records of the randomly selected patients during both preintervention and postintervention phases.\n[10] Pharmacists recorded all recommendations, which were then analyzed by type and acceptance.\n[11] RESULTS The rate of preventable ordering ADEs decreased by 66% from 10.4 per 1000 patient-days (95% confidence interval [CI], 7-14) before the intervention to 3.5 (95% CI, 1-5; P<.001) after the intervention.\n[12] In the control unit, the rate was essentially unchanged during the same time periods: 10.9 (95% CI, 6-16) and 12.4 (95% CI, 8-17) per 1000 patient-days.\n[13] The pharmacist made 366 recommendations related to drug ordering, of which 362 (99%) were accepted by physicians.\n[14] CONCLUSIONS The presence of a pharmacist on rounds as a full member of the patient care team in a medical ICU was associated with a substantially lower rate of ADEs caused by prescribing errors.\n[15] Nearly all the changes were readily accepted by physicians."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [14]\nExplanation: Evidence states: \"CONCLUSIONS The presence of a pharmacist on rounds as a full member of the patient care team in a medical ICU was associated with a substantially lower rate of ADEs caused by prescribing errors.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 941, "doc_id": 12258338, "label": "SUPPORTS", "evidence_sentence_ids": [14], "cited_doc_ids": [12258338], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Phase information is useful for predicting donor-recipient matches in organ transplantation.\n\nDocument title: MHC Haplotype Matching for Unrelated Hematopoietic Cell Transplantation\n\nAbstract sentences:\n[0] Background  Current criteria for the selection of unrelated donors for hematopoietic cell transplantation (HCT) include matching for the alleles of each human leukocyte antigen (HLA) locus within the major histocompatibility complex (MHC).\n[1] Graft-versus-host disease (GVHD), however, remains a significant and potentially life-threatening complication even after HLA-identical unrelated HCT.\n[2] The MHC harbors more than 400 genes, but the total number of transplantation antigens is unknown.\n[3] Genes that influence transplantation outcome could be identified by using linkage disequilibrium (LD)-mapping approaches, if the extended MHC haplotypes of the unrelated donor and recipient could be defined."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Genes that influence transplantation outcome could be identified by using linkage disequilibrium (LD)-mapping approaches, if the extended MHC haplotypes of the unrelated donor and recipient could be defined.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 942, "doc_id": 11527199, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [11527199], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Physical activity does not improve cognitive function in individuals with Alzheimers.\n\nDocument title: Effect of physical activity on cognitive function in older adults at risk for Alzheimer disease: a randomized trial.\n\nAbstract sentences:\n[0] CONTEXT Many observational studies have shown that physical activity reduces the risk of cognitive decline; however, evidence from randomized trials is lacking.\n[1] OBJECTIVE To determine whether physical activity reduces the rate of cognitive decline among older adults at risk.\n[2] DESIGN AND SETTING Randomized controlled trial of a 24-week physical activity intervention conducted between 2004 and 2007 in metropolitan Perth, Western Australia.\n[3] Assessors of cognitive function were blinded to group membership.\n[4] PARTICIPANTS We recruited volunteers who reported memory problems but did not meet criteria for dementia.\n[5] Three hundred eleven individuals aged 50 years or older were screened for eligibility, 89 were not eligible, and 52 refused to participate.\n[6] A total of 170 participants were randomized and 138 participants completed the 18-month assessment.\n[7] INTERVENTION Participants were randomly allocated to an education and usual care group or to a 24-week home-based program of physical activity.\n[8] MAIN OUTCOME MEASURE Change in Alzheimer Disease Assessment Scale-Cognitive Subscale (ADAS-Cog) scores (possible range, 0-70) over 18 months.\n[9] RESULTS In an intent-to-treat analysis, participants in the intervention group improved 0.26 points (95% confidence interval, -0.89 to 0.54) and those in the usual care group deteriorated 1.04 points (95% confidence interval, 0.32 to 1.82) on the ADAS-Cog at the end of the intervention.\n[10] The absolute difference of the outcome measure between the intervention and control groups was -1.3 points (95% confidence interval,-2.38 to -0.22) at the end of the intervention.\n[11] At 18 months, participants in the intervention group improved 0.73 points (95% confidence interval, -1.27 to 0.03) on the ADAS-Cog, and those in the usual care group improved 0.04 points (95% confidence interval, -0.46 to 0.88).\n[12] Word list delayed recall and Clinical Dementia Rating sum of boxes improved modestly as well, whereas word list total immediate recall, digit symbol coding, verbal fluency, Beck depression score, and Medical Outcomes 36-Item Short-Form physical and mental component summaries did not change significantly.\n[13] CONCLUSIONS In this study of adults with subjective memory impairment, a 6-month program of physical activity provided a modest improvement in cognition over an 18-month follow-up period.\n[14] TRIAL REGISTRATION anzctr.org.au Identifier: ACTRN12605000136606."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"RESULTS In an intent-to-treat analysis, participants in the intervention group improved 0.26 points (95% confidence interval, -0.89 to 0.54) and those in the usual care group deteriorated 1.04 points (95% confidence interval, 0.32 to 1.82) on the ADAS-Cog at the end of the intervention.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 944, "doc_id": 1642727, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [1642727], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Physical activity does not improve cognitive function in individuals with Alzheimers.\n\nDocument title: Effect of physical activity on cognitive function in older adults at risk for Alzheimer disease: a randomized trial.\n\nAbstract sentences:\n[0] CONTEXT Many observational studies have shown that physical activity reduces the risk of cognitive decline; however, evidence from randomized trials is lacking.\n[1] OBJECTIVE To determine whether physical activity reduces the rate of cognitive decline among older adults at risk.\n[2] DESIGN AND SETTING Randomized controlled trial of a 24-week physical activity intervention conducted between 2004 and 2007 in metropolitan Perth, Western Australia.\n[3] Assessors of cognitive function were blinded to group membership.\n[4] PARTICIPANTS We recruited volunteers who reported memory problems but did not meet criteria for dementia.\n[5] Three hundred eleven individuals aged 50 years or older were screened for eligibility, 89 were not eligible, and 52 refused to participate.\n[6] A total of 170 participants were randomized and 138 participants completed the 18-month assessment.\n[7] INTERVENTION Participants were randomly allocated to an education and usual care group or to a 24-week home-based program of physical activity.\n[8] MAIN OUTCOME MEASURE Change in Alzheimer Disease Assessment Scale-Cognitive Subscale (ADAS-Cog) scores (possible range, 0-70) over 18 months.\n[9] RESULTS In an intent-to-treat analysis, participants in the intervention group improved 0.26 points (95% confidence interval, -0.89 to 0.54) and those in the usual care group deteriorated 1.04 points (95% confidence interval, 0.32 to 1.82) on the ADAS-Cog at the end of the intervention.\n[10] The absolute difference of the outcome measure between the intervention and control groups was -1.3 points (95% confidence interval,-2.38 to -0.22) at the end of the intervention.\n[11] At 18 months, participants in the intervention group improved 0.73 points (95% confidence interval, -1.27 to 0.03) on the ADAS-Cog, and those in the usual care group improved 0.04 points (95% confidence interval, -0.46 to 0.88).\n[12] Word list delayed recall and Clinical Dementia Rating sum of boxes improved modestly as well, whereas word list total immediate recall, digit symbol coding, verbal fluency, Beck depression score, and Medical Outcomes 36-Item Short-Form physical and mental component summaries did not change significantly.\n[13] CONCLUSIONS In this study of adults with subjective memory impairment, a 6-month program of physical activity provided a modest improvement in cognition over an 18-month follow-up period.\n[14] TRIAL REGISTRATION anzctr.org.au Identifier: ACTRN12605000136606."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"CONCLUSIONS In this study of adults with subjective memory impairment, a 6-month program of physical activity provided a modest improvement in cognition over an 18-month follow-up period.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 944, "doc_id": 1642727, "label": "CONTRADICTS", "evidence_sentence_ids": [13], "cited_doc_ids": [1642727], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Physical activity level has no association with the difference in maximal oxygen consumption between black and white youth.\n\nDocument title: Relationship of physical activity and television watching with body weight and level of fatness among children: results from the Third National Health and Nutrition Examination Survey.\n\nAbstract sentences:\n[0] CONTEXT Physical inactivity contributes to weight gain in adults, but whether this relationship is true for children of different ethnic groups is not well established.\n[1] OBJECTIVE To assess participation in vigorous activity and television watching habits and their relationship to body weight and fatness in US children.\n[2] DESIGN Nationally representative cross-sectional survey with an in-person interview and medical examination.\n[3] SETTING AND PARTICIPANTS Between 1988 and 1994, 4063 children aged 8 through 16 years were examined as part of the National Health and Nutrition Examination Survey III.\n[4] Mexican Americans and non-Hispanic blacks were oversampled to produce reliable estimates for these groups.\n[5] MAIN OUTCOME MEASURES Episodes of weekly vigorous activity and daily hours of television watched, and their relationship to body mass index and body fatness.\n[6] RESULTS Eighty percent of US children reported performing 3 or more bouts of vigorous activity each week.\n[7] This rate was lower in non-Hispanic black and Mexican American girls (69% and 73%, respectively).\n[8] Twenty percent of US children participated in 2 or fewer bouts of vigorous activity perweek, and the rate was higher in girls (26%) than in boys (17%).\n[9] Overall, 26% of US children watched 4 or more hours of television per day and 67% watched at least 2 hours per day.\n[10] Non-Hispanic black children had the highest rates of watching 4 or more hours of television per day (42%).\n[11] Boys and girls who watch 4 or more hours of television each day had greater body fat (P<.001) and had a greater body mass index (P<.001) than those who watched less than 2 hours per day.\n[12] CONCLUSIONS Many US children watch a great deal of television and are inadequately vigorously active.\n[13] Vigorous activity levels are lowest among girls, non-Hispanic blacks, and Mexican Americans.\n[14] Intervention strategies to promote lifelong physical activity among US children are needed to stem the adverse health consequences of inactivity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 945, "doc_id": 8428935, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [8428935, 26112696, 4463588, 13083189], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Physical activity level is associated with the difference in maximal oxygen consumption between black and white youth.\n\nDocument title: Relationship of physical activity and television watching with body weight and level of fatness among children: results from the Third National Health and Nutrition Examination Survey.\n\nAbstract sentences:\n[0] CONTEXT Physical inactivity contributes to weight gain in adults, but whether this relationship is true for children of different ethnic groups is not well established.\n[1] OBJECTIVE To assess participation in vigorous activity and television watching habits and their relationship to body weight and fatness in US children.\n[2] DESIGN Nationally representative cross-sectional survey with an in-person interview and medical examination.\n[3] SETTING AND PARTICIPANTS Between 1988 and 1994, 4063 children aged 8 through 16 years were examined as part of the National Health and Nutrition Examination Survey III.\n[4] Mexican Americans and non-Hispanic blacks were oversampled to produce reliable estimates for these groups.\n[5] MAIN OUTCOME MEASURES Episodes of weekly vigorous activity and daily hours of television watched, and their relationship to body mass index and body fatness.\n[6] RESULTS Eighty percent of US children reported performing 3 or more bouts of vigorous activity each week.\n[7] This rate was lower in non-Hispanic black and Mexican American girls (69% and 73%, respectively).\n[8] Twenty percent of US children participated in 2 or fewer bouts of vigorous activity perweek, and the rate was higher in girls (26%) than in boys (17%).\n[9] Overall, 26% of US children watched 4 or more hours of television per day and 67% watched at least 2 hours per day.\n[10] Non-Hispanic black children had the highest rates of watching 4 or more hours of television per day (42%).\n[11] Boys and girls who watch 4 or more hours of television each day had greater body fat (P<.001) and had a greater body mass index (P<.001) than those who watched less than 2 hours per day.\n[12] CONCLUSIONS Many US children watch a great deal of television and are inadequately vigorously active.\n[13] Vigorous activity levels are lowest among girls, non-Hispanic blacks, and Mexican Americans.\n[14] Intervention strategies to promote lifelong physical activity among US children are needed to stem the adverse health consequences of inactivity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 946, "doc_id": 8428935, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [8428935, 26112696, 4463588, 13083189], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Physical injury represses transgultaminase activity.\n\nDocument title: Transglutaminase 2 Undergoes a Large Conformational Change upon Activation \n\nAbstract sentences:\n[0] Human transglutaminase 2 (TG2), a member of a large family of enzymes that catalyze protein crosslinking, plays an important role in the extracellular matrix biology of many tissues and is implicated in the gluten-induced pathogenesis of celiac sprue.\n[1] Although vertebrate transglutaminases have been studied extensively, thus far all structurally characterized members of this family have been crystallized in conformations with inaccessible active sites.\n[2] We have trapped human TG2 in complex with an inhibitor that mimics inflammatory gluten peptide substrates and have solved, at 2-A resolution, its x-ray crystal structure.\n[3] The inhibitor stabilizes TG2 in an extended conformation that is dramatically different from earlier transglutaminase structures.\n[4] The active site is exposed, revealing that catalysis takes place in a tunnel, bridged by two tryptophan residues that separate acyl-donor from acyl-acceptor and stabilize the tetrahedral reaction intermediates.\n[5] Site-directed mutagenesis was used to investigate the acyl-acceptor side of the tunnel, yielding mutants with a marked increase in preference for hydrolysis over transamidation.\n[6] By providing the ability to visualize this activated conformer, our results create a foundation for understanding the catalytic as well as the non-catalytic roles of TG2 in biology, and for dissecting the process by which the autoantibody response to TG2 is induced in celiac sprue patients."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 949, "doc_id": 13578199, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [13578199], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Piezo1 channels are sensors for cell migration in epithelial cells.\n\nDocument title: Piezo1 Is as a Novel Trefoil Factor Family 1 Binding Protein that Promotes Gastric Cancer Cell Mobility In Vitro\n\nAbstract sentences:\n[0] Trefoil factor family 1 (TFF1) is a member of the TFF-domain peptide family involved in epithelial restitution and cell motility.\n[1] Recently, we screened Piezo1 as a candidate TFF1-binding protein.\n[2] We aimed to confirm Piezo1 as a novel TFF1 binding protein and to assess the role of this interaction in mediating gastric cancer cell mobility.\n[3] This interaction was confirmed by co-immunoprecipitation and co-localisation of TFF1 and Piezo1 in GES-1 cells.\n[4] We used stable RNA interference to knockdown Piezo1 protein expression and restored the expression of TFF1 in the gastric cancer cell lines SGC-7901 and BGC-823.\n[5] Cell motility was evaluated using invasion assay and migration assay in vitro.\n[6] The expression levels of the integrin subunits β1, β5, α1 as well as the expression of β-catenin and E-cadherin were detected by Western blot.\n[7] We demonstrate that TFF1, but not TFF2 or TFF3, bind to and co-localize with Piezo1 in the cytoplasm in vitro.\n[8] TFF1 interacts with the C-terminal portion of the Piezo1 protein.\n[9] Wound healing and trans-well assays demonstrated that the restored expression of TFF1 promoted cell mobility in gastric cancer cells, and this effect was attenuated by the knockdown of Piezo1.\n[10] Western blots demonstrated the decreased expression of integrin β1 in Piezo1-knockdown cells.\n[11] Our data demonstrate that Piezo1 is a novel TFF1 binding protein that is important for TFF1-mediated cell migration and suggest that this interaction may be a therapeutic target in the invasion and metastasis of gastric cancer."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"This interaction was confirmed by co-immunoprecipitation and co-localisation of TFF1 and Piezo1 in GES-1 cells.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 951, "doc_id": 21414718, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [21414718], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Piezo1 channels are sensors for cell migration in epithelial cells.\n\nDocument title: Piezo1 Is as a Novel Trefoil Factor Family 1 Binding Protein that Promotes Gastric Cancer Cell Mobility In Vitro\n\nAbstract sentences:\n[0] Trefoil factor family 1 (TFF1) is a member of the TFF-domain peptide family involved in epithelial restitution and cell motility.\n[1] Recently, we screened Piezo1 as a candidate TFF1-binding protein.\n[2] We aimed to confirm Piezo1 as a novel TFF1 binding protein and to assess the role of this interaction in mediating gastric cancer cell mobility.\n[3] This interaction was confirmed by co-immunoprecipitation and co-localisation of TFF1 and Piezo1 in GES-1 cells.\n[4] We used stable RNA interference to knockdown Piezo1 protein expression and restored the expression of TFF1 in the gastric cancer cell lines SGC-7901 and BGC-823.\n[5] Cell motility was evaluated using invasion assay and migration assay in vitro.\n[6] The expression levels of the integrin subunits β1, β5, α1 as well as the expression of β-catenin and E-cadherin were detected by Western blot.\n[7] We demonstrate that TFF1, but not TFF2 or TFF3, bind to and co-localize with Piezo1 in the cytoplasm in vitro.\n[8] TFF1 interacts with the C-terminal portion of the Piezo1 protein.\n[9] Wound healing and trans-well assays demonstrated that the restored expression of TFF1 promoted cell mobility in gastric cancer cells, and this effect was attenuated by the knockdown of Piezo1.\n[10] Western blots demonstrated the decreased expression of integrin β1 in Piezo1-knockdown cells.\n[11] Our data demonstrate that Piezo1 is a novel TFF1 binding protein that is important for TFF1-mediated cell migration and suggest that this interaction may be a therapeutic target in the invasion and metastasis of gastric cancer."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"We demonstrate that TFF1, but not TFF2 or TFF3, bind to and co-localize with Piezo1 in the cytoplasm in vitro.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 951, "doc_id": 21414718, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [21414718], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Piezo1 channels are sensors for cell migration in epithelial cells.\n\nDocument title: Piezo1 Is as a Novel Trefoil Factor Family 1 Binding Protein that Promotes Gastric Cancer Cell Mobility In Vitro\n\nAbstract sentences:\n[0] Trefoil factor family 1 (TFF1) is a member of the TFF-domain peptide family involved in epithelial restitution and cell motility.\n[1] Recently, we screened Piezo1 as a candidate TFF1-binding protein.\n[2] We aimed to confirm Piezo1 as a novel TFF1 binding protein and to assess the role of this interaction in mediating gastric cancer cell mobility.\n[3] This interaction was confirmed by co-immunoprecipitation and co-localisation of TFF1 and Piezo1 in GES-1 cells.\n[4] We used stable RNA interference to knockdown Piezo1 protein expression and restored the expression of TFF1 in the gastric cancer cell lines SGC-7901 and BGC-823.\n[5] Cell motility was evaluated using invasion assay and migration assay in vitro.\n[6] The expression levels of the integrin subunits β1, β5, α1 as well as the expression of β-catenin and E-cadherin were detected by Western blot.\n[7] We demonstrate that TFF1, but not TFF2 or TFF3, bind to and co-localize with Piezo1 in the cytoplasm in vitro.\n[8] TFF1 interacts with the C-terminal portion of the Piezo1 protein.\n[9] Wound healing and trans-well assays demonstrated that the restored expression of TFF1 promoted cell mobility in gastric cancer cells, and this effect was attenuated by the knockdown of Piezo1.\n[10] Western blots demonstrated the decreased expression of integrin β1 in Piezo1-knockdown cells.\n[11] Our data demonstrate that Piezo1 is a novel TFF1 binding protein that is important for TFF1-mediated cell migration and suggest that this interaction may be a therapeutic target in the invasion and metastasis of gastric cancer."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"TFF1 interacts with the C-terminal portion of the Piezo1 protein.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 951, "doc_id": 21414718, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [21414718], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Piezo1 channels are sensors for cell migration in epithelial cells.\n\nDocument title: Piezo1 Is as a Novel Trefoil Factor Family 1 Binding Protein that Promotes Gastric Cancer Cell Mobility In Vitro\n\nAbstract sentences:\n[0] Trefoil factor family 1 (TFF1) is a member of the TFF-domain peptide family involved in epithelial restitution and cell motility.\n[1] Recently, we screened Piezo1 as a candidate TFF1-binding protein.\n[2] We aimed to confirm Piezo1 as a novel TFF1 binding protein and to assess the role of this interaction in mediating gastric cancer cell mobility.\n[3] This interaction was confirmed by co-immunoprecipitation and co-localisation of TFF1 and Piezo1 in GES-1 cells.\n[4] We used stable RNA interference to knockdown Piezo1 protein expression and restored the expression of TFF1 in the gastric cancer cell lines SGC-7901 and BGC-823.\n[5] Cell motility was evaluated using invasion assay and migration assay in vitro.\n[6] The expression levels of the integrin subunits β1, β5, α1 as well as the expression of β-catenin and E-cadherin were detected by Western blot.\n[7] We demonstrate that TFF1, but not TFF2 or TFF3, bind to and co-localize with Piezo1 in the cytoplasm in vitro.\n[8] TFF1 interacts with the C-terminal portion of the Piezo1 protein.\n[9] Wound healing and trans-well assays demonstrated that the restored expression of TFF1 promoted cell mobility in gastric cancer cells, and this effect was attenuated by the knockdown of Piezo1.\n[10] Western blots demonstrated the decreased expression of integrin β1 in Piezo1-knockdown cells.\n[11] Our data demonstrate that Piezo1 is a novel TFF1 binding protein that is important for TFF1-mediated cell migration and suggest that this interaction may be a therapeutic target in the invasion and metastasis of gastric cancer."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"Our data demonstrate that Piezo1 is a novel TFF1 binding protein that is important for TFF1-mediated cell migration and suggest that this interaction may be a therapeutic target in the invasion and metastasis of gastric cancer.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 951, "doc_id": 21414718, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [21414718], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pioglitazone use is not associated with an increased risk of prostate cancer.\n\nDocument title: Pioglitazone Use and Risk of Bladder Cancer and Other Common Cancers in Persons With Diabetes.\n\nAbstract sentences:\n[0] IMPORTANCE Studies suggest pioglitazone use may increase risk of cancers.\n[1] OBJECTIVE To examine whether pioglitazone use for diabetes is associated with risk of bladder and 10 additional cancers.\n[2] DESIGN, SETTING, AND PARTICIPANTS Cohort and nested case-control analyses among persons with diabetes.\n[3] A bladder cancer cohort followed 193,099 persons aged 40 years or older in 1997-2002 until December 2012; 464 case patients and 464 matched controls were surveyed about additional confounders.\n[4] A cohort analysis of 10 additional cancers included 236,507 persons aged 40 years or older in 1997-2005 and followed until June 2012.\n[5] Cohorts were from Kaiser Permanente Northern California.\n[6] EXPOSURES Ever use, duration, cumulative dose, and time since initiation of pioglitazone as time dependent.\n[7] MAIN OUTCOMES AND MEASURES Incident cancer, including bladder, prostate, female breast, lung/bronchus, endometrial, colon, non-Hodgkin lymphoma, pancreas, kidney/renal pelvis, rectum, and melanoma.\n[8] RESULTS Among 193,099 persons in the bladder cancer cohort, 34,181 (18%) received pioglitazone (median duration, 2.8 years; range, 0.2-13.2 years) and 1261 had incident bladder cancer.\n[9] Crude incidences of bladder cancer in pioglitazone users and nonusers were 89.8 and 75.9 per 100,000 person-years, respectively.\n[10] Ever use of pioglitazone was not associated with bladder cancer risk (adjusted hazard ratio [HR], 1.06; 95% CI, 0.89-1.26).\n[11] Results were similar in case-control analyses (pioglitazone use: 19.6% among case patients and 17.5% among controls; adjusted odds ratio, 1.18; 95% CI, 0.78-1.80).\n[12] In adjusted analyses, there was no association with 8 of the 10 additional cancers; ever use of pioglitazone was associated with increased risk of prostate cancer (HR, 1.13; 95% CI, 1.02-1.26) and pancreatic cancer (HR, 1.41; 95% CI, 1.16-1.71).\n[13] Crude incidences of prostate and pancreatic cancer in pioglitazone users vs nonusers were 453.3 vs 449.3 and 81.1 vs 48.4 per 100,000 person-years, respectively.\n[14] No clear patterns of risk for any cancer were observed for time since initiation, duration, or dose.\n[15] CONCLUSIONS AND RELEVANCE Pioglitazone use was not associated with a statistically significant increased risk of bladder cancer, although an increased risk, as previously observed, could not be excluded.\n[16] The increased prostate and pancreatic cancer risks associated with ever use of pioglitazone merit further investigation to assess whether they are causal or are due to chance, residual confounding, or reverse causality."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"In adjusted analyses, there was no association with 8 of the 10 additional cancers; ever use of pioglitazone was associated with increased risk of prostate cancer (HR, 1.13; 95% CI, 1.02-1.26) and pancreatic cancer (HR, 1.41; 95% CI, 1.16-1.71).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 952, "doc_id": 3355397, "label": "CONTRADICTS", "evidence_sentence_ids": [12], "cited_doc_ids": [3355397], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pioglitazone use is not associated with an increased risk of prostate cancer.\n\nDocument title: Pioglitazone Use and Risk of Bladder Cancer and Other Common Cancers in Persons With Diabetes.\n\nAbstract sentences:\n[0] IMPORTANCE Studies suggest pioglitazone use may increase risk of cancers.\n[1] OBJECTIVE To examine whether pioglitazone use for diabetes is associated with risk of bladder and 10 additional cancers.\n[2] DESIGN, SETTING, AND PARTICIPANTS Cohort and nested case-control analyses among persons with diabetes.\n[3] A bladder cancer cohort followed 193,099 persons aged 40 years or older in 1997-2002 until December 2012; 464 case patients and 464 matched controls were surveyed about additional confounders.\n[4] A cohort analysis of 10 additional cancers included 236,507 persons aged 40 years or older in 1997-2005 and followed until June 2012.\n[5] Cohorts were from Kaiser Permanente Northern California.\n[6] EXPOSURES Ever use, duration, cumulative dose, and time since initiation of pioglitazone as time dependent.\n[7] MAIN OUTCOMES AND MEASURES Incident cancer, including bladder, prostate, female breast, lung/bronchus, endometrial, colon, non-Hodgkin lymphoma, pancreas, kidney/renal pelvis, rectum, and melanoma.\n[8] RESULTS Among 193,099 persons in the bladder cancer cohort, 34,181 (18%) received pioglitazone (median duration, 2.8 years; range, 0.2-13.2 years) and 1261 had incident bladder cancer.\n[9] Crude incidences of bladder cancer in pioglitazone users and nonusers were 89.8 and 75.9 per 100,000 person-years, respectively.\n[10] Ever use of pioglitazone was not associated with bladder cancer risk (adjusted hazard ratio [HR], 1.06; 95% CI, 0.89-1.26).\n[11] Results were similar in case-control analyses (pioglitazone use: 19.6% among case patients and 17.5% among controls; adjusted odds ratio, 1.18; 95% CI, 0.78-1.80).\n[12] In adjusted analyses, there was no association with 8 of the 10 additional cancers; ever use of pioglitazone was associated with increased risk of prostate cancer (HR, 1.13; 95% CI, 1.02-1.26) and pancreatic cancer (HR, 1.41; 95% CI, 1.16-1.71).\n[13] Crude incidences of prostate and pancreatic cancer in pioglitazone users vs nonusers were 453.3 vs 449.3 and 81.1 vs 48.4 per 100,000 person-years, respectively.\n[14] No clear patterns of risk for any cancer were observed for time since initiation, duration, or dose.\n[15] CONCLUSIONS AND RELEVANCE Pioglitazone use was not associated with a statistically significant increased risk of bladder cancer, although an increased risk, as previously observed, could not be excluded.\n[16] The increased prostate and pancreatic cancer risks associated with ever use of pioglitazone merit further investigation to assess whether they are causal or are due to chance, residual confounding, or reverse causality."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [16]\nExplanation: Evidence states: \"The increased prostate and pancreatic cancer risks associated with ever use of pioglitazone merit further investigation to assess whether they are causal or are due to chance, residual confounding, or reverse causality.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 952, "doc_id": 3355397, "label": "CONTRADICTS", "evidence_sentence_ids": [16], "cited_doc_ids": [3355397], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pioglitazone use is significantly associated with an increased risk of pancreatic cancer.\n\nDocument title: Pioglitazone Use and Risk of Bladder Cancer and Other Common Cancers in Persons With Diabetes.\n\nAbstract sentences:\n[0] IMPORTANCE Studies suggest pioglitazone use may increase risk of cancers.\n[1] OBJECTIVE To examine whether pioglitazone use for diabetes is associated with risk of bladder and 10 additional cancers.\n[2] DESIGN, SETTING, AND PARTICIPANTS Cohort and nested case-control analyses among persons with diabetes.\n[3] A bladder cancer cohort followed 193,099 persons aged 40 years or older in 1997-2002 until December 2012; 464 case patients and 464 matched controls were surveyed about additional confounders.\n[4] A cohort analysis of 10 additional cancers included 236,507 persons aged 40 years or older in 1997-2005 and followed until June 2012.\n[5] Cohorts were from Kaiser Permanente Northern California.\n[6] EXPOSURES Ever use, duration, cumulative dose, and time since initiation of pioglitazone as time dependent.\n[7] MAIN OUTCOMES AND MEASURES Incident cancer, including bladder, prostate, female breast, lung/bronchus, endometrial, colon, non-Hodgkin lymphoma, pancreas, kidney/renal pelvis, rectum, and melanoma.\n[8] RESULTS Among 193,099 persons in the bladder cancer cohort, 34,181 (18%) received pioglitazone (median duration, 2.8 years; range, 0.2-13.2 years) and 1261 had incident bladder cancer.\n[9] Crude incidences of bladder cancer in pioglitazone users and nonusers were 89.8 and 75.9 per 100,000 person-years, respectively.\n[10] Ever use of pioglitazone was not associated with bladder cancer risk (adjusted hazard ratio [HR], 1.06; 95% CI, 0.89-1.26).\n[11] Results were similar in case-control analyses (pioglitazone use: 19.6% among case patients and 17.5% among controls; adjusted odds ratio, 1.18; 95% CI, 0.78-1.80).\n[12] In adjusted analyses, there was no association with 8 of the 10 additional cancers; ever use of pioglitazone was associated with increased risk of prostate cancer (HR, 1.13; 95% CI, 1.02-1.26) and pancreatic cancer (HR, 1.41; 95% CI, 1.16-1.71).\n[13] Crude incidences of prostate and pancreatic cancer in pioglitazone users vs nonusers were 453.3 vs 449.3 and 81.1 vs 48.4 per 100,000 person-years, respectively.\n[14] No clear patterns of risk for any cancer were observed for time since initiation, duration, or dose.\n[15] CONCLUSIONS AND RELEVANCE Pioglitazone use was not associated with a statistically significant increased risk of bladder cancer, although an increased risk, as previously observed, could not be excluded.\n[16] The increased prostate and pancreatic cancer risks associated with ever use of pioglitazone merit further investigation to assess whether they are causal or are due to chance, residual confounding, or reverse causality."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"In adjusted analyses, there was no association with 8 of the 10 additional cancers; ever use of pioglitazone was associated with increased risk of prostate cancer (HR, 1.13; 95% CI, 1.02-1.26) and pancreatic cancer (HR, 1.41; 95% CI, 1.16-1.71).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 953, "doc_id": 3355397, "label": "SUPPORTS", "evidence_sentence_ids": [12], "cited_doc_ids": [3355397], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pioglitazone use is significantly associated with an increased risk of pancreatic cancer.\n\nDocument title: Pioglitazone Use and Risk of Bladder Cancer and Other Common Cancers in Persons With Diabetes.\n\nAbstract sentences:\n[0] IMPORTANCE Studies suggest pioglitazone use may increase risk of cancers.\n[1] OBJECTIVE To examine whether pioglitazone use for diabetes is associated with risk of bladder and 10 additional cancers.\n[2] DESIGN, SETTING, AND PARTICIPANTS Cohort and nested case-control analyses among persons with diabetes.\n[3] A bladder cancer cohort followed 193,099 persons aged 40 years or older in 1997-2002 until December 2012; 464 case patients and 464 matched controls were surveyed about additional confounders.\n[4] A cohort analysis of 10 additional cancers included 236,507 persons aged 40 years or older in 1997-2005 and followed until June 2012.\n[5] Cohorts were from Kaiser Permanente Northern California.\n[6] EXPOSURES Ever use, duration, cumulative dose, and time since initiation of pioglitazone as time dependent.\n[7] MAIN OUTCOMES AND MEASURES Incident cancer, including bladder, prostate, female breast, lung/bronchus, endometrial, colon, non-Hodgkin lymphoma, pancreas, kidney/renal pelvis, rectum, and melanoma.\n[8] RESULTS Among 193,099 persons in the bladder cancer cohort, 34,181 (18%) received pioglitazone (median duration, 2.8 years; range, 0.2-13.2 years) and 1261 had incident bladder cancer.\n[9] Crude incidences of bladder cancer in pioglitazone users and nonusers were 89.8 and 75.9 per 100,000 person-years, respectively.\n[10] Ever use of pioglitazone was not associated with bladder cancer risk (adjusted hazard ratio [HR], 1.06; 95% CI, 0.89-1.26).\n[11] Results were similar in case-control analyses (pioglitazone use: 19.6% among case patients and 17.5% among controls; adjusted odds ratio, 1.18; 95% CI, 0.78-1.80).\n[12] In adjusted analyses, there was no association with 8 of the 10 additional cancers; ever use of pioglitazone was associated with increased risk of prostate cancer (HR, 1.13; 95% CI, 1.02-1.26) and pancreatic cancer (HR, 1.41; 95% CI, 1.16-1.71).\n[13] Crude incidences of prostate and pancreatic cancer in pioglitazone users vs nonusers were 453.3 vs 449.3 and 81.1 vs 48.4 per 100,000 person-years, respectively.\n[14] No clear patterns of risk for any cancer were observed for time since initiation, duration, or dose.\n[15] CONCLUSIONS AND RELEVANCE Pioglitazone use was not associated with a statistically significant increased risk of bladder cancer, although an increased risk, as previously observed, could not be excluded.\n[16] The increased prostate and pancreatic cancer risks associated with ever use of pioglitazone merit further investigation to assess whether they are causal or are due to chance, residual confounding, or reverse causality."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"Crude incidences of prostate and pancreatic cancer in pioglitazone users vs nonusers were 453.3 vs 449.3 and 81.1 vs 48.4 per 100,000 person-years, respectively.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 953, "doc_id": 3355397, "label": "SUPPORTS", "evidence_sentence_ids": [13], "cited_doc_ids": [3355397], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pioglitazone use is significantly associated with an increased risk of pancreatic cancer.\n\nDocument title: Pioglitazone Use and Risk of Bladder Cancer and Other Common Cancers in Persons With Diabetes.\n\nAbstract sentences:\n[0] IMPORTANCE Studies suggest pioglitazone use may increase risk of cancers.\n[1] OBJECTIVE To examine whether pioglitazone use for diabetes is associated with risk of bladder and 10 additional cancers.\n[2] DESIGN, SETTING, AND PARTICIPANTS Cohort and nested case-control analyses among persons with diabetes.\n[3] A bladder cancer cohort followed 193,099 persons aged 40 years or older in 1997-2002 until December 2012; 464 case patients and 464 matched controls were surveyed about additional confounders.\n[4] A cohort analysis of 10 additional cancers included 236,507 persons aged 40 years or older in 1997-2005 and followed until June 2012.\n[5] Cohorts were from Kaiser Permanente Northern California.\n[6] EXPOSURES Ever use, duration, cumulative dose, and time since initiation of pioglitazone as time dependent.\n[7] MAIN OUTCOMES AND MEASURES Incident cancer, including bladder, prostate, female breast, lung/bronchus, endometrial, colon, non-Hodgkin lymphoma, pancreas, kidney/renal pelvis, rectum, and melanoma.\n[8] RESULTS Among 193,099 persons in the bladder cancer cohort, 34,181 (18%) received pioglitazone (median duration, 2.8 years; range, 0.2-13.2 years) and 1261 had incident bladder cancer.\n[9] Crude incidences of bladder cancer in pioglitazone users and nonusers were 89.8 and 75.9 per 100,000 person-years, respectively.\n[10] Ever use of pioglitazone was not associated with bladder cancer risk (adjusted hazard ratio [HR], 1.06; 95% CI, 0.89-1.26).\n[11] Results were similar in case-control analyses (pioglitazone use: 19.6% among case patients and 17.5% among controls; adjusted odds ratio, 1.18; 95% CI, 0.78-1.80).\n[12] In adjusted analyses, there was no association with 8 of the 10 additional cancers; ever use of pioglitazone was associated with increased risk of prostate cancer (HR, 1.13; 95% CI, 1.02-1.26) and pancreatic cancer (HR, 1.41; 95% CI, 1.16-1.71).\n[13] Crude incidences of prostate and pancreatic cancer in pioglitazone users vs nonusers were 453.3 vs 449.3 and 81.1 vs 48.4 per 100,000 person-years, respectively.\n[14] No clear patterns of risk for any cancer were observed for time since initiation, duration, or dose.\n[15] CONCLUSIONS AND RELEVANCE Pioglitazone use was not associated with a statistically significant increased risk of bladder cancer, although an increased risk, as previously observed, could not be excluded.\n[16] The increased prostate and pancreatic cancer risks associated with ever use of pioglitazone merit further investigation to assess whether they are causal or are due to chance, residual confounding, or reverse causality."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [16]\nExplanation: Evidence states: \"The increased prostate and pancreatic cancer risks associated with ever use of pioglitazone merit further investigation to assess whether they are causal or are due to chance, residual confounding, or reverse causality.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 953, "doc_id": 3355397, "label": "SUPPORTS", "evidence_sentence_ids": [16], "cited_doc_ids": [3355397], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pioglitazone use is significantly associated with an increased risk of prostate cancer.\n\nDocument title: Pioglitazone Use and Risk of Bladder Cancer and Other Common Cancers in Persons With Diabetes.\n\nAbstract sentences:\n[0] IMPORTANCE Studies suggest pioglitazone use may increase risk of cancers.\n[1] OBJECTIVE To examine whether pioglitazone use for diabetes is associated with risk of bladder and 10 additional cancers.\n[2] DESIGN, SETTING, AND PARTICIPANTS Cohort and nested case-control analyses among persons with diabetes.\n[3] A bladder cancer cohort followed 193,099 persons aged 40 years or older in 1997-2002 until December 2012; 464 case patients and 464 matched controls were surveyed about additional confounders.\n[4] A cohort analysis of 10 additional cancers included 236,507 persons aged 40 years or older in 1997-2005 and followed until June 2012.\n[5] Cohorts were from Kaiser Permanente Northern California.\n[6] EXPOSURES Ever use, duration, cumulative dose, and time since initiation of pioglitazone as time dependent.\n[7] MAIN OUTCOMES AND MEASURES Incident cancer, including bladder, prostate, female breast, lung/bronchus, endometrial, colon, non-Hodgkin lymphoma, pancreas, kidney/renal pelvis, rectum, and melanoma.\n[8] RESULTS Among 193,099 persons in the bladder cancer cohort, 34,181 (18%) received pioglitazone (median duration, 2.8 years; range, 0.2-13.2 years) and 1261 had incident bladder cancer.\n[9] Crude incidences of bladder cancer in pioglitazone users and nonusers were 89.8 and 75.9 per 100,000 person-years, respectively.\n[10] Ever use of pioglitazone was not associated with bladder cancer risk (adjusted hazard ratio [HR], 1.06; 95% CI, 0.89-1.26).\n[11] Results were similar in case-control analyses (pioglitazone use: 19.6% among case patients and 17.5% among controls; adjusted odds ratio, 1.18; 95% CI, 0.78-1.80).\n[12] In adjusted analyses, there was no association with 8 of the 10 additional cancers; ever use of pioglitazone was associated with increased risk of prostate cancer (HR, 1.13; 95% CI, 1.02-1.26) and pancreatic cancer (HR, 1.41; 95% CI, 1.16-1.71).\n[13] Crude incidences of prostate and pancreatic cancer in pioglitazone users vs nonusers were 453.3 vs 449.3 and 81.1 vs 48.4 per 100,000 person-years, respectively.\n[14] No clear patterns of risk for any cancer were observed for time since initiation, duration, or dose.\n[15] CONCLUSIONS AND RELEVANCE Pioglitazone use was not associated with a statistically significant increased risk of bladder cancer, although an increased risk, as previously observed, could not be excluded.\n[16] The increased prostate and pancreatic cancer risks associated with ever use of pioglitazone merit further investigation to assess whether they are causal or are due to chance, residual confounding, or reverse causality."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"In adjusted analyses, there was no association with 8 of the 10 additional cancers; ever use of pioglitazone was associated with increased risk of prostate cancer (HR, 1.13; 95% CI, 1.02-1.26) and pancreatic cancer (HR, 1.41; 95% CI, 1.16-1.71).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 954, "doc_id": 3355397, "label": "SUPPORTS", "evidence_sentence_ids": [12], "cited_doc_ids": [3355397], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pioglitazone use is significantly associated with an increased risk of prostate cancer.\n\nDocument title: Pioglitazone Use and Risk of Bladder Cancer and Other Common Cancers in Persons With Diabetes.\n\nAbstract sentences:\n[0] IMPORTANCE Studies suggest pioglitazone use may increase risk of cancers.\n[1] OBJECTIVE To examine whether pioglitazone use for diabetes is associated with risk of bladder and 10 additional cancers.\n[2] DESIGN, SETTING, AND PARTICIPANTS Cohort and nested case-control analyses among persons with diabetes.\n[3] A bladder cancer cohort followed 193,099 persons aged 40 years or older in 1997-2002 until December 2012; 464 case patients and 464 matched controls were surveyed about additional confounders.\n[4] A cohort analysis of 10 additional cancers included 236,507 persons aged 40 years or older in 1997-2005 and followed until June 2012.\n[5] Cohorts were from Kaiser Permanente Northern California.\n[6] EXPOSURES Ever use, duration, cumulative dose, and time since initiation of pioglitazone as time dependent.\n[7] MAIN OUTCOMES AND MEASURES Incident cancer, including bladder, prostate, female breast, lung/bronchus, endometrial, colon, non-Hodgkin lymphoma, pancreas, kidney/renal pelvis, rectum, and melanoma.\n[8] RESULTS Among 193,099 persons in the bladder cancer cohort, 34,181 (18%) received pioglitazone (median duration, 2.8 years; range, 0.2-13.2 years) and 1261 had incident bladder cancer.\n[9] Crude incidences of bladder cancer in pioglitazone users and nonusers were 89.8 and 75.9 per 100,000 person-years, respectively.\n[10] Ever use of pioglitazone was not associated with bladder cancer risk (adjusted hazard ratio [HR], 1.06; 95% CI, 0.89-1.26).\n[11] Results were similar in case-control analyses (pioglitazone use: 19.6% among case patients and 17.5% among controls; adjusted odds ratio, 1.18; 95% CI, 0.78-1.80).\n[12] In adjusted analyses, there was no association with 8 of the 10 additional cancers; ever use of pioglitazone was associated with increased risk of prostate cancer (HR, 1.13; 95% CI, 1.02-1.26) and pancreatic cancer (HR, 1.41; 95% CI, 1.16-1.71).\n[13] Crude incidences of prostate and pancreatic cancer in pioglitazone users vs nonusers were 453.3 vs 449.3 and 81.1 vs 48.4 per 100,000 person-years, respectively.\n[14] No clear patterns of risk for any cancer were observed for time since initiation, duration, or dose.\n[15] CONCLUSIONS AND RELEVANCE Pioglitazone use was not associated with a statistically significant increased risk of bladder cancer, although an increased risk, as previously observed, could not be excluded.\n[16] The increased prostate and pancreatic cancer risks associated with ever use of pioglitazone merit further investigation to assess whether they are causal or are due to chance, residual confounding, or reverse causality."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [16]\nExplanation: Evidence states: \"The increased prostate and pancreatic cancer risks associated with ever use of pioglitazone merit further investigation to assess whether they are causal or are due to chance, residual confounding, or reverse causality.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 954, "doc_id": 3355397, "label": "SUPPORTS", "evidence_sentence_ids": [16], "cited_doc_ids": [3355397], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pioneer factor OCT3/4 interacts with major chromatin remodeling factors.\n\nDocument title: Oct4 links multiple epigenetic pathways to the pluripotency network\n\nAbstract sentences:\n[0] Oct4 is a well-known transcription factor that plays fundamental roles in stem cell self-renewal, pluripotency, and somatic cell reprogramming.\n[1] However, limited information is available on Oct4-associated protein complexes and their intrinsic protein-protein interactions that dictate Oct4's critical regulatory activities.\n[2] Here we employed an improved affinity purification approach combined with mass spectrometry to purify Oct4 protein complexes in mouse embryonic stem cells (mESCs), and discovered many novel Oct4 partners important for self-renewal and pluripotency of mESCs.\n[3] Notably, we found that Oct4 is associated with multiple chromatin-modifying complexes with documented as well as newly proved functional significance in stem cell maintenance and somatic cell reprogramming.\n[4] Our study establishes a solid biochemical basis for genetic and epigenetic regulation of stem cell pluripotency and provides a framework for exploring alternative factor-based reprogramming strategies."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Notably, we found that Oct4 is associated with multiple chromatin-modifying complexes with documented as well as newly proved functional significance in stem cell maintenance and somatic cell reprogramming.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 955, "doc_id": 2078658, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [2078658, 30507607], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pioneer factor OCT3/4 interacts with major chromatin remodeling factors.\n\nDocument title: An Oct4-Centered Protein Interaction Network in Embryonic Stem Cells\n\nAbstract sentences:\n[0] Transcription factors, such as Oct4, are critical for establishing and maintaining pluripotent cell identity.\n[1] Whereas the genomic locations of several pluripotency transcription factors have been reported, the spectrum of their interaction partners is underexplored.\n[2] Here, we use an improved affinity protocol to purify Oct4-interacting proteins from mouse embryonic stem cells (ESCs).\n[3] Subsequent purification of Oct4 partners Sall4, Tcfcp2l1, Dax1, and Esrrb resulted in an Oct4 interactome of 166 proteins, including transcription factors and chromatin-modifying complexes with documented roles in self-renewal, but also many factors not previously associated with the ESC network.\n[4] We find that Esrrb associated with the basal transcription machinery and also detect interactions between transcription factors and components of the TGF-beta, Notch, and Wnt signaling pathways.\n[5] Acute depletion of Oct4 reduced binding of Tcfcp2l1, Dax1, and Esrrb to several target genes.\n[6] In conclusion, our purification protocol allowed us to bring greater definition to the circuitry controlling pluripotent cell identity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Subsequent purification of Oct4 partners Sall4, Tcfcp2l1, Dax1, and Esrrb resulted in an Oct4 interactome of 166 proteins, including transcription factors and chromatin-modifying complexes with documented roles in self-renewal, but also many factors not previously associated with the ESC network.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 955, "doc_id": 30507607, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [2078658, 30507607], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Polymeal nutrition increases cardiovascular mortality.\n\nDocument title: The Polymeal: a more natural, safer, and probably tastier (than the Polypill) strategy to reduce cardiovascular disease by more than 75%.\n\nAbstract sentences:\n[0] OBJECTIVE Although the Polypill concept (proposed in 2003) is promising in terms of benefits for cardiovascular risk management, the potential costs and adverse effects are its main pitfalls.\n[1] The objective of this study was to identify a tastier and safer alternative to the Polypill: the Polymeal.\n[2] METHODS Data on the ingredients of the Polymeal were taken from the literature.\n[3] The evidence based recipe included wine, fish, dark chocolate, fruits, vegetables, garlic, and almonds.\n[4] Data from the Framingham heart study and the Framingham offspring study were used to build life tables to model the benefits of the Polymeal in the general population from age 50, assuming multiplicative correlations.\n[5] RESULTS Combining the ingredients of the Polymeal would reduce cardiovascular disease events by 76%.\n[6] For men, taking the Polymeal daily represented an increase in total life expectancy of 6.6 years, an increase in life expectancy free from cardiovascular disease of 9.0 years, and a decrease in life expectancy with cardiovascular disease of 2.4 years.\n[7] The corresponding differences for women were 4.8, 8.1, and 3.3 years.\n[8] CONCLUSION The Polymeal promises to be an effective, non-pharmacological, safe, cheap, and tasty alternative to reduce cardiovascular morbidity and increase life expectancy in the general population."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"For men, taking the Polymeal daily represented an increase in total life expectancy of 6.6 years, an increase in life expectancy free from cardiovascular disease of 9.0 years, and a decrease in life expectancy with cardiovascular disease of 2.4 years.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 959, "doc_id": 8780599, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [8780599], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Polymeal nutrition increases cardiovascular mortality.\n\nDocument title: The Polymeal: a more natural, safer, and probably tastier (than the Polypill) strategy to reduce cardiovascular disease by more than 75%.\n\nAbstract sentences:\n[0] OBJECTIVE Although the Polypill concept (proposed in 2003) is promising in terms of benefits for cardiovascular risk management, the potential costs and adverse effects are its main pitfalls.\n[1] The objective of this study was to identify a tastier and safer alternative to the Polypill: the Polymeal.\n[2] METHODS Data on the ingredients of the Polymeal were taken from the literature.\n[3] The evidence based recipe included wine, fish, dark chocolate, fruits, vegetables, garlic, and almonds.\n[4] Data from the Framingham heart study and the Framingham offspring study were used to build life tables to model the benefits of the Polymeal in the general population from age 50, assuming multiplicative correlations.\n[5] RESULTS Combining the ingredients of the Polymeal would reduce cardiovascular disease events by 76%.\n[6] For men, taking the Polymeal daily represented an increase in total life expectancy of 6.6 years, an increase in life expectancy free from cardiovascular disease of 9.0 years, and a decrease in life expectancy with cardiovascular disease of 2.4 years.\n[7] The corresponding differences for women were 4.8, 8.1, and 3.3 years.\n[8] CONCLUSION The Polymeal promises to be an effective, non-pharmacological, safe, cheap, and tasty alternative to reduce cardiovascular morbidity and increase life expectancy in the general population."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"CONCLUSION The Polymeal promises to be an effective, non-pharmacological, safe, cheap, and tasty alternative to reduce cardiovascular morbidity and increase life expectancy in the general population.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 959, "doc_id": 8780599, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [8780599], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Post-transcriptional handling of mitochondrial transcripts occurs in mitochondrial RNA granules.\n\nDocument title: GRSF1 Regulates RNA Processing in Mitochondrial RNA Granules\n\nAbstract sentences:\n[0] Various specialized domains have been described in the cytosol and the nucleus; however, little is known about compartmentalization within the mitochondrial matrix.\n[1] GRSF1 (G-rich sequence factor 1) is an RNA binding protein that was previously reported to localize in the cytosol.\n[2] We found that an isoform of GRSF1 accumulates in discrete foci in the mitochondrial matrix.\n[3] These foci are composed of nascent mitochondrial RNA and also contain RNase P, an enzyme that participates in mitochondrial RNA processing.\n[4] GRSF1 was found to interact with RNase P and to be required for processing of both classical and tRNA-less RNA precursors.\n[5] In its absence, cleavage of primary RNA transcripts is abnormal, leading to decreased expression of mitochondrially encoded proteins and mitochondrial dysfunction.\n[6] Our findings suggest that the foci containing GRSF1 and RNase P correspond to sites where primary RNA transcripts converge to be processed.\n[7] We have termed these large ribonucleoprotein structures \"mitochondrial RNA granules.\n[8] \""}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Our findings suggest that the foci containing GRSF1 and RNase P correspond to sites where primary RNA transcripts converge to be processed.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 962, "doc_id": 13931771, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [13931771, 935538, 4306711], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Post-transcriptional handling of mitochondrial transcripts occurs in mitochondrial RNA granules.\n\nDocument title: The mitochondrial RNA-binding protein GRSF1 localizes to RNA granules and is required for posttranscriptional mitochondrial gene expression.\n\nAbstract sentences:\n[0] RNA-binding proteins are at the heart of posttranscriptional gene regulation, coordinating the processing, storage, and handling of cellular RNAs.\n[1] We show here that GRSF1, previously implicated in the binding and selective translation of influenza mRNAs, is targeted to mitochondria where it forms granules that colocalize with foci of newly synthesized mtRNA next to mitochondrial nucleoids.\n[2] GRSF1 preferentially binds RNAs transcribed from three contiguous genes on the light strand of mtDNA, the ND6 mRNA, and the long noncoding RNAs for cytb and ND5, each of which contains multiple consensus binding sequences.\n[3] RNAi-mediated knockdown of GRSF1 leads to alterations in mitochondrial RNA stability, abnormal loading of mRNAs and lncRNAs on the mitochondrial ribosome, and impaired ribosome assembly.\n[4] This results in a specific protein synthesis defect and a failure to assemble normal amounts of the oxidative phosphorylation complexes.\n[5] These data implicate GRSF1 as a key regulator of posttranscriptional mitochondrial gene expression."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1, 5]\nExplanation: Evidence states: \"We show here that GRSF1, previously implicated in the binding and selective translation of influenza mRNAs, is targeted to mitochondria where it forms granules that colocalize with foci of newly synthesized mtRNA next to mitochondrial nucleoids. These data implicate GRSF1 as a key regulator of posttranscriptional mitochondrial gene expression.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 962, "doc_id": 935538, "label": "SUPPORTS", "evidence_sentence_ids": [1, 5], "cited_doc_ids": [13931771, 935538, 4306711], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Post-transcriptional handling of mitochondrial transcripts occurs in mitochondrial RNA granules.\n\nDocument title: The Human Mitochondrial DEAD-Box Protein DDX28 Resides in RNA Granules and Functions in Mitoribosome Assembly.\n\nAbstract sentences:\n[0] Human mitochondrial ribosomes are specialized in the synthesis of 13 proteins, which are fundamental components of the oxidative phosphorylation system.\n[1] The pathway of mitoribosome biogenesis, the compartmentalization of the process, and factors involved remain largely unknown.\n[2] Here, we have identified the DEAD-box protein DDX28 as an RNA granule component essential for the biogenesis of the mitoribosome large subunit (mt-LSU).\n[3] DDX28 interacts with the 16S rRNA and the mt-LSU.\n[4] RNAi-mediated DDX28 silencing in HEK293T cells does not affect mitochondrial mRNA stability or 16S rRNA processing or modification.\n[5] However, it leads to reduced levels of 16S rRNA and mt-LSU proteins, impaired mt-LSU assembly, deeply attenuated mitochondrial protein synthesis, and consequent failure to assemble oxidative phosphorylation complexes.\n[6] Our findings identify DDX28 as essential during the early stages of mitoribosome mt-LSU biogenesis, a process that takes place mainly near the mitochondrial nucleoids, in the compartment defined by the RNA granules."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here, we have identified the DEAD-box protein DDX28 as an RNA granule component essential for the biogenesis of the mitoribosome large subunit (mt-LSU).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 962, "doc_id": 4306711, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [13931771, 935538, 4306711], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Post-transcriptional handling of mitochondrial transcripts occurs in mitochondrial RNA granules.\n\nDocument title: The Human Mitochondrial DEAD-Box Protein DDX28 Resides in RNA Granules and Functions in Mitoribosome Assembly.\n\nAbstract sentences:\n[0] Human mitochondrial ribosomes are specialized in the synthesis of 13 proteins, which are fundamental components of the oxidative phosphorylation system.\n[1] The pathway of mitoribosome biogenesis, the compartmentalization of the process, and factors involved remain largely unknown.\n[2] Here, we have identified the DEAD-box protein DDX28 as an RNA granule component essential for the biogenesis of the mitoribosome large subunit (mt-LSU).\n[3] DDX28 interacts with the 16S rRNA and the mt-LSU.\n[4] RNAi-mediated DDX28 silencing in HEK293T cells does not affect mitochondrial mRNA stability or 16S rRNA processing or modification.\n[5] However, it leads to reduced levels of 16S rRNA and mt-LSU proteins, impaired mt-LSU assembly, deeply attenuated mitochondrial protein synthesis, and consequent failure to assemble oxidative phosphorylation complexes.\n[6] Our findings identify DDX28 as essential during the early stages of mitoribosome mt-LSU biogenesis, a process that takes place mainly near the mitochondrial nucleoids, in the compartment defined by the RNA granules."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Our findings identify DDX28 as essential during the early stages of mitoribosome mt-LSU biogenesis, a process that takes place mainly near the mitochondrial nucleoids, in the compartment defined by the RNA granules.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 962, "doc_id": 4306711, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [13931771, 935538, 4306711], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pre-mRNAs associated with spliceosomal components are less stable than unassociated splicing substrates.\n\nDocument title: Linking Splicing to Pol II Transcription Stabilizes Pre-mRNAs and Influences Splicing Patterns\n\nAbstract sentences:\n[0] RNA processing is carried out in close proximity to the site of transcription, suggesting a regulatory link between transcription and pre-mRNA splicing.\n[1] Using an in vitro transcription/splicing assay, we demonstrate that an association of RNA polymerase II (Pol II) transcription and pre-mRNA splicing is required for efficient gene expression.\n[2] Pol II-synthesized RNAs containing functional splice sites are protected from nuclear degradation, presumably because the local concentration of the splicing machinery is sufficiently high to ensure its association over interactions with nucleases.\n[3] Furthermore, the process of transcription influences alternative splicing of newly synthesized pre-mRNAs.\n[4] Because other RNA polymerases do not provide similar protection from nucleases, and their RNA products display altered splicing patterns, the link between transcription and RNA processing is RNA Pol II-specific.\n[5] We propose that the connection between transcription by Pol II and pre-mRNA splicing guarantees an extended half-life and proper processing of nascent pre-mRNAs."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"We propose that the connection between transcription by Pol II and pre-mRNA splicing guarantees an extended half-life and proper processing of nascent pre-mRNAs.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 963, "doc_id": 4162857, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [4162857, 29828242], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pre-mRNAs associated with spliceosomal components are more stable than unassociated splicing substrates.\n\nDocument title: Linking Splicing to Pol II Transcription Stabilizes Pre-mRNAs and Influences Splicing Patterns\n\nAbstract sentences:\n[0] RNA processing is carried out in close proximity to the site of transcription, suggesting a regulatory link between transcription and pre-mRNA splicing.\n[1] Using an in vitro transcription/splicing assay, we demonstrate that an association of RNA polymerase II (Pol II) transcription and pre-mRNA splicing is required for efficient gene expression.\n[2] Pol II-synthesized RNAs containing functional splice sites are protected from nuclear degradation, presumably because the local concentration of the splicing machinery is sufficiently high to ensure its association over interactions with nucleases.\n[3] Furthermore, the process of transcription influences alternative splicing of newly synthesized pre-mRNAs.\n[4] Because other RNA polymerases do not provide similar protection from nucleases, and their RNA products display altered splicing patterns, the link between transcription and RNA processing is RNA Pol II-specific.\n[5] We propose that the connection between transcription by Pol II and pre-mRNA splicing guarantees an extended half-life and proper processing of nascent pre-mRNAs."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"We propose that the connection between transcription by Pol II and pre-mRNA splicing guarantees an extended half-life and proper processing of nascent pre-mRNAs.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 964, "doc_id": 4162857, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [4162857, 29828242], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Prescribed exercise training improves quality of life.\n\nDocument title: Effects of exercise training on health status in patients with chronic heart failure: HF-ACTION randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Findings from previous studies of the effects of exercise training on patient-reported health status have been inconsistent.\n[1] OBJECTIVE To test the effects of exercise training on health status among patients with heart failure.\n[2] DESIGN, SETTING, AND PATIENTS Multicenter, randomized controlled trial among 2331 medically stable outpatients with heart failure with left ventricular ejection fraction of 35% or less.\n[3] Patients were randomized from April 2003 through February 2007.\n[4] INTERVENTIONS Usual care plus aerobic exercise training (n = 1172), consisting of 36 supervised sessions followed by home-based training, vs usual care alone (n = 1159).\n[5] Randomization was stratified by heart failure etiology, which was a covariate in all models.\n[6] MAIN OUTCOME MEASURES Kansas City Cardiomyopathy Questionnaire (KCCQ) overall summary scale and key subscales at baseline, every 3 months for 12 months, and annually thereafter for up to 4 years.\n[7] The KCCQ is scored from 0 to 100 with higher scores corresponding to better health status.\n[8] Treatment group effects were estimated using linear mixed models according to the intention-to-treat principle.\n[9] RESULTS Median follow-up was 2.5 years.\n[10] At 3 months, usual care plus exercise training led to greater improvement in the KCCQ overall summary score (mean, 5.21; 95% confidence interval, 4.42 to 6.00) compared with usual care alone (3.28; 95% confidence interval, 2.48 to 4.09).\n[11] The additional 1.93-point increase (95% confidence interval, 0.84 to 3.01) in the exercise training group was statistically significant (P < .001).\n[12] After 3 months, there were no further significant changes in KCCQ score for either group (P = .85 for the difference between slopes), resulting in a sustained, greater improvement overall for the exercise group (P < .001).\n[13] Results were similar on the KCCQ subscales, and no subgroup interactions were detected.\n[14] CONCLUSIONS Exercise training conferred modest but statistically significant improvements in self-reported health status compared with usual care without training.\n[15] Improvements occurred early and persisted over time.\n[16] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00047437."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"At 3 months, usual care plus exercise training led to greater improvement in the KCCQ overall summary score (mean, 5.21; 95% confidence interval, 4.42 to 6.00) compared with usual care alone (3.28; 95% confidence interval, 2.48 to 4.09).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 965, "doc_id": 40817021, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [40817021], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Prescribed exercise training improves quality of life.\n\nDocument title: Effects of exercise training on health status in patients with chronic heart failure: HF-ACTION randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Findings from previous studies of the effects of exercise training on patient-reported health status have been inconsistent.\n[1] OBJECTIVE To test the effects of exercise training on health status among patients with heart failure.\n[2] DESIGN, SETTING, AND PATIENTS Multicenter, randomized controlled trial among 2331 medically stable outpatients with heart failure with left ventricular ejection fraction of 35% or less.\n[3] Patients were randomized from April 2003 through February 2007.\n[4] INTERVENTIONS Usual care plus aerobic exercise training (n = 1172), consisting of 36 supervised sessions followed by home-based training, vs usual care alone (n = 1159).\n[5] Randomization was stratified by heart failure etiology, which was a covariate in all models.\n[6] MAIN OUTCOME MEASURES Kansas City Cardiomyopathy Questionnaire (KCCQ) overall summary scale and key subscales at baseline, every 3 months for 12 months, and annually thereafter for up to 4 years.\n[7] The KCCQ is scored from 0 to 100 with higher scores corresponding to better health status.\n[8] Treatment group effects were estimated using linear mixed models according to the intention-to-treat principle.\n[9] RESULTS Median follow-up was 2.5 years.\n[10] At 3 months, usual care plus exercise training led to greater improvement in the KCCQ overall summary score (mean, 5.21; 95% confidence interval, 4.42 to 6.00) compared with usual care alone (3.28; 95% confidence interval, 2.48 to 4.09).\n[11] The additional 1.93-point increase (95% confidence interval, 0.84 to 3.01) in the exercise training group was statistically significant (P < .001).\n[12] After 3 months, there were no further significant changes in KCCQ score for either group (P = .85 for the difference between slopes), resulting in a sustained, greater improvement overall for the exercise group (P < .001).\n[13] Results were similar on the KCCQ subscales, and no subgroup interactions were detected.\n[14] CONCLUSIONS Exercise training conferred modest but statistically significant improvements in self-reported health status compared with usual care without training.\n[15] Improvements occurred early and persisted over time.\n[16] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00047437."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"After 3 months, there were no further significant changes in KCCQ score for either group (P = .85 for the difference between slopes), resulting in a sustained, greater improvement overall for the exercise group (P < .001).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 965, "doc_id": 40817021, "label": "SUPPORTS", "evidence_sentence_ids": [12], "cited_doc_ids": [40817021], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Prescribed exercise training improves quality of life.\n\nDocument title: Effects of exercise training on health status in patients with chronic heart failure: HF-ACTION randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Findings from previous studies of the effects of exercise training on patient-reported health status have been inconsistent.\n[1] OBJECTIVE To test the effects of exercise training on health status among patients with heart failure.\n[2] DESIGN, SETTING, AND PATIENTS Multicenter, randomized controlled trial among 2331 medically stable outpatients with heart failure with left ventricular ejection fraction of 35% or less.\n[3] Patients were randomized from April 2003 through February 2007.\n[4] INTERVENTIONS Usual care plus aerobic exercise training (n = 1172), consisting of 36 supervised sessions followed by home-based training, vs usual care alone (n = 1159).\n[5] Randomization was stratified by heart failure etiology, which was a covariate in all models.\n[6] MAIN OUTCOME MEASURES Kansas City Cardiomyopathy Questionnaire (KCCQ) overall summary scale and key subscales at baseline, every 3 months for 12 months, and annually thereafter for up to 4 years.\n[7] The KCCQ is scored from 0 to 100 with higher scores corresponding to better health status.\n[8] Treatment group effects were estimated using linear mixed models according to the intention-to-treat principle.\n[9] RESULTS Median follow-up was 2.5 years.\n[10] At 3 months, usual care plus exercise training led to greater improvement in the KCCQ overall summary score (mean, 5.21; 95% confidence interval, 4.42 to 6.00) compared with usual care alone (3.28; 95% confidence interval, 2.48 to 4.09).\n[11] The additional 1.93-point increase (95% confidence interval, 0.84 to 3.01) in the exercise training group was statistically significant (P < .001).\n[12] After 3 months, there were no further significant changes in KCCQ score for either group (P = .85 for the difference between slopes), resulting in a sustained, greater improvement overall for the exercise group (P < .001).\n[13] Results were similar on the KCCQ subscales, and no subgroup interactions were detected.\n[14] CONCLUSIONS Exercise training conferred modest but statistically significant improvements in self-reported health status compared with usual care without training.\n[15] Improvements occurred early and persisted over time.\n[16] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00047437."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [14]\nExplanation: Evidence states: \"CONCLUSIONS Exercise training conferred modest but statistically significant improvements in self-reported health status compared with usual care without training.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 965, "doc_id": 40817021, "label": "SUPPORTS", "evidence_sentence_ids": [14], "cited_doc_ids": [40817021], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: PrimPol degrades short DNA replication intermediates on the leading strand during DNA replication.\n\nDocument title: hPrimpol1/CCDC111 is a human DNA primase-polymerase required for the maintenance of genome integrity.\n\nAbstract sentences:\n[0] Prim-pol is a recently identified DNA primase-polymerase belonging to the archaeao-eukaryotic primase (AEP) superfamily.\n[1] Here, we characterize a previously unrecognized prim-pol in human cells, which we designate hPrimpol1 (human primase-polymerase 1).\n[2] hPrimpol1 possesses primase and DNA polymerase activities in vitro, interacts directly with RPA1 and is recruited to sites of DNA damage and stalled replication forks in an RPA1-dependent manner.\n[3] Cells depleted of hPrimpol1 display increased spontaneous DNA damage and defects in the restart of stalled replication forks.\n[4] Both RPA1 binding and the primase activity of hPrimpol1 are required for its cellular function during DNA replication.\n[5] Our results indicate that hPrimpol1 is a novel factor involved in the response to DNA replication stress."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 969, "doc_id": 19356271, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [19356271, 17368516], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: PrimPol generates short DNA replication intermediates on the leading strand during DNA replication.\n\nDocument title: hPrimpol1/CCDC111 is a human DNA primase-polymerase required for the maintenance of genome integrity.\n\nAbstract sentences:\n[0] Prim-pol is a recently identified DNA primase-polymerase belonging to the archaeao-eukaryotic primase (AEP) superfamily.\n[1] Here, we characterize a previously unrecognized prim-pol in human cells, which we designate hPrimpol1 (human primase-polymerase 1).\n[2] hPrimpol1 possesses primase and DNA polymerase activities in vitro, interacts directly with RPA1 and is recruited to sites of DNA damage and stalled replication forks in an RPA1-dependent manner.\n[3] Cells depleted of hPrimpol1 display increased spontaneous DNA damage and defects in the restart of stalled replication forks.\n[4] Both RPA1 binding and the primase activity of hPrimpol1 are required for its cellular function during DNA replication.\n[5] Our results indicate that hPrimpol1 is a novel factor involved in the response to DNA replication stress."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 970, "doc_id": 19356271, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [19356271, 17368516], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Primary cervical cancer screening with HPV detection has lower longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nDocument title: Human papillomavirus and Papanicolaou tests to screen for cervical cancer.\n\nAbstract sentences:\n[0] BACKGROUND Screening for cervical cancer based on testing for human papillomavirus (HPV) increases the sensitivity of detection of high-grade (grade 2 or 3) cervical intraepithelial neoplasia, but whether this gain represents overdiagnosis or protection against future high-grade cervical epithelial neoplasia or cervical cancer is unknown.\n[1] METHODS In a population-based screening program in Sweden, 12,527 women 32 to 38 years of age were randomly assigned at a 1:1 ratio to have an HPV test plus a Papanicolaou (Pap) test (intervention group) or a Pap test alone (control group).\n[2] Women with a positive HPV test and a normal Pap test result were offered a second HPV test at least 1 year later, and those who were found to be persistently infected with the same high-risk type of HPV were then offered colposcopy with cervical biopsy.\n[3] A similar number of double-blinded Pap smears and colposcopies with biopsy were performed in randomly selected women in the control group.\n[4] Comprehensive registry data were used to follow the women for a mean of 4.1 years.\n[5] The relative rates of grade 2 or 3 cervical intraepithelial neoplasia or cancer detected at enrollment and at subsequent screening examinations were calculated.\n[6] RESULTS At enrollment, the proportion of women in the intervention group who were found to have lesions of grade 2 or 3 cervical intraepithelial neoplasia or cancer was 51% greater (95% confidence interval [CI], 13 to 102) than the proportion of women in the control group who were found to have such lesions.\n[7] At subsequent screening examinations, the proportion of women in the intervention group who were found to have grade 2 or 3 lesions or cancer was 42% less (95% CI, 4 to 64) and the proportion with grade 3 lesions or cancer was 47% less (95% CI, 2 to 71) than the proportions of control women who were found to have such lesions.\n[8] Women with persistent HPV infection remained at high risk for grade 2 or 3 lesions or cancer after referral for colposcopy.\n[9] CONCLUSIONS The addition of an HPV test to the Pap test to screen women in their mid-30s for cervical cancer reduces the incidence of grade 2 or 3 cervical intraepithelial neoplasia or cancer detected by subsequent screening examinations.\n[10] (ClinicalTrials.gov number, NCT00479375 [ClinicalTrials.gov].)."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"BACKGROUND Screening for cervical cancer based on testing for human papillomavirus (HPV) increases the sensitivity of detection of high-grade (grade 2 or 3) cervical intraepithelial neoplasia, but whether this gain represents overdiagnosis or protection against future high-grade cervical epithelial neoplasia or cervical cancer is unknown.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 972, "doc_id": 46695481, "label": "CONTRADICTS", "evidence_sentence_ids": [0], "cited_doc_ids": [46695481, 27873158, 28617573, 9764256], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Primary cervical cancer screening with HPV detection has lower longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nDocument title: Human papillomavirus and Papanicolaou tests to screen for cervical cancer.\n\nAbstract sentences:\n[0] BACKGROUND Screening for cervical cancer based on testing for human papillomavirus (HPV) increases the sensitivity of detection of high-grade (grade 2 or 3) cervical intraepithelial neoplasia, but whether this gain represents overdiagnosis or protection against future high-grade cervical epithelial neoplasia or cervical cancer is unknown.\n[1] METHODS In a population-based screening program in Sweden, 12,527 women 32 to 38 years of age were randomly assigned at a 1:1 ratio to have an HPV test plus a Papanicolaou (Pap) test (intervention group) or a Pap test alone (control group).\n[2] Women with a positive HPV test and a normal Pap test result were offered a second HPV test at least 1 year later, and those who were found to be persistently infected with the same high-risk type of HPV were then offered colposcopy with cervical biopsy.\n[3] A similar number of double-blinded Pap smears and colposcopies with biopsy were performed in randomly selected women in the control group.\n[4] Comprehensive registry data were used to follow the women for a mean of 4.1 years.\n[5] The relative rates of grade 2 or 3 cervical intraepithelial neoplasia or cancer detected at enrollment and at subsequent screening examinations were calculated.\n[6] RESULTS At enrollment, the proportion of women in the intervention group who were found to have lesions of grade 2 or 3 cervical intraepithelial neoplasia or cancer was 51% greater (95% confidence interval [CI], 13 to 102) than the proportion of women in the control group who were found to have such lesions.\n[7] At subsequent screening examinations, the proportion of women in the intervention group who were found to have grade 2 or 3 lesions or cancer was 42% less (95% CI, 4 to 64) and the proportion with grade 3 lesions or cancer was 47% less (95% CI, 2 to 71) than the proportions of control women who were found to have such lesions.\n[8] Women with persistent HPV infection remained at high risk for grade 2 or 3 lesions or cancer after referral for colposcopy.\n[9] CONCLUSIONS The addition of an HPV test to the Pap test to screen women in their mid-30s for cervical cancer reduces the incidence of grade 2 or 3 cervical intraepithelial neoplasia or cancer detected by subsequent screening examinations.\n[10] (ClinicalTrials.gov number, NCT00479375 [ClinicalTrials.gov].)."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"CONCLUSIONS The addition of an HPV test to the Pap test to screen women in their mid-30s for cervical cancer reduces the incidence of grade 2 or 3 cervical intraepithelial neoplasia or cancer detected by subsequent screening examinations.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 972, "doc_id": 46695481, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [46695481, 27873158, 28617573, 9764256], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Primary cervical cancer screening with HPV detection has lower longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nDocument title: Efficacy of human papillomavirus testing for the detection of invasive cervical cancers and cervical intraepithelial neoplasia: a randomised controlled trial.\n\nAbstract sentences:\n[0] BACKGROUND Human papillomavirus (HPV) testing is known to be more sensitive, but less specific than cytology for detecting cervical intraepithelial neoplasia (CIN).\n[1] We assessed the efficacy of cervical-cancer screening policies that are based on HPV testing.\n[2] METHODS Between March, 2004, and December, 2004, in two separate recruitment phases, women aged 25-60 years were randomly assigned to conventional cytology or to HPV testing in combination with liquid-based cytology (first phase) or alone (second phase).\n[3] Randomisation was done by computer in two screening centres and by sequential opening of numbered sealed envelopes in the remaining seven centres.\n[4] During phase one, women who were HPV-positive and aged 35-60 years were referred to colposcopy, whereas women aged 25-34 years were referred to colposcopy only if cytology was also abnormal or HPV testing was persistently positive.\n[5] During phase two, women in the HPV group were referred for colposcopy if the HPV test was positive.\n[6] Two rounds of screening occurred in each phase, and all women had cytology testing only at the second round.\n[7] The primary endpoint was the detection of grade 2 and 3 CIN, and of invasive cervical cancers during the first and second screening rounds.\n[8] Analysis was done by intention to screen.\n[9] This trial is registered, number ISRCTN81678807.\n[10] FINDINGS In total for both phases, 47,001 women were randomly assigned to the cytology group and 47,369 to HPV testing.\n[11] 33,851 women from the cytology group and 32,998 from the HPV-testing group had a second round of screening.\n[12] We also retrieved the histological diagnoses from screening done elsewhere.\n[13] The detection of invasive cervical cancers was similar for the two groups in the first round of screening (nine in the cytology group vs seven in the HPV group, p=0.62); no cases were detected in the HPV group during round two, compared with nine in the cytology group (p=0.004).\n[14] Overall, in the two rounds of screening, 18 invasive cancers were detected in the cytology group versus seven in the HPV group (p=0.028).\n[15] Among women aged 35-60 years, at round one the relative detection (HPV vs cytology) was 2.00 (95% CI 1.44-2.77) for CIN2, 2.08 (1.47-2.95) for CIN3, and 2.03 (1.60-2.57) for CIN2 and 3 together.\n[16] At round two the relative detection was 0.54 (0.23-1.28) for CIN2, 0.48 (0.21-1.11) for CIN3, and 0.51 (0.28-0.93) for CIN2 and 3 together.\n[17] Among women aged 25-34 years, there was significant heterogeneity between phases in the relative detection of CIN3.\n[18] At round one the relative detection was 0.93 (0.52-1.64) in phase one and 3.91 (2.02-7.57) in phase two.\n[19] At round two the relative detection was 1.34 (0.46-3.84) in phase one and 0.20 (0.04-0.93) in phase two.\n[20] Pooling both phases, the detection ratio of CIN2 for women aged 25-34 years was 4.09 (2.24-7.48) at round one and 0.64 (0.23-1.27) at round two.\n[21] INTERPRETATION HPV-based screening is more effective than cytology in preventing invasive cervical cancer, by detecting persistent high-grade lesions earlier and providing a longer low-risk period.\n[22] However, in younger women, HPV screening leads to over-diagnosis of regressive CIN2.\n[23] FUNDING European Union, Italian Ministry of Health, Regional Health Administrations of Piemonte, Tuscany, Veneto and Emilia-Romagna, and Public Health Agency of Lazio."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"BACKGROUND Human papillomavirus (HPV) testing is known to be more sensitive, but less specific than cytology for detecting cervical intraepithelial neoplasia (CIN).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 972, "doc_id": 27873158, "label": "CONTRADICTS", "evidence_sentence_ids": [0], "cited_doc_ids": [46695481, 27873158, 28617573, 9764256], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Primary cervical cancer screening with HPV detection has lower longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nDocument title: Efficacy of human papillomavirus testing for the detection of invasive cervical cancers and cervical intraepithelial neoplasia: a randomised controlled trial.\n\nAbstract sentences:\n[0] BACKGROUND Human papillomavirus (HPV) testing is known to be more sensitive, but less specific than cytology for detecting cervical intraepithelial neoplasia (CIN).\n[1] We assessed the efficacy of cervical-cancer screening policies that are based on HPV testing.\n[2] METHODS Between March, 2004, and December, 2004, in two separate recruitment phases, women aged 25-60 years were randomly assigned to conventional cytology or to HPV testing in combination with liquid-based cytology (first phase) or alone (second phase).\n[3] Randomisation was done by computer in two screening centres and by sequential opening of numbered sealed envelopes in the remaining seven centres.\n[4] During phase one, women who were HPV-positive and aged 35-60 years were referred to colposcopy, whereas women aged 25-34 years were referred to colposcopy only if cytology was also abnormal or HPV testing was persistently positive.\n[5] During phase two, women in the HPV group were referred for colposcopy if the HPV test was positive.\n[6] Two rounds of screening occurred in each phase, and all women had cytology testing only at the second round.\n[7] The primary endpoint was the detection of grade 2 and 3 CIN, and of invasive cervical cancers during the first and second screening rounds.\n[8] Analysis was done by intention to screen.\n[9] This trial is registered, number ISRCTN81678807.\n[10] FINDINGS In total for both phases, 47,001 women were randomly assigned to the cytology group and 47,369 to HPV testing.\n[11] 33,851 women from the cytology group and 32,998 from the HPV-testing group had a second round of screening.\n[12] We also retrieved the histological diagnoses from screening done elsewhere.\n[13] The detection of invasive cervical cancers was similar for the two groups in the first round of screening (nine in the cytology group vs seven in the HPV group, p=0.62); no cases were detected in the HPV group during round two, compared with nine in the cytology group (p=0.004).\n[14] Overall, in the two rounds of screening, 18 invasive cancers were detected in the cytology group versus seven in the HPV group (p=0.028).\n[15] Among women aged 35-60 years, at round one the relative detection (HPV vs cytology) was 2.00 (95% CI 1.44-2.77) for CIN2, 2.08 (1.47-2.95) for CIN3, and 2.03 (1.60-2.57) for CIN2 and 3 together.\n[16] At round two the relative detection was 0.54 (0.23-1.28) for CIN2, 0.48 (0.21-1.11) for CIN3, and 0.51 (0.28-0.93) for CIN2 and 3 together.\n[17] Among women aged 25-34 years, there was significant heterogeneity between phases in the relative detection of CIN3.\n[18] At round one the relative detection was 0.93 (0.52-1.64) in phase one and 3.91 (2.02-7.57) in phase two.\n[19] At round two the relative detection was 1.34 (0.46-3.84) in phase one and 0.20 (0.04-0.93) in phase two.\n[20] Pooling both phases, the detection ratio of CIN2 for women aged 25-34 years was 4.09 (2.24-7.48) at round one and 0.64 (0.23-1.27) at round two.\n[21] INTERPRETATION HPV-based screening is more effective than cytology in preventing invasive cervical cancer, by detecting persistent high-grade lesions earlier and providing a longer low-risk period.\n[22] However, in younger women, HPV screening leads to over-diagnosis of regressive CIN2.\n[23] FUNDING European Union, Italian Ministry of Health, Regional Health Administrations of Piemonte, Tuscany, Veneto and Emilia-Romagna, and Public Health Agency of Lazio."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [15]\nExplanation: Evidence states: \"Among women aged 35-60 years, at round one the relative detection (HPV vs cytology) was 2.00 (95% CI 1.44-2.77) for CIN2, 2.08 (1.47-2.95) for CIN3, and 2.03 (1.60-2.57) for CIN2 and 3 together.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 972, "doc_id": 27873158, "label": "CONTRADICTS", "evidence_sentence_ids": [15], "cited_doc_ids": [46695481, 27873158, 28617573, 9764256], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Primary cervical cancer screening with HPV detection has lower longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nDocument title: Efficacy of human papillomavirus testing for the detection of invasive cervical cancers and cervical intraepithelial neoplasia: a randomised controlled trial.\n\nAbstract sentences:\n[0] BACKGROUND Human papillomavirus (HPV) testing is known to be more sensitive, but less specific than cytology for detecting cervical intraepithelial neoplasia (CIN).\n[1] We assessed the efficacy of cervical-cancer screening policies that are based on HPV testing.\n[2] METHODS Between March, 2004, and December, 2004, in two separate recruitment phases, women aged 25-60 years were randomly assigned to conventional cytology or to HPV testing in combination with liquid-based cytology (first phase) or alone (second phase).\n[3] Randomisation was done by computer in two screening centres and by sequential opening of numbered sealed envelopes in the remaining seven centres.\n[4] During phase one, women who were HPV-positive and aged 35-60 years were referred to colposcopy, whereas women aged 25-34 years were referred to colposcopy only if cytology was also abnormal or HPV testing was persistently positive.\n[5] During phase two, women in the HPV group were referred for colposcopy if the HPV test was positive.\n[6] Two rounds of screening occurred in each phase, and all women had cytology testing only at the second round.\n[7] The primary endpoint was the detection of grade 2 and 3 CIN, and of invasive cervical cancers during the first and second screening rounds.\n[8] Analysis was done by intention to screen.\n[9] This trial is registered, number ISRCTN81678807.\n[10] FINDINGS In total for both phases, 47,001 women were randomly assigned to the cytology group and 47,369 to HPV testing.\n[11] 33,851 women from the cytology group and 32,998 from the HPV-testing group had a second round of screening.\n[12] We also retrieved the histological diagnoses from screening done elsewhere.\n[13] The detection of invasive cervical cancers was similar for the two groups in the first round of screening (nine in the cytology group vs seven in the HPV group, p=0.62); no cases were detected in the HPV group during round two, compared with nine in the cytology group (p=0.004).\n[14] Overall, in the two rounds of screening, 18 invasive cancers were detected in the cytology group versus seven in the HPV group (p=0.028).\n[15] Among women aged 35-60 years, at round one the relative detection (HPV vs cytology) was 2.00 (95% CI 1.44-2.77) for CIN2, 2.08 (1.47-2.95) for CIN3, and 2.03 (1.60-2.57) for CIN2 and 3 together.\n[16] At round two the relative detection was 0.54 (0.23-1.28) for CIN2, 0.48 (0.21-1.11) for CIN3, and 0.51 (0.28-0.93) for CIN2 and 3 together.\n[17] Among women aged 25-34 years, there was significant heterogeneity between phases in the relative detection of CIN3.\n[18] At round one the relative detection was 0.93 (0.52-1.64) in phase one and 3.91 (2.02-7.57) in phase two.\n[19] At round two the relative detection was 1.34 (0.46-3.84) in phase one and 0.20 (0.04-0.93) in phase two.\n[20] Pooling both phases, the detection ratio of CIN2 for women aged 25-34 years was 4.09 (2.24-7.48) at round one and 0.64 (0.23-1.27) at round two.\n[21] INTERPRETATION HPV-based screening is more effective than cytology in preventing invasive cervical cancer, by detecting persistent high-grade lesions earlier and providing a longer low-risk period.\n[22] However, in younger women, HPV screening leads to over-diagnosis of regressive CIN2.\n[23] FUNDING European Union, Italian Ministry of Health, Regional Health Administrations of Piemonte, Tuscany, Veneto and Emilia-Romagna, and Public Health Agency of Lazio."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [21]\nExplanation: Evidence states: \"INTERPRETATION HPV-based screening is more effective than cytology in preventing invasive cervical cancer, by detecting persistent high-grade lesions earlier and providing a longer low-risk period.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 972, "doc_id": 27873158, "label": "CONTRADICTS", "evidence_sentence_ids": [21], "cited_doc_ids": [46695481, 27873158, 28617573, 9764256], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Primary cervical cancer screening with HPV detection has lower longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nDocument title: Evidence regarding human papillomavirus testing in secondary prevention of cervical cancer.\n\nAbstract sentences:\n[0] More than ever, clinicians need regularly updated reviews given the continuously increasing amount of new information regarding innovative cervical cancer prevention methods.\n[1] A summary is given from recent meta-analyses and systematic reviews on 3 possible clinical applications of human papillomavirus (HPV) testing: triage of women with equivocal or low-grade cytologic abnormalities; prediction of the therapeutic outcome after treatment of cervical intraepithelial neoplasia (CIN) lesions, and last not but not least, primary screening for cervical cancer and pre-cancer.\n[2] Consistent evidence is available indicating that HPV-triage with the Hybrid Capture(®) 2 assay (Qiagen Gaithersburg, Inc., MD, USA [previously Digene Corp.] (HC2) is more accurate (higher sensitivity, similar specificity) than repeat cytology to triage women with equivocal Pap smear results.\n[3] Several other tests show at least similar accuracy but mRNA testing with the APTIMA(®) (Gen-Probe Inc., San Diego, CA, USA) test is similarly sensitive but more specific compared to HC2.\n[4] In triage of low-grade squamous intraepithelial lesions (LSIL), HC2 is more sensitive but its specificity is substantially lower compared to repeat cytology.\n[5] The APTIMA(®) test is more specific than HC2 without showing a loss in sensitivity.\n[6] Identification of DNA of HPV types 16 and/or 18, or RNA from the five most carcinogenic HPV types allow selecting women at highest risk for CIN3+ but the sensitivity and negative predictive value of these markers are lower than full-range high-risk HPV (hrHPV) testing.\n[7] After conservative treatment of cervical pre-cancer, HPV testing picks up more quickly, with higher sensitivity and not lower specificity, residual or recurrent high-grade CIN than follow-up cytology.\n[8] Primary screening for hrHPV generally detects more CIN2, CIN3 or cancer compared to cytology at cut-off atypical squamous cells of undetermined significance (ASC-US) or LSIL, but is less specific.\n[9] Combined HPV and cytology screening provides a further small gain in sensitivity at the expense of a considerable loss in specificity if positive by either test is referred to colposcopy, in comparison with HPV testing only.\n[10] Randomised trials and follow-up of cohort studies consistently demonstrate a significantly lower cumulative incidence of CIN3+ and even of cancer, in women aged 30 years or older, who were at enrollment hrHPV DNA negative compared to those who were cytologically negative.\n[11] The difference in cumulative risk of CIN3+ or cancer for double negative (cytology & HPV) versus only HPV-negative women is small.\n[12] HC2, GP5+/6+ PCR (polymerase chain reaction), cobas(®) 4800 PCR (Roche Molecular Systems Inc., Alameda, CA, USA) and Real Time PCR (Abbott Molecular, Des Plaines, IL, USA) can be considered as clinically validated for use in primary screening.\n[13] The loss in specificity associated with primary HPV-based screening can be compensated by appropriate algorithms involving reflex cytology and/or HPV genotyping for HPV16 or 18.\n[14] There exists a substantial evidence base to support that HPV testing is advantageous both in triage of women with equivocal abnormal cytology, in surveillance after treatment of CIN lesions and in primary screening of women aged 30 years or older.\n[15] However, the possible advantages offered by HPV-based screening require a well organised program with good compliance with screening and triage policies.\n[16] This article forms part of a special supplement entitled \"Comprehensive Control of HPV Infections and Related Diseases\" Vaccine Volume 30, Supplement 5, 2012."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Primary screening for hrHPV generally detects more CIN2, CIN3 or cancer compared to cytology at cut-off atypical squamous cells of undetermined significance (ASC-US) or LSIL, but is less specific.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 972, "doc_id": 28617573, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [46695481, 27873158, 28617573, 9764256], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Primary cervical cancer screening with HPV detection has lower longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nDocument title: Human papillomavirus testing for the detection of high-grade cervical intraepithelial neoplasia and cancer: final results of the POBASCAM randomised controlled trial.\n\nAbstract sentences:\n[0] BACKGROUND Human papillomavirus (HPV) testing is more sensitive for the detection of high-grade cervical lesions than is cytology, but detection of HPV by DNA screening in two screening rounds 5 years apart has not been assessed.\n[1] The aim of this study was to assess whether HPV DNA testing in the first screen decreases detection of cervical intraepithelial neoplasia (CIN) grade 3 or worse, CIN grade 2 or worse, and cervical cancer in the second screening.\n[2] METHODS In this randomised trial, women aged 29-56 years participating in the cervical screening programme in the Netherlands were randomly assigned to receive HPV DNA (GP5+/6+-PCR method) and cytology co-testing or cytology testing alone, from January, 1999, to September, 2002.\n[3] Randomisation (in a 1:1 ratio) was done with computer-generated random numbers after the cervical specimen had been taken.\n[4] At the second screening 5 years later, HPV DNA and cytology co-testing was done in both groups; researchers were masked to the patient's assignment.\n[5] The primary endpoint was the number of CIN grade 3 or worse detected.\n[6] Analysis was done by intention to screen.\n[7] The trial is now finished and is registered, number ISRCTN20781131.\n[8] FINDINGS 22,420 women were randomly assigned to the intervention group and 22 518 to the control group; 19 999 in the intervention group and 20,106 in the control group were eligible for analysis at the first screen.\n[9] At the second screen, 19 579 women in the intervention group and 19,731 in the control group were eligible, of whom 16,750 and 16,743, respectively, attended the second screen.\n[10] In the second round, CIN grade 3 or worse was less common in the intervention group than in the control group (88 of 19 579 in the intervention group vs 122 of 19,731 in the control group; relative risk 0·73, 95% CI 0·55-0·96; p=0·023).\n[11] Cervical cancer was also less common in the intervention group than in the control group (four of 19 579 in the intervention group vs 14 of 19,731; 0·29, 0·10-0·87; p=0·031).\n[12] In the baseline round, detection of CIN grade 3 or worse did not differ significantly between groups (171 of 19 999 vs 150 of 20,106; 1·15, 0·92-1·43; p=0·239) but was significantly more common in women with normal cytology (34 of 19,286 vs 12 of 19,373; 2·85, 1·47-5·49; p=0·001).\n[13] Furthermore, significantly more cases of CIN grade 2 or worse were detected in the intervention group than in the control group (267 of 19 999 vs 215 of 20,106; 1·25, 1·05-1·50; p=0·015).\n[14] In the second screen, fewer HPV16-positive CIN grade 3 or worse were detected in the intervention group than in the control group (17 of 9481 vs 35 of 9354; 0·48, 0·27-0·85; p=0·012); detection of non-HPV16-positive CIN grade 3 or worse did not differ between groups (25 of 9481 vs 25 of 9354; 0·99, 0·57-1·72; p=1·00).\n[15] The cumulative detection of CIN grade 3 or worse and CIN grade 2 or worse did not differ significantly between study arms, neither for the whole study group (CIN grade 3 or worse: 259 of 19 999 vs 272 of 20,106; 0·96, 0·81-1·14, p=0·631; CIN grade 2 or worse: 427 of 19 999 vs 399 of 20,106; 1·08, 0·94-1·24; p=0·292), nor for subgroups of women invited for the first time (CIN grade 3 or worse in women aged 29-33 years: 102 of 3139 vs 105 of 3128; 0·97, 0·74-1·27; CIN grade 2 or worse in women aged 29-33 years: 153 of 3139 vs 151 of 3128; 1·01, 0·81-1·26; CIN grade 3 or worse in women aged 34-56 years: 157 of 16,860 vs 167 of 16 978; 0·95, 0·76-1·18; CIN grade 2 or worse in women aged 34-56 years: 274 of 16,860 vs 248 of 16 978; 1·11, 0·94-1·32).\n[16] INTERPRETATION Implementation of HPV DNA testing in cervical screening leads to earlier detection of clinically relevant CIN grade 2 or worse, which when adequately treated, improves protection against CIN grade 3 or worse and cervical cancer.\n[17] Early detection of high-grade cervical legions caused by HPV16 was a major component of this benefit.\n[18] Our results lend support to the use of HPV DNA testing for all women aged 29 years and older.\n[19] FUNDING Zorg Onderzoek Nederland (Netherlands Organisation for Health Research and Development)."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"Furthermore, significantly more cases of CIN grade 2 or worse were detected in the intervention group than in the control group (267 of 19 999 vs 215 of 20,106; 1·25, 1·05-1·50; p=0·015).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 972, "doc_id": 9764256, "label": "CONTRADICTS", "evidence_sentence_ids": [13], "cited_doc_ids": [46695481, 27873158, 28617573, 9764256], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Primary cervical cytology screening with HPV detection has higher longitudinal sensitivity to detect severe cervical intraepithelial neoplasia than conventional cytology.\n\nDocument title: Rate of cervical cancer, severe intraepithelial neoplasia, and adenocarcinoma in situ in primary HPV DNA screening with cytology triage: randomised study within organised screening programme.\n\nAbstract sentences:\n[0] OBJECTIVE To assess the performance and impact of primary human papillomavirus (HPV) DNA screening with cytology triage compared with conventional cytology on cervical cancer and severe pre-cancerous lesions.\n[1] DESIGN Randomised trial.\n[2] SETTING Population based screening programme for cervical cancer in southern Finland in 2003-5.\n[3] PARTICIPANTS 58 076 women, aged 30-60, invited to the routine population based screening programme for cervical cancer.\n[4] INTERVENTIONS Primary HPV DNA test (hybrid capture II) with cytology triage if the result was positive or conventional cytological screening (reference).\n[5] MAIN OUTCOME MEASURES Rate of cervical cancer, cervical intraepithelial neoplasia (CIN) grade III, and adenocarcinoma in situ (as a composite outcome referred to as CIN III+) during 2003-7 through record linkage between files from the screening registry and the national cancer registry.\n[6] RESULTS In the HPV and conventional arms there were 95 600 and 95 700 woman years of follow-up and 76 and 53 cases of CIN III+, respectively (of which six and eight were cervical cancers).\n[7] The relative rate of CIN III+ in the HPV arm versus the conventional arm was 1.44 (95% confidence interval 1.01 to 2.05) among all women invited for screening and 1.77 (1.16 to 2.74) among those who attended.\n[8] Among women with a normal or negative test result, the relative rate of subsequent CIN III+ was 0.28 (0.04 to 1.17).\n[9] The rate of cervical cancer between arms was 0.75 (0.25 to 2.16) among women invited for screening and 1.98 (0.52 to 9.38) among those who attended.\n[10] CONCLUSIONS When incorporated into a well established organised screening programme, primary HPV screening with cytology triage was more sensitive than conventional cytology in detecting CIN III+ lesions.\n[11] The number of cases of cervical cancer was small, but considering the high probability of progression of CIN III the findings are of importance regarding cancer prevention.\n[12] TRIAL REGISTRATION Current Controlled Trials ISRCTN23885553."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"The relative rate of CIN III+ in the HPV arm versus the conventional arm was 1.44 (95% confidence interval 1.01 to 2.05) among all women invited for screening and 1.77 (1.16 to 2.74) among those who attended.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 973, "doc_id": 27446873, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [27446873, 27873158, 28617573, 9764256], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Primary cervical cytology screening with HPV detection has higher longitudinal sensitivity to detect severe cervical intraepithelial neoplasia than conventional cytology.\n\nDocument title: Rate of cervical cancer, severe intraepithelial neoplasia, and adenocarcinoma in situ in primary HPV DNA screening with cytology triage: randomised study within organised screening programme.\n\nAbstract sentences:\n[0] OBJECTIVE To assess the performance and impact of primary human papillomavirus (HPV) DNA screening with cytology triage compared with conventional cytology on cervical cancer and severe pre-cancerous lesions.\n[1] DESIGN Randomised trial.\n[2] SETTING Population based screening programme for cervical cancer in southern Finland in 2003-5.\n[3] PARTICIPANTS 58 076 women, aged 30-60, invited to the routine population based screening programme for cervical cancer.\n[4] INTERVENTIONS Primary HPV DNA test (hybrid capture II) with cytology triage if the result was positive or conventional cytological screening (reference).\n[5] MAIN OUTCOME MEASURES Rate of cervical cancer, cervical intraepithelial neoplasia (CIN) grade III, and adenocarcinoma in situ (as a composite outcome referred to as CIN III+) during 2003-7 through record linkage between files from the screening registry and the national cancer registry.\n[6] RESULTS In the HPV and conventional arms there were 95 600 and 95 700 woman years of follow-up and 76 and 53 cases of CIN III+, respectively (of which six and eight were cervical cancers).\n[7] The relative rate of CIN III+ in the HPV arm versus the conventional arm was 1.44 (95% confidence interval 1.01 to 2.05) among all women invited for screening and 1.77 (1.16 to 2.74) among those who attended.\n[8] Among women with a normal or negative test result, the relative rate of subsequent CIN III+ was 0.28 (0.04 to 1.17).\n[9] The rate of cervical cancer between arms was 0.75 (0.25 to 2.16) among women invited for screening and 1.98 (0.52 to 9.38) among those who attended.\n[10] CONCLUSIONS When incorporated into a well established organised screening programme, primary HPV screening with cytology triage was more sensitive than conventional cytology in detecting CIN III+ lesions.\n[11] The number of cases of cervical cancer was small, but considering the high probability of progression of CIN III the findings are of importance regarding cancer prevention.\n[12] TRIAL REGISTRATION Current Controlled Trials ISRCTN23885553."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"CONCLUSIONS When incorporated into a well established organised screening programme, primary HPV screening with cytology triage was more sensitive than conventional cytology in detecting CIN III+ lesions.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 973, "doc_id": 27446873, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [27446873, 27873158, 28617573, 9764256], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Primary cervical cytology screening with HPV detection has higher longitudinal sensitivity to detect severe cervical intraepithelial neoplasia than conventional cytology.\n\nDocument title: Efficacy of human papillomavirus testing for the detection of invasive cervical cancers and cervical intraepithelial neoplasia: a randomised controlled trial.\n\nAbstract sentences:\n[0] BACKGROUND Human papillomavirus (HPV) testing is known to be more sensitive, but less specific than cytology for detecting cervical intraepithelial neoplasia (CIN).\n[1] We assessed the efficacy of cervical-cancer screening policies that are based on HPV testing.\n[2] METHODS Between March, 2004, and December, 2004, in two separate recruitment phases, women aged 25-60 years were randomly assigned to conventional cytology or to HPV testing in combination with liquid-based cytology (first phase) or alone (second phase).\n[3] Randomisation was done by computer in two screening centres and by sequential opening of numbered sealed envelopes in the remaining seven centres.\n[4] During phase one, women who were HPV-positive and aged 35-60 years were referred to colposcopy, whereas women aged 25-34 years were referred to colposcopy only if cytology was also abnormal or HPV testing was persistently positive.\n[5] During phase two, women in the HPV group were referred for colposcopy if the HPV test was positive.\n[6] Two rounds of screening occurred in each phase, and all women had cytology testing only at the second round.\n[7] The primary endpoint was the detection of grade 2 and 3 CIN, and of invasive cervical cancers during the first and second screening rounds.\n[8] Analysis was done by intention to screen.\n[9] This trial is registered, number ISRCTN81678807.\n[10] FINDINGS In total for both phases, 47,001 women were randomly assigned to the cytology group and 47,369 to HPV testing.\n[11] 33,851 women from the cytology group and 32,998 from the HPV-testing group had a second round of screening.\n[12] We also retrieved the histological diagnoses from screening done elsewhere.\n[13] The detection of invasive cervical cancers was similar for the two groups in the first round of screening (nine in the cytology group vs seven in the HPV group, p=0.62); no cases were detected in the HPV group during round two, compared with nine in the cytology group (p=0.004).\n[14] Overall, in the two rounds of screening, 18 invasive cancers were detected in the cytology group versus seven in the HPV group (p=0.028).\n[15] Among women aged 35-60 years, at round one the relative detection (HPV vs cytology) was 2.00 (95% CI 1.44-2.77) for CIN2, 2.08 (1.47-2.95) for CIN3, and 2.03 (1.60-2.57) for CIN2 and 3 together.\n[16] At round two the relative detection was 0.54 (0.23-1.28) for CIN2, 0.48 (0.21-1.11) for CIN3, and 0.51 (0.28-0.93) for CIN2 and 3 together.\n[17] Among women aged 25-34 years, there was significant heterogeneity between phases in the relative detection of CIN3.\n[18] At round one the relative detection was 0.93 (0.52-1.64) in phase one and 3.91 (2.02-7.57) in phase two.\n[19] At round two the relative detection was 1.34 (0.46-3.84) in phase one and 0.20 (0.04-0.93) in phase two.\n[20] Pooling both phases, the detection ratio of CIN2 for women aged 25-34 years was 4.09 (2.24-7.48) at round one and 0.64 (0.23-1.27) at round two.\n[21] INTERPRETATION HPV-based screening is more effective than cytology in preventing invasive cervical cancer, by detecting persistent high-grade lesions earlier and providing a longer low-risk period.\n[22] However, in younger women, HPV screening leads to over-diagnosis of regressive CIN2.\n[23] FUNDING European Union, Italian Ministry of Health, Regional Health Administrations of Piemonte, Tuscany, Veneto and Emilia-Romagna, and Public Health Agency of Lazio."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"BACKGROUND Human papillomavirus (HPV) testing is known to be more sensitive, but less specific than cytology for detecting cervical intraepithelial neoplasia (CIN).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 973, "doc_id": 27873158, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [27446873, 27873158, 28617573, 9764256], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Primary cervical cytology screening with HPV detection has higher longitudinal sensitivity to detect severe cervical intraepithelial neoplasia than conventional cytology.\n\nDocument title: Efficacy of human papillomavirus testing for the detection of invasive cervical cancers and cervical intraepithelial neoplasia: a randomised controlled trial.\n\nAbstract sentences:\n[0] BACKGROUND Human papillomavirus (HPV) testing is known to be more sensitive, but less specific than cytology for detecting cervical intraepithelial neoplasia (CIN).\n[1] We assessed the efficacy of cervical-cancer screening policies that are based on HPV testing.\n[2] METHODS Between March, 2004, and December, 2004, in two separate recruitment phases, women aged 25-60 years were randomly assigned to conventional cytology or to HPV testing in combination with liquid-based cytology (first phase) or alone (second phase).\n[3] Randomisation was done by computer in two screening centres and by sequential opening of numbered sealed envelopes in the remaining seven centres.\n[4] During phase one, women who were HPV-positive and aged 35-60 years were referred to colposcopy, whereas women aged 25-34 years were referred to colposcopy only if cytology was also abnormal or HPV testing was persistently positive.\n[5] During phase two, women in the HPV group were referred for colposcopy if the HPV test was positive.\n[6] Two rounds of screening occurred in each phase, and all women had cytology testing only at the second round.\n[7] The primary endpoint was the detection of grade 2 and 3 CIN, and of invasive cervical cancers during the first and second screening rounds.\n[8] Analysis was done by intention to screen.\n[9] This trial is registered, number ISRCTN81678807.\n[10] FINDINGS In total for both phases, 47,001 women were randomly assigned to the cytology group and 47,369 to HPV testing.\n[11] 33,851 women from the cytology group and 32,998 from the HPV-testing group had a second round of screening.\n[12] We also retrieved the histological diagnoses from screening done elsewhere.\n[13] The detection of invasive cervical cancers was similar for the two groups in the first round of screening (nine in the cytology group vs seven in the HPV group, p=0.62); no cases were detected in the HPV group during round two, compared with nine in the cytology group (p=0.004).\n[14] Overall, in the two rounds of screening, 18 invasive cancers were detected in the cytology group versus seven in the HPV group (p=0.028).\n[15] Among women aged 35-60 years, at round one the relative detection (HPV vs cytology) was 2.00 (95% CI 1.44-2.77) for CIN2, 2.08 (1.47-2.95) for CIN3, and 2.03 (1.60-2.57) for CIN2 and 3 together.\n[16] At round two the relative detection was 0.54 (0.23-1.28) for CIN2, 0.48 (0.21-1.11) for CIN3, and 0.51 (0.28-0.93) for CIN2 and 3 together.\n[17] Among women aged 25-34 years, there was significant heterogeneity between phases in the relative detection of CIN3.\n[18] At round one the relative detection was 0.93 (0.52-1.64) in phase one and 3.91 (2.02-7.57) in phase two.\n[19] At round two the relative detection was 1.34 (0.46-3.84) in phase one and 0.20 (0.04-0.93) in phase two.\n[20] Pooling both phases, the detection ratio of CIN2 for women aged 25-34 years was 4.09 (2.24-7.48) at round one and 0.64 (0.23-1.27) at round two.\n[21] INTERPRETATION HPV-based screening is more effective than cytology in preventing invasive cervical cancer, by detecting persistent high-grade lesions earlier and providing a longer low-risk period.\n[22] However, in younger women, HPV screening leads to over-diagnosis of regressive CIN2.\n[23] FUNDING European Union, Italian Ministry of Health, Regional Health Administrations of Piemonte, Tuscany, Veneto and Emilia-Romagna, and Public Health Agency of Lazio."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [21]\nExplanation: Evidence states: \"INTERPRETATION HPV-based screening is more effective than cytology in preventing invasive cervical cancer, by detecting persistent high-grade lesions earlier and providing a longer low-risk period.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 973, "doc_id": 27873158, "label": "SUPPORTS", "evidence_sentence_ids": [21], "cited_doc_ids": [27446873, 27873158, 28617573, 9764256], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Primary cervical cytology screening with HPV detection has higher longitudinal sensitivity to detect severe cervical intraepithelial neoplasia than conventional cytology.\n\nDocument title: Evidence regarding human papillomavirus testing in secondary prevention of cervical cancer.\n\nAbstract sentences:\n[0] More than ever, clinicians need regularly updated reviews given the continuously increasing amount of new information regarding innovative cervical cancer prevention methods.\n[1] A summary is given from recent meta-analyses and systematic reviews on 3 possible clinical applications of human papillomavirus (HPV) testing: triage of women with equivocal or low-grade cytologic abnormalities; prediction of the therapeutic outcome after treatment of cervical intraepithelial neoplasia (CIN) lesions, and last not but not least, primary screening for cervical cancer and pre-cancer.\n[2] Consistent evidence is available indicating that HPV-triage with the Hybrid Capture(®) 2 assay (Qiagen Gaithersburg, Inc., MD, USA [previously Digene Corp.] (HC2) is more accurate (higher sensitivity, similar specificity) than repeat cytology to triage women with equivocal Pap smear results.\n[3] Several other tests show at least similar accuracy but mRNA testing with the APTIMA(®) (Gen-Probe Inc., San Diego, CA, USA) test is similarly sensitive but more specific compared to HC2.\n[4] In triage of low-grade squamous intraepithelial lesions (LSIL), HC2 is more sensitive but its specificity is substantially lower compared to repeat cytology.\n[5] The APTIMA(®) test is more specific than HC2 without showing a loss in sensitivity.\n[6] Identification of DNA of HPV types 16 and/or 18, or RNA from the five most carcinogenic HPV types allow selecting women at highest risk for CIN3+ but the sensitivity and negative predictive value of these markers are lower than full-range high-risk HPV (hrHPV) testing.\n[7] After conservative treatment of cervical pre-cancer, HPV testing picks up more quickly, with higher sensitivity and not lower specificity, residual or recurrent high-grade CIN than follow-up cytology.\n[8] Primary screening for hrHPV generally detects more CIN2, CIN3 or cancer compared to cytology at cut-off atypical squamous cells of undetermined significance (ASC-US) or LSIL, but is less specific.\n[9] Combined HPV and cytology screening provides a further small gain in sensitivity at the expense of a considerable loss in specificity if positive by either test is referred to colposcopy, in comparison with HPV testing only.\n[10] Randomised trials and follow-up of cohort studies consistently demonstrate a significantly lower cumulative incidence of CIN3+ and even of cancer, in women aged 30 years or older, who were at enrollment hrHPV DNA negative compared to those who were cytologically negative.\n[11] The difference in cumulative risk of CIN3+ or cancer for double negative (cytology & HPV) versus only HPV-negative women is small.\n[12] HC2, GP5+/6+ PCR (polymerase chain reaction), cobas(®) 4800 PCR (Roche Molecular Systems Inc., Alameda, CA, USA) and Real Time PCR (Abbott Molecular, Des Plaines, IL, USA) can be considered as clinically validated for use in primary screening.\n[13] The loss in specificity associated with primary HPV-based screening can be compensated by appropriate algorithms involving reflex cytology and/or HPV genotyping for HPV16 or 18.\n[14] There exists a substantial evidence base to support that HPV testing is advantageous both in triage of women with equivocal abnormal cytology, in surveillance after treatment of CIN lesions and in primary screening of women aged 30 years or older.\n[15] However, the possible advantages offered by HPV-based screening require a well organised program with good compliance with screening and triage policies.\n[16] This article forms part of a special supplement entitled \"Comprehensive Control of HPV Infections and Related Diseases\" Vaccine Volume 30, Supplement 5, 2012."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"After conservative treatment of cervical pre-cancer, HPV testing picks up more quickly, with higher sensitivity and not lower specificity, residual or recurrent high-grade CIN than follow-up cytology.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 973, "doc_id": 28617573, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [27446873, 27873158, 28617573, 9764256], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Primary cervical cytology screening with HPV detection has higher longitudinal sensitivity to detect severe cervical intraepithelial neoplasia than conventional cytology.\n\nDocument title: Evidence regarding human papillomavirus testing in secondary prevention of cervical cancer.\n\nAbstract sentences:\n[0] More than ever, clinicians need regularly updated reviews given the continuously increasing amount of new information regarding innovative cervical cancer prevention methods.\n[1] A summary is given from recent meta-analyses and systematic reviews on 3 possible clinical applications of human papillomavirus (HPV) testing: triage of women with equivocal or low-grade cytologic abnormalities; prediction of the therapeutic outcome after treatment of cervical intraepithelial neoplasia (CIN) lesions, and last not but not least, primary screening for cervical cancer and pre-cancer.\n[2] Consistent evidence is available indicating that HPV-triage with the Hybrid Capture(®) 2 assay (Qiagen Gaithersburg, Inc., MD, USA [previously Digene Corp.] (HC2) is more accurate (higher sensitivity, similar specificity) than repeat cytology to triage women with equivocal Pap smear results.\n[3] Several other tests show at least similar accuracy but mRNA testing with the APTIMA(®) (Gen-Probe Inc., San Diego, CA, USA) test is similarly sensitive but more specific compared to HC2.\n[4] In triage of low-grade squamous intraepithelial lesions (LSIL), HC2 is more sensitive but its specificity is substantially lower compared to repeat cytology.\n[5] The APTIMA(®) test is more specific than HC2 without showing a loss in sensitivity.\n[6] Identification of DNA of HPV types 16 and/or 18, or RNA from the five most carcinogenic HPV types allow selecting women at highest risk for CIN3+ but the sensitivity and negative predictive value of these markers are lower than full-range high-risk HPV (hrHPV) testing.\n[7] After conservative treatment of cervical pre-cancer, HPV testing picks up more quickly, with higher sensitivity and not lower specificity, residual or recurrent high-grade CIN than follow-up cytology.\n[8] Primary screening for hrHPV generally detects more CIN2, CIN3 or cancer compared to cytology at cut-off atypical squamous cells of undetermined significance (ASC-US) or LSIL, but is less specific.\n[9] Combined HPV and cytology screening provides a further small gain in sensitivity at the expense of a considerable loss in specificity if positive by either test is referred to colposcopy, in comparison with HPV testing only.\n[10] Randomised trials and follow-up of cohort studies consistently demonstrate a significantly lower cumulative incidence of CIN3+ and even of cancer, in women aged 30 years or older, who were at enrollment hrHPV DNA negative compared to those who were cytologically negative.\n[11] The difference in cumulative risk of CIN3+ or cancer for double negative (cytology & HPV) versus only HPV-negative women is small.\n[12] HC2, GP5+/6+ PCR (polymerase chain reaction), cobas(®) 4800 PCR (Roche Molecular Systems Inc., Alameda, CA, USA) and Real Time PCR (Abbott Molecular, Des Plaines, IL, USA) can be considered as clinically validated for use in primary screening.\n[13] The loss in specificity associated with primary HPV-based screening can be compensated by appropriate algorithms involving reflex cytology and/or HPV genotyping for HPV16 or 18.\n[14] There exists a substantial evidence base to support that HPV testing is advantageous both in triage of women with equivocal abnormal cytology, in surveillance after treatment of CIN lesions and in primary screening of women aged 30 years or older.\n[15] However, the possible advantages offered by HPV-based screening require a well organised program with good compliance with screening and triage policies.\n[16] This article forms part of a special supplement entitled \"Comprehensive Control of HPV Infections and Related Diseases\" Vaccine Volume 30, Supplement 5, 2012."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Primary screening for hrHPV generally detects more CIN2, CIN3 or cancer compared to cytology at cut-off atypical squamous cells of undetermined significance (ASC-US) or LSIL, but is less specific.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 973, "doc_id": 28617573, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [27446873, 27873158, 28617573, 9764256], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Primary cervical cytology screening with HPV detection has higher longitudinal sensitivity to detect severe cervical intraepithelial neoplasia than conventional cytology.\n\nDocument title: Human papillomavirus testing for the detection of high-grade cervical intraepithelial neoplasia and cancer: final results of the POBASCAM randomised controlled trial.\n\nAbstract sentences:\n[0] BACKGROUND Human papillomavirus (HPV) testing is more sensitive for the detection of high-grade cervical lesions than is cytology, but detection of HPV by DNA screening in two screening rounds 5 years apart has not been assessed.\n[1] The aim of this study was to assess whether HPV DNA testing in the first screen decreases detection of cervical intraepithelial neoplasia (CIN) grade 3 or worse, CIN grade 2 or worse, and cervical cancer in the second screening.\n[2] METHODS In this randomised trial, women aged 29-56 years participating in the cervical screening programme in the Netherlands were randomly assigned to receive HPV DNA (GP5+/6+-PCR method) and cytology co-testing or cytology testing alone, from January, 1999, to September, 2002.\n[3] Randomisation (in a 1:1 ratio) was done with computer-generated random numbers after the cervical specimen had been taken.\n[4] At the second screening 5 years later, HPV DNA and cytology co-testing was done in both groups; researchers were masked to the patient's assignment.\n[5] The primary endpoint was the number of CIN grade 3 or worse detected.\n[6] Analysis was done by intention to screen.\n[7] The trial is now finished and is registered, number ISRCTN20781131.\n[8] FINDINGS 22,420 women were randomly assigned to the intervention group and 22 518 to the control group; 19 999 in the intervention group and 20,106 in the control group were eligible for analysis at the first screen.\n[9] At the second screen, 19 579 women in the intervention group and 19,731 in the control group were eligible, of whom 16,750 and 16,743, respectively, attended the second screen.\n[10] In the second round, CIN grade 3 or worse was less common in the intervention group than in the control group (88 of 19 579 in the intervention group vs 122 of 19,731 in the control group; relative risk 0·73, 95% CI 0·55-0·96; p=0·023).\n[11] Cervical cancer was also less common in the intervention group than in the control group (four of 19 579 in the intervention group vs 14 of 19,731; 0·29, 0·10-0·87; p=0·031).\n[12] In the baseline round, detection of CIN grade 3 or worse did not differ significantly between groups (171 of 19 999 vs 150 of 20,106; 1·15, 0·92-1·43; p=0·239) but was significantly more common in women with normal cytology (34 of 19,286 vs 12 of 19,373; 2·85, 1·47-5·49; p=0·001).\n[13] Furthermore, significantly more cases of CIN grade 2 or worse were detected in the intervention group than in the control group (267 of 19 999 vs 215 of 20,106; 1·25, 1·05-1·50; p=0·015).\n[14] In the second screen, fewer HPV16-positive CIN grade 3 or worse were detected in the intervention group than in the control group (17 of 9481 vs 35 of 9354; 0·48, 0·27-0·85; p=0·012); detection of non-HPV16-positive CIN grade 3 or worse did not differ between groups (25 of 9481 vs 25 of 9354; 0·99, 0·57-1·72; p=1·00).\n[15] The cumulative detection of CIN grade 3 or worse and CIN grade 2 or worse did not differ significantly between study arms, neither for the whole study group (CIN grade 3 or worse: 259 of 19 999 vs 272 of 20,106; 0·96, 0·81-1·14, p=0·631; CIN grade 2 or worse: 427 of 19 999 vs 399 of 20,106; 1·08, 0·94-1·24; p=0·292), nor for subgroups of women invited for the first time (CIN grade 3 or worse in women aged 29-33 years: 102 of 3139 vs 105 of 3128; 0·97, 0·74-1·27; CIN grade 2 or worse in women aged 29-33 years: 153 of 3139 vs 151 of 3128; 1·01, 0·81-1·26; CIN grade 3 or worse in women aged 34-56 years: 157 of 16,860 vs 167 of 16 978; 0·95, 0·76-1·18; CIN grade 2 or worse in women aged 34-56 years: 274 of 16,860 vs 248 of 16 978; 1·11, 0·94-1·32).\n[16] INTERPRETATION Implementation of HPV DNA testing in cervical screening leads to earlier detection of clinically relevant CIN grade 2 or worse, which when adequately treated, improves protection against CIN grade 3 or worse and cervical cancer.\n[17] Early detection of high-grade cervical legions caused by HPV16 was a major component of this benefit.\n[18] Our results lend support to the use of HPV DNA testing for all women aged 29 years and older.\n[19] FUNDING Zorg Onderzoek Nederland (Netherlands Organisation for Health Research and Development)."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"Furthermore, significantly more cases of CIN grade 2 or worse were detected in the intervention group than in the control group (267 of 19 999 vs 215 of 20,106; 1·25, 1·05-1·50; p=0·015).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 973, "doc_id": 9764256, "label": "SUPPORTS", "evidence_sentence_ids": [13], "cited_doc_ids": [27446873, 27873158, 28617573, 9764256], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Primary cervical cytology screening with HPV detection has higher longitudinal sensitivity to detect severe cervical intraepithelial neoplasia than conventional cytology.\n\nDocument title: Human papillomavirus testing for the detection of high-grade cervical intraepithelial neoplasia and cancer: final results of the POBASCAM randomised controlled trial.\n\nAbstract sentences:\n[0] BACKGROUND Human papillomavirus (HPV) testing is more sensitive for the detection of high-grade cervical lesions than is cytology, but detection of HPV by DNA screening in two screening rounds 5 years apart has not been assessed.\n[1] The aim of this study was to assess whether HPV DNA testing in the first screen decreases detection of cervical intraepithelial neoplasia (CIN) grade 3 or worse, CIN grade 2 or worse, and cervical cancer in the second screening.\n[2] METHODS In this randomised trial, women aged 29-56 years participating in the cervical screening programme in the Netherlands were randomly assigned to receive HPV DNA (GP5+/6+-PCR method) and cytology co-testing or cytology testing alone, from January, 1999, to September, 2002.\n[3] Randomisation (in a 1:1 ratio) was done with computer-generated random numbers after the cervical specimen had been taken.\n[4] At the second screening 5 years later, HPV DNA and cytology co-testing was done in both groups; researchers were masked to the patient's assignment.\n[5] The primary endpoint was the number of CIN grade 3 or worse detected.\n[6] Analysis was done by intention to screen.\n[7] The trial is now finished and is registered, number ISRCTN20781131.\n[8] FINDINGS 22,420 women were randomly assigned to the intervention group and 22 518 to the control group; 19 999 in the intervention group and 20,106 in the control group were eligible for analysis at the first screen.\n[9] At the second screen, 19 579 women in the intervention group and 19,731 in the control group were eligible, of whom 16,750 and 16,743, respectively, attended the second screen.\n[10] In the second round, CIN grade 3 or worse was less common in the intervention group than in the control group (88 of 19 579 in the intervention group vs 122 of 19,731 in the control group; relative risk 0·73, 95% CI 0·55-0·96; p=0·023).\n[11] Cervical cancer was also less common in the intervention group than in the control group (four of 19 579 in the intervention group vs 14 of 19,731; 0·29, 0·10-0·87; p=0·031).\n[12] In the baseline round, detection of CIN grade 3 or worse did not differ significantly between groups (171 of 19 999 vs 150 of 20,106; 1·15, 0·92-1·43; p=0·239) but was significantly more common in women with normal cytology (34 of 19,286 vs 12 of 19,373; 2·85, 1·47-5·49; p=0·001).\n[13] Furthermore, significantly more cases of CIN grade 2 or worse were detected in the intervention group than in the control group (267 of 19 999 vs 215 of 20,106; 1·25, 1·05-1·50; p=0·015).\n[14] In the second screen, fewer HPV16-positive CIN grade 3 or worse were detected in the intervention group than in the control group (17 of 9481 vs 35 of 9354; 0·48, 0·27-0·85; p=0·012); detection of non-HPV16-positive CIN grade 3 or worse did not differ between groups (25 of 9481 vs 25 of 9354; 0·99, 0·57-1·72; p=1·00).\n[15] The cumulative detection of CIN grade 3 or worse and CIN grade 2 or worse did not differ significantly between study arms, neither for the whole study group (CIN grade 3 or worse: 259 of 19 999 vs 272 of 20,106; 0·96, 0·81-1·14, p=0·631; CIN grade 2 or worse: 427 of 19 999 vs 399 of 20,106; 1·08, 0·94-1·24; p=0·292), nor for subgroups of women invited for the first time (CIN grade 3 or worse in women aged 29-33 years: 102 of 3139 vs 105 of 3128; 0·97, 0·74-1·27; CIN grade 2 or worse in women aged 29-33 years: 153 of 3139 vs 151 of 3128; 1·01, 0·81-1·26; CIN grade 3 or worse in women aged 34-56 years: 157 of 16,860 vs 167 of 16 978; 0·95, 0·76-1·18; CIN grade 2 or worse in women aged 34-56 years: 274 of 16,860 vs 248 of 16 978; 1·11, 0·94-1·32).\n[16] INTERPRETATION Implementation of HPV DNA testing in cervical screening leads to earlier detection of clinically relevant CIN grade 2 or worse, which when adequately treated, improves protection against CIN grade 3 or worse and cervical cancer.\n[17] Early detection of high-grade cervical legions caused by HPV16 was a major component of this benefit.\n[18] Our results lend support to the use of HPV DNA testing for all women aged 29 years and older.\n[19] FUNDING Zorg Onderzoek Nederland (Netherlands Organisation for Health Research and Development)."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [16]\nExplanation: Evidence states: \"INTERPRETATION Implementation of HPV DNA testing in cervical screening leads to earlier detection of clinically relevant CIN grade 2 or worse, which when adequately treated, improves protection against CIN grade 3 or worse and cervical cancer.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 973, "doc_id": 9764256, "label": "SUPPORTS", "evidence_sentence_ids": [16], "cited_doc_ids": [27446873, 27873158, 28617573, 9764256], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Primary pro-inflammatory cytokines suppress secondary pro- and anti-inflammatory mediators.\n\nDocument title: Inter-individual variability and genetic influences on cytokine responses to bacteria and fungi\n\nAbstract sentences:\n[0] Little is known about the inter-individual variation of cytokine responses to different pathogens in healthy individuals.\n[1] To systematically describe cytokine responses elicited by distinct pathogens and to determine the effect of genetic variation on cytokine production, we profiled cytokines produced by peripheral blood mononuclear cells from 197 individuals of European origin from the 200 Functional Genomics (200FG) cohort in the Human Functional Genomics Project (http://www.humanfunctionalgenomics.org), obtained over three different years.\n[2] We compared bacteria- and fungi-induced cytokine profiles and found that most cytokine responses were organized around a physiological response to specific pathogens, rather than around a particular immune pathway or cytokine.\n[3] We then correlated genome-wide single-nucleotide polymorphism (SNP) genotypes with cytokine abundance and identified six cytokine quantitative trait loci (QTLs).\n[4] Among them, a cytokine QTL at the NAA35-GOLM1 locus markedly modulated interleukin (IL)-6 production in response to multiple pathogens and was associated with susceptibility to candidemia.\n[5] Furthermore, the cytokine QTLs that we identified were enriched among SNPs previously associated with infectious diseases and heart diseases.\n[6] These data reveal and begin to explain the variability in cytokine production by human immune cells in response to pathogens."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 976, "doc_id": 5304891, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [5304891], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pro-inflammatory cytokines are up regulated during tumor development.\n\nDocument title: Impact of TNF-alpha and IL-6 levels on development of cachexia in newly diagnosed NSCLC patients.\n\nAbstract sentences:\n[0] OBJECTIVES We investigated the role of cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) in cachexia development in newly diagnosed nonsmall cell lung cancer (NSCLC) patients.\n[1] METHODS : We evaluated 44 (M/F:41/3) NSCLC patients and 12 (M/F:10/2) age matched healthy smokers.\n[2] NSCLC cases with a weight loss of > or =10% consisted the cachectic group (n:23, M/F:21/2) and the ones with <10% weight loss consisted the noncachectic group (n:21, M/F:19/2).\n[3] RESULTS Body mass index (BMI) of cachectics was significantly lower than that of noncachectics (21.0 +/- 2.9 versus 24.5 +/-\n[4] 3.6, P = 0.02) and controls (21.0 +/- 2.9 versus 25.5 +/- 2.6, P = 0.01).\n[5] Serum TNF-alpha level did not differ between cachectic and noncachectics (37.3 +/-\n[6] 39.1 and 51.6 +/-\n[7] 84.2 pg/mL, respectively).\n[8] However, it was significantly higher in NSCLC patients compared with controls (44.1 +/- 64.3 and 15.1 +/-\n[9] 14.3 pg/mL, P = 0.03).\n[10] Serum IL-6 level was not different between 3 groups (6.4 +/- 4.1, 8.9 +/-\n[11] 16.3, and 4.1 +/-\n[12] 3.5 pg/mL, respectively)\n[13] but it correlated significantly with TNF-alpha (r = 0.4, P = 0.006) and BMI (r = -0.3, P = 0.03).\n[14] Erythrocyte sedimentation rate (ESR) correlated significantly with TNF-alpha (r = 0.4, P = 0.003) and BMI (r = -0.3, P = 0.03).\n[15] Among 44 cases, survival of 12 and 17 patients was recorded in cachectics and noncachectics, with no statistical difference (12.2 +/- 3.7 and 11.2 +/-\n[16] 1.0 months, respectively).\n[17] CONCLUSIONS TNF-alpha and IL-6 levels did not differ significantly between cachectics and noncachectics.\n[18] However, significant correlations between IL-6, BMI, and TNF-alpha suggested that these cytokines acted as cofactors in weight loss.\n[19] Survival was neither influenced by BMI, nor the cytokine levels in the present study.\n[20] The significant correlation of ESR with TNF-alpha suggested that ESR could provide valuable clue for considerable weight loss in the follow-up of NSCLC patients."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8, 9]\nExplanation: Evidence states: \"However, it was significantly higher in NSCLC patients compared with controls (44.1 +/- 64.3 and 15.1 +/- 14.3 pg/mL, P = 0.03).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 977, "doc_id": 39264456, "label": "SUPPORTS", "evidence_sentence_ids": [8, 9], "cited_doc_ids": [14075252, 39264456], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pro-inflammatory cytokines are up repressed during tumor development.\n\nDocument title: Paraneoplastic thrombocytosis: the secrets of tumor self-promotion.\n\nAbstract sentences:\n[0] Paraneoplastic thrombocytosis is associated with many solid tumors and often correlates with reduced survival.\n[1] Recent studies suggest that a pathogenic feed back loop may be operative between platelets and tumor cells, with reciprocal interactions between tumor growth/metastasis and thrombocytosis/platelet activation.\n[2] Specific molecular pathways have been identified in which tumors can stimulate platelet production and activation; activated platelets can, in turn, promote tumor growth and metastasis.\n[3] Taken together, these findings provide exciting new potential targets for therapeutic intervention."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 978, "doc_id": 14075252, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14075252], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Progerin induces premature aging in stem cells.\n\nDocument title: Human iPSC-based modeling of late-onset disease via progerin-induced aging.\n\nAbstract sentences:\n[0] Reprogramming somatic cells to induced pluripotent stem cells (iPSCs) resets their identity back to an embryonic age and, thus, presents a significant hurdle for modeling late-onset disorders.\n[1] In this study, we describe a strategy for inducing aging-related features in human iPSC-derived lineages and apply it to the modeling of Parkinson's disease (PD).\n[2] Our approach involves expression of progerin, a truncated form of lamin A associated with premature aging.\n[3] We found that expression of progerin in iPSC-derived fibroblasts and neurons induces multiple aging-related markers and characteristics, including dopamine-specific phenotypes such as neuromelanin accumulation.\n[4] Induced aging in PD iPSC-derived dopamine neurons revealed disease phenotypes that require both aging and genetic susceptibility, such as pronounced dendrite degeneration, progressive loss of tyrosine hydroxylase (TH) expression, and enlarged mitochondria or Lewy-body-precursor inclusions.\n[5] Thus, our study suggests that progerin-induced aging can be used to reveal late-onset age-related disease features in hiPSC-based disease models."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"We found that expression of progerin in iPSC-derived fibroblasts and neurons induces multiple aging-related markers and characteristics, including dopamine-specific phenotypes such as neuromelanin accumulation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 979, "doc_id": 11659421, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [11659421], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Progerin induces premature aging in stem cells.\n\nDocument title: Human iPSC-based modeling of late-onset disease via progerin-induced aging.\n\nAbstract sentences:\n[0] Reprogramming somatic cells to induced pluripotent stem cells (iPSCs) resets their identity back to an embryonic age and, thus, presents a significant hurdle for modeling late-onset disorders.\n[1] In this study, we describe a strategy for inducing aging-related features in human iPSC-derived lineages and apply it to the modeling of Parkinson's disease (PD).\n[2] Our approach involves expression of progerin, a truncated form of lamin A associated with premature aging.\n[3] We found that expression of progerin in iPSC-derived fibroblasts and neurons induces multiple aging-related markers and characteristics, including dopamine-specific phenotypes such as neuromelanin accumulation.\n[4] Induced aging in PD iPSC-derived dopamine neurons revealed disease phenotypes that require both aging and genetic susceptibility, such as pronounced dendrite degeneration, progressive loss of tyrosine hydroxylase (TH) expression, and enlarged mitochondria or Lewy-body-precursor inclusions.\n[5] Thus, our study suggests that progerin-induced aging can be used to reveal late-onset age-related disease features in hiPSC-based disease models."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Thus, our study suggests that progerin-induced aging can be used to reveal late-onset age-related disease features in hiPSC-based disease models.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 979, "doc_id": 11659421, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [11659421], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Propriospinal interneurons that play a role in the plastic reorganization of spinal circuits are integral for recovery from spinal cord injury.\n\nDocument title: Recovery of supraspinal control of stepping via indirect propriospinal relay connections after spinal cord injury\n\nAbstract sentences:\n[0] Spinal cord injuries (SCIs) in humans and experimental animals are often associated with varying degrees of spontaneous functional recovery during the first months after injury.\n[1] Such recovery is widely attributed to axons spared from injury that descend from the brain and bypass incomplete lesions, but its mechanisms are uncertain.\n[2] To investigate the neural basis of spontaneous recovery, we used kinematic, physiological and anatomical analyses to evaluate mice with various combinations of spatially and temporally separated lateral hemisections with or without the excitotoxic ablation of intrinsic spinal cord neurons.\n[3] We show that propriospinal relay connections that bypass one or more injury sites are able to mediate spontaneous functional recovery and supraspinal control of stepping, even when there has been essentially total and irreversible interruption of long descending supraspinal pathways in mice.\n[4] Our findings show that pronounced functional recovery can occur after severe SCI without the maintenance or regeneration of direct projections from the brain past the lesion and can be mediated by the reorganization of descending and propriospinal connections.\n[5] Targeting interventions toward augmenting the remodeling of relay connections may provide new therapeutic strategies to bypass lesions and restore function after SCI and in other conditions such as stroke and multiple sclerosis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"We show that propriospinal relay connections that bypass one or more injury sites are able to mediate spontaneous functional recovery and supraspinal control of stepping, even when there has been essentially total and irreversible interruption of long descending supraspinal pathways in mice.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 980, "doc_id": 20128547, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [20128547], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Propriospinal interneurons that play a role in the plastic reorganization of spinal circuits are integral for recovery from spinal cord injury.\n\nDocument title: Recovery of supraspinal control of stepping via indirect propriospinal relay connections after spinal cord injury\n\nAbstract sentences:\n[0] Spinal cord injuries (SCIs) in humans and experimental animals are often associated with varying degrees of spontaneous functional recovery during the first months after injury.\n[1] Such recovery is widely attributed to axons spared from injury that descend from the brain and bypass incomplete lesions, but its mechanisms are uncertain.\n[2] To investigate the neural basis of spontaneous recovery, we used kinematic, physiological and anatomical analyses to evaluate mice with various combinations of spatially and temporally separated lateral hemisections with or without the excitotoxic ablation of intrinsic spinal cord neurons.\n[3] We show that propriospinal relay connections that bypass one or more injury sites are able to mediate spontaneous functional recovery and supraspinal control of stepping, even when there has been essentially total and irreversible interruption of long descending supraspinal pathways in mice.\n[4] Our findings show that pronounced functional recovery can occur after severe SCI without the maintenance or regeneration of direct projections from the brain past the lesion and can be mediated by the reorganization of descending and propriospinal connections.\n[5] Targeting interventions toward augmenting the remodeling of relay connections may provide new therapeutic strategies to bypass lesions and restore function after SCI and in other conditions such as stroke and multiple sclerosis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Our findings show that pronounced functional recovery can occur after severe SCI without the maintenance or regeneration of direct projections from the brain past the lesion and can be mediated by the reorganization of descending and propriospinal connections.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 980, "doc_id": 20128547, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [20128547], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pseudogene PTENP1 encodes a transcript that regulates PTEN expression.\n\nDocument title: A coding-independent function of gene and pseudogene mRNAs regulates tumour biology\n\nAbstract sentences:\n[0] The canonical role of messenger RNA (mRNA) is to deliver protein-coding information to sites of protein synthesis.\n[1] However, given that microRNAs bind to RNAs, we hypothesized that RNAs could possess a regulatory role that relies on their ability to compete for microRNA binding, independently of their protein-coding function.\n[2] As a model for the protein-coding-independent role of RNAs, we describe the functional relationship between the mRNAs produced by the PTEN tumour suppressor gene and its pseudogene PTENP1 and the critical consequences of this interaction.\n[3] We find that PTENP1 is biologically active as it can regulate cellular levels of PTEN and exert a growth-suppressive role.\n[4] We also show that the PTENP1 locus is selectively lost in human cancer.\n[5] We extended our analysis to other cancer-related genes that possess pseudogenes, such as oncogenic KRAS.\n[6] We also demonstrate that the transcripts of protein-coding genes such as PTEN are biologically active.\n[7] These findings attribute a novel biological role to expressed pseudogenes, as they can regulate coding gene expression, and reveal a non-coding function for mRNAs."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"We find that PTENP1 is biologically active as it can regulate cellular levels of PTEN and exert a growth-suppressive role.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 984, "doc_id": 6828370, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [6828370], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pseudoknots are not evolutionarily conserved in most eukaryotes.\n\nDocument title: Identification and analysis of ribonuclease P and MRP RNA in a broad range of eukaryotes\n\nAbstract sentences:\n[0] RNases P and MRP are ribonucleoprotein complexes involved in tRNA and rRNA processing, respectively.\n[1] The RNA subunits of these two enzymes are structurally related to each other and play an essential role in the enzymatic reaction.\n[2] Both of the RNAs have a highly conserved helical region, P4, which is important in the catalytic reaction.\n[3] We have used a bioinformatics approach based on conserved elements to computationally analyze available genomic sequences of eukaryotic organisms and have identified a large number of novel nuclear RNase P and MRP RNA genes.\n[4] For MRP RNA for instance, this investigation increases the number of known sequences by a factor of three.\n[5] We present secondary structure models of many of the predicted RNAs.\n[6] Although all sequences are able to fold into the consensus secondary structure of P and MRP RNAs, a striking variation in size is observed, ranging from a Nosema locustae MRP RNA of 160 nt to much larger RNAs, e.g. a Plasmodium knowlesi P RNA of 696 nt.\n[7] The P and MRP RNA genes appear in tandem in some protists, further emphasizing the close evolutionary relationship of these RNAs."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 988, "doc_id": 3033830, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [3033830], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pure neural progenitor cell (NPC) populations can only be obtained from cell cultures that undergo passaging, filtration, or other isolation and cell sorting methods.\n\nDocument title: Niche-Independent Symmetrical Self-Renewal of a Mammalian Tissue Stem Cell\n\nAbstract sentences:\n[0] Pluripotent mouse embryonic stem (ES) cells multiply in simple monoculture by symmetrical divisions.\n[1] In vivo, however, stem cells are generally thought to depend on specialised cellular microenvironments and to undergo predominantly asymmetric divisions.\n[2] Ex vivo expansion of pure populations of tissue stem cells has proven elusive.\n[3] Neural progenitor cells are propagated in combination with differentiating progeny in floating clusters called neurospheres.\n[4] The proportion of stem cells in neurospheres is low, however, and they cannot be directly observed or interrogated.\n[5] Here we demonstrate that the complex neurosphere environment is dispensable for stem cell maintenance, and that the combination of fibroblast growth factor 2 (FGF-2) and epidermal growth factor (EGF) is sufficient for derivation and continuous expansion by symmetrical division of pure cultures of neural stem (NS) cells.\n[6] NS cells were derived first from mouse ES cells.\n[7] Neural lineage induction was followed by growth factor addition in basal culture media.\n[8] In the presence of only EGF and FGF-2, resulting NS cells proliferate continuously, are diploid, and clonogenic.\n[9] After prolonged expansion, they remain able to differentiate efficiently into neurons and astrocytes in vitro and upon transplantation into the adult brain.\n[10] Colonies generated from single NS cells all produce neurons upon growth factor withdrawal.\n[11] NS cells uniformly express morphological, cell biological, and molecular features of radial glia, developmental precursors of neurons and glia.\n[12] Consistent with this profile, adherent NS cell lines can readily be established from foetal mouse brain.\n[13] Similar NS cells can be generated from human ES cells and human foetal brain.\n[14] The extrinsic factors EGF plus FGF-2 are sufficient to sustain pure symmetrical self-renewing divisions of NS cells.\n[15] The resultant cultures constitute the first known example of tissue-specific stem cells that can be propagated without accompanying differentiation.\n[16] These homogenous cultures will enable delineation of molecular mechanisms that define a tissue-specific stem cell and allow direct comparison with pluripotent ES cells."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 989, "doc_id": 9988425, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [9988425], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pyridostatin decreases telomere fragility in BRCA2-deficient cells.\n\nDocument title: Targeting BRCA1 and BRCA2 Deficiencies with G-Quadruplex-Interacting Compounds\n\nAbstract sentences:\n[0] G-quadruplex (G4)-forming genomic sequences, including telomeres, represent natural replication fork barriers.\n[1] Stalled replication forks can be stabilized and restarted by homologous recombination (HR), which also repairs DNA double-strand breaks (DSBs) arising at collapsed forks.\n[2] We have previously shown that HR facilitates telomere replication.\n[3] Here, we demonstrate that the replication efficiency of guanine-rich (G-rich) telomeric repeats is decreased significantly in cells lacking HR.\n[4] Treatment with the G4-stabilizing compound pyridostatin (PDS) increases telomere fragility in BRCA2-deficient cells, suggesting that G4 formation drives telomere instability.\n[5] Remarkably, PDS reduces proliferation of HR-defective cells by inducing DSB accumulation, checkpoint activation, and deregulated G2/M progression and by enhancing the replication defect intrinsic to HR deficiency.\n[6] PDS toxicity extends to HR-defective cells that have acquired olaparib resistance through loss of 53BP1 or REV7.\n[7] Altogether, these results highlight the therapeutic potential of G4-stabilizing drugs to selectively eliminate HR-compromised cells and tumors, including those resistant to PARP inhibition."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Treatment with the G4-stabilizing compound pyridostatin (PDS) increases telomere fragility in BRCA2-deficient cells, suggesting that G4 formation drives telomere instability.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 990, "doc_id": 16472469, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [16472469], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pyridostatin deregulates G2/M progression.\n\nDocument title: Targeting BRCA1 and BRCA2 Deficiencies with G-Quadruplex-Interacting Compounds\n\nAbstract sentences:\n[0] G-quadruplex (G4)-forming genomic sequences, including telomeres, represent natural replication fork barriers.\n[1] Stalled replication forks can be stabilized and restarted by homologous recombination (HR), which also repairs DNA double-strand breaks (DSBs) arising at collapsed forks.\n[2] We have previously shown that HR facilitates telomere replication.\n[3] Here, we demonstrate that the replication efficiency of guanine-rich (G-rich) telomeric repeats is decreased significantly in cells lacking HR.\n[4] Treatment with the G4-stabilizing compound pyridostatin (PDS) increases telomere fragility in BRCA2-deficient cells, suggesting that G4 formation drives telomere instability.\n[5] Remarkably, PDS reduces proliferation of HR-defective cells by inducing DSB accumulation, checkpoint activation, and deregulated G2/M progression and by enhancing the replication defect intrinsic to HR deficiency.\n[6] PDS toxicity extends to HR-defective cells that have acquired olaparib resistance through loss of 53BP1 or REV7.\n[7] Altogether, these results highlight the therapeutic potential of G4-stabilizing drugs to selectively eliminate HR-compromised cells and tumors, including those resistant to PARP inhibition."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Remarkably, PDS reduces proliferation of HR-defective cells by inducing DSB accumulation, checkpoint activation, and deregulated G2/M progression and by enhancing the replication defect intrinsic to HR deficiency.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 992, "doc_id": 16472469, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [16472469], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pyridostatin encourages proliferation of homologous recombination - defective cells.\n\nDocument title: Targeting BRCA1 and BRCA2 Deficiencies with G-Quadruplex-Interacting Compounds\n\nAbstract sentences:\n[0] G-quadruplex (G4)-forming genomic sequences, including telomeres, represent natural replication fork barriers.\n[1] Stalled replication forks can be stabilized and restarted by homologous recombination (HR), which also repairs DNA double-strand breaks (DSBs) arising at collapsed forks.\n[2] We have previously shown that HR facilitates telomere replication.\n[3] Here, we demonstrate that the replication efficiency of guanine-rich (G-rich) telomeric repeats is decreased significantly in cells lacking HR.\n[4] Treatment with the G4-stabilizing compound pyridostatin (PDS) increases telomere fragility in BRCA2-deficient cells, suggesting that G4 formation drives telomere instability.\n[5] Remarkably, PDS reduces proliferation of HR-defective cells by inducing DSB accumulation, checkpoint activation, and deregulated G2/M progression and by enhancing the replication defect intrinsic to HR deficiency.\n[6] PDS toxicity extends to HR-defective cells that have acquired olaparib resistance through loss of 53BP1 or REV7.\n[7] Altogether, these results highlight the therapeutic potential of G4-stabilizing drugs to selectively eliminate HR-compromised cells and tumors, including those resistant to PARP inhibition."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Remarkably, PDS reduces proliferation of HR-defective cells by inducing DSB accumulation, checkpoint activation, and deregulated G2/M progression and by enhancing the replication defect intrinsic to HR deficiency.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 994, "doc_id": 16472469, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [16472469], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pyridostatin induces checkpoint activation.\n\nDocument title: Targeting BRCA1 and BRCA2 Deficiencies with G-Quadruplex-Interacting Compounds\n\nAbstract sentences:\n[0] G-quadruplex (G4)-forming genomic sequences, including telomeres, represent natural replication fork barriers.\n[1] Stalled replication forks can be stabilized and restarted by homologous recombination (HR), which also repairs DNA double-strand breaks (DSBs) arising at collapsed forks.\n[2] We have previously shown that HR facilitates telomere replication.\n[3] Here, we demonstrate that the replication efficiency of guanine-rich (G-rich) telomeric repeats is decreased significantly in cells lacking HR.\n[4] Treatment with the G4-stabilizing compound pyridostatin (PDS) increases telomere fragility in BRCA2-deficient cells, suggesting that G4 formation drives telomere instability.\n[5] Remarkably, PDS reduces proliferation of HR-defective cells by inducing DSB accumulation, checkpoint activation, and deregulated G2/M progression and by enhancing the replication defect intrinsic to HR deficiency.\n[6] PDS toxicity extends to HR-defective cells that have acquired olaparib resistance through loss of 53BP1 or REV7.\n[7] Altogether, these results highlight the therapeutic potential of G4-stabilizing drugs to selectively eliminate HR-compromised cells and tumors, including those resistant to PARP inhibition."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Remarkably, PDS reduces proliferation of HR-defective cells by inducing DSB accumulation, checkpoint activation, and deregulated G2/M progression and by enhancing the replication defect intrinsic to HR deficiency.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 996, "doc_id": 16472469, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [16472469], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pyridostatin induces double-strand breaks accumulation.\n\nDocument title: Targeting BRCA1 and BRCA2 Deficiencies with G-Quadruplex-Interacting Compounds\n\nAbstract sentences:\n[0] G-quadruplex (G4)-forming genomic sequences, including telomeres, represent natural replication fork barriers.\n[1] Stalled replication forks can be stabilized and restarted by homologous recombination (HR), which also repairs DNA double-strand breaks (DSBs) arising at collapsed forks.\n[2] We have previously shown that HR facilitates telomere replication.\n[3] Here, we demonstrate that the replication efficiency of guanine-rich (G-rich) telomeric repeats is decreased significantly in cells lacking HR.\n[4] Treatment with the G4-stabilizing compound pyridostatin (PDS) increases telomere fragility in BRCA2-deficient cells, suggesting that G4 formation drives telomere instability.\n[5] Remarkably, PDS reduces proliferation of HR-defective cells by inducing DSB accumulation, checkpoint activation, and deregulated G2/M progression and by enhancing the replication defect intrinsic to HR deficiency.\n[6] PDS toxicity extends to HR-defective cells that have acquired olaparib resistance through loss of 53BP1 or REV7.\n[7] Altogether, these results highlight the therapeutic potential of G4-stabilizing drugs to selectively eliminate HR-compromised cells and tumors, including those resistant to PARP inhibition."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Remarkably, PDS reduces proliferation of HR-defective cells by inducing DSB accumulation, checkpoint activation, and deregulated G2/M progression and by enhancing the replication defect intrinsic to HR deficiency.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 997, "doc_id": 16472469, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [16472469], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pyridostatin prevents double-strand breaks accumulation.\n\nDocument title: Targeting BRCA1 and BRCA2 Deficiencies with G-Quadruplex-Interacting Compounds\n\nAbstract sentences:\n[0] G-quadruplex (G4)-forming genomic sequences, including telomeres, represent natural replication fork barriers.\n[1] Stalled replication forks can be stabilized and restarted by homologous recombination (HR), which also repairs DNA double-strand breaks (DSBs) arising at collapsed forks.\n[2] We have previously shown that HR facilitates telomere replication.\n[3] Here, we demonstrate that the replication efficiency of guanine-rich (G-rich) telomeric repeats is decreased significantly in cells lacking HR.\n[4] Treatment with the G4-stabilizing compound pyridostatin (PDS) increases telomere fragility in BRCA2-deficient cells, suggesting that G4 formation drives telomere instability.\n[5] Remarkably, PDS reduces proliferation of HR-defective cells by inducing DSB accumulation, checkpoint activation, and deregulated G2/M progression and by enhancing the replication defect intrinsic to HR deficiency.\n[6] PDS toxicity extends to HR-defective cells that have acquired olaparib resistance through loss of 53BP1 or REV7.\n[7] Altogether, these results highlight the therapeutic potential of G4-stabilizing drugs to selectively eliminate HR-compromised cells and tumors, including those resistant to PARP inhibition."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Remarkably, PDS reduces proliferation of HR-defective cells by inducing DSB accumulation, checkpoint activation, and deregulated G2/M progression and by enhancing the replication defect intrinsic to HR deficiency.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 998, "doc_id": 16472469, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [16472469], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pyridostatin reduces proliferation of homologous recombination - defective cells.\n\nDocument title: Targeting BRCA1 and BRCA2 Deficiencies with G-Quadruplex-Interacting Compounds\n\nAbstract sentences:\n[0] G-quadruplex (G4)-forming genomic sequences, including telomeres, represent natural replication fork barriers.\n[1] Stalled replication forks can be stabilized and restarted by homologous recombination (HR), which also repairs DNA double-strand breaks (DSBs) arising at collapsed forks.\n[2] We have previously shown that HR facilitates telomere replication.\n[3] Here, we demonstrate that the replication efficiency of guanine-rich (G-rich) telomeric repeats is decreased significantly in cells lacking HR.\n[4] Treatment with the G4-stabilizing compound pyridostatin (PDS) increases telomere fragility in BRCA2-deficient cells, suggesting that G4 formation drives telomere instability.\n[5] Remarkably, PDS reduces proliferation of HR-defective cells by inducing DSB accumulation, checkpoint activation, and deregulated G2/M progression and by enhancing the replication defect intrinsic to HR deficiency.\n[6] PDS toxicity extends to HR-defective cells that have acquired olaparib resistance through loss of 53BP1 or REV7.\n[7] Altogether, these results highlight the therapeutic potential of G4-stabilizing drugs to selectively eliminate HR-compromised cells and tumors, including those resistant to PARP inhibition."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Remarkably, PDS reduces proliferation of HR-defective cells by inducing DSB accumulation, checkpoint activation, and deregulated G2/M progression and by enhancing the replication defect intrinsic to HR deficiency.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 999, "doc_id": 16472469, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [16472469], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Pyridostatin stabilizes the G - quadruplex in the telomeric region.\n\nDocument title: Targeting BRCA1 and BRCA2 Deficiencies with G-Quadruplex-Interacting Compounds\n\nAbstract sentences:\n[0] G-quadruplex (G4)-forming genomic sequences, including telomeres, represent natural replication fork barriers.\n[1] Stalled replication forks can be stabilized and restarted by homologous recombination (HR), which also repairs DNA double-strand breaks (DSBs) arising at collapsed forks.\n[2] We have previously shown that HR facilitates telomere replication.\n[3] Here, we demonstrate that the replication efficiency of guanine-rich (G-rich) telomeric repeats is decreased significantly in cells lacking HR.\n[4] Treatment with the G4-stabilizing compound pyridostatin (PDS) increases telomere fragility in BRCA2-deficient cells, suggesting that G4 formation drives telomere instability.\n[5] Remarkably, PDS reduces proliferation of HR-defective cells by inducing DSB accumulation, checkpoint activation, and deregulated G2/M progression and by enhancing the replication defect intrinsic to HR deficiency.\n[6] PDS toxicity extends to HR-defective cells that have acquired olaparib resistance through loss of 53BP1 or REV7.\n[7] Altogether, these results highlight the therapeutic potential of G4-stabilizing drugs to selectively eliminate HR-compromised cells and tumors, including those resistant to PARP inhibition."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Treatment with the G4-stabilizing compound pyridostatin (PDS) increases telomere fragility in BRCA2-deficient cells, suggesting that G4 formation drives telomere instability.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1000, "doc_id": 16472469, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [16472469], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: R2D2 stops miRNA production by increasing the selectivity of Dcr2 for long dsRNA.\n\nDocument title: Phosphate and R2D2 restrict the substrate specificity of Dicer-2, an ATP-driven ribonuclease.\n\nAbstract sentences:\n[0] Drosophila Dicer-2 generates small interfering RNAs (siRNAs) from long double-stranded RNA (dsRNA), whereas Dicer-1 produces microRNAs (miRNAs) from pre-miRNA.\n[1] What makes the two Dicers specific for their biological substrates?\n[2] We find that purified Dicer-2 can efficiently cleave pre-miRNA, but that inorganic phosphate and the Dicer-2 partner protein R2D2 inhibit pre-miRNA cleavage.\n[3] Dicer-2 contains C-terminal RNase III domains that mediate RNA cleavage and an N-terminal helicase motif, whose function is unclear.\n[4] We show that Dicer-2 is a dsRNA-stimulated ATPase that hydrolyzes ATP to ADP; ATP hydrolysis is required for Dicer-2 to process long dsRNA, but not pre-miRNA.\n[5] Wild-type Dicer-2, but not a mutant defective in ATP hydrolysis, can generate siRNAs faster than it can dissociate from a long dsRNA substrate.\n[6] We propose that the Dicer-2 helicase domain uses ATP to generate many siRNAs from a single molecule of dsRNA before dissociating from its substrate."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1001, "doc_id": 5702790, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [5702790], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RA activation of DIF2 and NB4 cells induces hallmarks of transcriptionally active promoters.\n\nDocument title: Histone Methylation-Dependent Mechanisms Impose Ligand Dependency for Gene Activation by Nuclear Receptors\n\nAbstract sentences:\n[0] Nuclear receptors undergo ligand-dependent conformational changes that are required for corepressor-coactivator exchange, but whether there is an actual requirement for specific epigenetic landmarks to impose ligand dependency for gene activation remains unknown.\n[1] Here we report an unexpected and general strategy that is based on the requirement for specific cohorts of inhibitory histone methyltransferases (HMTs) to impose gene-specific gatekeeper functions that prevent unliganded nuclear receptors and other classes of regulated transcription factors from binding to their target gene promoters and causing constitutive gene activation in the absence of stimulating signals.\n[2] This strategy, based at least in part on an HMT-dependent inhibitory histone code, imposes a requirement for specific histone demethylases, including LSD1, to permit ligand- and signal-dependent activation of regulated gene expression.\n[3] These events link an inhibitory methylation component of the histone code to a broadly used strategy that circumvents pathological constitutive gene induction by physiologically regulated transcription factors."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1002, "doc_id": 13639330, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [13639330], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RAD52 is involved in break-induced DNA replication (BIR).\n\nDocument title: Mammalian RAD52 Functions in Break-Induced Replication Repair of Collapsed DNA Replication Forks\n\nAbstract sentences:\n[0] Human cancers are characterized by the presence of oncogene-induced DNA replication stress (DRS), making them dependent on repair pathways such as break-induced replication (BIR) for damaged DNA replication forks.\n[1] To better understand BIR, we performed a targeted siRNA screen for genes whose depletion inhibited G1 to S phase progression when oncogenic cyclin E was overexpressed.\n[2] RAD52, a gene dispensable for normal development in mice, was among the top hits.\n[3] In cells in which fork collapse was induced by oncogenes or chemicals, the Rad52 protein localized to DRS foci.\n[4] Depletion of Rad52 by siRNA or knockout of the gene by CRISPR/Cas9 compromised restart of collapsed forks and led to DNA damage in cells experiencing DRS.\n[5] Furthermore, in cancer-prone, heterozygous APC mutant mice, homozygous deletion of the Rad52 gene suppressed tumor growth and prolonged lifespan.\n[6] We therefore propose that mammalian RAD52 facilitates repair of collapsed DNA replication forks in cancer cells."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"We therefore propose that mammalian RAD52 facilitates repair of collapsed DNA replication forks in cancer cells.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1003, "doc_id": 14332945, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [14332945, 4319844, 4899981], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RAD52 is involved in break-induced DNA replication (BIR).\n\nDocument title: Alternative Lengthening of Telomeres Mediated by Mitotic DNA Synthesis Engages Break-Induced Replication Processes.\n\nAbstract sentences:\n[0] Alternative lengthening of telomeres (ALT) is a telomerase-independent telomere maintenance mechanism that occurs in a subset of cancers.\n[1] By analyzing telomerase-positive cells and their human TERC knockout-derived ALT human cell lines, we show that ALT cells harbor more fragile telomeres representing telomere replication problems.\n[2] ALT-associated replication defects trigger mitotic DNA synthesis (MiDAS) at telomeres in a RAD52-dependent, but RAD51-independent, manner.\n[3] Telomeric MiDAS is a conservative DNA synthesis process, potentially mediated by break-induced replication, similar to type II ALT survivors in Saccharomyces cerevisiae Replication stresses induced by ectopic oncogenic expression of cyclin E, G-quadruplexes, or R-loop formation facilitate the ALT pathway and lead to telomere clustering, a hallmark of ALT cancers.\n[4] The TIMELESS/TIPIN complex suppresses telomere clustering and telomeric MiDAS, whereas the SMC5/6 complex promotes them.\n[5] In summary, ALT cells exhibit more telomere replication defects that result in persistent DNA damage responses at telomeres, leading to the engagement of telomeric MiDAS (spontaneous mitotic telomere synthesis) that is triggered by DNA replication stress, a potential driver of genomic duplications in cancer."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"ALT-associated replication defects trigger mitotic DNA synthesis (MiDAS) at telomeres in a RAD52-dependent, but RAD51-independent, manner.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1003, "doc_id": 4319844, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [14332945, 4319844, 4899981], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RAD52 is involved in break-induced DNA replication (BIR).\n\nDocument title: Human cancer cells utilize mitotic DNA synthesis to resist replication stress at telomeres regardless of their telomere maintenance mechanism\n\nAbstract sentences:\n[0] Telomeres resemble common fragile sites (CFSs) in that they are difficult-to-replicate and exhibit fragility in mitosis in response to DNA replication stress.\n[1] At CFSs, this fragility is associated with a delay in the completion of DNA replication until early mitosis, whereupon cells are proposed to switch to a RAD52-dependent form of break-induced replication.\n[2] Here, we show that this mitotic DNA synthesis (MiDAS) is also a feature of human telomeres.\n[3] Telomeric MiDAS is not restricted to those telomeres displaying overt fragility, and is a feature of a wide range of cell lines irrespective of whether their telomeres are maintained by telomerase or by the alternative lengthening of telomeres (ALT) mechanism.\n[4] MiDAS at telomeres requires RAD52, and is mechanistically similar to CFS-associated MiDAS, with the notable exception that telomeric MiDAS does not require the MUS81-EME1 endonuclease.\n[5] We propose a model whereby replication stress initiates a RAD52-dependent form of break-induced replication that bypasses a requirement for MUS81-EME1 to complete DNA synthesis in mitosis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"At CFSs, this fragility is associated with a delay in the completion of DNA replication until early mitosis, whereupon cells are proposed to switch to a RAD52-dependent form of break-induced replication.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1003, "doc_id": 4899981, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [14332945, 4319844, 4899981], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RAD52 is involved in break-induced DNA replication (BIR).\n\nDocument title: Human cancer cells utilize mitotic DNA synthesis to resist replication stress at telomeres regardless of their telomere maintenance mechanism\n\nAbstract sentences:\n[0] Telomeres resemble common fragile sites (CFSs) in that they are difficult-to-replicate and exhibit fragility in mitosis in response to DNA replication stress.\n[1] At CFSs, this fragility is associated with a delay in the completion of DNA replication until early mitosis, whereupon cells are proposed to switch to a RAD52-dependent form of break-induced replication.\n[2] Here, we show that this mitotic DNA synthesis (MiDAS) is also a feature of human telomeres.\n[3] Telomeric MiDAS is not restricted to those telomeres displaying overt fragility, and is a feature of a wide range of cell lines irrespective of whether their telomeres are maintained by telomerase or by the alternative lengthening of telomeres (ALT) mechanism.\n[4] MiDAS at telomeres requires RAD52, and is mechanistically similar to CFS-associated MiDAS, with the notable exception that telomeric MiDAS does not require the MUS81-EME1 endonuclease.\n[5] We propose a model whereby replication stress initiates a RAD52-dependent form of break-induced replication that bypasses a requirement for MUS81-EME1 to complete DNA synthesis in mitosis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"We propose a model whereby replication stress initiates a RAD52-dependent form of break-induced replication that bypasses a requirement for MUS81-EME1 to complete DNA synthesis in mitosis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1003, "doc_id": 4899981, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [14332945, 4319844, 4899981], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RANK-RANKL pathway signalling has no known association with development of Aire-expressing medullary thymic epithelial cells.\n\nDocument title: Rank Signaling Links the Development of Invariant γδ T Cell Progenitors and Aire+ Medullary Epithelium\n\nAbstract sentences:\n[0] The thymic medulla provides a specialized microenvironment for the negative selection of T cells, with the presence of autoimmune regulator (Aire)-expressing medullary thymic epithelial cells (mTECs) during the embryonic-neonatal period being both necessary and sufficient to establish long-lasting tolerance.\n[1] Here we showed that emergence of the first cohorts of Aire(+) mTECs at this key developmental stage, prior to αβ T cell repertoire selection, was jointly directed by Rankl(+) lymphoid tissue inducer cells and invariant Vγ5(+) dendritic epidermal T cell (DETC) progenitors that are the first thymocytes to express the products of gene rearrangement.\n[2] In turn, generation of Aire(+) mTECs then fostered Skint-1-dependent, but Aire-independent, DETC progenitor maturation and the emergence of an invariant DETC repertoire.\n[3] Hence, our data attributed a functional importance to the temporal development of Vγ5(+) γδ T cells during thymus medulla formation for αβ T cell tolerance induction and demonstrated a Rank-mediated reciprocal link between DETC and Aire(+) mTEC maturation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Here we showed that emergence of the first cohorts of Aire(+) mTECs at this key developmental stage, prior to αβ T cell repertoire selection, was jointly directed by Rankl(+) lymphoid tissue inducer cells and invariant Vγ5(+) dendritic epidermal T cell (DETC) progenitors that are the first thymocytes to express the products of gene rearrangement.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1004, "doc_id": 301838, "label": "CONTRADICTS", "evidence_sentence_ids": [1], "cited_doc_ids": [301838, 2734421, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RANK-RANKL pathway signalling has no known association with development of Aire-expressing medullary thymic epithelial cells.\n\nDocument title: Rank Signaling Links the Development of Invariant γδ T Cell Progenitors and Aire+ Medullary Epithelium\n\nAbstract sentences:\n[0] The thymic medulla provides a specialized microenvironment for the negative selection of T cells, with the presence of autoimmune regulator (Aire)-expressing medullary thymic epithelial cells (mTECs) during the embryonic-neonatal period being both necessary and sufficient to establish long-lasting tolerance.\n[1] Here we showed that emergence of the first cohorts of Aire(+) mTECs at this key developmental stage, prior to αβ T cell repertoire selection, was jointly directed by Rankl(+) lymphoid tissue inducer cells and invariant Vγ5(+) dendritic epidermal T cell (DETC) progenitors that are the first thymocytes to express the products of gene rearrangement.\n[2] In turn, generation of Aire(+) mTECs then fostered Skint-1-dependent, but Aire-independent, DETC progenitor maturation and the emergence of an invariant DETC repertoire.\n[3] Hence, our data attributed a functional importance to the temporal development of Vγ5(+) γδ T cells during thymus medulla formation for αβ T cell tolerance induction and demonstrated a Rank-mediated reciprocal link between DETC and Aire(+) mTEC maturation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Hence, our data attributed a functional importance to the temporal development of Vγ5(+) γδ T cells during thymus medulla formation for αβ T cell tolerance induction and demonstrated a Rank-mediated reciprocal link between DETC and Aire(+) mTEC maturation.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1004, "doc_id": 301838, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [301838, 2734421, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RANK-RANKL pathway signalling has no known association with development of Aire-expressing medullary thymic epithelial cells.\n\nDocument title: The tumor necrosis factor family receptors RANK and CD40 cooperatively establish the thymic medullary microenvironment and self-tolerance.\n\nAbstract sentences:\n[0] Medullary thymic epithelial cells (mTECs) establish T cell self-tolerance through the expression of autoimmune regulator (Aire) and peripheral tissue-specific self-antigens.\n[1] However, signals underlying mTEC development remain largely unclear.\n[2] Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals.\n[3] Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment.\n[4] Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner.\n[5] These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1004, "doc_id": 2734421, "label": "CONTRADICTS", "evidence_sentence_ids": [2], "cited_doc_ids": [301838, 2734421, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RANK-RANKL pathway signalling has no known association with development of Aire-expressing medullary thymic epithelial cells.\n\nDocument title: The tumor necrosis factor family receptors RANK and CD40 cooperatively establish the thymic medullary microenvironment and self-tolerance.\n\nAbstract sentences:\n[0] Medullary thymic epithelial cells (mTECs) establish T cell self-tolerance through the expression of autoimmune regulator (Aire) and peripheral tissue-specific self-antigens.\n[1] However, signals underlying mTEC development remain largely unclear.\n[2] Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals.\n[3] Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment.\n[4] Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner.\n[5] These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1004, "doc_id": 2734421, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [301838, 2734421, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RANK-RANKL pathway signalling has no known association with development of Aire-expressing medullary thymic epithelial cells.\n\nDocument title: The tumor necrosis factor family receptors RANK and CD40 cooperatively establish the thymic medullary microenvironment and self-tolerance.\n\nAbstract sentences:\n[0] Medullary thymic epithelial cells (mTECs) establish T cell self-tolerance through the expression of autoimmune regulator (Aire) and peripheral tissue-specific self-antigens.\n[1] However, signals underlying mTEC development remain largely unclear.\n[2] Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals.\n[3] Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment.\n[4] Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner.\n[5] These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1004, "doc_id": 2734421, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [301838, 2734421, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RANK-RANKL pathway signalling has no known association with development of Aire-expressing medullary thymic epithelial cells.\n\nDocument title: The tumor necrosis factor family receptors RANK and CD40 cooperatively establish the thymic medullary microenvironment and self-tolerance.\n\nAbstract sentences:\n[0] Medullary thymic epithelial cells (mTECs) establish T cell self-tolerance through the expression of autoimmune regulator (Aire) and peripheral tissue-specific self-antigens.\n[1] However, signals underlying mTEC development remain largely unclear.\n[2] Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals.\n[3] Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment.\n[4] Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner.\n[5] These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1004, "doc_id": 2734421, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [301838, 2734421, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RANK-RANKL pathway signalling has no known association with development of Aire-expressing medullary thymic epithelial cells.\n\nDocument title: RANK signals from CD4+3− inducer cells regulate development of Aire-expressing epithelial cells in the thymic medulla\n\nAbstract sentences:\n[0] Aire-expressing medullary thymic epithelial cells (mTECs) play a key role in preventing autoimmunity by expressing tissue-restricted antigens to help purge the emerging T cell receptor repertoire of self-reactive specificities.\n[1] Here we demonstrate a novel role for a CD4+3− inducer cell population, previously linked to development of organized secondary lymphoid structures and maintenance of T cell memory in the functional regulation of Aire-mediated promiscuous gene expression in the thymus.\n[2] CD4+3− cells are closely associated with mTECs in adult thymus, and in fetal thymus their appearance is temporally linked with the appearance of Aire+ mTECs.\n[3] We show that RANKL signals from this cell promote the maturation of RANK-expressing CD80−Aire− mTEC progenitors into CD80+Aire+ mTECs, and that transplantation of RANK-deficient thymic stroma into immunodeficient hosts induces autoimmunity.\n[4] Collectively, our data reveal cellular and molecular mechanisms leading to the generation of Aire+ mTECs and highlight a previously unrecognized role for CD4+3−RANKL+ inducer cells in intrathymic self-tolerance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"We show that RANKL signals from this cell promote the maturation of RANK-expressing CD80−Aire− mTEC progenitors into CD80+Aire+ mTECs, and that transplantation of RANK-deficient thymic stroma into immunodeficient hosts induces autoimmunity.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1004, "doc_id": 3952288, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [301838, 2734421, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RANK-RANKL pathway signalling has no known association with development of Aire-expressing medullary thymic epithelial cells.\n\nDocument title: RANK signals from CD4+3− inducer cells regulate development of Aire-expressing epithelial cells in the thymic medulla\n\nAbstract sentences:\n[0] Aire-expressing medullary thymic epithelial cells (mTECs) play a key role in preventing autoimmunity by expressing tissue-restricted antigens to help purge the emerging T cell receptor repertoire of self-reactive specificities.\n[1] Here we demonstrate a novel role for a CD4+3− inducer cell population, previously linked to development of organized secondary lymphoid structures and maintenance of T cell memory in the functional regulation of Aire-mediated promiscuous gene expression in the thymus.\n[2] CD4+3− cells are closely associated with mTECs in adult thymus, and in fetal thymus their appearance is temporally linked with the appearance of Aire+ mTECs.\n[3] We show that RANKL signals from this cell promote the maturation of RANK-expressing CD80−Aire− mTEC progenitors into CD80+Aire+ mTECs, and that transplantation of RANK-deficient thymic stroma into immunodeficient hosts induces autoimmunity.\n[4] Collectively, our data reveal cellular and molecular mechanisms leading to the generation of Aire+ mTECs and highlight a previously unrecognized role for CD4+3−RANKL+ inducer cells in intrathymic self-tolerance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Collectively, our data reveal cellular and molecular mechanisms leading to the generation of Aire+ mTECs and highlight a previously unrecognized role for CD4+3−RANKL+ inducer cells in intrathymic self-tolerance.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1004, "doc_id": 3952288, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [301838, 2734421, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RANK-RANKL pathway signalling is linked to development of Aire-expressing medullary thymic epithelial cells.\n\nDocument title: Rank Signaling Links the Development of Invariant γδ T Cell Progenitors and Aire+ Medullary Epithelium\n\nAbstract sentences:\n[0] The thymic medulla provides a specialized microenvironment for the negative selection of T cells, with the presence of autoimmune regulator (Aire)-expressing medullary thymic epithelial cells (mTECs) during the embryonic-neonatal period being both necessary and sufficient to establish long-lasting tolerance.\n[1] Here we showed that emergence of the first cohorts of Aire(+) mTECs at this key developmental stage, prior to αβ T cell repertoire selection, was jointly directed by Rankl(+) lymphoid tissue inducer cells and invariant Vγ5(+) dendritic epidermal T cell (DETC) progenitors that are the first thymocytes to express the products of gene rearrangement.\n[2] In turn, generation of Aire(+) mTECs then fostered Skint-1-dependent, but Aire-independent, DETC progenitor maturation and the emergence of an invariant DETC repertoire.\n[3] Hence, our data attributed a functional importance to the temporal development of Vγ5(+) γδ T cells during thymus medulla formation for αβ T cell tolerance induction and demonstrated a Rank-mediated reciprocal link between DETC and Aire(+) mTEC maturation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Here we showed that emergence of the first cohorts of Aire(+) mTECs at this key developmental stage, prior to αβ T cell repertoire selection, was jointly directed by Rankl(+) lymphoid tissue inducer cells and invariant Vγ5(+) dendritic epidermal T cell (DETC) progenitors that are the first thymocytes to express the products of gene rearrangement.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1005, "doc_id": 301838, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [301838, 2734421, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RANK-RANKL pathway signalling is linked to development of Aire-expressing medullary thymic epithelial cells.\n\nDocument title: Rank Signaling Links the Development of Invariant γδ T Cell Progenitors and Aire+ Medullary Epithelium\n\nAbstract sentences:\n[0] The thymic medulla provides a specialized microenvironment for the negative selection of T cells, with the presence of autoimmune regulator (Aire)-expressing medullary thymic epithelial cells (mTECs) during the embryonic-neonatal period being both necessary and sufficient to establish long-lasting tolerance.\n[1] Here we showed that emergence of the first cohorts of Aire(+) mTECs at this key developmental stage, prior to αβ T cell repertoire selection, was jointly directed by Rankl(+) lymphoid tissue inducer cells and invariant Vγ5(+) dendritic epidermal T cell (DETC) progenitors that are the first thymocytes to express the products of gene rearrangement.\n[2] In turn, generation of Aire(+) mTECs then fostered Skint-1-dependent, but Aire-independent, DETC progenitor maturation and the emergence of an invariant DETC repertoire.\n[3] Hence, our data attributed a functional importance to the temporal development of Vγ5(+) γδ T cells during thymus medulla formation for αβ T cell tolerance induction and demonstrated a Rank-mediated reciprocal link between DETC and Aire(+) mTEC maturation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Hence, our data attributed a functional importance to the temporal development of Vγ5(+) γδ T cells during thymus medulla formation for αβ T cell tolerance induction and demonstrated a Rank-mediated reciprocal link between DETC and Aire(+) mTEC maturation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1005, "doc_id": 301838, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [301838, 2734421, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RANK-RANKL pathway signalling is linked to development of Aire-expressing medullary thymic epithelial cells.\n\nDocument title: The tumor necrosis factor family receptors RANK and CD40 cooperatively establish the thymic medullary microenvironment and self-tolerance.\n\nAbstract sentences:\n[0] Medullary thymic epithelial cells (mTECs) establish T cell self-tolerance through the expression of autoimmune regulator (Aire) and peripheral tissue-specific self-antigens.\n[1] However, signals underlying mTEC development remain largely unclear.\n[2] Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals.\n[3] Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment.\n[4] Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner.\n[5] These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1005, "doc_id": 2734421, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [301838, 2734421, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RANK-RANKL pathway signalling is linked to development of Aire-expressing medullary thymic epithelial cells.\n\nDocument title: The tumor necrosis factor family receptors RANK and CD40 cooperatively establish the thymic medullary microenvironment and self-tolerance.\n\nAbstract sentences:\n[0] Medullary thymic epithelial cells (mTECs) establish T cell self-tolerance through the expression of autoimmune regulator (Aire) and peripheral tissue-specific self-antigens.\n[1] However, signals underlying mTEC development remain largely unclear.\n[2] Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals.\n[3] Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment.\n[4] Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner.\n[5] These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1005, "doc_id": 2734421, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [301838, 2734421, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RANK-RANKL pathway signalling is linked to development of Aire-expressing medullary thymic epithelial cells.\n\nDocument title: The tumor necrosis factor family receptors RANK and CD40 cooperatively establish the thymic medullary microenvironment and self-tolerance.\n\nAbstract sentences:\n[0] Medullary thymic epithelial cells (mTECs) establish T cell self-tolerance through the expression of autoimmune regulator (Aire) and peripheral tissue-specific self-antigens.\n[1] However, signals underlying mTEC development remain largely unclear.\n[2] Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals.\n[3] Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment.\n[4] Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner.\n[5] These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1005, "doc_id": 2734421, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [301838, 2734421, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RANK-RANKL pathway signalling is linked to development of Aire-expressing medullary thymic epithelial cells.\n\nDocument title: The tumor necrosis factor family receptors RANK and CD40 cooperatively establish the thymic medullary microenvironment and self-tolerance.\n\nAbstract sentences:\n[0] Medullary thymic epithelial cells (mTECs) establish T cell self-tolerance through the expression of autoimmune regulator (Aire) and peripheral tissue-specific self-antigens.\n[1] However, signals underlying mTEC development remain largely unclear.\n[2] Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals.\n[3] Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment.\n[4] Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner.\n[5] These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1005, "doc_id": 2734421, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [301838, 2734421, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RANK-RANKL pathway signalling is linked to development of Aire-expressing medullary thymic epithelial cells.\n\nDocument title: RANK signals from CD4+3− inducer cells regulate development of Aire-expressing epithelial cells in the thymic medulla\n\nAbstract sentences:\n[0] Aire-expressing medullary thymic epithelial cells (mTECs) play a key role in preventing autoimmunity by expressing tissue-restricted antigens to help purge the emerging T cell receptor repertoire of self-reactive specificities.\n[1] Here we demonstrate a novel role for a CD4+3− inducer cell population, previously linked to development of organized secondary lymphoid structures and maintenance of T cell memory in the functional regulation of Aire-mediated promiscuous gene expression in the thymus.\n[2] CD4+3− cells are closely associated with mTECs in adult thymus, and in fetal thymus their appearance is temporally linked with the appearance of Aire+ mTECs.\n[3] We show that RANKL signals from this cell promote the maturation of RANK-expressing CD80−Aire− mTEC progenitors into CD80+Aire+ mTECs, and that transplantation of RANK-deficient thymic stroma into immunodeficient hosts induces autoimmunity.\n[4] Collectively, our data reveal cellular and molecular mechanisms leading to the generation of Aire+ mTECs and highlight a previously unrecognized role for CD4+3−RANKL+ inducer cells in intrathymic self-tolerance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"We show that RANKL signals from this cell promote the maturation of RANK-expressing CD80−Aire− mTEC progenitors into CD80+Aire+ mTECs, and that transplantation of RANK-deficient thymic stroma into immunodeficient hosts induces autoimmunity.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1005, "doc_id": 3952288, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [301838, 2734421, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RANK-RANKL pathway signalling is linked to development of Aire-expressing medullary thymic epithelial cells.\n\nDocument title: RANK signals from CD4+3− inducer cells regulate development of Aire-expressing epithelial cells in the thymic medulla\n\nAbstract sentences:\n[0] Aire-expressing medullary thymic epithelial cells (mTECs) play a key role in preventing autoimmunity by expressing tissue-restricted antigens to help purge the emerging T cell receptor repertoire of self-reactive specificities.\n[1] Here we demonstrate a novel role for a CD4+3− inducer cell population, previously linked to development of organized secondary lymphoid structures and maintenance of T cell memory in the functional regulation of Aire-mediated promiscuous gene expression in the thymus.\n[2] CD4+3− cells are closely associated with mTECs in adult thymus, and in fetal thymus their appearance is temporally linked with the appearance of Aire+ mTECs.\n[3] We show that RANKL signals from this cell promote the maturation of RANK-expressing CD80−Aire− mTEC progenitors into CD80+Aire+ mTECs, and that transplantation of RANK-deficient thymic stroma into immunodeficient hosts induces autoimmunity.\n[4] Collectively, our data reveal cellular and molecular mechanisms leading to the generation of Aire+ mTECs and highlight a previously unrecognized role for CD4+3−RANKL+ inducer cells in intrathymic self-tolerance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Collectively, our data reveal cellular and molecular mechanisms leading to the generation of Aire+ mTECs and highlight a previously unrecognized role for CD4+3−RANKL+ inducer cells in intrathymic self-tolerance.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1005, "doc_id": 3952288, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [301838, 2734421, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RTEL1 interacts with TRF2 through a C4C4 motif\n\nDocument title: TRF2 Recruits RTEL1 to Telomeres in S Phase to Promote T-Loop Unwinding\n\nAbstract sentences:\n[0] The helicase RTEL1 promotes t-loop unwinding and suppresses telomere fragility to maintain the integrity of vertebrate telomeres.\n[1] An interaction between RTEL1 and PCNA is important to prevent telomere fragility, but how RTEL1 engages with the telomere to promote t-loop unwinding is unclear.\n[2] Here, we establish that the shelterin protein TRF2 recruits RTEL1 to telomeres in S phase, which is required to prevent catastrophic t-loop processing by structure-specific nucleases.\n[3] We show that the TRF2-RTEL1 interaction is mediated by a metal-coordinating C4C4 motif in RTEL1, which is compromised by the Hoyeraal-Hreidarsson syndrome (HHS) mutation, RTEL1(R1264H).\n[4] Conversely, we define a TRF2(I124D) substitution mutation within the TRFH domain of TRF2, which eliminates RTEL1 binding and phenocopies the RTEL1(R1264H) mutation, giving rise to aberrant t-loop excision, telomere length heterogeneity, and loss of the telomere as a circle.\n[5] These results implicate TRF2 in the recruitment of RTEL1 to facilitate t-loop disassembly at telomeres in S phase."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"We show that the TRF2-RTEL1 interaction is mediated by a metal-coordinating C4C4 motif in RTEL1, which is compromised by the Hoyeraal-Hreidarsson syndrome (HHS) mutation, RTEL1(R1264H).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1006, "doc_id": 4926049, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [4926049], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RUNX is not expressed in skin tissue.\n\nDocument title: Human epidermal stem cell function is regulated by circadian oscillations.\n\nAbstract sentences:\n[0] Human skin copes with harmful environmental factors that are circadian in nature, yet how circadian rhythms modulate the function of human epidermal stem cells is mostly unknown.\n[1] Here we show that in human epidermal stem cells and their differentiated counterparts, core clock genes peak in a successive and phased manner, establishing distinct temporal intervals during the 24 hr day period.\n[2] Each of these successive clock waves is associated with a peak in the expression of subsets of transcripts that temporally segregate the predisposition of epidermal stem cells to respond to cues that regulate their proliferation or differentiation, such as TGFβ and calcium.\n[3] Accordingly, circadian arrhythmia profoundly affects stem cell function in culture and in vivo.\n[4] We hypothesize that this intricate mechanism ensures homeostasis by providing epidermal stem cells with environmentally relevant temporal functional cues during the course of the day and that its perturbation may contribute to aging and carcinogenesis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1008, "doc_id": 2547636, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [2547636], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RUNX1 is downregulated or mutated in TLX1 T-ALL.\n\nDocument title: Reverse engineering of TLX oncogenic transcriptional networks identifies RUNX1 as tumor suppressor in T-ALL\n\nAbstract sentences:\n[0] The TLX1 and TLX3 transcription factor oncogenes have a key role in the pathogenesis of T cell acute lymphoblastic leukemia (T-ALL).\n[1] Here we used reverse engineering of global transcriptional networks to decipher the oncogenic regulatory circuit controlled by TLX1 and TLX3.\n[2] This systems biology analysis defined T cell leukemia homeobox 1 (TLX1) and TLX3 as master regulators of an oncogenic transcriptional circuit governing T-ALL.\n[3] Notably, a network structure analysis of this hierarchical network identified RUNX1 as a key mediator of the T-ALL induced by TLX1 and TLX3 and predicted a tumor-suppressor role for RUNX1 in T cell transformation.\n[4] Consistent with these results, we identified recurrent somatic loss-of-function mutations in RUNX1 in human T-ALL.\n[5] Overall, these results place TLX1 and TLX3 at the top of an oncogenic transcriptional network controlling leukemia development, show the power of network analyses to identify key elements in the regulatory circuits governing human cancer and identify RUNX1 as a tumor-suppressor gene in T-ALL."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Notably, a network structure analysis of this hierarchical network identified RUNX1 as a key mediator of the T-ALL induced by TLX1 and TLX3 and predicted a tumor-suppressor role for RUNX1 in T cell transformation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1009, "doc_id": 1982286, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [1982286], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: RUNX1 is downregulated or mutated in TLX1 T-ALL.\n\nDocument title: Reverse engineering of TLX oncogenic transcriptional networks identifies RUNX1 as tumor suppressor in T-ALL\n\nAbstract sentences:\n[0] The TLX1 and TLX3 transcription factor oncogenes have a key role in the pathogenesis of T cell acute lymphoblastic leukemia (T-ALL).\n[1] Here we used reverse engineering of global transcriptional networks to decipher the oncogenic regulatory circuit controlled by TLX1 and TLX3.\n[2] This systems biology analysis defined T cell leukemia homeobox 1 (TLX1) and TLX3 as master regulators of an oncogenic transcriptional circuit governing T-ALL.\n[3] Notably, a network structure analysis of this hierarchical network identified RUNX1 as a key mediator of the T-ALL induced by TLX1 and TLX3 and predicted a tumor-suppressor role for RUNX1 in T cell transformation.\n[4] Consistent with these results, we identified recurrent somatic loss-of-function mutations in RUNX1 in human T-ALL.\n[5] Overall, these results place TLX1 and TLX3 at the top of an oncogenic transcriptional network controlling leukemia development, show the power of network analyses to identify key elements in the regulatory circuits governing human cancer and identify RUNX1 as a tumor-suppressor gene in T-ALL."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Overall, these results place TLX1 and TLX3 at the top of an oncogenic transcriptional network controlling leukemia development, show the power of network analyses to identify key elements in the regulatory circuits governing human cancer and identify RUNX1 as a tumor-suppressor gene in T-ALL.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1009, "doc_id": 1982286, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [1982286], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Radioiodine treatment of non-toxic multinodular goitre increases thyroid volume.\n\nDocument title: Radioiodine treatment of multinodular non-toxic goitre.\n\nAbstract sentences:\n[0] OBJECTIVE To investigate the long term effect of radioactive iodine on thyroid function and size in patients with non-toxic multinodular goitre.\n[1] DESIGN Consecutive patients with multinodular non-toxic goitre selected for radioactive iodine treatment and followed for a minimum of 12 months (median 48 months) after an intended dose of 3.7 MBq/g thyroid tissue corrected to a 100% uptake of iodine-131 in 24 hours.\n[2] PATIENTS 69 patients with a growing multinodular non-toxic goitre causing local compression symptoms or cosmetic inconveniences.\n[3] The treatment was chosen because of a high operative risk, previous thyroidectomy, or refusal to be operated on.\n[4] MAIN OUTCOME MEASUREMENTS Standard thyroid function variables and ultrasonically determined thyroid volume before treatment as well as 1, 2, 3, 6, and 12 months after treatment and then once a year.\n[5] RESULTS 56 patients were treated with a single dose of 131I, 12 with two doses, and one with four doses.\n[6] In 45 patients treated with one dose and remaining euthyroid the median thyroid volume was reduced from 73 (interquartile range 50-106) ml to 29 (23-48) ml at 24 months in the 39 patients in whom this was measured during follow up.\n[7] The median reduction was 40 (22-48) ml (60% reduction, p < 0.0001), half of which occurred within three months.\n[8] Patients treated with two doses as well as those developing hypothyroidism and hyperthyroidism had a significant reduction in thyroid volume.\n[9] Eleven patients developed hypothyroidism (cumulative five year risk 22%, 95% confidence interval 4.8% to 38.4%).\n[10] Side effects were few: three cases of hyperthyroidism and two cases of radiation thyroiditis.\n[11] Only one patient was dissatisfied with the result; she was referred for operation six months after treatment.\n[12] CONCLUSIONS A substantial reduction in thyroid volume accompanied by a low incidence of hypothyroidism and few side effects makes the use of radioactive iodine an attractive alternative to surgery in selected cases of non-toxic multinodular goitre."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"In 45 patients treated with one dose and remaining euthyroid the median thyroid volume was reduced from 73 (interquartile range 50-106) ml to 29 (23-48) ml at 24 months in the 39 patients in whom this was measured during follow up.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1011, "doc_id": 9745001, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [9745001], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Radioiodine treatment of non-toxic multinodular goitre increases thyroid volume.\n\nDocument title: Radioiodine treatment of multinodular non-toxic goitre.\n\nAbstract sentences:\n[0] OBJECTIVE To investigate the long term effect of radioactive iodine on thyroid function and size in patients with non-toxic multinodular goitre.\n[1] DESIGN Consecutive patients with multinodular non-toxic goitre selected for radioactive iodine treatment and followed for a minimum of 12 months (median 48 months) after an intended dose of 3.7 MBq/g thyroid tissue corrected to a 100% uptake of iodine-131 in 24 hours.\n[2] PATIENTS 69 patients with a growing multinodular non-toxic goitre causing local compression symptoms or cosmetic inconveniences.\n[3] The treatment was chosen because of a high operative risk, previous thyroidectomy, or refusal to be operated on.\n[4] MAIN OUTCOME MEASUREMENTS Standard thyroid function variables and ultrasonically determined thyroid volume before treatment as well as 1, 2, 3, 6, and 12 months after treatment and then once a year.\n[5] RESULTS 56 patients were treated with a single dose of 131I, 12 with two doses, and one with four doses.\n[6] In 45 patients treated with one dose and remaining euthyroid the median thyroid volume was reduced from 73 (interquartile range 50-106) ml to 29 (23-48) ml at 24 months in the 39 patients in whom this was measured during follow up.\n[7] The median reduction was 40 (22-48) ml (60% reduction, p < 0.0001), half of which occurred within three months.\n[8] Patients treated with two doses as well as those developing hypothyroidism and hyperthyroidism had a significant reduction in thyroid volume.\n[9] Eleven patients developed hypothyroidism (cumulative five year risk 22%, 95% confidence interval 4.8% to 38.4%).\n[10] Side effects were few: three cases of hyperthyroidism and two cases of radiation thyroiditis.\n[11] Only one patient was dissatisfied with the result; she was referred for operation six months after treatment.\n[12] CONCLUSIONS A substantial reduction in thyroid volume accompanied by a low incidence of hypothyroidism and few side effects makes the use of radioactive iodine an attractive alternative to surgery in selected cases of non-toxic multinodular goitre."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"CONCLUSIONS A substantial reduction in thyroid volume accompanied by a low incidence of hypothyroidism and few side effects makes the use of radioactive iodine an attractive alternative to surgery in selected cases of non-toxic multinodular goitre.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1011, "doc_id": 9745001, "label": "CONTRADICTS", "evidence_sentence_ids": [12], "cited_doc_ids": [9745001], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Rapamycin delays aging in fruit flies.\n\nDocument title: Mechanisms of Life Span Extension by Rapamycin in the Fruit Fly Drosophila melanogaster\n\nAbstract sentences:\n[0] The target of rapamycin (TOR) pathway is a major nutrient-sensing pathway that, when genetically downregulated, increases life span in evolutionarily diverse organisms including mammals.\n[1] The central component of this pathway, TOR kinase, is the target of the inhibitory drug rapamycin, a highly specific and well-described drug approved for human use.\n[2] We show here that feeding rapamycin to adult Drosophila produces the life span extension seen in some TOR mutants.\n[3] Increase in life span by rapamycin was associated with increased resistance to both starvation and paraquat.\n[4] Analysis of the underlying mechanisms revealed that rapamycin increased longevity specifically through the TORC1 branch of the TOR pathway, through alterations to both autophagy and translation.\n[5] Rapamycin could increase life span of weak insulin/Igf signaling (IIS) pathway mutants and of flies with life span maximized by dietary restriction, indicating additional mechanisms."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"We show here that feeding rapamycin to adult Drosophila produces the life span extension seen in some TOR mutants.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1015, "doc_id": 6277638, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [6277638], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Rapamycin increases the concentration of triacylglycerols in fruit flies.\n\nDocument title: Mechanisms of Life Span Extension by Rapamycin in the Fruit Fly Drosophila melanogaster\n\nAbstract sentences:\n[0] The target of rapamycin (TOR) pathway is a major nutrient-sensing pathway that, when genetically downregulated, increases life span in evolutionarily diverse organisms including mammals.\n[1] The central component of this pathway, TOR kinase, is the target of the inhibitory drug rapamycin, a highly specific and well-described drug approved for human use.\n[2] We show here that feeding rapamycin to adult Drosophila produces the life span extension seen in some TOR mutants.\n[3] Increase in life span by rapamycin was associated with increased resistance to both starvation and paraquat.\n[4] Analysis of the underlying mechanisms revealed that rapamycin increased longevity specifically through the TORC1 branch of the TOR pathway, through alterations to both autophagy and translation.\n[5] Rapamycin could increase life span of weak insulin/Igf signaling (IIS) pathway mutants and of flies with life span maximized by dietary restriction, indicating additional mechanisms."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1016, "doc_id": 6277638, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [6277638], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Rapid phosphotransfer rates are correlated with histidine kinase regulator specificity.\n\nDocument title: Using Structural Information to Change the Phosphotransfer Specificity of a Two-Component Chemotaxis Signalling Complex\n\nAbstract sentences:\n[0] Two-component signal transduction pathways comprising histidine protein kinases (HPKs) and their response regulators (RRs) are widely used to control bacterial responses to environmental challenges.\n[1] Some bacteria have over 150 different two-component pathways, and the specificity of the phosphotransfer reactions within these systems is tightly controlled to prevent unwanted crosstalk.\n[2] One of the best understood two-component signalling pathways is the chemotaxis pathway.\n[3] Here, we present the 1.40 A crystal structure of the histidine-containing phosphotransfer domain of the chemotaxis HPK, CheA(3), in complex with its cognate RR, CheY(6).\n[4] A methionine finger on CheY(6) that nestles in a hydrophobic pocket in CheA(3) was shown to be important for the interaction and was found to only occur in the cognate RRs of CheA(3), CheY(6), and CheB(2).\n[5] Site-directed mutagenesis of this methionine in combination with two adjacent residues abolished binding, as shown by surface plasmon resonance studies, and phosphotransfer from CheA(3)-P to CheY(6).\n[6] Introduction of this methionine and an adjacent alanine residue into a range of noncognate CheYs, dramatically changed their specificity, allowing protein interaction and rapid phosphotransfer from CheA(3)-P. The structure presented here has allowed us to identify specificity determinants for the CheA-CheY interaction and subsequently to successfully reengineer phosphotransfer signalling.\n[7] In summary, our results provide valuable insight into how cells mediate specificity in one of the most abundant signalling pathways in biology, two-component signal transduction."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Introduction of this methionine and an adjacent alanine residue into a range of noncognate CheYs, dramatically changed their specificity, allowing protein interaction and rapid phosphotransfer from CheA(3)-P. The structure presented here has allowed us to identify specificity determinants for the CheA-CheY interaction and subsequently to successfully reengineer phosphotransfer signalling.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1018, "doc_id": 11603066, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [11603066], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Recognition of start codons depends on the translation initiation factor IF3.\n\nDocument title: Large-Scale Movements of IF3 and tRNA during Bacterial Translation Initiation\n\nAbstract sentences:\n[0] In bacterial translational initiation, three initiation factors (IFs 1-3) enable the selection of initiator tRNA and the start codon in the P site of the 30S ribosomal subunit.\n[1] Here, we report 11 single-particle cryo-electron microscopy (cryoEM) reconstructions of the complex of bacterial 30S subunit with initiator tRNA, mRNA, and IFs 1-3, representing different steps along the initiation pathway.\n[2] IF1 provides key anchoring points for IF2 and IF3, thereby enhancing their activities.\n[3] IF2 positions a domain in an extended conformation appropriate for capturing the formylmethionyl moiety charged on tRNA.\n[4] IF3 and tRNA undergo large conformational changes to facilitate the accommodation of the formylmethionyl-tRNA (fMet-tRNA(fMet)) into the P site for start codon recognition."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"IF3 and tRNA undergo large conformational changes to facilitate the accommodation of the formylmethionyl-tRNA (fMet-tRNA(fMet)) into the P site for start codon recognition.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1023, "doc_id": 16927286, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [16927286], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Reduced levels of lipolysis leads to higher P38 phosphorylation in adipose tissue.\n\nDocument title: Activation of AMPKα2 in adipocytes is essential for nicotine-induced insulin resistance in vivo\n\nAbstract sentences:\n[0] Cigarette smoking promotes body weight reduction in humans while paradoxically also promoting insulin resistance (IR) and hyperinsulinemia.\n[1] However, the mechanisms behind these effects are unclear.\n[2] Here we show that nicotine, a major constituent of cigarette smoke, selectively activates AMP-activated protein kinase α2 (AMPKα2) in adipocytes, which in turn phosphorylates MAP kinase phosphatase-1 (MKP1) at serine 334, initiating its proteasome-dependent degradation.\n[3] The nicotine-dependent reduction of MKP1 induces the aberrant activation of both p38 mitogen-activated protein kinase and c-Jun N-terminal kinase, leading to increased phosphorylation of insulin receptor substrate 1 (IRS1) at serine 307.\n[4] Phosphorylation of IRS1 leads to its degradation, protein kinase B inhibition, and the loss of insulin-mediated inhibition of lipolysis.\n[5] Consequently, nicotine increases lipolysis, which results in body weight reduction, but this increase also elevates the levels of circulating free fatty acids and thus causes IR in insulin-sensitive tissues.\n[6] These results establish AMPKα2 as an essential mediator of nicotine-induced whole-body IR in spite of reductions in adiposity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1025, "doc_id": 32408470, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [32408470], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Reduced phosphorylation of PP2A increases HDAC4 dephosphorylation by enhancing PP2A-HDAC4 interaction.\n\nDocument title: Nuclear accumulation of HDAC4 in ATM deficiency promotes neurodegeneration in ataxia-telangiectasia\n\nAbstract sentences:\n[0] Ataxia telangiectasia is a neurodegenerative disease caused by mutation of the Atm gene.\n[1] Here we report that ataxia telangiectasia mutated (ATM) deficiency causes nuclear accumulation of histone deacetylase 4 (HDAC4) in neurons and promotes neurodegeneration.\n[2] Nuclear HDAC4 binds to chromatin, as well as to myocyte enhancer factor 2A (MEF2A) and cAMP-responsive element binding protein (CREB), leading to histone deacetylation and altered neuronal gene expression.\n[3] Blocking either HDAC4 activity or its nuclear accumulation blunts these neurodegenerative changes and rescues several behavioral abnormalities of ATM-deficient mice.\n[4] Full rescue of the neurodegeneration, however, also requires the presence of HDAC4 in the cytoplasm, suggesting that the ataxia telangiectasia phenotype results both from a loss of cytoplasmic HDAC4 as well as its nuclear accumulation.\n[5] To remain cytoplasmic, HDAC4 must be phosphorylated.\n[6] The activity of the HDAC4 phosphatase, protein phosphatase 2A (PP2A), is downregulated by ATM-mediated phosphorylation.\n[7] In ATM deficiency, enhanced PP2A activity leads to HDAC4 dephosphorylation and the nuclear accumulation of HDAC4.\n[8] Our results define a crucial role of the cellular localization of HDAC4 in the events leading to ataxia telangiectasia neurodegeneration."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1026, "doc_id": 3113630, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [3113630], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Reduced phosphorylation of PP2A suppresses HDAC4 dephosphorylation.\n\nDocument title: Nuclear accumulation of HDAC4 in ATM deficiency promotes neurodegeneration in ataxia-telangiectasia\n\nAbstract sentences:\n[0] Ataxia telangiectasia is a neurodegenerative disease caused by mutation of the Atm gene.\n[1] Here we report that ataxia telangiectasia mutated (ATM) deficiency causes nuclear accumulation of histone deacetylase 4 (HDAC4) in neurons and promotes neurodegeneration.\n[2] Nuclear HDAC4 binds to chromatin, as well as to myocyte enhancer factor 2A (MEF2A) and cAMP-responsive element binding protein (CREB), leading to histone deacetylation and altered neuronal gene expression.\n[3] Blocking either HDAC4 activity or its nuclear accumulation blunts these neurodegenerative changes and rescues several behavioral abnormalities of ATM-deficient mice.\n[4] Full rescue of the neurodegeneration, however, also requires the presence of HDAC4 in the cytoplasm, suggesting that the ataxia telangiectasia phenotype results both from a loss of cytoplasmic HDAC4 as well as its nuclear accumulation.\n[5] To remain cytoplasmic, HDAC4 must be phosphorylated.\n[6] The activity of the HDAC4 phosphatase, protein phosphatase 2A (PP2A), is downregulated by ATM-mediated phosphorylation.\n[7] In ATM deficiency, enhanced PP2A activity leads to HDAC4 dephosphorylation and the nuclear accumulation of HDAC4.\n[8] Our results define a crucial role of the cellular localization of HDAC4 in the events leading to ataxia telangiectasia neurodegeneration."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1027, "doc_id": 3113630, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [3113630], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Reduced responsiveness to interleukin-2 in regulatory T cells is associated with autoimmune diseases such as Type 1 Diabetes.\n\nDocument title: Interleukin-2 gene variation impairs regulatory T cell function and causes autoimmunity\n\nAbstract sentences:\n[0] Autoimmune diseases are thought to result from imbalances in normal immune physiology and regulation.\n[1] Here, we show that autoimmune disease susceptibility and resistance alleles on mouse chromosome 3 (Idd3) correlate with differential expression of the key immunoregulatory cytokine interleukin-2 (IL-2).\n[2] In order to test directly that an approximately twofold reduction in IL-2 underpins the Idd3-linked destabilization of immune homeostasis, we show that engineered haplodeficiency of Il2 gene expression not only reduces T cell IL-2 production by twofold but also mimics the autoimmune dysregulatory effects of the naturally occurring susceptibility alleles of Il2.\n[3] Reduced IL-2 production achieved by either genetic mechanism correlates with reduced function of CD4+ CD25+ regulatory T cells, which are critical for maintaining immune homeostasis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2, 3]\nExplanation: Evidence states: \"In order to test directly that an approximately twofold reduction in IL-2 underpins the Idd3-linked destabilization of immune homeostasis, we show that engineered haplodeficiency of Il2 gene expression not only reduces T cell IL-2 production by twofold but also mimics the autoimmune dysregulatory effects of the naturally occurring susceptibility alleles of Il2. Reduced IL-2 production achieved by either genetic mechanism correlates with reduced function of CD4+ CD25+ regulatory T cells, which are critical for maintaining immune homeostasis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1028, "doc_id": 13923140, "label": "SUPPORTS", "evidence_sentence_ids": [2, 3], "cited_doc_ids": [13923140, 11899391], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Reduced responsiveness to interleukin-2 in regulatory T cells is associated with autoimmune diseases such as Type 1 Diabetes.\n\nDocument title: Type 1 diabetes-associated IL2RA variation lowers IL-2 signaling and contributes to diminished CD4+CD25+ regulatory T cell function.\n\nAbstract sentences:\n[0] Numerous reports have demonstrated that CD4(+)CD25(+) regulatory T cells (Tregs) from individuals with a range of human autoimmune diseases, including type 1 diabetes, are deficient in their ability to control autologous proinflammatory responses when compared with nondiseased, control individuals.\n[1] Treg dysfunction could be a primary, causal event or may result from perturbations in the immune system during disease development.\n[2] Polymorphisms in genes associated with Treg function, such as IL2RA, confer a higher risk of autoimmune disease.\n[3] Although this suggests a primary role for defective Tregs in autoimmunity, a link between IL2RA gene polymorphisms and Treg function has not been examined.\n[4] We addressed this by examining the impact of an IL2RA haplotype associated with type 1 diabetes on Treg fitness and suppressive function.\n[5] Studies were conducted using healthy human subjects to avoid any confounding effects of disease.\n[6] We demonstrated that the presence of an autoimmune disease-associated IL2RA haplotype correlates with diminished IL-2 responsiveness in Ag-experienced CD4(+) T cells, as measured by phosphorylation of STAT5a, and is associated with lower levels of FOXP3 expression by Tregs and a reduction in their ability to suppress proliferation of autologous effector T cells.\n[7] These data offer a rationale that contributes to the molecular and cellular mechanisms through which polymorphisms in the IL-2RA gene affect immune regulation, and consequently upon susceptibility to autoimmune and inflammatory diseases."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"We demonstrated that the presence of an autoimmune disease-associated IL2RA haplotype correlates with diminished IL-2 responsiveness in Ag-experienced CD4(+) T cells, as measured by phosphorylation of STAT5a, and is associated with lower levels of FOXP3 expression by Tregs and a reduction in their ability to suppress proliferation of autologous effector T cells.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1028, "doc_id": 11899391, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [13923140, 11899391], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Reducing H3k4me3 methylation induces mouse epiblast stem cells to naive pluripotency efficiently.\n\nDocument title: MLL1 Inhibition Reprograms Epiblast Stem Cells to Naive Pluripotency.\n\nAbstract sentences:\n[0] The interconversion between naive and primed pluripotent states is accompanied by drastic epigenetic rearrangements.\n[1] However, it is unclear whether intrinsic epigenetic events can drive reprogramming to naive pluripotency or if distinct chromatin states are instead simply a reflection of discrete pluripotent states.\n[2] Here, we show that blocking histone H3K4 methyltransferase MLL1 activity with the small-molecule inhibitor MM-401 reprograms mouse epiblast stem cells (EpiSCs) to naive pluripotency.\n[3] This reversion is highly efficient and synchronized, with more than 50% of treated EpiSCs exhibiting features of naive embryonic stem cells (ESCs) within 3 days.\n[4] Reverted ESCs reactivate the silenced X chromosome and contribute to embryos following blastocyst injection, generating germline-competent chimeras.\n[5] Importantly, blocking MLL1 leads to global redistribution of H3K4me1 at enhancers and represses lineage determinant factors and EpiSC markers, which indirectly regulate ESC transcription circuitry.\n[6] These findings show that discrete perturbation of H3K4 methylation is sufficient to drive reprogramming to naive pluripotency."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here, we show that blocking histone H3K4 methyltransferase MLL1 activity with the small-molecule inhibitor MM-401 reprograms mouse epiblast stem cells (EpiSCs) to naive pluripotency.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1030, "doc_id": 6441369, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [6441369], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Reduction of Rpl38 alters the composition of the Hox gene mRNAs translation in mice without lowering overall protein synthesis.\n\nDocument title: Ribosome-Mediated Specificity in Hox mRNA Translation and Vertebrate Tissue Patterning\n\nAbstract sentences:\n[0] Historically, the ribosome has been viewed as a complex ribozyme with constitutive rather than regulatory capacity in mRNA translation.\n[1] Here we identify mutations of the Ribosomal Protein L38 (Rpl38) gene in mice exhibiting surprising tissue-specific patterning defects, including pronounced homeotic transformations of the axial skeleton.\n[2] In Rpl38 mutant embryos, global protein synthesis is unchanged; however the translation of a select subset of Homeobox mRNAs is perturbed.\n[3] Our data reveal that RPL38 facilitates 80S complex formation on these mRNAs as a regulatory component of the ribosome to confer transcript-specific translational control.\n[4] We further show that Rpl38 expression is markedly enriched in regions of the embryo where loss-of-function phenotypes occur.\n[5] Unexpectedly, a ribosomal protein (RP) expression screen reveals dynamic regulation of individual RPs within the vertebrate embryo.\n[6] Collectively, these findings suggest that RP activity may be highly regulated to impart a new layer of specificity in the control of gene expression and mammalian development."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"In Rpl38 mutant embryos, global protein synthesis is unchanged; however the translation of a select subset of Homeobox mRNAs is perturbed.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1031, "doc_id": 12486491, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [12486491], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Reduction of purity of cytoplasmic membranes isolated from overexpressors is indicated by stronger spots for OmpA in 2D BN-PAGE gels.\n\nDocument title: Identification of a Multicomponent Complex Required for Outer Membrane Biogenesis in Escherichia coli\n\nAbstract sentences:\n[0] Gram-negative bacteria have an outer membrane (OM) that functions as a barrier to protect the cell from toxic compounds such as antibiotics and detergents.\n[1] The OM is a highly asymmetric bilayer composed of phospholipids, glycolipids, and proteins.\n[2] Assembly of this essential organelle occurs outside the cytoplasm in an environment that lacks obvious energy sources such as ATP, and the mechanisms involved are poorly understood.\n[3] We describe the identification of a multiprotein complex required for the assembly of proteins in the OM of Escherichia coli.\n[4] We also demonstrate genetic interactions between genes encoding components of this protein assembly complex and imp, which encodes a protein involved in the assembly of lipopolysaccharides (LPS) in the OM.\n[5] These genetic interactions suggest a role for YfgL, one of the lipoprotein components of the protein assembly complex, in a homeostatic control mechanism that coordinates the overall OM assembly process."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1032, "doc_id": 6836086, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [6836086], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Reduction of purity of cytoplasmic membranes isolated from overexpressors is indicated by stronger spots for OmpF in 2D BN-PAGE gels.\n\nDocument title: Identification of a Multicomponent Complex Required for Outer Membrane Biogenesis in Escherichia coli\n\nAbstract sentences:\n[0] Gram-negative bacteria have an outer membrane (OM) that functions as a barrier to protect the cell from toxic compounds such as antibiotics and detergents.\n[1] The OM is a highly asymmetric bilayer composed of phospholipids, glycolipids, and proteins.\n[2] Assembly of this essential organelle occurs outside the cytoplasm in an environment that lacks obvious energy sources such as ATP, and the mechanisms involved are poorly understood.\n[3] We describe the identification of a multiprotein complex required for the assembly of proteins in the OM of Escherichia coli.\n[4] We also demonstrate genetic interactions between genes encoding components of this protein assembly complex and imp, which encodes a protein involved in the assembly of lipopolysaccharides (LPS) in the OM.\n[5] These genetic interactions suggest a role for YfgL, one of the lipoprotein components of the protein assembly complex, in a homeostatic control mechanism that coordinates the overall OM assembly process."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1033, "doc_id": 6836086, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [6836086], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Removal of H3K9me3 by ectopic expression of other H3K9 demethylases decreases reprogramming efficiency in SCNT experiments.\n\nDocument title: H3K9 demethylase KDM4E is an epigenetic regulator for bovine embryonic development and a defective factor for nuclear reprogramming.\n\nAbstract sentences:\n[0] Aberrant epigenetic reprogramming often results in developmental defects in somatic cell nuclear transfer (SCNT) embryos during embryonic genome activation (EGA).\n[1] Bovine eight-cell SCNT embryos exhibit global hypermethylation of histone H3 lysine 9 tri- and di-methylation (H3K9me3/2), but the intrinsic reason for this remains elusive.\n[2] Here, we provide evidence that two H3K9 demethylase genes, lysine-specific demethylase 4D (KDM4D) and 4E (KDM4E), are related to active H3K9me3/2 demethylation in in vitro fertilized (IVF) embryos and are deficiently expressed in cloned embryos at the time of EGA.\n[3] Moreover, KDM4E plays a more crucial role in IVF and SCNT embryonic development, and overexpression of KDM4E can restore the global transcriptome, improve blastocyst formation and increase the cloning efficiency of SCNT embryos.\n[4] Our results thereby indicate that KDM4E can function as a crucial epigenetic regulator of EGA and as an internal defective factor responsible for persistent H3K9me3/2 barriers to SCNT-mediated reprogramming.\n[5] Furthermore, we show that interactions between RNA and KDM4E are essential for H3K9 demethylation during EGA.\n[6] These observations advance the understanding of incomplete nuclear reprogramming and are of great importance for transgenic cattle procreation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Moreover, KDM4E plays a more crucial role in IVF and SCNT embryonic development, and overexpression of KDM4E can restore the global transcriptome, improve blastocyst formation and increase the cloning efficiency of SCNT embryos.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1034, "doc_id": 4547102, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [4547102], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Removal of H3K9me3 by ectopic expression of other H3K9 demethylases improves reprogramming efficiency in SCNT experiments.\n\nDocument title: H3K9 demethylase KDM4E is an epigenetic regulator for bovine embryonic development and a defective factor for nuclear reprogramming.\n\nAbstract sentences:\n[0] Aberrant epigenetic reprogramming often results in developmental defects in somatic cell nuclear transfer (SCNT) embryos during embryonic genome activation (EGA).\n[1] Bovine eight-cell SCNT embryos exhibit global hypermethylation of histone H3 lysine 9 tri- and di-methylation (H3K9me3/2), but the intrinsic reason for this remains elusive.\n[2] Here, we provide evidence that two H3K9 demethylase genes, lysine-specific demethylase 4D (KDM4D) and 4E (KDM4E), are related to active H3K9me3/2 demethylation in in vitro fertilized (IVF) embryos and are deficiently expressed in cloned embryos at the time of EGA.\n[3] Moreover, KDM4E plays a more crucial role in IVF and SCNT embryonic development, and overexpression of KDM4E can restore the global transcriptome, improve blastocyst formation and increase the cloning efficiency of SCNT embryos.\n[4] Our results thereby indicate that KDM4E can function as a crucial epigenetic regulator of EGA and as an internal defective factor responsible for persistent H3K9me3/2 barriers to SCNT-mediated reprogramming.\n[5] Furthermore, we show that interactions between RNA and KDM4E are essential for H3K9 demethylation during EGA.\n[6] These observations advance the understanding of incomplete nuclear reprogramming and are of great importance for transgenic cattle procreation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Moreover, KDM4E plays a more crucial role in IVF and SCNT embryonic development, and overexpression of KDM4E can restore the global transcriptome, improve blastocyst formation and increase the cloning efficiency of SCNT embryos.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1035, "doc_id": 4547102, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [4547102], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Removal of H3K9me3 improves reprogramming efficiency in human somatic cell nuclear transfer experiments.\n\nDocument title: H3K9 demethylase KDM4E is an epigenetic regulator for bovine embryonic development and a defective factor for nuclear reprogramming.\n\nAbstract sentences:\n[0] Aberrant epigenetic reprogramming often results in developmental defects in somatic cell nuclear transfer (SCNT) embryos during embryonic genome activation (EGA).\n[1] Bovine eight-cell SCNT embryos exhibit global hypermethylation of histone H3 lysine 9 tri- and di-methylation (H3K9me3/2), but the intrinsic reason for this remains elusive.\n[2] Here, we provide evidence that two H3K9 demethylase genes, lysine-specific demethylase 4D (KDM4D) and 4E (KDM4E), are related to active H3K9me3/2 demethylation in in vitro fertilized (IVF) embryos and are deficiently expressed in cloned embryos at the time of EGA.\n[3] Moreover, KDM4E plays a more crucial role in IVF and SCNT embryonic development, and overexpression of KDM4E can restore the global transcriptome, improve blastocyst formation and increase the cloning efficiency of SCNT embryos.\n[4] Our results thereby indicate that KDM4E can function as a crucial epigenetic regulator of EGA and as an internal defective factor responsible for persistent H3K9me3/2 barriers to SCNT-mediated reprogramming.\n[5] Furthermore, we show that interactions between RNA and KDM4E are essential for H3K9 demethylation during EGA.\n[6] These observations advance the understanding of incomplete nuclear reprogramming and are of great importance for transgenic cattle procreation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Moreover, KDM4E plays a more crucial role in IVF and SCNT embryonic development, and overexpression of KDM4E can restore the global transcriptome, improve blastocyst formation and increase the cloning efficiency of SCNT embryos.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1036, "doc_id": 4547102, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [4547102], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Replacement of OCT4 and SOX2 genes with GATA3 has the ability to reprogram human cells.\n\nDocument title: Reprogramming of human fibroblasts to pluripotency with lineage specifiers.\n\nAbstract sentences:\n[0] Since the initial discovery that OCT4, SOX2, KLF4, and c-MYC overexpression sufficed for the induction of pluripotency in somatic cells, methodologies replacing the original factors have enhanced our understanding of the reprogramming process.\n[1] However, unlike in mouse, OCT4 has not been replaced successfully during reprogramming of human cells.\n[2] Here we report on a strategy to accomplish this replacement.\n[3] Through a combination of transcriptome and bioinformatic analysis we have identified factors previously characterized as being lineage specifiers that are able to replace OCT4 and SOX2 in the reprogramming of human fibroblasts.\n[4] Our results show that it is possible to replace OCT4 and SOX2 simultaneously with alternative lineage specifiers in the reprogramming of human cells.\n[5] At a broader level, they also support a model in which counteracting lineage specification networks underlies the induction of pluripotency."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1037, "doc_id": 16287725, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [16287725], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Replacement of OCT4 and SOX2 genes with GATA3 is not capable of reprogramming human cells.\n\nDocument title: Reprogramming of human fibroblasts to pluripotency with lineage specifiers.\n\nAbstract sentences:\n[0] Since the initial discovery that OCT4, SOX2, KLF4, and c-MYC overexpression sufficed for the induction of pluripotency in somatic cells, methodologies replacing the original factors have enhanced our understanding of the reprogramming process.\n[1] However, unlike in mouse, OCT4 has not been replaced successfully during reprogramming of human cells.\n[2] Here we report on a strategy to accomplish this replacement.\n[3] Through a combination of transcriptome and bioinformatic analysis we have identified factors previously characterized as being lineage specifiers that are able to replace OCT4 and SOX2 in the reprogramming of human fibroblasts.\n[4] Our results show that it is possible to replace OCT4 and SOX2 simultaneously with alternative lineage specifiers in the reprogramming of human cells.\n[5] At a broader level, they also support a model in which counteracting lineage specification networks underlies the induction of pluripotency."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1038, "doc_id": 16287725, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [16287725], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Replacement of histone H2A with H2A.Z accelerates gene activation in yeasts by destabilizing +1 nucleosomes.\n\nDocument title: Nucleosome stability mediated by histone variants H3.3 and H2A.Z.\n\nAbstract sentences:\n[0] Nucleosomes containing the histone variant H3.3 tend to be clustered in vivo in the neighborhood of transcriptionally active genes and over regulatory elements.\n[1] It has not been clear, however, whether H3.3-containing nucleosomes possess unique properties that would affect transcription.\n[2] We report here that H3.3 nucleosomes isolated from vertebrates, regardless of whether they are partnered with H2A or H2A.Z, are unusually sensitive to salt-dependent disruption, losing H2A/H2B or H2A.Z/H2B dimers.\n[3] Immunoprecipitation studies of nucleosome core particles (NCPs) show that NCPs that contain both H3.3 and H2A.Z are even less stable than NCPs containing H3.3 and H2A.\n[4] Intriguingly, NCPs containing H3 and H2A.Z are at least as stable as H3/H2A NCPs.\n[5] These results establish an hierarchy of stabilities for native nucleosomes carrying different complements of variants, and suggest how H2A.Z could play different roles depending on its partners within the NCP.\n[6] They also are consistent with the idea that H3.3 plays an active role in maintaining accessible chromatin structures in enhancer regions and transcribed regions.\n[7] Consistent with this idea, promoters and enhancers at transcriptionally active genes and coding regions at highly expressed genes have nucleosomes that simultaneously carry both H3.3 and H2A.Z, and should therefore be extremely sensitive to disruption."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Immunoprecipitation studies of nucleosome core particles (NCPs) show that NCPs that contain both H3.3 and H2A.Z are even less stable than NCPs containing H3.3 and H2A.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1040, "doc_id": 25254425, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [25254425, 16626264], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Repressing IL-18 has negative effects on atherosclerotic lesion composition and progression.\n\nDocument title: Expression of interleukin-18 in human atherosclerotic plaques and relation to plaque instability.\n\nAbstract sentences:\n[0] BACKGROUND Interleukin (IL)-18 is a potent proinflammatory cytokine with potential atherogenic properties.\n[1] Its expression and role in atherosclerosis, however, are unknown.\n[2] METHODS AND RESULTS In the present study, we examined stable and unstable human carotid atherosclerotic plaques retrieved by endarterectomy for the presence of IL-18 using reverse transcription-polymerase chain reaction (PCR), Western blot, and immunohistochemical techniques.\n[3] IL-18 was highly expressed in the atherosclerotic plaques compared with control normal arteries and was localized mainly in plaque macrophages.\n[4] IL-18 receptor was also upregulated in plaque macrophages and endothelial cells, suggesting potential biological effects.\n[5] To examine the role of IL-18 in atherosclerosis, we determined the relation between IL-18 mRNA expression and signs of plaque instability using real-time quantitative PCR.\n[6] Interestingly, significantly higher levels of IL-18 mRNA were found in symptomatic (unstable) plaques than asymptomatic (stable) plaques (P<0.01).\n[7] CONCLUSIONS These results suggest, for the first time, a major role for IL-18 in atherosclerotic plaque destabilization leading to acute ischemic syndromes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Interestingly, significantly higher levels of IL-18 mRNA were found in symptomatic (unstable) plaques than asymptomatic (stable) plaques (P<0.01).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1042, "doc_id": 17421851, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [17421851], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Repressing IL-18 has negative effects on atherosclerotic lesion composition and progression.\n\nDocument title: Expression of interleukin-18 in human atherosclerotic plaques and relation to plaque instability.\n\nAbstract sentences:\n[0] BACKGROUND Interleukin (IL)-18 is a potent proinflammatory cytokine with potential atherogenic properties.\n[1] Its expression and role in atherosclerosis, however, are unknown.\n[2] METHODS AND RESULTS In the present study, we examined stable and unstable human carotid atherosclerotic plaques retrieved by endarterectomy for the presence of IL-18 using reverse transcription-polymerase chain reaction (PCR), Western blot, and immunohistochemical techniques.\n[3] IL-18 was highly expressed in the atherosclerotic plaques compared with control normal arteries and was localized mainly in plaque macrophages.\n[4] IL-18 receptor was also upregulated in plaque macrophages and endothelial cells, suggesting potential biological effects.\n[5] To examine the role of IL-18 in atherosclerosis, we determined the relation between IL-18 mRNA expression and signs of plaque instability using real-time quantitative PCR.\n[6] Interestingly, significantly higher levels of IL-18 mRNA were found in symptomatic (unstable) plaques than asymptomatic (stable) plaques (P<0.01).\n[7] CONCLUSIONS These results suggest, for the first time, a major role for IL-18 in atherosclerotic plaque destabilization leading to acute ischemic syndromes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"CONCLUSIONS These results suggest, for the first time, a major role for IL-18 in atherosclerotic plaque destabilization leading to acute ischemic syndromes.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1042, "doc_id": 17421851, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [17421851], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Retinoic acid receptor-related orphan receptor gamma (RORγ) is a therapeutic target for castration-resistant prostate cancer (CRPC)\n\nDocument title: ROR-γ drives androgen receptor expression and represents a therapeutic target in castration-resistant prostate cancer\n\nAbstract sentences:\n[0] The androgen receptor (AR) is overexpressed and hyperactivated in human castration-resistant prostate cancer (CRPC).\n[1] However, the determinants of AR overexpression in CRPC are poorly defined.\n[2] Here we show that retinoic acid receptor-related orphan receptor γ (ROR-γ) is overexpressed and amplified in metastatic CRPC tumors, and that ROR-γ drives AR expression in the tumors.\n[3] ROR-γ recruits nuclear receptor coactivator 1 and 3 (NCOA1 and NCOA3, also known as SRC-1 and SRC-3) to an AR-ROR response element (RORE) to stimulate AR gene transcription.\n[4] ROR-γ antagonists suppress the expression of both AR and its variant AR-V7 in prostate cancer (PCa) cell lines and tumors.\n[5] ROR-γ antagonists also markedly diminish genome-wide AR binding, H3K27ac abundance and expression of the AR target gene network.\n[6] Finally, ROR-γ antagonists suppressed tumor growth in multiple AR-expressing, but not AR-negative, xenograft PCa models, and they effectively sensitized CRPC tumors to enzalutamide, without overt toxicity, in mice.\n[7] Taken together, these results establish ROR-γ as a key player in CRPC by acting upstream of AR and as a potential therapeutic target for advanced PCa."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Finally, ROR-γ antagonists suppressed tumor growth in multiple AR-expressing, but not AR-negative, xenograft PCa models, and they effectively sensitized CRPC tumors to enzalutamide, without overt toxicity, in mice.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1043, "doc_id": 17671145, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [17671145], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Retinoic acid receptor-related orphan receptor gamma (RORγ) is a therapeutic target for castration-resistant prostate cancer (CRPC)\n\nDocument title: ROR-γ drives androgen receptor expression and represents a therapeutic target in castration-resistant prostate cancer\n\nAbstract sentences:\n[0] The androgen receptor (AR) is overexpressed and hyperactivated in human castration-resistant prostate cancer (CRPC).\n[1] However, the determinants of AR overexpression in CRPC are poorly defined.\n[2] Here we show that retinoic acid receptor-related orphan receptor γ (ROR-γ) is overexpressed and amplified in metastatic CRPC tumors, and that ROR-γ drives AR expression in the tumors.\n[3] ROR-γ recruits nuclear receptor coactivator 1 and 3 (NCOA1 and NCOA3, also known as SRC-1 and SRC-3) to an AR-ROR response element (RORE) to stimulate AR gene transcription.\n[4] ROR-γ antagonists suppress the expression of both AR and its variant AR-V7 in prostate cancer (PCa) cell lines and tumors.\n[5] ROR-γ antagonists also markedly diminish genome-wide AR binding, H3K27ac abundance and expression of the AR target gene network.\n[6] Finally, ROR-γ antagonists suppressed tumor growth in multiple AR-expressing, but not AR-negative, xenograft PCa models, and they effectively sensitized CRPC tumors to enzalutamide, without overt toxicity, in mice.\n[7] Taken together, these results establish ROR-γ as a key player in CRPC by acting upstream of AR and as a potential therapeutic target for advanced PCa."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Taken together, these results establish ROR-γ as a key player in CRPC by acting upstream of AR and as a potential therapeutic target for advanced PCa.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1043, "doc_id": 17671145, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [17671145], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Rhythmic expression of Cry1 translates directly into a circadian regulation of cAMP signaling in gluconeogenesis.\n\nDocument title: Cryptochrome Mediates Circadian Regulation of cAMP Signaling and Hepatic Gluconeogenesis\n\nAbstract sentences:\n[0] During fasting, mammals maintain normal glucose homeostasis by stimulating hepatic gluconeogenesis.\n[1] Elevations in circulating glucagon and epinephrine, two hormones that activate hepatic gluconeogenesis, trigger the cAMP-mediated phosphorylation of cAMP response element-binding protein (Creb) and dephosphorylation of the Creb-regulated transcription coactivator-2 (Crtc2)--two key transcriptional regulators of this process.\n[2] Although the underlying mechanism is unclear, hepatic gluconeogenesis is also regulated by the circadian clock, which coordinates glucose metabolism with changes in the external environment.\n[3] Circadian control of gene expression is achieved by two transcriptional activators, Clock and Bmal1, which stimulate cryptochrome (Cry1 and Cry2) and Period (Per1, Per2 and Per3) repressors that feed back on Clock-Bmal1 activity.\n[4] Here we show that Creb activity during fasting is modulated by Cry1 and Cry2, which are rhythmically expressed in the liver.\n[5] Cry1 expression was elevated during the night-day transition, when it reduced fasting gluconeogenic gene expression by blocking glucagon-mediated increases in intracellular cAMP concentrations and in the protein kinase A-mediated phosphorylation of Creb.\n[6] In biochemical reconstitution studies, we found that Cry1 inhibited accumulation of cAMP in response to G protein-coupled receptor (GPCR) activation but not to forskolin, a direct activator of adenyl cyclase.\n[7] Cry proteins seemed to modulate GPCR activity directly through interaction with G(s)α.\n[8] As hepatic overexpression of Cry1 lowered blood glucose concentrations and improved insulin sensitivity in insulin-resistant db/db mice, our results suggest that compounds that enhance cryptochrome activity may provide therapeutic benefit to individuals with type 2 diabetes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Here we show that Creb activity during fasting is modulated by Cry1 and Cry2, which are rhythmically expressed in the liver.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1044, "doc_id": 22500262, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [22500262], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Rhythmic expression of Cry1 translates directly into a circadian regulation of cAMP signaling in gluconeogenesis.\n\nDocument title: Cryptochrome Mediates Circadian Regulation of cAMP Signaling and Hepatic Gluconeogenesis\n\nAbstract sentences:\n[0] During fasting, mammals maintain normal glucose homeostasis by stimulating hepatic gluconeogenesis.\n[1] Elevations in circulating glucagon and epinephrine, two hormones that activate hepatic gluconeogenesis, trigger the cAMP-mediated phosphorylation of cAMP response element-binding protein (Creb) and dephosphorylation of the Creb-regulated transcription coactivator-2 (Crtc2)--two key transcriptional regulators of this process.\n[2] Although the underlying mechanism is unclear, hepatic gluconeogenesis is also regulated by the circadian clock, which coordinates glucose metabolism with changes in the external environment.\n[3] Circadian control of gene expression is achieved by two transcriptional activators, Clock and Bmal1, which stimulate cryptochrome (Cry1 and Cry2) and Period (Per1, Per2 and Per3) repressors that feed back on Clock-Bmal1 activity.\n[4] Here we show that Creb activity during fasting is modulated by Cry1 and Cry2, which are rhythmically expressed in the liver.\n[5] Cry1 expression was elevated during the night-day transition, when it reduced fasting gluconeogenic gene expression by blocking glucagon-mediated increases in intracellular cAMP concentrations and in the protein kinase A-mediated phosphorylation of Creb.\n[6] In biochemical reconstitution studies, we found that Cry1 inhibited accumulation of cAMP in response to G protein-coupled receptor (GPCR) activation but not to forskolin, a direct activator of adenyl cyclase.\n[7] Cry proteins seemed to modulate GPCR activity directly through interaction with G(s)α.\n[8] As hepatic overexpression of Cry1 lowered blood glucose concentrations and improved insulin sensitivity in insulin-resistant db/db mice, our results suggest that compounds that enhance cryptochrome activity may provide therapeutic benefit to individuals with type 2 diabetes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Cry1 expression was elevated during the night-day transition, when it reduced fasting gluconeogenic gene expression by blocking glucagon-mediated increases in intracellular cAMP concentrations and in the protein kinase A-mediated phosphorylation of Creb.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1044, "doc_id": 22500262, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [22500262], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Rhythmic expression of Cry1 translates directly into a circadian regulation of cAMP signaling in hepatic glucose metabolism.\n\nDocument title: Cryptochrome Mediates Circadian Regulation of cAMP Signaling and Hepatic Gluconeogenesis\n\nAbstract sentences:\n[0] During fasting, mammals maintain normal glucose homeostasis by stimulating hepatic gluconeogenesis.\n[1] Elevations in circulating glucagon and epinephrine, two hormones that activate hepatic gluconeogenesis, trigger the cAMP-mediated phosphorylation of cAMP response element-binding protein (Creb) and dephosphorylation of the Creb-regulated transcription coactivator-2 (Crtc2)--two key transcriptional regulators of this process.\n[2] Although the underlying mechanism is unclear, hepatic gluconeogenesis is also regulated by the circadian clock, which coordinates glucose metabolism with changes in the external environment.\n[3] Circadian control of gene expression is achieved by two transcriptional activators, Clock and Bmal1, which stimulate cryptochrome (Cry1 and Cry2) and Period (Per1, Per2 and Per3) repressors that feed back on Clock-Bmal1 activity.\n[4] Here we show that Creb activity during fasting is modulated by Cry1 and Cry2, which are rhythmically expressed in the liver.\n[5] Cry1 expression was elevated during the night-day transition, when it reduced fasting gluconeogenic gene expression by blocking glucagon-mediated increases in intracellular cAMP concentrations and in the protein kinase A-mediated phosphorylation of Creb.\n[6] In biochemical reconstitution studies, we found that Cry1 inhibited accumulation of cAMP in response to G protein-coupled receptor (GPCR) activation but not to forskolin, a direct activator of adenyl cyclase.\n[7] Cry proteins seemed to modulate GPCR activity directly through interaction with G(s)α.\n[8] As hepatic overexpression of Cry1 lowered blood glucose concentrations and improved insulin sensitivity in insulin-resistant db/db mice, our results suggest that compounds that enhance cryptochrome activity may provide therapeutic benefit to individuals with type 2 diabetes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2, 3]\nExplanation: Evidence states: \"Although the underlying mechanism is unclear, hepatic gluconeogenesis is also regulated by the circadian clock, which coordinates glucose metabolism with changes in the external environment. Circadian control of gene expression is achieved by two transcriptional activators, Clock and Bmal1, which stimulate cryptochrome (Cry1 and Cry2) and Period (Per1, Per2 and Per3) repressors that feed back on Clock-Bmal1 activity.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1045, "doc_id": 22500262, "label": "SUPPORTS", "evidence_sentence_ids": [2, 3], "cited_doc_ids": [22500262], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Rhythmic expression of Cry1 translates directly into a circadian regulation of cAMP signaling in hepatic glucose metabolism.\n\nDocument title: Cryptochrome Mediates Circadian Regulation of cAMP Signaling and Hepatic Gluconeogenesis\n\nAbstract sentences:\n[0] During fasting, mammals maintain normal glucose homeostasis by stimulating hepatic gluconeogenesis.\n[1] Elevations in circulating glucagon and epinephrine, two hormones that activate hepatic gluconeogenesis, trigger the cAMP-mediated phosphorylation of cAMP response element-binding protein (Creb) and dephosphorylation of the Creb-regulated transcription coactivator-2 (Crtc2)--two key transcriptional regulators of this process.\n[2] Although the underlying mechanism is unclear, hepatic gluconeogenesis is also regulated by the circadian clock, which coordinates glucose metabolism with changes in the external environment.\n[3] Circadian control of gene expression is achieved by two transcriptional activators, Clock and Bmal1, which stimulate cryptochrome (Cry1 and Cry2) and Period (Per1, Per2 and Per3) repressors that feed back on Clock-Bmal1 activity.\n[4] Here we show that Creb activity during fasting is modulated by Cry1 and Cry2, which are rhythmically expressed in the liver.\n[5] Cry1 expression was elevated during the night-day transition, when it reduced fasting gluconeogenic gene expression by blocking glucagon-mediated increases in intracellular cAMP concentrations and in the protein kinase A-mediated phosphorylation of Creb.\n[6] In biochemical reconstitution studies, we found that Cry1 inhibited accumulation of cAMP in response to G protein-coupled receptor (GPCR) activation but not to forskolin, a direct activator of adenyl cyclase.\n[7] Cry proteins seemed to modulate GPCR activity directly through interaction with G(s)α.\n[8] As hepatic overexpression of Cry1 lowered blood glucose concentrations and improved insulin sensitivity in insulin-resistant db/db mice, our results suggest that compounds that enhance cryptochrome activity may provide therapeutic benefit to individuals with type 2 diabetes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Here we show that Creb activity during fasting is modulated by Cry1 and Cry2, which are rhythmically expressed in the liver.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1045, "doc_id": 22500262, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [22500262], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Rhythmic expression of Cry1 translates directly into a circadian regulation of cAMP signaling in hepatic glucose metabolism.\n\nDocument title: Cryptochrome Mediates Circadian Regulation of cAMP Signaling and Hepatic Gluconeogenesis\n\nAbstract sentences:\n[0] During fasting, mammals maintain normal glucose homeostasis by stimulating hepatic gluconeogenesis.\n[1] Elevations in circulating glucagon and epinephrine, two hormones that activate hepatic gluconeogenesis, trigger the cAMP-mediated phosphorylation of cAMP response element-binding protein (Creb) and dephosphorylation of the Creb-regulated transcription coactivator-2 (Crtc2)--two key transcriptional regulators of this process.\n[2] Although the underlying mechanism is unclear, hepatic gluconeogenesis is also regulated by the circadian clock, which coordinates glucose metabolism with changes in the external environment.\n[3] Circadian control of gene expression is achieved by two transcriptional activators, Clock and Bmal1, which stimulate cryptochrome (Cry1 and Cry2) and Period (Per1, Per2 and Per3) repressors that feed back on Clock-Bmal1 activity.\n[4] Here we show that Creb activity during fasting is modulated by Cry1 and Cry2, which are rhythmically expressed in the liver.\n[5] Cry1 expression was elevated during the night-day transition, when it reduced fasting gluconeogenic gene expression by blocking glucagon-mediated increases in intracellular cAMP concentrations and in the protein kinase A-mediated phosphorylation of Creb.\n[6] In biochemical reconstitution studies, we found that Cry1 inhibited accumulation of cAMP in response to G protein-coupled receptor (GPCR) activation but not to forskolin, a direct activator of adenyl cyclase.\n[7] Cry proteins seemed to modulate GPCR activity directly through interaction with G(s)α.\n[8] As hepatic overexpression of Cry1 lowered blood glucose concentrations and improved insulin sensitivity in insulin-resistant db/db mice, our results suggest that compounds that enhance cryptochrome activity may provide therapeutic benefit to individuals with type 2 diabetes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Cry1 expression was elevated during the night-day transition, when it reduced fasting gluconeogenic gene expression by blocking glucagon-mediated increases in intracellular cAMP concentrations and in the protein kinase A-mediated phosphorylation of Creb.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1045, "doc_id": 22500262, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [22500262], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ribosomal protein (RP) expression is controlled in part by stress-activated regulators.\n\nDocument title: Pathway connectivity and signaling coordination in the yeast stress-activated signaling network\n\nAbstract sentences:\n[0] Stressed cells coordinate a multi-faceted response spanning many levels of physiology.\n[1] Yet knowledge of the complete stress-activated regulatory network as well as design principles for signal integration remains incomplete.\n[2] We developed an experimental and computational approach to integrate available protein interaction data with gene fitness contributions, mutant transcriptome profiles, and phospho-proteome changes in cells responding to salt stress, to infer the salt-responsive signaling network in yeast.\n[3] The inferred subnetwork presented many novel predictions by implicating new regulators, uncovering unrecognized crosstalk between known pathways, and pointing to previously unknown 'hubs' of signal integration.\n[4] We exploited these predictions to show that Cdc14 phosphatase is a central hub in the network and that modification of RNA polymerase II coordinates induction of stress-defense genes with reduction of growth-related transcripts.\n[5] We find that the orthologous human network is enriched for cancer-causing genes, underscoring the importance of the subnetwork's predictions in understanding stress biology."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1046, "doc_id": 418246, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [418246, 4324278, 16712164], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ribosome-inactivating protein-2 (RIP-2) interacts with the p75 NTR death domain\n\nDocument title: Gamma-Secretase Represents a Therapeutic Target for the Treatment of Invasive Glioma Mediated by the p75 Neurotrophin Receptor\n\nAbstract sentences:\n[0] The multifunctional signaling protein p75 neurotrophin receptor (p75(NTR)) is a central regulator and major contributor to the highly invasive nature of malignant gliomas.\n[1] Here, we show that neurotrophin-dependent regulated intramembrane proteolysis (RIP) of p75(NTR) is required for p75(NTR)-mediated glioma invasion, and identify a previously unnamed process for targeted glioma therapy.\n[2] Expression of cleavage-resistant chimeras of p75(NTR) or treatment of animals bearing p75(NTR)-positive intracranial tumors with clinically applicable gamma-secretase inhibitors resulted in dramatically decreased glioma invasion and prolonged survival.\n[3] Importantly, proteolytic processing of p75(NTR) was observed in p75(NTR)-positive patient tumor specimens and brain tumor initiating cells.\n[4] This work highlights the importance of p75(NTR) as a therapeutic target, suggesting that gamma-secretase inhibitors may have direct clinical application for the treatment of malignant glioma."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1047, "doc_id": 14706752, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14706752], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ribosomopathies have a high degree of cell and tissue specific pathology.\n\nDocument title: Ribosome-Mediated Specificity in Hox mRNA Translation and Vertebrate Tissue Patterning\n\nAbstract sentences:\n[0] Historically, the ribosome has been viewed as a complex ribozyme with constitutive rather than regulatory capacity in mRNA translation.\n[1] Here we identify mutations of the Ribosomal Protein L38 (Rpl38) gene in mice exhibiting surprising tissue-specific patterning defects, including pronounced homeotic transformations of the axial skeleton.\n[2] In Rpl38 mutant embryos, global protein synthesis is unchanged; however the translation of a select subset of Homeobox mRNAs is perturbed.\n[3] Our data reveal that RPL38 facilitates 80S complex formation on these mRNAs as a regulatory component of the ribosome to confer transcript-specific translational control.\n[4] We further show that Rpl38 expression is markedly enriched in regions of the embryo where loss-of-function phenotypes occur.\n[5] Unexpectedly, a ribosomal protein (RP) expression screen reveals dynamic regulation of individual RPs within the vertebrate embryo.\n[6] Collectively, these findings suggest that RP activity may be highly regulated to impart a new layer of specificity in the control of gene expression and mammalian development."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5, 6]\nExplanation: Evidence states: \"Unexpectedly, a ribosomal protein (RP) expression screen reveals dynamic regulation of individual RPs within the vertebrate embryo. Collectively, these findings suggest that RP activity may be highly regulated to impart a new layer of specificity in the control of gene expression and mammalian development.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1048, "doc_id": 12486491, "label": "SUPPORTS", "evidence_sentence_ids": [5, 6], "cited_doc_ids": [12486491], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Risedronate increases risk of vertebral and non-vertebral fractures.\n\nDocument title: Effects of risedronate treatment on vertebral and nonvertebral fractures in women with postmenopausal osteoporosis: a randomized controlled trial. Vertebral Efficacy With Risedronate Therapy (VERT) Study Group.\n\nAbstract sentences:\n[0] CONTEXT Risedronate, a potent bisphosphonate, has been shown to be effective in the treatment of Paget disease of bone and other metabolic bone diseases but, to our knowledge, it has not been evaluated in the treatment of established postmenopausal osteoporosis.\n[1] OBJECTIVE To test the efficacy and safety of daily treatment with risedronate to reduce the risk of vertebral and other fractures in postmenopausal women with established osteoporosis.\n[2] DESIGN, SETTING, AND PARTICIPANTS Randomized, double-blind, placebo-controlled trial of 2458 ambulatory postmenopausal women younger than 85 years with at least 1 vertebral fracture at baseline who were enrolled at 1 of 110 centers in North America conducted between December 1993 and January 1998.\n[3] INTERVENTIONS Subjects were randomly assigned to receive oral treatment for 3 years with risedronate (2.5 or 5 mg/d) or placebo.\n[4] All subjects received calcium, 1000 mg/d.\n[5] Vitamin D (cholecalciferol, up to 500 IU/d) was provided if baseline levels of 25-hydroxyvitamin D were low.\n[6] MAIN OUTCOME MEASURES Incidence of new vertebral fractures as detected by quantitative and semiquantitative assessments of radiographs; incidence of radiographically confirmed nonvertebral fractures and change from baseline in bone mineral density as determined by dual x-ray absorptiometry.\n[7] RESULTS The 2.5 mg/d of risedronate arm was discontinued after 1 year; in the placebo and 5 mg/d of risedronate arms, 450 and 489 subjects, respectively, completed all 3 years of the trial.\n[8] Treatment with 5 mg/d of risedronate, compared with placebo, decreased the cumulative incidence of new vertebral fractures by 41 % (95% confidence interval [CI], 18%-58%) over 3 years (11.3 % vs 16.3%; P= .003).\n[9] A fracture reduction of 65% (95% CI, 38%-81 %) was observed after the first year (2.4% vs 6.4%; P<.001).\n[10] The cumulative incidence of nonvertebral fractures over 3 years was reduced by 39% (95% CI, 6%-61 %) (5.2 % vs 8.4%; P = .02).\n[11] Bone mineral density increased significantly compared with placebo at the lumbar spine (5.4% vs 1.1 %), femoral neck (1.6% vs -1.2%), femoral trochanter (3.3% vs -0.7%), and midshaft of the radius (0.2% vs -1.4%).\n[12] Bone formed during risedronate treatment was histologically normal.\n[13] The overall safety profile of risedronate, including gastrointestinal safety, was similar to that of placebo.\n[14] CONCLUSIONS These data suggest that risedronate therapy is effective and well tolerated in the treatment of women with established postmenopausal osteoporosis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8, 10]\nExplanation: Evidence states: \"Treatment with 5 mg/d of risedronate, compared with placebo, decreased the cumulative incidence of new vertebral fractures by 41 % (95% confidence interval [CI], 18%-58%) over 3 years (11.3 % vs 16.3%; P= .003). The cumulative incidence of nonvertebral fractures over 3 years was reduced by 39% (95% CI, 6%-61 %) (5.2 % vs 8.4%; P = .02).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1050, "doc_id": 19878070, "label": "CONTRADICTS", "evidence_sentence_ids": [8, 10], "cited_doc_ids": [19878070], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Rising temperatures caused by global warming increases risk of dengue fever transmission.\n\nDocument title: Spatial and Temporal Clustering of Dengue Virus Transmission in Thai Villages\n\nAbstract sentences:\n[0] BACKGROUND Transmission of dengue viruses (DENV), the leading cause of arboviral disease worldwide, is known to vary through time and space, likely owing to a combination of factors related to the human host, virus, mosquito vector, and environment.\n[1] An improved understanding of variation in transmission patterns is fundamental to conducting surveillance and implementing disease prevention strategies.\n[2] To test the hypothesis that DENV transmission is spatially and temporally focal, we compared geographic and temporal characteristics within Thai villages where DENV are and are not being actively transmitted.\n[3] METHODS AND FINDINGS Cluster investigations were conducted within 100 m of homes where febrile index children with (positive clusters) and without (negative clusters) acute dengue lived during two seasons of peak DENV transmission.\n[4] Data on human infection and mosquito infection/density were examined to precisely (1) define the spatial and temporal dimensions of DENV transmission, (2) correlate these factors with variation in DENV transmission, and (3) determine the burden of inapparent and symptomatic infections.\n[5] Among 556 village children enrolled as neighbors of 12 dengue-positive and 22 dengue-negative index cases, all 27 DENV infections (4.9% of enrollees) occurred in positive clusters (p < 0.01; attributable risk [AR] = 10.4 per 100; 95% confidence interval 1-19.8 per 100].\n[6] In positive clusters, 12.4% of enrollees became infected in a 15-d period and DENV infections were aggregated centrally near homes of index cases.\n[7] As only 1 of 217 pairs of serologic specimens tested in positive clusters revealed a recent DENV infection that occurred prior to cluster initiation, we attribute the observed DENV transmission subsequent to cluster investigation to recent DENV transmission activity.\n[8] Of the 1,022 female adult Ae.\n[9] aegypti collected, all eight (0.8%) dengue-infected mosquitoes came from houses in positive clusters; none from control clusters or schools.\n[10] Distinguishing features between positive and negative clusters were greater availability of piped water in negative clusters (p < 0.01) and greater number of Ae.\n[11] aegypti pupae per person in positive clusters (p = 0.04).\n[12] During primarily DENV-4 transmission seasons, the ratio of inapparent to symptomatic infections was nearly 1:1 among child enrollees.\n[13] Study limitations included inability to sample all children and mosquitoes within each cluster and our reliance on serologic rather than virologic evidence of interval infections in enrollees given restrictions on the frequency of blood collections in children.\n[14] CONCLUSIONS Our data reveal the remarkably focal nature of DENV transmission within a hyperendemic rural area of Thailand.\n[15] These data suggest that active school-based dengue case detection prompting local spraying could contain recent virus introductions and reduce the longitudinal risk of virus spread within rural areas.\n[16] Our results should prompt future cluster studies to explore how host immune and behavioral aspects may impact DENV transmission and prevention strategies.\n[17] Cluster methodology could serve as a useful research tool for investigation of other temporally and spatially clustered infectious diseases."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1052, "doc_id": 18816720, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [18816720], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Rising temperatures caused by global warming lowers the risk of dengue fever transmission.\n\nDocument title: Spatial and Temporal Clustering of Dengue Virus Transmission in Thai Villages\n\nAbstract sentences:\n[0] BACKGROUND Transmission of dengue viruses (DENV), the leading cause of arboviral disease worldwide, is known to vary through time and space, likely owing to a combination of factors related to the human host, virus, mosquito vector, and environment.\n[1] An improved understanding of variation in transmission patterns is fundamental to conducting surveillance and implementing disease prevention strategies.\n[2] To test the hypothesis that DENV transmission is spatially and temporally focal, we compared geographic and temporal characteristics within Thai villages where DENV are and are not being actively transmitted.\n[3] METHODS AND FINDINGS Cluster investigations were conducted within 100 m of homes where febrile index children with (positive clusters) and without (negative clusters) acute dengue lived during two seasons of peak DENV transmission.\n[4] Data on human infection and mosquito infection/density were examined to precisely (1) define the spatial and temporal dimensions of DENV transmission, (2) correlate these factors with variation in DENV transmission, and (3) determine the burden of inapparent and symptomatic infections.\n[5] Among 556 village children enrolled as neighbors of 12 dengue-positive and 22 dengue-negative index cases, all 27 DENV infections (4.9% of enrollees) occurred in positive clusters (p < 0.01; attributable risk [AR] = 10.4 per 100; 95% confidence interval 1-19.8 per 100].\n[6] In positive clusters, 12.4% of enrollees became infected in a 15-d period and DENV infections were aggregated centrally near homes of index cases.\n[7] As only 1 of 217 pairs of serologic specimens tested in positive clusters revealed a recent DENV infection that occurred prior to cluster initiation, we attribute the observed DENV transmission subsequent to cluster investigation to recent DENV transmission activity.\n[8] Of the 1,022 female adult Ae.\n[9] aegypti collected, all eight (0.8%) dengue-infected mosquitoes came from houses in positive clusters; none from control clusters or schools.\n[10] Distinguishing features between positive and negative clusters were greater availability of piped water in negative clusters (p < 0.01) and greater number of Ae.\n[11] aegypti pupae per person in positive clusters (p = 0.04).\n[12] During primarily DENV-4 transmission seasons, the ratio of inapparent to symptomatic infections was nearly 1:1 among child enrollees.\n[13] Study limitations included inability to sample all children and mosquitoes within each cluster and our reliance on serologic rather than virologic evidence of interval infections in enrollees given restrictions on the frequency of blood collections in children.\n[14] CONCLUSIONS Our data reveal the remarkably focal nature of DENV transmission within a hyperendemic rural area of Thailand.\n[15] These data suggest that active school-based dengue case detection prompting local spraying could contain recent virus introductions and reduce the longitudinal risk of virus spread within rural areas.\n[16] Our results should prompt future cluster studies to explore how host immune and behavioral aspects may impact DENV transmission and prevention strategies.\n[17] Cluster methodology could serve as a useful research tool for investigation of other temporally and spatially clustered infectious diseases."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1053, "doc_id": 18816720, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [18816720], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Risk of cardiovascular events can be cut by a third by using antihypertensive drug therapy among hemodialysis patients.\n\nDocument title: Cardiovascular protection with antihypertensive drugs in dialysis patients: systematic review and meta-analysis.\n\nAbstract sentences:\n[0] Epidemiological studies demonstrate that a lower blood pressure and decline in blood pressure over months or years are associated with higher mortality in dialysis patients.\n[1] In contrast, randomized, controlled trials lack power to establish benefits of antihypertensive therapy.\n[2] Patients on long-term dialysis participating in randomized, controlled trials and receiving antihypertensive drug therapy were the subject of this meta-analysis.\n[3] Outcomes assessed were the hazard ratio of cardiovascular events and all-cause mortality in treated group compared with controls.\n[4] Among 1202 patients who we identified in 5 studies, the overall benefit of antihypertensive therapy compared with the control or placebo group had a combined hazard ratio for cardiovascular events of 0.69 (95% CI: 0.56 to 0.84) using a fixed-effects model and 0.62 (95% CI: 0.45 to 0.86) using a random-effects model.\n[5] In a sensitivity analysis, we found that the hypertensive group had a pooled hazard ratio of 0.49 (95% CI: 0.35 to 0.67), but when normotensives were included in the trial, lesser cardiovascular protection was seen (pooled hazard ratio of 0.86 [95% CI: 0.67 to 1.12]).\n[6] Test for heterogeneity between hypertensive and \"normotensive-included\" groups was significant (P<0.006).\n[7] Similar results were seen for risk ratio for death and cardiovascular events.\n[8] There was evidence of publication bias based on Egger's test and funnel plot.\n[9] Randomized trials suggested a benefit of antihypertensive therapy among hemodialysis patients.\n[10] Adequately powered randomized trials are required to confirm these observations, especially among those with hypertension."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Among 1202 patients who we identified in 5 studies, the overall benefit of antihypertensive therapy compared with the control or placebo group had a combined hazard ratio for cardiovascular events of 0.69 (95% CI: 0.56 to 0.84) using a fixed-effects model and 0.62 (95% CI: 0.45 to 0.86) using a random-effects model.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1054, "doc_id": 10072941, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [10072941], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Risk-adjusted mortality rates are similar in teaching and non-teaching hospitals.\n\nDocument title: Patient Outcomes with Teaching Versus Nonteaching Healthcare: A Systematic Review\n\nAbstract sentences:\n[0] Background  Extensive debate exists in the healthcare community over whether outcomes of medical care at teaching hospitals and other healthcare units are better or worse than those at the respective nonteaching ones.\n[1] Thus, our goal was to systematically evaluate the evidence pertaining to this question.\n[2] Methods and Findings  We reviewed all studies that compared teaching versus nonteaching healthcare structures for mortality or any other patient outcome, regardless of health condition.\n[3] Studies were retrieved from PubMed, contact with experts, and literature cross-referencing.\n[4] Data were extracted on setting, patients, data sources, author affiliations, definition of compared groups, types of diagnoses considered, adjusting covariates, and estimates of effect for mortality and for each other outcome.\n[5] Overall, 132 eligible studies were identified, including 93 on mortality and 61 on other eligible outcomes (22 addressed both).\n[6] Synthesis of the available adjusted estimates on mortality yielded a summary relative risk of 0.96 (95% confidence interval [CI], 0.93–1.00) for teaching versus nonteaching healthcare structures and 1.04 (95% CI, 0.99–1.10) for minor teaching versus nonteaching ones.\n[7] There was considerable heterogeneity between studies (I2 = 72% for the main analysis).\n[8] Results were similar in studies using clinical and those using administrative databases.\n[9] No differences were seen in the 14 studies fully adjusting for volume/experience, severity, and comorbidity (relative risk 1.01).\n[10] Smaller studies did not differ in their results from larger studies.\n[11] Differences were seen for some diagnoses (e.g., significantly better survival for breast cancer and cerebrovascular accidents in teaching hospitals and significantly better survival from cholecystectomy in nonteaching hospitals), but these were small in magnitude.\n[12] Other outcomes were diverse, but typically teaching healthcare structures did not do better than nonteaching ones.\n[13] Conclusions  The available data are limited by their nonrandomized design, but overall they do not suggest that a healthcare facility's teaching status on its own markedly improves or worsens patient outcomes.\n[14] Differences for specific diseases cannot be excluded, but are likely to be small."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Synthesis of the available adjusted estimates on mortality yielded a summary relative risk of 0.96 (95% confidence interval [CI], 0.93–1.00) for teaching versus nonteaching healthcare structures and 1.04 (95% CI, 0.99–1.10) for minor teaching versus nonteaching ones.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1055, "doc_id": 13906581, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [13906581], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Risk-adjusted mortality rates are similar in teaching and non-teaching hospitals.\n\nDocument title: Patient Outcomes with Teaching Versus Nonteaching Healthcare: A Systematic Review\n\nAbstract sentences:\n[0] Background  Extensive debate exists in the healthcare community over whether outcomes of medical care at teaching hospitals and other healthcare units are better or worse than those at the respective nonteaching ones.\n[1] Thus, our goal was to systematically evaluate the evidence pertaining to this question.\n[2] Methods and Findings  We reviewed all studies that compared teaching versus nonteaching healthcare structures for mortality or any other patient outcome, regardless of health condition.\n[3] Studies were retrieved from PubMed, contact with experts, and literature cross-referencing.\n[4] Data were extracted on setting, patients, data sources, author affiliations, definition of compared groups, types of diagnoses considered, adjusting covariates, and estimates of effect for mortality and for each other outcome.\n[5] Overall, 132 eligible studies were identified, including 93 on mortality and 61 on other eligible outcomes (22 addressed both).\n[6] Synthesis of the available adjusted estimates on mortality yielded a summary relative risk of 0.96 (95% confidence interval [CI], 0.93–1.00) for teaching versus nonteaching healthcare structures and 1.04 (95% CI, 0.99–1.10) for minor teaching versus nonteaching ones.\n[7] There was considerable heterogeneity between studies (I2 = 72% for the main analysis).\n[8] Results were similar in studies using clinical and those using administrative databases.\n[9] No differences were seen in the 14 studies fully adjusting for volume/experience, severity, and comorbidity (relative risk 1.01).\n[10] Smaller studies did not differ in their results from larger studies.\n[11] Differences were seen for some diagnoses (e.g., significantly better survival for breast cancer and cerebrovascular accidents in teaching hospitals and significantly better survival from cholecystectomy in nonteaching hospitals), but these were small in magnitude.\n[12] Other outcomes were diverse, but typically teaching healthcare structures did not do better than nonteaching ones.\n[13] Conclusions  The available data are limited by their nonrandomized design, but overall they do not suggest that a healthcare facility's teaching status on its own markedly improves or worsens patient outcomes.\n[14] Differences for specific diseases cannot be excluded, but are likely to be small."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"Conclusions  The available data are limited by their nonrandomized design, but overall they do not suggest that a healthcare facility's teaching status on its own markedly improves or worsens patient outcomes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1055, "doc_id": 13906581, "label": "SUPPORTS", "evidence_sentence_ids": [13], "cited_doc_ids": [13906581], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Rotator cuff exercises are more effective than general exercise therapy in reducing pain and improving function of the shoulder.\n\nDocument title: Effect of specific exercise strategy on need for surgery in patients with subacromial impingement syndrome: randomised controlled study\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate if a specific exercise strategy, targeting the rotator cuff and scapula stabilisers, improves shoulder function and pain more than unspecific exercises in patients with subacromial impingement syndrome, thereby decreasing the need for arthroscopic subacromial decompression.\n[1] DESIGN Randomised, participant and single assessor blinded, controlled study.\n[2] SETTING Department of orthopaedics in a Swedish university hospital.\n[3] PARTICIPANTS 102 patients with long standing (over six months) persistent subacromial impingement syndrome in whom earlier conservative treatment had failed, recruited through orthopaedic specialists.\n[4] INTERVENTIONS The specific exercise strategy consisted of strengthening eccentric exercises for the rotator cuff and concentric/eccentric exercises for the scapula stabilisers in combination with manual mobilisation.\n[5] The control exercise programme consisted of unspecific movement exercises for the neck and shoulder.\n[6] Patients in both groups received five to six individual guided treatment sessions during 12 weeks.\n[7] In between these supervised sessions the participants performed home exercises once or twice a day for 12 weeks.\n[8] MAIN OUTCOME MEASURES The primary outcome was the Constant-Murley shoulder assessment score evaluating shoulder function and pain.\n[9] Secondary outcomes were patients' global impression of change because of treatment and decision regarding surgery.\n[10] RESULTS Most (97, 95%) participants completed the 12 week study.\n[11] There was a significantly greater improvement in the Constant-Murley score in the specific exercise group than in the control exercise group (24 points (95% confidence interval 19 to 28.0) v 9 points (5 to 13); mean difference between group: 15 points (8.5 to 20.6)).\n[12] Significantly more patients in the specific exercise group reported successful outcome (defined as large improvement or recovered) in the patients' global assessment of change because of treatment: 69% (35/51) v 24% (11/46); odds ratio 7.6, 3.1 to 18.9; P<0.001.\n[13] A significantly lower proportion of patients in the specific exercise group subsequently chose to undergo surgery: 20% (10/51) v 63% (29/46); odds ratio 7.7, 3.1 to 19.4; P<0.001).\n[14] CONCLUSION A specific exercise strategy, focusing on strengthening eccentric exercises for the rotator cuff and concentric/eccentric exercises for the scapula stabilisers, is effective in reducing pain and improving shoulder function in patients with persistent subacromial impingement syndrome.\n[15] By extension, this exercise strategy reduces the need for arthroscopic subacromial decompression within the three month timeframe used in the study.\n[16] TRIAL REGISTRATION Clinical trials NCT01037673."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"There was a significantly greater improvement in the Constant-Murley score in the specific exercise group than in the control exercise group (24 points (95% confidence interval 19 to 28.0) v 9 points (5 to 13); mean difference between group: 15 points (8.5 to 20.6)).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1056, "doc_id": 4200695, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [4200695], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Roughly 55% of women with chronic pelvic pain have no underlying pathology.\n\nDocument title: Laparoscopic uterosacral nerve ablation for alleviating chronic pelvic pain: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Chronic pelvic pain is a common condition with a major effect on health-related quality of life, work productivity, and health care use.\n[1] Operative interruption of nerve trunks in the uterosacral ligaments by laparoscopic uterosacral nerve ablation (LUNA) is a treatment option for patients with chronic pelvic pain.\n[2] OBJECTIVE To assess the effectiveness of LUNA in patients with chronic pelvic pain.\n[3] DESIGN, SETTING, AND PARTICIPANTS Randomized controlled trial of 487 women with chronic pelvic pain lasting longer than 6 months without or with minimal endometriosis, adhesions, or pelvic inflammatory disease, who were recruited to the study by consultant gynecological surgeons from 18 UK hospitals between February 1998 and December 2005.\n[4] Follow-up was conducted by questionnaires mailed at 3 and 6 months and at 1, 2, 3, and 5 years.\n[5] INTERVENTION Bilateral LUNA or laparoscopy without pelvic denervation (no LUNA); participants were blinded to the treatment allocation.\n[6] MAIN OUTCOME MEASURES\n[7] The primary outcome was pain, which was assessed by a visual analogue scale.\n[8] Data concerning the 3 types of pain (noncyclical pain, dysmenorrhea, and dyspareunia) were analyzed separately as was the worst pain level experienced from any of these 3 types of pain.\n[9] The secondary outcome was health-related quality of life, which was measured using a generic instrument (EuroQoL EQ-5D and EQ-VAS).\n[10] RESULTS After a median follow-up of 69 months, there were no significant differences reported on the visual analogue pain scales for the worst pain (mean difference between the LUNA group and the no LUNA group, -0.04 cm [95% confidence interval {CI}, -0.33 to 0.25 cm]; P = .80), noncyclical pain (-0.11 cm [95% CI, -0.50 to 0.29 cm]; P = .60), dysmenorrhea (-0.09 cm [95% CI, -0.49 to 0.30 cm]; P = .60), or dyspareunia (0.18 cm [95% CI, -0.22 to 0.62 cm]; P = .40).\n[11] No differences were observed between the LUNA group and the no LUNA group for quality of life.\n[12] CONCLUSION Among women with chronic pelvic pain, LUNA did not result in improvements in pain, dysmenorrhea, dyspareunia, or quality of life compared with laparoscopy without pelvic denervation.\n[13] TRIAL REGISTRATION controlled-trials.com Identifier: ISRCTN41196151."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1058, "doc_id": 13027590, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [13027590], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Satellite cell dysfunction is a key factor in sarcopenia development.\n\nDocument title: Inducible depletion of satellite cells in adult, sedentary mice impairs muscle regenerative capacity without affecting sarcopenia\n\nAbstract sentences:\n[0] A key determinant of geriatric frailty is sarcopenia, the age-associated loss of skeletal muscle mass and strength.\n[1] Although the etiology of sarcopenia is unknown, the correlation during aging between the loss of activity of satellite cells, which are endogenous muscle stem cells, and impaired muscle regenerative capacity has led to the hypothesis that the loss of satellite cell activity is also a cause of sarcopenia.\n[2] We tested this hypothesis in male sedentary mice by experimentally depleting satellite cells in young adult animals to a degree sufficient to impair regeneration throughout the rest of their lives.\n[3] A detailed analysis of multiple muscles harvested at various time points during aging in different cohorts of these mice showed that the muscles were of normal size, despite low regenerative capacity, but did have increased fibrosis.\n[4] These results suggest that lifelong reduction of satellite cells neither accelerated nor exacerbated sarcopenia and that satellite cells did not contribute to the maintenance of muscle size or fiber type composition during aging, but that their loss may contribute to age-related muscle fibrosis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"A detailed analysis of multiple muscles harvested at various time points during aging in different cohorts of these mice showed that the muscles were of normal size, despite low regenerative capacity, but did have increased fibrosis.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1065, "doc_id": 20418809, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [20418809], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Satellite cell dysfunction is a key factor in sarcopenia development.\n\nDocument title: Inducible depletion of satellite cells in adult, sedentary mice impairs muscle regenerative capacity without affecting sarcopenia\n\nAbstract sentences:\n[0] A key determinant of geriatric frailty is sarcopenia, the age-associated loss of skeletal muscle mass and strength.\n[1] Although the etiology of sarcopenia is unknown, the correlation during aging between the loss of activity of satellite cells, which are endogenous muscle stem cells, and impaired muscle regenerative capacity has led to the hypothesis that the loss of satellite cell activity is also a cause of sarcopenia.\n[2] We tested this hypothesis in male sedentary mice by experimentally depleting satellite cells in young adult animals to a degree sufficient to impair regeneration throughout the rest of their lives.\n[3] A detailed analysis of multiple muscles harvested at various time points during aging in different cohorts of these mice showed that the muscles were of normal size, despite low regenerative capacity, but did have increased fibrosis.\n[4] These results suggest that lifelong reduction of satellite cells neither accelerated nor exacerbated sarcopenia and that satellite cells did not contribute to the maintenance of muscle size or fiber type composition during aging, but that their loss may contribute to age-related muscle fibrosis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"These results suggest that lifelong reduction of satellite cells neither accelerated nor exacerbated sarcopenia and that satellite cells did not contribute to the maintenance of muscle size or fiber type composition during aging, but that their loss may contribute to age-related muscle fibrosis.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1065, "doc_id": 20418809, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [20418809], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: ScPif1p has higher binding ability to G-rich ssDNA than to non-G-rich ssDNA.\n\nDocument title: Pif1 family helicases suppress genome instability at G-quadruplex motifs\n\nAbstract sentences:\n[0] The Saccharomyces cerevisiae Pif1 helicase is the prototypical member of the Pif1 DNA helicase family, which is conserved from bacteria to humans.\n[1] Here we show that exceptionally potent G-quadruplex unwinding is conserved among Pif1 helicases.\n[2] Moreover, Pif1 helicases from organisms separated by more than 3 billion years of evolution suppressed DNA damage at G-quadruplex motifs in yeast.\n[3] The G-quadruplex-induced damage generated in the absence of Pif1 helicases led to new genetic and epigenetic changes.\n[4] Furthermore, when expressed in yeast, human PIF1 suppressed both G-quadruplex-associated DNA damage and telomere lengthening."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1067, "doc_id": 4429668, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4429668], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: ScPif1p has reduced binding ability to G-rich ssDNA compared to non-G-rich ssDNA.\n\nDocument title: Pif1 family helicases suppress genome instability at G-quadruplex motifs\n\nAbstract sentences:\n[0] The Saccharomyces cerevisiae Pif1 helicase is the prototypical member of the Pif1 DNA helicase family, which is conserved from bacteria to humans.\n[1] Here we show that exceptionally potent G-quadruplex unwinding is conserved among Pif1 helicases.\n[2] Moreover, Pif1 helicases from organisms separated by more than 3 billion years of evolution suppressed DNA damage at G-quadruplex motifs in yeast.\n[3] The G-quadruplex-induced damage generated in the absence of Pif1 helicases led to new genetic and epigenetic changes.\n[4] Furthermore, when expressed in yeast, human PIF1 suppressed both G-quadruplex-associated DNA damage and telomere lengthening."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1068, "doc_id": 4429668, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4429668], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Scapular stabilizer exercises are more effective than general exercise therapy in reducing pain and improving function of the shoulder.\n\nDocument title: Effect of specific exercise strategy on need for surgery in patients with subacromial impingement syndrome: randomised controlled study\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate if a specific exercise strategy, targeting the rotator cuff and scapula stabilisers, improves shoulder function and pain more than unspecific exercises in patients with subacromial impingement syndrome, thereby decreasing the need for arthroscopic subacromial decompression.\n[1] DESIGN Randomised, participant and single assessor blinded, controlled study.\n[2] SETTING Department of orthopaedics in a Swedish university hospital.\n[3] PARTICIPANTS 102 patients with long standing (over six months) persistent subacromial impingement syndrome in whom earlier conservative treatment had failed, recruited through orthopaedic specialists.\n[4] INTERVENTIONS The specific exercise strategy consisted of strengthening eccentric exercises for the rotator cuff and concentric/eccentric exercises for the scapula stabilisers in combination with manual mobilisation.\n[5] The control exercise programme consisted of unspecific movement exercises for the neck and shoulder.\n[6] Patients in both groups received five to six individual guided treatment sessions during 12 weeks.\n[7] In between these supervised sessions the participants performed home exercises once or twice a day for 12 weeks.\n[8] MAIN OUTCOME MEASURES The primary outcome was the Constant-Murley shoulder assessment score evaluating shoulder function and pain.\n[9] Secondary outcomes were patients' global impression of change because of treatment and decision regarding surgery.\n[10] RESULTS Most (97, 95%) participants completed the 12 week study.\n[11] There was a significantly greater improvement in the Constant-Murley score in the specific exercise group than in the control exercise group (24 points (95% confidence interval 19 to 28.0) v 9 points (5 to 13); mean difference between group: 15 points (8.5 to 20.6)).\n[12] Significantly more patients in the specific exercise group reported successful outcome (defined as large improvement or recovered) in the patients' global assessment of change because of treatment: 69% (35/51) v 24% (11/46); odds ratio 7.6, 3.1 to 18.9; P<0.001.\n[13] A significantly lower proportion of patients in the specific exercise group subsequently chose to undergo surgery: 20% (10/51) v 63% (29/46); odds ratio 7.7, 3.1 to 19.4; P<0.001).\n[14] CONCLUSION A specific exercise strategy, focusing on strengthening eccentric exercises for the rotator cuff and concentric/eccentric exercises for the scapula stabilisers, is effective in reducing pain and improving shoulder function in patients with persistent subacromial impingement syndrome.\n[15] By extension, this exercise strategy reduces the need for arthroscopic subacromial decompression within the three month timeframe used in the study.\n[16] TRIAL REGISTRATION Clinical trials NCT01037673."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"There was a significantly greater improvement in the Constant-Murley score in the specific exercise group than in the control exercise group (24 points (95% confidence interval 19 to 28.0) v 9 points (5 to 13); mean difference between group: 15 points (8.5 to 20.6)).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1069, "doc_id": 4200695, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [4200695], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Scapular stabilizer exercises are more effective than general exercise therapy in reducing pain and improving function of the shoulder.\n\nDocument title: Effect of specific exercise strategy on need for surgery in patients with subacromial impingement syndrome: randomised controlled study\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate if a specific exercise strategy, targeting the rotator cuff and scapula stabilisers, improves shoulder function and pain more than unspecific exercises in patients with subacromial impingement syndrome, thereby decreasing the need for arthroscopic subacromial decompression.\n[1] DESIGN Randomised, participant and single assessor blinded, controlled study.\n[2] SETTING Department of orthopaedics in a Swedish university hospital.\n[3] PARTICIPANTS 102 patients with long standing (over six months) persistent subacromial impingement syndrome in whom earlier conservative treatment had failed, recruited through orthopaedic specialists.\n[4] INTERVENTIONS The specific exercise strategy consisted of strengthening eccentric exercises for the rotator cuff and concentric/eccentric exercises for the scapula stabilisers in combination with manual mobilisation.\n[5] The control exercise programme consisted of unspecific movement exercises for the neck and shoulder.\n[6] Patients in both groups received five to six individual guided treatment sessions during 12 weeks.\n[7] In between these supervised sessions the participants performed home exercises once or twice a day for 12 weeks.\n[8] MAIN OUTCOME MEASURES The primary outcome was the Constant-Murley shoulder assessment score evaluating shoulder function and pain.\n[9] Secondary outcomes were patients' global impression of change because of treatment and decision regarding surgery.\n[10] RESULTS Most (97, 95%) participants completed the 12 week study.\n[11] There was a significantly greater improvement in the Constant-Murley score in the specific exercise group than in the control exercise group (24 points (95% confidence interval 19 to 28.0) v 9 points (5 to 13); mean difference between group: 15 points (8.5 to 20.6)).\n[12] Significantly more patients in the specific exercise group reported successful outcome (defined as large improvement or recovered) in the patients' global assessment of change because of treatment: 69% (35/51) v 24% (11/46); odds ratio 7.6, 3.1 to 18.9; P<0.001.\n[13] A significantly lower proportion of patients in the specific exercise group subsequently chose to undergo surgery: 20% (10/51) v 63% (29/46); odds ratio 7.7, 3.1 to 19.4; P<0.001).\n[14] CONCLUSION A specific exercise strategy, focusing on strengthening eccentric exercises for the rotator cuff and concentric/eccentric exercises for the scapula stabilisers, is effective in reducing pain and improving shoulder function in patients with persistent subacromial impingement syndrome.\n[15] By extension, this exercise strategy reduces the need for arthroscopic subacromial decompression within the three month timeframe used in the study.\n[16] TRIAL REGISTRATION Clinical trials NCT01037673."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"Significantly more patients in the specific exercise group reported successful outcome (defined as large improvement or recovered) in the patients' global assessment of change because of treatment: 69% (35/51) v 24% (11/46); odds ratio 7.6, 3.1 to 18.9; P<0.001.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1069, "doc_id": 4200695, "label": "SUPPORTS", "evidence_sentence_ids": [12], "cited_doc_ids": [4200695], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Scapular stabilizer exercises are more effective than general exercise therapy in reducing pain and improving function of the shoulder.\n\nDocument title: Effect of specific exercise strategy on need for surgery in patients with subacromial impingement syndrome: randomised controlled study\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate if a specific exercise strategy, targeting the rotator cuff and scapula stabilisers, improves shoulder function and pain more than unspecific exercises in patients with subacromial impingement syndrome, thereby decreasing the need for arthroscopic subacromial decompression.\n[1] DESIGN Randomised, participant and single assessor blinded, controlled study.\n[2] SETTING Department of orthopaedics in a Swedish university hospital.\n[3] PARTICIPANTS 102 patients with long standing (over six months) persistent subacromial impingement syndrome in whom earlier conservative treatment had failed, recruited through orthopaedic specialists.\n[4] INTERVENTIONS The specific exercise strategy consisted of strengthening eccentric exercises for the rotator cuff and concentric/eccentric exercises for the scapula stabilisers in combination with manual mobilisation.\n[5] The control exercise programme consisted of unspecific movement exercises for the neck and shoulder.\n[6] Patients in both groups received five to six individual guided treatment sessions during 12 weeks.\n[7] In between these supervised sessions the participants performed home exercises once or twice a day for 12 weeks.\n[8] MAIN OUTCOME MEASURES The primary outcome was the Constant-Murley shoulder assessment score evaluating shoulder function and pain.\n[9] Secondary outcomes were patients' global impression of change because of treatment and decision regarding surgery.\n[10] RESULTS Most (97, 95%) participants completed the 12 week study.\n[11] There was a significantly greater improvement in the Constant-Murley score in the specific exercise group than in the control exercise group (24 points (95% confidence interval 19 to 28.0) v 9 points (5 to 13); mean difference between group: 15 points (8.5 to 20.6)).\n[12] Significantly more patients in the specific exercise group reported successful outcome (defined as large improvement or recovered) in the patients' global assessment of change because of treatment: 69% (35/51) v 24% (11/46); odds ratio 7.6, 3.1 to 18.9; P<0.001.\n[13] A significantly lower proportion of patients in the specific exercise group subsequently chose to undergo surgery: 20% (10/51) v 63% (29/46); odds ratio 7.7, 3.1 to 19.4; P<0.001).\n[14] CONCLUSION A specific exercise strategy, focusing on strengthening eccentric exercises for the rotator cuff and concentric/eccentric exercises for the scapula stabilisers, is effective in reducing pain and improving shoulder function in patients with persistent subacromial impingement syndrome.\n[15] By extension, this exercise strategy reduces the need for arthroscopic subacromial decompression within the three month timeframe used in the study.\n[16] TRIAL REGISTRATION Clinical trials NCT01037673."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [14]\nExplanation: Evidence states: \"CONCLUSION A specific exercise strategy, focusing on strengthening eccentric exercises for the rotator cuff and concentric/eccentric exercises for the scapula stabilisers, is effective in reducing pain and improving shoulder function in patients with persistent subacromial impingement syndrome.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1069, "doc_id": 4200695, "label": "SUPPORTS", "evidence_sentence_ids": [14], "cited_doc_ids": [4200695], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Self-advocacy training is effective at decreasing homelessness.\n\nDocument title: Mental health problems of homeless children and families: longitudinal study.\n\nAbstract sentences:\n[0] OBJECTIVE To establish the mental health needs of homeless children and families before and after rehousing.\n[1] DESIGN Cross sectional, longitudinal study.\n[2] SETTING City of Birmingham.\n[3] SUBJECTS 58 rehoused families with 103 children aged 2-16 years and 21 comparison families of low socioeconomic status in stable housing, with 54 children.\n[4] MAIN OUTCOME MEASURES Children's mental health problems and level of communication; mothers' mental health problems and social support one year after rehousing.\n[5] RESULTS Mental health problems remained significantly higher in rehoused mothers and their children than in the comparison group (mothers 26% v 5%, P = 0.04; children 39% v 11%, P = 0.0003).\n[6] Homeless mothers continued to have significantly less social support at follow up.\n[7] Mothers with a history of abuse and poor social integration were more likely to have children with persistent mental health problems.\n[8] CONCLUSIONS Homeless families have a high level of complex needs that cannot be met by conventional health services and arrangements.\n[9] Local strategies for rapid rehousing into permanent accommodation, effective social support and health care for parents and children, and protection from violence and intimidation should be developed and implemented."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1070, "doc_id": 25649714, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [25649714], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Sepsis related mortality has remained stable between 2009-2014.\n\nDocument title: Incidence and Trends of Sepsis in US Hospitals Using Clinical vs Claims Data, 2009-2014\n\nAbstract sentences:\n[0] Importance Estimates from claims-based analyses suggest that the incidence of sepsis is increasing and mortality rates from sepsis are decreasing.\n[1] However, estimates from claims data may lack clinical fidelity and can be affected by changing diagnosis and coding practices over time.\n[2] Objective To estimate the US national incidence of sepsis and trends using detailed clinical data from the electronic health record (EHR) systems of diverse hospitals.\n[3] Design, Setting, and Population Retrospective cohort study of adult patients admitted to 409 academic, community, and federal hospitals from 2009-2014.\n[4] Exposures Sepsis was identified using clinical indicators of presumed infection and concurrent acute organ dysfunction, adapting Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) criteria for objective and consistent EHR-based surveillance.\n[5] Main Outcomes and Measures Sepsis incidence, outcomes, and trends from 2009-2014 were calculated using regression models and compared with claims-based estimates using International Classification of Diseases, Ninth Revision, Clinical Modification codes for severe sepsis or septic shock.\n[6] Case-finding criteria were validated against Sepsis-3 criteria using medical record reviews.\n[7] Results A total of 173 690 sepsis cases (mean age, 66.5 [SD, 15.5] y; 77 660 [42.4%] women) were identified using clinical criteria among 2 901 019 adults admitted to study hospitals in 2014 (6.0% incidence).\n[8] Of these, 26 061 (15.0%) died in the hospital and 10 731 (6.2%) were discharged to hospice.\n[9] From 2009-2014, sepsis incidence using clinical criteria was stable (+0.6% relative change/y [95% CI, −2.3% to 3.5%], P = .67) whereas incidence per claims increased (+10.3%/y [95% CI, 7.2% to 13.3%], P < .001).\n[10] In-hospital mortality using clinical criteria declined (−3.3%/y [95% CI, −5.6% to −1.0%], P = .004), but there was no significant change in the combined outcome of death or discharge to hospice (−1.3%/y [95% CI, −3.2% to 0.6%], P = .19).\n[11] In contrast, mortality using claims declined significantly (−7.0%/y [95% CI, −8.8% to −5.2%], P < .001), as did death or discharge to hospice (−4.5%/y [95% CI, −6.1% to −2.8%], P < .001).\n[12] Clinical criteria were more sensitive in identifying sepsis than claims (69.7% [95% CI, 52.9% to 92.0%] vs 32.3% [95% CI, 24.4% to 43.0%], P < .001), with comparable positive predictive value (70.4% [95% CI, 64.0% to 76.8%] vs 75.2% [95% CI, 69.8% to 80.6%], P = .23).\n[13] Conclusions and Relevance In clinical data from 409 hospitals, sepsis was present in 6% of adult hospitalizations, and in contrast to claims-based analyses, neither the incidence of sepsis nor the combined outcome of death or discharge to hospice changed significantly between 2009-2014.\n[14] The findings also suggest that EHR-based clinical data provide more objective estimates than claims-based data for sepsis surveillance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"In-hospital mortality using clinical criteria declined (−3.3%/y [95% CI, −5.6% to −1.0%], P = .004), but there was no significant change in the combined outcome of death or discharge to hospice (−1.3%/y [95% CI, −3.2% to 0.6%], P = .19).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1072, "doc_id": 4824840, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [4824840], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Sepsis related mortality has remained stable between 2009-2014.\n\nDocument title: Incidence and Trends of Sepsis in US Hospitals Using Clinical vs Claims Data, 2009-2014\n\nAbstract sentences:\n[0] Importance Estimates from claims-based analyses suggest that the incidence of sepsis is increasing and mortality rates from sepsis are decreasing.\n[1] However, estimates from claims data may lack clinical fidelity and can be affected by changing diagnosis and coding practices over time.\n[2] Objective To estimate the US national incidence of sepsis and trends using detailed clinical data from the electronic health record (EHR) systems of diverse hospitals.\n[3] Design, Setting, and Population Retrospective cohort study of adult patients admitted to 409 academic, community, and federal hospitals from 2009-2014.\n[4] Exposures Sepsis was identified using clinical indicators of presumed infection and concurrent acute organ dysfunction, adapting Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) criteria for objective and consistent EHR-based surveillance.\n[5] Main Outcomes and Measures Sepsis incidence, outcomes, and trends from 2009-2014 were calculated using regression models and compared with claims-based estimates using International Classification of Diseases, Ninth Revision, Clinical Modification codes for severe sepsis or septic shock.\n[6] Case-finding criteria were validated against Sepsis-3 criteria using medical record reviews.\n[7] Results A total of 173 690 sepsis cases (mean age, 66.5 [SD, 15.5] y; 77 660 [42.4%] women) were identified using clinical criteria among 2 901 019 adults admitted to study hospitals in 2014 (6.0% incidence).\n[8] Of these, 26 061 (15.0%) died in the hospital and 10 731 (6.2%) were discharged to hospice.\n[9] From 2009-2014, sepsis incidence using clinical criteria was stable (+0.6% relative change/y [95% CI, −2.3% to 3.5%], P = .67) whereas incidence per claims increased (+10.3%/y [95% CI, 7.2% to 13.3%], P < .001).\n[10] In-hospital mortality using clinical criteria declined (−3.3%/y [95% CI, −5.6% to −1.0%], P = .004), but there was no significant change in the combined outcome of death or discharge to hospice (−1.3%/y [95% CI, −3.2% to 0.6%], P = .19).\n[11] In contrast, mortality using claims declined significantly (−7.0%/y [95% CI, −8.8% to −5.2%], P < .001), as did death or discharge to hospice (−4.5%/y [95% CI, −6.1% to −2.8%], P < .001).\n[12] Clinical criteria were more sensitive in identifying sepsis than claims (69.7% [95% CI, 52.9% to 92.0%] vs 32.3% [95% CI, 24.4% to 43.0%], P < .001), with comparable positive predictive value (70.4% [95% CI, 64.0% to 76.8%] vs 75.2% [95% CI, 69.8% to 80.6%], P = .23).\n[13] Conclusions and Relevance In clinical data from 409 hospitals, sepsis was present in 6% of adult hospitalizations, and in contrast to claims-based analyses, neither the incidence of sepsis nor the combined outcome of death or discharge to hospice changed significantly between 2009-2014.\n[14] The findings also suggest that EHR-based clinical data provide more objective estimates than claims-based data for sepsis surveillance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"Conclusions and Relevance In clinical data from 409 hospitals, sepsis was present in 6% of adult hospitalizations, and in contrast to claims-based analyses, neither the incidence of sepsis nor the combined outcome of death or discharge to hospice changed significantly between 2009-2014.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1072, "doc_id": 4824840, "label": "SUPPORTS", "evidence_sentence_ids": [13], "cited_doc_ids": [4824840], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Sepsis related mortality has risen from 2009 to 2014.\n\nDocument title: Incidence and Trends of Sepsis in US Hospitals Using Clinical vs Claims Data, 2009-2014\n\nAbstract sentences:\n[0] Importance Estimates from claims-based analyses suggest that the incidence of sepsis is increasing and mortality rates from sepsis are decreasing.\n[1] However, estimates from claims data may lack clinical fidelity and can be affected by changing diagnosis and coding practices over time.\n[2] Objective To estimate the US national incidence of sepsis and trends using detailed clinical data from the electronic health record (EHR) systems of diverse hospitals.\n[3] Design, Setting, and Population Retrospective cohort study of adult patients admitted to 409 academic, community, and federal hospitals from 2009-2014.\n[4] Exposures Sepsis was identified using clinical indicators of presumed infection and concurrent acute organ dysfunction, adapting Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) criteria for objective and consistent EHR-based surveillance.\n[5] Main Outcomes and Measures Sepsis incidence, outcomes, and trends from 2009-2014 were calculated using regression models and compared with claims-based estimates using International Classification of Diseases, Ninth Revision, Clinical Modification codes for severe sepsis or septic shock.\n[6] Case-finding criteria were validated against Sepsis-3 criteria using medical record reviews.\n[7] Results A total of 173 690 sepsis cases (mean age, 66.5 [SD, 15.5] y; 77 660 [42.4%] women) were identified using clinical criteria among 2 901 019 adults admitted to study hospitals in 2014 (6.0% incidence).\n[8] Of these, 26 061 (15.0%) died in the hospital and 10 731 (6.2%) were discharged to hospice.\n[9] From 2009-2014, sepsis incidence using clinical criteria was stable (+0.6% relative change/y [95% CI, −2.3% to 3.5%], P = .67) whereas incidence per claims increased (+10.3%/y [95% CI, 7.2% to 13.3%], P < .001).\n[10] In-hospital mortality using clinical criteria declined (−3.3%/y [95% CI, −5.6% to −1.0%], P = .004), but there was no significant change in the combined outcome of death or discharge to hospice (−1.3%/y [95% CI, −3.2% to 0.6%], P = .19).\n[11] In contrast, mortality using claims declined significantly (−7.0%/y [95% CI, −8.8% to −5.2%], P < .001), as did death or discharge to hospice (−4.5%/y [95% CI, −6.1% to −2.8%], P < .001).\n[12] Clinical criteria were more sensitive in identifying sepsis than claims (69.7% [95% CI, 52.9% to 92.0%] vs 32.3% [95% CI, 24.4% to 43.0%], P < .001), with comparable positive predictive value (70.4% [95% CI, 64.0% to 76.8%] vs 75.2% [95% CI, 69.8% to 80.6%], P = .23).\n[13] Conclusions and Relevance In clinical data from 409 hospitals, sepsis was present in 6% of adult hospitalizations, and in contrast to claims-based analyses, neither the incidence of sepsis nor the combined outcome of death or discharge to hospice changed significantly between 2009-2014.\n[14] The findings also suggest that EHR-based clinical data provide more objective estimates than claims-based data for sepsis surveillance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"In-hospital mortality using clinical criteria declined (−3.3%/y [95% CI, −5.6% to −1.0%], P = .004), but there was no significant change in the combined outcome of death or discharge to hospice (−1.3%/y [95% CI, −3.2% to 0.6%], P = .19).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1073, "doc_id": 4824840, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [4824840], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Sepsis related mortality has risen from 2009 to 2014.\n\nDocument title: Incidence and Trends of Sepsis in US Hospitals Using Clinical vs Claims Data, 2009-2014\n\nAbstract sentences:\n[0] Importance Estimates from claims-based analyses suggest that the incidence of sepsis is increasing and mortality rates from sepsis are decreasing.\n[1] However, estimates from claims data may lack clinical fidelity and can be affected by changing diagnosis and coding practices over time.\n[2] Objective To estimate the US national incidence of sepsis and trends using detailed clinical data from the electronic health record (EHR) systems of diverse hospitals.\n[3] Design, Setting, and Population Retrospective cohort study of adult patients admitted to 409 academic, community, and federal hospitals from 2009-2014.\n[4] Exposures Sepsis was identified using clinical indicators of presumed infection and concurrent acute organ dysfunction, adapting Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) criteria for objective and consistent EHR-based surveillance.\n[5] Main Outcomes and Measures Sepsis incidence, outcomes, and trends from 2009-2014 were calculated using regression models and compared with claims-based estimates using International Classification of Diseases, Ninth Revision, Clinical Modification codes for severe sepsis or septic shock.\n[6] Case-finding criteria were validated against Sepsis-3 criteria using medical record reviews.\n[7] Results A total of 173 690 sepsis cases (mean age, 66.5 [SD, 15.5] y; 77 660 [42.4%] women) were identified using clinical criteria among 2 901 019 adults admitted to study hospitals in 2014 (6.0% incidence).\n[8] Of these, 26 061 (15.0%) died in the hospital and 10 731 (6.2%) were discharged to hospice.\n[9] From 2009-2014, sepsis incidence using clinical criteria was stable (+0.6% relative change/y [95% CI, −2.3% to 3.5%], P = .67) whereas incidence per claims increased (+10.3%/y [95% CI, 7.2% to 13.3%], P < .001).\n[10] In-hospital mortality using clinical criteria declined (−3.3%/y [95% CI, −5.6% to −1.0%], P = .004), but there was no significant change in the combined outcome of death or discharge to hospice (−1.3%/y [95% CI, −3.2% to 0.6%], P = .19).\n[11] In contrast, mortality using claims declined significantly (−7.0%/y [95% CI, −8.8% to −5.2%], P < .001), as did death or discharge to hospice (−4.5%/y [95% CI, −6.1% to −2.8%], P < .001).\n[12] Clinical criteria were more sensitive in identifying sepsis than claims (69.7% [95% CI, 52.9% to 92.0%] vs 32.3% [95% CI, 24.4% to 43.0%], P < .001), with comparable positive predictive value (70.4% [95% CI, 64.0% to 76.8%] vs 75.2% [95% CI, 69.8% to 80.6%], P = .23).\n[13] Conclusions and Relevance In clinical data from 409 hospitals, sepsis was present in 6% of adult hospitalizations, and in contrast to claims-based analyses, neither the incidence of sepsis nor the combined outcome of death or discharge to hospice changed significantly between 2009-2014.\n[14] The findings also suggest that EHR-based clinical data provide more objective estimates than claims-based data for sepsis surveillance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"Conclusions and Relevance In clinical data from 409 hospitals, sepsis was present in 6% of adult hospitalizations, and in contrast to claims-based analyses, neither the incidence of sepsis nor the combined outcome of death or discharge to hospice changed significantly between 2009-2014.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1073, "doc_id": 4824840, "label": "CONTRADICTS", "evidence_sentence_ids": [13], "cited_doc_ids": [4824840], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Sequence conservation in gene regulatory regions between species is a high-accuracy predictor of conserved functionality.\n\nDocument title: Enhancer Evolution across 20 Mammalian Species\n\nAbstract sentences:\n[0] The mammalian radiation has corresponded with rapid changes in noncoding regions of the genome, but we lack a comprehensive understanding of regulatory evolution in mammals.\n[1] Here, we track the evolution of promoters and enhancers active in liver across 20 mammalian species from six diverse orders by profiling genomic enrichment of H3K27 acetylation and H3K4 trimethylation.\n[2] We report that rapid evolution of enhancers is a universal feature of mammalian genomes.\n[3] Most of the recently evolved enhancers arise from ancestral DNA exaptation, rather than lineage-specific expansions of repeat elements.\n[4] In contrast, almost all liver promoters are partially or fully conserved across these species.\n[5] Our data further reveal that recently evolved enhancers can be associated with genes under positive selection, demonstrating the power of this approach for annotating regulatory adaptations in genomic sequences.\n[6] These results provide important insight into the functional genetics underpinning mammalian regulatory evolution."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1074, "doc_id": 14658685, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14658685], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Sequence conservation in gene regulatory regions between species is a poor predictor of conserved functionality.\n\nDocument title: Enhancer Evolution across 20 Mammalian Species\n\nAbstract sentences:\n[0] The mammalian radiation has corresponded with rapid changes in noncoding regions of the genome, but we lack a comprehensive understanding of regulatory evolution in mammals.\n[1] Here, we track the evolution of promoters and enhancers active in liver across 20 mammalian species from six diverse orders by profiling genomic enrichment of H3K27 acetylation and H3K4 trimethylation.\n[2] We report that rapid evolution of enhancers is a universal feature of mammalian genomes.\n[3] Most of the recently evolved enhancers arise from ancestral DNA exaptation, rather than lineage-specific expansions of repeat elements.\n[4] In contrast, almost all liver promoters are partially or fully conserved across these species.\n[5] Our data further reveal that recently evolved enhancers can be associated with genes under positive selection, demonstrating the power of this approach for annotating regulatory adaptations in genomic sequences.\n[6] These results provide important insight into the functional genetics underpinning mammalian regulatory evolution."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1075, "doc_id": 14658685, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14658685], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Side effects associated with antidepressants do not represent a mortality risk to postmenopausal women.\n\nDocument title: Antidepressant use and risk of adverse outcomes in older people: population based cohort study\n\nAbstract sentences:\n[0] OBJECTIVES To investigate the association between antidepressant treatment and risk of several potential adverse outcomes in older people with depression and to examine risks by class of antidepressant, duration of use, and dose.\n[1] DESIGN Cohort study of people aged 65 and over diagnosed as having depression.\n[2] SETTING 570 general practices in the United Kingdom supplying data to the QResearch primary care database.\n[3] PARTICIPANTS 60,746 patients diagnosed as having a new episode of depression between the ages of 65 and 100 years from 1 January 1996 to 31 December 2007 and followed up until 31 December 2008.\n[4] MAIN OUTCOME MEASURES Hazard ratios associated with antidepressant use for all cause mortality, attempted suicide/self harm, myocardial infarction, stroke/transient ischaemic attack, falls, fractures, upper gastrointestinal bleeding, epilepsy/seizures, road traffic accidents, adverse drug reactions, and hyponatraemia, adjusted for a range of potential confounding variables.\n[5] Hazard ratios were calculated for antidepressant class (tricyclic and related antidepressants, selective serotonin reuptake inhibitors, other antidepressants), dose, and duration of use and for commonly prescribed individual drugs.\n[6] RESULTS 54,038 (89.0%) patients received at least one prescription for an antidepressant during follow-up.\n[7] A total of 1,398,359 antidepressant prescriptions were issued: 764,659 (54.7%) for selective serotonin reuptake inhibitors, 442,192 (31.6%) for tricyclic antidepressants, 2203 (0.2%) for monoamine oxidase inhibitors, and 189,305 (13.5%) for the group of other antidepressants.\n[8] The associations with the adverse outcomes differed significantly between the antidepressant classes for seven outcomes.\n[9] Selective serotonin reuptake inhibitors were associated with the highest adjusted hazard ratios for falls (1.66, 95% confidence interval 1.58 to 1.73) and hyponatraemia (1.52, 1.33 to 1.75) compared with when antidepressants were not being used.\n[10] The group of other antidepressants was associated with the highest adjusted hazard ratios for all cause mortality (1.66, 1.56 to 1.77), attempted suicide/self harm (5.16, 3.90 to 6.83), stroke/transient ischaemic attack (1.37, 1.22 to 1.55), fracture (1.64, 1.46 to 1.84), and epilepsy/seizures (2.24, 1.60 to 3.15), compared with when antidepressants were not being used.\n[11] Tricyclic antidepressants did not have the highest hazard ratio for any of the outcomes.\n[12] Significantly different associations also existed between the individual drugs for the same seven outcomes; trazodone (tricyclic antidepressant), mirtazapine, and venlafaxine (both in the group of other antidepressants) were associated with the highest rates for some of these outcomes.\n[13] Absolute risks over 1 year for all cause mortality were 7.04% for patients while not taking antidepressants, 8.12% for those taking tricyclic antidepressants, 10.61% for selective serotonin reuptake inhibitors, and 11.43% for other antidepressants.\n[14] CONCLUSIONS Selective serotonin reuptake inhibitors and drugs in the group of other antidepressants were associated with an increased risk of several adverse outcomes compared with tricyclic antidepressants.\n[15] Among individual drugs, trazodone, mirtazapine, and venlafaxine were associated with the highest risks for some outcomes.\n[16] As this is an observational study, it is susceptible to confounding by indication, channelling bias, and residual confounding, so differences in characteristics between patients prescribed different antidepressant drugs that could account for some of the associations between the drugs and the adverse outcomes may remain.\n[17] Further research is needed to confirm these findings, but the risks and benefits of different antidepressants should be carefully evaluated when these drugs are prescribed to older people."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"The group of other antidepressants was associated with the highest adjusted hazard ratios for all cause mortality (1.66, 1.56 to 1.77), attempted suicide/self harm (5.16, 3.90 to 6.83), stroke/transient ischaemic attack (1.37, 1.22 to 1.55), fracture (1.64, 1.46 to 1.84), and epilepsy/seizures (2.24, 1.60 to 3.15), compared with when antidepressants were not being used.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1081, "doc_id": 5691302, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [5691302], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Side effects associated with antidepressants do not represent a mortality risk to postmenopausal women.\n\nDocument title: Antidepressant use and risk of adverse outcomes in older people: population based cohort study\n\nAbstract sentences:\n[0] OBJECTIVES To investigate the association between antidepressant treatment and risk of several potential adverse outcomes in older people with depression and to examine risks by class of antidepressant, duration of use, and dose.\n[1] DESIGN Cohort study of people aged 65 and over diagnosed as having depression.\n[2] SETTING 570 general practices in the United Kingdom supplying data to the QResearch primary care database.\n[3] PARTICIPANTS 60,746 patients diagnosed as having a new episode of depression between the ages of 65 and 100 years from 1 January 1996 to 31 December 2007 and followed up until 31 December 2008.\n[4] MAIN OUTCOME MEASURES Hazard ratios associated with antidepressant use for all cause mortality, attempted suicide/self harm, myocardial infarction, stroke/transient ischaemic attack, falls, fractures, upper gastrointestinal bleeding, epilepsy/seizures, road traffic accidents, adverse drug reactions, and hyponatraemia, adjusted for a range of potential confounding variables.\n[5] Hazard ratios were calculated for antidepressant class (tricyclic and related antidepressants, selective serotonin reuptake inhibitors, other antidepressants), dose, and duration of use and for commonly prescribed individual drugs.\n[6] RESULTS 54,038 (89.0%) patients received at least one prescription for an antidepressant during follow-up.\n[7] A total of 1,398,359 antidepressant prescriptions were issued: 764,659 (54.7%) for selective serotonin reuptake inhibitors, 442,192 (31.6%) for tricyclic antidepressants, 2203 (0.2%) for monoamine oxidase inhibitors, and 189,305 (13.5%) for the group of other antidepressants.\n[8] The associations with the adverse outcomes differed significantly between the antidepressant classes for seven outcomes.\n[9] Selective serotonin reuptake inhibitors were associated with the highest adjusted hazard ratios for falls (1.66, 95% confidence interval 1.58 to 1.73) and hyponatraemia (1.52, 1.33 to 1.75) compared with when antidepressants were not being used.\n[10] The group of other antidepressants was associated with the highest adjusted hazard ratios for all cause mortality (1.66, 1.56 to 1.77), attempted suicide/self harm (5.16, 3.90 to 6.83), stroke/transient ischaemic attack (1.37, 1.22 to 1.55), fracture (1.64, 1.46 to 1.84), and epilepsy/seizures (2.24, 1.60 to 3.15), compared with when antidepressants were not being used.\n[11] Tricyclic antidepressants did not have the highest hazard ratio for any of the outcomes.\n[12] Significantly different associations also existed between the individual drugs for the same seven outcomes; trazodone (tricyclic antidepressant), mirtazapine, and venlafaxine (both in the group of other antidepressants) were associated with the highest rates for some of these outcomes.\n[13] Absolute risks over 1 year for all cause mortality were 7.04% for patients while not taking antidepressants, 8.12% for those taking tricyclic antidepressants, 10.61% for selective serotonin reuptake inhibitors, and 11.43% for other antidepressants.\n[14] CONCLUSIONS Selective serotonin reuptake inhibitors and drugs in the group of other antidepressants were associated with an increased risk of several adverse outcomes compared with tricyclic antidepressants.\n[15] Among individual drugs, trazodone, mirtazapine, and venlafaxine were associated with the highest risks for some outcomes.\n[16] As this is an observational study, it is susceptible to confounding by indication, channelling bias, and residual confounding, so differences in characteristics between patients prescribed different antidepressant drugs that could account for some of the associations between the drugs and the adverse outcomes may remain.\n[17] Further research is needed to confirm these findings, but the risks and benefits of different antidepressants should be carefully evaluated when these drugs are prescribed to older people."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"Absolute risks over 1 year for all cause mortality were 7.04% for patients while not taking antidepressants, 8.12% for those taking tricyclic antidepressants, 10.61% for selective serotonin reuptake inhibitors, and 11.43% for other antidepressants.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1081, "doc_id": 5691302, "label": "CONTRADICTS", "evidence_sentence_ids": [13], "cited_doc_ids": [5691302], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Side effects associated with antidepressants increases risk of stroke.\n\nDocument title: Antidepressant use and risk of adverse outcomes in older people: population based cohort study\n\nAbstract sentences:\n[0] OBJECTIVES To investigate the association between antidepressant treatment and risk of several potential adverse outcomes in older people with depression and to examine risks by class of antidepressant, duration of use, and dose.\n[1] DESIGN Cohort study of people aged 65 and over diagnosed as having depression.\n[2] SETTING 570 general practices in the United Kingdom supplying data to the QResearch primary care database.\n[3] PARTICIPANTS 60,746 patients diagnosed as having a new episode of depression between the ages of 65 and 100 years from 1 January 1996 to 31 December 2007 and followed up until 31 December 2008.\n[4] MAIN OUTCOME MEASURES Hazard ratios associated with antidepressant use for all cause mortality, attempted suicide/self harm, myocardial infarction, stroke/transient ischaemic attack, falls, fractures, upper gastrointestinal bleeding, epilepsy/seizures, road traffic accidents, adverse drug reactions, and hyponatraemia, adjusted for a range of potential confounding variables.\n[5] Hazard ratios were calculated for antidepressant class (tricyclic and related antidepressants, selective serotonin reuptake inhibitors, other antidepressants), dose, and duration of use and for commonly prescribed individual drugs.\n[6] RESULTS 54,038 (89.0%) patients received at least one prescription for an antidepressant during follow-up.\n[7] A total of 1,398,359 antidepressant prescriptions were issued: 764,659 (54.7%) for selective serotonin reuptake inhibitors, 442,192 (31.6%) for tricyclic antidepressants, 2203 (0.2%) for monoamine oxidase inhibitors, and 189,305 (13.5%) for the group of other antidepressants.\n[8] The associations with the adverse outcomes differed significantly between the antidepressant classes for seven outcomes.\n[9] Selective serotonin reuptake inhibitors were associated with the highest adjusted hazard ratios for falls (1.66, 95% confidence interval 1.58 to 1.73) and hyponatraemia (1.52, 1.33 to 1.75) compared with when antidepressants were not being used.\n[10] The group of other antidepressants was associated with the highest adjusted hazard ratios for all cause mortality (1.66, 1.56 to 1.77), attempted suicide/self harm (5.16, 3.90 to 6.83), stroke/transient ischaemic attack (1.37, 1.22 to 1.55), fracture (1.64, 1.46 to 1.84), and epilepsy/seizures (2.24, 1.60 to 3.15), compared with when antidepressants were not being used.\n[11] Tricyclic antidepressants did not have the highest hazard ratio for any of the outcomes.\n[12] Significantly different associations also existed between the individual drugs for the same seven outcomes; trazodone (tricyclic antidepressant), mirtazapine, and venlafaxine (both in the group of other antidepressants) were associated with the highest rates for some of these outcomes.\n[13] Absolute risks over 1 year for all cause mortality were 7.04% for patients while not taking antidepressants, 8.12% for those taking tricyclic antidepressants, 10.61% for selective serotonin reuptake inhibitors, and 11.43% for other antidepressants.\n[14] CONCLUSIONS Selective serotonin reuptake inhibitors and drugs in the group of other antidepressants were associated with an increased risk of several adverse outcomes compared with tricyclic antidepressants.\n[15] Among individual drugs, trazodone, mirtazapine, and venlafaxine were associated with the highest risks for some outcomes.\n[16] As this is an observational study, it is susceptible to confounding by indication, channelling bias, and residual confounding, so differences in characteristics between patients prescribed different antidepressant drugs that could account for some of the associations between the drugs and the adverse outcomes may remain.\n[17] Further research is needed to confirm these findings, but the risks and benefits of different antidepressants should be carefully evaluated when these drugs are prescribed to older people."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"The group of other antidepressants was associated with the highest adjusted hazard ratios for all cause mortality (1.66, 1.56 to 1.77), attempted suicide/self harm (5.16, 3.90 to 6.83), stroke/transient ischaemic attack (1.37, 1.22 to 1.55), fracture (1.64, 1.46 to 1.84), and epilepsy/seizures (2.24, 1.60 to 3.15), compared with when antidepressants were not being used.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1084, "doc_id": 5691302, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [5691302], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Side effects associated with antidepressants lower risk of myocardial infarction.\n\nDocument title: Antidepressant use and risk of adverse outcomes in older people: population based cohort study\n\nAbstract sentences:\n[0] OBJECTIVES To investigate the association between antidepressant treatment and risk of several potential adverse outcomes in older people with depression and to examine risks by class of antidepressant, duration of use, and dose.\n[1] DESIGN Cohort study of people aged 65 and over diagnosed as having depression.\n[2] SETTING 570 general practices in the United Kingdom supplying data to the QResearch primary care database.\n[3] PARTICIPANTS 60,746 patients diagnosed as having a new episode of depression between the ages of 65 and 100 years from 1 January 1996 to 31 December 2007 and followed up until 31 December 2008.\n[4] MAIN OUTCOME MEASURES Hazard ratios associated with antidepressant use for all cause mortality, attempted suicide/self harm, myocardial infarction, stroke/transient ischaemic attack, falls, fractures, upper gastrointestinal bleeding, epilepsy/seizures, road traffic accidents, adverse drug reactions, and hyponatraemia, adjusted for a range of potential confounding variables.\n[5] Hazard ratios were calculated for antidepressant class (tricyclic and related antidepressants, selective serotonin reuptake inhibitors, other antidepressants), dose, and duration of use and for commonly prescribed individual drugs.\n[6] RESULTS 54,038 (89.0%) patients received at least one prescription for an antidepressant during follow-up.\n[7] A total of 1,398,359 antidepressant prescriptions were issued: 764,659 (54.7%) for selective serotonin reuptake inhibitors, 442,192 (31.6%) for tricyclic antidepressants, 2203 (0.2%) for monoamine oxidase inhibitors, and 189,305 (13.5%) for the group of other antidepressants.\n[8] The associations with the adverse outcomes differed significantly between the antidepressant classes for seven outcomes.\n[9] Selective serotonin reuptake inhibitors were associated with the highest adjusted hazard ratios for falls (1.66, 95% confidence interval 1.58 to 1.73) and hyponatraemia (1.52, 1.33 to 1.75) compared with when antidepressants were not being used.\n[10] The group of other antidepressants was associated with the highest adjusted hazard ratios for all cause mortality (1.66, 1.56 to 1.77), attempted suicide/self harm (5.16, 3.90 to 6.83), stroke/transient ischaemic attack (1.37, 1.22 to 1.55), fracture (1.64, 1.46 to 1.84), and epilepsy/seizures (2.24, 1.60 to 3.15), compared with when antidepressants were not being used.\n[11] Tricyclic antidepressants did not have the highest hazard ratio for any of the outcomes.\n[12] Significantly different associations also existed between the individual drugs for the same seven outcomes; trazodone (tricyclic antidepressant), mirtazapine, and venlafaxine (both in the group of other antidepressants) were associated with the highest rates for some of these outcomes.\n[13] Absolute risks over 1 year for all cause mortality were 7.04% for patients while not taking antidepressants, 8.12% for those taking tricyclic antidepressants, 10.61% for selective serotonin reuptake inhibitors, and 11.43% for other antidepressants.\n[14] CONCLUSIONS Selective serotonin reuptake inhibitors and drugs in the group of other antidepressants were associated with an increased risk of several adverse outcomes compared with tricyclic antidepressants.\n[15] Among individual drugs, trazodone, mirtazapine, and venlafaxine were associated with the highest risks for some outcomes.\n[16] As this is an observational study, it is susceptible to confounding by indication, channelling bias, and residual confounding, so differences in characteristics between patients prescribed different antidepressant drugs that could account for some of the associations between the drugs and the adverse outcomes may remain.\n[17] Further research is needed to confirm these findings, but the risks and benefits of different antidepressants should be carefully evaluated when these drugs are prescribed to older people."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1085, "doc_id": 5691302, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [5691302], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Sildenafil worsens erectile function in men who experience sexual dysfunction as a result of the use of SSRI antidepressants.\n\nDocument title: Treatment of antidepressant-associated sexual dysfunction with sildenafil: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Sexual dysfunction is a common adverse effect of antidepressants that frequently results in treatment noncompliance.\n[1] OBJECTIVE To assess the efficacy of sildenafil citrate in men with sexual dysfunction associated with the use of selective and nonselective serotonin reuptake inhibitor (SRI) antidepressants.\n[2] DESIGN, SETTING, AND PATIENTS Prospective, parallel-group, randomized, double-blind, placebo-controlled trial conducted between November 1, 2000, and January 1, 2001, at 3 US university medical centers among 90 male outpatients (mean [SD] age, 45 [8] years) with major depression in remission and sexual dysfunction associated with SRI antidepressant treatment.\n[3] INTERVENTION Patients were randomly assigned to take sildenafil (n = 45) or placebo (n = 45) at a flexible dose starting at 50 mg and adjustable to 100 mg before sexual activity for 6 weeks.\n[4] MAIN OUTCOME MEASURES The primary outcome measure was score on the Clinical Global Impression-Sexual Function (CGI-SF); secondary measures were scores on the International Index of Erectile Function, Arizona Sexual Experience Scale, Massachusetts General Hospital-Sexual Functioning Questionnaire, and Hamilton Rating Scale for Depression (HAM-D).\n[5] RESULTS Among the 90 randomized patients, 93% (83/89) of patients treated per protocol took at least 1 dose of study drug and 85% (76/89) completed week 6 end-point assessments with last observation carried forward analyses.\n[6] At a CGI-SF score of 2 or lower, 54.5% (24/44) of sildenafil compared with 4.4% (2/45) of placebo patients were much or very much improved (P<.001).\n[7] Erectile function, arousal, ejaculation, orgasm, and overall satisfaction domain measures improved significantly in sildenafil compared with placebo patients.\n[8] Mean depression scores remained consistent with remission (HAM-D score < or =10) in both groups for the study duration.\n[9] CONCLUSION In our study, sildenafil effectively improved erectile function and other aspects of sexual function in men with sexual dysfunction associated with the use of SRI antidepressants.\n[10] These improvements may allow patients to maintain adherence with effective antidepressant treatment."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Erectile function, arousal, ejaculation, orgasm, and overall satisfaction domain measures improved significantly in sildenafil compared with placebo patients.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1087, "doc_id": 39281140, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [39281140], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Sildenafil worsens erectile function in men who experience sexual dysfunction as a result of the use of SSRI antidepressants.\n\nDocument title: Treatment of antidepressant-associated sexual dysfunction with sildenafil: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Sexual dysfunction is a common adverse effect of antidepressants that frequently results in treatment noncompliance.\n[1] OBJECTIVE To assess the efficacy of sildenafil citrate in men with sexual dysfunction associated with the use of selective and nonselective serotonin reuptake inhibitor (SRI) antidepressants.\n[2] DESIGN, SETTING, AND PATIENTS Prospective, parallel-group, randomized, double-blind, placebo-controlled trial conducted between November 1, 2000, and January 1, 2001, at 3 US university medical centers among 90 male outpatients (mean [SD] age, 45 [8] years) with major depression in remission and sexual dysfunction associated with SRI antidepressant treatment.\n[3] INTERVENTION Patients were randomly assigned to take sildenafil (n = 45) or placebo (n = 45) at a flexible dose starting at 50 mg and adjustable to 100 mg before sexual activity for 6 weeks.\n[4] MAIN OUTCOME MEASURES The primary outcome measure was score on the Clinical Global Impression-Sexual Function (CGI-SF); secondary measures were scores on the International Index of Erectile Function, Arizona Sexual Experience Scale, Massachusetts General Hospital-Sexual Functioning Questionnaire, and Hamilton Rating Scale for Depression (HAM-D).\n[5] RESULTS Among the 90 randomized patients, 93% (83/89) of patients treated per protocol took at least 1 dose of study drug and 85% (76/89) completed week 6 end-point assessments with last observation carried forward analyses.\n[6] At a CGI-SF score of 2 or lower, 54.5% (24/44) of sildenafil compared with 4.4% (2/45) of placebo patients were much or very much improved (P<.001).\n[7] Erectile function, arousal, ejaculation, orgasm, and overall satisfaction domain measures improved significantly in sildenafil compared with placebo patients.\n[8] Mean depression scores remained consistent with remission (HAM-D score < or =10) in both groups for the study duration.\n[9] CONCLUSION In our study, sildenafil effectively improved erectile function and other aspects of sexual function in men with sexual dysfunction associated with the use of SRI antidepressants.\n[10] These improvements may allow patients to maintain adherence with effective antidepressant treatment."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"CONCLUSION In our study, sildenafil effectively improved erectile function and other aspects of sexual function in men with sexual dysfunction associated with the use of SRI antidepressants.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1087, "doc_id": 39281140, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [39281140], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Smc5/6 engagment halts the activation of SUMO E3 ligase Mms21 by ATP-dependent remolding.\n\nDocument title: ATPase-Dependent Control of the Mms21 SUMO Ligase during DNA Repair\n\nAbstract sentences:\n[0] Modification of proteins by SUMO is essential for the maintenance of genome integrity.\n[1] During DNA replication, the Mms21-branch of the SUMO pathway counteracts recombination intermediates at damaged replication forks, thus facilitating sister chromatid disjunction.\n[2] The Mms21 SUMO ligase docks to the arm region of the Smc5 protein in the Smc5/6 complex; together, they cooperate during recombinational DNA repair.\n[3] Yet how the activity of the SUMO ligase is controlled remains unknown.\n[4] Here we show that the SUMO ligase and the chromosome disjunction functions of Mms21 depend on its docking to an intact and active Smc5/6 complex, indicating that the Smc5/6-Mms21 complex operates as a large SUMO ligase in vivo.\n[5] In spite of the physical distance separating the E3 and the nucleotide-binding domains in Smc5/6, Mms21-dependent sumoylation requires binding of ATP to Smc5, a step that is part of the ligase mechanism that assists Ubc9 function.\n[6] The communication is enabled by the presence of a conserved disruption in the coiled coil domain of Smc5, pointing to potential conformational changes for SUMO ligase activation.\n[7] In accordance, scanning force microscopy of the Smc5-Mms21 heterodimer shows that the molecule is physically remodeled in an ATP-dependent manner.\n[8] Our results demonstrate that the ATP-binding activity of the Smc5/6 complex is coordinated with its SUMO ligase, through the coiled coil domain of Smc5 and the physical remodeling of the molecule, to promote sumoylation and chromosome disjunction during DNA repair."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"In accordance, scanning force microscopy of the Smc5-Mms21 heterodimer shows that the molecule is physically remodeled in an ATP-dependent manner.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1090, "doc_id": 17628888, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [17628888], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Sn is present on mature DCs during inflammation in vivo.\n\nDocument title: Siglec-1 Is a Novel Dendritic Cell Receptor That Mediates HIV-1 Trans-Infection Through Recognition of Viral Membrane Gangliosides\n\nAbstract sentences:\n[0] Dendritic cells (DCs) are essential antigen-presenting cells for the induction of immunity against pathogens.\n[1] However, HIV-1 spread is strongly enhanced in clusters of DCs and CD4(+) T cells.\n[2] Uninfected DCs capture HIV-1 and mediate viral transfer to bystander CD4(+) T cells through a process termed trans-infection.\n[3] Initial studies identified the C-type lectin DC-SIGN as the HIV-1 binding factor on DCs, which interacts with the viral envelope glycoproteins.\n[4] Upon DC maturation, however, DC-SIGN is down-regulated, while HIV-1 capture and trans-infection is strongly enhanced via a glycoprotein-independent capture pathway that recognizes sialyllactose-containing membrane gangliosides.\n[5] Here we show that the sialic acid-binding Ig-like lectin 1 (Siglec-1, CD169), which is highly expressed on mature DCs, specifically binds HIV-1 and vesicles carrying sialyllactose.\n[6] Furthermore, Siglec-1 is essential for trans-infection by mature DCs.\n[7] These findings identify Siglec-1 as a key factor for HIV-1 spread via infectious DC/T-cell synapses, highlighting a novel mechanism that mediates HIV-1 dissemination in activated tissues."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1091, "doc_id": 2603304, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [2603304], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Specialized functional cell types can be derived from human pluripotent stem cells.\n\nDocument title: Complex Tissue and Disease Modeling using hiPSCs.\n\nAbstract sentences:\n[0] Defined genetic models based on human pluripotent stem cells have opened new avenues for understanding disease mechanisms and drug screening.\n[1] Many of these models assume cell-autonomous mechanisms of disease but it is possible that disease phenotypes or drug responses will only be evident if all cellular and extracellular components of a tissue are present and functionally mature.\n[2] To derive optimal benefit from such models, complex multicellular structures with vascular components that mimic tissue niches will thus likely be necessary.\n[3] Here we consider emerging research creating human tissue mimics and provide some recommendations for moving the field forward."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1096, "doc_id": 29638116, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [29638116], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Splenomegaly is observed in knockin mouse lacking the SHP-2 MAPK pathway.\n\nDocument title: Dissection of signaling cascades through gp130 in vivo: reciprocal roles for STAT3- and SHP2-mediated signals in immune responses.\n\nAbstract sentences:\n[0] We generated a series of knockin mouse lines, in which the cytokine receptor gp130-dependent STAT3 and/or SHP2 signals were disrupted, by replacing the mouse gp130 gene with human gp130 mutant cDNAs.\n[1] The SHP2 signal-deficient mice (gp130F759/F759 were born normal but displayed splenomegaly and lymphadenopathy and an enhanced acute phase reaction.\n[2] In contrast, the STAT3 signal-deficient mice (gp130FXQ/FXXQ) died perinatally, like the gp130-deficient mice (gp130D/D).\n[3] The gp130F759/F759 mice showed prolonged gp130-induced STAT3 activation, indicating a negative regulatory role for SHP2.\n[4] Th1-type cytokine production and IgG2a and IgG2b production were increased in the gp130F759/F759 mice, while they were decreased in the gp130FXXQ/FXXQ immune system.\n[5] These results indicate that the balance of positive and negative signals generated through gp130 regulates the immune responses."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"The SHP2 signal-deficient mice (gp130F759/F759 were born normal but displayed splenomegaly and lymphadenopathy and an enhanced acute phase reaction.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1097, "doc_id": 26851674, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [26851674], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Stacking is more stable when a purine is present in the +5 position (C1698).\n\nDocument title: Decoding Mammalian Ribosome-mRNA States by Translational GTPase Complexes\n\nAbstract sentences:\n[0] In eukaryotes, accurate protein synthesis relies on a family of translational GTPases that pair with specific decoding factors to decipher the mRNA code on ribosomes.\n[1] We present structures of the mammalian ribosome engaged with decoding factor⋅GTPase complexes representing intermediates of translation elongation (aminoacyl-tRNA⋅eEF1A), termination (eRF1⋅eRF3), and ribosome rescue (Pelota⋅Hbs1l).\n[2] Comparative analyses reveal that each decoding factor exploits the plasticity of the ribosomal decoding center to differentially remodel ribosomal proteins and rRNA.\n[3] This leads to varying degrees of large-scale ribosome movements and implies distinct mechanisms for communicating information from the decoding center to each GTPase.\n[4] Additional structural snapshots of the translation termination pathway reveal the conformational changes that choreograph the accommodation of decoding factors into the peptidyl transferase center.\n[5] Our results provide a structural framework for how different states of the mammalian ribosome are selectively recognized by the appropriate decoding factor⋅GTPase complex to ensure translational fidelity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1098, "doc_id": 13552682, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [13552682], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Stiff substrates encourage mesodermal differentiation by degrading beta-catenin in an integrin-dependent manner.\n\nDocument title: Tissue Mechanics Orchestrate Wnt-Dependent Human Embryonic Stem Cell Differentiation.\n\nAbstract sentences:\n[0] Regenerative medicine is predicated on understanding the mechanisms regulating development and applying these conditions to direct stem cell fate.\n[1] Embryogenesis is guided by cell-cell and cell-matrix interactions, but it is unclear how these physical cues influence stem cells in culture.\n[2] We used human embryonic stem cells (hESCs) to examine whether mechanical features of the extracellular microenvironment could differentially modulate mesoderm specification.\n[3] We found that, on a hydrogel-based compliant matrix, hESCs accumulate β-catenin at cell-cell adhesions and show enhanced Wnt-dependent mesoderm differentiation.\n[4] Mechanistically, Src-driven ubiquitination of E-cadherin by Cbl-like ubiquitin ligase releases P120-catenin to facilitate transcriptional activity of β-catenin, which initiates and reinforces mesoderm differentiation.\n[5] By contrast, on a stiff hydrogel matrix, hESCs show elevated integrin-dependent GSK3 and Src activity that promotes β-catenin degradation and inhibits differentiation.\n[6] Thus, we found that mechanical features of the microenvironmental matrix influence tissue-specific differentiation of hESCs by altering the cellular response to morphogens."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"By contrast, on a stiff hydrogel matrix, hESCs show elevated integrin-dependent GSK3 and Src activity that promotes β-catenin degradation and inhibits differentiation.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1101, "doc_id": 3874000, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [3874000], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Stiff substrates inhibit mesodermal differentiation by degrading beta-catenin in an integrin-dependent manner.\n\nDocument title: Tissue Mechanics Orchestrate Wnt-Dependent Human Embryonic Stem Cell Differentiation.\n\nAbstract sentences:\n[0] Regenerative medicine is predicated on understanding the mechanisms regulating development and applying these conditions to direct stem cell fate.\n[1] Embryogenesis is guided by cell-cell and cell-matrix interactions, but it is unclear how these physical cues influence stem cells in culture.\n[2] We used human embryonic stem cells (hESCs) to examine whether mechanical features of the extracellular microenvironment could differentially modulate mesoderm specification.\n[3] We found that, on a hydrogel-based compliant matrix, hESCs accumulate β-catenin at cell-cell adhesions and show enhanced Wnt-dependent mesoderm differentiation.\n[4] Mechanistically, Src-driven ubiquitination of E-cadherin by Cbl-like ubiquitin ligase releases P120-catenin to facilitate transcriptional activity of β-catenin, which initiates and reinforces mesoderm differentiation.\n[5] By contrast, on a stiff hydrogel matrix, hESCs show elevated integrin-dependent GSK3 and Src activity that promotes β-catenin degradation and inhibits differentiation.\n[6] Thus, we found that mechanical features of the microenvironmental matrix influence tissue-specific differentiation of hESCs by altering the cellular response to morphogens."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"By contrast, on a stiff hydrogel matrix, hESCs show elevated integrin-dependent GSK3 and Src activity that promotes β-catenin degradation and inhibits differentiation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1102, "doc_id": 3874000, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [3874000], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Stroke patients with prior use of direct oral anticoagulants have a higher risk of in-hospital mortality than stroke patients with prior use of warfarin.\n\nDocument title: Association of Intracerebral Hemorrhage Among Patients Taking Non–Vitamin K Antagonist vs Vitamin K Antagonist Oral Anticoagulants With In-Hospital Mortality\n\nAbstract sentences:\n[0] Importance Although non–vitamin K antagonist oral anticoagulants (NOACs) are increasingly used to prevent thromboembolic disease, there are limited data on NOAC-related intracerebral hemorrhage (ICH).\n[1] Objective To assess the association between preceding oral anticoagulant use (warfarin, NOACs, and no oral anticoagulants [OACs]) and in-hospital mortality among patients with ICH.\n[2] Design, Setting, and Participants Retrospective cohort study of 141 311 patients with ICH admitted from October 2013 to December 2016 to 1662 Get With The Guidelines–Stroke hospitals.\n[3] Exposures Anticoagulation therapy before ICH, defined as any use of OACs within 7 days prior to hospital arrival.\n[4] Main Outcomes and Measures In-hospital mortality.\n[5] Results Among 141 311 patients with ICH (mean [SD] age, 68.3 [15.3] years; 48.1% women), 15 036 (10.6%) were taking warfarin and 4918 (3.5%) were taking NOACs preceding ICH, and 39 585 (28.0%) and 5783 (4.1%) were taking concomitant single and dual antiplatelet agents, respectively.\n[6] Patients with prior use of warfarin or NOACs were older and had higher prevalence of atrial fibrillation and prior stroke.\n[7] Acute ICH stroke severity (measured by the National Institutes of Health Stroke Scale) was not significantly different across the 3 groups (median, 9 [interquartile range, 2-21] for warfarin, 8 [2-20] for NOACs, and 8 [2-19] for no OACs).\n[8] The unadjusted in-hospital mortality rates were 32.6% for warfarin, 26.5% for NOACs, and 22.5% for no OACs.\n[9] Compared with patients without prior use of OACs, the risk of in-hospital mortality was higher among patients with prior use of warfarin (adjusted risk difference [ARD], 9.0% [97.5% CI, 7.9% to 10.1%]; adjusted odds ratio [AOR], 1.62 [97.5% CI, 1.53 to 1.71]) and higher among patients with prior use of NOACs (ARD, 3.3% [97.5% CI, 1.7% to 4.8%]; AOR, 1.21 [97.5% CI, 1.11-1.32]).\n[10] Compared with patients with prior use of warfarin, patients with prior use of NOACs had a lower risk of in-hospital mortality (ARD, −5.7% [97.5% CI, −7.3% to −4.2%]; AOR, 0.75 [97.5% CI, 0.69 to 0.81]).\n[11] The difference in mortality between NOAC-treated patients and warfarin-treated patients was numerically greater among patients with prior use of dual antiplatelet agents (32.7% vs 47.1%; ARD, −15.0% [95.5% CI, −26.3% to −3.8%]; AOR, 0.50 [97.5% CI, 0.29 to 0.86]) than among those taking these agents without prior antiplatelet therapy (26.4% vs 31.7%; ARD, −5.0% [97.5% CI, −6.8% to −3.2%]; AOR, 0.77 [97.5% CI, 0.70 to 0.85]), although the interaction P value (.07) was not statistically significant.\n[12] Conclusions and Relevance Among patients with ICH, prior use of NOACs or warfarin was associated with higher in-hospital mortality compared with no OACs.\n[13] Prior use of NOACs, compared with prior use of warfarin, was associated with lower risk of in-hospital mortality."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"The unadjusted in-hospital mortality rates were 32.6% for warfarin, 26.5% for NOACs, and 22.5% for no OACs.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1103, "doc_id": 3898784, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [3898784], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Stroke patients with prior use of direct oral anticoagulants have a higher risk of in-hospital mortality than stroke patients with prior use of warfarin.\n\nDocument title: Association of Intracerebral Hemorrhage Among Patients Taking Non–Vitamin K Antagonist vs Vitamin K Antagonist Oral Anticoagulants With In-Hospital Mortality\n\nAbstract sentences:\n[0] Importance Although non–vitamin K antagonist oral anticoagulants (NOACs) are increasingly used to prevent thromboembolic disease, there are limited data on NOAC-related intracerebral hemorrhage (ICH).\n[1] Objective To assess the association between preceding oral anticoagulant use (warfarin, NOACs, and no oral anticoagulants [OACs]) and in-hospital mortality among patients with ICH.\n[2] Design, Setting, and Participants Retrospective cohort study of 141 311 patients with ICH admitted from October 2013 to December 2016 to 1662 Get With The Guidelines–Stroke hospitals.\n[3] Exposures Anticoagulation therapy before ICH, defined as any use of OACs within 7 days prior to hospital arrival.\n[4] Main Outcomes and Measures In-hospital mortality.\n[5] Results Among 141 311 patients with ICH (mean [SD] age, 68.3 [15.3] years; 48.1% women), 15 036 (10.6%) were taking warfarin and 4918 (3.5%) were taking NOACs preceding ICH, and 39 585 (28.0%) and 5783 (4.1%) were taking concomitant single and dual antiplatelet agents, respectively.\n[6] Patients with prior use of warfarin or NOACs were older and had higher prevalence of atrial fibrillation and prior stroke.\n[7] Acute ICH stroke severity (measured by the National Institutes of Health Stroke Scale) was not significantly different across the 3 groups (median, 9 [interquartile range, 2-21] for warfarin, 8 [2-20] for NOACs, and 8 [2-19] for no OACs).\n[8] The unadjusted in-hospital mortality rates were 32.6% for warfarin, 26.5% for NOACs, and 22.5% for no OACs.\n[9] Compared with patients without prior use of OACs, the risk of in-hospital mortality was higher among patients with prior use of warfarin (adjusted risk difference [ARD], 9.0% [97.5% CI, 7.9% to 10.1%]; adjusted odds ratio [AOR], 1.62 [97.5% CI, 1.53 to 1.71]) and higher among patients with prior use of NOACs (ARD, 3.3% [97.5% CI, 1.7% to 4.8%]; AOR, 1.21 [97.5% CI, 1.11-1.32]).\n[10] Compared with patients with prior use of warfarin, patients with prior use of NOACs had a lower risk of in-hospital mortality (ARD, −5.7% [97.5% CI, −7.3% to −4.2%]; AOR, 0.75 [97.5% CI, 0.69 to 0.81]).\n[11] The difference in mortality between NOAC-treated patients and warfarin-treated patients was numerically greater among patients with prior use of dual antiplatelet agents (32.7% vs 47.1%; ARD, −15.0% [95.5% CI, −26.3% to −3.8%]; AOR, 0.50 [97.5% CI, 0.29 to 0.86]) than among those taking these agents without prior antiplatelet therapy (26.4% vs 31.7%; ARD, −5.0% [97.5% CI, −6.8% to −3.2%]; AOR, 0.77 [97.5% CI, 0.70 to 0.85]), although the interaction P value (.07) was not statistically significant.\n[12] Conclusions and Relevance Among patients with ICH, prior use of NOACs or warfarin was associated with higher in-hospital mortality compared with no OACs.\n[13] Prior use of NOACs, compared with prior use of warfarin, was associated with lower risk of in-hospital mortality."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Compared with patients without prior use of OACs, the risk of in-hospital mortality was higher among patients with prior use of warfarin (adjusted risk difference [ARD], 9.0% [97.5% CI, 7.9% to 10.1%]; adjusted odds ratio [AOR], 1.62 [97.5% CI, 1.53 to 1.71]) and higher among patients with prior use of NOACs (ARD, 3.3% [97.5% CI, 1.7% to 4.8%]; AOR, 1.21 [97.5% CI, 1.11-1.32]).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1103, "doc_id": 3898784, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [3898784], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Stroke patients with prior use of direct oral anticoagulants have a higher risk of in-hospital mortality than stroke patients with prior use of warfarin.\n\nDocument title: Association of Intracerebral Hemorrhage Among Patients Taking Non–Vitamin K Antagonist vs Vitamin K Antagonist Oral Anticoagulants With In-Hospital Mortality\n\nAbstract sentences:\n[0] Importance Although non–vitamin K antagonist oral anticoagulants (NOACs) are increasingly used to prevent thromboembolic disease, there are limited data on NOAC-related intracerebral hemorrhage (ICH).\n[1] Objective To assess the association between preceding oral anticoagulant use (warfarin, NOACs, and no oral anticoagulants [OACs]) and in-hospital mortality among patients with ICH.\n[2] Design, Setting, and Participants Retrospective cohort study of 141 311 patients with ICH admitted from October 2013 to December 2016 to 1662 Get With The Guidelines–Stroke hospitals.\n[3] Exposures Anticoagulation therapy before ICH, defined as any use of OACs within 7 days prior to hospital arrival.\n[4] Main Outcomes and Measures In-hospital mortality.\n[5] Results Among 141 311 patients with ICH (mean [SD] age, 68.3 [15.3] years; 48.1% women), 15 036 (10.6%) were taking warfarin and 4918 (3.5%) were taking NOACs preceding ICH, and 39 585 (28.0%) and 5783 (4.1%) were taking concomitant single and dual antiplatelet agents, respectively.\n[6] Patients with prior use of warfarin or NOACs were older and had higher prevalence of atrial fibrillation and prior stroke.\n[7] Acute ICH stroke severity (measured by the National Institutes of Health Stroke Scale) was not significantly different across the 3 groups (median, 9 [interquartile range, 2-21] for warfarin, 8 [2-20] for NOACs, and 8 [2-19] for no OACs).\n[8] The unadjusted in-hospital mortality rates were 32.6% for warfarin, 26.5% for NOACs, and 22.5% for no OACs.\n[9] Compared with patients without prior use of OACs, the risk of in-hospital mortality was higher among patients with prior use of warfarin (adjusted risk difference [ARD], 9.0% [97.5% CI, 7.9% to 10.1%]; adjusted odds ratio [AOR], 1.62 [97.5% CI, 1.53 to 1.71]) and higher among patients with prior use of NOACs (ARD, 3.3% [97.5% CI, 1.7% to 4.8%]; AOR, 1.21 [97.5% CI, 1.11-1.32]).\n[10] Compared with patients with prior use of warfarin, patients with prior use of NOACs had a lower risk of in-hospital mortality (ARD, −5.7% [97.5% CI, −7.3% to −4.2%]; AOR, 0.75 [97.5% CI, 0.69 to 0.81]).\n[11] The difference in mortality between NOAC-treated patients and warfarin-treated patients was numerically greater among patients with prior use of dual antiplatelet agents (32.7% vs 47.1%; ARD, −15.0% [95.5% CI, −26.3% to −3.8%]; AOR, 0.50 [97.5% CI, 0.29 to 0.86]) than among those taking these agents without prior antiplatelet therapy (26.4% vs 31.7%; ARD, −5.0% [97.5% CI, −6.8% to −3.2%]; AOR, 0.77 [97.5% CI, 0.70 to 0.85]), although the interaction P value (.07) was not statistically significant.\n[12] Conclusions and Relevance Among patients with ICH, prior use of NOACs or warfarin was associated with higher in-hospital mortality compared with no OACs.\n[13] Prior use of NOACs, compared with prior use of warfarin, was associated with lower risk of in-hospital mortality."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Compared with patients with prior use of warfarin, patients with prior use of NOACs had a lower risk of in-hospital mortality (ARD, −5.7% [97.5% CI, −7.3% to −4.2%]; AOR, 0.75 [97.5% CI, 0.69 to 0.81]).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1103, "doc_id": 3898784, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [3898784], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Stroke patients with prior use of direct oral anticoagulants have a higher risk of in-hospital mortality than stroke patients with prior use of warfarin.\n\nDocument title: Association of Intracerebral Hemorrhage Among Patients Taking Non–Vitamin K Antagonist vs Vitamin K Antagonist Oral Anticoagulants With In-Hospital Mortality\n\nAbstract sentences:\n[0] Importance Although non–vitamin K antagonist oral anticoagulants (NOACs) are increasingly used to prevent thromboembolic disease, there are limited data on NOAC-related intracerebral hemorrhage (ICH).\n[1] Objective To assess the association between preceding oral anticoagulant use (warfarin, NOACs, and no oral anticoagulants [OACs]) and in-hospital mortality among patients with ICH.\n[2] Design, Setting, and Participants Retrospective cohort study of 141 311 patients with ICH admitted from October 2013 to December 2016 to 1662 Get With The Guidelines–Stroke hospitals.\n[3] Exposures Anticoagulation therapy before ICH, defined as any use of OACs within 7 days prior to hospital arrival.\n[4] Main Outcomes and Measures In-hospital mortality.\n[5] Results Among 141 311 patients with ICH (mean [SD] age, 68.3 [15.3] years; 48.1% women), 15 036 (10.6%) were taking warfarin and 4918 (3.5%) were taking NOACs preceding ICH, and 39 585 (28.0%) and 5783 (4.1%) were taking concomitant single and dual antiplatelet agents, respectively.\n[6] Patients with prior use of warfarin or NOACs were older and had higher prevalence of atrial fibrillation and prior stroke.\n[7] Acute ICH stroke severity (measured by the National Institutes of Health Stroke Scale) was not significantly different across the 3 groups (median, 9 [interquartile range, 2-21] for warfarin, 8 [2-20] for NOACs, and 8 [2-19] for no OACs).\n[8] The unadjusted in-hospital mortality rates were 32.6% for warfarin, 26.5% for NOACs, and 22.5% for no OACs.\n[9] Compared with patients without prior use of OACs, the risk of in-hospital mortality was higher among patients with prior use of warfarin (adjusted risk difference [ARD], 9.0% [97.5% CI, 7.9% to 10.1%]; adjusted odds ratio [AOR], 1.62 [97.5% CI, 1.53 to 1.71]) and higher among patients with prior use of NOACs (ARD, 3.3% [97.5% CI, 1.7% to 4.8%]; AOR, 1.21 [97.5% CI, 1.11-1.32]).\n[10] Compared with patients with prior use of warfarin, patients with prior use of NOACs had a lower risk of in-hospital mortality (ARD, −5.7% [97.5% CI, −7.3% to −4.2%]; AOR, 0.75 [97.5% CI, 0.69 to 0.81]).\n[11] The difference in mortality between NOAC-treated patients and warfarin-treated patients was numerically greater among patients with prior use of dual antiplatelet agents (32.7% vs 47.1%; ARD, −15.0% [95.5% CI, −26.3% to −3.8%]; AOR, 0.50 [97.5% CI, 0.29 to 0.86]) than among those taking these agents without prior antiplatelet therapy (26.4% vs 31.7%; ARD, −5.0% [97.5% CI, −6.8% to −3.2%]; AOR, 0.77 [97.5% CI, 0.70 to 0.85]), although the interaction P value (.07) was not statistically significant.\n[12] Conclusions and Relevance Among patients with ICH, prior use of NOACs or warfarin was associated with higher in-hospital mortality compared with no OACs.\n[13] Prior use of NOACs, compared with prior use of warfarin, was associated with lower risk of in-hospital mortality."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"Prior use of NOACs, compared with prior use of warfarin, was associated with lower risk of in-hospital mortality.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1103, "doc_id": 3898784, "label": "CONTRADICTS", "evidence_sentence_ids": [13], "cited_doc_ids": [3898784], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Students who perform poorly in the early years of medical school are at increased risk for professional misconduct later in their careers.\n\nDocument title: Risk factors at medical school for subsequent professional misconduct: multicentre retrospective case-control study\n\nAbstract sentences:\n[0] OBJECTIVE To determine whether there are risk factors in a doctor's time at medical school that are associated with subsequent professional misconduct.\n[1] DESIGN Matched case-control study.\n[2] Setting Records from medical schools and the General Medical Council (GMC).\n[3] PARTICIPANTS 59 doctors who had graduated from any one of eight medical schools in the United Kingdom in 1958-97 and had a proved finding of serious professional misconduct in GMC proceedings in 1999-2004 (cases); 236 controls (four for each case) were selected by systematic sampling from matching graduation cohorts.\n[4] Case-control status was revealed by the GMC after completion of data entry.\n[5] MAIN OUTCOME MEASURE Odds ratios for being a \"case,\" with multivariable conditional logistic regression of potential risk factors including pre-admission characteristics and progress during the course.\n[6] These data were obtained from anonymised copies of the students' progress files held by their original medical schools.\n[7] RESULTS Univariate conditional logistic regression analysis found that cases were more likely to be men, to be of lower estimated social class, and to have had academic difficulties during their medical course, especially in the early years.\n[8] Multivariable analysis showed that male sex (odds ratio 9.80, 95% confidence interval 2.43 to 39.44, P=0.001), lower social class (4.28, 1.52 to 12.09, P=0.006), and failure of early or preclinical examinations (5.47, 2.17 to 13.79, P<0.001) were independently associated with being a case.\n[9] CONCLUSIONS This small study suggests that male sex, a lower socioeconomic background, and early academic difficulties at medical school could be risk factors for subsequent professional misconduct.\n[10] The findings are preliminary and should be interpreted with caution.\n[11] Most doctors with risk factors will not come before the GMC's disciplinary panels."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"RESULTS Univariate conditional logistic regression analysis found that cases were more likely to be men, to be of lower estimated social class, and to have had academic difficulties during their medical course, especially in the early years.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1105, "doc_id": 6710713, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [6710713], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Students who perform poorly in the early years of medical school are at increased risk for professional misconduct later in their careers.\n\nDocument title: Risk factors at medical school for subsequent professional misconduct: multicentre retrospective case-control study\n\nAbstract sentences:\n[0] OBJECTIVE To determine whether there are risk factors in a doctor's time at medical school that are associated with subsequent professional misconduct.\n[1] DESIGN Matched case-control study.\n[2] Setting Records from medical schools and the General Medical Council (GMC).\n[3] PARTICIPANTS 59 doctors who had graduated from any one of eight medical schools in the United Kingdom in 1958-97 and had a proved finding of serious professional misconduct in GMC proceedings in 1999-2004 (cases); 236 controls (four for each case) were selected by systematic sampling from matching graduation cohorts.\n[4] Case-control status was revealed by the GMC after completion of data entry.\n[5] MAIN OUTCOME MEASURE Odds ratios for being a \"case,\" with multivariable conditional logistic regression of potential risk factors including pre-admission characteristics and progress during the course.\n[6] These data were obtained from anonymised copies of the students' progress files held by their original medical schools.\n[7] RESULTS Univariate conditional logistic regression analysis found that cases were more likely to be men, to be of lower estimated social class, and to have had academic difficulties during their medical course, especially in the early years.\n[8] Multivariable analysis showed that male sex (odds ratio 9.80, 95% confidence interval 2.43 to 39.44, P=0.001), lower social class (4.28, 1.52 to 12.09, P=0.006), and failure of early or preclinical examinations (5.47, 2.17 to 13.79, P<0.001) were independently associated with being a case.\n[9] CONCLUSIONS This small study suggests that male sex, a lower socioeconomic background, and early academic difficulties at medical school could be risk factors for subsequent professional misconduct.\n[10] The findings are preliminary and should be interpreted with caution.\n[11] Most doctors with risk factors will not come before the GMC's disciplinary panels."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Multivariable analysis showed that male sex (odds ratio 9.80, 95% confidence interval 2.43 to 39.44, P=0.001), lower social class (4.28, 1.52 to 12.09, P=0.006), and failure of early or preclinical examinations (5.47, 2.17 to 13.79, P<0.001) were independently associated with being a case.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1105, "doc_id": 6710713, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [6710713], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Students who perform poorly in the early years of medical school are at increased risk for professional misconduct later in their careers.\n\nDocument title: Risk factors at medical school for subsequent professional misconduct: multicentre retrospective case-control study\n\nAbstract sentences:\n[0] OBJECTIVE To determine whether there are risk factors in a doctor's time at medical school that are associated with subsequent professional misconduct.\n[1] DESIGN Matched case-control study.\n[2] Setting Records from medical schools and the General Medical Council (GMC).\n[3] PARTICIPANTS 59 doctors who had graduated from any one of eight medical schools in the United Kingdom in 1958-97 and had a proved finding of serious professional misconduct in GMC proceedings in 1999-2004 (cases); 236 controls (four for each case) were selected by systematic sampling from matching graduation cohorts.\n[4] Case-control status was revealed by the GMC after completion of data entry.\n[5] MAIN OUTCOME MEASURE Odds ratios for being a \"case,\" with multivariable conditional logistic regression of potential risk factors including pre-admission characteristics and progress during the course.\n[6] These data were obtained from anonymised copies of the students' progress files held by their original medical schools.\n[7] RESULTS Univariate conditional logistic regression analysis found that cases were more likely to be men, to be of lower estimated social class, and to have had academic difficulties during their medical course, especially in the early years.\n[8] Multivariable analysis showed that male sex (odds ratio 9.80, 95% confidence interval 2.43 to 39.44, P=0.001), lower social class (4.28, 1.52 to 12.09, P=0.006), and failure of early or preclinical examinations (5.47, 2.17 to 13.79, P<0.001) were independently associated with being a case.\n[9] CONCLUSIONS This small study suggests that male sex, a lower socioeconomic background, and early academic difficulties at medical school could be risk factors for subsequent professional misconduct.\n[10] The findings are preliminary and should be interpreted with caution.\n[11] Most doctors with risk factors will not come before the GMC's disciplinary panels."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"CONCLUSIONS This small study suggests that male sex, a lower socioeconomic background, and early academic difficulties at medical school could be risk factors for subsequent professional misconduct.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1105, "doc_id": 6710713, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [6710713], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Students who perform poorly in the early years of medical school are less likely to commit professional misconduct later in their careers.\n\nDocument title: Risk factors at medical school for subsequent professional misconduct: multicentre retrospective case-control study\n\nAbstract sentences:\n[0] OBJECTIVE To determine whether there are risk factors in a doctor's time at medical school that are associated with subsequent professional misconduct.\n[1] DESIGN Matched case-control study.\n[2] Setting Records from medical schools and the General Medical Council (GMC).\n[3] PARTICIPANTS 59 doctors who had graduated from any one of eight medical schools in the United Kingdom in 1958-97 and had a proved finding of serious professional misconduct in GMC proceedings in 1999-2004 (cases); 236 controls (four for each case) were selected by systematic sampling from matching graduation cohorts.\n[4] Case-control status was revealed by the GMC after completion of data entry.\n[5] MAIN OUTCOME MEASURE Odds ratios for being a \"case,\" with multivariable conditional logistic regression of potential risk factors including pre-admission characteristics and progress during the course.\n[6] These data were obtained from anonymised copies of the students' progress files held by their original medical schools.\n[7] RESULTS Univariate conditional logistic regression analysis found that cases were more likely to be men, to be of lower estimated social class, and to have had academic difficulties during their medical course, especially in the early years.\n[8] Multivariable analysis showed that male sex (odds ratio 9.80, 95% confidence interval 2.43 to 39.44, P=0.001), lower social class (4.28, 1.52 to 12.09, P=0.006), and failure of early or preclinical examinations (5.47, 2.17 to 13.79, P<0.001) were independently associated with being a case.\n[9] CONCLUSIONS This small study suggests that male sex, a lower socioeconomic background, and early academic difficulties at medical school could be risk factors for subsequent professional misconduct.\n[10] The findings are preliminary and should be interpreted with caution.\n[11] Most doctors with risk factors will not come before the GMC's disciplinary panels."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"RESULTS Univariate conditional logistic regression analysis found that cases were more likely to be men, to be of lower estimated social class, and to have had academic difficulties during their medical course, especially in the early years.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1106, "doc_id": 6710713, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [6710713], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Students who perform poorly in the early years of medical school are less likely to commit professional misconduct later in their careers.\n\nDocument title: Risk factors at medical school for subsequent professional misconduct: multicentre retrospective case-control study\n\nAbstract sentences:\n[0] OBJECTIVE To determine whether there are risk factors in a doctor's time at medical school that are associated with subsequent professional misconduct.\n[1] DESIGN Matched case-control study.\n[2] Setting Records from medical schools and the General Medical Council (GMC).\n[3] PARTICIPANTS 59 doctors who had graduated from any one of eight medical schools in the United Kingdom in 1958-97 and had a proved finding of serious professional misconduct in GMC proceedings in 1999-2004 (cases); 236 controls (four for each case) were selected by systematic sampling from matching graduation cohorts.\n[4] Case-control status was revealed by the GMC after completion of data entry.\n[5] MAIN OUTCOME MEASURE Odds ratios for being a \"case,\" with multivariable conditional logistic regression of potential risk factors including pre-admission characteristics and progress during the course.\n[6] These data were obtained from anonymised copies of the students' progress files held by their original medical schools.\n[7] RESULTS Univariate conditional logistic regression analysis found that cases were more likely to be men, to be of lower estimated social class, and to have had academic difficulties during their medical course, especially in the early years.\n[8] Multivariable analysis showed that male sex (odds ratio 9.80, 95% confidence interval 2.43 to 39.44, P=0.001), lower social class (4.28, 1.52 to 12.09, P=0.006), and failure of early or preclinical examinations (5.47, 2.17 to 13.79, P<0.001) were independently associated with being a case.\n[9] CONCLUSIONS This small study suggests that male sex, a lower socioeconomic background, and early academic difficulties at medical school could be risk factors for subsequent professional misconduct.\n[10] The findings are preliminary and should be interpreted with caution.\n[11] Most doctors with risk factors will not come before the GMC's disciplinary panels."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Multivariable analysis showed that male sex (odds ratio 9.80, 95% confidence interval 2.43 to 39.44, P=0.001), lower social class (4.28, 1.52 to 12.09, P=0.006), and failure of early or preclinical examinations (5.47, 2.17 to 13.79, P<0.001) were independently associated with being a case.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1106, "doc_id": 6710713, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [6710713], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Students who perform poorly in the early years of medical school are less likely to commit professional misconduct later in their careers.\n\nDocument title: Risk factors at medical school for subsequent professional misconduct: multicentre retrospective case-control study\n\nAbstract sentences:\n[0] OBJECTIVE To determine whether there are risk factors in a doctor's time at medical school that are associated with subsequent professional misconduct.\n[1] DESIGN Matched case-control study.\n[2] Setting Records from medical schools and the General Medical Council (GMC).\n[3] PARTICIPANTS 59 doctors who had graduated from any one of eight medical schools in the United Kingdom in 1958-97 and had a proved finding of serious professional misconduct in GMC proceedings in 1999-2004 (cases); 236 controls (four for each case) were selected by systematic sampling from matching graduation cohorts.\n[4] Case-control status was revealed by the GMC after completion of data entry.\n[5] MAIN OUTCOME MEASURE Odds ratios for being a \"case,\" with multivariable conditional logistic regression of potential risk factors including pre-admission characteristics and progress during the course.\n[6] These data were obtained from anonymised copies of the students' progress files held by their original medical schools.\n[7] RESULTS Univariate conditional logistic regression analysis found that cases were more likely to be men, to be of lower estimated social class, and to have had academic difficulties during their medical course, especially in the early years.\n[8] Multivariable analysis showed that male sex (odds ratio 9.80, 95% confidence interval 2.43 to 39.44, P=0.001), lower social class (4.28, 1.52 to 12.09, P=0.006), and failure of early or preclinical examinations (5.47, 2.17 to 13.79, P<0.001) were independently associated with being a case.\n[9] CONCLUSIONS This small study suggests that male sex, a lower socioeconomic background, and early academic difficulties at medical school could be risk factors for subsequent professional misconduct.\n[10] The findings are preliminary and should be interpreted with caution.\n[11] Most doctors with risk factors will not come before the GMC's disciplinary panels."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"CONCLUSIONS This small study suggests that male sex, a lower socioeconomic background, and early academic difficulties at medical school could be risk factors for subsequent professional misconduct.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1106, "doc_id": 6710713, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [6710713], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Suboptimal nutrition is a leading cause of premature death\n\nDocument title: Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015\n\nAbstract sentences:\n[0] BACKGROUND The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease.\n[1] By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context.\n[2] METHODS We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015.\n[3] This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence.\n[4] We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources.\n[5] We used statistical models to pool data, adjust for bias, and incorporate covariates.\n[6] We developed a metric that allows comparisons of exposure across risk factors-the summary exposure value.\n[7] Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk.\n[8] We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates.\n[9] We characterised risk exposure in relation to a Socio-demographic Index (SDI).\n[10] FINDINGS Between 1990 and 2015, global exposure to unsafe sanitation, household air pollution, childhood underweight, childhood stunting, and smoking each decreased by more than 25%.\n[11] Global exposure for several occupational risks, high body-mass index (BMI), and drug use increased by more than 25% over the same period.\n[12] All risks jointly evaluated in 2015 accounted for 57·8% (95% CI 56·6-58·8) of global deaths and 41·2% (39·8-42·8) of DALYs.\n[13] In 2015, the ten largest contributors to global DALYs among Level 3 risks were high systolic blood pressure (211·8 million [192·7 million to 231·1 million] global DALYs), smoking (148·6 million [134·2 million to 163·1 million]), high fasting plasma glucose (143·1 million [125·1 million to 163·5 million]), high BMI (120·1 million [83·8 million to 158·4 million]), childhood undernutrition (113·3 million [103·9 million to 123·4 million]), ambient particulate matter (103·1 million [90·8 million to 115·1 million]), high total cholesterol (88·7 million [74·6 million to 105·7 million]), household air pollution (85·6 million [66·7 million to 106·1 million]), alcohol use (85·0 million [77·2 million to 93·0 million]), and diets high in sodium (83·0 million [49·3 million to 127·5 million]).\n[14] From 1990 to 2015, attributable DALYs declined for micronutrient deficiencies, childhood undernutrition, unsafe sanitation and water, and household air pollution; reductions in risk-deleted DALY rates rather than reductions in exposure drove these declines.\n[15] Rising exposure contributed to notable increases in attributable DALYs from high BMI, high fasting plasma glucose, occupational carcinogens, and drug use.\n[16] Environmental risks and childhood undernutrition declined steadily with SDI; low physical activity, high BMI, and high fasting plasma glucose increased with SDI.\n[17] In 119 countries, metabolic risks, such as high BMI and fasting plasma glucose, contributed the most attributable DALYs in 2015.\n[18] Regionally, smoking still ranked among the leading five risk factors for attributable DALYs in 109 countries; childhood underweight and unsafe sex remained primary drivers of early death and disability in much of sub-Saharan Africa.\n[19] INTERPRETATION Declines in some key environmental risks have contributed to declines in critical infectious diseases.\n[20] Some risks appear to be invariant to SDI.\n[21] Increasing risks, including high BMI, high fasting plasma glucose, drug use, and some occupational exposures, contribute to rising burden from some conditions, but also provide opportunities for intervention.\n[22] Some highly preventable risks, such as smoking, remain major causes of attributable DALYs, even as exposure is declining.\n[23] Public policy makers need to pay attention to the risks that are increasingly major contributors to global burden.\n[24] FUNDING Bill & Melinda Gates Foundation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"In 2015, the ten largest contributors to global DALYs among Level 3 risks were high systolic blood pressure (211·8 million [192·7 million to 231·1 million] global DALYs), smoking (148·6 million [134·2 million to 163·1 million]), high fasting plasma glucose (143·1 million [125·1 million to 163·5 million]), high BMI (120·1 million [83·8 million to 158·4 million]), childhood undernutrition (113·3 million [103·9 million to 123·4 million]), ambient particulate matter (103·1 million [90·8 million to 115·1 million]), high total cholesterol (88·7 million [74·6 million to 105·7 million]), household air pollution (85·6 million [66·7 million to 106·1 million]), alcohol use (85·0 million [77·2 million to 93·0 million]), and diets high in sodium (83·0 million [49·3 million to 127·5 million]).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1109, "doc_id": 13770184, "label": "SUPPORTS", "evidence_sentence_ids": [13], "cited_doc_ids": [13770184, 8582337], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Suboptimal nutrition is a leading cause of premature death\n\nDocument title: The state of US health, 1990-2010: burden of diseases, injuries, and risk factors.\n\nAbstract sentences:\n[0] IMPORTANCE Understanding the major health problems in the United States and how they are changing over time is critical for informing national health policy.\n[1] OBJECTIVES To measure the burden of diseases, injuries, and leading risk factors in the United States from 1990 to 2010 and to compare these measurements with those of the 34 countries in the Organisation for Economic Co-operation and Development (OECD) countries.\n[2] DESIGN We used the systematic analysis of descriptive epidemiology of 291 diseases and injuries, 1160 sequelae of these diseases and injuries, and 67 risk factors or clusters of risk factors from 1990 to 2010 for 187 countries developed for the Global Burden of Disease 2010 Study to describe the health status of the United States and to compare US health outcomes with those of 34 OECD countries.\n[3] Years of life lost due to premature mortality (YLLs) were computed by multiplying the number of deaths at each age by a reference life expectancy at that age.\n[4] Years lived with disability (YLDs) were calculated by multiplying prevalence (based on systematic reviews) by the disability weight (based on population-based surveys) for each sequela; disability in this study refers to any short- or long-term loss of health.\n[5] Disability-adjusted life-years (DALYs) were estimated as the sum of YLDs and YLLs.\n[6] Deaths and DALYs related to risk factors were based on systematic reviews and meta-analyses of exposure data and relative risks for risk-outcome pairs.\n[7] Healthy life expectancy (HALE) was used to summarize overall population health, accounting for both length of life and levels of ill health experienced at different ages.\n[8] RESULTS US life expectancy for both sexes combined increased from 75.2 years in 1990 to 78.2 years in 2010; during the same period, HALE increased from 65.8 years to 68.1 years.\n[9] The diseases and injuries with the largest number of YLLs in 2010 were ischemic heart disease, lung cancer, stroke, chronic obstructive pulmonary disease, and road injury.\n[10] Age-standardized YLL rates increased for Alzheimer disease, drug use disorders, chronic kidney disease, kidney cancer, and falls.\n[11] The diseases with the largest number of YLDs in 2010 were low back pain, major depressive disorder, other musculoskeletal disorders, neck pain, and anxiety disorders.\n[12] As the US population has aged, YLDs have comprised a larger share of DALYs than have YLLs.\n[13] The leading risk factors related to DALYs were dietary risks, tobacco smoking, high body mass index, high blood pressure, high fasting plasma glucose, physical inactivity, and alcohol use.\n[14] Among 34 OECD countries between 1990 and 2010, the US rank for the age-standardized death rate changed from 18th to 27th, for the age-standardized YLL rate from 23rd to 28th, for the age-standardized YLD rate from 5th to 6th, for life expectancy at birth from 20th to 27th, and for HALE from 14th to 26th.\n[15] CONCLUSIONS AND RELEVANCE From 1990 to 2010, the United States made substantial progress in improving health.\n[16] Life expectancy at birth and HALE increased, all-cause death rates at all ages decreased, and age-specific rates of years lived with disability remained stable.\n[17] However, morbidity and chronic disability now account for nearly half of the US health burden, and improvements in population health in the United States have not kept pace with advances in population health in other wealthy nations."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"The leading risk factors related to DALYs were dietary risks, tobacco smoking, high body mass index, high blood pressure, high fasting plasma glucose, physical inactivity, and alcohol use.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1109, "doc_id": 8582337, "label": "SUPPORTS", "evidence_sentence_ids": [13], "cited_doc_ids": [13770184, 8582337], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Sudden death can occur in patients with complex ventricular arrhythmias.\n\nDocument title: Myocardial muscarinic receptor upregulation and normal response to isoproterenol in denervated hearts by familial amyloid polyneuropathy.\n\nAbstract sentences:\n[0] BACKGROUND Patients with familial amyloid polyneuropathy, a rare hereditary form of amyloidosis, have progressive autonomic neuropathy.\n[1] The disease usually does not induce heart failure but is associated with sudden death, conduction disturbances, and an increased risk of complications during anesthesia.\n[2] Although cardiac sympathetic denervation has been clearly demonstrated, the postsynaptic status of the cardiac autonomic nervous system remains unelucidated.\n[3] METHODS AND RESULTS Twenty-one patients were studied (age, 39+/-11 years; normal coronary arteries; left ventricular ejection fraction 68+/-9%).\n[4] To evaluate the density and affinity constants of myocardial muscarinic receptors, PET with (11)C-MQNB (methylquinuclidinyl benzilate), a specific hydrophilic antagonist, was used.\n[5] Cardiac beta-receptor functional efficiency was studied by the heart rate (HR) response to intravenous infusion of isoproterenol (5 minutes after 2 mg of atropine, 5, 10, and 15 ng/kg per minute during 5 minutes per step).\n[6] The mean muscarinic receptor density was higher in patients than in control subjects (B'(max), 35.5+/-8.9 versus 26.1+/-6.7 pmol/mL, P=0.003), without change in receptor affinity.\n[7] The increase in HR after injection of atropine as well as of MQNB was lower in patients compared with control subjects despite a similar basal HR (DeltaHR after atropine, 11+/-21% versus 62+/-17%; P<0.001), consistent with parasympathetic denervation.\n[8] Incremental infusion of isoproterenol induced a similar increase in HR in patients and control subjects.\n[9] CONCLUSIONS Cardiac autonomic denervation in familial amyloid polyneuropathy results in an upregulation of myocardial muscarinic receptors but without change in cardiac beta-receptor responsiveness to catecholamines."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1111, "doc_id": 1686881, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [1686881], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Sudden death can occur in patients with orthostatic hypertension without cardiac conduction abnormalities.\n\nDocument title: Myocardial muscarinic receptor upregulation and normal response to isoproterenol in denervated hearts by familial amyloid polyneuropathy.\n\nAbstract sentences:\n[0] BACKGROUND Patients with familial amyloid polyneuropathy, a rare hereditary form of amyloidosis, have progressive autonomic neuropathy.\n[1] The disease usually does not induce heart failure but is associated with sudden death, conduction disturbances, and an increased risk of complications during anesthesia.\n[2] Although cardiac sympathetic denervation has been clearly demonstrated, the postsynaptic status of the cardiac autonomic nervous system remains unelucidated.\n[3] METHODS AND RESULTS Twenty-one patients were studied (age, 39+/-11 years; normal coronary arteries; left ventricular ejection fraction 68+/-9%).\n[4] To evaluate the density and affinity constants of myocardial muscarinic receptors, PET with (11)C-MQNB (methylquinuclidinyl benzilate), a specific hydrophilic antagonist, was used.\n[5] Cardiac beta-receptor functional efficiency was studied by the heart rate (HR) response to intravenous infusion of isoproterenol (5 minutes after 2 mg of atropine, 5, 10, and 15 ng/kg per minute during 5 minutes per step).\n[6] The mean muscarinic receptor density was higher in patients than in control subjects (B'(max), 35.5+/-8.9 versus 26.1+/-6.7 pmol/mL, P=0.003), without change in receptor affinity.\n[7] The increase in HR after injection of atropine as well as of MQNB was lower in patients compared with control subjects despite a similar basal HR (DeltaHR after atropine, 11+/-21% versus 62+/-17%; P<0.001), consistent with parasympathetic denervation.\n[8] Incremental infusion of isoproterenol induced a similar increase in HR in patients and control subjects.\n[9] CONCLUSIONS Cardiac autonomic denervation in familial amyloid polyneuropathy results in an upregulation of myocardial muscarinic receptors but without change in cardiac beta-receptor responsiveness to catecholamines."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1112, "doc_id": 1686881, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [1686881], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Surfactin producing cells and exopolymer producing cells cooperate to generate \"Van Gogh\" bundles that have sliding abilities on specialized media.\n\nDocument title: From Cell Differentiation to Cell Collectives: Bacillus subtilis Uses Division of Labor to Migrate\n\nAbstract sentences:\n[0] The organization of cells, emerging from cell-cell interactions, can give rise to collective properties.\n[1] These properties are adaptive when together cells can face environmental challenges that they separately cannot.\n[2] One particular challenge that is important for microorganisms is migration.\n[3] In this study, we show how flagellum-independent migration is driven by the division of labor of two cell types that appear during Bacillus subtilis sliding motility.\n[4] Cell collectives organize themselves into bundles (called \"van Gogh bundles\") of tightly aligned cell chains that form filamentous loops at the colony edge.\n[5] We show, by time-course microscopy, that these loops migrate by pushing themselves away from the colony.\n[6] The formation of van Gogh bundles depends critically on the synergistic interaction of surfactin-producing and matrix-producing cells.\n[7] We propose that surfactin-producing cells reduce the friction between cells and their substrate, thereby facilitating matrix-producing cells to form bundles.\n[8] The folding properties of these bundles determine the rate of colony expansion.\n[9] Our study illustrates how the simple organization of cells within a community can yield a strong ecological advantage.\n[10] This is a key factor underlying the diverse origins of multicellularity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"The formation of van Gogh bundles depends critically on the synergistic interaction of surfactin-producing and matrix-producing cells.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1114, "doc_id": 12824568, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [12824568], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Surfactin producing cells and exopolymer producing cells cooperate to generate \"Van Gogh\" bundles that have sliding abilities on specialized media.\n\nDocument title: From Cell Differentiation to Cell Collectives: Bacillus subtilis Uses Division of Labor to Migrate\n\nAbstract sentences:\n[0] The organization of cells, emerging from cell-cell interactions, can give rise to collective properties.\n[1] These properties are adaptive when together cells can face environmental challenges that they separately cannot.\n[2] One particular challenge that is important for microorganisms is migration.\n[3] In this study, we show how flagellum-independent migration is driven by the division of labor of two cell types that appear during Bacillus subtilis sliding motility.\n[4] Cell collectives organize themselves into bundles (called \"van Gogh bundles\") of tightly aligned cell chains that form filamentous loops at the colony edge.\n[5] We show, by time-course microscopy, that these loops migrate by pushing themselves away from the colony.\n[6] The formation of van Gogh bundles depends critically on the synergistic interaction of surfactin-producing and matrix-producing cells.\n[7] We propose that surfactin-producing cells reduce the friction between cells and their substrate, thereby facilitating matrix-producing cells to form bundles.\n[8] The folding properties of these bundles determine the rate of colony expansion.\n[9] Our study illustrates how the simple organization of cells within a community can yield a strong ecological advantage.\n[10] This is a key factor underlying the diverse origins of multicellularity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"We propose that surfactin-producing cells reduce the friction between cells and their substrate, thereby facilitating matrix-producing cells to form bundles.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1114, "doc_id": 12824568, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [12824568], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Surgical treatment is not superior to non-surgical in treating adults with displaced fractures of the proximal humerus.\n\nDocument title: Surgical vs nonsurgical treatment of adults with displaced fractures of the proximal humerus: the PROFHER randomized clinical trial.\n\nAbstract sentences:\n[0] IMPORTANCE The need for surgery for the majority of patients with displaced proximal humeral fractures is unclear, but its use is increasing.\n[1] OBJECTIVE To evaluate the clinical effectiveness of surgical vs nonsurgical treatment for adults with displaced fractures of the proximal humerus involving the surgical neck.\n[2] DESIGN, SETTING, AND PARTICIPANTS A pragmatic, multicenter, parallel-group, randomized clinical trial, the Proximal Fracture of the Humerus Evaluation by Randomization (PROFHER) trial, recruited 250 patients aged 16 years or older (mean age, 66 years [range, 24-92 years]; 192 [77%] were female; and 249 [99.6%] were white) who presented at the orthopedic departments of 32 acute UK National Health Service hospitals between September 2008 and April 2011 within 3 weeks after sustaining a displaced fracture of the proximal humerus involving the surgical neck.\n[3] Patients were followed up for 2 years (up to April 2013) and 215 had complete follow-up data.\n[4] The data for 231 patients (114 in surgical group and 117 in nonsurgical group) were included in the primary analysis.\n[5] INTERVENTIONS Fracture fixation or humeral head replacement were performed by surgeons experienced in these techniques.\n[6] Nonsurgical treatment was sling immobilization.\n[7] Standardized outpatient and community-based rehabilitation was provided to both groups.\n[8] MAIN OUTCOMES AND MEASURES Primary outcome was the Oxford Shoulder Score (range, 0-48; higher scores indicate better outcomes) assessed during a 2-year period, with assessment and data collection at 6, 12, and 24 months.\n[9] Sample size was based on a minimal clinically important difference of 5 points for the Oxford Shoulder Score.\n[10] Secondary outcomes were the Short-Form 12 (SF-12), complications, subsequent therapy, and mortality.\n[11] RESULTS There was no significant mean treatment group difference in the Oxford Shoulder Score averaged over 2 years (39.07 points for the surgical group vs 38.32 points for the nonsurgical group; difference of 0.75 points [95% CI, -1.33 to 2.84 points]; P = .48) or at individual time points.\n[12] There were also no significant between-group differences over 2 years in the mean SF-12 physical component score (surgical group: 1.77 points higher [95% CI, -0.84 to 4.39 points];\n[13] P = .18); the mean SF-12 mental component score (surgical group: 1.28 points lower [95% CI, -3.80 to 1.23 points]; P = .32); complications related to surgery or shoulder fracture (30 patients in surgical group vs 23 patients in nonsurgical group; P = .28), requiring secondary surgery to the shoulder (11 patients in both groups), and increased or new shoulder-related therapy (7 patients vs 4 patients, respectively; P = .58); and mortality (9 patients vs 5 patients; P = .27).\n[14] Ten medical complications (2 cardiovascular events, 2 respiratory events, 2 gastrointestinal events, and 4 others) occurred in the surgical group during the postoperative hospital stay.\n[15] CONCLUSIONS AND RELEVANCE Among patients with displaced proximal humeral fractures involving the surgical neck, there was no significant difference between surgical treatment compared with nonsurgical treatment in patient-reported clinical outcomes over 2 years following fracture occurrence.\n[16] These results do not support the trend of increased surgery for patients with displaced fractures of the proximal humerus.\n[17] TRIAL REGISTRATION isrctn.com Identifier: ISRCTN50850043."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"RESULTS There was no significant mean treatment group difference in the Oxford Shoulder Score averaged over 2 years (39.07 points for the surgical group vs 38.32 points for the nonsurgical group; difference of 0.75 points [95% CI, -1.33 to 2.84 points]; P = .48) or at individual time points.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1115, "doc_id": 44048701, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [44048701], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Surgical treatment is not superior to non-surgical in treating adults with displaced fractures of the proximal humerus.\n\nDocument title: Surgical vs nonsurgical treatment of adults with displaced fractures of the proximal humerus: the PROFHER randomized clinical trial.\n\nAbstract sentences:\n[0] IMPORTANCE The need for surgery for the majority of patients with displaced proximal humeral fractures is unclear, but its use is increasing.\n[1] OBJECTIVE To evaluate the clinical effectiveness of surgical vs nonsurgical treatment for adults with displaced fractures of the proximal humerus involving the surgical neck.\n[2] DESIGN, SETTING, AND PARTICIPANTS A pragmatic, multicenter, parallel-group, randomized clinical trial, the Proximal Fracture of the Humerus Evaluation by Randomization (PROFHER) trial, recruited 250 patients aged 16 years or older (mean age, 66 years [range, 24-92 years]; 192 [77%] were female; and 249 [99.6%] were white) who presented at the orthopedic departments of 32 acute UK National Health Service hospitals between September 2008 and April 2011 within 3 weeks after sustaining a displaced fracture of the proximal humerus involving the surgical neck.\n[3] Patients were followed up for 2 years (up to April 2013) and 215 had complete follow-up data.\n[4] The data for 231 patients (114 in surgical group and 117 in nonsurgical group) were included in the primary analysis.\n[5] INTERVENTIONS Fracture fixation or humeral head replacement were performed by surgeons experienced in these techniques.\n[6] Nonsurgical treatment was sling immobilization.\n[7] Standardized outpatient and community-based rehabilitation was provided to both groups.\n[8] MAIN OUTCOMES AND MEASURES Primary outcome was the Oxford Shoulder Score (range, 0-48; higher scores indicate better outcomes) assessed during a 2-year period, with assessment and data collection at 6, 12, and 24 months.\n[9] Sample size was based on a minimal clinically important difference of 5 points for the Oxford Shoulder Score.\n[10] Secondary outcomes were the Short-Form 12 (SF-12), complications, subsequent therapy, and mortality.\n[11] RESULTS There was no significant mean treatment group difference in the Oxford Shoulder Score averaged over 2 years (39.07 points for the surgical group vs 38.32 points for the nonsurgical group; difference of 0.75 points [95% CI, -1.33 to 2.84 points]; P = .48) or at individual time points.\n[12] There were also no significant between-group differences over 2 years in the mean SF-12 physical component score (surgical group: 1.77 points higher [95% CI, -0.84 to 4.39 points];\n[13] P = .18); the mean SF-12 mental component score (surgical group: 1.28 points lower [95% CI, -3.80 to 1.23 points]; P = .32); complications related to surgery or shoulder fracture (30 patients in surgical group vs 23 patients in nonsurgical group; P = .28), requiring secondary surgery to the shoulder (11 patients in both groups), and increased or new shoulder-related therapy (7 patients vs 4 patients, respectively; P = .58); and mortality (9 patients vs 5 patients; P = .27).\n[14] Ten medical complications (2 cardiovascular events, 2 respiratory events, 2 gastrointestinal events, and 4 others) occurred in the surgical group during the postoperative hospital stay.\n[15] CONCLUSIONS AND RELEVANCE Among patients with displaced proximal humeral fractures involving the surgical neck, there was no significant difference between surgical treatment compared with nonsurgical treatment in patient-reported clinical outcomes over 2 years following fracture occurrence.\n[16] These results do not support the trend of increased surgery for patients with displaced fractures of the proximal humerus.\n[17] TRIAL REGISTRATION isrctn.com Identifier: ISRCTN50850043."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"There were also no significant between-group differences over 2 years in the mean SF-12 physical component score (surgical group: 1.77 points higher [95% CI, -0.84 to 4.39 points];\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1115, "doc_id": 44048701, "label": "SUPPORTS", "evidence_sentence_ids": [12], "cited_doc_ids": [44048701], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Surgical treatment is not superior to non-surgical in treating adults with displaced fractures of the proximal humerus.\n\nDocument title: Surgical vs nonsurgical treatment of adults with displaced fractures of the proximal humerus: the PROFHER randomized clinical trial.\n\nAbstract sentences:\n[0] IMPORTANCE The need for surgery for the majority of patients with displaced proximal humeral fractures is unclear, but its use is increasing.\n[1] OBJECTIVE To evaluate the clinical effectiveness of surgical vs nonsurgical treatment for adults with displaced fractures of the proximal humerus involving the surgical neck.\n[2] DESIGN, SETTING, AND PARTICIPANTS A pragmatic, multicenter, parallel-group, randomized clinical trial, the Proximal Fracture of the Humerus Evaluation by Randomization (PROFHER) trial, recruited 250 patients aged 16 years or older (mean age, 66 years [range, 24-92 years]; 192 [77%] were female; and 249 [99.6%] were white) who presented at the orthopedic departments of 32 acute UK National Health Service hospitals between September 2008 and April 2011 within 3 weeks after sustaining a displaced fracture of the proximal humerus involving the surgical neck.\n[3] Patients were followed up for 2 years (up to April 2013) and 215 had complete follow-up data.\n[4] The data for 231 patients (114 in surgical group and 117 in nonsurgical group) were included in the primary analysis.\n[5] INTERVENTIONS Fracture fixation or humeral head replacement were performed by surgeons experienced in these techniques.\n[6] Nonsurgical treatment was sling immobilization.\n[7] Standardized outpatient and community-based rehabilitation was provided to both groups.\n[8] MAIN OUTCOMES AND MEASURES Primary outcome was the Oxford Shoulder Score (range, 0-48; higher scores indicate better outcomes) assessed during a 2-year period, with assessment and data collection at 6, 12, and 24 months.\n[9] Sample size was based on a minimal clinically important difference of 5 points for the Oxford Shoulder Score.\n[10] Secondary outcomes were the Short-Form 12 (SF-12), complications, subsequent therapy, and mortality.\n[11] RESULTS There was no significant mean treatment group difference in the Oxford Shoulder Score averaged over 2 years (39.07 points for the surgical group vs 38.32 points for the nonsurgical group; difference of 0.75 points [95% CI, -1.33 to 2.84 points]; P = .48) or at individual time points.\n[12] There were also no significant between-group differences over 2 years in the mean SF-12 physical component score (surgical group: 1.77 points higher [95% CI, -0.84 to 4.39 points];\n[13] P = .18); the mean SF-12 mental component score (surgical group: 1.28 points lower [95% CI, -3.80 to 1.23 points]; P = .32); complications related to surgery or shoulder fracture (30 patients in surgical group vs 23 patients in nonsurgical group; P = .28), requiring secondary surgery to the shoulder (11 patients in both groups), and increased or new shoulder-related therapy (7 patients vs 4 patients, respectively; P = .58); and mortality (9 patients vs 5 patients; P = .27).\n[14] Ten medical complications (2 cardiovascular events, 2 respiratory events, 2 gastrointestinal events, and 4 others) occurred in the surgical group during the postoperative hospital stay.\n[15] CONCLUSIONS AND RELEVANCE Among patients with displaced proximal humeral fractures involving the surgical neck, there was no significant difference between surgical treatment compared with nonsurgical treatment in patient-reported clinical outcomes over 2 years following fracture occurrence.\n[16] These results do not support the trend of increased surgery for patients with displaced fractures of the proximal humerus.\n[17] TRIAL REGISTRATION isrctn.com Identifier: ISRCTN50850043."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"P = .18); the mean SF-12 mental component score (surgical group: 1.28 points lower [95% CI, -3.80 to 1.23 points]; P = .32); complications related to surgery or shoulder fracture (30 patients in surgical group vs 23 patients in nonsurgical group; P = .28), requiring secondary surgery to the shoulder (11 patients in both groups), and increased or new shoulder-related therapy (7 patients vs 4 patients, respectively; P = .58); and mortality (9 patients vs 5 patients; P = .27).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1115, "doc_id": 44048701, "label": "SUPPORTS", "evidence_sentence_ids": [13], "cited_doc_ids": [44048701], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Surgical treatment is not superior to non-surgical in treating adults with displaced fractures of the proximal humerus.\n\nDocument title: Surgical vs nonsurgical treatment of adults with displaced fractures of the proximal humerus: the PROFHER randomized clinical trial.\n\nAbstract sentences:\n[0] IMPORTANCE The need for surgery for the majority of patients with displaced proximal humeral fractures is unclear, but its use is increasing.\n[1] OBJECTIVE To evaluate the clinical effectiveness of surgical vs nonsurgical treatment for adults with displaced fractures of the proximal humerus involving the surgical neck.\n[2] DESIGN, SETTING, AND PARTICIPANTS A pragmatic, multicenter, parallel-group, randomized clinical trial, the Proximal Fracture of the Humerus Evaluation by Randomization (PROFHER) trial, recruited 250 patients aged 16 years or older (mean age, 66 years [range, 24-92 years]; 192 [77%] were female; and 249 [99.6%] were white) who presented at the orthopedic departments of 32 acute UK National Health Service hospitals between September 2008 and April 2011 within 3 weeks after sustaining a displaced fracture of the proximal humerus involving the surgical neck.\n[3] Patients were followed up for 2 years (up to April 2013) and 215 had complete follow-up data.\n[4] The data for 231 patients (114 in surgical group and 117 in nonsurgical group) were included in the primary analysis.\n[5] INTERVENTIONS Fracture fixation or humeral head replacement were performed by surgeons experienced in these techniques.\n[6] Nonsurgical treatment was sling immobilization.\n[7] Standardized outpatient and community-based rehabilitation was provided to both groups.\n[8] MAIN OUTCOMES AND MEASURES Primary outcome was the Oxford Shoulder Score (range, 0-48; higher scores indicate better outcomes) assessed during a 2-year period, with assessment and data collection at 6, 12, and 24 months.\n[9] Sample size was based on a minimal clinically important difference of 5 points for the Oxford Shoulder Score.\n[10] Secondary outcomes were the Short-Form 12 (SF-12), complications, subsequent therapy, and mortality.\n[11] RESULTS There was no significant mean treatment group difference in the Oxford Shoulder Score averaged over 2 years (39.07 points for the surgical group vs 38.32 points for the nonsurgical group; difference of 0.75 points [95% CI, -1.33 to 2.84 points]; P = .48) or at individual time points.\n[12] There were also no significant between-group differences over 2 years in the mean SF-12 physical component score (surgical group: 1.77 points higher [95% CI, -0.84 to 4.39 points];\n[13] P = .18); the mean SF-12 mental component score (surgical group: 1.28 points lower [95% CI, -3.80 to 1.23 points]; P = .32); complications related to surgery or shoulder fracture (30 patients in surgical group vs 23 patients in nonsurgical group; P = .28), requiring secondary surgery to the shoulder (11 patients in both groups), and increased or new shoulder-related therapy (7 patients vs 4 patients, respectively; P = .58); and mortality (9 patients vs 5 patients; P = .27).\n[14] Ten medical complications (2 cardiovascular events, 2 respiratory events, 2 gastrointestinal events, and 4 others) occurred in the surgical group during the postoperative hospital stay.\n[15] CONCLUSIONS AND RELEVANCE Among patients with displaced proximal humeral fractures involving the surgical neck, there was no significant difference between surgical treatment compared with nonsurgical treatment in patient-reported clinical outcomes over 2 years following fracture occurrence.\n[16] These results do not support the trend of increased surgery for patients with displaced fractures of the proximal humerus.\n[17] TRIAL REGISTRATION isrctn.com Identifier: ISRCTN50850043."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [15]\nExplanation: Evidence states: \"CONCLUSIONS AND RELEVANCE Among patients with displaced proximal humeral fractures involving the surgical neck, there was no significant difference between surgical treatment compared with nonsurgical treatment in patient-reported clinical outcomes over 2 years following fracture occurrence.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1115, "doc_id": 44048701, "label": "SUPPORTS", "evidence_sentence_ids": [15], "cited_doc_ids": [44048701], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Sweet taste receptors on the tongue are deactivated by between 1 and 10 mM glucose.\n\nDocument title: Detection of sweet and umami taste in the absence of taste receptor T1r3.\n\nAbstract sentences:\n[0] The tastes of sugars (sweet) and glutamate (umami) are thought to be detected by T1r receptors expressed in taste cells.\n[1] Molecular genetics and heterologous expression implicate T1r2 plus T1r3 as a sweet-responsive receptor,and T1r1 plus T1r3,as well as a truncated form of the type 4 metabotropic glutamate receptor (taste-mGluR4),as umami-responsive receptors.\n[2] Here,we show that mice lacking T1r3 showed no preference for artificial sweeteners and had diminished but not abolished behavioral and nerve responses to sugars and umami compounds.\n[3] These results indicate that T1r3-independent sweet- and umami-responsive receptors and/or pathways exist in taste cells."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1118, "doc_id": 23351136, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [23351136], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Sympathetic nerve activity is elevated throughout normal pregnancy.\n\nDocument title: Sympathetic neural mechanisms in normal and hypertensive pregnancy in humans.\n\nAbstract sentences:\n[0] BACKGROUND Direct recordings from peripheral sympathetic nerves have shown an increased sympathetic drive in pregnancy-induced hypertension (PIH) and preeclampsia (PE).\n[1] It is unknown whether sympathetic drive is altered in normal pregnancy, when arterial blood pressure can be normal or relatively low.\n[2] The aim of this study was to measure and compare peripheral sympathetic discharge, its vasoconstrictor effect and its baroreceptor control, during pregnancy and postpartum in women with normal pregnancy (NP) and PIH and in normotensive nonpregnant (NN) women.\n[3] METHODS AND RESULTS Twenty-one women with NP, 18 women with PIH, and 21 NN women had muscle sympathetic nerve activity assessed from multiunit discharges (MSNA) and from single units with defined vasoconstrictor properties (s-MSNA).\n[4] The s-MSNA in NP (38+/-6.6 impulses/100 beats) was greater (P<0.05) than in NN women (19+/-1.8 impulses/100 beats) despite similar age and body weight but less than in PIH women (P<0.001) (146+/-23.5 impulses/100 beats).\n[5] MSNA followed a similar trend.\n[6] Cardiac baroreceptor reflex sensitivity (BRS) was impaired in NP and PIH women relative to NN.\n[7] After delivery, sympathetic activity decreased to values similar to those obtained in NN, and there was an increase in BRS.\n[8] In women with NP, the decrease in sympathetic output occurred despite an insignificant change in blood pressure.\n[9] CONCLUSIONS Central sympathetic output was increased in women with normal pregnancy and was even greater in the hypertensive pregnant group.\n[10] The findings suggest that the moderate sympathetic hyperactivity during the latter months of normal pregnancy may help to return the arterial pressure to nonpregnant levels, although when the increase in activity is excessive, hypertension may ensue."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"The s-MSNA in NP (38+/-6.6 impulses/100 beats) was greater (P<0.05) than in NN women (19+/-1.8 impulses/100 beats) despite similar age and body weight but less than in PIH women (P<0.001) (146+/-23.5 impulses/100 beats).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1119, "doc_id": 5323845, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [5323845, 18997216, 13907928], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Sympathetic nerve activity is elevated throughout normal pregnancy.\n\nDocument title: Sympathetic neural mechanisms in normal and hypertensive pregnancy in humans.\n\nAbstract sentences:\n[0] BACKGROUND Direct recordings from peripheral sympathetic nerves have shown an increased sympathetic drive in pregnancy-induced hypertension (PIH) and preeclampsia (PE).\n[1] It is unknown whether sympathetic drive is altered in normal pregnancy, when arterial blood pressure can be normal or relatively low.\n[2] The aim of this study was to measure and compare peripheral sympathetic discharge, its vasoconstrictor effect and its baroreceptor control, during pregnancy and postpartum in women with normal pregnancy (NP) and PIH and in normotensive nonpregnant (NN) women.\n[3] METHODS AND RESULTS Twenty-one women with NP, 18 women with PIH, and 21 NN women had muscle sympathetic nerve activity assessed from multiunit discharges (MSNA) and from single units with defined vasoconstrictor properties (s-MSNA).\n[4] The s-MSNA in NP (38+/-6.6 impulses/100 beats) was greater (P<0.05) than in NN women (19+/-1.8 impulses/100 beats) despite similar age and body weight but less than in PIH women (P<0.001) (146+/-23.5 impulses/100 beats).\n[5] MSNA followed a similar trend.\n[6] Cardiac baroreceptor reflex sensitivity (BRS) was impaired in NP and PIH women relative to NN.\n[7] After delivery, sympathetic activity decreased to values similar to those obtained in NN, and there was an increase in BRS.\n[8] In women with NP, the decrease in sympathetic output occurred despite an insignificant change in blood pressure.\n[9] CONCLUSIONS Central sympathetic output was increased in women with normal pregnancy and was even greater in the hypertensive pregnant group.\n[10] The findings suggest that the moderate sympathetic hyperactivity during the latter months of normal pregnancy may help to return the arterial pressure to nonpregnant levels, although when the increase in activity is excessive, hypertension may ensue."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"The findings suggest that the moderate sympathetic hyperactivity during the latter months of normal pregnancy may help to return the arterial pressure to nonpregnant levels, although when the increase in activity is excessive, hypertension may ensue.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1119, "doc_id": 5323845, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [5323845, 18997216, 13907928], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Sympathetic nerve activity is elevated throughout normal pregnancy.\n\nDocument title: Sympathetic baroreflex gain in normotensive pregnant women.\n\nAbstract sentences:\n[0] Muscle sympathetic nerve activity is increased during normotensive pregnancy while mean arterial pressure is maintained or reduced, suggesting baroreflex resetting.\n[1] We hypothesized spontaneous sympathetic baroreflex gain would be reduced in normotensive pregnant women relative to nonpregnant matched controls.\n[2] Integrated muscle sympathetic burst incidence and total sympathetic activity (microneurography), blood pressure (Finometer), and R-R interval (ECG) were assessed at rest in 11 pregnant women (33 ± 1 wk gestation, 31 ± 1 yr, prepregnancy BMI: 23.5 ± 0.9 kg/m(2)) and 11 nonpregnant controls (29 ± 1 yr; BMI: 25.2 ± 1.7 kg/m(2)).\n[3] Pregnant women had elevated baseline sympathetic burst incidence (43 ± 2 vs. 33 ± 2 bursts/100 heart beats, P = 0.01) and total sympathetic activity (1,811 ± 148 vs. 1,140 ± 55 au, P < 0.01) relative to controls.\n[4] Both mean (88 ± 3 vs. 91 ± 2 mmHg, P = 0.4) and diastolic (DBP) (72 ± 3 vs. 73 ± 2 mmHg, P = 0.7) pressures were similar between pregnant and nonpregnant women, respectively, indicating an upward resetting of the baroreflex set point with pregnancy.\n[5] Baroreflex gain, calculated as the linear relationship between sympathetic burst incidence and DBP, was reduced in pregnant women relative to controls (-3.7 ± 0.5 vs. -5.4 ± 0.5 bursts·100 heart beats(-1)·mmHg(-1), P = 0.03), as was baroreflex gain calculated with total sympathetic activity (-294 ± 24 vs. -210 ± 24 au·100 heart beats(-1)·mmHg(-1); P = 0.03).\n[6] Cardiovagal baroreflex gain (sequence method) was not different between nonpregnant controls and pregnant women (49 ± 8 vs. 36 ± 8 ms/mmHg; P = 0.2).\n[7] However, sympathetic (burst incidence) and cardiovagal gains were negatively correlated in pregnant women (R = -0.7; P = 0.02).\n[8] Together, these data indicate that the influence of the sympathetic nervous system over arterial blood pressure is reduced in normotensive pregnancy, in terms of both long-term and beat-to-beat regulation of arterial pressure, likely through a baroreceptor-dependent mechanism."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Muscle sympathetic nerve activity is increased during normotensive pregnancy while mean arterial pressure is maintained or reduced, suggesting baroreflex resetting.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1119, "doc_id": 18997216, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [5323845, 18997216, 13907928], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Sympathetic nerve activity is elevated throughout normal pregnancy.\n\nDocument title: Sympathetic baroreflex gain in normotensive pregnant women.\n\nAbstract sentences:\n[0] Muscle sympathetic nerve activity is increased during normotensive pregnancy while mean arterial pressure is maintained or reduced, suggesting baroreflex resetting.\n[1] We hypothesized spontaneous sympathetic baroreflex gain would be reduced in normotensive pregnant women relative to nonpregnant matched controls.\n[2] Integrated muscle sympathetic burst incidence and total sympathetic activity (microneurography), blood pressure (Finometer), and R-R interval (ECG) were assessed at rest in 11 pregnant women (33 ± 1 wk gestation, 31 ± 1 yr, prepregnancy BMI: 23.5 ± 0.9 kg/m(2)) and 11 nonpregnant controls (29 ± 1 yr; BMI: 25.2 ± 1.7 kg/m(2)).\n[3] Pregnant women had elevated baseline sympathetic burst incidence (43 ± 2 vs. 33 ± 2 bursts/100 heart beats, P = 0.01) and total sympathetic activity (1,811 ± 148 vs. 1,140 ± 55 au, P < 0.01) relative to controls.\n[4] Both mean (88 ± 3 vs. 91 ± 2 mmHg, P = 0.4) and diastolic (DBP) (72 ± 3 vs. 73 ± 2 mmHg, P = 0.7) pressures were similar between pregnant and nonpregnant women, respectively, indicating an upward resetting of the baroreflex set point with pregnancy.\n[5] Baroreflex gain, calculated as the linear relationship between sympathetic burst incidence and DBP, was reduced in pregnant women relative to controls (-3.7 ± 0.5 vs. -5.4 ± 0.5 bursts·100 heart beats(-1)·mmHg(-1), P = 0.03), as was baroreflex gain calculated with total sympathetic activity (-294 ± 24 vs. -210 ± 24 au·100 heart beats(-1)·mmHg(-1); P = 0.03).\n[6] Cardiovagal baroreflex gain (sequence method) was not different between nonpregnant controls and pregnant women (49 ± 8 vs. 36 ± 8 ms/mmHg; P = 0.2).\n[7] However, sympathetic (burst incidence) and cardiovagal gains were negatively correlated in pregnant women (R = -0.7; P = 0.02).\n[8] Together, these data indicate that the influence of the sympathetic nervous system over arterial blood pressure is reduced in normotensive pregnancy, in terms of both long-term and beat-to-beat regulation of arterial pressure, likely through a baroreceptor-dependent mechanism."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Pregnant women had elevated baseline sympathetic burst incidence (43 ± 2 vs. 33 ± 2 bursts/100 heart beats, P = 0.01) and total sympathetic activity (1,811 ± 148 vs. 1,140 ± 55 au, P < 0.01) relative to controls.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1119, "doc_id": 18997216, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [5323845, 18997216, 13907928], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Sympathetic nerve activity is elevated throughout normal pregnancy.\n\nDocument title: Regulation of sympathetic nerve activity during the cold pressor test in normotensive pregnant and nonpregnant women.\n\nAbstract sentences:\n[0] Baseline neurovascular transduction is reduced in normotensive pregnancy; however, little is known about changes to neurovascular transduction during periods of heightened sympathetic activation.\n[1] We tested the hypothesis that, despite an exacerbated muscle sympathetic nerve activity (microneurography) response to cold pressor stimulation, the blunting of neurovascular transduction in normotensive pregnant women would result in similar changes in vascular resistance and mean arterial pressure (Finometer) relative to nonpregnant controls.\n[2] Baseline neurovascular transduction was reduced in pregnant women relative to controls when expressed as the quotient of both total resistance and mean arterial pressure and sympathetic burst frequency (0.32±0.07 versus 0.58±0.16 mm Hg/L/min/bursts/min, P<0.001 and 2.4±0.7 versus 3.6±0.8 mm Hg/bursts/min, P=0.001).\n[3] Sympathetic activation was greater across all 3 minutes of cold pressor stimulation in the pregnant women relative to the nonpregnant controls.\n[4] Peak sympathoexcitation was also greater in pregnant than in nonpregnant women, whether expressed as sympathetic burst frequency (+17±13 versus +7±8 bursts/min, P=0.049), burst incidence (+17±9 versus +6±11 bursts/100 hb, P=0.03), or total activity (+950±660 versus +363±414 arbitrary units, P=0.04).\n[5] However, neurovascular transduction during peak cold pressor-induced sympathoexcitation remained blunted in pregnant women (0.25±0.11 versus 0.45±0.08 mm Hg/L/min/bursts/min, P<0.001 and 1.9±1.0 versus 3.2±0.9 mm Hg/bursts/min, P=0.006).\n[6] Therefore, mean arterial pressure (93±21 versus 99±6 mm Hg, P=0.4) and total peripheral resistance (12±3 versus 14±3 mm Hg/L/min) were not different between pregnant and nonpregnant women during peak sympathoexcitation.\n[7] These data indicate that the third trimester of normotensive pregnancy is associated with reductions in neurovascular transduction, which result in the dissociation of sympathetic outflow from hemodynamic outcomes, even during cold pressor-induced sympathoexcitation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Sympathetic activation was greater across all 3 minutes of cold pressor stimulation in the pregnant women relative to the nonpregnant controls.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1119, "doc_id": 13907928, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [5323845, 18997216, 13907928], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Sympathetic nerve activity is elevated throughout normal pregnancy.\n\nDocument title: Regulation of sympathetic nerve activity during the cold pressor test in normotensive pregnant and nonpregnant women.\n\nAbstract sentences:\n[0] Baseline neurovascular transduction is reduced in normotensive pregnancy; however, little is known about changes to neurovascular transduction during periods of heightened sympathetic activation.\n[1] We tested the hypothesis that, despite an exacerbated muscle sympathetic nerve activity (microneurography) response to cold pressor stimulation, the blunting of neurovascular transduction in normotensive pregnant women would result in similar changes in vascular resistance and mean arterial pressure (Finometer) relative to nonpregnant controls.\n[2] Baseline neurovascular transduction was reduced in pregnant women relative to controls when expressed as the quotient of both total resistance and mean arterial pressure and sympathetic burst frequency (0.32±0.07 versus 0.58±0.16 mm Hg/L/min/bursts/min, P<0.001 and 2.4±0.7 versus 3.6±0.8 mm Hg/bursts/min, P=0.001).\n[3] Sympathetic activation was greater across all 3 minutes of cold pressor stimulation in the pregnant women relative to the nonpregnant controls.\n[4] Peak sympathoexcitation was also greater in pregnant than in nonpregnant women, whether expressed as sympathetic burst frequency (+17±13 versus +7±8 bursts/min, P=0.049), burst incidence (+17±9 versus +6±11 bursts/100 hb, P=0.03), or total activity (+950±660 versus +363±414 arbitrary units, P=0.04).\n[5] However, neurovascular transduction during peak cold pressor-induced sympathoexcitation remained blunted in pregnant women (0.25±0.11 versus 0.45±0.08 mm Hg/L/min/bursts/min, P<0.001 and 1.9±1.0 versus 3.2±0.9 mm Hg/bursts/min, P=0.006).\n[6] Therefore, mean arterial pressure (93±21 versus 99±6 mm Hg, P=0.4) and total peripheral resistance (12±3 versus 14±3 mm Hg/L/min) were not different between pregnant and nonpregnant women during peak sympathoexcitation.\n[7] These data indicate that the third trimester of normotensive pregnancy is associated with reductions in neurovascular transduction, which result in the dissociation of sympathetic outflow from hemodynamic outcomes, even during cold pressor-induced sympathoexcitation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Peak sympathoexcitation was also greater in pregnant than in nonpregnant women, whether expressed as sympathetic burst frequency (+17±13 versus +7±8 bursts/min, P=0.049), burst incidence (+17±9 versus +6±11 bursts/100 hb, P=0.03), or total activity (+950±660 versus +363±414 arbitrary units, P=0.04).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1119, "doc_id": 13907928, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [5323845, 18997216, 13907928], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Sympathetic nerve activity is reduced throughout normal pregnancy.\n\nDocument title: Sympathetic neural mechanisms in normal and hypertensive pregnancy in humans.\n\nAbstract sentences:\n[0] BACKGROUND Direct recordings from peripheral sympathetic nerves have shown an increased sympathetic drive in pregnancy-induced hypertension (PIH) and preeclampsia (PE).\n[1] It is unknown whether sympathetic drive is altered in normal pregnancy, when arterial blood pressure can be normal or relatively low.\n[2] The aim of this study was to measure and compare peripheral sympathetic discharge, its vasoconstrictor effect and its baroreceptor control, during pregnancy and postpartum in women with normal pregnancy (NP) and PIH and in normotensive nonpregnant (NN) women.\n[3] METHODS AND RESULTS Twenty-one women with NP, 18 women with PIH, and 21 NN women had muscle sympathetic nerve activity assessed from multiunit discharges (MSNA) and from single units with defined vasoconstrictor properties (s-MSNA).\n[4] The s-MSNA in NP (38+/-6.6 impulses/100 beats) was greater (P<0.05) than in NN women (19+/-1.8 impulses/100 beats) despite similar age and body weight but less than in PIH women (P<0.001) (146+/-23.5 impulses/100 beats).\n[5] MSNA followed a similar trend.\n[6] Cardiac baroreceptor reflex sensitivity (BRS) was impaired in NP and PIH women relative to NN.\n[7] After delivery, sympathetic activity decreased to values similar to those obtained in NN, and there was an increase in BRS.\n[8] In women with NP, the decrease in sympathetic output occurred despite an insignificant change in blood pressure.\n[9] CONCLUSIONS Central sympathetic output was increased in women with normal pregnancy and was even greater in the hypertensive pregnant group.\n[10] The findings suggest that the moderate sympathetic hyperactivity during the latter months of normal pregnancy may help to return the arterial pressure to nonpregnant levels, although when the increase in activity is excessive, hypertension may ensue."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"The s-MSNA in NP (38+/-6.6 impulses/100 beats) was greater (P<0.05) than in NN women (19+/-1.8 impulses/100 beats) despite similar age and body weight but less than in PIH women (P<0.001) (146+/-23.5 impulses/100 beats).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1120, "doc_id": 5323845, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [5323845, 18997216, 13907928], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Sympathetic nerve activity is reduced throughout normal pregnancy.\n\nDocument title: Sympathetic neural mechanisms in normal and hypertensive pregnancy in humans.\n\nAbstract sentences:\n[0] BACKGROUND Direct recordings from peripheral sympathetic nerves have shown an increased sympathetic drive in pregnancy-induced hypertension (PIH) and preeclampsia (PE).\n[1] It is unknown whether sympathetic drive is altered in normal pregnancy, when arterial blood pressure can be normal or relatively low.\n[2] The aim of this study was to measure and compare peripheral sympathetic discharge, its vasoconstrictor effect and its baroreceptor control, during pregnancy and postpartum in women with normal pregnancy (NP) and PIH and in normotensive nonpregnant (NN) women.\n[3] METHODS AND RESULTS Twenty-one women with NP, 18 women with PIH, and 21 NN women had muscle sympathetic nerve activity assessed from multiunit discharges (MSNA) and from single units with defined vasoconstrictor properties (s-MSNA).\n[4] The s-MSNA in NP (38+/-6.6 impulses/100 beats) was greater (P<0.05) than in NN women (19+/-1.8 impulses/100 beats) despite similar age and body weight but less than in PIH women (P<0.001) (146+/-23.5 impulses/100 beats).\n[5] MSNA followed a similar trend.\n[6] Cardiac baroreceptor reflex sensitivity (BRS) was impaired in NP and PIH women relative to NN.\n[7] After delivery, sympathetic activity decreased to values similar to those obtained in NN, and there was an increase in BRS.\n[8] In women with NP, the decrease in sympathetic output occurred despite an insignificant change in blood pressure.\n[9] CONCLUSIONS Central sympathetic output was increased in women with normal pregnancy and was even greater in the hypertensive pregnant group.\n[10] The findings suggest that the moderate sympathetic hyperactivity during the latter months of normal pregnancy may help to return the arterial pressure to nonpregnant levels, although when the increase in activity is excessive, hypertension may ensue."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"The findings suggest that the moderate sympathetic hyperactivity during the latter months of normal pregnancy may help to return the arterial pressure to nonpregnant levels, although when the increase in activity is excessive, hypertension may ensue.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1120, "doc_id": 5323845, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [5323845, 18997216, 13907928], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Sympathetic nerve activity is reduced throughout normal pregnancy.\n\nDocument title: Sympathetic baroreflex gain in normotensive pregnant women.\n\nAbstract sentences:\n[0] Muscle sympathetic nerve activity is increased during normotensive pregnancy while mean arterial pressure is maintained or reduced, suggesting baroreflex resetting.\n[1] We hypothesized spontaneous sympathetic baroreflex gain would be reduced in normotensive pregnant women relative to nonpregnant matched controls.\n[2] Integrated muscle sympathetic burst incidence and total sympathetic activity (microneurography), blood pressure (Finometer), and R-R interval (ECG) were assessed at rest in 11 pregnant women (33 ± 1 wk gestation, 31 ± 1 yr, prepregnancy BMI: 23.5 ± 0.9 kg/m(2)) and 11 nonpregnant controls (29 ± 1 yr; BMI: 25.2 ± 1.7 kg/m(2)).\n[3] Pregnant women had elevated baseline sympathetic burst incidence (43 ± 2 vs. 33 ± 2 bursts/100 heart beats, P = 0.01) and total sympathetic activity (1,811 ± 148 vs. 1,140 ± 55 au, P < 0.01) relative to controls.\n[4] Both mean (88 ± 3 vs. 91 ± 2 mmHg, P = 0.4) and diastolic (DBP) (72 ± 3 vs. 73 ± 2 mmHg, P = 0.7) pressures were similar between pregnant and nonpregnant women, respectively, indicating an upward resetting of the baroreflex set point with pregnancy.\n[5] Baroreflex gain, calculated as the linear relationship between sympathetic burst incidence and DBP, was reduced in pregnant women relative to controls (-3.7 ± 0.5 vs. -5.4 ± 0.5 bursts·100 heart beats(-1)·mmHg(-1), P = 0.03), as was baroreflex gain calculated with total sympathetic activity (-294 ± 24 vs. -210 ± 24 au·100 heart beats(-1)·mmHg(-1); P = 0.03).\n[6] Cardiovagal baroreflex gain (sequence method) was not different between nonpregnant controls and pregnant women (49 ± 8 vs. 36 ± 8 ms/mmHg; P = 0.2).\n[7] However, sympathetic (burst incidence) and cardiovagal gains were negatively correlated in pregnant women (R = -0.7; P = 0.02).\n[8] Together, these data indicate that the influence of the sympathetic nervous system over arterial blood pressure is reduced in normotensive pregnancy, in terms of both long-term and beat-to-beat regulation of arterial pressure, likely through a baroreceptor-dependent mechanism."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Muscle sympathetic nerve activity is increased during normotensive pregnancy while mean arterial pressure is maintained or reduced, suggesting baroreflex resetting.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1120, "doc_id": 18997216, "label": "CONTRADICTS", "evidence_sentence_ids": [0], "cited_doc_ids": [5323845, 18997216, 13907928], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Sympathetic nerve activity is reduced throughout normal pregnancy.\n\nDocument title: Sympathetic baroreflex gain in normotensive pregnant women.\n\nAbstract sentences:\n[0] Muscle sympathetic nerve activity is increased during normotensive pregnancy while mean arterial pressure is maintained or reduced, suggesting baroreflex resetting.\n[1] We hypothesized spontaneous sympathetic baroreflex gain would be reduced in normotensive pregnant women relative to nonpregnant matched controls.\n[2] Integrated muscle sympathetic burst incidence and total sympathetic activity (microneurography), blood pressure (Finometer), and R-R interval (ECG) were assessed at rest in 11 pregnant women (33 ± 1 wk gestation, 31 ± 1 yr, prepregnancy BMI: 23.5 ± 0.9 kg/m(2)) and 11 nonpregnant controls (29 ± 1 yr; BMI: 25.2 ± 1.7 kg/m(2)).\n[3] Pregnant women had elevated baseline sympathetic burst incidence (43 ± 2 vs. 33 ± 2 bursts/100 heart beats, P = 0.01) and total sympathetic activity (1,811 ± 148 vs. 1,140 ± 55 au, P < 0.01) relative to controls.\n[4] Both mean (88 ± 3 vs. 91 ± 2 mmHg, P = 0.4) and diastolic (DBP) (72 ± 3 vs. 73 ± 2 mmHg, P = 0.7) pressures were similar between pregnant and nonpregnant women, respectively, indicating an upward resetting of the baroreflex set point with pregnancy.\n[5] Baroreflex gain, calculated as the linear relationship between sympathetic burst incidence and DBP, was reduced in pregnant women relative to controls (-3.7 ± 0.5 vs. -5.4 ± 0.5 bursts·100 heart beats(-1)·mmHg(-1), P = 0.03), as was baroreflex gain calculated with total sympathetic activity (-294 ± 24 vs. -210 ± 24 au·100 heart beats(-1)·mmHg(-1); P = 0.03).\n[6] Cardiovagal baroreflex gain (sequence method) was not different between nonpregnant controls and pregnant women (49 ± 8 vs. 36 ± 8 ms/mmHg; P = 0.2).\n[7] However, sympathetic (burst incidence) and cardiovagal gains were negatively correlated in pregnant women (R = -0.7; P = 0.02).\n[8] Together, these data indicate that the influence of the sympathetic nervous system over arterial blood pressure is reduced in normotensive pregnancy, in terms of both long-term and beat-to-beat regulation of arterial pressure, likely through a baroreceptor-dependent mechanism."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Pregnant women had elevated baseline sympathetic burst incidence (43 ± 2 vs. 33 ± 2 bursts/100 heart beats, P = 0.01) and total sympathetic activity (1,811 ± 148 vs. 1,140 ± 55 au, P < 0.01) relative to controls.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1120, "doc_id": 18997216, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [5323845, 18997216, 13907928], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Sympathetic nerve activity is reduced throughout normal pregnancy.\n\nDocument title: Regulation of sympathetic nerve activity during the cold pressor test in normotensive pregnant and nonpregnant women.\n\nAbstract sentences:\n[0] Baseline neurovascular transduction is reduced in normotensive pregnancy; however, little is known about changes to neurovascular transduction during periods of heightened sympathetic activation.\n[1] We tested the hypothesis that, despite an exacerbated muscle sympathetic nerve activity (microneurography) response to cold pressor stimulation, the blunting of neurovascular transduction in normotensive pregnant women would result in similar changes in vascular resistance and mean arterial pressure (Finometer) relative to nonpregnant controls.\n[2] Baseline neurovascular transduction was reduced in pregnant women relative to controls when expressed as the quotient of both total resistance and mean arterial pressure and sympathetic burst frequency (0.32±0.07 versus 0.58±0.16 mm Hg/L/min/bursts/min, P<0.001 and 2.4±0.7 versus 3.6±0.8 mm Hg/bursts/min, P=0.001).\n[3] Sympathetic activation was greater across all 3 minutes of cold pressor stimulation in the pregnant women relative to the nonpregnant controls.\n[4] Peak sympathoexcitation was also greater in pregnant than in nonpregnant women, whether expressed as sympathetic burst frequency (+17±13 versus +7±8 bursts/min, P=0.049), burst incidence (+17±9 versus +6±11 bursts/100 hb, P=0.03), or total activity (+950±660 versus +363±414 arbitrary units, P=0.04).\n[5] However, neurovascular transduction during peak cold pressor-induced sympathoexcitation remained blunted in pregnant women (0.25±0.11 versus 0.45±0.08 mm Hg/L/min/bursts/min, P<0.001 and 1.9±1.0 versus 3.2±0.9 mm Hg/bursts/min, P=0.006).\n[6] Therefore, mean arterial pressure (93±21 versus 99±6 mm Hg, P=0.4) and total peripheral resistance (12±3 versus 14±3 mm Hg/L/min) were not different between pregnant and nonpregnant women during peak sympathoexcitation.\n[7] These data indicate that the third trimester of normotensive pregnancy is associated with reductions in neurovascular transduction, which result in the dissociation of sympathetic outflow from hemodynamic outcomes, even during cold pressor-induced sympathoexcitation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Sympathetic activation was greater across all 3 minutes of cold pressor stimulation in the pregnant women relative to the nonpregnant controls.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1120, "doc_id": 13907928, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [5323845, 18997216, 13907928], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Sympathetic nerve activity is reduced throughout normal pregnancy.\n\nDocument title: Regulation of sympathetic nerve activity during the cold pressor test in normotensive pregnant and nonpregnant women.\n\nAbstract sentences:\n[0] Baseline neurovascular transduction is reduced in normotensive pregnancy; however, little is known about changes to neurovascular transduction during periods of heightened sympathetic activation.\n[1] We tested the hypothesis that, despite an exacerbated muscle sympathetic nerve activity (microneurography) response to cold pressor stimulation, the blunting of neurovascular transduction in normotensive pregnant women would result in similar changes in vascular resistance and mean arterial pressure (Finometer) relative to nonpregnant controls.\n[2] Baseline neurovascular transduction was reduced in pregnant women relative to controls when expressed as the quotient of both total resistance and mean arterial pressure and sympathetic burst frequency (0.32±0.07 versus 0.58±0.16 mm Hg/L/min/bursts/min, P<0.001 and 2.4±0.7 versus 3.6±0.8 mm Hg/bursts/min, P=0.001).\n[3] Sympathetic activation was greater across all 3 minutes of cold pressor stimulation in the pregnant women relative to the nonpregnant controls.\n[4] Peak sympathoexcitation was also greater in pregnant than in nonpregnant women, whether expressed as sympathetic burst frequency (+17±13 versus +7±8 bursts/min, P=0.049), burst incidence (+17±9 versus +6±11 bursts/100 hb, P=0.03), or total activity (+950±660 versus +363±414 arbitrary units, P=0.04).\n[5] However, neurovascular transduction during peak cold pressor-induced sympathoexcitation remained blunted in pregnant women (0.25±0.11 versus 0.45±0.08 mm Hg/L/min/bursts/min, P<0.001 and 1.9±1.0 versus 3.2±0.9 mm Hg/bursts/min, P=0.006).\n[6] Therefore, mean arterial pressure (93±21 versus 99±6 mm Hg, P=0.4) and total peripheral resistance (12±3 versus 14±3 mm Hg/L/min) were not different between pregnant and nonpregnant women during peak sympathoexcitation.\n[7] These data indicate that the third trimester of normotensive pregnancy is associated with reductions in neurovascular transduction, which result in the dissociation of sympathetic outflow from hemodynamic outcomes, even during cold pressor-induced sympathoexcitation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Peak sympathoexcitation was also greater in pregnant than in nonpregnant women, whether expressed as sympathetic burst frequency (+17±13 versus +7±8 bursts/min, P=0.049), burst incidence (+17±9 versus +6±11 bursts/100 hb, P=0.03), or total activity (+950±660 versus +363±414 arbitrary units, P=0.04).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1120, "doc_id": 13907928, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [5323845, 18997216, 13907928], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Systemic immunosuppressive (IS) therapy does not enhance the chance of cancer mortality in patients with inflammatory eye disease (IED)\n\nDocument title: Overall and cancer related mortality among patients with ocular inflammation treated with immunosuppressive drugs: retrospective cohort study.\n\nAbstract sentences:\n[0] CONTEXT Whether immunosuppressive treatment adversely affects survival is unclear.\n[1] OBJECTIVE To assess whether immunosuppressive drugs increase mortality.\n[2] DESIGN Retrospective cohort study evaluating overall and cancer mortality in relation to immunosuppressive drug exposure among patients with ocular inflammatory diseases.\n[3] Demographic, clinical, and treatment data derived from medical records, and mortality results from United States National Death Index linkage.\n[4] The cohort's mortality risk was compared with US vital statistics using standardised mortality ratios.\n[5] Overall and cancer mortality in relation to use or non-use of immunosuppressive drugs within the cohort was studied with survival analysis.\n[6] SETTING Five tertiary ocular inflammation clinics.\n[7] Patients 7957 US residents with non-infectious ocular inflammation, 2340 of whom received immunosuppressive drugs during follow up.\n[8] Exposures Use of antimetabolites, T cell inhibitors, alkylating agents, and tumour necrosis factor inhibitors.\n[9] MAIN OUTCOME MEASURES Overall mortality, cancer mortality.\n[10] RESULTS Over 66 802 person years (17 316 after exposure to immunosuppressive drugs), 936 patients died (1.4/100 person years), 230 (24.6%) from cancer.\n[11] For patients unexposed to immunosuppressive treatment, risks of death overall (standardised mortality ratio 1.02, 95% confidence interval [CI] 0.94 to 1.11) and from cancer (1.10, 0.93 to 1.29) were similar to those of the US population.\n[12] Patients who used azathioprine, methotrexate, mycophenolate mofetil, ciclosporin, systemic corticosteroids, or dapsone had overall and cancer mortality similar to that of patients who never took immunosuppressive drugs.\n[13] In patients who used cyclophosphamide, overall mortality was not increased and cancer mortality was non-significantly increased.\n[14] Tumour necrosis factor inhibitors were associated with increased overall (adjusted hazard ratio [HR] 1.99, 95% CI 1.00 to 3.98) and cancer mortality (adjusted HR 3.83, 1.13 to 13.01).\n[15] CONCLUSIONS Most commonly used immunosuppressive drugs do not seem to increase overall or cancer mortality.\n[16] Our results suggesting that tumour necrosis factor inhibitors might increase mortality are less robust than the other findings; additional evidence is needed."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"Patients who used azathioprine, methotrexate, mycophenolate mofetil, ciclosporin, systemic corticosteroids, or dapsone had overall and cancer mortality similar to that of patients who never took immunosuppressive drugs.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1125, "doc_id": 21009874, "label": "SUPPORTS", "evidence_sentence_ids": [12], "cited_doc_ids": [21009874], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Systemic immunosuppressive (IS) therapy does not enhance the chance of cancer mortality in patients with inflammatory eye disease (IED)\n\nDocument title: Overall and cancer related mortality among patients with ocular inflammation treated with immunosuppressive drugs: retrospective cohort study.\n\nAbstract sentences:\n[0] CONTEXT Whether immunosuppressive treatment adversely affects survival is unclear.\n[1] OBJECTIVE To assess whether immunosuppressive drugs increase mortality.\n[2] DESIGN Retrospective cohort study evaluating overall and cancer mortality in relation to immunosuppressive drug exposure among patients with ocular inflammatory diseases.\n[3] Demographic, clinical, and treatment data derived from medical records, and mortality results from United States National Death Index linkage.\n[4] The cohort's mortality risk was compared with US vital statistics using standardised mortality ratios.\n[5] Overall and cancer mortality in relation to use or non-use of immunosuppressive drugs within the cohort was studied with survival analysis.\n[6] SETTING Five tertiary ocular inflammation clinics.\n[7] Patients 7957 US residents with non-infectious ocular inflammation, 2340 of whom received immunosuppressive drugs during follow up.\n[8] Exposures Use of antimetabolites, T cell inhibitors, alkylating agents, and tumour necrosis factor inhibitors.\n[9] MAIN OUTCOME MEASURES Overall mortality, cancer mortality.\n[10] RESULTS Over 66 802 person years (17 316 after exposure to immunosuppressive drugs), 936 patients died (1.4/100 person years), 230 (24.6%) from cancer.\n[11] For patients unexposed to immunosuppressive treatment, risks of death overall (standardised mortality ratio 1.02, 95% confidence interval [CI] 0.94 to 1.11) and from cancer (1.10, 0.93 to 1.29) were similar to those of the US population.\n[12] Patients who used azathioprine, methotrexate, mycophenolate mofetil, ciclosporin, systemic corticosteroids, or dapsone had overall and cancer mortality similar to that of patients who never took immunosuppressive drugs.\n[13] In patients who used cyclophosphamide, overall mortality was not increased and cancer mortality was non-significantly increased.\n[14] Tumour necrosis factor inhibitors were associated with increased overall (adjusted hazard ratio [HR] 1.99, 95% CI 1.00 to 3.98) and cancer mortality (adjusted HR 3.83, 1.13 to 13.01).\n[15] CONCLUSIONS Most commonly used immunosuppressive drugs do not seem to increase overall or cancer mortality.\n[16] Our results suggesting that tumour necrosis factor inhibitors might increase mortality are less robust than the other findings; additional evidence is needed."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [15]\nExplanation: Evidence states: \"CONCLUSIONS Most commonly used immunosuppressive drugs do not seem to increase overall or cancer mortality.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1125, "doc_id": 21009874, "label": "SUPPORTS", "evidence_sentence_ids": [15], "cited_doc_ids": [21009874], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Systemic immunosuppressive (IS) therapy increases the chance of cancer mortality in patients with inflammatory eye disease (IED)\n\nDocument title: Overall and cancer related mortality among patients with ocular inflammation treated with immunosuppressive drugs: retrospective cohort study.\n\nAbstract sentences:\n[0] CONTEXT Whether immunosuppressive treatment adversely affects survival is unclear.\n[1] OBJECTIVE To assess whether immunosuppressive drugs increase mortality.\n[2] DESIGN Retrospective cohort study evaluating overall and cancer mortality in relation to immunosuppressive drug exposure among patients with ocular inflammatory diseases.\n[3] Demographic, clinical, and treatment data derived from medical records, and mortality results from United States National Death Index linkage.\n[4] The cohort's mortality risk was compared with US vital statistics using standardised mortality ratios.\n[5] Overall and cancer mortality in relation to use or non-use of immunosuppressive drugs within the cohort was studied with survival analysis.\n[6] SETTING Five tertiary ocular inflammation clinics.\n[7] Patients 7957 US residents with non-infectious ocular inflammation, 2340 of whom received immunosuppressive drugs during follow up.\n[8] Exposures Use of antimetabolites, T cell inhibitors, alkylating agents, and tumour necrosis factor inhibitors.\n[9] MAIN OUTCOME MEASURES Overall mortality, cancer mortality.\n[10] RESULTS Over 66 802 person years (17 316 after exposure to immunosuppressive drugs), 936 patients died (1.4/100 person years), 230 (24.6%) from cancer.\n[11] For patients unexposed to immunosuppressive treatment, risks of death overall (standardised mortality ratio 1.02, 95% confidence interval [CI] 0.94 to 1.11) and from cancer (1.10, 0.93 to 1.29) were similar to those of the US population.\n[12] Patients who used azathioprine, methotrexate, mycophenolate mofetil, ciclosporin, systemic corticosteroids, or dapsone had overall and cancer mortality similar to that of patients who never took immunosuppressive drugs.\n[13] In patients who used cyclophosphamide, overall mortality was not increased and cancer mortality was non-significantly increased.\n[14] Tumour necrosis factor inhibitors were associated with increased overall (adjusted hazard ratio [HR] 1.99, 95% CI 1.00 to 3.98) and cancer mortality (adjusted HR 3.83, 1.13 to 13.01).\n[15] CONCLUSIONS Most commonly used immunosuppressive drugs do not seem to increase overall or cancer mortality.\n[16] Our results suggesting that tumour necrosis factor inhibitors might increase mortality are less robust than the other findings; additional evidence is needed."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"Patients who used azathioprine, methotrexate, mycophenolate mofetil, ciclosporin, systemic corticosteroids, or dapsone had overall and cancer mortality similar to that of patients who never took immunosuppressive drugs.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1126, "doc_id": 21009874, "label": "CONTRADICTS", "evidence_sentence_ids": [12], "cited_doc_ids": [21009874], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Systemic immunosuppressive (IS) therapy increases the chance of cancer mortality in patients with inflammatory eye disease (IED)\n\nDocument title: Overall and cancer related mortality among patients with ocular inflammation treated with immunosuppressive drugs: retrospective cohort study.\n\nAbstract sentences:\n[0] CONTEXT Whether immunosuppressive treatment adversely affects survival is unclear.\n[1] OBJECTIVE To assess whether immunosuppressive drugs increase mortality.\n[2] DESIGN Retrospective cohort study evaluating overall and cancer mortality in relation to immunosuppressive drug exposure among patients with ocular inflammatory diseases.\n[3] Demographic, clinical, and treatment data derived from medical records, and mortality results from United States National Death Index linkage.\n[4] The cohort's mortality risk was compared with US vital statistics using standardised mortality ratios.\n[5] Overall and cancer mortality in relation to use or non-use of immunosuppressive drugs within the cohort was studied with survival analysis.\n[6] SETTING Five tertiary ocular inflammation clinics.\n[7] Patients 7957 US residents with non-infectious ocular inflammation, 2340 of whom received immunosuppressive drugs during follow up.\n[8] Exposures Use of antimetabolites, T cell inhibitors, alkylating agents, and tumour necrosis factor inhibitors.\n[9] MAIN OUTCOME MEASURES Overall mortality, cancer mortality.\n[10] RESULTS Over 66 802 person years (17 316 after exposure to immunosuppressive drugs), 936 patients died (1.4/100 person years), 230 (24.6%) from cancer.\n[11] For patients unexposed to immunosuppressive treatment, risks of death overall (standardised mortality ratio 1.02, 95% confidence interval [CI] 0.94 to 1.11) and from cancer (1.10, 0.93 to 1.29) were similar to those of the US population.\n[12] Patients who used azathioprine, methotrexate, mycophenolate mofetil, ciclosporin, systemic corticosteroids, or dapsone had overall and cancer mortality similar to that of patients who never took immunosuppressive drugs.\n[13] In patients who used cyclophosphamide, overall mortality was not increased and cancer mortality was non-significantly increased.\n[14] Tumour necrosis factor inhibitors were associated with increased overall (adjusted hazard ratio [HR] 1.99, 95% CI 1.00 to 3.98) and cancer mortality (adjusted HR 3.83, 1.13 to 13.01).\n[15] CONCLUSIONS Most commonly used immunosuppressive drugs do not seem to increase overall or cancer mortality.\n[16] Our results suggesting that tumour necrosis factor inhibitors might increase mortality are less robust than the other findings; additional evidence is needed."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [15]\nExplanation: Evidence states: \"CONCLUSIONS Most commonly used immunosuppressive drugs do not seem to increase overall or cancer mortality.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1126, "doc_id": 21009874, "label": "CONTRADICTS", "evidence_sentence_ids": [15], "cited_doc_ids": [21009874], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Systemic lupus erythematosus is a risk factor for cardiovascular disease.\n\nDocument title: Development and validation of QRISK3 risk prediction algorithms to estimate future risk of cardiovascular disease: prospective cohort study\n\nAbstract sentences:\n[0] Objectives To develop and validate updated QRISK3 prediction algorithms to estimate the 10 year risk of cardiovascular disease in women and men accounting for potential new risk factors.\n[1] Design Prospective open cohort study.\n[2] Setting General practices in England providing data for the QResearch database.\n[3] Participants 1309 QResearch general practices in England: 981 practices were used to develop the scores and a separate set of 328 practices were used to validate the scores.\n[4] 7.89 million patients aged 25-84 years were in the derivation cohort and 2.67 million patients in the validation cohort.\n[5] Patients were free of cardiovascular disease and not prescribed statins at baseline.\n[6] Methods Cox proportional hazards models in the derivation cohort to derive separate risk equations in men and women for evaluation at 10 years.\n[7] Risk factors considered included those already in QRISK2 (age, ethnicity, deprivation, systolic blood pressure, body mass index, total cholesterol: high density lipoprotein cholesterol ratio, smoking, family history of coronary heart disease in a first degree relative aged less than 60 years, type 1 diabetes, type 2 diabetes, treated hypertension, rheumatoid arthritis, atrial fibrillation, chronic kidney disease (stage 4 or 5)) and new risk factors (chronic kidney disease (stage 3, 4, or 5), a measure of systolic blood pressure variability (standard deviation of repeated measures), migraine, corticosteroids, systemic lupus erythematosus (SLE), atypical antipsychotics, severe mental illness, and HIV/AIDs).\n[8] We also considered erectile dysfunction diagnosis or treatment in men.\n[9] Measures of calibration and discrimination were determined in the validation cohort for men and women separately and for individual subgroups by age group, ethnicity, and baseline disease status.\n[10] Main outcome measures Incident cardiovascular disease recorded on any of the following three linked data sources: general practice, mortality, or hospital admission records.\n[11] Results 363 565 incident cases of cardiovascular disease were identified in the derivation cohort during follow-up arising from 50.8 million person years of observation.\n[12] All new risk factors considered met the model inclusion criteria except for HIV/AIDS, which was not statistically significant.\n[13] The models had good calibration and high levels of explained variation and discrimination.\n[14] In women, the algorithm explained 59.6% of the variation in time to diagnosis of cardiovascular disease (R2, with higher values indicating more variation), and the D statistic was 2.48 and Harrell's C statistic was 0.88 (both measures of discrimination, with higher values indicating better discrimination).\n[15] The corresponding values for men were 54.8%, 2.26, and 0.86.\n[16] Overall performance of the updated QRISK3 algorithms was similar to the QRISK2 algorithms.\n[17] Conclusion Updated QRISK3 risk prediction models were developed and validated.\n[18] The inclusion of additional clinical variables in QRISK3 (chronic kidney disease, a measure of systolic blood pressure variability (standard deviation of repeated measures), migraine, corticosteroids, SLE, atypical antipsychotics, severe mental illness, and erectile dysfunction) can help enable doctors to identify those at most risk of heart disease and stroke."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Risk factors considered included those already in QRISK2 (age, ethnicity, deprivation, systolic blood pressure, body mass index, total cholesterol: high density lipoprotein cholesterol ratio, smoking, family history of coronary heart disease in a first degree relative aged less than 60 years, type 1 diabetes, type 2 diabetes, treated hypertension, rheumatoid arthritis, atrial fibrillation, chronic kidney disease (stage 4 or 5)) and new risk factors (chronic kidney disease (stage 3, 4, or 5), a measure of systolic blood pressure variability (standard deviation of repeated measures), migraine, corticosteroids, systemic lupus erythematosus (SLE), atypical antipsychotics, severe mental illness, and HIV/AIDs).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1127, "doc_id": 27466734, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [27466734], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: T cell receptor /CD3 microdomains are required to induce the immunologic synapse.\n\nDocument title: Full activation of the T cell receptor requires both clustering and conformational changes at CD3.\n\nAbstract sentences:\n[0] T cell receptor (TCR-CD3) triggering involves both receptor clustering and conformational changes at the cytoplasmic tails of the CD3 subunits.\n[1] The mechanism by which TCRalphabeta ligand binding confers conformational changes to CD3 is unknown.\n[2] By using well-defined ligands, we showed that induction of the conformational change requires both multivalent engagement and the mobility restriction of the TCR-CD3 imposed by the plasma membrane.\n[3] The conformational change is elicited by cooperative rearrangements of two TCR-CD3 complexes and does not require accompanying changes in the structure of the TCRalphabeta ectodomains.\n[4] This conformational change at CD3 reverts upon ligand dissociation and is required for T cell activation.\n[5] Thus, our permissive geometry model provides a molecular mechanism that rationalizes how the information of ligand binding to TCRalphabeta is transmitted to the CD3 subunits and to the intracellular signaling machinery."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"T cell receptor (TCR-CD3) triggering involves both receptor clustering and conformational changes at the cytoplasmic tails of the CD3 subunits.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1128, "doc_id": 33499189, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [33499189, 9283422], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: T cell receptor /CD3 microdomains are required to induce the immunologic synapse.\n\nDocument title: Full activation of the T cell receptor requires both clustering and conformational changes at CD3.\n\nAbstract sentences:\n[0] T cell receptor (TCR-CD3) triggering involves both receptor clustering and conformational changes at the cytoplasmic tails of the CD3 subunits.\n[1] The mechanism by which TCRalphabeta ligand binding confers conformational changes to CD3 is unknown.\n[2] By using well-defined ligands, we showed that induction of the conformational change requires both multivalent engagement and the mobility restriction of the TCR-CD3 imposed by the plasma membrane.\n[3] The conformational change is elicited by cooperative rearrangements of two TCR-CD3 complexes and does not require accompanying changes in the structure of the TCRalphabeta ectodomains.\n[4] This conformational change at CD3 reverts upon ligand dissociation and is required for T cell activation.\n[5] Thus, our permissive geometry model provides a molecular mechanism that rationalizes how the information of ligand binding to TCRalphabeta is transmitted to the CD3 subunits and to the intracellular signaling machinery."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"This conformational change at CD3 reverts upon ligand dissociation and is required for T cell activation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1128, "doc_id": 33499189, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [33499189, 9283422], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: TMEM27 is a marker for beta cells.\n\nDocument title: Tmem27: a cleaved and shed plasma membrane protein that stimulates pancreatic beta cell proliferation.\n\nAbstract sentences:\n[0] The signals and molecular mechanisms that regulate the replication of terminally differentiated beta cells are unknown.\n[1] Here, we report the identification and characterization of transmembrane protein 27 (Tmem27, collectrin) in pancreatic beta cells.\n[2] Expression of Tmem27 is reduced in Tcf1(-/-) mice and is increased in islets of mouse models with hypertrophy of the endocrine pancreas.\n[3] Tmem27 forms dimers and its extracellular domain is glycosylated, cleaved and shed from the plasma membrane of beta cells.\n[4] This cleavage process is beta cell specific and does not occur in other cell types.\n[5] Overexpression of full-length Tmem27, but not the truncated or soluble protein, leads to increased thymidine incorporation, whereas silencing of Tmem27 using RNAi results in a reduction of cell replication.\n[6] Furthermore, transgenic mice with increased expression of Tmem27 in pancreatic beta cells exhibit increased beta cell mass.\n[7] Our results identify a pancreatic beta cell transmembrane protein that regulates cell growth of pancreatic islets."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Here, we report the identification and characterization of transmembrane protein 27 (Tmem27, collectrin) in pancreatic beta cells.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1133, "doc_id": 24142891, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [24142891], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: TMEM27 is a marker for beta cells.\n\nDocument title: Tmem27: a cleaved and shed plasma membrane protein that stimulates pancreatic beta cell proliferation.\n\nAbstract sentences:\n[0] The signals and molecular mechanisms that regulate the replication of terminally differentiated beta cells are unknown.\n[1] Here, we report the identification and characterization of transmembrane protein 27 (Tmem27, collectrin) in pancreatic beta cells.\n[2] Expression of Tmem27 is reduced in Tcf1(-/-) mice and is increased in islets of mouse models with hypertrophy of the endocrine pancreas.\n[3] Tmem27 forms dimers and its extracellular domain is glycosylated, cleaved and shed from the plasma membrane of beta cells.\n[4] This cleavage process is beta cell specific and does not occur in other cell types.\n[5] Overexpression of full-length Tmem27, but not the truncated or soluble protein, leads to increased thymidine incorporation, whereas silencing of Tmem27 using RNAi results in a reduction of cell replication.\n[6] Furthermore, transgenic mice with increased expression of Tmem27 in pancreatic beta cells exhibit increased beta cell mass.\n[7] Our results identify a pancreatic beta cell transmembrane protein that regulates cell growth of pancreatic islets."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"This cleavage process is beta cell specific and does not occur in other cell types.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1133, "doc_id": 24142891, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [24142891], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: TMEM27 is a marker for beta cells.\n\nDocument title: Tmem27: a cleaved and shed plasma membrane protein that stimulates pancreatic beta cell proliferation.\n\nAbstract sentences:\n[0] The signals and molecular mechanisms that regulate the replication of terminally differentiated beta cells are unknown.\n[1] Here, we report the identification and characterization of transmembrane protein 27 (Tmem27, collectrin) in pancreatic beta cells.\n[2] Expression of Tmem27 is reduced in Tcf1(-/-) mice and is increased in islets of mouse models with hypertrophy of the endocrine pancreas.\n[3] Tmem27 forms dimers and its extracellular domain is glycosylated, cleaved and shed from the plasma membrane of beta cells.\n[4] This cleavage process is beta cell specific and does not occur in other cell types.\n[5] Overexpression of full-length Tmem27, but not the truncated or soluble protein, leads to increased thymidine incorporation, whereas silencing of Tmem27 using RNAi results in a reduction of cell replication.\n[6] Furthermore, transgenic mice with increased expression of Tmem27 in pancreatic beta cells exhibit increased beta cell mass.\n[7] Our results identify a pancreatic beta cell transmembrane protein that regulates cell growth of pancreatic islets."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Furthermore, transgenic mice with increased expression of Tmem27 in pancreatic beta cells exhibit increased beta cell mass.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1133, "doc_id": 24142891, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [24142891], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: TNFAIP3 is a glioblastoma tumor enhancer.\n\nDocument title: Targeting A20 Decreases Glioma Stem Cell Survival and Tumor Growth\n\nAbstract sentences:\n[0] Glioblastomas are deadly cancers that display a functional cellular hierarchy maintained by self-renewing glioblastoma stem cells (GSCs).\n[1] GSCs are regulated by molecular pathways distinct from the bulk tumor that may be useful therapeutic targets.\n[2] We determined that A20 (TNFAIP3), a regulator of cell survival and the NF-kappaB pathway, is overexpressed in GSCs relative to non-stem glioblastoma cells at both the mRNA and protein levels.\n[3] To determine the functional significance of A20 in GSCs, we targeted A20 expression with lentiviral-mediated delivery of short hairpin RNA (shRNA).\n[4] Inhibiting A20 expression decreased GSC growth and survival through mechanisms associated with decreased cell-cycle progression and decreased phosphorylation of p65/RelA. Elevated levels of A20 in GSCs contributed to apoptotic resistance: GSCs were less susceptible to TNFalpha-induced cell death than matched non-stem glioma cells, but A20 knockdown sensitized GSCs to TNFalpha-mediated apoptosis.\n[5] The decreased survival of GSCs upon A20 knockdown contributed to the reduced ability of these cells to self-renew in primary and secondary neurosphere formation assays.\n[6] The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts.\n[7] In silico analysis of a glioma patient genomic database indicates that A20 overexpression and amplification is inversely correlated with survival.\n[8] Together these data indicate that A20 contributes to glioma maintenance through effects on the glioma stem cell subpopulation.\n[9] Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through glioma genomic sequencing: in fact, our data suggest A20 may function as a tumor enhancer in glioma through promotion of GSC survival.\n[10] A20 anticancer therapies should therefore be viewed with caution as effects will likely differ depending on the tumor type."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Inhibiting A20 expression decreased GSC growth and survival through mechanisms associated with decreased cell-cycle progression and decreased phosphorylation of p65/RelA. Elevated levels of A20 in GSCs contributed to apoptotic resistance: GSCs were less susceptible to TNFalpha-induced cell death than matched non-stem glioma cells, but A20 knockdown sensitized GSCs to TNFalpha-mediated apoptosis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1134, "doc_id": 33370, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [33370], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: TNFAIP3 is a glioblastoma tumor enhancer.\n\nDocument title: Targeting A20 Decreases Glioma Stem Cell Survival and Tumor Growth\n\nAbstract sentences:\n[0] Glioblastomas are deadly cancers that display a functional cellular hierarchy maintained by self-renewing glioblastoma stem cells (GSCs).\n[1] GSCs are regulated by molecular pathways distinct from the bulk tumor that may be useful therapeutic targets.\n[2] We determined that A20 (TNFAIP3), a regulator of cell survival and the NF-kappaB pathway, is overexpressed in GSCs relative to non-stem glioblastoma cells at both the mRNA and protein levels.\n[3] To determine the functional significance of A20 in GSCs, we targeted A20 expression with lentiviral-mediated delivery of short hairpin RNA (shRNA).\n[4] Inhibiting A20 expression decreased GSC growth and survival through mechanisms associated with decreased cell-cycle progression and decreased phosphorylation of p65/RelA. Elevated levels of A20 in GSCs contributed to apoptotic resistance: GSCs were less susceptible to TNFalpha-induced cell death than matched non-stem glioma cells, but A20 knockdown sensitized GSCs to TNFalpha-mediated apoptosis.\n[5] The decreased survival of GSCs upon A20 knockdown contributed to the reduced ability of these cells to self-renew in primary and secondary neurosphere formation assays.\n[6] The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts.\n[7] In silico analysis of a glioma patient genomic database indicates that A20 overexpression and amplification is inversely correlated with survival.\n[8] Together these data indicate that A20 contributes to glioma maintenance through effects on the glioma stem cell subpopulation.\n[9] Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through glioma genomic sequencing: in fact, our data suggest A20 may function as a tumor enhancer in glioma through promotion of GSC survival.\n[10] A20 anticancer therapies should therefore be viewed with caution as effects will likely differ depending on the tumor type."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through glioma genomic sequencing: in fact, our data suggest A20 may function as a tumor enhancer in glioma through promotion of GSC survival.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1134, "doc_id": 33370, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [33370], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: TNFAIP3 is a glioblastoma tumor suppressor.\n\nDocument title: Targeting A20 Decreases Glioma Stem Cell Survival and Tumor Growth\n\nAbstract sentences:\n[0] Glioblastomas are deadly cancers that display a functional cellular hierarchy maintained by self-renewing glioblastoma stem cells (GSCs).\n[1] GSCs are regulated by molecular pathways distinct from the bulk tumor that may be useful therapeutic targets.\n[2] We determined that A20 (TNFAIP3), a regulator of cell survival and the NF-kappaB pathway, is overexpressed in GSCs relative to non-stem glioblastoma cells at both the mRNA and protein levels.\n[3] To determine the functional significance of A20 in GSCs, we targeted A20 expression with lentiviral-mediated delivery of short hairpin RNA (shRNA).\n[4] Inhibiting A20 expression decreased GSC growth and survival through mechanisms associated with decreased cell-cycle progression and decreased phosphorylation of p65/RelA. Elevated levels of A20 in GSCs contributed to apoptotic resistance: GSCs were less susceptible to TNFalpha-induced cell death than matched non-stem glioma cells, but A20 knockdown sensitized GSCs to TNFalpha-mediated apoptosis.\n[5] The decreased survival of GSCs upon A20 knockdown contributed to the reduced ability of these cells to self-renew in primary and secondary neurosphere formation assays.\n[6] The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts.\n[7] In silico analysis of a glioma patient genomic database indicates that A20 overexpression and amplification is inversely correlated with survival.\n[8] Together these data indicate that A20 contributes to glioma maintenance through effects on the glioma stem cell subpopulation.\n[9] Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through glioma genomic sequencing: in fact, our data suggest A20 may function as a tumor enhancer in glioma through promotion of GSC survival.\n[10] A20 anticancer therapies should therefore be viewed with caution as effects will likely differ depending on the tumor type."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Inhibiting A20 expression decreased GSC growth and survival through mechanisms associated with decreased cell-cycle progression and decreased phosphorylation of p65/RelA. Elevated levels of A20 in GSCs contributed to apoptotic resistance: GSCs were less susceptible to TNFalpha-induced cell death than matched non-stem glioma cells, but A20 knockdown sensitized GSCs to TNFalpha-mediated apoptosis.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1135, "doc_id": 33370, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [33370], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: TNFAIP3 is a glioblastoma tumor suppressor.\n\nDocument title: Targeting A20 Decreases Glioma Stem Cell Survival and Tumor Growth\n\nAbstract sentences:\n[0] Glioblastomas are deadly cancers that display a functional cellular hierarchy maintained by self-renewing glioblastoma stem cells (GSCs).\n[1] GSCs are regulated by molecular pathways distinct from the bulk tumor that may be useful therapeutic targets.\n[2] We determined that A20 (TNFAIP3), a regulator of cell survival and the NF-kappaB pathway, is overexpressed in GSCs relative to non-stem glioblastoma cells at both the mRNA and protein levels.\n[3] To determine the functional significance of A20 in GSCs, we targeted A20 expression with lentiviral-mediated delivery of short hairpin RNA (shRNA).\n[4] Inhibiting A20 expression decreased GSC growth and survival through mechanisms associated with decreased cell-cycle progression and decreased phosphorylation of p65/RelA. Elevated levels of A20 in GSCs contributed to apoptotic resistance: GSCs were less susceptible to TNFalpha-induced cell death than matched non-stem glioma cells, but A20 knockdown sensitized GSCs to TNFalpha-mediated apoptosis.\n[5] The decreased survival of GSCs upon A20 knockdown contributed to the reduced ability of these cells to self-renew in primary and secondary neurosphere formation assays.\n[6] The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts.\n[7] In silico analysis of a glioma patient genomic database indicates that A20 overexpression and amplification is inversely correlated with survival.\n[8] Together these data indicate that A20 contributes to glioma maintenance through effects on the glioma stem cell subpopulation.\n[9] Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through glioma genomic sequencing: in fact, our data suggest A20 may function as a tumor enhancer in glioma through promotion of GSC survival.\n[10] A20 anticancer therapies should therefore be viewed with caution as effects will likely differ depending on the tumor type."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through glioma genomic sequencing: in fact, our data suggest A20 may function as a tumor enhancer in glioma through promotion of GSC survival.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1135, "doc_id": 33370, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [33370], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: TNFAIP3 is a tumor enhancer in glioblastoma.\n\nDocument title: Targeting A20 Decreases Glioma Stem Cell Survival and Tumor Growth\n\nAbstract sentences:\n[0] Glioblastomas are deadly cancers that display a functional cellular hierarchy maintained by self-renewing glioblastoma stem cells (GSCs).\n[1] GSCs are regulated by molecular pathways distinct from the bulk tumor that may be useful therapeutic targets.\n[2] We determined that A20 (TNFAIP3), a regulator of cell survival and the NF-kappaB pathway, is overexpressed in GSCs relative to non-stem glioblastoma cells at both the mRNA and protein levels.\n[3] To determine the functional significance of A20 in GSCs, we targeted A20 expression with lentiviral-mediated delivery of short hairpin RNA (shRNA).\n[4] Inhibiting A20 expression decreased GSC growth and survival through mechanisms associated with decreased cell-cycle progression and decreased phosphorylation of p65/RelA. Elevated levels of A20 in GSCs contributed to apoptotic resistance: GSCs were less susceptible to TNFalpha-induced cell death than matched non-stem glioma cells, but A20 knockdown sensitized GSCs to TNFalpha-mediated apoptosis.\n[5] The decreased survival of GSCs upon A20 knockdown contributed to the reduced ability of these cells to self-renew in primary and secondary neurosphere formation assays.\n[6] The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts.\n[7] In silico analysis of a glioma patient genomic database indicates that A20 overexpression and amplification is inversely correlated with survival.\n[8] Together these data indicate that A20 contributes to glioma maintenance through effects on the glioma stem cell subpopulation.\n[9] Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through glioma genomic sequencing: in fact, our data suggest A20 may function as a tumor enhancer in glioma through promotion of GSC survival.\n[10] A20 anticancer therapies should therefore be viewed with caution as effects will likely differ depending on the tumor type."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1136, "doc_id": 33370, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [33370], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: TNFAIP3 is a tumor enhancer in glioblastoma.\n\nDocument title: Targeting A20 Decreases Glioma Stem Cell Survival and Tumor Growth\n\nAbstract sentences:\n[0] Glioblastomas are deadly cancers that display a functional cellular hierarchy maintained by self-renewing glioblastoma stem cells (GSCs).\n[1] GSCs are regulated by molecular pathways distinct from the bulk tumor that may be useful therapeutic targets.\n[2] We determined that A20 (TNFAIP3), a regulator of cell survival and the NF-kappaB pathway, is overexpressed in GSCs relative to non-stem glioblastoma cells at both the mRNA and protein levels.\n[3] To determine the functional significance of A20 in GSCs, we targeted A20 expression with lentiviral-mediated delivery of short hairpin RNA (shRNA).\n[4] Inhibiting A20 expression decreased GSC growth and survival through mechanisms associated with decreased cell-cycle progression and decreased phosphorylation of p65/RelA. Elevated levels of A20 in GSCs contributed to apoptotic resistance: GSCs were less susceptible to TNFalpha-induced cell death than matched non-stem glioma cells, but A20 knockdown sensitized GSCs to TNFalpha-mediated apoptosis.\n[5] The decreased survival of GSCs upon A20 knockdown contributed to the reduced ability of these cells to self-renew in primary and secondary neurosphere formation assays.\n[6] The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts.\n[7] In silico analysis of a glioma patient genomic database indicates that A20 overexpression and amplification is inversely correlated with survival.\n[8] Together these data indicate that A20 contributes to glioma maintenance through effects on the glioma stem cell subpopulation.\n[9] Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through glioma genomic sequencing: in fact, our data suggest A20 may function as a tumor enhancer in glioma through promotion of GSC survival.\n[10] A20 anticancer therapies should therefore be viewed with caution as effects will likely differ depending on the tumor type."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through glioma genomic sequencing: in fact, our data suggest A20 may function as a tumor enhancer in glioma through promotion of GSC survival.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1136, "doc_id": 33370, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [33370], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: TRAP+ osteoclasts regulate mature osteoblast maintenance.\n\nDocument title: PDGF-BB secreted by preosteoclasts induces angiogenesis during coupling with osteogenesis\n\nAbstract sentences:\n[0] Osteogenesis during bone modeling and remodeling is coupled with angiogenesis.\n[1] A recent study showed that a specific vessel subtype, strongly positive for CD31 and endomucin (CD31hiEmcnhi), couples angiogenesis and osteogenesis.\n[2] Here, we found that platelet-derived growth factor-BB (PDGF-BB) secreted by preosteoclasts induces CD31hiEmcnhi vessel formation during bone modeling and remodeling.\n[3] Mice with depletion of PDGF-BB in the tartrate-resistant acid phosphatase–positive cell lineage show significantly lower trabecular and cortical bone mass, serum and bone marrow PDGF-BB concentrations, and fewer CD31hiEmcnhi vessels compared to wild-type mice.\n[4] In the ovariectomy (OVX)-induced osteoporotic mouse model, serum and bone marrow levels of PDGF-BB and numbers of CD31hiEmcnhi vessels are significantly lower compared to sham-operated controls.\n[5] Treatment with exogenous PDGF-BB or inhibition of cathepsin K to increase the number of preosteoclasts, and thus the endogenous levels of PDGF-BB, increases CD31hiEmcnhi vessel number and stimulates bone formation in OVX mice.\n[6] Thus, pharmacotherapies that increase PDGF-BB secretion from preosteoclasts offer a new therapeutic target for treating osteoporosis by promoting angiogenesis and thus bone formation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Mice with depletion of PDGF-BB in the tartrate-resistant acid phosphatase–positive cell lineage show significantly lower trabecular and cortical bone mass, serum and bone marrow PDGF-BB concentrations, and fewer CD31hiEmcnhi vessels compared to wild-type mice.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1138, "doc_id": 6796297, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [6796297], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Taking 400mg of α-tocopheryl acetate does not prevent prostate cancer.\n\nDocument title: Vitamins E and C in the prevention of prostate and total cancer in men: the Physicians' Health Study II randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Many individuals take vitamins in the hopes of preventing chronic diseases such as cancer, and vitamins E and C are among the most common individual supplements.\n[1] A large-scale randomized trial suggested that vitamin E may reduce risk of prostate cancer; however, few trials have been powered to address this relationship.\n[2] No previous trial in men at usual risk has examined vitamin C alone in the prevention of cancer.\n[3] OBJECTIVE To evaluate whether long-term vitamin E or C supplementation decreases risk of prostate and total cancer events among men.\n[4] DESIGN, SETTING, AND PARTICIPANTS The Physicians' Health Study II is a randomized, double-blind, placebo-controlled factorial trial of vitamins E and C that began in 1997 and continued until its scheduled completion on August 31, 2007.\n[5] A total of 14,641 male physicians in the United States initially aged 50 years or older, including 1307 men with a history of prior cancer at randomization, were enrolled.\n[6] INTERVENTION Individual supplements of 400 IU of vitamin E every other day and 500 mg of vitamin C daily.\n[7] MAIN OUTCOME MEASURES Prostate and total cancer.\n[8] RESULTS During a mean follow-up of 8.0 years, there were 1008 confirmed incident cases of prostate cancer and 1943 total cancers.\n[9] Compared with placebo, vitamin E had no effect on the incidence of prostate cancer (active and placebo vitamin E groups, 9.1 and 9.5 events per 1000 person-years; hazard ratio [HR], 0.97; 95% confidence interval [CI], 0.85-1.09; P = .58) or total cancer (active and placebo vitamin E groups, 17.8 and 17.3 cases per 1000 person-years; HR, 1.04; 95% CI, 0.95-1.13; P = .41).\n[10] There was also no significant effect of vitamin C on total cancer (active and placebo vitamin C groups, 17.6 and 17.5 events per 1000 person-years; HR, 1.01; 95% CI, 0.92-1.10; P = .86) or prostate cancer (active and placebo vitamin C groups, 9.4 and 9.2 cases per 1000 person-years; HR, 1.02; 95% CI, 0.90-1.15; P = .80).\n[11] Neither vitamin E nor vitamin C had a significant effect on colorectal, lung, or other site-specific cancers.\n[12] Adjustment for adherence and exclusion of the first 4 or 6 years of follow-up did not alter the results.\n[13] Stratification by various cancer risk factors demonstrated no significant modification of the effect of vitamin E on prostate cancer risk or either agent on total cancer risk.\n[14] CONCLUSIONS In this large, long-term trial of male physicians, neither vitamin E nor C supplementation reduced the risk of prostate or total cancer.\n[15] These data provide no support for the use of these supplements for the prevention of cancer in middle-aged and older men.\n[16] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00270647."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Compared with placebo, vitamin E had no effect on the incidence of prostate cancer (active and placebo vitamin E groups, 9.1 and 9.5 events per 1000 person-years; hazard ratio [HR], 0.97; 95% confidence interval [CI], 0.85-1.09; P = .58) or total cancer (active and placebo vitamin E groups, 17.8 and 17.3 cases per 1000 person-years; HR, 1.04; 95% CI, 0.95-1.13; P = .41).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1139, "doc_id": 12009265, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [12009265], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Taking 400mg of α-tocopheryl acetate does not prevent prostate cancer.\n\nDocument title: Vitamins E and C in the prevention of prostate and total cancer in men: the Physicians' Health Study II randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Many individuals take vitamins in the hopes of preventing chronic diseases such as cancer, and vitamins E and C are among the most common individual supplements.\n[1] A large-scale randomized trial suggested that vitamin E may reduce risk of prostate cancer; however, few trials have been powered to address this relationship.\n[2] No previous trial in men at usual risk has examined vitamin C alone in the prevention of cancer.\n[3] OBJECTIVE To evaluate whether long-term vitamin E or C supplementation decreases risk of prostate and total cancer events among men.\n[4] DESIGN, SETTING, AND PARTICIPANTS The Physicians' Health Study II is a randomized, double-blind, placebo-controlled factorial trial of vitamins E and C that began in 1997 and continued until its scheduled completion on August 31, 2007.\n[5] A total of 14,641 male physicians in the United States initially aged 50 years or older, including 1307 men with a history of prior cancer at randomization, were enrolled.\n[6] INTERVENTION Individual supplements of 400 IU of vitamin E every other day and 500 mg of vitamin C daily.\n[7] MAIN OUTCOME MEASURES Prostate and total cancer.\n[8] RESULTS During a mean follow-up of 8.0 years, there were 1008 confirmed incident cases of prostate cancer and 1943 total cancers.\n[9] Compared with placebo, vitamin E had no effect on the incidence of prostate cancer (active and placebo vitamin E groups, 9.1 and 9.5 events per 1000 person-years; hazard ratio [HR], 0.97; 95% confidence interval [CI], 0.85-1.09; P = .58) or total cancer (active and placebo vitamin E groups, 17.8 and 17.3 cases per 1000 person-years; HR, 1.04; 95% CI, 0.95-1.13; P = .41).\n[10] There was also no significant effect of vitamin C on total cancer (active and placebo vitamin C groups, 17.6 and 17.5 events per 1000 person-years; HR, 1.01; 95% CI, 0.92-1.10; P = .86) or prostate cancer (active and placebo vitamin C groups, 9.4 and 9.2 cases per 1000 person-years; HR, 1.02; 95% CI, 0.90-1.15; P = .80).\n[11] Neither vitamin E nor vitamin C had a significant effect on colorectal, lung, or other site-specific cancers.\n[12] Adjustment for adherence and exclusion of the first 4 or 6 years of follow-up did not alter the results.\n[13] Stratification by various cancer risk factors demonstrated no significant modification of the effect of vitamin E on prostate cancer risk or either agent on total cancer risk.\n[14] CONCLUSIONS In this large, long-term trial of male physicians, neither vitamin E nor C supplementation reduced the risk of prostate or total cancer.\n[15] These data provide no support for the use of these supplements for the prevention of cancer in middle-aged and older men.\n[16] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00270647."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [14]\nExplanation: Evidence states: \"CONCLUSIONS In this large, long-term trial of male physicians, neither vitamin E nor C supplementation reduced the risk of prostate or total cancer.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1139, "doc_id": 12009265, "label": "SUPPORTS", "evidence_sentence_ids": [14], "cited_doc_ids": [12009265], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Taking 400mg of α-tocopheryl acetate in combination with vitamin C reduces the risk of prostate cancer.\n\nDocument title: Vitamins E and C in the prevention of prostate and total cancer in men: the Physicians' Health Study II randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Many individuals take vitamins in the hopes of preventing chronic diseases such as cancer, and vitamins E and C are among the most common individual supplements.\n[1] A large-scale randomized trial suggested that vitamin E may reduce risk of prostate cancer; however, few trials have been powered to address this relationship.\n[2] No previous trial in men at usual risk has examined vitamin C alone in the prevention of cancer.\n[3] OBJECTIVE To evaluate whether long-term vitamin E or C supplementation decreases risk of prostate and total cancer events among men.\n[4] DESIGN, SETTING, AND PARTICIPANTS The Physicians' Health Study II is a randomized, double-blind, placebo-controlled factorial trial of vitamins E and C that began in 1997 and continued until its scheduled completion on August 31, 2007.\n[5] A total of 14,641 male physicians in the United States initially aged 50 years or older, including 1307 men with a history of prior cancer at randomization, were enrolled.\n[6] INTERVENTION Individual supplements of 400 IU of vitamin E every other day and 500 mg of vitamin C daily.\n[7] MAIN OUTCOME MEASURES Prostate and total cancer.\n[8] RESULTS During a mean follow-up of 8.0 years, there were 1008 confirmed incident cases of prostate cancer and 1943 total cancers.\n[9] Compared with placebo, vitamin E had no effect on the incidence of prostate cancer (active and placebo vitamin E groups, 9.1 and 9.5 events per 1000 person-years; hazard ratio [HR], 0.97; 95% confidence interval [CI], 0.85-1.09; P = .58) or total cancer (active and placebo vitamin E groups, 17.8 and 17.3 cases per 1000 person-years; HR, 1.04; 95% CI, 0.95-1.13; P = .41).\n[10] There was also no significant effect of vitamin C on total cancer (active and placebo vitamin C groups, 17.6 and 17.5 events per 1000 person-years; HR, 1.01; 95% CI, 0.92-1.10; P = .86) or prostate cancer (active and placebo vitamin C groups, 9.4 and 9.2 cases per 1000 person-years; HR, 1.02; 95% CI, 0.90-1.15; P = .80).\n[11] Neither vitamin E nor vitamin C had a significant effect on colorectal, lung, or other site-specific cancers.\n[12] Adjustment for adherence and exclusion of the first 4 or 6 years of follow-up did not alter the results.\n[13] Stratification by various cancer risk factors demonstrated no significant modification of the effect of vitamin E on prostate cancer risk or either agent on total cancer risk.\n[14] CONCLUSIONS In this large, long-term trial of male physicians, neither vitamin E nor C supplementation reduced the risk of prostate or total cancer.\n[15] These data provide no support for the use of these supplements for the prevention of cancer in middle-aged and older men.\n[16] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00270647."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9, 10]\nExplanation: Evidence states: \"Compared with placebo, vitamin E had no effect on the incidence of prostate cancer (active and placebo vitamin E groups, 9.1 and 9.5 events per 1000 person-years; hazard ratio [HR], 0.97; 95% confidence interval [CI], 0.85-1.09; P = .58) or total cancer (active and placebo vitamin E groups, 17.8 and 17.3 cases per 1000 person-years; HR, 1.04; 95% CI, 0.95-1.13; P = .41). There was also no significant effect of vitamin C on total cancer (active and placebo vitamin C groups, 17.6 and 17.5 events per 1000 person-years; HR, 1.01; 95% CI, 0.92-1.10; P = .86) or prostate cancer (active and placebo vitamin C groups, 9.4 and 9.2 cases per 1000 person-years; HR, 1.02; 95% CI, 0.90-1.15; P = .80).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1141, "doc_id": 12009265, "label": "CONTRADICTS", "evidence_sentence_ids": [9, 10], "cited_doc_ids": [12009265], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Taking 400mg of α-tocopheryl acetate in combination with vitamin C reduces the risk of prostate cancer.\n\nDocument title: Vitamins E and C in the prevention of prostate and total cancer in men: the Physicians' Health Study II randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT Many individuals take vitamins in the hopes of preventing chronic diseases such as cancer, and vitamins E and C are among the most common individual supplements.\n[1] A large-scale randomized trial suggested that vitamin E may reduce risk of prostate cancer; however, few trials have been powered to address this relationship.\n[2] No previous trial in men at usual risk has examined vitamin C alone in the prevention of cancer.\n[3] OBJECTIVE To evaluate whether long-term vitamin E or C supplementation decreases risk of prostate and total cancer events among men.\n[4] DESIGN, SETTING, AND PARTICIPANTS The Physicians' Health Study II is a randomized, double-blind, placebo-controlled factorial trial of vitamins E and C that began in 1997 and continued until its scheduled completion on August 31, 2007.\n[5] A total of 14,641 male physicians in the United States initially aged 50 years or older, including 1307 men with a history of prior cancer at randomization, were enrolled.\n[6] INTERVENTION Individual supplements of 400 IU of vitamin E every other day and 500 mg of vitamin C daily.\n[7] MAIN OUTCOME MEASURES Prostate and total cancer.\n[8] RESULTS During a mean follow-up of 8.0 years, there were 1008 confirmed incident cases of prostate cancer and 1943 total cancers.\n[9] Compared with placebo, vitamin E had no effect on the incidence of prostate cancer (active and placebo vitamin E groups, 9.1 and 9.5 events per 1000 person-years; hazard ratio [HR], 0.97; 95% confidence interval [CI], 0.85-1.09; P = .58) or total cancer (active and placebo vitamin E groups, 17.8 and 17.3 cases per 1000 person-years; HR, 1.04; 95% CI, 0.95-1.13; P = .41).\n[10] There was also no significant effect of vitamin C on total cancer (active and placebo vitamin C groups, 17.6 and 17.5 events per 1000 person-years; HR, 1.01; 95% CI, 0.92-1.10; P = .86) or prostate cancer (active and placebo vitamin C groups, 9.4 and 9.2 cases per 1000 person-years; HR, 1.02; 95% CI, 0.90-1.15; P = .80).\n[11] Neither vitamin E nor vitamin C had a significant effect on colorectal, lung, or other site-specific cancers.\n[12] Adjustment for adherence and exclusion of the first 4 or 6 years of follow-up did not alter the results.\n[13] Stratification by various cancer risk factors demonstrated no significant modification of the effect of vitamin E on prostate cancer risk or either agent on total cancer risk.\n[14] CONCLUSIONS In this large, long-term trial of male physicians, neither vitamin E nor C supplementation reduced the risk of prostate or total cancer.\n[15] These data provide no support for the use of these supplements for the prevention of cancer in middle-aged and older men.\n[16] TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00270647."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [14]\nExplanation: Evidence states: \"CONCLUSIONS In this large, long-term trial of male physicians, neither vitamin E nor C supplementation reduced the risk of prostate or total cancer.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1141, "doc_id": 12009265, "label": "CONTRADICTS", "evidence_sentence_ids": [14], "cited_doc_ids": [12009265], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Taking anti-depresents is associated with a decrease in the Aβ level in the brain of experimental animals.\n\nDocument title: An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice\n\nAbstract sentences:\n[0] Serotonin signaling suppresses generation of amyloid-β (Aβ) in vitro and in animal models of Alzheimer’s disease (AD).\n[1] We show that in an aged transgenic AD mouse model (APP/PS1 plaque-bearing mice), the antidepressant citalopram, a selective serotonin reuptake inhibitor, decreased Aβ in brain interstitial fluid in a dose-dependent manner.\n[2] Growth of individual amyloid plaques was assessed in plaque-bearing mice that were chronically administered citalopram.\n[3] Citalopram arrested the growth of preexisting plaques and reduced the appearance of new plaques by 78%.\n[4] In healthy human volunteers, citalopram’s effects on Aβ production and Aβ concentrations in cerebrospinal fluid (CSF) were measured prospectively using stable isotope labeling kinetics, with CSF sampling during acute dosing of citalopram.\n[5] Aβ production in CSF was slowed by 37% in the citalopram group compared to placebo.\n[6] This change was associated with a 38% decrease in total CSF Aβ concentrations in the drug-treated group.\n[7] The ability to safely decrease Aβ concentrations is potentially important as a preventive strategy for AD.\n[8] This study demonstrates key target engagement for future AD prevention trials."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Aβ production in CSF was slowed by 37% in the citalopram group compared to placebo.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1142, "doc_id": 5260382, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [5260382], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Taxation of sugar-sweetened beverages reduced the incidence rate of type II diabetes in India.\n\nDocument title: Averting Obesity and Type 2 Diabetes in India through Sugar-Sweetened Beverage Taxation: An Economic-Epidemiologic Modeling Study\n\nAbstract sentences:\n[0] BACKGROUND Taxing sugar-sweetened beverages (SSBs) has been proposed in high-income countries to reduce obesity and type 2 diabetes.\n[1] We sought to estimate the potential health effects of such a fiscal strategy in the middle-income country of India, where there is heterogeneity in SSB consumption, patterns of substitution between SSBs and other beverages after tax increases, and vast differences in chronic disease risk within the population.\n[2] METHODS AND FINDINGS Using consumption and price variations data from a nationally representative survey of 100,855 Indian households, we first calculated how changes in SSB price alter per capita consumption of SSBs and substitution with other beverages.\n[3] We then incorporated SSB sales trends, body mass index (BMI), and diabetes incidence data stratified by age, sex, income, and urban/rural residence into a validated microsimulation of caloric consumption, glycemic load, overweight/obesity prevalence, and type 2 diabetes incidence among Indian subpopulations facing a 20% SSB excise tax.\n[4] The 20% SSB tax was anticipated to reduce overweight and obesity prevalence by 3.0% (95% CI 1.6%-5.9%) and type 2 diabetes incidence by 1.6% (95% CI 1.2%-1.9%) among various Indian subpopulations over the period 2014-2023, if SSB consumption continued to increase linearly in accordance with secular trends.\n[5] However, acceleration in SSB consumption trends consistent with industry marketing models would be expected to increase the impact efficacy of taxation, averting 4.2% of prevalent overweight/obesity (95% CI 2.5-10.0%) and 2.5% (95% CI 1.0-2.8%) of incident type 2 diabetes from 2014-2023.\n[6] Given current consumption and BMI distributions, our results suggest the largest relative effect would be expected among young rural men, refuting our a priori hypothesis that urban populations would be isolated beneficiaries of SSB taxation.\n[7] Key limitations of this estimation approach include the assumption that consumer expenditure behavior from prior years, captured in price elasticities, will reflect future behavior among consumers, and potential underreporting of consumption in dietary recall data used to inform our calculations.\n[8] CONCLUSION Sustained SSB taxation at a high tax rate could mitigate rising obesity and type 2 diabetes in India among both urban and rural subpopulations."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"The 20% SSB tax was anticipated to reduce overweight and obesity prevalence by 3.0% (95% CI 1.6%-5.9%) and type 2 diabetes incidence by 1.6% (95% CI 1.2%-1.9%) among various Indian subpopulations over the period 2014-2023, if SSB consumption continued to increase linearly in accordance with secular trends.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1145, "doc_id": 10071552, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [10071552], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Taxation of sugar-sweetened beverages reduced the incidence rate of type II diabetes in India.\n\nDocument title: Averting Obesity and Type 2 Diabetes in India through Sugar-Sweetened Beverage Taxation: An Economic-Epidemiologic Modeling Study\n\nAbstract sentences:\n[0] BACKGROUND Taxing sugar-sweetened beverages (SSBs) has been proposed in high-income countries to reduce obesity and type 2 diabetes.\n[1] We sought to estimate the potential health effects of such a fiscal strategy in the middle-income country of India, where there is heterogeneity in SSB consumption, patterns of substitution between SSBs and other beverages after tax increases, and vast differences in chronic disease risk within the population.\n[2] METHODS AND FINDINGS Using consumption and price variations data from a nationally representative survey of 100,855 Indian households, we first calculated how changes in SSB price alter per capita consumption of SSBs and substitution with other beverages.\n[3] We then incorporated SSB sales trends, body mass index (BMI), and diabetes incidence data stratified by age, sex, income, and urban/rural residence into a validated microsimulation of caloric consumption, glycemic load, overweight/obesity prevalence, and type 2 diabetes incidence among Indian subpopulations facing a 20% SSB excise tax.\n[4] The 20% SSB tax was anticipated to reduce overweight and obesity prevalence by 3.0% (95% CI 1.6%-5.9%) and type 2 diabetes incidence by 1.6% (95% CI 1.2%-1.9%) among various Indian subpopulations over the period 2014-2023, if SSB consumption continued to increase linearly in accordance with secular trends.\n[5] However, acceleration in SSB consumption trends consistent with industry marketing models would be expected to increase the impact efficacy of taxation, averting 4.2% of prevalent overweight/obesity (95% CI 2.5-10.0%) and 2.5% (95% CI 1.0-2.8%) of incident type 2 diabetes from 2014-2023.\n[6] Given current consumption and BMI distributions, our results suggest the largest relative effect would be expected among young rural men, refuting our a priori hypothesis that urban populations would be isolated beneficiaries of SSB taxation.\n[7] Key limitations of this estimation approach include the assumption that consumer expenditure behavior from prior years, captured in price elasticities, will reflect future behavior among consumers, and potential underreporting of consumption in dietary recall data used to inform our calculations.\n[8] CONCLUSION Sustained SSB taxation at a high tax rate could mitigate rising obesity and type 2 diabetes in India among both urban and rural subpopulations."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"However, acceleration in SSB consumption trends consistent with industry marketing models would be expected to increase the impact efficacy of taxation, averting 4.2% of prevalent overweight/obesity (95% CI 2.5-10.0%) and 2.5% (95% CI 1.0-2.8%) of incident type 2 diabetes from 2014-2023.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1145, "doc_id": 10071552, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [10071552], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Taxation of sugar-sweetened beverages reduced the incidence rate of type II diabetes in India.\n\nDocument title: Averting Obesity and Type 2 Diabetes in India through Sugar-Sweetened Beverage Taxation: An Economic-Epidemiologic Modeling Study\n\nAbstract sentences:\n[0] BACKGROUND Taxing sugar-sweetened beverages (SSBs) has been proposed in high-income countries to reduce obesity and type 2 diabetes.\n[1] We sought to estimate the potential health effects of such a fiscal strategy in the middle-income country of India, where there is heterogeneity in SSB consumption, patterns of substitution between SSBs and other beverages after tax increases, and vast differences in chronic disease risk within the population.\n[2] METHODS AND FINDINGS Using consumption and price variations data from a nationally representative survey of 100,855 Indian households, we first calculated how changes in SSB price alter per capita consumption of SSBs and substitution with other beverages.\n[3] We then incorporated SSB sales trends, body mass index (BMI), and diabetes incidence data stratified by age, sex, income, and urban/rural residence into a validated microsimulation of caloric consumption, glycemic load, overweight/obesity prevalence, and type 2 diabetes incidence among Indian subpopulations facing a 20% SSB excise tax.\n[4] The 20% SSB tax was anticipated to reduce overweight and obesity prevalence by 3.0% (95% CI 1.6%-5.9%) and type 2 diabetes incidence by 1.6% (95% CI 1.2%-1.9%) among various Indian subpopulations over the period 2014-2023, if SSB consumption continued to increase linearly in accordance with secular trends.\n[5] However, acceleration in SSB consumption trends consistent with industry marketing models would be expected to increase the impact efficacy of taxation, averting 4.2% of prevalent overweight/obesity (95% CI 2.5-10.0%) and 2.5% (95% CI 1.0-2.8%) of incident type 2 diabetes from 2014-2023.\n[6] Given current consumption and BMI distributions, our results suggest the largest relative effect would be expected among young rural men, refuting our a priori hypothesis that urban populations would be isolated beneficiaries of SSB taxation.\n[7] Key limitations of this estimation approach include the assumption that consumer expenditure behavior from prior years, captured in price elasticities, will reflect future behavior among consumers, and potential underreporting of consumption in dietary recall data used to inform our calculations.\n[8] CONCLUSION Sustained SSB taxation at a high tax rate could mitigate rising obesity and type 2 diabetes in India among both urban and rural subpopulations."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"CONCLUSION Sustained SSB taxation at a high tax rate could mitigate rising obesity and type 2 diabetes in India among both urban and rural subpopulations.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1145, "doc_id": 10071552, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [10071552], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ten percent (10%) of kidney cancers in the UK are attributable to excess weight.\n\nDocument title: Body-mass index and risk of 22 specific cancers: a population-based cohort study of 5·24 million UK adults\n\nAbstract sentences:\n[0] BACKGROUND High body-mass index (BMI) predisposes to several site-specific cancers, but a large-scale systematic and detailed characterisation of patterns of risk across all common cancers adjusted for potential confounders has not previously been undertaken.\n[1] We aimed to investigate the links between BMI and the most common site-specific cancers.\n[2] METHODS With primary care data from individuals in the Clinical Practice Research Datalink with BMI data, we fitted Cox models to investigate associations between BMI and 22 of the most common cancers, adjusting for potential confounders.\n[3] We fitted linear then non-linear (spline) models; investigated effect modification by sex, menopausal status, smoking, and age; and calculated population effects.\n[4] FINDINGS 5·24 million individuals were included; 166,955 developed cancers of interest.\n[5] BMI was associated with 17 of 22 cancers, but effects varied substantially by site.\n[6] Each 5 kg/m(2) increase in BMI was roughly linearly associated with cancers of the uterus (hazard ratio [HR] 1·62, 99% CI 1·56-1·69; p<0·0001), gallbladder (1·31, 1·12-1·52; p<0·0001), kidney (1·25, 1·17-1·33; p<0·0001), cervix (1·10, 1·03-1·17; p=0·00035), thyroid (1·09, 1·00-1·19; p=0·0088), and leukaemia (1·09, 1·05-1·13; p≤0·0001).\n[7] BMI was positively associated with liver (1·19, 1·12-1·27), colon (1·10, 1·07-1·13), ovarian (1·09, 1.04-1.14), and postmenopausal breast cancers (1·05, 1·03-1·07) overall (all p<0·0001), but these effects varied by underlying BMI or individual-level characteristics.\n[8] We estimated inverse associations with prostate and premenopausal breast cancer risk, both overall (prostate 0·98, 0·95-1·00; premenopausal breast cancer 0·89, 0·86-0·92) and in never-smokers (prostate 0·96, 0·93-0·99; premenopausal breast cancer 0·89, 0·85-0·94).\n[9] By contrast, for lung and oral cavity cancer, we observed no association in never smokers (lung 0·99, 0·93-1·05; oral cavity 1·07, 0·91-1·26): inverse associations overall were driven by current smokers and ex-smokers, probably because of residual confounding by smoking amount.\n[10] Assuming causality, 41% of uterine and 10% or more of gallbladder, kidney, liver, and colon cancers could be attributable to excess weight.\n[11] We estimated that a 1 kg/m(2) population-wide increase in BMI would result in 3790 additional annual UK patients developing one of the ten cancers positively associated with BMI.\n[12] INTERPRETATION BMI is associated with cancer risk, with substantial population-level effects.\n[13] The heterogeneity in the effects suggests that different mechanisms are associated with different cancer sites and different patient subgroups.\n[14] FUNDING National Institute for Health Research, Wellcome Trust, and Medical Research Council."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Assuming causality, 41% of uterine and 10% or more of gallbladder, kidney, liver, and colon cancers could be attributable to excess weight.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1148, "doc_id": 4828631, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [4828631], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The C-type lectin receptor (CLEC-2) rearranges the actin cytoskeleton in dendritic cells to promote efficient motility along stromal surfaces.\n\nDocument title: Podoplanin-Rich Stromal Networks Induce Dendritic Cell Motility via Activation of the C-type Lectin Receptor CLEC-2\n\nAbstract sentences:\n[0] To initiate adaptive immunity, dendritic cells (DCs) move from parenchymal tissues to lymphoid organs by migrating along stromal scaffolds that display the glycoprotein podoplanin (PDPN).\n[1] PDPN is expressed by lymphatic endothelial and fibroblastic reticular cells and promotes blood-lymph separation during development by activating the C-type lectin receptor, CLEC-2, on platelets.\n[2] Here, we describe a role for CLEC-2 in the morphodynamic behavior and motility of DCs.\n[3] CLEC-2 deficiency in DCs impaired their entry into lymphatics and trafficking to and within lymph nodes, thereby reducing T cell priming.\n[4] CLEC-2 engagement of PDPN was necessary for DCs to spread and migrate along stromal surfaces and sufficient to induce membrane protrusions.\n[5] CLEC-2 activation triggered cell spreading via downregulation of RhoA activity and myosin light-chain phosphorylation and triggered F-actin-rich protrusions via Vav signaling and Rac1 activation.\n[6] Thus, activation of CLEC-2 by PDPN rearranges the actin cytoskeleton in DCs to promote efficient motility along stromal surfaces."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"CLEC-2 activation triggered cell spreading via downregulation of RhoA activity and myosin light-chain phosphorylation and triggered F-actin-rich protrusions via Vav signaling and Rac1 activation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1153, "doc_id": 7370282, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [7370282], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The C-type lectin receptor (CLEC-2) rearranges the actin cytoskeleton in dendritic cells to promote efficient motility along stromal surfaces.\n\nDocument title: Podoplanin-Rich Stromal Networks Induce Dendritic Cell Motility via Activation of the C-type Lectin Receptor CLEC-2\n\nAbstract sentences:\n[0] To initiate adaptive immunity, dendritic cells (DCs) move from parenchymal tissues to lymphoid organs by migrating along stromal scaffolds that display the glycoprotein podoplanin (PDPN).\n[1] PDPN is expressed by lymphatic endothelial and fibroblastic reticular cells and promotes blood-lymph separation during development by activating the C-type lectin receptor, CLEC-2, on platelets.\n[2] Here, we describe a role for CLEC-2 in the morphodynamic behavior and motility of DCs.\n[3] CLEC-2 deficiency in DCs impaired their entry into lymphatics and trafficking to and within lymph nodes, thereby reducing T cell priming.\n[4] CLEC-2 engagement of PDPN was necessary for DCs to spread and migrate along stromal surfaces and sufficient to induce membrane protrusions.\n[5] CLEC-2 activation triggered cell spreading via downregulation of RhoA activity and myosin light-chain phosphorylation and triggered F-actin-rich protrusions via Vav signaling and Rac1 activation.\n[6] Thus, activation of CLEC-2 by PDPN rearranges the actin cytoskeleton in DCs to promote efficient motility along stromal surfaces."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Thus, activation of CLEC-2 by PDPN rearranges the actin cytoskeleton in DCs to promote efficient motility along stromal surfaces.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1153, "doc_id": 7370282, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [7370282], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The DESMOND program caused substantial weight loss in most participants.\n\nDocument title: Effectiveness of a diabetes education and self management programme (DESMOND) for people with newly diagnosed type 2 diabetes mellitus: three year follow-up of a cluster randomised controlled trial in primary care\n\nAbstract sentences:\n[0] OBJECTIVE To measure whether the benefits of a single education and self management structured programme for people with newly diagnosed type 2 diabetes mellitus are sustained at three years.\n[1] DESIGN Three year follow-up of a multicentre cluster randomised controlled trial in primary care, with randomisation at practice level.\n[2] SETTING 207 general practices in 13 primary care sites in the United Kingdom.\n[3] PARTICIPANTS 731 of the 824 participants included in the original trial were eligible for follow-up.\n[4] Biomedical data were collected on 604 (82.6%) and questionnaire data on 513 (70.1%) participants.\n[5] INTERVENTION A structured group education programme for six hours delivered in the community by two trained healthcare professional educators compared with usual care.\n[6] MAIN OUTCOME MEASURES The primary outcome was glycated haemoglobin (HbA(1c)) levels.\n[7] The secondary outcomes were blood pressure, weight, blood lipid levels, smoking status, physical activity, quality of life, beliefs about illness, depression, emotional impact of diabetes, and drug use at three years.\n[8] RESULTS HbA(1c) levels at three years had decreased in both groups.\n[9] After adjusting for baseline and cluster the difference was not significant (difference -0.02, 95% confidence interval -0.22 to 0.17).\n[10] The groups did not differ for the other biomedical and lifestyle outcomes and drug use.\n[11] The significant benefits in the intervention group across four out of five health beliefs seen at 12 months were sustained at three years (P<0.01).\n[12] Depression scores and quality of life did not differ at three years.\n[13] CONCLUSION A single programme for people with newly diagnosed type 2 diabetes mellitus showed no difference in biomedical or lifestyle outcomes at three years although there were sustained improvements in some illness beliefs.\n[14] TRIAL REGISTRATION Current Controlled Trials ISRCTN17844016."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"CONCLUSION A single programme for people with newly diagnosed type 2 diabetes mellitus showed no difference in biomedical or lifestyle outcomes at three years although there were sustained improvements in some illness beliefs.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1156, "doc_id": 12584053, "label": "CONTRADICTS", "evidence_sentence_ids": [13], "cited_doc_ids": [12584053], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The DESMOND program demonstrates no significant impact on biochemical outcomes.\n\nDocument title: Effectiveness of a diabetes education and self management programme (DESMOND) for people with newly diagnosed type 2 diabetes mellitus: three year follow-up of a cluster randomised controlled trial in primary care\n\nAbstract sentences:\n[0] OBJECTIVE To measure whether the benefits of a single education and self management structured programme for people with newly diagnosed type 2 diabetes mellitus are sustained at three years.\n[1] DESIGN Three year follow-up of a multicentre cluster randomised controlled trial in primary care, with randomisation at practice level.\n[2] SETTING 207 general practices in 13 primary care sites in the United Kingdom.\n[3] PARTICIPANTS 731 of the 824 participants included in the original trial were eligible for follow-up.\n[4] Biomedical data were collected on 604 (82.6%) and questionnaire data on 513 (70.1%) participants.\n[5] INTERVENTION A structured group education programme for six hours delivered in the community by two trained healthcare professional educators compared with usual care.\n[6] MAIN OUTCOME MEASURES The primary outcome was glycated haemoglobin (HbA(1c)) levels.\n[7] The secondary outcomes were blood pressure, weight, blood lipid levels, smoking status, physical activity, quality of life, beliefs about illness, depression, emotional impact of diabetes, and drug use at three years.\n[8] RESULTS HbA(1c) levels at three years had decreased in both groups.\n[9] After adjusting for baseline and cluster the difference was not significant (difference -0.02, 95% confidence interval -0.22 to 0.17).\n[10] The groups did not differ for the other biomedical and lifestyle outcomes and drug use.\n[11] The significant benefits in the intervention group across four out of five health beliefs seen at 12 months were sustained at three years (P<0.01).\n[12] Depression scores and quality of life did not differ at three years.\n[13] CONCLUSION A single programme for people with newly diagnosed type 2 diabetes mellitus showed no difference in biomedical or lifestyle outcomes at three years although there were sustained improvements in some illness beliefs.\n[14] TRIAL REGISTRATION Current Controlled Trials ISRCTN17844016."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"After adjusting for baseline and cluster the difference was not significant (difference -0.02, 95% confidence interval -0.22 to 0.17).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1157, "doc_id": 12584053, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [12584053], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The DESMOND program demonstrates no significant impact on biochemical outcomes.\n\nDocument title: Effectiveness of a diabetes education and self management programme (DESMOND) for people with newly diagnosed type 2 diabetes mellitus: three year follow-up of a cluster randomised controlled trial in primary care\n\nAbstract sentences:\n[0] OBJECTIVE To measure whether the benefits of a single education and self management structured programme for people with newly diagnosed type 2 diabetes mellitus are sustained at three years.\n[1] DESIGN Three year follow-up of a multicentre cluster randomised controlled trial in primary care, with randomisation at practice level.\n[2] SETTING 207 general practices in 13 primary care sites in the United Kingdom.\n[3] PARTICIPANTS 731 of the 824 participants included in the original trial were eligible for follow-up.\n[4] Biomedical data were collected on 604 (82.6%) and questionnaire data on 513 (70.1%) participants.\n[5] INTERVENTION A structured group education programme for six hours delivered in the community by two trained healthcare professional educators compared with usual care.\n[6] MAIN OUTCOME MEASURES The primary outcome was glycated haemoglobin (HbA(1c)) levels.\n[7] The secondary outcomes were blood pressure, weight, blood lipid levels, smoking status, physical activity, quality of life, beliefs about illness, depression, emotional impact of diabetes, and drug use at three years.\n[8] RESULTS HbA(1c) levels at three years had decreased in both groups.\n[9] After adjusting for baseline and cluster the difference was not significant (difference -0.02, 95% confidence interval -0.22 to 0.17).\n[10] The groups did not differ for the other biomedical and lifestyle outcomes and drug use.\n[11] The significant benefits in the intervention group across four out of five health beliefs seen at 12 months were sustained at three years (P<0.01).\n[12] Depression scores and quality of life did not differ at three years.\n[13] CONCLUSION A single programme for people with newly diagnosed type 2 diabetes mellitus showed no difference in biomedical or lifestyle outcomes at three years although there were sustained improvements in some illness beliefs.\n[14] TRIAL REGISTRATION Current Controlled Trials ISRCTN17844016."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"The groups did not differ for the other biomedical and lifestyle outcomes and drug use.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1157, "doc_id": 12584053, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [12584053], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The DESMOND program demonstrates no significant impact on biochemical outcomes.\n\nDocument title: Effectiveness of a diabetes education and self management programme (DESMOND) for people with newly diagnosed type 2 diabetes mellitus: three year follow-up of a cluster randomised controlled trial in primary care\n\nAbstract sentences:\n[0] OBJECTIVE To measure whether the benefits of a single education and self management structured programme for people with newly diagnosed type 2 diabetes mellitus are sustained at three years.\n[1] DESIGN Three year follow-up of a multicentre cluster randomised controlled trial in primary care, with randomisation at practice level.\n[2] SETTING 207 general practices in 13 primary care sites in the United Kingdom.\n[3] PARTICIPANTS 731 of the 824 participants included in the original trial were eligible for follow-up.\n[4] Biomedical data were collected on 604 (82.6%) and questionnaire data on 513 (70.1%) participants.\n[5] INTERVENTION A structured group education programme for six hours delivered in the community by two trained healthcare professional educators compared with usual care.\n[6] MAIN OUTCOME MEASURES The primary outcome was glycated haemoglobin (HbA(1c)) levels.\n[7] The secondary outcomes were blood pressure, weight, blood lipid levels, smoking status, physical activity, quality of life, beliefs about illness, depression, emotional impact of diabetes, and drug use at three years.\n[8] RESULTS HbA(1c) levels at three years had decreased in both groups.\n[9] After adjusting for baseline and cluster the difference was not significant (difference -0.02, 95% confidence interval -0.22 to 0.17).\n[10] The groups did not differ for the other biomedical and lifestyle outcomes and drug use.\n[11] The significant benefits in the intervention group across four out of five health beliefs seen at 12 months were sustained at three years (P<0.01).\n[12] Depression scores and quality of life did not differ at three years.\n[13] CONCLUSION A single programme for people with newly diagnosed type 2 diabetes mellitus showed no difference in biomedical or lifestyle outcomes at three years although there were sustained improvements in some illness beliefs.\n[14] TRIAL REGISTRATION Current Controlled Trials ISRCTN17844016."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"CONCLUSION A single programme for people with newly diagnosed type 2 diabetes mellitus showed no difference in biomedical or lifestyle outcomes at three years although there were sustained improvements in some illness beliefs.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1157, "doc_id": 12584053, "label": "SUPPORTS", "evidence_sentence_ids": [13], "cited_doc_ids": [12584053], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The DESMOND program demonstrates no significant impact on lifestyles outcomes.\n\nDocument title: Effectiveness of a diabetes education and self management programme (DESMOND) for people with newly diagnosed type 2 diabetes mellitus: three year follow-up of a cluster randomised controlled trial in primary care\n\nAbstract sentences:\n[0] OBJECTIVE To measure whether the benefits of a single education and self management structured programme for people with newly diagnosed type 2 diabetes mellitus are sustained at three years.\n[1] DESIGN Three year follow-up of a multicentre cluster randomised controlled trial in primary care, with randomisation at practice level.\n[2] SETTING 207 general practices in 13 primary care sites in the United Kingdom.\n[3] PARTICIPANTS 731 of the 824 participants included in the original trial were eligible for follow-up.\n[4] Biomedical data were collected on 604 (82.6%) and questionnaire data on 513 (70.1%) participants.\n[5] INTERVENTION A structured group education programme for six hours delivered in the community by two trained healthcare professional educators compared with usual care.\n[6] MAIN OUTCOME MEASURES The primary outcome was glycated haemoglobin (HbA(1c)) levels.\n[7] The secondary outcomes were blood pressure, weight, blood lipid levels, smoking status, physical activity, quality of life, beliefs about illness, depression, emotional impact of diabetes, and drug use at three years.\n[8] RESULTS HbA(1c) levels at three years had decreased in both groups.\n[9] After adjusting for baseline and cluster the difference was not significant (difference -0.02, 95% confidence interval -0.22 to 0.17).\n[10] The groups did not differ for the other biomedical and lifestyle outcomes and drug use.\n[11] The significant benefits in the intervention group across four out of five health beliefs seen at 12 months were sustained at three years (P<0.01).\n[12] Depression scores and quality of life did not differ at three years.\n[13] CONCLUSION A single programme for people with newly diagnosed type 2 diabetes mellitus showed no difference in biomedical or lifestyle outcomes at three years although there were sustained improvements in some illness beliefs.\n[14] TRIAL REGISTRATION Current Controlled Trials ISRCTN17844016."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"CONCLUSION A single programme for people with newly diagnosed type 2 diabetes mellitus showed no difference in biomedical or lifestyle outcomes at three years although there were sustained improvements in some illness beliefs.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1158, "doc_id": 12584053, "label": "SUPPORTS", "evidence_sentence_ids": [13], "cited_doc_ids": [12584053], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The DESMOND program demonstrates no significant impact on weight loss.\n\nDocument title: Effectiveness of a diabetes education and self management programme (DESMOND) for people with newly diagnosed type 2 diabetes mellitus: three year follow-up of a cluster randomised controlled trial in primary care\n\nAbstract sentences:\n[0] OBJECTIVE To measure whether the benefits of a single education and self management structured programme for people with newly diagnosed type 2 diabetes mellitus are sustained at three years.\n[1] DESIGN Three year follow-up of a multicentre cluster randomised controlled trial in primary care, with randomisation at practice level.\n[2] SETTING 207 general practices in 13 primary care sites in the United Kingdom.\n[3] PARTICIPANTS 731 of the 824 participants included in the original trial were eligible for follow-up.\n[4] Biomedical data were collected on 604 (82.6%) and questionnaire data on 513 (70.1%) participants.\n[5] INTERVENTION A structured group education programme for six hours delivered in the community by two trained healthcare professional educators compared with usual care.\n[6] MAIN OUTCOME MEASURES The primary outcome was glycated haemoglobin (HbA(1c)) levels.\n[7] The secondary outcomes were blood pressure, weight, blood lipid levels, smoking status, physical activity, quality of life, beliefs about illness, depression, emotional impact of diabetes, and drug use at three years.\n[8] RESULTS HbA(1c) levels at three years had decreased in both groups.\n[9] After adjusting for baseline and cluster the difference was not significant (difference -0.02, 95% confidence interval -0.22 to 0.17).\n[10] The groups did not differ for the other biomedical and lifestyle outcomes and drug use.\n[11] The significant benefits in the intervention group across four out of five health beliefs seen at 12 months were sustained at three years (P<0.01).\n[12] Depression scores and quality of life did not differ at three years.\n[13] CONCLUSION A single programme for people with newly diagnosed type 2 diabetes mellitus showed no difference in biomedical or lifestyle outcomes at three years although there were sustained improvements in some illness beliefs.\n[14] TRIAL REGISTRATION Current Controlled Trials ISRCTN17844016."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"CONCLUSION A single programme for people with newly diagnosed type 2 diabetes mellitus showed no difference in biomedical or lifestyle outcomes at three years although there were sustained improvements in some illness beliefs.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1159, "doc_id": 12584053, "label": "SUPPORTS", "evidence_sentence_ids": [13], "cited_doc_ids": [12584053], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The DEXI promoter region is bound by multiple transcription factors in a murine haematopoietic progenitor cell line.\n\nDocument title: Combinatorial transcriptional control in blood stem/progenitor cells: genome-wide analysis of ten major transcriptional regulators.\n\nAbstract sentences:\n[0] Combinatorial transcription factor (TF) interactions control cellular phenotypes and, therefore, underpin stem cell formation, maintenance, and differentiation.\n[1] Here, we report the genome-wide binding patterns and combinatorial interactions for ten key regulators of blood stem/progenitor cells (SCL/TAL1, LYL1, LMO2, GATA2, RUNX1, MEIS1, PU.1, ERG, FLI-1, and GFI1B), thus providing the most comprehensive TF data set for any adult stem/progenitor cell type to date.\n[2] Genome-wide computational analysis of complex binding patterns, followed by functional validation, revealed the following: first, a previously unrecognized combinatorial interaction between a heptad of TFs (SCL, LYL1, LMO2, GATA2, RUNX1, ERG, and FLI-1).\n[3] Second, we implicate direct protein-protein interactions between four key regulators (RUNX1, GATA2, SCL, and ERG) in stabilizing complex binding to DNA.\n[4] Third, Runx1(+/-)::Gata2(+/-) compound heterozygous mice are not viable with severe hematopoietic defects at midgestation.\n[5] Taken together, this study demonstrates the power of genome-wide analysis in generating novel functional insights into the transcriptional control of stem and progenitor cells."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1161, "doc_id": 13048272, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [13048272], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The DdrB protein from Deinococcus radiodurans functions as a pentamer.\n\nDocument title: The structure of DdrB from Deinococcus: a new fold for single-stranded DNA binding proteins\n\nAbstract sentences:\n[0] Deinococcus spp. are renowned for their amazing ability to recover rapidly from severe genomic fragmentation as a result of exposure to extreme levels of ionizing radiation or desiccation.\n[1] Despite having been originally characterized over 50 years ago, the mechanism underlying this remarkable repair process is still poorly understood.\n[2] Here, we report the 2.8 A structure of DdrB, a single-stranded DNA (ssDNA) binding protein unique to Deinococcus spp.\n[3] that is crucial for recovery following DNA damage.\n[4] DdrB forms a pentameric ring capable of binding single-stranded but not double-stranded DNA.\n[5] Unexpectedly, the crystal structure reveals that DdrB comprises a novel fold that is structurally and topologically distinct from all other single-stranded binding (SSB) proteins characterized to date.\n[6] The need for a unique ssDNA binding function in response to severe damage, suggests a distinct role for DdrB which may encompass not only standard SSB protein function in protection of ssDNA, but also more specialized roles in protein recruitment or DNA architecture maintenance.\n[7] Possible mechanisms of DdrB action in damage recovery are discussed."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"DdrB forms a pentameric ring capable of binding single-stranded but not double-stranded DNA.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1162, "doc_id": 15305881, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [15305881], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The G34R/V mutation creates a hypomethylated phenotype at the H3K36 histone.\n\nDocument title: ZMYND11 links histone H3.3K36me3 to transcription elongation and tumour suppression\n\nAbstract sentences:\n[0] Recognition of modified histones by ‘reader’ proteins plays a critical role in the regulation of chromatin.\n[1] H3K36 trimethylation (H3K36me3) is deposited onto the nucleosomes in the transcribed regions after RNA polymerase II elongation.\n[2] In yeast, this mark in turn recruits epigenetic regulators to reset the chromatin to a relatively repressive state, thus suppressing cryptic transcription.\n[3] However, much less is known about the role of H3K36me3 in transcription regulation in mammals.\n[4] This is further complicated by the transcription-coupled incorporation of the histone variant H3.3 in gene bodies.\n[5] Here we show that the candidate tumour suppressor ZMYND11 specifically recognizes H3K36me3 on H3.3 (H3.3K36me3) and regulates RNA polymerase II elongation.\n[6] Structural studies show that in addition to the trimethyl-lysine binding by an aromatic cage within the PWWP domain, the H3.3-dependent recognition is mediated by the encapsulation of the H3.3-specific ‘Ser 31’ residue in a composite pocket formed by the tandem bromo–PWWP domains of ZMYND11.\n[7] Chromatin immunoprecipitation followed by sequencing shows a genome-wide co-localization of ZMYND11 with H3K36me3 and H3.3 in gene bodies, and its occupancy requires the pre-deposition of H3.3K36me3.\n[8] Although ZMYND11 is associated with highly expressed genes, it functions as an unconventional transcription co-repressor by modulating RNA polymerase II at the elongation stage.\n[9] ZMYND11 is critical for the repression of a transcriptional program that is essential for tumour cell growth; low expression levels of ZMYND11 in breast cancer patients correlate with worse prognosis.\n[10] Consistently, overexpression of ZMYND11 suppresses cancer cell growth in vitro and tumour formation in mice.\n[11] Together, this study identifies ZMYND11 as an H3.3-specific reader of H3K36me3 that links the histone-variant-mediated transcription elongation control to tumour suppression."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1164, "doc_id": 4455466, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4455466], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The G34R/V mutation does not create a hypomethylated phenotype at the H3K36 histone.\n\nDocument title: ZMYND11 links histone H3.3K36me3 to transcription elongation and tumour suppression\n\nAbstract sentences:\n[0] Recognition of modified histones by ‘reader’ proteins plays a critical role in the regulation of chromatin.\n[1] H3K36 trimethylation (H3K36me3) is deposited onto the nucleosomes in the transcribed regions after RNA polymerase II elongation.\n[2] In yeast, this mark in turn recruits epigenetic regulators to reset the chromatin to a relatively repressive state, thus suppressing cryptic transcription.\n[3] However, much less is known about the role of H3K36me3 in transcription regulation in mammals.\n[4] This is further complicated by the transcription-coupled incorporation of the histone variant H3.3 in gene bodies.\n[5] Here we show that the candidate tumour suppressor ZMYND11 specifically recognizes H3K36me3 on H3.3 (H3.3K36me3) and regulates RNA polymerase II elongation.\n[6] Structural studies show that in addition to the trimethyl-lysine binding by an aromatic cage within the PWWP domain, the H3.3-dependent recognition is mediated by the encapsulation of the H3.3-specific ‘Ser 31’ residue in a composite pocket formed by the tandem bromo–PWWP domains of ZMYND11.\n[7] Chromatin immunoprecipitation followed by sequencing shows a genome-wide co-localization of ZMYND11 with H3K36me3 and H3.3 in gene bodies, and its occupancy requires the pre-deposition of H3.3K36me3.\n[8] Although ZMYND11 is associated with highly expressed genes, it functions as an unconventional transcription co-repressor by modulating RNA polymerase II at the elongation stage.\n[9] ZMYND11 is critical for the repression of a transcriptional program that is essential for tumour cell growth; low expression levels of ZMYND11 in breast cancer patients correlate with worse prognosis.\n[10] Consistently, overexpression of ZMYND11 suppresses cancer cell growth in vitro and tumour formation in mice.\n[11] Together, this study identifies ZMYND11 as an H3.3-specific reader of H3K36me3 that links the histone-variant-mediated transcription elongation control to tumour suppression."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1165, "doc_id": 4455466, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4455466], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The H2A-H2B eviction defect is compensated for by other histone chaperone(s).\n\nDocument title: FACT Disrupts Nucleosome Structure by Binding H2A-H2B with Conserved Peptide Motifs.\n\nAbstract sentences:\n[0] FACT, a heterodimer of Spt16 and Pob3, is an essential histone chaperone.\n[1] We show that the H2A-H2B binding activity that is central to FACT function resides in short acidic regions near the C termini of each subunit.\n[2] Mutations throughout these regions affect binding and cause correlated phenotypes that range from mild to lethal, with the largest individual contributions unexpectedly coming from an aromatic residue and a nearby carboxylate residue within each domain.\n[3] Spt16 and Pob3 bind overlapping sites on H2A-H2B, and Spt16-Pob3 heterodimers simultaneously bind two H2A-H2B dimers, the same stoichiometry as the components of a nucleosome.\n[4] An Spt16:H2A-H2B crystal structure explains the biochemical and genetic data, provides a model for Pob3 binding, and implies a mechanism for FACT reorganization that we confirm biochemically.\n[5] Moreover, unexpected similarity to binding of ANP32E and Swr1 with H2A.Z-H2B reveals that diverse H2A-H2B chaperones use common mechanisms of histone binding and regulating nucleosome functions."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1166, "doc_id": 9889151, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [9889151], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The HSV-2 infection is typically asymptomatic.\n\nDocument title: Persistence of HIV-1 Receptor-Positive Cells after HSV-2 Reactivation: A Potential Mechanism for Increased HIV-1 Acquisition\n\nAbstract sentences:\n[0] To explore the mechanism by which herpes simplex virus (HSV)-2 infection is related to HIV-1 acquisition, we conducted in situ analysis of the cellular infiltrate from sequential biopsies of HSV-2 lesions from patients on and off antiviral therapy.\n[1] CD4(+) and CD8(+) T cells and a mixed population of plasmacytoid and myeloid dendritic cells (DCs), including cells expressing the C-type lectin receptor DC-SIGN, persisted at sites of HSV-2 reactivation for months after healing, even with daily antiviral therapy.\n[2] The CD4(+) T cells that persisted reacted to HSV-2 antigen, were enriched for expression of the chemokine receptor CCR5, and were contiguous to DCs expressing the interleukin-3 receptor CD123 or DC-SIGN.\n[3] Ex vivo infection with a CCR5-tropic strain of HIV-1 revealed greater concentrations of integrated HIV-1 DNA in cells derived from healed genital lesion biopsies than in cells from control skin biopsies.\n[4] The persistence and enrichment of HIV receptor-positive inflammatory cells in the genitalia help explain the inability of anti-HSV-2 therapy to reduce HIV acquisition."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1168, "doc_id": 8563659, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [8563659], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The M2-phenotype in brown adipose tissue macrophages increases brown adipose tissue thermogenic activity.\n\nDocument title: Alternatively activated macrophages produce catecholamines to sustain adaptive thermogenesis\n\nAbstract sentences:\n[0] All homeotherms use thermogenesis to maintain their core body temperature, ensuring that cellular functions and physiological processes can continue in cold environments.\n[1] In the prevailing model of thermogenesis, when the hypothalamus senses cold temperatures it triggers sympathetic discharge, resulting in the release of noradrenaline in brown adipose tissue and white adipose tissue.\n[2] Acting via the β(3)-adrenergic receptors, noradrenaline induces lipolysis in white adipocytes, whereas it stimulates the expression of thermogenic genes, such as PPAR-γ coactivator 1a (Ppargc1a), uncoupling protein 1 (Ucp1) and acyl-CoA synthetase long-chain family member 1 (Acsl1), in brown adipocytes.\n[3] However, the precise nature of all the cell types involved in this efferent loop is not well established.\n[4] Here we report in mice an unexpected requirement for the interleukin-4 (IL-4)-stimulated program of alternative macrophage activation in adaptive thermogenesis.\n[5] Exposure to cold temperature rapidly promoted alternative activation of adipose tissue macrophages, which secrete catecholamines to induce thermogenic gene expression in brown adipose tissue and lipolysis in white adipose tissue.\n[6] Absence of alternatively activated macrophages impaired metabolic adaptations to cold, whereas administration of IL-4 increased thermogenic gene expression, fatty acid mobilization and energy expenditure, all in a macrophage-dependent manner.\n[7] Thus, we have discovered a role for alternatively activated macrophages in the orchestration of an important mammalian stress response, the response to cold."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Exposure to cold temperature rapidly promoted alternative activation of adipose tissue macrophages, which secrete catecholamines to induce thermogenic gene expression in brown adipose tissue and lipolysis in white adipose tissue.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1169, "doc_id": 4319174, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [4319174], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The M2-phenotype in brown adipose tissue macrophages increases brown adipose tissue thermogenic activity.\n\nDocument title: Alternatively activated macrophages produce catecholamines to sustain adaptive thermogenesis\n\nAbstract sentences:\n[0] All homeotherms use thermogenesis to maintain their core body temperature, ensuring that cellular functions and physiological processes can continue in cold environments.\n[1] In the prevailing model of thermogenesis, when the hypothalamus senses cold temperatures it triggers sympathetic discharge, resulting in the release of noradrenaline in brown adipose tissue and white adipose tissue.\n[2] Acting via the β(3)-adrenergic receptors, noradrenaline induces lipolysis in white adipocytes, whereas it stimulates the expression of thermogenic genes, such as PPAR-γ coactivator 1a (Ppargc1a), uncoupling protein 1 (Ucp1) and acyl-CoA synthetase long-chain family member 1 (Acsl1), in brown adipocytes.\n[3] However, the precise nature of all the cell types involved in this efferent loop is not well established.\n[4] Here we report in mice an unexpected requirement for the interleukin-4 (IL-4)-stimulated program of alternative macrophage activation in adaptive thermogenesis.\n[5] Exposure to cold temperature rapidly promoted alternative activation of adipose tissue macrophages, which secrete catecholamines to induce thermogenic gene expression in brown adipose tissue and lipolysis in white adipose tissue.\n[6] Absence of alternatively activated macrophages impaired metabolic adaptations to cold, whereas administration of IL-4 increased thermogenic gene expression, fatty acid mobilization and energy expenditure, all in a macrophage-dependent manner.\n[7] Thus, we have discovered a role for alternatively activated macrophages in the orchestration of an important mammalian stress response, the response to cold."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Absence of alternatively activated macrophages impaired metabolic adaptations to cold, whereas administration of IL-4 increased thermogenic gene expression, fatty acid mobilization and energy expenditure, all in a macrophage-dependent manner.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1169, "doc_id": 4319174, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [4319174], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The NF-κB essential modulator gene induces intestinal inflammation by promoting receptor-interacting protein (RIP) kinase 1 kinase activity-mediated epithelial cell death.\n\nDocument title: NEMO Prevents RIP Kinase 1-Mediated Epithelial Cell Death and Chronic Intestinal Inflammation by NF-κB-Dependent and -Independent Functions\n\nAbstract sentences:\n[0] Intestinal epithelial cells (IECs) regulate gut immune homeostasis, and impaired epithelial responses are implicated in the pathogenesis of inflammatory bowel diseases (IBD).\n[1] IEC-specific ablation of nuclear factor κB (NF-κB) essential modulator (NEMO) caused Paneth cell apoptosis and impaired antimicrobial factor expression in the ileum, as well as colonocyte apoptosis and microbiota-driven chronic inflammation in the colon.\n[2] Combined RelA, c-Rel, and RelB deficiency in IECs caused Paneth cell apoptosis but not colitis, suggesting that NEMO prevents colon inflammation by NF-κB-independent functions.\n[3] Inhibition of receptor-interacting protein kinase 1 (RIPK1) kinase activity or combined deficiency of Fas-associated via death domain protein (FADD) and RIPK3 prevented epithelial cell death, Paneth cell loss, and colitis development in mice with epithelial NEMO deficiency.\n[4] Therefore, NEMO prevents intestinal inflammation by inhibiting RIPK1 kinase activity-mediated IEC death, suggesting that RIPK1 inhibitors could be effective in the treatment of colitis in patients with NEMO mutations and possibly in IBD."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Inhibition of receptor-interacting protein kinase 1 (RIPK1) kinase activity or combined deficiency of Fas-associated via death domain protein (FADD) and RIPK3 prevented epithelial cell death, Paneth cell loss, and colitis development in mice with epithelial NEMO deficiency.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1170, "doc_id": 18956141, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [18956141], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The NF-κB essential modulator gene induces intestinal inflammation by promoting receptor-interacting protein (RIP) kinase 1 kinase activity-mediated epithelial cell death.\n\nDocument title: NEMO Prevents RIP Kinase 1-Mediated Epithelial Cell Death and Chronic Intestinal Inflammation by NF-κB-Dependent and -Independent Functions\n\nAbstract sentences:\n[0] Intestinal epithelial cells (IECs) regulate gut immune homeostasis, and impaired epithelial responses are implicated in the pathogenesis of inflammatory bowel diseases (IBD).\n[1] IEC-specific ablation of nuclear factor κB (NF-κB) essential modulator (NEMO) caused Paneth cell apoptosis and impaired antimicrobial factor expression in the ileum, as well as colonocyte apoptosis and microbiota-driven chronic inflammation in the colon.\n[2] Combined RelA, c-Rel, and RelB deficiency in IECs caused Paneth cell apoptosis but not colitis, suggesting that NEMO prevents colon inflammation by NF-κB-independent functions.\n[3] Inhibition of receptor-interacting protein kinase 1 (RIPK1) kinase activity or combined deficiency of Fas-associated via death domain protein (FADD) and RIPK3 prevented epithelial cell death, Paneth cell loss, and colitis development in mice with epithelial NEMO deficiency.\n[4] Therefore, NEMO prevents intestinal inflammation by inhibiting RIPK1 kinase activity-mediated IEC death, suggesting that RIPK1 inhibitors could be effective in the treatment of colitis in patients with NEMO mutations and possibly in IBD."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Therefore, NEMO prevents intestinal inflammation by inhibiting RIPK1 kinase activity-mediated IEC death, suggesting that RIPK1 inhibitors could be effective in the treatment of colitis in patients with NEMO mutations and possibly in IBD.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1170, "doc_id": 18956141, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [18956141], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The NF-κB essential modulator gene prevents intestinal inflammation by inhibiting receptor-interacting protein (RIP) kinase 1 kinase activity-mediated epithelial cell death.\n\nDocument title: NEMO Prevents RIP Kinase 1-Mediated Epithelial Cell Death and Chronic Intestinal Inflammation by NF-κB-Dependent and -Independent Functions\n\nAbstract sentences:\n[0] Intestinal epithelial cells (IECs) regulate gut immune homeostasis, and impaired epithelial responses are implicated in the pathogenesis of inflammatory bowel diseases (IBD).\n[1] IEC-specific ablation of nuclear factor κB (NF-κB) essential modulator (NEMO) caused Paneth cell apoptosis and impaired antimicrobial factor expression in the ileum, as well as colonocyte apoptosis and microbiota-driven chronic inflammation in the colon.\n[2] Combined RelA, c-Rel, and RelB deficiency in IECs caused Paneth cell apoptosis but not colitis, suggesting that NEMO prevents colon inflammation by NF-κB-independent functions.\n[3] Inhibition of receptor-interacting protein kinase 1 (RIPK1) kinase activity or combined deficiency of Fas-associated via death domain protein (FADD) and RIPK3 prevented epithelial cell death, Paneth cell loss, and colitis development in mice with epithelial NEMO deficiency.\n[4] Therefore, NEMO prevents intestinal inflammation by inhibiting RIPK1 kinase activity-mediated IEC death, suggesting that RIPK1 inhibitors could be effective in the treatment of colitis in patients with NEMO mutations and possibly in IBD."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Inhibition of receptor-interacting protein kinase 1 (RIPK1) kinase activity or combined deficiency of Fas-associated via death domain protein (FADD) and RIPK3 prevented epithelial cell death, Paneth cell loss, and colitis development in mice with epithelial NEMO deficiency.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1171, "doc_id": 18956141, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [18956141], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The NF-κB essential modulator gene prevents intestinal inflammation by inhibiting receptor-interacting protein (RIP) kinase 1 kinase activity-mediated epithelial cell death.\n\nDocument title: NEMO Prevents RIP Kinase 1-Mediated Epithelial Cell Death and Chronic Intestinal Inflammation by NF-κB-Dependent and -Independent Functions\n\nAbstract sentences:\n[0] Intestinal epithelial cells (IECs) regulate gut immune homeostasis, and impaired epithelial responses are implicated in the pathogenesis of inflammatory bowel diseases (IBD).\n[1] IEC-specific ablation of nuclear factor κB (NF-κB) essential modulator (NEMO) caused Paneth cell apoptosis and impaired antimicrobial factor expression in the ileum, as well as colonocyte apoptosis and microbiota-driven chronic inflammation in the colon.\n[2] Combined RelA, c-Rel, and RelB deficiency in IECs caused Paneth cell apoptosis but not colitis, suggesting that NEMO prevents colon inflammation by NF-κB-independent functions.\n[3] Inhibition of receptor-interacting protein kinase 1 (RIPK1) kinase activity or combined deficiency of Fas-associated via death domain protein (FADD) and RIPK3 prevented epithelial cell death, Paneth cell loss, and colitis development in mice with epithelial NEMO deficiency.\n[4] Therefore, NEMO prevents intestinal inflammation by inhibiting RIPK1 kinase activity-mediated IEC death, suggesting that RIPK1 inhibitors could be effective in the treatment of colitis in patients with NEMO mutations and possibly in IBD."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Therefore, NEMO prevents intestinal inflammation by inhibiting RIPK1 kinase activity-mediated IEC death, suggesting that RIPK1 inhibitors could be effective in the treatment of colitis in patients with NEMO mutations and possibly in IBD.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1171, "doc_id": 18956141, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [18956141], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The PDPN gene deactivates the C-type lectin receptor (CLEC-2).\n\nDocument title: Podoplanin-Rich Stromal Networks Induce Dendritic Cell Motility via Activation of the C-type Lectin Receptor CLEC-2\n\nAbstract sentences:\n[0] To initiate adaptive immunity, dendritic cells (DCs) move from parenchymal tissues to lymphoid organs by migrating along stromal scaffolds that display the glycoprotein podoplanin (PDPN).\n[1] PDPN is expressed by lymphatic endothelial and fibroblastic reticular cells and promotes blood-lymph separation during development by activating the C-type lectin receptor, CLEC-2, on platelets.\n[2] Here, we describe a role for CLEC-2 in the morphodynamic behavior and motility of DCs.\n[3] CLEC-2 deficiency in DCs impaired their entry into lymphatics and trafficking to and within lymph nodes, thereby reducing T cell priming.\n[4] CLEC-2 engagement of PDPN was necessary for DCs to spread and migrate along stromal surfaces and sufficient to induce membrane protrusions.\n[5] CLEC-2 activation triggered cell spreading via downregulation of RhoA activity and myosin light-chain phosphorylation and triggered F-actin-rich protrusions via Vav signaling and Rac1 activation.\n[6] Thus, activation of CLEC-2 by PDPN rearranges the actin cytoskeleton in DCs to promote efficient motility along stromal surfaces."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"PDPN is expressed by lymphatic endothelial and fibroblastic reticular cells and promotes blood-lymph separation during development by activating the C-type lectin receptor, CLEC-2, on platelets.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1173, "doc_id": 7370282, "label": "CONTRADICTS", "evidence_sentence_ids": [1], "cited_doc_ids": [7370282], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The PDPN gene deactivates the C-type lectin receptor (CLEC-2).\n\nDocument title: Podoplanin-Rich Stromal Networks Induce Dendritic Cell Motility via Activation of the C-type Lectin Receptor CLEC-2\n\nAbstract sentences:\n[0] To initiate adaptive immunity, dendritic cells (DCs) move from parenchymal tissues to lymphoid organs by migrating along stromal scaffolds that display the glycoprotein podoplanin (PDPN).\n[1] PDPN is expressed by lymphatic endothelial and fibroblastic reticular cells and promotes blood-lymph separation during development by activating the C-type lectin receptor, CLEC-2, on platelets.\n[2] Here, we describe a role for CLEC-2 in the morphodynamic behavior and motility of DCs.\n[3] CLEC-2 deficiency in DCs impaired their entry into lymphatics and trafficking to and within lymph nodes, thereby reducing T cell priming.\n[4] CLEC-2 engagement of PDPN was necessary for DCs to spread and migrate along stromal surfaces and sufficient to induce membrane protrusions.\n[5] CLEC-2 activation triggered cell spreading via downregulation of RhoA activity and myosin light-chain phosphorylation and triggered F-actin-rich protrusions via Vav signaling and Rac1 activation.\n[6] Thus, activation of CLEC-2 by PDPN rearranges the actin cytoskeleton in DCs to promote efficient motility along stromal surfaces."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Thus, activation of CLEC-2 by PDPN rearranges the actin cytoskeleton in DCs to promote efficient motility along stromal surfaces.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1173, "doc_id": 7370282, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [7370282], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The PPR MDA5 has twenty N-terminal CARD domains.\n\nDocument title: Immune signaling by RIG-I-like receptors.\n\nAbstract sentences:\n[0] The RIG-I-like receptors (RLRs) RIG-I, MDA5, and LGP2 play a major role in pathogen sensing of RNA virus infection to initiate and modulate antiviral immunity.\n[1] The RLRs detect viral RNA ligands or processed self RNA in the cytoplasm to trigger innate immunity and inflammation and to impart gene expression that serves to control infection.\n[2] Importantly, RLRs cooperate in signaling crosstalk networks with Toll-like receptors and other factors to impart innate immunity and to modulate the adaptive immune response.\n[3] RLR regulation occurs at a variety of levels ranging from autoregulation to ligand and cofactor interactions and posttranslational modifications.\n[4] Abberant RLR signaling or dysregulation of RLR expression is now implicated in the development of autoimmune diseases.\n[5] Understanding the processes of RLR signaling and response will provide insights to guide RLR-targeted therapeutics for antiviral and immune-modifying applications."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1174, "doc_id": 31272411, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [31272411], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The PRDM1 gene is a key determinant of primordial germ cells.\n\nDocument title: The Germ Cell Determinant Blimp1 Is Not Required for Derivation of Pluripotent Stem Cells\n\nAbstract sentences:\n[0] Blimp1 (Prdm1), the key determinant of primordial germ cells (PGCs), plays a combinatorial role with Prdm14 during PGC specification from postimplantation epiblast cells.\n[1] They together initiate epigenetic reprogramming in early germ cells toward an underlying pluripotent state, which is equivalent to embryonic stem cells (ESCs).\n[2] Whereas Prdm14 alone can promote reprogramming and is important for the propagation of the pluripotent state, it is not known whether Blimp1 is similarly involved.\n[3] By using a genetic approach, we demonstrate that Blimp1 is dispensable for the derivation and maintenance of ESCs and postimplantation epiblast stem cells (epiSCs).\n[4] Notably, Blimp1 is also dispensable for reprogramming epiSCs to ESCs.\n[5] Thus, although Blimp1 is obligatory for PGC specification, it is not required for the reversion of epiSCs to ESCs and for their maintenance thereafter.\n[6] This study suggests that reprogramming, including that of somatic cells to ESCs, may not entail an obligatory route through a Blimp1-positive PGC-like state."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Blimp1 (Prdm1), the key determinant of primordial germ cells (PGCs), plays a combinatorial role with Prdm14 during PGC specification from postimplantation epiblast cells.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1176, "doc_id": 13910150, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [13910150], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The PRDM1 gene, when combined with the PRDM14 gene, plays an important role during primordial germ cell specification.\n\nDocument title: The Germ Cell Determinant Blimp1 Is Not Required for Derivation of Pluripotent Stem Cells\n\nAbstract sentences:\n[0] Blimp1 (Prdm1), the key determinant of primordial germ cells (PGCs), plays a combinatorial role with Prdm14 during PGC specification from postimplantation epiblast cells.\n[1] They together initiate epigenetic reprogramming in early germ cells toward an underlying pluripotent state, which is equivalent to embryonic stem cells (ESCs).\n[2] Whereas Prdm14 alone can promote reprogramming and is important for the propagation of the pluripotent state, it is not known whether Blimp1 is similarly involved.\n[3] By using a genetic approach, we demonstrate that Blimp1 is dispensable for the derivation and maintenance of ESCs and postimplantation epiblast stem cells (epiSCs).\n[4] Notably, Blimp1 is also dispensable for reprogramming epiSCs to ESCs.\n[5] Thus, although Blimp1 is obligatory for PGC specification, it is not required for the reversion of epiSCs to ESCs and for their maintenance thereafter.\n[6] This study suggests that reprogramming, including that of somatic cells to ESCs, may not entail an obligatory route through a Blimp1-positive PGC-like state."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Blimp1 (Prdm1), the key determinant of primordial germ cells (PGCs), plays a combinatorial role with Prdm14 during PGC specification from postimplantation epiblast cells.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1177, "doc_id": 13910150, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [13910150], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The PRR MDA5 has a C-terminal domain.\n\nDocument title: Immune signaling by RIG-I-like receptors.\n\nAbstract sentences:\n[0] The RIG-I-like receptors (RLRs) RIG-I, MDA5, and LGP2 play a major role in pathogen sensing of RNA virus infection to initiate and modulate antiviral immunity.\n[1] The RLRs detect viral RNA ligands or processed self RNA in the cytoplasm to trigger innate immunity and inflammation and to impart gene expression that serves to control infection.\n[2] Importantly, RLRs cooperate in signaling crosstalk networks with Toll-like receptors and other factors to impart innate immunity and to modulate the adaptive immune response.\n[3] RLR regulation occurs at a variety of levels ranging from autoregulation to ligand and cofactor interactions and posttranslational modifications.\n[4] Abberant RLR signaling or dysregulation of RLR expression is now implicated in the development of autoimmune diseases.\n[5] Understanding the processes of RLR signaling and response will provide insights to guide RLR-targeted therapeutics for antiviral and immune-modifying applications."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1178, "doc_id": 31272411, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [31272411], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The RANK-RANK-Ligand (RANKL) pathway is involved in the development of Aire-expressing medullary thymic epithelial cells (mTECs).\n\nDocument title: Rank Signaling Links the Development of Invariant γδ T Cell Progenitors and Aire+ Medullary Epithelium\n\nAbstract sentences:\n[0] The thymic medulla provides a specialized microenvironment for the negative selection of T cells, with the presence of autoimmune regulator (Aire)-expressing medullary thymic epithelial cells (mTECs) during the embryonic-neonatal period being both necessary and sufficient to establish long-lasting tolerance.\n[1] Here we showed that emergence of the first cohorts of Aire(+) mTECs at this key developmental stage, prior to αβ T cell repertoire selection, was jointly directed by Rankl(+) lymphoid tissue inducer cells and invariant Vγ5(+) dendritic epidermal T cell (DETC) progenitors that are the first thymocytes to express the products of gene rearrangement.\n[2] In turn, generation of Aire(+) mTECs then fostered Skint-1-dependent, but Aire-independent, DETC progenitor maturation and the emergence of an invariant DETC repertoire.\n[3] Hence, our data attributed a functional importance to the temporal development of Vγ5(+) γδ T cells during thymus medulla formation for αβ T cell tolerance induction and demonstrated a Rank-mediated reciprocal link between DETC and Aire(+) mTEC maturation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Here we showed that emergence of the first cohorts of Aire(+) mTECs at this key developmental stage, prior to αβ T cell repertoire selection, was jointly directed by Rankl(+) lymphoid tissue inducer cells and invariant Vγ5(+) dendritic epidermal T cell (DETC) progenitors that are the first thymocytes to express the products of gene rearrangement.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1181, "doc_id": 301838, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [301838, 2734421, 39128592, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The RANK-RANK-Ligand (RANKL) pathway is involved in the development of Aire-expressing medullary thymic epithelial cells (mTECs).\n\nDocument title: Rank Signaling Links the Development of Invariant γδ T Cell Progenitors and Aire+ Medullary Epithelium\n\nAbstract sentences:\n[0] The thymic medulla provides a specialized microenvironment for the negative selection of T cells, with the presence of autoimmune regulator (Aire)-expressing medullary thymic epithelial cells (mTECs) during the embryonic-neonatal period being both necessary and sufficient to establish long-lasting tolerance.\n[1] Here we showed that emergence of the first cohorts of Aire(+) mTECs at this key developmental stage, prior to αβ T cell repertoire selection, was jointly directed by Rankl(+) lymphoid tissue inducer cells and invariant Vγ5(+) dendritic epidermal T cell (DETC) progenitors that are the first thymocytes to express the products of gene rearrangement.\n[2] In turn, generation of Aire(+) mTECs then fostered Skint-1-dependent, but Aire-independent, DETC progenitor maturation and the emergence of an invariant DETC repertoire.\n[3] Hence, our data attributed a functional importance to the temporal development of Vγ5(+) γδ T cells during thymus medulla formation for αβ T cell tolerance induction and demonstrated a Rank-mediated reciprocal link between DETC and Aire(+) mTEC maturation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Hence, our data attributed a functional importance to the temporal development of Vγ5(+) γδ T cells during thymus medulla formation for αβ T cell tolerance induction and demonstrated a Rank-mediated reciprocal link between DETC and Aire(+) mTEC maturation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1181, "doc_id": 301838, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [301838, 2734421, 39128592, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The RANK-RANK-Ligand (RANKL) pathway is involved in the development of Aire-expressing medullary thymic epithelial cells (mTECs).\n\nDocument title: The tumor necrosis factor family receptors RANK and CD40 cooperatively establish the thymic medullary microenvironment and self-tolerance.\n\nAbstract sentences:\n[0] Medullary thymic epithelial cells (mTECs) establish T cell self-tolerance through the expression of autoimmune regulator (Aire) and peripheral tissue-specific self-antigens.\n[1] However, signals underlying mTEC development remain largely unclear.\n[2] Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals.\n[3] Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment.\n[4] Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner.\n[5] These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1181, "doc_id": 2734421, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [301838, 2734421, 39128592, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The RANK-RANK-Ligand (RANKL) pathway is involved in the development of Aire-expressing medullary thymic epithelial cells (mTECs).\n\nDocument title: The tumor necrosis factor family receptors RANK and CD40 cooperatively establish the thymic medullary microenvironment and self-tolerance.\n\nAbstract sentences:\n[0] Medullary thymic epithelial cells (mTECs) establish T cell self-tolerance through the expression of autoimmune regulator (Aire) and peripheral tissue-specific self-antigens.\n[1] However, signals underlying mTEC development remain largely unclear.\n[2] Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals.\n[3] Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment.\n[4] Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner.\n[5] These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1181, "doc_id": 2734421, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [301838, 2734421, 39128592, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The RANK-RANK-Ligand (RANKL) pathway is involved in the development of Aire-expressing medullary thymic epithelial cells (mTECs).\n\nDocument title: The tumor necrosis factor family receptors RANK and CD40 cooperatively establish the thymic medullary microenvironment and self-tolerance.\n\nAbstract sentences:\n[0] Medullary thymic epithelial cells (mTECs) establish T cell self-tolerance through the expression of autoimmune regulator (Aire) and peripheral tissue-specific self-antigens.\n[1] However, signals underlying mTEC development remain largely unclear.\n[2] Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals.\n[3] Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment.\n[4] Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner.\n[5] These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1181, "doc_id": 2734421, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [301838, 2734421, 39128592, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The RANK-RANK-Ligand (RANKL) pathway is involved in the development of Aire-expressing medullary thymic epithelial cells (mTECs).\n\nDocument title: The tumor necrosis factor family receptors RANK and CD40 cooperatively establish the thymic medullary microenvironment and self-tolerance.\n\nAbstract sentences:\n[0] Medullary thymic epithelial cells (mTECs) establish T cell self-tolerance through the expression of autoimmune regulator (Aire) and peripheral tissue-specific self-antigens.\n[1] However, signals underlying mTEC development remain largely unclear.\n[2] Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals.\n[3] Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment.\n[4] Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner.\n[5] These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1181, "doc_id": 2734421, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [301838, 2734421, 39128592, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The RANK-RANK-Ligand (RANKL) pathway is involved in the development of Aire-expressing medullary thymic epithelial cells (mTECs).\n\nDocument title: The cytokine RANKL produced by positively selected thymocytes fosters medullary thymic epithelial cells that express autoimmune regulator.\n\nAbstract sentences:\n[0] The thymic medulla provides a microenvironment where medullary thymic epithelial cells (mTECs) express autoimmune regulator and diverse tissue-restricted genes, contributing to launching self-tolerance.\n[1] Positive selection is essential for thymic medulla formation via a previously unknown mechanism.\n[2] Here we show that the cytokine RANK ligand (RANKL) was produced by positively selected thymocytes and regulated the cellularity of mTEC by interacting with RANK and osteoprotegerin.\n[3] Forced expression of RANKL restored thymic medulla in mice lacking positive selection, whereas RANKL perturbation impaired medulla formation.\n[4] These results indicate that RANKL produced by positively selected thymocytes is responsible for fostering thymic medulla formation, thereby establishing central tolerance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here we show that the cytokine RANK ligand (RANKL) was produced by positively selected thymocytes and regulated the cellularity of mTEC by interacting with RANK and osteoprotegerin.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1181, "doc_id": 39128592, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [301838, 2734421, 39128592, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The RANK-RANK-Ligand (RANKL) pathway is involved in the development of Aire-expressing medullary thymic epithelial cells (mTECs).\n\nDocument title: RANK signals from CD4+3− inducer cells regulate development of Aire-expressing epithelial cells in the thymic medulla\n\nAbstract sentences:\n[0] Aire-expressing medullary thymic epithelial cells (mTECs) play a key role in preventing autoimmunity by expressing tissue-restricted antigens to help purge the emerging T cell receptor repertoire of self-reactive specificities.\n[1] Here we demonstrate a novel role for a CD4+3− inducer cell population, previously linked to development of organized secondary lymphoid structures and maintenance of T cell memory in the functional regulation of Aire-mediated promiscuous gene expression in the thymus.\n[2] CD4+3− cells are closely associated with mTECs in adult thymus, and in fetal thymus their appearance is temporally linked with the appearance of Aire+ mTECs.\n[3] We show that RANKL signals from this cell promote the maturation of RANK-expressing CD80−Aire− mTEC progenitors into CD80+Aire+ mTECs, and that transplantation of RANK-deficient thymic stroma into immunodeficient hosts induces autoimmunity.\n[4] Collectively, our data reveal cellular and molecular mechanisms leading to the generation of Aire+ mTECs and highlight a previously unrecognized role for CD4+3−RANKL+ inducer cells in intrathymic self-tolerance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"We show that RANKL signals from this cell promote the maturation of RANK-expressing CD80−Aire− mTEC progenitors into CD80+Aire+ mTECs, and that transplantation of RANK-deficient thymic stroma into immunodeficient hosts induces autoimmunity.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1181, "doc_id": 3952288, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [301838, 2734421, 39128592, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The RANK-RANK-Ligand (RANKL) pathway is involved in the development of Aire-expressing medullary thymic epithelial cells (mTECs).\n\nDocument title: RANK signals from CD4+3− inducer cells regulate development of Aire-expressing epithelial cells in the thymic medulla\n\nAbstract sentences:\n[0] Aire-expressing medullary thymic epithelial cells (mTECs) play a key role in preventing autoimmunity by expressing tissue-restricted antigens to help purge the emerging T cell receptor repertoire of self-reactive specificities.\n[1] Here we demonstrate a novel role for a CD4+3− inducer cell population, previously linked to development of organized secondary lymphoid structures and maintenance of T cell memory in the functional regulation of Aire-mediated promiscuous gene expression in the thymus.\n[2] CD4+3− cells are closely associated with mTECs in adult thymus, and in fetal thymus their appearance is temporally linked with the appearance of Aire+ mTECs.\n[3] We show that RANKL signals from this cell promote the maturation of RANK-expressing CD80−Aire− mTEC progenitors into CD80+Aire+ mTECs, and that transplantation of RANK-deficient thymic stroma into immunodeficient hosts induces autoimmunity.\n[4] Collectively, our data reveal cellular and molecular mechanisms leading to the generation of Aire+ mTECs and highlight a previously unrecognized role for CD4+3−RANKL+ inducer cells in intrathymic self-tolerance."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Collectively, our data reveal cellular and molecular mechanisms leading to the generation of Aire+ mTECs and highlight a previously unrecognized role for CD4+3−RANKL+ inducer cells in intrathymic self-tolerance.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1181, "doc_id": 3952288, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [301838, 2734421, 39128592, 3952288], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The Snf1 complex regulates carbon and energy metabolism in baker's yeast (Saccharomyces cerevisiae).\n\nDocument title: Reconstruction of the yeast Snf1 kinase regulatory network reveals its role as a global energy regulator\n\nAbstract sentences:\n[0] Highly conserved among eukaryotic cells, the AMP-activated kinase (AMPK) is a central regulator of carbon metabolism.\n[1] To map the complete network of interactions around AMPK in yeast (Snf1) and to evaluate the role of its regulatory subunit Snf4, we measured global mRNA, protein and metabolite levels in wild type, Deltasnf1, Deltasnf4, and Deltasnf1Deltasnf4 knockout strains.\n[2] Using four newly developed computational tools, including novel DOGMA sub-network analysis, we showed the benefits of three-level ome-data integration to uncover the global Snf1 kinase role in yeast.\n[3] We for the first time identified Snf1's global regulation on gene and protein expression levels, and showed that yeast Snf1 has a far more extensive function in controlling energy metabolism than reported earlier.\n[4] Additionally, we identified complementary roles of Snf1 and Snf4.\n[5] Similar to the function of AMPK in humans, our findings showed that Snf1 is a low-energy checkpoint and that yeast can be used more extensively as a model system for studying the molecular mechanisms underlying the global regulation of AMPK in mammals, failure of which leads to metabolic diseases."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"We for the first time identified Snf1's global regulation on gene and protein expression levels, and showed that yeast Snf1 has a far more extensive function in controlling energy metabolism than reported earlier.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1182, "doc_id": 14541844, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [14541844], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The TRaF1/C5 rs10818488 allele polymorphism regulates the neighboring C5 gene.\n\nDocument title: A Candidate Gene Approach Identifies the TRAF1/C5 Region as a Risk Factor for Rheumatoid Arthritis\n\nAbstract sentences:\n[0] Correction for:    Kurreeman FAS, Padyukov L, Marques RB, Schrodi SJ, Seddighzadeh M, et al. (2007)\n[1] A Candidate Gene Approach Identifies the TRAF1/C5 Region as a Risk Factor for Rheumatoid Arthritis.\n[2] PLoS Med 4(9): e278.\n[3] doi:10.1371/journal.pmed.0040278    In Table 1, the allele ratio in column eight (Allele Ratiosb: Cases, Controls) refers to allele A: allele B and not allele1:allele2 as described in footnote b, with Allele A being the Susceptibility Allele as denoted in column seven.\n[4] The footnote should read:    bNumber of alleles were compared in cases versus controls: allele A: allele B cases, allele A: allele B controls.\n[5] Allele A refers to the susceptibility alleles as given in column seven."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1183, "doc_id": 1967017, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [1967017], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The US health care system can save up to $5 billion if 7% of patients waiting for kidney transplants participate in the optimized national kidney paired donation program.\n\nDocument title: Kidney paired donation and optimizing the use of live donor organs.\n\nAbstract sentences:\n[0] CONTEXT Blood type and crossmatch incompatibility will exclude at least one third of patients in need from receiving a live donor kidney transplant.\n[1] Kidney paired donation (KPD) offers incompatible donor/recipient pairs the opportunity to match for compatible transplants.\n[2] Despite its increasing popularity, very few transplants have resulted from KPD.\n[3] OBJECTIVE To determine the potential impact of improved matching schemes on the number and quality of transplants achievable with KPD.\n[4] DESIGN, SETTING, AND POPULATION We developed a model that simulates pools of incompatible donor/recipient pairs.\n[5] We designed a mathematically verifiable optimized matching algorithm and compared it with the scheme currently used in some centers and regions.\n[6] Simulated patients from the general community with characteristics drawn from distributions describing end-stage renal disease patients eligible for renal transplantation and their willing and eligible live donors.\n[7] MAIN OUTCOME MEASURES Number of kidneys matched, HLA mismatch of matched kidneys, and number of grafts surviving 5 years after transplantation.\n[8] RESULTS A national optimized matching algorithm would result in more transplants (47.7% vs 42.0%, P<.001), better HLA concordance (3.0 vs 4.5 mismatched antigens; P<.001), more grafts surviving at 5 years (34.9% vs 28.7%; P<.001), and a reduction in the number of pairs required to travel (2.9% vs 18.4%; P<.001) when compared with an extension of the currently used first-accept scheme to a national level.\n[9] Furthermore, highly sensitized patients would benefit 6-fold from a national optimized scheme (2.3% vs 14.1% successfully matched; P<.001).\n[10] Even if only 7% of patients awaiting kidney transplantation participated in an optimized national KPD program, the health care system could save as much as $750 million.\n[11] CONCLUSIONS The combination of a national KPD program and a mathematically optimized matching algorithm yields more matches with lower HLA disparity.\n[12] Optimized matching affords patients the flexibility of customizing their matching priorities and the security of knowing that the greatest number of high-quality matches will be found and distributed equitably."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Even if only 7% of patients awaiting kidney transplantation participated in an optimized national KPD program, the health care system could save as much as $750 million.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1184, "doc_id": 16737210, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [16737210], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The World Health Organization's (WHO) data collection process is biased downward by unequal selection of larger outbreaks.\n\nDocument title: Using Routine Surveillance Data to Estimate the Epidemic Potential of Emerging Zoonoses: Application to the Emergence of US Swine Origin Influenza A H3N2v Virus\n\nAbstract sentences:\n[0] BACKGROUND Prior to emergence in human populations, zoonoses such as SARS cause occasional infections in human populations exposed to reservoir species.\n[1] The risk of widespread epidemics in humans can be assessed by monitoring the reproduction number R (average number of persons infected by a human case).\n[2] However, until now, estimating R required detailed outbreak investigations of human clusters, for which resources and expertise are not always available.\n[3] Additionally, existing methods do not correct for important selection and under-ascertainment biases.\n[4] Here, we present simple estimation methods that overcome many of these limitations.\n[5] METHODS AND FINDINGS Our approach is based on a parsimonious mathematical model of disease transmission and only requires data collected through routine surveillance and standard case investigations.\n[6] We apply it to assess the transmissibility of swine-origin influenza A H3N2v-M virus in the US, Nipah virus in Malaysia and Bangladesh, and also present a non-zoonotic example (cholera in the Dominican Republic).\n[7] Estimation is based on two simple summary statistics, the proportion infected by the natural reservoir among detected cases (G) and among the subset of the first detected cases in each cluster (F).\n[8] If detection of a case does not affect detection of other cases from the same cluster, we find that R can be estimated by 1-G; otherwise R can be estimated by 1-F when the case detection rate is low.\n[9] In more general cases, bounds on R can still be derived.\n[10] CONCLUSIONS We have developed a simple approach with limited data requirements that enables robust assessment of the risks posed by emerging zoonoses.\n[11] We illustrate this by deriving transmissibility estimates for the H3N2v-M virus, an important step in evaluating the possible pandemic threat posed by this virus.\n[12] Please see later in the article for the Editors' Summary."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1186, "doc_id": 7485455, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [7485455], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The ability of activator E2Fs in preventing cell death is limited to terminally differentiated cells.\n\nDocument title: E2F1-3 Switch from Activators in Progenitor Cells to Repressors in Differentiating Cells\n\nAbstract sentences:\n[0] In the established model of mammalian cell cycle control, the retinoblastoma protein (Rb) functions to restrict cells from entering S phase by binding and sequestering E2f activators (E2f1, E2f2 and E2f3), which are invariably portrayed as the ultimate effectors of a transcriptional program that commit cells to enter and progress through S phase.\n[1] Using a panel of tissue-specific cre-transgenic mice and conditional E2f alleles we examined the effects of E2f1, E2f2 and E2f3 triple deficiency in murine embryonic stem cells, embryos and small intestines.\n[2] We show that in normal dividing progenitor cells E2f1-3 function as transcriptional activators, but contrary to the current view, are dispensable for cell division and instead are necessary for cell survival.\n[3] In differentiating cells E2f1-3 function in a complex with Rb as repressors to silence E2f targets and facilitate exit from the cell cycle.\n[4] The inactivation of Rb in differentiating cells resulted in a switch of E2f1-3 from repressors to activators, leading to the superactivation of E2f responsive targets and ectopic cell divisions.\n[5] Loss of E2f1-3 completely suppressed these phenotypes caused by Rb deficiency.\n[6] This work contextualizes the activator versus repressor functions of E2f1-3 in vivo, revealing distinct roles in dividing versus differentiating cells and in normal versus cancer-like cell cycles."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1188, "doc_id": 4394817, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4394817], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The amount of publicly available DNA data doubles every 10 months.\n\nDocument title: The EMBL nucleotide sequence database.\n\nAbstract sentences:\n[0] The EMBL Nucleotide Sequence Database (http://www.ebi.ac.uk/embl. html ) constitutes Europe's primary nucleotide sequence resource.\n[1] DNA and RNA sequences are directly submitted from researchers and genome sequencing groups and collected from the scientific literature and patent applications (Fig. 1).\n[2] In collaboration with DDBJ and GenBank the database is produced, maintained and distributed at the European Bioinformatics Institute.\n[3] Database releases are produced quarterly and are distributed on CD-ROM.\n[4] EBI's network services allow access to the most up-to-date data collection via Internet and World Wide Web interface, providing database searching and sequence similarity facilities plus access to a large number of additional databases."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1190, "doc_id": 30655442, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [30655442], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The appearance of brown-like or beige cells primarily occurs in visceral fat, not subcutaneous fat.\n\nDocument title: Tracking adipogenesis during white adipose tissue development, expansion and regeneration\n\nAbstract sentences:\n[0] White adipose tissue displays high plasticity.\n[1] We developed a system for the inducible, permanent labeling of mature adipocytes that we called the AdipoChaser mouse.\n[2] We monitored adipogenesis during development, high-fat diet (HFD) feeding and cold exposure.\n[3] During cold-induced 'browning' of subcutaneous fat, most 'beige' adipocytes stem from de novo–differentiated adipocytes.\n[4] During HFD feeding, epididymal fat initiates adipogenesis after 4 weeks, whereas subcutaneous fat undergoes hypertrophy for a period of up to 12 weeks.\n[5] Gonadal fat develops postnatally, whereas subcutaneous fat develops between embryonic days 14 and 18.\n[6] Our results highlight the extensive differences in adipogenic potential in various fat depots."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1193, "doc_id": 20532591, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [20532591], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The artifactual C-terminal helix swapping in the StART domain is observed in the Ups1-Mdm35 heterodimer of the StARkin superfamily.\n\nDocument title: Structural and mechanistic insights into phospholipid transfer by Ups1–Mdm35 in mitochondria\n\nAbstract sentences:\n[0] Eukaryotic cells are compartmentalized into membrane-bounded organelles whose functions rely on lipid trafficking to achieve membrane-specific compositions of lipids.\n[1] Here we focused on the Ups1-Mdm35 system, which mediates phosphatidic acid (PA) transfer between the outer and inner mitochondrial membranes, and determined the X-ray structures of Mdm35 and Ups1-Mdm35 with and without PA.\n[2] The Ups1-Mdm35 complex constitutes a single domain that has a deep pocket and flexible Ω-loop lid.\n[3] Structure-based mutational analyses revealed that a basic residue at the pocket bottom and the Ω-loop lid are important for PA extraction from the membrane following Ups1 binding.\n[4] Ups1 binding to the membrane is enhanced by the dissociation of Mdm35.\n[5] We also show that basic residues around the pocket entrance are important for Ups1 binding to the membrane and PA extraction.\n[6] These results provide a structural basis for understanding the mechanism of PA transfer between mitochondrial membranes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1195, "doc_id": 26283293, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [26283293], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The combination of physical examinations with C-reactive protein values do not improve the accuracy of radiographic verified pneumonia predictions.\n\nDocument title: Use of serum C reactive protein and procalcitonin concentrations in addition to symptoms and signs to predict pneumonia in patients presenting to primary care with acute cough: diagnostic study\n\nAbstract sentences:\n[0] OBJECTIVES To quantify the diagnostic accuracy of selected inflammatory markers in addition to symptoms and signs for predicting pneumonia and to derive a diagnostic tool.\n[1] DESIGN Diagnostic study performed between 2007 and 2010.\n[2] Participants had their history taken, underwent physical examination and measurement of C reactive protein (CRP) and procalcitonin in venous blood on the day they first consulted, and underwent chest radiography within seven days.\n[3] SETTING Primary care centres in 12 European countries.\n[4] PARTICIPANTS Adults presenting with acute cough.\n[5] MAIN OUTCOME MEASURES Pneumonia as determined by radiologists, who were blind to all other information when they judged chest radiographs.\n[6] RESULTS Of 3106 eligible patients, 286 were excluded because of missing or inadequate chest radiographs, leaving 2820 patients (mean age 50, 40% men) of whom 140 (5%) had pneumonia.\n[7] Re-assessment of a subset of 1675 chest radiographs showed agreement in 94% (κ 0.45, 95% confidence interval 0.36 to 0.54).\n[8] Six published \"symptoms and signs models\" varied in their discrimination (area under receiver operating characteristics curve (ROC) ranged from 0.55 (95% confidence interval 0.50 to 0.61) to 0.71 (0.66 to 0.76)).\n[9] The optimal combination of clinical prediction items derived from our patients included absence of runny nose and presence of breathlessness, crackles and diminished breath sounds on auscultation, tachycardia, and fever, with an ROC area of 0.70 (0.65 to 0.75).\n[10] Addition of CRP at the optimal cut off of >30 mg/L increased the ROC area to 0.77 (0.73 to 0.81) and improved the diagnostic classification (net reclassification improvement 28%).\n[11] In the 1556 patients classified according to symptoms, signs, and CRP >30 mg/L as \"low risk\" (<2.5%) for pneumonia, the prevalence of pneumonia was 2%.\n[12] In the 132 patients classified as \"high risk\" (>20%), the prevalence of pneumonia was 31%.\n[13] The positive likelihood ratio of low, intermediate, and high risk for pneumonia was 0.4, 1.2, and 8.6 respectively.\n[14] Measurement of procalcitonin added no relevant additional diagnostic information.\n[15] A simplified diagnostic score based on symptoms, signs, and CRP >30 mg/L resulted in proportions of pneumonia of 0.7%, 3.8%, and 18.2% in the low, intermediate, and high risk group respectively.\n[16] CONCLUSIONS A clinical rule based on symptoms and signs to predict pneumonia in patients presenting to primary care with acute cough performed best in patients with mild or severe clinical presentation.\n[17] Addition of CRP concentration at the optimal cut off of >30 mg/L improved diagnostic information, but measurement of procalcitonin concentration did not add clinically relevant information in this group."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Addition of CRP at the optimal cut off of >30 mg/L increased the ROC area to 0.77 (0.73 to 0.81) and improved the diagnostic classification (net reclassification improvement 28%).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1205, "doc_id": 5558754, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [5558754], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The combination of physical examinations with C-reactive protein values do not improve the accuracy of radiographic verified pneumonia predictions.\n\nDocument title: Use of serum C reactive protein and procalcitonin concentrations in addition to symptoms and signs to predict pneumonia in patients presenting to primary care with acute cough: diagnostic study\n\nAbstract sentences:\n[0] OBJECTIVES To quantify the diagnostic accuracy of selected inflammatory markers in addition to symptoms and signs for predicting pneumonia and to derive a diagnostic tool.\n[1] DESIGN Diagnostic study performed between 2007 and 2010.\n[2] Participants had their history taken, underwent physical examination and measurement of C reactive protein (CRP) and procalcitonin in venous blood on the day they first consulted, and underwent chest radiography within seven days.\n[3] SETTING Primary care centres in 12 European countries.\n[4] PARTICIPANTS Adults presenting with acute cough.\n[5] MAIN OUTCOME MEASURES Pneumonia as determined by radiologists, who were blind to all other information when they judged chest radiographs.\n[6] RESULTS Of 3106 eligible patients, 286 were excluded because of missing or inadequate chest radiographs, leaving 2820 patients (mean age 50, 40% men) of whom 140 (5%) had pneumonia.\n[7] Re-assessment of a subset of 1675 chest radiographs showed agreement in 94% (κ 0.45, 95% confidence interval 0.36 to 0.54).\n[8] Six published \"symptoms and signs models\" varied in their discrimination (area under receiver operating characteristics curve (ROC) ranged from 0.55 (95% confidence interval 0.50 to 0.61) to 0.71 (0.66 to 0.76)).\n[9] The optimal combination of clinical prediction items derived from our patients included absence of runny nose and presence of breathlessness, crackles and diminished breath sounds on auscultation, tachycardia, and fever, with an ROC area of 0.70 (0.65 to 0.75).\n[10] Addition of CRP at the optimal cut off of >30 mg/L increased the ROC area to 0.77 (0.73 to 0.81) and improved the diagnostic classification (net reclassification improvement 28%).\n[11] In the 1556 patients classified according to symptoms, signs, and CRP >30 mg/L as \"low risk\" (<2.5%) for pneumonia, the prevalence of pneumonia was 2%.\n[12] In the 132 patients classified as \"high risk\" (>20%), the prevalence of pneumonia was 31%.\n[13] The positive likelihood ratio of low, intermediate, and high risk for pneumonia was 0.4, 1.2, and 8.6 respectively.\n[14] Measurement of procalcitonin added no relevant additional diagnostic information.\n[15] A simplified diagnostic score based on symptoms, signs, and CRP >30 mg/L resulted in proportions of pneumonia of 0.7%, 3.8%, and 18.2% in the low, intermediate, and high risk group respectively.\n[16] CONCLUSIONS A clinical rule based on symptoms and signs to predict pneumonia in patients presenting to primary care with acute cough performed best in patients with mild or severe clinical presentation.\n[17] Addition of CRP concentration at the optimal cut off of >30 mg/L improved diagnostic information, but measurement of procalcitonin concentration did not add clinically relevant information in this group."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [17]\nExplanation: Evidence states: \"Addition of CRP concentration at the optimal cut off of >30 mg/L improved diagnostic information, but measurement of procalcitonin concentration did not add clinically relevant information in this group.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1205, "doc_id": 5558754, "label": "CONTRADICTS", "evidence_sentence_ids": [17], "cited_doc_ids": [5558754], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The composition of myosin-II isoform switches from the A isoform to the B isoform during hematopoietic differentiation.\n\nDocument title: Contractile forces sustain and polarize hematopoiesis from stem and progenitor cells.\n\nAbstract sentences:\n[0] Self-renewal and differentiation of stem cells depend on asymmetric division and polarized motility processes that in other cell types are modulated by nonmuscle myosin-II (MII) forces and matrix mechanics.\n[1] Here, mass spectrometry-calibrated intracellular flow cytometry of human hematopoiesis reveals MIIB to be a major isoform that is strongly polarized in hematopoietic stem cells and progenitors (HSC/Ps) and thereby downregulated in differentiated cells via asymmetric division.\n[2] MIIA is constitutive and activated by dephosphorylation during cytokine-triggered differentiation of cells grown on stiff, endosteum-like matrix, but not soft, marrow-like matrix.\n[3] In vivo, MIIB is required for generation of blood, while MIIA is required for sustained HSC/P engraftment.\n[4] Reversible inhibition of both isoforms in culture with blebbistatin enriches for long-term hematopoietic multilineage reconstituting cells by 5-fold or more as assessed in vivo.\n[5] Megakaryocytes also become more polyploid, producing 4-fold more platelets.\n[6] MII is thus a multifunctional node in polarized division and niche sensing."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1206, "doc_id": 18909530, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [18909530], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The cytokine receptor which regulates chemotaxis and formation of lymph nodes is involved in production of myeloperoxidase in the left atrium.\n\nDocument title: Myeloperoxidase acts as a profibrotic mediator of atrial fibrillation\n\nAbstract sentences:\n[0] Observational clinical and ex vivo studies have established a strong association between atrial fibrillation and inflammation.\n[1] However, whether inflammation is the cause or the consequence of atrial fibrillation and which specific inflammatory mediators may increase the atria's susceptibility to fibrillation remain elusive.\n[2] Here we provide experimental and clinical evidence for the mechanistic involvement of myeloperoxidase (MPO), a heme enzyme abundantly expressed by neutrophils, in the pathophysiology of atrial fibrillation.\n[3] MPO-deficient mice pretreated with angiotensin II (AngII) to provoke leukocyte activation showed lower atrial tissue abundance of the MPO product 3-chlorotyrosine, reduced activity of matrix metalloproteinases and blunted atrial fibrosis as compared to wild-type mice.\n[4] Upon right atrial electrophysiological stimulation, MPO-deficient mice were protected from atrial fibrillation, which was reversed when MPO was restored.\n[5] Humans with atrial fibrillation had higher plasma concentrations of MPO and a larger MPO burden in right atrial tissue as compared to individuals devoid of atrial fibrillation.\n[6] In the atria, MPO colocalized with markedly increased formation of 3-chlorotyrosine.\n[7] Our data demonstrate that MPO is a crucial prerequisite for structural remodeling of the myocardium, leading to an increased vulnerability to atrial fibrillation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1208, "doc_id": 10284593, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [10284593], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The deamination of cytidine to uridine on the minus strand of viral DNA can inactivate the viral genome by inducing G-to-A mutations.\n\nDocument title: Broad antiretroviral defence by human APOBEC3G through lethal editing of nascent reverse transcripts\n\nAbstract sentences:\n[0] Viral replication usually requires that innate intracellular lines of defence be overcome, a task usually accomplished by specialized viral gene products.\n[1] The virion infectivity factor (Vif) protein of human immunodeficiency virus (HIV) is required during the late stages of viral production to counter the antiviral activity of APOBEC3G (apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like 3G; also known as CEM15), a protein expressed notably in human T lymphocytes.\n[2] When produced in the presence of APOBEC3G, vif-defective virus is non-infectious.\n[3] APOBEC3G is closely related to APOBEC1, the central component of an RNA-editing complex that deaminates a cytosine residue in apoB messenger RNA.\n[4] APOBEC family members also have potent DNA mutator activity through dC deamination; however, whether the editing potential of APOBEC3G has any relevance to HIV inhibition is unknown.\n[5] Here, we demonstrate that it does, as APOBEC3G exerts its antiviral effect during reverse transcription to trigger G-to-A hypermutation in the nascent retroviral DNA.\n[6] We also find that APOBEC3G can act on a broad range of retroviruses in addition to HIV, suggesting that hypermutation by editing is a general innate defence mechanism against this important group of pathogens."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3, 5]\nExplanation: Evidence states: \"APOBEC3G is closely related to APOBEC1, the central component of an RNA-editing complex that deaminates a cytosine residue in apoB messenger RNA. Here, we demonstrate that it does, as APOBEC3G exerts its antiviral effect during reverse transcription to trigger G-to-A hypermutation in the nascent retroviral DNA.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1209, "doc_id": 4347374, "label": "SUPPORTS", "evidence_sentence_ids": [3, 5], "cited_doc_ids": [4347374], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The density of cytokine receptor bearing cells affects the distance over which cytokines act.\n\nDocument title: A Tunable Diffusion‐Consumption Mechanism of Cytokine Propagation Enables Plasticity in Cell‐to‐Cell Communication in the Immune System\n\nAbstract sentences:\n[0] &NA; Immune cells communicate by exchanging cytokines to achieve a context‐appropriate response, but the distances over which such communication happens are not known.\n[1] Here, we used theoretical considerations and experimental models of immune responses in vitro and in vivo to quantify the spatial extent of cytokine communications in dense tissues.\n[2] We established that competition between cytokine diffusion and consumption generated spatial niches of high cytokine concentrations with sharp boundaries.\n[3] The size of these self‐assembled niches scaled with the density of cytokine‐consuming cells, a parameter that gets tuned during immune responses.\n[4] In vivo, we measured interactions on length scales of 80–120 &mgr;m, which resulted in a high degree of cell‐to‐cell variance in cytokine exposure.\n[5] Such heterogeneous distributions of cytokines were a source of non‐genetic cell‐to‐cell variability that is often overlooked in single‐cell studies.\n[6] Our findings thus provide a basis for understanding variability in the patterning of immune responses by diffusible factors.\n[7] Graphical Abstract Figure.\n[8] No caption available.\n[9] HighlightsCytokine penetration in tissues is governed by a diffusion‐consumption mechanismSpherical cytokine niches are generated around cytokine‐producing cellsThe characteristic niche size depends on the density of cytokine consumersCytokine niches are a source of variability in otherwise identical cells &NA; Cytokine‐mediated communication allows immune cells to achieve a context‐appropriate response, but the distance over which this communication happens is unclear.\n[10] Oyler‐Yaniv et al. (2017) show that a simple diffusion‐consumption mechanism quantitatively describes the spatial spread of cytokines in vivo and results in localized niches of high cytokine concentrations that contribute to cell‐to‐cell variability."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"HighlightsCytokine penetration in tissues is governed by a diffusion‐consumption mechanismSpherical cytokine niches are generated around cytokine‐producing cellsThe characteristic niche size depends on the density of cytokine consumersCytokine niches are a source of variability in otherwise identical cells &NA; Cytokine‐mediated communication allows immune cells to achieve a context‐appropriate response, but the distance over which this communication happens is unclear.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1210, "doc_id": 4928282, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [4928282], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The density of cytokine receptor bearing cells has no effect on the distance over which cytokines act.\n\nDocument title: A Tunable Diffusion‐Consumption Mechanism of Cytokine Propagation Enables Plasticity in Cell‐to‐Cell Communication in the Immune System\n\nAbstract sentences:\n[0] &NA; Immune cells communicate by exchanging cytokines to achieve a context‐appropriate response, but the distances over which such communication happens are not known.\n[1] Here, we used theoretical considerations and experimental models of immune responses in vitro and in vivo to quantify the spatial extent of cytokine communications in dense tissues.\n[2] We established that competition between cytokine diffusion and consumption generated spatial niches of high cytokine concentrations with sharp boundaries.\n[3] The size of these self‐assembled niches scaled with the density of cytokine‐consuming cells, a parameter that gets tuned during immune responses.\n[4] In vivo, we measured interactions on length scales of 80–120 &mgr;m, which resulted in a high degree of cell‐to‐cell variance in cytokine exposure.\n[5] Such heterogeneous distributions of cytokines were a source of non‐genetic cell‐to‐cell variability that is often overlooked in single‐cell studies.\n[6] Our findings thus provide a basis for understanding variability in the patterning of immune responses by diffusible factors.\n[7] Graphical Abstract Figure.\n[8] No caption available.\n[9] HighlightsCytokine penetration in tissues is governed by a diffusion‐consumption mechanismSpherical cytokine niches are generated around cytokine‐producing cellsThe characteristic niche size depends on the density of cytokine consumersCytokine niches are a source of variability in otherwise identical cells &NA; Cytokine‐mediated communication allows immune cells to achieve a context‐appropriate response, but the distance over which this communication happens is unclear.\n[10] Oyler‐Yaniv et al. (2017) show that a simple diffusion‐consumption mechanism quantitatively describes the spatial spread of cytokines in vivo and results in localized niches of high cytokine concentrations that contribute to cell‐to‐cell variability."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"HighlightsCytokine penetration in tissues is governed by a diffusion‐consumption mechanismSpherical cytokine niches are generated around cytokine‐producing cellsThe characteristic niche size depends on the density of cytokine consumersCytokine niches are a source of variability in otherwise identical cells &NA; Cytokine‐mediated communication allows immune cells to achieve a context‐appropriate response, but the distance over which this communication happens is unclear.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1211, "doc_id": 4928282, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [4928282], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The deregulated and prolonged activation of monocytes has deleterious effects in chronic infectious conditions.\n\nDocument title: The myeloid transcription factor KLF2 regulates the host response to polymicrobial infection and endotoxic shock.\n\nAbstract sentences:\n[0] Precise control of myeloid cell activation is required for optimal host defense.\n[1] However, this activation process must be under exquisite control to prevent uncontrolled inflammation.\n[2] Herein, we identify the Kruppel-like transcription factor 2 (KLF2) as a potent regulator of myeloid cell activation in vivo.\n[3] Exposure of myeloid cells to hypoxia and/or bacterial products reduced KLF2 expression while inducing hypoxia inducible factor-1α (HIF-1α), findings that were recapitulated in human septic patients.\n[4] Myeloid KLF2 was found to be a potent inhibitor of nuclear factor-kappaB (NF-κB)-dependent HIF-1α transcription and, consequently, a critical determinant of outcome in models of polymicrobial infection and endotoxemia.\n[5] Collectively, these observations identify KLF2 as a tonic repressor of myeloid cell activation in vivo and an essential regulator of the innate immune system."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1212, "doc_id": 6493422, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [6493422, 44724517], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The deregulated and prolonged activation of monocytes improves inflammatory disease outcomes.\n\nDocument title: The myeloid transcription factor KLF2 regulates the host response to polymicrobial infection and endotoxic shock.\n\nAbstract sentences:\n[0] Precise control of myeloid cell activation is required for optimal host defense.\n[1] However, this activation process must be under exquisite control to prevent uncontrolled inflammation.\n[2] Herein, we identify the Kruppel-like transcription factor 2 (KLF2) as a potent regulator of myeloid cell activation in vivo.\n[3] Exposure of myeloid cells to hypoxia and/or bacterial products reduced KLF2 expression while inducing hypoxia inducible factor-1α (HIF-1α), findings that were recapitulated in human septic patients.\n[4] Myeloid KLF2 was found to be a potent inhibitor of nuclear factor-kappaB (NF-κB)-dependent HIF-1α transcription and, consequently, a critical determinant of outcome in models of polymicrobial infection and endotoxemia.\n[5] Collectively, these observations identify KLF2 as a tonic repressor of myeloid cell activation in vivo and an essential regulator of the innate immune system."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1214, "doc_id": 6493422, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [6493422, 14407673], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The effect of Lipopolysaccharides on kidney barrier function is dependent on inflammation levels.\n\nDocument title: Modification of kidney barrier function by the urokinase receptor\n\nAbstract sentences:\n[0] Podocyte dysfunction, represented by foot process effacement and proteinuria, is often the starting point for progressive kidney disease.\n[1] Therapies aimed at the cellular level of the disease are currently not available.\n[2] Here we show that induction of urokinase receptor (uPAR) signaling in podocytes leads to foot process effacement and urinary protein loss via a mechanism that includes lipid-dependent activation of αvβ3 integrin.\n[3] Mice lacking uPAR (Plaur−/−) are protected from lipopolysaccharide (LPS)-mediated proteinuria but develop disease after expression of a constitutively active β3 integrin.\n[4] Gene transfer studies reveal a prerequisite for uPAR expression in podocytes, but not in endothelial cells, for the development of LPS-mediated proteinuria.\n[5] Mechanistically, uPAR is required to activate αvβ3 integrin in podocytes, promoting cell motility and activation of the small GTPases Cdc42 and Rac1.\n[6] Blockade of αvβ3 integrin reduces podocyte motility in vitro and lowers proteinuria in mice.\n[7] Our findings show a physiological role for uPAR signaling in the regulation of kidney permeability."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1215, "doc_id": 16355392, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [16355392], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The first MBT repeat of the four malignant brain tumor (4MBT) domain of Drosophila's Sfmbt and of the orthologous mammalian L3MBTL2 is required for the interaction with the spacer region of Drosophila's Pleiohomeotic (Pho) or its human ortholog YY1.\n\nDocument title: The polycomb group protein L3mbtl2 assembles an atypical PRC1-family complex that is essential in pluripotent stem cells and early development.\n\nAbstract sentences:\n[0] L3mbtl2 has been implicated in transcriptional repression and chromatin compaction but its biological function has not been defined.\n[1] Here we show that disruption of L3mbtl2 results in embryonic lethality with failure of gastrulation.\n[2] This correlates with compromised proliferation and abnormal differentiation of L3mbtl2(-/-) embryonic stem (ES) cells.\n[3] L3mbtl2 regulates genes by recruiting a Polycomb Repressive Complex1 (PRC1)-related complex, resembling the previously described E2F6-complex, and including G9A, Hdac1, and Ring1b.\n[4] The presence of L3mbtl2 at target genes is associated with H3K9 dimethylation, low histone acetylation, and H2AK119 ubiquitination, but the latter is neither dependent on L3mbtl2 nor sufficient for repression.\n[5] Genome-wide studies revealed that the L3mbtl2-dependent complex predominantly regulates genes not bound by canonical PRC1 and PRC2.\n[6] However, some developmental regulators are repressed by the combined activity of all three complexes.\n[7] Together, we have uncovered a highly selective, essential role for an atypical PRC1-family complex in ES cells and early development."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1218, "doc_id": 15635366, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [15635366], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The gene daf-16, which encodes forkhead Box O (FOXO), is required for all phenotypes associated with reduced insulin/insulin-like growth factor (Igf) signaling.\n\nDocument title: DAF-16/FOXO employs the chromatin remodeller SWI/SNF to promote stress resistance and longevity\n\nAbstract sentences:\n[0] Organisms are constantly challenged by stresses and privations and require adaptive responses for their survival.\n[1] The forkhead box O (FOXO) transcription factor DAF-16 (hereafter referred to as DAF-16/FOXO) is a central nexus in these responses, but despite its importance little is known about how it regulates its target genes.\n[2] Proteomic identification of DAF-16/FOXO-binding partners in Caenorhabditis elegans and their subsequent functional evaluation by RNA interference revealed several candidate DAF-16/FOXO cofactors, most notably the chromatin remodeller SWI/SNF.\n[3] DAF-16/FOXO and SWI/SNF form a complex and globally co-localize at DAF-16/FOXO target promoters.\n[4] We show that specifically for gene activation, DAF-16/FOXO depends on SWI/SNF, facilitating SWI/SNF recruitment to target promoters, to activate transcription by presumed remodelling of local chromatin.\n[5] For the animal, this translates into an essential role for SWI/SNF in DAF-16/FOXO-mediated processes, in particular dauer formation, stress resistance and the promotion of longevity.\n[6] Thus, we give insight into the mechanisms of DAF-16/FOXO-mediated transcriptional regulation and establish a critical link between ATP-dependent chromatin remodelling and lifespan regulation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1219, "doc_id": 9393969, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [9393969, 14864285], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The generation of reactive oxygen species by activated oncogenes contributes to the increased genomic instability of leukaemia cells.\n\nDocument title: BCR/ABL oncogenic kinase promotes unfaithful repair of the reactive oxygen species-dependent DNA double-strand breaks.\n\nAbstract sentences:\n[0] The oncogenic BCR/ABL tyrosine kinase induces constitutive DNA damage in Philadelphia chromosome (Ph)-positive leukemia cells.\n[1] We find that BCR/ABL-induced reactive oxygen species (ROSs) cause chronic oxidative DNA damage resulting in double-strand breaks (DSBs) in S and G(2)/M cell cycle phases.\n[2] These lesions are repaired by BCR/ABL-stimulated homologous recombination repair (HRR) and nonhomologous end-joining (NHEJ) mechanisms.\n[3] A high mutation rate is detected in HRR products in BCR/ABL-positive cells, but not in the normal counterparts.\n[4] In addition, large deletions are found in NHEJ products exclusively in BCR/ABL cells.\n[5] We propose that the following series of events may contribute to genomic instability of Ph-positive leukemias: BCR/ABL --> ROSs --> oxidative DNA damage --> DSBs in proliferating cells --> unfaithful HRR and NHEJ repair."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0, 1]\nExplanation: Evidence states: \"The oncogenic BCR/ABL tyrosine kinase induces constitutive DNA damage in Philadelphia chromosome (Ph)-positive leukemia cells. We find that BCR/ABL-induced reactive oxygen species (ROSs) cause chronic oxidative DNA damage resulting in double-strand breaks (DSBs) in S and G(2)/M cell cycle phases.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1220, "doc_id": 13023410, "label": "SUPPORTS", "evidence_sentence_ids": [0, 1], "cited_doc_ids": [13023410], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The generation of reactive oxygen species by activated oncogenes contributes to the increased genomic instability of leukaemia cells.\n\nDocument title: BCR/ABL oncogenic kinase promotes unfaithful repair of the reactive oxygen species-dependent DNA double-strand breaks.\n\nAbstract sentences:\n[0] The oncogenic BCR/ABL tyrosine kinase induces constitutive DNA damage in Philadelphia chromosome (Ph)-positive leukemia cells.\n[1] We find that BCR/ABL-induced reactive oxygen species (ROSs) cause chronic oxidative DNA damage resulting in double-strand breaks (DSBs) in S and G(2)/M cell cycle phases.\n[2] These lesions are repaired by BCR/ABL-stimulated homologous recombination repair (HRR) and nonhomologous end-joining (NHEJ) mechanisms.\n[3] A high mutation rate is detected in HRR products in BCR/ABL-positive cells, but not in the normal counterparts.\n[4] In addition, large deletions are found in NHEJ products exclusively in BCR/ABL cells.\n[5] We propose that the following series of events may contribute to genomic instability of Ph-positive leukemias: BCR/ABL --> ROSs --> oxidative DNA damage --> DSBs in proliferating cells --> unfaithful HRR and NHEJ repair."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"We propose that the following series of events may contribute to genomic instability of Ph-positive leukemias: BCR/ABL --> ROSs --> oxidative DNA damage --> DSBs in proliferating cells --> unfaithful HRR and NHEJ repair.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1220, "doc_id": 13023410, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [13023410], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The innate immune response struggles to remove small numbers of parasites.\n\nDocument title: Partitioning regulatory mechanisms of within-host malaria dynamics using the effective propagation number.\n\nAbstract sentences:\n[0] Immune clearance and resource limitation (via red blood cell depletion) shape the peaks and troughs of malaria parasitemia, which in turn affect disease severity and transmission.\n[1] Quantitatively partitioning the relative roles of these effects through time is challenging.\n[2] Using data from rodent malaria, we estimated the effective propagation number, which reflects the relative importance of contrasting within-host control mechanisms through time and is sensitive to the inoculating parasite dose.\n[3] Our analysis showed that the capacity of innate responses to restrict initial parasite growth saturates with parasite dose and that experimentally enhanced innate immunity can affect parasite density indirectly via resource depletion.\n[4] Such a statistical approach offers a tool to improve targeting of drugs or vaccines for human therapy by revealing the dynamics and interactions of within-host regulatory mechanisms."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Our analysis showed that the capacity of innate responses to restrict initial parasite growth saturates with parasite dose and that experimentally enhanced innate immunity can affect parasite density indirectly via resource depletion.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1223, "doc_id": 5289038, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [5289038], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The latent infection of myeloid cells with human cytomegalovirus induces a number of changes in gene expression.\n\nDocument title: Microarrays for the study of viral gene expression during human cytomegalovirus latent infection.\n\nAbstract sentences:\n[0] Human cytomegalovirus (HCMV) is one of the largest known DNA viruses.\n[1] It is ubiquitous, and following resolution of primary productive infection, it persists in the human host by establishing a lifelong latent infection in myeloid lineage cells such as monocytes and their progenitors.\n[2] Most adults with HCMV infection are healthy but it can cause neurologic deficits in infants, and remains an important cause of morbidity and mortality in the immunosuppressed patient.\n[3] Microarray-based studies of HCMV have provided useful information about genes that are transcriptionally active during both productive and latent phases of infection.\n[4] This chapter describes how to study genes in HCMV using microarrays and two cell types (productively infected human foreskin fibroblasts, and latently infected primary human myeloid progenitor cells)."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Microarray-based studies of HCMV have provided useful information about genes that are transcriptionally active during both productive and latent phases of infection.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1224, "doc_id": 21932050, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [21932050, 34016987], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The latent infection of myeloid cells with human cytomegalovirus induces a number of changes in gene expression.\n\nDocument title: Transcriptome analysis reveals human cytomegalovirus reprograms monocyte differentiation toward an M1 macrophage.\n\nAbstract sentences:\n[0] Monocytes are primary targets for human CMV (HCMV) infection and are proposed to be responsible for hematogenous dissemination of the virus.\n[1] Monocytes acquire different functional traits during polarization to the classical proinflammatory M1 macrophage or the alternative antiinflammatory M2 macrophage.\n[2] We hypothesized that HCMV induced a proinflammatory M1 macrophage following infection to promote viral dissemination because, biologically, a proinflammatory state provides the tools to drive infected monocytes from the blood into the tissue.\n[3] To test this hypothesis of monocyte conversion from a normal quiescent phenotype to an inflammatory phenotype, we used Affymetrix Microarray to acquire a transcriptional profile of infected monocytes at a time point our data emphasized is a key temporal regulatory point following infection.\n[4] We found that HCMV significantly up-regulated 583 (5.2%) of the total genes and down-regulated 621 (5.5%) of the total genes>or=1.5-fold at 4 h postinfection.\n[5] Further ontology analysis revealed that genes implicated in classical M1 macrophage activation were stimulated by HCMV infection.\n[6] We found that 65% of genes strictly associated with M1 polarization were up-regulated, while only 4% of genes solely associated with M2 polarization were up-regulated.\n[7] Analysis of the monocyte chemokinome at the transcriptional level showed that 44% of M1 and 33% of M2 macrophage chemokines were up-regulated.\n[8] Proteomic analysis using chemokine Ab arrays confirmed the secretion of these chemotactic proteins from HCMV-infected monocytes.\n[9] Overall, the results identify that the HCMV-infected monocyte transcriptome displayed a unique M1/M2 polarization signature that was skewed toward the classical M1 activation phenotype."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"We found that HCMV significantly up-regulated 583 (5.2%) of the total genes and down-regulated 621 (5.5%) of the total genes>or=1.5-fold at 4 h postinfection.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1224, "doc_id": 34016987, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [21932050, 34016987], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The latent infection of myeloid cells with human cytomegalovirus induces a number of changes in gene expression.\n\nDocument title: Transcriptome analysis reveals human cytomegalovirus reprograms monocyte differentiation toward an M1 macrophage.\n\nAbstract sentences:\n[0] Monocytes are primary targets for human CMV (HCMV) infection and are proposed to be responsible for hematogenous dissemination of the virus.\n[1] Monocytes acquire different functional traits during polarization to the classical proinflammatory M1 macrophage or the alternative antiinflammatory M2 macrophage.\n[2] We hypothesized that HCMV induced a proinflammatory M1 macrophage following infection to promote viral dissemination because, biologically, a proinflammatory state provides the tools to drive infected monocytes from the blood into the tissue.\n[3] To test this hypothesis of monocyte conversion from a normal quiescent phenotype to an inflammatory phenotype, we used Affymetrix Microarray to acquire a transcriptional profile of infected monocytes at a time point our data emphasized is a key temporal regulatory point following infection.\n[4] We found that HCMV significantly up-regulated 583 (5.2%) of the total genes and down-regulated 621 (5.5%) of the total genes>or=1.5-fold at 4 h postinfection.\n[5] Further ontology analysis revealed that genes implicated in classical M1 macrophage activation were stimulated by HCMV infection.\n[6] We found that 65% of genes strictly associated with M1 polarization were up-regulated, while only 4% of genes solely associated with M2 polarization were up-regulated.\n[7] Analysis of the monocyte chemokinome at the transcriptional level showed that 44% of M1 and 33% of M2 macrophage chemokines were up-regulated.\n[8] Proteomic analysis using chemokine Ab arrays confirmed the secretion of these chemotactic proteins from HCMV-infected monocytes.\n[9] Overall, the results identify that the HCMV-infected monocyte transcriptome displayed a unique M1/M2 polarization signature that was skewed toward the classical M1 activation phenotype."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Further ontology analysis revealed that genes implicated in classical M1 macrophage activation were stimulated by HCMV infection.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1224, "doc_id": 34016987, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [21932050, 34016987], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The latent infection of myeloid cells with human cytomegalovirus induces a number of changes in gene expression.\n\nDocument title: Transcriptome analysis reveals human cytomegalovirus reprograms monocyte differentiation toward an M1 macrophage.\n\nAbstract sentences:\n[0] Monocytes are primary targets for human CMV (HCMV) infection and are proposed to be responsible for hematogenous dissemination of the virus.\n[1] Monocytes acquire different functional traits during polarization to the classical proinflammatory M1 macrophage or the alternative antiinflammatory M2 macrophage.\n[2] We hypothesized that HCMV induced a proinflammatory M1 macrophage following infection to promote viral dissemination because, biologically, a proinflammatory state provides the tools to drive infected monocytes from the blood into the tissue.\n[3] To test this hypothesis of monocyte conversion from a normal quiescent phenotype to an inflammatory phenotype, we used Affymetrix Microarray to acquire a transcriptional profile of infected monocytes at a time point our data emphasized is a key temporal regulatory point following infection.\n[4] We found that HCMV significantly up-regulated 583 (5.2%) of the total genes and down-regulated 621 (5.5%) of the total genes>or=1.5-fold at 4 h postinfection.\n[5] Further ontology analysis revealed that genes implicated in classical M1 macrophage activation were stimulated by HCMV infection.\n[6] We found that 65% of genes strictly associated with M1 polarization were up-regulated, while only 4% of genes solely associated with M2 polarization were up-regulated.\n[7] Analysis of the monocyte chemokinome at the transcriptional level showed that 44% of M1 and 33% of M2 macrophage chemokines were up-regulated.\n[8] Proteomic analysis using chemokine Ab arrays confirmed the secretion of these chemotactic proteins from HCMV-infected monocytes.\n[9] Overall, the results identify that the HCMV-infected monocyte transcriptome displayed a unique M1/M2 polarization signature that was skewed toward the classical M1 activation phenotype."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Overall, the results identify that the HCMV-infected monocyte transcriptome displayed a unique M1/M2 polarization signature that was skewed toward the classical M1 activation phenotype.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1224, "doc_id": 34016987, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [21932050, 34016987], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The mean suicide rate in women is higher after miscarriage than live birth.\n\nDocument title: Suicides after pregnancy in Finland, 1987-94: register linkage study.\n\nAbstract sentences:\n[0] OBJECTIVE To determine rates of suicide associated with pregnancy by the type of pregnancy.\n[1] DESIGN Register linkage study.\n[2] Information on suicides in women of reproductive age was linked with the Finnish birth, abortion, and hospital discharge registers to find out how many women who committed suicide had had a completed pregnancy during her last year of life.\n[3] SETTING Nationwide data from Finland.\n[4] SUBJECTS Women who committed suicide in 1987-94.\n[5] RESULTS There were 73 suicides associated with pregnancy, representing 5.4% of all suicides in women in this age group.\n[6] The mean annual suicide rate was 11.3 per 100,000.\n[7] The suicide rate associated with birth was significantly lower (5.9) and the rates associated with miscarriage (18.1) and induced abortion (34.7) were significantly higher than in the population.\n[8] The risk associated with birth was higher among teenagers and that associated with abortion was increased in all age groups.\n[9] Women who had committed a suicide tended to come from lower social classes and were more likely to be unmarried than other women who had had a completed pregnancy.\n[10] CONCLUSIONS The increased risk of suicide after an induced abortion indicates either common risk factors for both or harmful effects of induced abortion on mental health."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"The suicide rate associated with birth was significantly lower (5.9) and the rates associated with miscarriage (18.1) and induced abortion (34.7) were significantly higher than in the population.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1227, "doc_id": 25641414, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [25641414], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The mean suicide rate in women is lower after miscarriage than live birth.\n\nDocument title: Suicides after pregnancy in Finland, 1987-94: register linkage study.\n\nAbstract sentences:\n[0] OBJECTIVE To determine rates of suicide associated with pregnancy by the type of pregnancy.\n[1] DESIGN Register linkage study.\n[2] Information on suicides in women of reproductive age was linked with the Finnish birth, abortion, and hospital discharge registers to find out how many women who committed suicide had had a completed pregnancy during her last year of life.\n[3] SETTING Nationwide data from Finland.\n[4] SUBJECTS Women who committed suicide in 1987-94.\n[5] RESULTS There were 73 suicides associated with pregnancy, representing 5.4% of all suicides in women in this age group.\n[6] The mean annual suicide rate was 11.3 per 100,000.\n[7] The suicide rate associated with birth was significantly lower (5.9) and the rates associated with miscarriage (18.1) and induced abortion (34.7) were significantly higher than in the population.\n[8] The risk associated with birth was higher among teenagers and that associated with abortion was increased in all age groups.\n[9] Women who had committed a suicide tended to come from lower social classes and were more likely to be unmarried than other women who had had a completed pregnancy.\n[10] CONCLUSIONS The increased risk of suicide after an induced abortion indicates either common risk factors for both or harmful effects of induced abortion on mental health."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"The suicide rate associated with birth was significantly lower (5.9) and the rates associated with miscarriage (18.1) and induced abortion (34.7) were significantly higher than in the population.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1228, "doc_id": 25641414, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [25641414], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The microtubule-dependent delivery and secretion of matrix metalloproteases (MMPs) is partially responsible for the disassembly of adhesion sites.\n\nDocument title: CLASPs link focal adhesion-associated microtubule capture to localized exocytosis and adhesion site turnover\n\nAbstract sentences:\n[0] Turnover of integrin-based focal adhesions (FAs) with the extracellular matrix (ECM) is essential for coordinated cell movement.\n[1] In collectively migrating human keratinocytes, FAs assemble near the leading edge, grow and mature as a result of contractile forces and disassemble underneath the advancing cell body.\n[2] We report that clustering of microtubule-associated CLASP1 and CLASP2 proteins around FAs temporally correlates with FA turnover.\n[3] CLASPs and LL5β (also known as PHLDB2), which recruits CLASPs to FAs, facilitate FA disassembly.\n[4] CLASPs are further required for FA-associated ECM degradation, and matrix metalloprotease inhibition slows FA disassembly similarly to CLASP or PHLDB2 (LL5β) depletion.\n[5] Finally, CLASP-mediated microtubule tethering at FAs establishes an FA-directed transport pathway for delivery, docking and localized fusion of exocytic vesicles near FAs.\n[6] We propose that CLASPs couple microtubule organization, vesicle transport and cell interactions with the ECM, establishing a local secretion pathway that facilitates FA turnover by severing cell-matrix connections."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"CLASPs are further required for FA-associated ECM degradation, and matrix metalloprotease inhibition slows FA disassembly similarly to CLASP or PHLDB2 (LL5β) depletion.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1229, "doc_id": 1676568, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [1676568], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The minor G allele of FOXO3 downregulates pro-inflammatory cytokines.\n\nDocument title: Human SNP Links Differential Outcomes in Inflammatory and Infectious Disease to a FOXO3-Regulated Pathway\n\nAbstract sentences:\n[0] The clinical course and eventual outcome, or prognosis, of complex diseases varies enormously between affected individuals.\n[1] This variability critically determines the impact a disease has on a patient's life but is very poorly understood.\n[2] Here, we exploit existing genome-wide association study data to gain insight into the role of genetics in prognosis.\n[3] We identify a noncoding polymorphism in FOXO3A (rs12212067: T > G) at which the minor (G) allele, despite not being associated with disease susceptibility, is associated with a milder course of Crohn's disease and rheumatoid arthritis and with increased risk of severe malaria.\n[4] Minor allele carriage is shown to limit inflammatory responses in monocytes via a FOXO3-driven pathway, which through TGFβ1 reduces production of proinflammatory cytokines, including TNFα, and increases production of anti-inflammatory cytokines, including IL-10.\n[5] Thus, we uncover a shared genetic contribution to prognosis in distinct diseases that operates via a FOXO3-driven pathway modulating inflammatory responses."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Minor allele carriage is shown to limit inflammatory responses in monocytes via a FOXO3-driven pathway, which through TGFβ1 reduces production of proinflammatory cytokines, including TNFα, and increases production of anti-inflammatory cytokines, including IL-10.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1230, "doc_id": 13905670, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [13905670], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The minor G allele of FOXO3 is related to less severe symptoms of Crohn's Disease.\n\nDocument title: Human SNP Links Differential Outcomes in Inflammatory and Infectious Disease to a FOXO3-Regulated Pathway\n\nAbstract sentences:\n[0] The clinical course and eventual outcome, or prognosis, of complex diseases varies enormously between affected individuals.\n[1] This variability critically determines the impact a disease has on a patient's life but is very poorly understood.\n[2] Here, we exploit existing genome-wide association study data to gain insight into the role of genetics in prognosis.\n[3] We identify a noncoding polymorphism in FOXO3A (rs12212067: T > G) at which the minor (G) allele, despite not being associated with disease susceptibility, is associated with a milder course of Crohn's disease and rheumatoid arthritis and with increased risk of severe malaria.\n[4] Minor allele carriage is shown to limit inflammatory responses in monocytes via a FOXO3-driven pathway, which through TGFβ1 reduces production of proinflammatory cytokines, including TNFα, and increases production of anti-inflammatory cytokines, including IL-10.\n[5] Thus, we uncover a shared genetic contribution to prognosis in distinct diseases that operates via a FOXO3-driven pathway modulating inflammatory responses."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"We identify a noncoding polymorphism in FOXO3A (rs12212067: T > G) at which the minor (G) allele, despite not being associated with disease susceptibility, is associated with a milder course of Crohn's disease and rheumatoid arthritis and with increased risk of severe malaria.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1231, "doc_id": 13905670, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [13905670], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The minor G allele of FOXO3 up-regulates IL-10.\n\nDocument title: Human SNP Links Differential Outcomes in Inflammatory and Infectious Disease to a FOXO3-Regulated Pathway\n\nAbstract sentences:\n[0] The clinical course and eventual outcome, or prognosis, of complex diseases varies enormously between affected individuals.\n[1] This variability critically determines the impact a disease has on a patient's life but is very poorly understood.\n[2] Here, we exploit existing genome-wide association study data to gain insight into the role of genetics in prognosis.\n[3] We identify a noncoding polymorphism in FOXO3A (rs12212067: T > G) at which the minor (G) allele, despite not being associated with disease susceptibility, is associated with a milder course of Crohn's disease and rheumatoid arthritis and with increased risk of severe malaria.\n[4] Minor allele carriage is shown to limit inflammatory responses in monocytes via a FOXO3-driven pathway, which through TGFβ1 reduces production of proinflammatory cytokines, including TNFα, and increases production of anti-inflammatory cytokines, including IL-10.\n[5] Thus, we uncover a shared genetic contribution to prognosis in distinct diseases that operates via a FOXO3-driven pathway modulating inflammatory responses."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Minor allele carriage is shown to limit inflammatory responses in monocytes via a FOXO3-driven pathway, which through TGFβ1 reduces production of proinflammatory cytokines, including TNFα, and increases production of anti-inflammatory cytokines, including IL-10.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1234, "doc_id": 13905670, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [13905670], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The morphology change from large white adipocytes to small brown adipocytes is a sign of decreased energy expenditure potential in white adipose tissue.\n\nDocument title: Human ‘brite / beige’ adipocytes develop from capillary networks and their implantation improves metabolic homeostasis in mice\n\nAbstract sentences:\n[0] Uncoupling protein 1 (UCP1) is highly expressed in brown adipose tissue, where it generates heat by uncoupling electron transport from ATP production.\n[1] UCP1 is also found outside classical brown adipose tissue depots, in adipocytes that are termed 'brite' (brown-in-white) or 'beige'.\n[2] In humans, the presence of brite or beige (brite/beige) adipocytes is correlated with a lean, metabolically healthy phenotype, but whether a causal relationship exists is not clear.\n[3] Here we report that human brite/beige adipocyte progenitors proliferate in response to pro-angiogenic factors, in association with expanding capillary networks.\n[4] Adipocytes formed from these progenitors transform in response to adenylate cyclase activation from being UCP1 negative to being UCP1 positive, which is a defining feature of the beige/brite phenotype, while displaying uncoupled respiration.\n[5] When implanted into normal chow-fed, or into high-fat diet (HFD)-fed, glucose-intolerant NOD-scid IL2rg(null) (NSG) mice, brite/beige adipocytes activated in vitro enhance systemic glucose tolerance.\n[6] These adipocytes express neuroendocrine and secreted factors, including the pro-protein convertase PCSK1, which is strongly associated with human obesity.\n[7] Pro-angiogenic conditions therefore drive the proliferation of human beige/brite adipocyte progenitors, and activated beige/brite adipocytes can affect systemic glucose homeostasis, potentially through a neuroendocrine mechanism."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1235, "doc_id": 17973161, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [17973161], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The morphology change from large white adipocytes to small brown adipocytes is a sign of increased energy expenditure potential in white adipose tissue.\n\nDocument title: Human ‘brite / beige’ adipocytes develop from capillary networks and their implantation improves metabolic homeostasis in mice\n\nAbstract sentences:\n[0] Uncoupling protein 1 (UCP1) is highly expressed in brown adipose tissue, where it generates heat by uncoupling electron transport from ATP production.\n[1] UCP1 is also found outside classical brown adipose tissue depots, in adipocytes that are termed 'brite' (brown-in-white) or 'beige'.\n[2] In humans, the presence of brite or beige (brite/beige) adipocytes is correlated with a lean, metabolically healthy phenotype, but whether a causal relationship exists is not clear.\n[3] Here we report that human brite/beige adipocyte progenitors proliferate in response to pro-angiogenic factors, in association with expanding capillary networks.\n[4] Adipocytes formed from these progenitors transform in response to adenylate cyclase activation from being UCP1 negative to being UCP1 positive, which is a defining feature of the beige/brite phenotype, while displaying uncoupled respiration.\n[5] When implanted into normal chow-fed, or into high-fat diet (HFD)-fed, glucose-intolerant NOD-scid IL2rg(null) (NSG) mice, brite/beige adipocytes activated in vitro enhance systemic glucose tolerance.\n[6] These adipocytes express neuroendocrine and secreted factors, including the pro-protein convertase PCSK1, which is strongly associated with human obesity.\n[7] Pro-angiogenic conditions therefore drive the proliferation of human beige/brite adipocyte progenitors, and activated beige/brite adipocytes can affect systemic glucose homeostasis, potentially through a neuroendocrine mechanism."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1236, "doc_id": 17973161, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [17973161], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The most prevalent adverse events to Semaglutide are cardiovascular.\n\nDocument title: Effect of Oral Semaglutide Compared With Placebo and Subcutaneous Semaglutide on Glycemic Control in Patients With Type 2 Diabetes: A Randomized Clinical Trial\n\nAbstract sentences:\n[0] Importance Glucagon-like peptide-1 (GLP-1) receptor agonists are effective therapies for the treatment of type 2 diabetes and are all currently available as an injection.\n[1] Objectives To compare the effects of oral semaglutide with placebo (primary) and open-label subcutaneous semaglutide (secondary) on glycemic control in patients with type 2 diabetes.\n[2] Design, Setting, and Patients Phase 2, randomized, parallel-group, dosage-finding, 26-week trial with 5-week follow-up at 100 sites (hospital clinics, general practices, and clinical research centers) in 14 countries conducted between December 2013 and December 2014.\n[3] Of 1106 participants assessed, 632 with type 2 diabetes and insufficient glycemic control using diet and exercise alone or a stable dose of metformin were randomized.\n[4] Randomization was stratified by metformin use.\n[5] Interventions Once-daily oral semaglutide of 2.5 mg (n = 70), 5 mg (n = 70), 10 mg (n = 70), 20 mg (n = 70), 40-mg 4-week dose escalation (standard escalation; n = 71), 40-mg 8-week dose escalation (slow escalation; n = 70), 40-mg 2-week dose escalation (fast escalation, n = 70), oral placebo (n = 71; double-blind) or once-weekly subcutaneous semaglutide of 1.0 mg (n = 70) for 26 weeks.\n[6] Main Outcomes and Measures The primary end point was change in hemoglobing A1c (HbA1c) from baseline to week 26.\n[7] Secondary end points included change from baseline in body weight and adverse events.\n[8] Results Baseline characteristics were comparable across treatment groups.\n[9] Of the 632 randomized patients (mean age, 57.1 years [SD, 10.6]; men, 395 (62.7%); diabetes duration, 6.3 years [SD, 5.2]; body weight, 92.3 kg [SD, 16.8]; BMI, 31.7 [SD, 4.3]), 583 (92%) completed the trial.\n[10] Mean change in HbA1c level from baseline to week 26 decreased with oral semaglutide (dosage-dependent range, −0.7% to −1.9%) and subcutaneous semaglutide (−1.9%) and placebo (−0.3%); oral semaglutide reductions were significant vs placebo (dosage-dependent estimated treatment difference [ETD] range for oral semaglutide vs placebo, –0.4% to –1.6%; P = .01 for 2.5 mg, <.001 for all other dosages).\n[11] Reductions in body weight were greater with oral semaglutide (dosage-dependent range, −2.1 kg to −6.9 kg) and subcutaneous semaglutide (−6.4 kg) vs placebo (−1.2 kg), and significant for oral semaglutide dosages of 10 mg or more vs placebo (dosage-dependent ETD range, –0.9 to –5.7 kg; P < .001).\n[12] Adverse events were reported by 63% to 86% (371 of 490 patients) in the oral semaglutide groups, 81% (56 of 69 patients) in the subcutaneous semaglutide group, and 68% (48 of 71 patients) in the placebo group; mild to moderate gastrointestinal events were most common.\n[13] Conclusions and Relevance Among patients with type 2 diabetes, oral semaglutide resulted in better glycemic control than placebo over 26 weeks.\n[14] These findings support phase 3 studies to assess longer-term and clinical outcomes, as well as safety.\n[15] Trial Registration clinicaltrials.gov Identifier: NCT01923181"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"Adverse events were reported by 63% to 86% (371 of 490 patients) in the oral semaglutide groups, 81% (56 of 69 patients) in the subcutaneous semaglutide group, and 68% (48 of 71 patients) in the placebo group; mild to moderate gastrointestinal events were most common.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1237, "doc_id": 3654468, "label": "CONTRADICTS", "evidence_sentence_ids": [12], "cited_doc_ids": [3654468], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The most prevalent adverse events to Semaglutide are gastrointestinal.\n\nDocument title: Effect of Oral Semaglutide Compared With Placebo and Subcutaneous Semaglutide on Glycemic Control in Patients With Type 2 Diabetes: A Randomized Clinical Trial\n\nAbstract sentences:\n[0] Importance Glucagon-like peptide-1 (GLP-1) receptor agonists are effective therapies for the treatment of type 2 diabetes and are all currently available as an injection.\n[1] Objectives To compare the effects of oral semaglutide with placebo (primary) and open-label subcutaneous semaglutide (secondary) on glycemic control in patients with type 2 diabetes.\n[2] Design, Setting, and Patients Phase 2, randomized, parallel-group, dosage-finding, 26-week trial with 5-week follow-up at 100 sites (hospital clinics, general practices, and clinical research centers) in 14 countries conducted between December 2013 and December 2014.\n[3] Of 1106 participants assessed, 632 with type 2 diabetes and insufficient glycemic control using diet and exercise alone or a stable dose of metformin were randomized.\n[4] Randomization was stratified by metformin use.\n[5] Interventions Once-daily oral semaglutide of 2.5 mg (n = 70), 5 mg (n = 70), 10 mg (n = 70), 20 mg (n = 70), 40-mg 4-week dose escalation (standard escalation; n = 71), 40-mg 8-week dose escalation (slow escalation; n = 70), 40-mg 2-week dose escalation (fast escalation, n = 70), oral placebo (n = 71; double-blind) or once-weekly subcutaneous semaglutide of 1.0 mg (n = 70) for 26 weeks.\n[6] Main Outcomes and Measures The primary end point was change in hemoglobing A1c (HbA1c) from baseline to week 26.\n[7] Secondary end points included change from baseline in body weight and adverse events.\n[8] Results Baseline characteristics were comparable across treatment groups.\n[9] Of the 632 randomized patients (mean age, 57.1 years [SD, 10.6]; men, 395 (62.7%); diabetes duration, 6.3 years [SD, 5.2]; body weight, 92.3 kg [SD, 16.8]; BMI, 31.7 [SD, 4.3]), 583 (92%) completed the trial.\n[10] Mean change in HbA1c level from baseline to week 26 decreased with oral semaglutide (dosage-dependent range, −0.7% to −1.9%) and subcutaneous semaglutide (−1.9%) and placebo (−0.3%); oral semaglutide reductions were significant vs placebo (dosage-dependent estimated treatment difference [ETD] range for oral semaglutide vs placebo, –0.4% to –1.6%; P = .01 for 2.5 mg, <.001 for all other dosages).\n[11] Reductions in body weight were greater with oral semaglutide (dosage-dependent range, −2.1 kg to −6.9 kg) and subcutaneous semaglutide (−6.4 kg) vs placebo (−1.2 kg), and significant for oral semaglutide dosages of 10 mg or more vs placebo (dosage-dependent ETD range, –0.9 to –5.7 kg; P < .001).\n[12] Adverse events were reported by 63% to 86% (371 of 490 patients) in the oral semaglutide groups, 81% (56 of 69 patients) in the subcutaneous semaglutide group, and 68% (48 of 71 patients) in the placebo group; mild to moderate gastrointestinal events were most common.\n[13] Conclusions and Relevance Among patients with type 2 diabetes, oral semaglutide resulted in better glycemic control than placebo over 26 weeks.\n[14] These findings support phase 3 studies to assess longer-term and clinical outcomes, as well as safety.\n[15] Trial Registration clinicaltrials.gov Identifier: NCT01923181"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"Adverse events were reported by 63% to 86% (371 of 490 patients) in the oral semaglutide groups, 81% (56 of 69 patients) in the subcutaneous semaglutide group, and 68% (48 of 71 patients) in the placebo group; mild to moderate gastrointestinal events were most common.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1238, "doc_id": 3654468, "label": "SUPPORTS", "evidence_sentence_ids": [12], "cited_doc_ids": [3654468], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The myocardial cell lineage originally develops from cardiac progenitors of exclusively endodermal origin.\n\nDocument title: Human cardiovascular progenitor cells develop from a KDR+ embryonic-stem-cell-derived population\n\nAbstract sentences:\n[0] The functional heart is comprised of distinct mesoderm-derived lineages including cardiomyocytes, endothelial cells and vascular smooth muscle cells.\n[1] Studies in the mouse embryo and the mouse embryonic stem cell differentiation model have provided evidence indicating that these three lineages develop from a common Flk-1+ (kinase insert domain protein receptor, also known as Kdr) cardiovascular progenitor that represents one of the earliest stages in mesoderm specification to the cardiovascular lineages.\n[2] To determine whether a comparable progenitor is present during human cardiogenesis, we analysed the development of the cardiovascular lineages in human embryonic stem cell differentiation cultures.\n[3] Here we show that after induction with combinations of activin A, bone morphogenetic protein 4 (BMP4), basic fibroblast growth factor (bFGF, also known as FGF2), vascular endothelial growth factor (VEGF, also known as VEGFA) and dickkopf homolog 1 (DKK1) in serum-free media, human embryonic-stem-cell-derived embryoid bodies generate a KDRlow/C-KIT(CD117)neg population that displays cardiac, endothelial and vascular smooth muscle potential in vitro and, after transplantation, in vivo.\n[4] When plated in monolayer cultures, these KDRlow/C-KITneg cells differentiate to generate populations consisting of greater than 50% contracting cardiomyocytes.\n[5] Populations derived from the KDRlow/C-KITneg fraction give rise to colonies that contain all three lineages when plated in methylcellulose cultures.\n[6] Results from limiting dilution studies and cell-mixing experiments support the interpretation that these colonies are clones, indicating that they develop from a cardiovascular colony-forming cell.\n[7] Together, these findings identify a human cardiovascular progenitor that defines one of the earliest stages of human cardiac development."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Studies in the mouse embryo and the mouse embryonic stem cell differentiation model have provided evidence indicating that these three lineages develop from a common Flk-1+ (kinase insert domain protein receptor, also known as Kdr) cardiovascular progenitor that represents one of the earliest stages in mesoderm specification to the cardiovascular lineages.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1239, "doc_id": 4427392, "label": "CONTRADICTS", "evidence_sentence_ids": [1], "cited_doc_ids": [21387297, 4427392], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The number of unfertilized oocytes in mated hermaphrodites increases with age.\n\nDocument title: TGF-β and Insulin Signaling Regulate Reproductive Aging via Oocyte and Germline Quality Maintenance\n\nAbstract sentences:\n[0] Reproductive cessation is perhaps the earliest aging phenotype that humans experience.\n[1] Similarly, reproduction of Caenorhabditis elegans ceases in mid-adulthood.\n[2] Although somatic aging has been studied in both worms and humans, mechanisms regulating reproductive aging are not yet understood.\n[3] Here, we show that TGF-β Sma/Mab and Insulin/IGF-1 signaling regulate C. elegans reproductive aging by modulating multiple aspects of the reproductive process, including embryo integrity, oocyte fertilizability, chromosome segregation fidelity, DNA damage resistance, and oocyte and germline morphology.\n[4] TGF-β activity regulates reproductive span and germline/oocyte quality noncell-autonomously and is temporally and transcriptionally separable from its regulation of growth.\n[5] Chromosome segregation, cell cycle, and DNA damage response genes are upregulated in TGF-β mutant oocytes, decline in aged mammalian oocytes, and are critical for oocyte quality maintenance.\n[6] Our data suggest that C. elegans and humans share many aspects of reproductive aging, including the correlation between reproductive aging and declining oocyte quality and mechanisms determining oocyte quality."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1244, "doc_id": 18949516, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [18949516], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The one-child policy has created a hospitable environment for female infants.\n\nDocument title: Perinatal mortality in rural China: retrospective cohort study.\n\nAbstract sentences:\n[0] OBJECTIVES To explore the use of local civil registration data to assess the perinatal mortality in a typical rural county in a less developed province in China, 1999-2000.\n[1] DESIGN Retrospective cohort study.\n[2] Pregnancies in a cohort of women followed from registration of pregnancy to outcome of infant seven days after birth.\n[3] SETTING Routine family planning records in 20 rural townships in eastern China.\n[4] SUBJECTS 3697 pregnancies registered by the local family planning system during 1999.\n[5] MAIN OUTCOME MEASURES Abortions, stillbirths, early neonatal mortality, perinatal mortality.\n[6] RESULTS Only three cases were lost to follow up.\n[7] The average age of the women at pregnancy was 25.9 years.\n[8] Three hundred and twelve pregnancies were aborted and 240 ended in miscarriage (total 552, 15%).\n[9] The perinatal mortality rate was 69 per 1000 births, the rate of stillbirth was 24 per 1000 births, and the early neonatal mortality was 46 per 1000 live births.\n[10] The early neonatal mortality was 29 in boys and 69 in girls per 1000 live births.\n[11] The perinatal mortality rate increased notably with parity and was higher in townships having lower income per capita.\n[12] CONCLUSIONS The family planning system at the most local level is a useful data source for studying perinatal mortality in rural China.\n[13] The perinatal mortality rate in the study county was higher than previously reported for both rural and urban areas in China.\n[14] The results by parity and sex of the infant raise concern over the impact of the one child policy."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"The early neonatal mortality was 29 in boys and 69 in girls per 1000 live births.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1246, "doc_id": 7662395, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [7662395], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The origin of the CRF01_1b2k protein occurred between 1923 and 1956.\n\nDocument title: The Global Spread of Hepatitis C Virus 1a and 1b: A Phylodynamic and Phylogeographic Analysis\n\nAbstract sentences:\n[0] BACKGROUND Hepatitis C virus (HCV) is estimated to affect 130-180 million people worldwide.\n[1] Although its origin is unknown, patterns of viral diversity suggest that HCV genotype 1 probably originated from West Africa.\n[2] Previous attempts to estimate the spatiotemporal parameters of the virus, both globally and regionally, have suggested that epidemic HCV transmission began in 1900 and grew steadily until the late 1980s.\n[3] However, epidemiological data suggest that the expansion of HCV may have occurred after the Second World War.\n[4] The aim of our study was to elucidate the timescale and route of the global spread of HCV.\n[5] METHODS AND FINDINGS We show that the rarely sequenced HCV region (E2P7NS2) is more informative for molecular epidemiology studies than the more commonly used NS5B region.\n[6] We applied phylodynamic methods to a substantial set of new E2P7NS2 and NS5B sequences, together with all available global HCV sequences with information in both of these genomic regions, in order to estimate the timescale and nature of the global expansion of the most prevalent HCV subtypes, 1a and 1b.\n[7] We showed that transmission of subtypes 1a and 1b \"exploded\" between 1940 and 1980, with the spread of 1b preceding that of 1a by at least 16 y (95% confidence interval 15-17).\n[8] Phylogeographic analysis of all available NS5B sequences suggests that HCV subtypes 1a and 1b disseminated from the developed world to the developing countries.\n[9] CONCLUSIONS The evolutionary rate of HCV appears faster than previously suggested.\n[10] The global spread of HCV coincided with the widespread use of transfused blood and blood products and with the expansion of intravenous drug use but slowed prior to the wide implementation of anti-HCV screening.\n[11] Differences in the transmission routes associated with subtypes 1a and 1b provide an explanation of the relatively earlier expansion of 1b.\n[12] Our data show that the most plausible route of the HCV dispersal was from developed countries to the developing world.\n[13] Please see later in the article for the Editors' Summary."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1247, "doc_id": 5114282, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [5114282], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The peak incidence of fractures occurs during pubertal growth spurt in early adolescents.\n\nDocument title: Incidence of childhood distal forearm fractures over 30 years: a population-based study.\n\nAbstract sentences:\n[0] CONTEXT The incidence of distal forearm fractures in children peaks around the time of the pubertal growth spurt, possibly because physical activity increases at the time of a transient deficit in cortical bone mass due to the increased calcium demand during maximal skeletal growth.\n[1] Changes in physical activity or diet may therefore influence risk of forearm fracture.\n[2] OBJECTIVE To determine whether there has been a change in the incidence of distal forearm fractures in children in recent years.\n[3] DESIGN, SETTING, AND PATIENTS Population-based study among Rochester, Minn, residents younger than 35 years with distal forearm fractures in 1969-1971, 1979-1981, 1989-1991, and 1999-2001.\n[4] MAIN OUTCOME MEASURE Estimated incidence of distal forearm fractures in 4 time periods.\n[5] RESULTS Comparably age- and sex-adjusted annual incidence rates per 100 000 increased from 263.3 (95% confidence interval [CI], 231.1-295.4) in 1969-1971 to 322.3 (95% CI, 285.3-359.4) in 1979-1981 and to 399.8 (95% CI, 361.0-438.6) in 1989-1991 before leveling off at 372.9 (95% CI, 339.1-406.7) in 1999-2001.\n[6] Age-adjusted incidence rates per 100 000 were 32% greater among male residents in 1999-2001 compared with 1969-1971 (409.4 [95% CI, 359.9-459.0] vs 309.4 [95% CI, 259.3-359.5]; P =.01) and 56% greater among female residents in the same time periods (334.3 [95% CI, 288.6-380.1] vs 214.6 [95% CI, 174.9-254.4]; P<.001).\n[7] The peak incidence and greatest increase occurred between ages 11 and 14 years in boys and 8 and 11 years in girls.\n[8] CONCLUSIONS There has been a statistically significant increase in the incidence of distal forearm fractures in children and adolescents, but whether this is due to changing patterns of physical activity, decreased bone acquisition due to poor calcium intake, or both is unclear at present.\n[9] Given the large number of childhood fractures, however, studies are needed to define the cause(s) of this increase."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"CONTEXT The incidence of distal forearm fractures in children peaks around the time of the pubertal growth spurt, possibly because physical activity increases at the time of a transient deficit in cortical bone mass due to the increased calcium demand during maximal skeletal growth.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1248, "doc_id": 7209559, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [7209559], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The peak incidence of fractures occurs in toddlers.\n\nDocument title: Incidence of childhood distal forearm fractures over 30 years: a population-based study.\n\nAbstract sentences:\n[0] CONTEXT The incidence of distal forearm fractures in children peaks around the time of the pubertal growth spurt, possibly because physical activity increases at the time of a transient deficit in cortical bone mass due to the increased calcium demand during maximal skeletal growth.\n[1] Changes in physical activity or diet may therefore influence risk of forearm fracture.\n[2] OBJECTIVE To determine whether there has been a change in the incidence of distal forearm fractures in children in recent years.\n[3] DESIGN, SETTING, AND PATIENTS Population-based study among Rochester, Minn, residents younger than 35 years with distal forearm fractures in 1969-1971, 1979-1981, 1989-1991, and 1999-2001.\n[4] MAIN OUTCOME MEASURE Estimated incidence of distal forearm fractures in 4 time periods.\n[5] RESULTS Comparably age- and sex-adjusted annual incidence rates per 100 000 increased from 263.3 (95% confidence interval [CI], 231.1-295.4) in 1969-1971 to 322.3 (95% CI, 285.3-359.4) in 1979-1981 and to 399.8 (95% CI, 361.0-438.6) in 1989-1991 before leveling off at 372.9 (95% CI, 339.1-406.7) in 1999-2001.\n[6] Age-adjusted incidence rates per 100 000 were 32% greater among male residents in 1999-2001 compared with 1969-1971 (409.4 [95% CI, 359.9-459.0] vs 309.4 [95% CI, 259.3-359.5]; P =.01) and 56% greater among female residents in the same time periods (334.3 [95% CI, 288.6-380.1] vs 214.6 [95% CI, 174.9-254.4]; P<.001).\n[7] The peak incidence and greatest increase occurred between ages 11 and 14 years in boys and 8 and 11 years in girls.\n[8] CONCLUSIONS There has been a statistically significant increase in the incidence of distal forearm fractures in children and adolescents, but whether this is due to changing patterns of physical activity, decreased bone acquisition due to poor calcium intake, or both is unclear at present.\n[9] Given the large number of childhood fractures, however, studies are needed to define the cause(s) of this increase."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"CONTEXT The incidence of distal forearm fractures in children peaks around the time of the pubertal growth spurt, possibly because physical activity increases at the time of a transient deficit in cortical bone mass due to the increased calcium demand during maximal skeletal growth.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1249, "doc_id": 7209559, "label": "CONTRADICTS", "evidence_sentence_ids": [0], "cited_doc_ids": [7209559], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The predominant localization of Linc00173 is in mononuclear macrophage nuclei.\n\nDocument title: The non-coding RNA landscape of human hematopoiesis and leukemia\n\nAbstract sentences:\n[0] Non-coding RNAs have emerged as crucial regulators of gene expression and cell fate decisions.\n[1] However, their expression patterns and regulatory functions during normal and malignant human hematopoiesis are incompletely understood.\n[2] Here we present a comprehensive resource defining the non-coding RNA landscape of the human hematopoietic system.\n[3] Based on highly specific non-coding RNA expression portraits per blood cell population, we identify unique fingerprint non-coding RNAs-such as LINC00173 in granulocytes-and assign these to critical regulatory circuits involved in blood homeostasis.\n[4] Following the incorporation of acute myeloid leukemia samples into the landscape, we further uncover prognostically relevant non-coding RNA stem cell signatures shared between acute myeloid leukemia blasts and healthy hematopoietic stem cells.\n[5] Our findings highlight the importance of the non-coding transcriptome in the formation and maintenance of the human blood hierarchy.\n[6] While micro-RNAs are known regulators of haematopoiesis and leukemogenesis, the role of long non-coding RNAs is less clear.\n[7] Here the authors provide a non-coding RNA expression landscape of the human hematopoietic system, highlighting their role in the formation and maintenance of the human blood hierarchy."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1253, "doc_id": 3321943, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [3321943], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The proliferative capacity of neural progenitors differs across species.\n\nDocument title: 2D and 3D Stem Cell Models of Primate Cortical Development Identify Species-Specific Differences in Progenitor Behavior Contributing to Brain Size.\n\nAbstract sentences:\n[0] Variation in cerebral cortex size and complexity is thought to contribute to differences in cognitive ability between humans and other animals.\n[1] Here we compare cortical progenitor cell output in humans and three nonhuman primates using directed differentiation of pluripotent stem cells (PSCs) in adherent two-dimensional (2D) and organoid three-dimensional (3D) culture systems.\n[2] Clonal lineage analysis showed that primate cortical progenitors proliferate for a protracted period of time, during which they generate early-born neurons, in contrast to rodents, where this expansion phase largely ceases before neurogenesis begins.\n[3] The extent of this additional cortical progenitor expansion differs among primates, leading to differences in the number of neurons generated by each progenitor cell.\n[4] We found that this mechanism for controlling cortical size is regulated cell autonomously in culture, suggesting that primate cerebral cortex size is regulated at least in part at the level of individual cortical progenitor cell clonal output."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Clonal lineage analysis showed that primate cortical progenitors proliferate for a protracted period of time, during which they generate early-born neurons, in contrast to rodents, where this expansion phase largely ceases before neurogenesis begins.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1254, "doc_id": 16939583, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [16939583], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The proliferative capacity of neural progenitors differs across species.\n\nDocument title: 2D and 3D Stem Cell Models of Primate Cortical Development Identify Species-Specific Differences in Progenitor Behavior Contributing to Brain Size.\n\nAbstract sentences:\n[0] Variation in cerebral cortex size and complexity is thought to contribute to differences in cognitive ability between humans and other animals.\n[1] Here we compare cortical progenitor cell output in humans and three nonhuman primates using directed differentiation of pluripotent stem cells (PSCs) in adherent two-dimensional (2D) and organoid three-dimensional (3D) culture systems.\n[2] Clonal lineage analysis showed that primate cortical progenitors proliferate for a protracted period of time, during which they generate early-born neurons, in contrast to rodents, where this expansion phase largely ceases before neurogenesis begins.\n[3] The extent of this additional cortical progenitor expansion differs among primates, leading to differences in the number of neurons generated by each progenitor cell.\n[4] We found that this mechanism for controlling cortical size is regulated cell autonomously in culture, suggesting that primate cerebral cortex size is regulated at least in part at the level of individual cortical progenitor cell clonal output."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"The extent of this additional cortical progenitor expansion differs among primates, leading to differences in the number of neurons generated by each progenitor cell.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1254, "doc_id": 16939583, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [16939583], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The proliferative capacity of progenitors is regulated cell-autonomously.\n\nDocument title: 2D and 3D Stem Cell Models of Primate Cortical Development Identify Species-Specific Differences in Progenitor Behavior Contributing to Brain Size.\n\nAbstract sentences:\n[0] Variation in cerebral cortex size and complexity is thought to contribute to differences in cognitive ability between humans and other animals.\n[1] Here we compare cortical progenitor cell output in humans and three nonhuman primates using directed differentiation of pluripotent stem cells (PSCs) in adherent two-dimensional (2D) and organoid three-dimensional (3D) culture systems.\n[2] Clonal lineage analysis showed that primate cortical progenitors proliferate for a protracted period of time, during which they generate early-born neurons, in contrast to rodents, where this expansion phase largely ceases before neurogenesis begins.\n[3] The extent of this additional cortical progenitor expansion differs among primates, leading to differences in the number of neurons generated by each progenitor cell.\n[4] We found that this mechanism for controlling cortical size is regulated cell autonomously in culture, suggesting that primate cerebral cortex size is regulated at least in part at the level of individual cortical progenitor cell clonal output."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"We found that this mechanism for controlling cortical size is regulated cell autonomously in culture, suggesting that primate cerebral cortex size is regulated at least in part at the level of individual cortical progenitor cell clonal output.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1255, "doc_id": 16939583, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [16939583], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The proportion of people with visual difficulty is two times higher in low-income countries than in high-income countries.\n\nDocument title: Global, regional, and national disability-adjusted life-years (DALYs) for 315 diseases and injuries and healthy life expectancy (HALE), 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015\n\nAbstract sentences:\n[0] BACKGROUND Healthy life expectancy (HALE) and disability-adjusted life-years (DALYs) provide summary measures of health across geographies and time that can inform assessments of epidemiological patterns and health system performance, help to prioritise investments in research and development, and monitor progress toward the Sustainable Development Goals (SDGs).\n[1] We aimed to provide updated HALE and DALYs for geographies worldwide and evaluate how disease burden changes with development.\n[2] METHODS We used results from the Global Burden of Diseases, Injuries, and Risk Factors Study 2015 (GBD 2015) for all-cause mortality, cause-specific mortality, and non-fatal disease burden to derive HALE and DALYs by sex for 195 countries and territories from 1990 to 2015.\n[3] We calculated DALYs by summing years of life lost (YLLs) and years of life lived with disability (YLDs) for each geography, age group, sex, and year.\n[4] We estimated HALE using the Sullivan method, which draws from age-specific death rates and YLDs per capita.\n[5] We then assessed how observed levels of DALYs and HALE differed from expected trends calculated with the Socio-demographic Index (SDI), a composite indicator constructed from measures of income per capita, average years of schooling, and total fertility rate.\n[6] FINDINGS Total global DALYs remained largely unchanged from 1990 to 2015, with decreases in communicable, neonatal, maternal, and nutritional (Group 1) disease DALYs offset by increased DALYs due to non-communicable diseases (NCDs).\n[7] Much of this epidemiological transition was caused by changes in population growth and ageing, but it was accelerated by widespread improvements in SDI that also correlated strongly with the increasing importance of NCDs.\n[8] Both total DALYs and age-standardised DALY rates due to most Group 1 causes significantly decreased by 2015, and although total burden climbed for the majority of NCDs, age-standardised DALY rates due to NCDs declined.\n[9] Nonetheless, age-standardised DALY rates due to several high-burden NCDs (including osteoarthritis, drug use disorders, depression, diabetes, congenital birth defects, and skin, oral, and sense organ diseases) either increased or remained unchanged, leading to increases in their relative ranking in many geographies.\n[10] From 2005 to 2015, HALE at birth increased by an average of 2·9 years (95% uncertainty interval 2·9-3·0) for men and 3·5 years (3·4-3·7) for women, while HALE at age 65 years improved by 0·85 years (0·78-0·92) and 1·2 years (1·1-1·3), respectively.\n[11] Rising SDI was associated with consistently higher HALE and a somewhat smaller proportion of life spent with functional health loss; however, rising SDI was related to increases in total disability.\n[12] Many countries and territories in central America and eastern sub-Saharan Africa had increasingly lower rates of disease burden than expected given their SDI.\n[13] At the same time, a subset of geographies recorded a growing gap between observed and expected levels of DALYs, a trend driven mainly by rising burden due to war, interpersonal violence, and various NCDs.\n[14] INTERPRETATION Health is improving globally, but this means more populations are spending more time with functional health loss, an absolute expansion of morbidity.\n[15] The proportion of life spent in ill health decreases somewhat with increasing SDI, a relative compression of morbidity, which supports continued efforts to elevate personal income, improve education, and limit fertility.\n[16] Our analysis of DALYs and HALE and their relationship to SDI represents a robust framework on which to benchmark geography-specific health performance and SDG progress.\n[17] Country-specific drivers of disease burden, particularly for causes with higher-than-expected DALYs, should inform financial and research investments, prevention efforts, health policies, and health system improvement initiatives for all countries along the development continuum.\n[18] FUNDING Bill & Melinda Gates Foundation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1257, "doc_id": 581832, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [581832], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The recruitment of Wdr5 to its target loci depends on Kat8.\n\nDocument title: The histone acetyltransferase MOF is a key regulator of the embryonic stem cell core transcriptional network.\n\nAbstract sentences:\n[0] Pluripotent embryonic stem cells (ESCs) maintain self-renewal and the potential for rapid response to differentiation cues.\n[1] Both ESC features are subject to epigenetic regulation.\n[2] Here we show that the histone acetyltransferase Mof plays an essential role in the maintenance of ESC self-renewal and pluripotency.\n[3] ESCs with Mof deletion lose characteristic morphology, alkaline phosphatase (AP) staining, and differentiation potential.\n[4] They also have aberrant expression of the core transcription factors Nanog, Oct4, and Sox2.\n[5] Importantly, the phenotypes of Mof null ESCs can be partially suppressed by Nanog overexpression, supporting the idea that Mof functions as an upstream regulator of Nanog in ESCs.\n[6] Genome-wide ChIP-sequencing and transcriptome analyses further demonstrate that Mof is an integral component of the ESC core transcriptional network and that Mof primes genes for diverse developmental programs.\n[7] Mof is also required for Wdr5 recruitment and H3K4 methylation at key regulatory loci, highlighting the complexity and interconnectivity of various chromatin regulators in ESCs."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Mof is also required for Wdr5 recruitment and H3K4 methylation at key regulatory loci, highlighting the complexity and interconnectivity of various chromatin regulators in ESCs.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1258, "doc_id": 12040627, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [12040627], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The relationship between a breast cancer patient's capacity to metabolize tamoxifen and treatment outcome is independent of the patient's genetic make-up.\n\nDocument title: Association between CYP2D6 polymorphisms and outcomes among women with early stage breast cancer treated with tamoxifen.\n\nAbstract sentences:\n[0] CONTEXT The growth inhibitory effect of tamoxifen, which is used for the treatment of hormone receptor-positive breast cancer, is mediated by its metabolites, 4-hydroxytamoxifen and endoxifen.\n[1] The formation of active metabolites is catalyzed by the polymorphic cytochrome P450 2D6 (CYP2D6) enzyme.\n[2] OBJECTIVE To determine whether CYP2D6 variation is associated with clinical outcomes in women receiving adjuvant tamoxifen.\n[3] DESIGN, SETTING, AND PATIENTS Retrospective analysis of German and US cohorts of patients treated with adjuvant tamoxifen for early stage breast cancer.\n[4] The 1325 patients had diagnoses between 1986 and 2005 of stage I through III breast cancer and were mainly postmenopausal (95.4%).\n[5] Last follow-up was in December 2008; inclusion criteria were hormone receptor positivity, no metastatic disease at diagnosis, adjuvant tamoxifen therapy, and no chemotherapy.\n[6] DNA from tumor tissue or blood was genotyped for CYP2D6 variants associated with reduced (*10, *41) or absent (*3, *4, *5) enzyme activity.\n[7] Women were classified as having an extensive (n=609), heterozygous extensive/intermediate (n=637), or poor (n=79) CYP2D6 metabolism.\n[8] MAIN OUTCOME MEASURES Time to recurrence, event-free survival, disease-free survival, and overall survival.\n[9] RESULTS Median follow-up was 6.3 years.\n[10] At 9 years of follow-up, the recurrence rates were 14.9% for extensive metabolizers, 20.9% for heterozygous extensive/intermediate metabolizers, and 29.0% for poor metabolizers, and all-cause mortality rates were 16.7%, 18.0%, and 22.8%, respectively.\n[11] Compared with extensive metabolizers, there was a significantly increased risk of recurrence for heterozygous extensive/intermediate metabolizers (time to recurrence adjusted hazard ratio [HR], 1.40; 95% confidence interval [CI], 1.04-1.90) and for poor metabolizers (time to recurrence HR, 1.90; 95% CI, 1.10-3.28).\n[12] Compared with extensive metabolizers, those with decreased CYP2D6 activity (heterozygous extensive/intermediate and poor metabolism) had worse event-free survival (HR, 1.33; 95% CI, 1.06-1.68) and disease-free survival (HR, 1.29; 95% CI, 1.03-1.61), but there was no significant difference in overall survival (HR, 1.15; 95% CI, 0.88-1.51).\n[13] CONCLUSION Among women with breast cancer treated with tamoxifen, there was an association between CYP2D6 variation and clinical outcomes, such that the presence of 2 functional CYP2D6 alleles was associated with better clinical outcomes and the presence of nonfunctional or reduced-function alleles with worse outcomes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"Compared with extensive metabolizers, there was a significantly increased risk of recurrence for heterozygous extensive/intermediate metabolizers (time to recurrence adjusted hazard ratio [HR], 1.40; 95% confidence interval [CI], 1.04-1.90) and for poor metabolizers (time to recurrence HR, 1.90; 95% CI, 1.10-3.28).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1260, "doc_id": 24341590, "label": "CONTRADICTS", "evidence_sentence_ids": [11], "cited_doc_ids": [24341590], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The relationship between a breast cancer patient's capacity to metabolize tamoxifen and treatment outcome is independent of the patient's genetic make-up.\n\nDocument title: Association between CYP2D6 polymorphisms and outcomes among women with early stage breast cancer treated with tamoxifen.\n\nAbstract sentences:\n[0] CONTEXT The growth inhibitory effect of tamoxifen, which is used for the treatment of hormone receptor-positive breast cancer, is mediated by its metabolites, 4-hydroxytamoxifen and endoxifen.\n[1] The formation of active metabolites is catalyzed by the polymorphic cytochrome P450 2D6 (CYP2D6) enzyme.\n[2] OBJECTIVE To determine whether CYP2D6 variation is associated with clinical outcomes in women receiving adjuvant tamoxifen.\n[3] DESIGN, SETTING, AND PATIENTS Retrospective analysis of German and US cohorts of patients treated with adjuvant tamoxifen for early stage breast cancer.\n[4] The 1325 patients had diagnoses between 1986 and 2005 of stage I through III breast cancer and were mainly postmenopausal (95.4%).\n[5] Last follow-up was in December 2008; inclusion criteria were hormone receptor positivity, no metastatic disease at diagnosis, adjuvant tamoxifen therapy, and no chemotherapy.\n[6] DNA from tumor tissue or blood was genotyped for CYP2D6 variants associated with reduced (*10, *41) or absent (*3, *4, *5) enzyme activity.\n[7] Women were classified as having an extensive (n=609), heterozygous extensive/intermediate (n=637), or poor (n=79) CYP2D6 metabolism.\n[8] MAIN OUTCOME MEASURES Time to recurrence, event-free survival, disease-free survival, and overall survival.\n[9] RESULTS Median follow-up was 6.3 years.\n[10] At 9 years of follow-up, the recurrence rates were 14.9% for extensive metabolizers, 20.9% for heterozygous extensive/intermediate metabolizers, and 29.0% for poor metabolizers, and all-cause mortality rates were 16.7%, 18.0%, and 22.8%, respectively.\n[11] Compared with extensive metabolizers, there was a significantly increased risk of recurrence for heterozygous extensive/intermediate metabolizers (time to recurrence adjusted hazard ratio [HR], 1.40; 95% confidence interval [CI], 1.04-1.90) and for poor metabolizers (time to recurrence HR, 1.90; 95% CI, 1.10-3.28).\n[12] Compared with extensive metabolizers, those with decreased CYP2D6 activity (heterozygous extensive/intermediate and poor metabolism) had worse event-free survival (HR, 1.33; 95% CI, 1.06-1.68) and disease-free survival (HR, 1.29; 95% CI, 1.03-1.61), but there was no significant difference in overall survival (HR, 1.15; 95% CI, 0.88-1.51).\n[13] CONCLUSION Among women with breast cancer treated with tamoxifen, there was an association between CYP2D6 variation and clinical outcomes, such that the presence of 2 functional CYP2D6 alleles was associated with better clinical outcomes and the presence of nonfunctional or reduced-function alleles with worse outcomes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"Compared with extensive metabolizers, those with decreased CYP2D6 activity (heterozygous extensive/intermediate and poor metabolism) had worse event-free survival (HR, 1.33; 95% CI, 1.06-1.68) and disease-free survival (HR, 1.29; 95% CI, 1.03-1.61), but there was no significant difference in overall survival (HR, 1.15; 95% CI, 0.88-1.51).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1260, "doc_id": 24341590, "label": "CONTRADICTS", "evidence_sentence_ids": [12], "cited_doc_ids": [24341590], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The relationship between a breast cancer patient's capacity to metabolize tamoxifen and treatment outcome is independent of the patient's genetic make-up.\n\nDocument title: Association between CYP2D6 polymorphisms and outcomes among women with early stage breast cancer treated with tamoxifen.\n\nAbstract sentences:\n[0] CONTEXT The growth inhibitory effect of tamoxifen, which is used for the treatment of hormone receptor-positive breast cancer, is mediated by its metabolites, 4-hydroxytamoxifen and endoxifen.\n[1] The formation of active metabolites is catalyzed by the polymorphic cytochrome P450 2D6 (CYP2D6) enzyme.\n[2] OBJECTIVE To determine whether CYP2D6 variation is associated with clinical outcomes in women receiving adjuvant tamoxifen.\n[3] DESIGN, SETTING, AND PATIENTS Retrospective analysis of German and US cohorts of patients treated with adjuvant tamoxifen for early stage breast cancer.\n[4] The 1325 patients had diagnoses between 1986 and 2005 of stage I through III breast cancer and were mainly postmenopausal (95.4%).\n[5] Last follow-up was in December 2008; inclusion criteria were hormone receptor positivity, no metastatic disease at diagnosis, adjuvant tamoxifen therapy, and no chemotherapy.\n[6] DNA from tumor tissue or blood was genotyped for CYP2D6 variants associated with reduced (*10, *41) or absent (*3, *4, *5) enzyme activity.\n[7] Women were classified as having an extensive (n=609), heterozygous extensive/intermediate (n=637), or poor (n=79) CYP2D6 metabolism.\n[8] MAIN OUTCOME MEASURES Time to recurrence, event-free survival, disease-free survival, and overall survival.\n[9] RESULTS Median follow-up was 6.3 years.\n[10] At 9 years of follow-up, the recurrence rates were 14.9% for extensive metabolizers, 20.9% for heterozygous extensive/intermediate metabolizers, and 29.0% for poor metabolizers, and all-cause mortality rates were 16.7%, 18.0%, and 22.8%, respectively.\n[11] Compared with extensive metabolizers, there was a significantly increased risk of recurrence for heterozygous extensive/intermediate metabolizers (time to recurrence adjusted hazard ratio [HR], 1.40; 95% confidence interval [CI], 1.04-1.90) and for poor metabolizers (time to recurrence HR, 1.90; 95% CI, 1.10-3.28).\n[12] Compared with extensive metabolizers, those with decreased CYP2D6 activity (heterozygous extensive/intermediate and poor metabolism) had worse event-free survival (HR, 1.33; 95% CI, 1.06-1.68) and disease-free survival (HR, 1.29; 95% CI, 1.03-1.61), but there was no significant difference in overall survival (HR, 1.15; 95% CI, 0.88-1.51).\n[13] CONCLUSION Among women with breast cancer treated with tamoxifen, there was an association between CYP2D6 variation and clinical outcomes, such that the presence of 2 functional CYP2D6 alleles was associated with better clinical outcomes and the presence of nonfunctional or reduced-function alleles with worse outcomes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"CONCLUSION Among women with breast cancer treated with tamoxifen, there was an association between CYP2D6 variation and clinical outcomes, such that the presence of 2 functional CYP2D6 alleles was associated with better clinical outcomes and the presence of nonfunctional or reduced-function alleles with worse outcomes.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1260, "doc_id": 24341590, "label": "CONTRADICTS", "evidence_sentence_ids": [13], "cited_doc_ids": [24341590], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The removal of reactive oxygen species by activated oncogenes contributes to the increased genomic instability of leukaemia cells.\n\nDocument title: BCR/ABL oncogenic kinase promotes unfaithful repair of the reactive oxygen species-dependent DNA double-strand breaks.\n\nAbstract sentences:\n[0] The oncogenic BCR/ABL tyrosine kinase induces constitutive DNA damage in Philadelphia chromosome (Ph)-positive leukemia cells.\n[1] We find that BCR/ABL-induced reactive oxygen species (ROSs) cause chronic oxidative DNA damage resulting in double-strand breaks (DSBs) in S and G(2)/M cell cycle phases.\n[2] These lesions are repaired by BCR/ABL-stimulated homologous recombination repair (HRR) and nonhomologous end-joining (NHEJ) mechanisms.\n[3] A high mutation rate is detected in HRR products in BCR/ABL-positive cells, but not in the normal counterparts.\n[4] In addition, large deletions are found in NHEJ products exclusively in BCR/ABL cells.\n[5] We propose that the following series of events may contribute to genomic instability of Ph-positive leukemias: BCR/ABL --> ROSs --> oxidative DNA damage --> DSBs in proliferating cells --> unfaithful HRR and NHEJ repair."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [0, 1]\nExplanation: Evidence states: \"The oncogenic BCR/ABL tyrosine kinase induces constitutive DNA damage in Philadelphia chromosome (Ph)-positive leukemia cells. We find that BCR/ABL-induced reactive oxygen species (ROSs) cause chronic oxidative DNA damage resulting in double-strand breaks (DSBs) in S and G(2)/M cell cycle phases.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1261, "doc_id": 13023410, "label": "CONTRADICTS", "evidence_sentence_ids": [0, 1], "cited_doc_ids": [13023410], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The removal of reactive oxygen species by activated oncogenes contributes to the increased genomic instability of leukaemia cells.\n\nDocument title: BCR/ABL oncogenic kinase promotes unfaithful repair of the reactive oxygen species-dependent DNA double-strand breaks.\n\nAbstract sentences:\n[0] The oncogenic BCR/ABL tyrosine kinase induces constitutive DNA damage in Philadelphia chromosome (Ph)-positive leukemia cells.\n[1] We find that BCR/ABL-induced reactive oxygen species (ROSs) cause chronic oxidative DNA damage resulting in double-strand breaks (DSBs) in S and G(2)/M cell cycle phases.\n[2] These lesions are repaired by BCR/ABL-stimulated homologous recombination repair (HRR) and nonhomologous end-joining (NHEJ) mechanisms.\n[3] A high mutation rate is detected in HRR products in BCR/ABL-positive cells, but not in the normal counterparts.\n[4] In addition, large deletions are found in NHEJ products exclusively in BCR/ABL cells.\n[5] We propose that the following series of events may contribute to genomic instability of Ph-positive leukemias: BCR/ABL --> ROSs --> oxidative DNA damage --> DSBs in proliferating cells --> unfaithful HRR and NHEJ repair."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"We propose that the following series of events may contribute to genomic instability of Ph-positive leukemias: BCR/ABL --> ROSs --> oxidative DNA damage --> DSBs in proliferating cells --> unfaithful HRR and NHEJ repair.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1261, "doc_id": 13023410, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [13023410], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The repeat-variable diresidue (RVD) in the loop of Transcription-Activator Like (TAL) effectors specifies the nucleotides-amino acid contact at the target promoter element.\n\nDocument title: Structural basis for sequence-specific recognition of DNA by TAL effectors.\n\nAbstract sentences:\n[0] TAL (transcription activator-like) effectors, secreted by phytopathogenic bacteria, recognize host DNA sequences through a central domain of tandem repeats.\n[1] Each repeat comprises 33 to 35 conserved amino acids and targets a specific base pair by using two hypervariable residues [known as repeat variable diresidues (RVDs)] at positions 12 and 13.\n[2] Here, we report the crystal structures of an 11.5-repeat TAL effector in both DNA-free and DNA-bound states.\n[3] Each TAL repeat comprises two helices connected by a short RVD-containing loop.\n[4] The 11.5 repeats form a right-handed, superhelical structure that tracks along the sense strand of DNA duplex, with RVDs contacting the major groove.\n[5] The 12th residue stabilizes the RVD loop, whereas the 13th residue makes a base-specific contact.\n[6] Understanding DNA recognition by TAL effectors may facilitate rational design of DNA-binding proteins with biotechnological applications."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0, 1]\nExplanation: Evidence states: \"TAL (transcription activator-like) effectors, secreted by phytopathogenic bacteria, recognize host DNA sequences through a central domain of tandem repeats. Each repeat comprises 33 to 35 conserved amino acids and targets a specific base pair by using two hypervariable residues [known as repeat variable diresidues (RVDs)] at positions 12 and 13.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1263, "doc_id": 3981729, "label": "SUPPORTS", "evidence_sentence_ids": [0, 1], "cited_doc_ids": [3981729], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The risk of breast cancer among parous women decreases with placental weight of pregnancies.\n\nDocument title: Pregnancy characteristics and maternal risk of breast cancer.\n\nAbstract sentences:\n[0] CONTEXT During pregnancy, serum levels of estrogen, progesterone, and other hormones are markedly higher than during other periods of life.\n[1] Pregnancy hormones primarily are produced in the placenta, and signs of placental impairment may serve as indirect markers of hormone exposures during pregnancy.\n[2] During pregnancy, these markers have been inconsistently associated with subsequent risk of breast cancer in the mother.\n[3] OBJECTIVE To examine associations between indirect markers of hormonal exposures, such as placental weight and other pregnancy characteristics, and maternal risk of developing breast cancer.\n[4] DESIGN AND SETTING Population-based cohort study using data from the Swedish Birth Register, the Swedish Cancer Register, the Swedish Cause of Death Register, and the Swedish Register of Population and Population Changes.\n[5] PARTICIPANTS Women included in the Sweden Birth Register who delivered singletons between 1982 and 1989, with complete information on date of birth and gestational age.\n[6] Women were followed up until the occurrence of breast cancer, death, or end of follow-up (December 31, 2001).\n[7] Cox proportional hazards models were used to estimate associations between hormone exposures and risks of breast cancer.\n[8] MAIN OUTCOME MEASURE Incidence of invasive breast cancer.\n[9] RESULTS Of 314,019 women in the cohort, 2216 (0.7%) developed breast cancer during the follow-up through 2001, of whom 2100 (95%) were diagnosed before age 50 years.\n[10] Compared with women who had placentas weighing less than 500 g in 2 consecutive pregnancies, the risk of breast cancer was increased among women whose placentas weighed between 500 and 699 g in their first pregnancy and at least 700 g in their second pregnancy (or vice versa) (adjusted hazard ratio, 1.82; 95% confidence interval [CI], 1.07-3.08), and the corresponding risk was doubled among women whose placentas weighed at least 700 g in both pregnancies (adjusted hazard ratio, 2.05; 95% CI, 1.15-3.64).\n[11] A high birth weight (> or =4000 g) in 2 successive births was associated with an increased risk of breast cancer before but not after adjusting for placental weight and other covariates (adjusted hazard ratio, 1.10; 95% CI, 0.76-1.59).\n[12] CONCLUSIONS Placental weight is positively associated with maternal risk of breast cancer.\n[13] These results further support the hypothesis that pregnancy hormones are important modifiers of subsequent maternal breast cancer risk."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Compared with women who had placentas weighing less than 500 g in 2 consecutive pregnancies, the risk of breast cancer was increased among women whose placentas weighed between 500 and 699 g in their first pregnancy and at least 700 g in their second pregnancy (or vice versa) (adjusted hazard ratio, 1.82; 95% confidence interval [CI], 1.07-3.08), and the corresponding risk was doubled among women whose placentas weighed at least 700 g in both pregnancies (adjusted hazard ratio, 2.05; 95% CI, 1.15-3.64).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1265, "doc_id": 37480103, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [37480103], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The risk of breast cancer among parous women decreases with placental weight of pregnancies.\n\nDocument title: Pregnancy characteristics and maternal risk of breast cancer.\n\nAbstract sentences:\n[0] CONTEXT During pregnancy, serum levels of estrogen, progesterone, and other hormones are markedly higher than during other periods of life.\n[1] Pregnancy hormones primarily are produced in the placenta, and signs of placental impairment may serve as indirect markers of hormone exposures during pregnancy.\n[2] During pregnancy, these markers have been inconsistently associated with subsequent risk of breast cancer in the mother.\n[3] OBJECTIVE To examine associations between indirect markers of hormonal exposures, such as placental weight and other pregnancy characteristics, and maternal risk of developing breast cancer.\n[4] DESIGN AND SETTING Population-based cohort study using data from the Swedish Birth Register, the Swedish Cancer Register, the Swedish Cause of Death Register, and the Swedish Register of Population and Population Changes.\n[5] PARTICIPANTS Women included in the Sweden Birth Register who delivered singletons between 1982 and 1989, with complete information on date of birth and gestational age.\n[6] Women were followed up until the occurrence of breast cancer, death, or end of follow-up (December 31, 2001).\n[7] Cox proportional hazards models were used to estimate associations between hormone exposures and risks of breast cancer.\n[8] MAIN OUTCOME MEASURE Incidence of invasive breast cancer.\n[9] RESULTS Of 314,019 women in the cohort, 2216 (0.7%) developed breast cancer during the follow-up through 2001, of whom 2100 (95%) were diagnosed before age 50 years.\n[10] Compared with women who had placentas weighing less than 500 g in 2 consecutive pregnancies, the risk of breast cancer was increased among women whose placentas weighed between 500 and 699 g in their first pregnancy and at least 700 g in their second pregnancy (or vice versa) (adjusted hazard ratio, 1.82; 95% confidence interval [CI], 1.07-3.08), and the corresponding risk was doubled among women whose placentas weighed at least 700 g in both pregnancies (adjusted hazard ratio, 2.05; 95% CI, 1.15-3.64).\n[11] A high birth weight (> or =4000 g) in 2 successive births was associated with an increased risk of breast cancer before but not after adjusting for placental weight and other covariates (adjusted hazard ratio, 1.10; 95% CI, 0.76-1.59).\n[12] CONCLUSIONS Placental weight is positively associated with maternal risk of breast cancer.\n[13] These results further support the hypothesis that pregnancy hormones are important modifiers of subsequent maternal breast cancer risk."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"CONCLUSIONS Placental weight is positively associated with maternal risk of breast cancer.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1265, "doc_id": 37480103, "label": "CONTRADICTS", "evidence_sentence_ids": [12], "cited_doc_ids": [37480103], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The risk of cancer rises with level of alcohol consumption.\n\nDocument title: Alcohol use and burden for 195 countries and territories, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016\n\nAbstract sentences:\n[0] Summary Background Alcohol use is a leading risk factor for death and disability, but its overall association with health remains complex given the possible protective effects of moderate alcohol consumption on some conditions.\n[1] With our comprehensive approach to health accounting within the Global Burden of Diseases, Injuries, and Risk Factors Study 2016, we generated improved estimates of alcohol use and alcohol-attributable deaths and disability-adjusted life-years (DALYs) for 195 locations from 1990 to 2016, for both sexes and for 5-year age groups between the ages of 15 years and 95 years and older.\n[2] Methods Using 694 data sources of individual and population-level alcohol consumption, along with 592 prospective and retrospective studies on the risk of alcohol use, we produced estimates of the prevalence of current drinking, abstention, the distribution of alcohol consumption among current drinkers in standard drinks daily (defined as 10 g of pure ethyl alcohol), and alcohol-attributable deaths and DALYs.\n[3] We made several methodological improvements compared with previous estimates: first, we adjusted alcohol sales estimates to take into account tourist and unrecorded consumption; second, we did a new meta-analysis of relative risks for 23 health outcomes associated with alcohol use; and third, we developed a new method to quantify the level of alcohol consumption that minimises the overall risk to individual health.\n[4] Findings Globally, alcohol use was the seventh leading risk factor for both deaths and DALYs in 2016, accounting for 2·2% (95% uncertainty interval [UI] 1·5–3·0) of age-standardised female deaths and 6·8% (5·8–8·0) of age-standardised male deaths.\n[5] Among the population aged 15–49 years, alcohol use was the leading risk factor globally in 2016, with 3·8% (95% UI 3·2–4·3) of female deaths and 12·2% (10·8–13·6) of male deaths attributable to alcohol use.\n[6] For the population aged 15–49 years, female attributable DALYs were 2·3% (95% UI 2·0–2·6) and male attributable DALYs were 8·9% (7·8–9·9).\n[7] The three leading causes of attributable deaths in this age group were tuberculosis (1·4% [95% UI 1·0–1·7] of total deaths), road injuries (1·2% [0·7–1·9]), and self-harm (1·1% [0·6–1·5]).\n[8] For populations aged 50 years and older, cancers accounted for a large proportion of total alcohol-attributable deaths in 2016, constituting 27·1% (95% UI 21·2–33·3) of total alcohol-attributable female deaths and 18·9% (15·3–22·6) of male deaths.\n[9] The level of alcohol consumption that minimised harm across health outcomes was zero (95% UI 0·0–0·8) standard drinks per week.\n[10] Interpretation Alcohol use is a leading risk factor for global disease burden and causes substantial health loss.\n[11] We found that the risk of all-cause mortality, and of cancers specifically, rises with increasing levels of consumption, and the level of consumption that minimises health loss is zero.\n[12] These results suggest that alcohol control policies might need to be revised worldwide, refocusing on efforts to lower overall population-level consumption.\n[13] Funding Bill & Melinda Gates Foundation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"For populations aged 50 years and older, cancers accounted for a large proportion of total alcohol-attributable deaths in 2016, constituting 27·1% (95% UI 21·2–33·3) of total alcohol-attributable female deaths and 18·9% (15·3–22·6) of male deaths.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1268, "doc_id": 52072815, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [52072815], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The risk of cancer rises with level of alcohol consumption.\n\nDocument title: Alcohol use and burden for 195 countries and territories, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016\n\nAbstract sentences:\n[0] Summary Background Alcohol use is a leading risk factor for death and disability, but its overall association with health remains complex given the possible protective effects of moderate alcohol consumption on some conditions.\n[1] With our comprehensive approach to health accounting within the Global Burden of Diseases, Injuries, and Risk Factors Study 2016, we generated improved estimates of alcohol use and alcohol-attributable deaths and disability-adjusted life-years (DALYs) for 195 locations from 1990 to 2016, for both sexes and for 5-year age groups between the ages of 15 years and 95 years and older.\n[2] Methods Using 694 data sources of individual and population-level alcohol consumption, along with 592 prospective and retrospective studies on the risk of alcohol use, we produced estimates of the prevalence of current drinking, abstention, the distribution of alcohol consumption among current drinkers in standard drinks daily (defined as 10 g of pure ethyl alcohol), and alcohol-attributable deaths and DALYs.\n[3] We made several methodological improvements compared with previous estimates: first, we adjusted alcohol sales estimates to take into account tourist and unrecorded consumption; second, we did a new meta-analysis of relative risks for 23 health outcomes associated with alcohol use; and third, we developed a new method to quantify the level of alcohol consumption that minimises the overall risk to individual health.\n[4] Findings Globally, alcohol use was the seventh leading risk factor for both deaths and DALYs in 2016, accounting for 2·2% (95% uncertainty interval [UI] 1·5–3·0) of age-standardised female deaths and 6·8% (5·8–8·0) of age-standardised male deaths.\n[5] Among the population aged 15–49 years, alcohol use was the leading risk factor globally in 2016, with 3·8% (95% UI 3·2–4·3) of female deaths and 12·2% (10·8–13·6) of male deaths attributable to alcohol use.\n[6] For the population aged 15–49 years, female attributable DALYs were 2·3% (95% UI 2·0–2·6) and male attributable DALYs were 8·9% (7·8–9·9).\n[7] The three leading causes of attributable deaths in this age group were tuberculosis (1·4% [95% UI 1·0–1·7] of total deaths), road injuries (1·2% [0·7–1·9]), and self-harm (1·1% [0·6–1·5]).\n[8] For populations aged 50 years and older, cancers accounted for a large proportion of total alcohol-attributable deaths in 2016, constituting 27·1% (95% UI 21·2–33·3) of total alcohol-attributable female deaths and 18·9% (15·3–22·6) of male deaths.\n[9] The level of alcohol consumption that minimised harm across health outcomes was zero (95% UI 0·0–0·8) standard drinks per week.\n[10] Interpretation Alcohol use is a leading risk factor for global disease burden and causes substantial health loss.\n[11] We found that the risk of all-cause mortality, and of cancers specifically, rises with increasing levels of consumption, and the level of consumption that minimises health loss is zero.\n[12] These results suggest that alcohol control policies might need to be revised worldwide, refocusing on efforts to lower overall population-level consumption.\n[13] Funding Bill & Melinda Gates Foundation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"We found that the risk of all-cause mortality, and of cancers specifically, rises with increasing levels of consumption, and the level of consumption that minimises health loss is zero.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1268, "doc_id": 52072815, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [52072815], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The risk of female prisoners harming themselves is ten times that of male prisoners.\n\nDocument title: Self-harm in prisons in England and Wales: an epidemiological study of prevalence, risk factors, clustering, and subsequent suicide\n\nAbstract sentences:\n[0] BACKGROUND Self-harm and suicide are common in prisoners, yet robust information on the full extent and characteristics of people at risk of self-harm is scant.\n[1] Furthermore, understanding how frequently self-harm is followed by suicide, and in which prisoners this progression is most likely to happen, is important.\n[2] We did a case-control study of all prisoners in England and Wales to ascertain the prevalence of self-harm in this population, associated risk factors, clustering effects, and risk of subsequent suicide after self-harm.\n[3] METHODS Records of self-harm incidents in all prisons in England and Wales were gathered routinely between January, 2004, and December, 2009.\n[4] We did a case-control comparison of prisoners who self-harmed and those who did not between January, 2006, and December, 2009.\n[5] We also used a Bayesian approach to look at clustering of people who self-harmed.\n[6] Prisoners who self-harmed and subsequently died by suicide in prison were compared with other inmates who self-harmed.\n[7] FINDINGS 139,195 self-harm incidents were recorded in 26,510 individual prisoners between 2004 and 2009; 5-6% of male prisoners and 20-24% of female inmates self-harmed every year.\n[8] Self-harm rates were more than ten times higher in female prisoners than in male inmates.\n[9] Repetition of self-harm was common, particularly in women and teenage girls, in whom a subgroup of 102 prisoners accounted for 17,307 episodes.\n[10] In both sexes, self-harm was associated with younger age, white ethnic origin, prison type, and a life sentence or being unsentenced; in female inmates, committing a violent offence against an individual was also a factor.\n[11] Substantial evidence was noted of clustering in time and location of prisoners who self-harmed (adjusted intra-class correlation 0·15, 95% CI 0·11-0·18).\n[12] 109 subsequent suicides in prison were reported in individuals who self-harmed; the risk was higher in those who self-harmed than in the general prison population, and more than half the deaths occurred within a month of self-harm.\n[13] Risk factors for suicide after self-harm in male prisoners were older age and a previous self-harm incident of high or moderate lethality; in female inmates, a history of more than five self-harm incidents within a year was associated with subsequent suicide.\n[14] INTERPRETATION The burden of self-harm in prisoners is substantial, particularly in women.\n[15] Self-harm in prison is associated with subsequent suicide in this setting.\n[16] Prevention and treatment of self-harm in prisoners is an essential component of suicide prevention in prisons.\n[17] FUNDING Wellcome Trust, National Institute for Health Research, National Offender Management Service, and Department of Health."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"FINDINGS 139,195 self-harm incidents were recorded in 26,510 individual prisoners between 2004 and 2009; 5-6% of male prisoners and 20-24% of female inmates self-harmed every year.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1269, "doc_id": 13900610, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [13900610], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The risk of female prisoners harming themselves is ten times that of male prisoners.\n\nDocument title: Self-harm in prisons in England and Wales: an epidemiological study of prevalence, risk factors, clustering, and subsequent suicide\n\nAbstract sentences:\n[0] BACKGROUND Self-harm and suicide are common in prisoners, yet robust information on the full extent and characteristics of people at risk of self-harm is scant.\n[1] Furthermore, understanding how frequently self-harm is followed by suicide, and in which prisoners this progression is most likely to happen, is important.\n[2] We did a case-control study of all prisoners in England and Wales to ascertain the prevalence of self-harm in this population, associated risk factors, clustering effects, and risk of subsequent suicide after self-harm.\n[3] METHODS Records of self-harm incidents in all prisons in England and Wales were gathered routinely between January, 2004, and December, 2009.\n[4] We did a case-control comparison of prisoners who self-harmed and those who did not between January, 2006, and December, 2009.\n[5] We also used a Bayesian approach to look at clustering of people who self-harmed.\n[6] Prisoners who self-harmed and subsequently died by suicide in prison were compared with other inmates who self-harmed.\n[7] FINDINGS 139,195 self-harm incidents were recorded in 26,510 individual prisoners between 2004 and 2009; 5-6% of male prisoners and 20-24% of female inmates self-harmed every year.\n[8] Self-harm rates were more than ten times higher in female prisoners than in male inmates.\n[9] Repetition of self-harm was common, particularly in women and teenage girls, in whom a subgroup of 102 prisoners accounted for 17,307 episodes.\n[10] In both sexes, self-harm was associated with younger age, white ethnic origin, prison type, and a life sentence or being unsentenced; in female inmates, committing a violent offence against an individual was also a factor.\n[11] Substantial evidence was noted of clustering in time and location of prisoners who self-harmed (adjusted intra-class correlation 0·15, 95% CI 0·11-0·18).\n[12] 109 subsequent suicides in prison were reported in individuals who self-harmed; the risk was higher in those who self-harmed than in the general prison population, and more than half the deaths occurred within a month of self-harm.\n[13] Risk factors for suicide after self-harm in male prisoners were older age and a previous self-harm incident of high or moderate lethality; in female inmates, a history of more than five self-harm incidents within a year was associated with subsequent suicide.\n[14] INTERPRETATION The burden of self-harm in prisoners is substantial, particularly in women.\n[15] Self-harm in prison is associated with subsequent suicide in this setting.\n[16] Prevention and treatment of self-harm in prisoners is an essential component of suicide prevention in prisons.\n[17] FUNDING Wellcome Trust, National Institute for Health Research, National Offender Management Service, and Department of Health."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Self-harm rates were more than ten times higher in female prisoners than in male inmates.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1269, "doc_id": 13900610, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [13900610], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The tip of the inner tube of the toxic type VI secretion system (T6SS) antibacterial effector in Escherichia coli (E. coli) is decorated with VgrG and PAAR proteins.\n\nDocument title: A view to a kill: the bacterial type VI secretion system.\n\nAbstract sentences:\n[0] The bacterial type VI secretion system (T6SS) is an organelle that is structurally and mechanistically analogous to an intracellular membrane-attached contractile phage tail.\n[1] Recent studies determined that a rapid conformational change in the structure of a sheath protein complex propels T6SS spike and tube components along with antibacterial and antieukaryotic effectors out of predatory T6SS(+) cells and into prey cells.\n[2] The contracted organelle is then recycled in an ATP-dependent process.\n[3] T6SS is regulated at transcriptional and posttranslational levels, the latter involving detection of membrane perturbation in some species.\n[4] In addition to directly targeting eukaryotic cells, the T6SS can also target other bacteria coinfecting a mammalian host, highlighting the importance of the T6SS not only for bacterial survival in environmental ecosystems, but also in the context of infection and disease.\n[5] This review highlights these and other advances in our understanding of the structure, mechanical function, assembly, and regulation of the T6SS."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1275, "doc_id": 27731651, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [27731651], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: The tissue surrounding the granuloma in an immune cell induces an anti-inflammatory immune response.\n\nDocument title: Inflammatory signaling in human Tuberculosis granulomas is spatially organized\n\nAbstract sentences:\n[0] Granulomas are the pathological hallmark of tuberculosis (TB).\n[1] However, their function and mechanisms of formation remain poorly understood.\n[2] To understand the role of granulomas in TB, we analyzed the proteomes of granulomas from subjects with tuberculosis in an unbiased manner.\n[3] Using laser-capture microdissection, mass spectrometry and confocal microscopy, we generated detailed molecular maps of human granulomas.\n[4] We found that the centers of granulomas have a pro-inflammatory environment that is characterized by the presence of antimicrobial peptides, reactive oxygen species and pro-inflammatory eicosanoids.\n[5] Conversely, the tissue surrounding the caseum has a comparatively anti-inflammatory signature.\n[6] These findings are consistent across a set of six human subjects and in rabbits.\n[7] Although the balance between systemic pro- and anti-inflammatory signals is crucial to TB disease outcome, here we find that these signals are physically segregated within each granuloma.\n[8] From the protein and lipid snapshots of human and rabbit lesions analyzed here, we hypothesize that the pathologic response to TB is shaped by the precise anatomical localization of these inflammatory pathways during the development of the granuloma."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Conversely, the tissue surrounding the caseum has a comparatively anti-inflammatory signature.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1276, "doc_id": 3475317, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [3475317], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Therapeutics receiving accelerated approval encounter a lower frequency of post-marketing safety events\n\nDocument title: Postmarket Safety Events Among Novel Therapeutics Approved by the US Food and Drug Administration Between 2001 and 2010\n\nAbstract sentences:\n[0] Importance Postmarket safety events of novel pharmaceuticals and biologics occur when new safety risks are identified after initial regulatory approval of these therapeutics.\n[1] These safety events can change how novel therapeutics are used in clinical practice and inform patient and clinician decision making.\n[2] Objectives To characterize the frequency of postmarket safety events among novel therapeutics approved by the US Food and Drug Administration (FDA), and to examine whether any novel therapeutic characteristics known at the time of FDA approval were associated with increased risk.\n[3] Design and Setting Cohort study of all novel therapeutics approved by the FDA between January 1, 2001, and December 31, 2010, followed up through February 28, 2017.\n[4] Exposures Novel therapeutic characteristics known at the time of FDA approval, including drug class, therapeutic area, priority review, accelerated approval, orphan status, near–regulatory deadline approval, and regulatory review time.\n[5] Main Outcomes and Measures A composite of (1) withdrawals due to safety concerns, (2) FDA issuance of incremental boxed warnings added in the postmarket period, and (3) FDA issuance of safety communications.\n[6] Results From 2001 through 2010, the FDA approved 222 novel therapeutics (183 pharmaceuticals and 39 biologics).\n[7] There were 123 new postmarket safety events (3 withdrawals, 61 boxed warnings, and 59 safety communications) during a median follow-up period of 11.7 years (interquartile range [IQR], 8.7-13.8 years), affecting 71 (32.0%) of the novel therapeutics.\n[8] The median time from approval to first postmarket safety event was 4.2 years (IQR, 2.5-6.0 years), and the proportion of novel therapeutics affected by a postmarket safety event at 10 years was 30.8% (95% CI, 25.1%-37.5%).\n[9] In multivariable analysis, postmarket safety events were statistically significantly more frequent among biologics (incidence rate ratio [IRR] = 1.93; 95% CI, 1.06-3.52; P = .03), therapeutics indicated for the treatment of psychiatric disease (IRR = 3.78; 95% CI, 1.77-8.06; P < .001), those receiving accelerated approval (IRR = 2.20; 95% CI, 1.15-4.21; P = .02), and those with near–regulatory deadline approval (IRR = 1.90; 95% CI, 1.19-3.05; P = .008); events were statistically significantly less frequent among those with regulatory review times less than 200 days (IRR = 0.46; 95% CI, 0.24-0.87; P = .02).\n[10] Conclusions and Relevance Among 222 novel therapeutics approved by the FDA from 2001 through 2010, 32% were affected by a postmarket safety event.\n[11] Biologics, psychiatric therapeutics, and accelerated and near–regulatory deadline approval were statistically significantly associated with higher rates of events, highlighting the need for continuous monitoring of the safety of novel therapeutics throughout their life cycle."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"In multivariable analysis, postmarket safety events were statistically significantly more frequent among biologics (incidence rate ratio [IRR] = 1.93; 95% CI, 1.06-3.52; P = .03), therapeutics indicated for the treatment of psychiatric disease (IRR = 3.78; 95% CI, 1.77-8.06; P < .001), those receiving accelerated approval (IRR = 2.20; 95% CI, 1.15-4.21; P = .02), and those with near–regulatory deadline approval (IRR = 1.90; 95% CI, 1.19-3.05; P = .008); events were statistically significantly less frequent among those with regulatory review times less than 200 days (IRR = 0.46; 95% CI, 0.24-0.87; P = .02).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1284, "doc_id": 3578380, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [3578380], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: There is a positive correlation between hip fractures and statin use.\n\nDocument title: HMG-CoA reductase inhibitors and the risk of hip fractures in elderly patients.\n\nAbstract sentences:\n[0] CONTEXT Recent animal studies have found that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) lipid-lowering drugs (statins) substantially increase bone formation, but whether statin use in humans results in clinically meaningful bone formation or a reduction in the risk of osteoporotic fractures is not known.\n[1] OBJECTIVE To determine whether the use of statins is associated with reduced hip fracture risk.\n[2] DESIGN Case-control study.\n[3] SETTING AND PATIENTS A total of 6110 New Jersey residents aged 65 years or older and enrolled in Medicare and either Medicaid or the Pharmacy Assistance for the Aged and Disabled program.\n[4] Case patients (n=1222) underwent surgical repair of a hip fracture in 1994.\n[5] Control patients (n=4888) were identified at a ratio of 4:1 and frequency-matched to case patients for age and sex.\n[6] MAIN OUTCOME MEASURE Adjusted odds ratio (OR) of hip fracture by statin use in the 180 days and 3 years prior to the index date (the earliest date of admission for surgery), adjusted for demographic and clinical characteristics and health care utilization.\n[7] RESULTS Use of statins in either the prior 180 days (adjusted OR, 0.50; 95% confidence interval [CI], 0.33-0.76) or prior 3 years (adjusted OR, 0.57; 95% CI, 0.40-0.82) was associated with a significant reduction in the risk of hip fracture, even after controlling for variables such as race, insurance status, psychoactive medications, estrogen and thiazide use, ischemic heart disease, cancer, and diabetes mellitus.\n[8] No significant relationship was observed between use of nonstatin lipid-lowering agents and hip fracture risk.\n[9] Clear relationships were observed between the degree of reduction in hip fracture risk and the extent of statin use; there was no evidence of such relationships with nonstatin lipid-lowering agents.\n[10] After adjusting for extent of statin use in the prior 3 years, current use (on the index date) was associated with a 71% reduction in risk (adjusted OR, 0.29; 95% CI, 0.10-0.81).\n[11] The relationship between statin use and hip fracture risk persisted after controlling for variables such as the number of medications, the Charlson comorbidity index score, and hospitalization or nursing home stay in the last 180 days, as well as after excluding patients who were in a nursing home prior to their index date or who died in the year after their index date.\n[12] Use of nonstatin lipid-lowering agents was not observed to be associated with reduction in hip fracture risk in any of these alternative models or analyses.\n[13] CONCLUSIONS These findings support an association between statin use by elderly patients and reduction in the risk of hip fracture.\n[14] Controlled trials are needed to exclude the possibility of unmeasured confounders.\n[15] JAMA.\n[16] 2000;283:3211-3216"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"RESULTS Use of statins in either the prior 180 days (adjusted OR, 0.50; 95% confidence interval [CI], 0.33-0.76) or prior 3 years (adjusted OR, 0.57; 95% CI, 0.40-0.82) was associated with a significant reduction in the risk of hip fracture, even after controlling for variables such as race, insurance status, psychoactive medications, estrogen and thiazide use, ischemic heart disease, cancer, and diabetes mellitus.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1288, "doc_id": 4687948, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [4687948], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: There is a positive correlation between hip fractures and statin use.\n\nDocument title: HMG-CoA reductase inhibitors and the risk of hip fractures in elderly patients.\n\nAbstract sentences:\n[0] CONTEXT Recent animal studies have found that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) lipid-lowering drugs (statins) substantially increase bone formation, but whether statin use in humans results in clinically meaningful bone formation or a reduction in the risk of osteoporotic fractures is not known.\n[1] OBJECTIVE To determine whether the use of statins is associated with reduced hip fracture risk.\n[2] DESIGN Case-control study.\n[3] SETTING AND PATIENTS A total of 6110 New Jersey residents aged 65 years or older and enrolled in Medicare and either Medicaid or the Pharmacy Assistance for the Aged and Disabled program.\n[4] Case patients (n=1222) underwent surgical repair of a hip fracture in 1994.\n[5] Control patients (n=4888) were identified at a ratio of 4:1 and frequency-matched to case patients for age and sex.\n[6] MAIN OUTCOME MEASURE Adjusted odds ratio (OR) of hip fracture by statin use in the 180 days and 3 years prior to the index date (the earliest date of admission for surgery), adjusted for demographic and clinical characteristics and health care utilization.\n[7] RESULTS Use of statins in either the prior 180 days (adjusted OR, 0.50; 95% confidence interval [CI], 0.33-0.76) or prior 3 years (adjusted OR, 0.57; 95% CI, 0.40-0.82) was associated with a significant reduction in the risk of hip fracture, even after controlling for variables such as race, insurance status, psychoactive medications, estrogen and thiazide use, ischemic heart disease, cancer, and diabetes mellitus.\n[8] No significant relationship was observed between use of nonstatin lipid-lowering agents and hip fracture risk.\n[9] Clear relationships were observed between the degree of reduction in hip fracture risk and the extent of statin use; there was no evidence of such relationships with nonstatin lipid-lowering agents.\n[10] After adjusting for extent of statin use in the prior 3 years, current use (on the index date) was associated with a 71% reduction in risk (adjusted OR, 0.29; 95% CI, 0.10-0.81).\n[11] The relationship between statin use and hip fracture risk persisted after controlling for variables such as the number of medications, the Charlson comorbidity index score, and hospitalization or nursing home stay in the last 180 days, as well as after excluding patients who were in a nursing home prior to their index date or who died in the year after their index date.\n[12] Use of nonstatin lipid-lowering agents was not observed to be associated with reduction in hip fracture risk in any of these alternative models or analyses.\n[13] CONCLUSIONS These findings support an association between statin use by elderly patients and reduction in the risk of hip fracture.\n[14] Controlled trials are needed to exclude the possibility of unmeasured confounders.\n[15] JAMA.\n[16] 2000;283:3211-3216"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Clear relationships were observed between the degree of reduction in hip fracture risk and the extent of statin use; there was no evidence of such relationships with nonstatin lipid-lowering agents.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1288, "doc_id": 4687948, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [4687948], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: There is a positive correlation between hip fractures and statin use.\n\nDocument title: HMG-CoA reductase inhibitors and the risk of hip fractures in elderly patients.\n\nAbstract sentences:\n[0] CONTEXT Recent animal studies have found that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) lipid-lowering drugs (statins) substantially increase bone formation, but whether statin use in humans results in clinically meaningful bone formation or a reduction in the risk of osteoporotic fractures is not known.\n[1] OBJECTIVE To determine whether the use of statins is associated with reduced hip fracture risk.\n[2] DESIGN Case-control study.\n[3] SETTING AND PATIENTS A total of 6110 New Jersey residents aged 65 years or older and enrolled in Medicare and either Medicaid or the Pharmacy Assistance for the Aged and Disabled program.\n[4] Case patients (n=1222) underwent surgical repair of a hip fracture in 1994.\n[5] Control patients (n=4888) were identified at a ratio of 4:1 and frequency-matched to case patients for age and sex.\n[6] MAIN OUTCOME MEASURE Adjusted odds ratio (OR) of hip fracture by statin use in the 180 days and 3 years prior to the index date (the earliest date of admission for surgery), adjusted for demographic and clinical characteristics and health care utilization.\n[7] RESULTS Use of statins in either the prior 180 days (adjusted OR, 0.50; 95% confidence interval [CI], 0.33-0.76) or prior 3 years (adjusted OR, 0.57; 95% CI, 0.40-0.82) was associated with a significant reduction in the risk of hip fracture, even after controlling for variables such as race, insurance status, psychoactive medications, estrogen and thiazide use, ischemic heart disease, cancer, and diabetes mellitus.\n[8] No significant relationship was observed between use of nonstatin lipid-lowering agents and hip fracture risk.\n[9] Clear relationships were observed between the degree of reduction in hip fracture risk and the extent of statin use; there was no evidence of such relationships with nonstatin lipid-lowering agents.\n[10] After adjusting for extent of statin use in the prior 3 years, current use (on the index date) was associated with a 71% reduction in risk (adjusted OR, 0.29; 95% CI, 0.10-0.81).\n[11] The relationship between statin use and hip fracture risk persisted after controlling for variables such as the number of medications, the Charlson comorbidity index score, and hospitalization or nursing home stay in the last 180 days, as well as after excluding patients who were in a nursing home prior to their index date or who died in the year after their index date.\n[12] Use of nonstatin lipid-lowering agents was not observed to be associated with reduction in hip fracture risk in any of these alternative models or analyses.\n[13] CONCLUSIONS These findings support an association between statin use by elderly patients and reduction in the risk of hip fracture.\n[14] Controlled trials are needed to exclude the possibility of unmeasured confounders.\n[15] JAMA.\n[16] 2000;283:3211-3216"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"After adjusting for extent of statin use in the prior 3 years, current use (on the index date) was associated with a 71% reduction in risk (adjusted OR, 0.29; 95% CI, 0.10-0.81).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1288, "doc_id": 4687948, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [4687948], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: There is a positive correlation between hip fractures and statin use.\n\nDocument title: HMG-CoA reductase inhibitors and the risk of hip fractures in elderly patients.\n\nAbstract sentences:\n[0] CONTEXT Recent animal studies have found that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) lipid-lowering drugs (statins) substantially increase bone formation, but whether statin use in humans results in clinically meaningful bone formation or a reduction in the risk of osteoporotic fractures is not known.\n[1] OBJECTIVE To determine whether the use of statins is associated with reduced hip fracture risk.\n[2] DESIGN Case-control study.\n[3] SETTING AND PATIENTS A total of 6110 New Jersey residents aged 65 years or older and enrolled in Medicare and either Medicaid or the Pharmacy Assistance for the Aged and Disabled program.\n[4] Case patients (n=1222) underwent surgical repair of a hip fracture in 1994.\n[5] Control patients (n=4888) were identified at a ratio of 4:1 and frequency-matched to case patients for age and sex.\n[6] MAIN OUTCOME MEASURE Adjusted odds ratio (OR) of hip fracture by statin use in the 180 days and 3 years prior to the index date (the earliest date of admission for surgery), adjusted for demographic and clinical characteristics and health care utilization.\n[7] RESULTS Use of statins in either the prior 180 days (adjusted OR, 0.50; 95% confidence interval [CI], 0.33-0.76) or prior 3 years (adjusted OR, 0.57; 95% CI, 0.40-0.82) was associated with a significant reduction in the risk of hip fracture, even after controlling for variables such as race, insurance status, psychoactive medications, estrogen and thiazide use, ischemic heart disease, cancer, and diabetes mellitus.\n[8] No significant relationship was observed between use of nonstatin lipid-lowering agents and hip fracture risk.\n[9] Clear relationships were observed between the degree of reduction in hip fracture risk and the extent of statin use; there was no evidence of such relationships with nonstatin lipid-lowering agents.\n[10] After adjusting for extent of statin use in the prior 3 years, current use (on the index date) was associated with a 71% reduction in risk (adjusted OR, 0.29; 95% CI, 0.10-0.81).\n[11] The relationship between statin use and hip fracture risk persisted after controlling for variables such as the number of medications, the Charlson comorbidity index score, and hospitalization or nursing home stay in the last 180 days, as well as after excluding patients who were in a nursing home prior to their index date or who died in the year after their index date.\n[12] Use of nonstatin lipid-lowering agents was not observed to be associated with reduction in hip fracture risk in any of these alternative models or analyses.\n[13] CONCLUSIONS These findings support an association between statin use by elderly patients and reduction in the risk of hip fracture.\n[14] Controlled trials are needed to exclude the possibility of unmeasured confounders.\n[15] JAMA.\n[16] 2000;283:3211-3216"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"CONCLUSIONS These findings support an association between statin use by elderly patients and reduction in the risk of hip fracture.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1288, "doc_id": 4687948, "label": "CONTRADICTS", "evidence_sentence_ids": [13], "cited_doc_ids": [4687948], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: There is a relation between Erythromycin use and hypertrophic pyloric stenosis.\n\nDocument title: Use of macrolides in mother and child and risk of infantile hypertrophic pyloric stenosis: nationwide cohort study\n\nAbstract sentences:\n[0] OBJECTIVE To assess the association between use of macrolide antibiotics in mothers and infants from pregnancy onset until 120 days after birth and infantile hypertrophic pyloric stenosis (IHPS).\n[1] DESIGN Nationwide register based cohort study.\n[2] SETTING Denmark, 1996-2011.\n[3] PARTICIPANTS 999,378 liveborn singletons and linked individual level information on macrolide prescriptions (maternal use during pregnancy, n=30,091; maternal use after birth, n=21,557; use in infants, n=6591), surgery for IHPS, and potential confounders.\n[4] MAIN OUTCOME MEASURES Surgery for IHPS by three categories of macrolide use: in mothers during pregnancy, in mothers after birth, and in infants after birth.\n[5] RESULTS 880 infants developed IHPS (0.9 cases per 1000 births).\n[6] Compared with infants with no use of macrolides, the adjusted rate ratio for IHPS in infants with use of macrolides during days 0 to 13 after birth was 29.8 (95% confidence interval 16.4 to 54.1) and during days 14 to 120 was 3.24 (1.20 to 8.74); the corresponding absolute risk differences were 24.4 (95% confidence interval 13.0 to 44.1) and 0.65 (0.06 to 2.21) cases per 1000 infants exposed to macrolides, respectively.\n[7] The rate ratio for maternal use of macrolides for days 0 to 13 after birth was 3.49 (1.92 to 6.34) and for days 14 to 120 was 0.70 (0.26 to 1.90); the corresponding absolute risk differences were 2.15 (0.82 to 4.64) and -0.11 (-0.26 to 0.31).\n[8] The rate ratios for maternal use of macrolides during pregnancy were 1.02 (0.65 to 1.59) for weeks 0 to 27 and 1.77 (0.95 to 3.31) for weeks 28 to birth; the corresponding absolute risk differences were 0.01 (-0.31 to 0.50) and 0.67 (-0.06 to 2.02).\n[9] CONCLUSIONS Treatment of young infants with macrolide antibiotics was strongly associated with IHPS and should therefore only be administered if potential treatment benefits outweigh the risk.\n[10] Maternal use of macrolides during the first two weeks after birth was also associated with an increased risk of IHPS.\n[11] A possible association was also found with use during late pregnancy."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"CONCLUSIONS Treatment of young infants with macrolide antibiotics was strongly associated with IHPS and should therefore only be administered if potential treatment benefits outweigh the risk.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1289, "doc_id": 21239672, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [21239672], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: There is a relation between Erythromycin use and hypertrophic pyloric stenosis.\n\nDocument title: Use of macrolides in mother and child and risk of infantile hypertrophic pyloric stenosis: nationwide cohort study\n\nAbstract sentences:\n[0] OBJECTIVE To assess the association between use of macrolide antibiotics in mothers and infants from pregnancy onset until 120 days after birth and infantile hypertrophic pyloric stenosis (IHPS).\n[1] DESIGN Nationwide register based cohort study.\n[2] SETTING Denmark, 1996-2011.\n[3] PARTICIPANTS 999,378 liveborn singletons and linked individual level information on macrolide prescriptions (maternal use during pregnancy, n=30,091; maternal use after birth, n=21,557; use in infants, n=6591), surgery for IHPS, and potential confounders.\n[4] MAIN OUTCOME MEASURES Surgery for IHPS by three categories of macrolide use: in mothers during pregnancy, in mothers after birth, and in infants after birth.\n[5] RESULTS 880 infants developed IHPS (0.9 cases per 1000 births).\n[6] Compared with infants with no use of macrolides, the adjusted rate ratio for IHPS in infants with use of macrolides during days 0 to 13 after birth was 29.8 (95% confidence interval 16.4 to 54.1) and during days 14 to 120 was 3.24 (1.20 to 8.74); the corresponding absolute risk differences were 24.4 (95% confidence interval 13.0 to 44.1) and 0.65 (0.06 to 2.21) cases per 1000 infants exposed to macrolides, respectively.\n[7] The rate ratio for maternal use of macrolides for days 0 to 13 after birth was 3.49 (1.92 to 6.34) and for days 14 to 120 was 0.70 (0.26 to 1.90); the corresponding absolute risk differences were 2.15 (0.82 to 4.64) and -0.11 (-0.26 to 0.31).\n[8] The rate ratios for maternal use of macrolides during pregnancy were 1.02 (0.65 to 1.59) for weeks 0 to 27 and 1.77 (0.95 to 3.31) for weeks 28 to birth; the corresponding absolute risk differences were 0.01 (-0.31 to 0.50) and 0.67 (-0.06 to 2.02).\n[9] CONCLUSIONS Treatment of young infants with macrolide antibiotics was strongly associated with IHPS and should therefore only be administered if potential treatment benefits outweigh the risk.\n[10] Maternal use of macrolides during the first two weeks after birth was also associated with an increased risk of IHPS.\n[11] A possible association was also found with use during late pregnancy."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Maternal use of macrolides during the first two weeks after birth was also associated with an increased risk of IHPS.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1289, "doc_id": 21239672, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [21239672], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: There is no association between HNF4A mutations and diabetes risks.\n\nDocument title: Macrosomia and Hyperinsulinaemic Hypoglycaemia in Patients with Heterozygous Mutations in the HNF4A Gene\n\nAbstract sentences:\n[0] Background  Macrosomia is associated with considerable neonatal and maternal morbidity.\n[1] Factors that predict macrosomia are poorly understood.\n[2] The increased rate of macrosomia in the offspring of pregnant women with diabetes and in congenital hyperinsulinaemia is mediated by increased foetal insulin secretion.\n[3] We assessed the in utero and neonatal role of two key regulators of pancreatic insulin secretion by studying birthweight and the incidence of neonatal hypoglycaemia in patients with heterozygous mutations in the maturity-onset diabetes of the young (MODY) genes HNF4A (encoding HNF-4α) and HNF1A/TCF1 (encoding HNF-1α), and the effect of pancreatic deletion of Hnf4a on foetal and neonatal insulin secretion in mice."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1291, "doc_id": 56893404, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [56893404], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: There is no increased risk of hypospadias with clomiphene.\n\nDocument title: Use of clomifene during early pregnancy and risk of hypospadias: population based case-control study.\n\nAbstract sentences:\n[0] Clomifene is widely used for inducing ovulation.1 It is structurally related to diethylstilbestrol, which has been linked to vaginal and cervical clear cell adenocarcinoma in women exposed in utero.\n[1] The adverse effect is less severe in sons, although links to testicular cancer and urogenital anomalies, such as epididymal cysts, have been reported.2 3 A recent study also found an increased risk of hypospadias in the sons of women exposed to diethylstilbestrol in utero.4 Clomifene has a half life of about five days, but its metabolites have been found in blood samples on day 22 of the menstrual cycle and in faeces up to six weeks after administration.5 The occurrence of hypospadias may be increasing.\n[2] Little is known about the risk of hypospadias in boys born to women who have used clomifene to induce ovulation.\n[3] ### Methods and results  Our case-control study was done in the Danish counties of North Jutland, Aarhus, Viborg, and …"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"The adverse effect is less severe in sons, although links to testicular cancer and urogenital anomalies, such as epididymal cysts, have been reported.2 3 A recent study also found an increased risk of hypospadias in the sons of women exposed to diethylstilbestrol in utero.4 Clomifene has a half life of about five days, but its metabolites have been found in blood samples on day 22 of the menstrual cycle and in faeces up to six weeks after administration.5 The occurrence of hypospadias may be increasing.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1293, "doc_id": 43329366, "label": "CONTRADICTS", "evidence_sentence_ids": [1], "cited_doc_ids": [43329366], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: There is no known interaction between Pioneer factor OCT3/4 and major chromatin remodeling factors.\n\nDocument title: Oct4 links multiple epigenetic pathways to the pluripotency network\n\nAbstract sentences:\n[0] Oct4 is a well-known transcription factor that plays fundamental roles in stem cell self-renewal, pluripotency, and somatic cell reprogramming.\n[1] However, limited information is available on Oct4-associated protein complexes and their intrinsic protein-protein interactions that dictate Oct4's critical regulatory activities.\n[2] Here we employed an improved affinity purification approach combined with mass spectrometry to purify Oct4 protein complexes in mouse embryonic stem cells (mESCs), and discovered many novel Oct4 partners important for self-renewal and pluripotency of mESCs.\n[3] Notably, we found that Oct4 is associated with multiple chromatin-modifying complexes with documented as well as newly proved functional significance in stem cell maintenance and somatic cell reprogramming.\n[4] Our study establishes a solid biochemical basis for genetic and epigenetic regulation of stem cell pluripotency and provides a framework for exploring alternative factor-based reprogramming strategies."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Notably, we found that Oct4 is associated with multiple chromatin-modifying complexes with documented as well as newly proved functional significance in stem cell maintenance and somatic cell reprogramming.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1294, "doc_id": 2078658, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [2078658, 30507607], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: There is no known interaction between Pioneer factor OCT3/4 and major chromatin remodeling factors.\n\nDocument title: An Oct4-Centered Protein Interaction Network in Embryonic Stem Cells\n\nAbstract sentences:\n[0] Transcription factors, such as Oct4, are critical for establishing and maintaining pluripotent cell identity.\n[1] Whereas the genomic locations of several pluripotency transcription factors have been reported, the spectrum of their interaction partners is underexplored.\n[2] Here, we use an improved affinity protocol to purify Oct4-interacting proteins from mouse embryonic stem cells (ESCs).\n[3] Subsequent purification of Oct4 partners Sall4, Tcfcp2l1, Dax1, and Esrrb resulted in an Oct4 interactome of 166 proteins, including transcription factors and chromatin-modifying complexes with documented roles in self-renewal, but also many factors not previously associated with the ESC network.\n[4] We find that Esrrb associated with the basal transcription machinery and also detect interactions between transcription factors and components of the TGF-beta, Notch, and Wnt signaling pathways.\n[5] Acute depletion of Oct4 reduced binding of Tcfcp2l1, Dax1, and Esrrb to several target genes.\n[6] In conclusion, our purification protocol allowed us to bring greater definition to the circuitry controlling pluripotent cell identity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Subsequent purification of Oct4 partners Sall4, Tcfcp2l1, Dax1, and Esrrb resulted in an Oct4 interactome of 166 proteins, including transcription factors and chromatin-modifying complexes with documented roles in self-renewal, but also many factors not previously associated with the ESC network.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1294, "doc_id": 30507607, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [2078658, 30507607], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: There is no relation between Erythromycin use and hypertrophic pyloric stenosis.\n\nDocument title: Use of macrolides in mother and child and risk of infantile hypertrophic pyloric stenosis: nationwide cohort study\n\nAbstract sentences:\n[0] OBJECTIVE To assess the association between use of macrolide antibiotics in mothers and infants from pregnancy onset until 120 days after birth and infantile hypertrophic pyloric stenosis (IHPS).\n[1] DESIGN Nationwide register based cohort study.\n[2] SETTING Denmark, 1996-2011.\n[3] PARTICIPANTS 999,378 liveborn singletons and linked individual level information on macrolide prescriptions (maternal use during pregnancy, n=30,091; maternal use after birth, n=21,557; use in infants, n=6591), surgery for IHPS, and potential confounders.\n[4] MAIN OUTCOME MEASURES Surgery for IHPS by three categories of macrolide use: in mothers during pregnancy, in mothers after birth, and in infants after birth.\n[5] RESULTS 880 infants developed IHPS (0.9 cases per 1000 births).\n[6] Compared with infants with no use of macrolides, the adjusted rate ratio for IHPS in infants with use of macrolides during days 0 to 13 after birth was 29.8 (95% confidence interval 16.4 to 54.1) and during days 14 to 120 was 3.24 (1.20 to 8.74); the corresponding absolute risk differences were 24.4 (95% confidence interval 13.0 to 44.1) and 0.65 (0.06 to 2.21) cases per 1000 infants exposed to macrolides, respectively.\n[7] The rate ratio for maternal use of macrolides for days 0 to 13 after birth was 3.49 (1.92 to 6.34) and for days 14 to 120 was 0.70 (0.26 to 1.90); the corresponding absolute risk differences were 2.15 (0.82 to 4.64) and -0.11 (-0.26 to 0.31).\n[8] The rate ratios for maternal use of macrolides during pregnancy were 1.02 (0.65 to 1.59) for weeks 0 to 27 and 1.77 (0.95 to 3.31) for weeks 28 to birth; the corresponding absolute risk differences were 0.01 (-0.31 to 0.50) and 0.67 (-0.06 to 2.02).\n[9] CONCLUSIONS Treatment of young infants with macrolide antibiotics was strongly associated with IHPS and should therefore only be administered if potential treatment benefits outweigh the risk.\n[10] Maternal use of macrolides during the first two weeks after birth was also associated with an increased risk of IHPS.\n[11] A possible association was also found with use during late pregnancy."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"CONCLUSIONS Treatment of young infants with macrolide antibiotics was strongly associated with IHPS and should therefore only be administered if potential treatment benefits outweigh the risk.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1295, "doc_id": 21239672, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [21239672], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: There is no relation between Erythromycin use and hypertrophic pyloric stenosis.\n\nDocument title: Use of macrolides in mother and child and risk of infantile hypertrophic pyloric stenosis: nationwide cohort study\n\nAbstract sentences:\n[0] OBJECTIVE To assess the association between use of macrolide antibiotics in mothers and infants from pregnancy onset until 120 days after birth and infantile hypertrophic pyloric stenosis (IHPS).\n[1] DESIGN Nationwide register based cohort study.\n[2] SETTING Denmark, 1996-2011.\n[3] PARTICIPANTS 999,378 liveborn singletons and linked individual level information on macrolide prescriptions (maternal use during pregnancy, n=30,091; maternal use after birth, n=21,557; use in infants, n=6591), surgery for IHPS, and potential confounders.\n[4] MAIN OUTCOME MEASURES Surgery for IHPS by three categories of macrolide use: in mothers during pregnancy, in mothers after birth, and in infants after birth.\n[5] RESULTS 880 infants developed IHPS (0.9 cases per 1000 births).\n[6] Compared with infants with no use of macrolides, the adjusted rate ratio for IHPS in infants with use of macrolides during days 0 to 13 after birth was 29.8 (95% confidence interval 16.4 to 54.1) and during days 14 to 120 was 3.24 (1.20 to 8.74); the corresponding absolute risk differences were 24.4 (95% confidence interval 13.0 to 44.1) and 0.65 (0.06 to 2.21) cases per 1000 infants exposed to macrolides, respectively.\n[7] The rate ratio for maternal use of macrolides for days 0 to 13 after birth was 3.49 (1.92 to 6.34) and for days 14 to 120 was 0.70 (0.26 to 1.90); the corresponding absolute risk differences were 2.15 (0.82 to 4.64) and -0.11 (-0.26 to 0.31).\n[8] The rate ratios for maternal use of macrolides during pregnancy were 1.02 (0.65 to 1.59) for weeks 0 to 27 and 1.77 (0.95 to 3.31) for weeks 28 to birth; the corresponding absolute risk differences were 0.01 (-0.31 to 0.50) and 0.67 (-0.06 to 2.02).\n[9] CONCLUSIONS Treatment of young infants with macrolide antibiotics was strongly associated with IHPS and should therefore only be administered if potential treatment benefits outweigh the risk.\n[10] Maternal use of macrolides during the first two weeks after birth was also associated with an increased risk of IHPS.\n[11] A possible association was also found with use during late pregnancy."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Maternal use of macrolides during the first two weeks after birth was also associated with an increased risk of IHPS.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1295, "doc_id": 21239672, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [21239672], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: There was an estimated 30 million cases of pneumonia in young children worldwide in 2010.\n\nDocument title: Global and regional burden of hospital admissions for severe acute lower respiratory infections in young children in 2010: a systematic analysis\n\nAbstract sentences:\n[0] BACKGROUND The annual number of hospital admissions and in-hospital deaths due to severe acute lower respiratory infections (ALRI) in young children worldwide is unknown.\n[1] We aimed to estimate the incidence of admissions and deaths for such infections in children younger than 5 years in 2010.\n[2] METHODS We estimated the incidence of admissions for severe and very severe ALRI in children younger than 5 years, stratified by age and region, with data from a systematic review of studies published between Jan 1, 1990, and March 31, 2012, and from 28 unpublished population-based studies.\n[3] We applied these incidence estimates to population estimates for 2010, to calculate the global and regional burden in children admitted with severe ALRI in that year.\n[4] We estimated in-hospital mortality due to severe and very severe ALRI by combining incidence estimates with case fatality ratios from hospital-based studies.\n[5] FINDINGS We identified 89 eligible studies and estimated that in 2010, 11·9 million (95% CI 10·3-13·9 million) episodes of severe and 3·0 million (2·1-4·2 million) episodes of very severe ALRI resulted in hospital admissions in young children worldwide.\n[6] Incidence was higher in boys than in girls, the sex disparity being greatest in South Asian studies.\n[7] On the basis of data from 37 hospital studies reporting case fatality ratios for severe ALRI, we estimated that roughly 265,000 (95% CI 160,000-450,000) in-hospital deaths took place in young children, with 99% of these deaths in developing countries.\n[8] Therefore, the data suggest that although 62% of children with severe ALRI are treated in hospitals, 81% of deaths happen outside hospitals.\n[9] INTERPRETATION Severe ALRI is a substantial burden on health services worldwide and a major cause of hospital referral and admission in young children.\n[10] Improved hospital access and reduced inequities, such as those related to sex and rural status, could substantially decrease mortality related to such infection.\n[11] Community-based management of severe disease could be an important complementary strategy to reduce pneumonia mortality and health inequities.\n[12] FUNDING WHO."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"FINDINGS We identified 89 eligible studies and estimated that in 2010, 11·9 million (95% CI 10·3-13·9 million) episodes of severe and 3·0 million (2·1-4·2 million) episodes of very severe ALRI resulted in hospital admissions in young children worldwide.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1297, "doc_id": 9167230, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [9167230], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Thiopurine active metabolites can be catabolized through dephosphorylation of thioguanine nucleotides.\n\nDocument title: Activating mutations in the NT5C2 nucleotidase gene drive chemotherapy resistance in relapsed ALL\n\nAbstract sentences:\n[0] Acute lymphoblastic leukemia (ALL) is an aggressive hematological tumor resulting from the malignant transformation of lymphoid progenitors.\n[1] Despite intensive chemotherapy, 20% of pediatric patients and over 50% of adult patients with ALL do not achieve a complete remission or relapse after intensified chemotherapy, making disease relapse and resistance to therapy the most substantial challenge in the treatment of this disease.\n[2] Using whole-exome sequencing, we identify mutations in the cytosolic 5'-nucleotidase II gene (NT5C2), which encodes a 5'-nucleotidase enzyme that is responsible for the inactivation of nucleoside-analog chemotherapy drugs, in 20/103 (19%) relapse T cell ALLs and 1/35 (3%) relapse B-precursor ALLs.\n[3] NT5C2 mutant proteins show increased nucleotidase activity in vitro and conferred resistance to chemotherapy with 6-mercaptopurine and 6-thioguanine when expressed in ALL lymphoblasts.\n[4] These results support a prominent role for activating mutations in NT5C2 and increased nucleoside-analog metabolism in disease progression and chemotherapy resistance in ALL."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1300, "doc_id": 6421792, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [6421792], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Tirasemtiv has no effect on cardiac muscle.\n\nDocument title: Activation of fast skeletal muscle troponin as a potential therapeutic approach for treating neuromuscular diseases\n\nAbstract sentences:\n[0] Limited neural input results in muscle weakness in neuromuscular disease because of a reduction in the density of muscle innervation, the rate of neuromuscular junction activation or the efficiency of synaptic transmission.\n[1] We developed a small-molecule fast-skeletal-troponin activator, CK-2017357, as a means to increase muscle strength by amplifying the response of muscle when neural input is otherwise diminished secondary to neuromuscular disease.\n[2] Binding selectively to the fast-skeletal-troponin complex, CK-2017357 slows the rate of calcium release from troponin C and sensitizes muscle to calcium.\n[3] As a consequence, the force-calcium relationship of muscle fibers shifts leftwards, as does the force-frequency relationship of a nerve-muscle pair, so that CK-2017357 increases the production of muscle force in situ at sub-maximal nerve stimulation rates.\n[4] Notably, we show that sensitization of the fast-skeletal-troponin complex to calcium improves muscle force and grip strength immediately after administration of single doses of CK-2017357 in a model of the neuromuscular disease myasthenia gravis.\n[5] Troponin activation may provide a new therapeutic approach to improve physical activity in diseases where neuromuscular function is compromised."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1302, "doc_id": 12631697, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [12631697], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Tirasemtiv targets cardiac muscle.\n\nDocument title: Activation of fast skeletal muscle troponin as a potential therapeutic approach for treating neuromuscular diseases\n\nAbstract sentences:\n[0] Limited neural input results in muscle weakness in neuromuscular disease because of a reduction in the density of muscle innervation, the rate of neuromuscular junction activation or the efficiency of synaptic transmission.\n[1] We developed a small-molecule fast-skeletal-troponin activator, CK-2017357, as a means to increase muscle strength by amplifying the response of muscle when neural input is otherwise diminished secondary to neuromuscular disease.\n[2] Binding selectively to the fast-skeletal-troponin complex, CK-2017357 slows the rate of calcium release from troponin C and sensitizes muscle to calcium.\n[3] As a consequence, the force-calcium relationship of muscle fibers shifts leftwards, as does the force-frequency relationship of a nerve-muscle pair, so that CK-2017357 increases the production of muscle force in situ at sub-maximal nerve stimulation rates.\n[4] Notably, we show that sensitization of the fast-skeletal-troponin complex to calcium improves muscle force and grip strength immediately after administration of single doses of CK-2017357 in a model of the neuromuscular disease myasthenia gravis.\n[5] Troponin activation may provide a new therapeutic approach to improve physical activity in diseases where neuromuscular function is compromised."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1304, "doc_id": 12631697, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [12631697], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Tirasemtiv targets fast-twitch muscle.\n\nDocument title: Activation of fast skeletal muscle troponin as a potential therapeutic approach for treating neuromuscular diseases\n\nAbstract sentences:\n[0] Limited neural input results in muscle weakness in neuromuscular disease because of a reduction in the density of muscle innervation, the rate of neuromuscular junction activation or the efficiency of synaptic transmission.\n[1] We developed a small-molecule fast-skeletal-troponin activator, CK-2017357, as a means to increase muscle strength by amplifying the response of muscle when neural input is otherwise diminished secondary to neuromuscular disease.\n[2] Binding selectively to the fast-skeletal-troponin complex, CK-2017357 slows the rate of calcium release from troponin C and sensitizes muscle to calcium.\n[3] As a consequence, the force-calcium relationship of muscle fibers shifts leftwards, as does the force-frequency relationship of a nerve-muscle pair, so that CK-2017357 increases the production of muscle force in situ at sub-maximal nerve stimulation rates.\n[4] Notably, we show that sensitization of the fast-skeletal-troponin complex to calcium improves muscle force and grip strength immediately after administration of single doses of CK-2017357 in a model of the neuromuscular disease myasthenia gravis.\n[5] Troponin activation may provide a new therapeutic approach to improve physical activity in diseases where neuromuscular function is compromised."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"We developed a small-molecule fast-skeletal-troponin activator, CK-2017357, as a means to increase muscle strength by amplifying the response of muscle when neural input is otherwise diminished secondary to neuromuscular disease.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1305, "doc_id": 12631697, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [12631697], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Tirasemtiv targets fast-twitch muscle.\n\nDocument title: Activation of fast skeletal muscle troponin as a potential therapeutic approach for treating neuromuscular diseases\n\nAbstract sentences:\n[0] Limited neural input results in muscle weakness in neuromuscular disease because of a reduction in the density of muscle innervation, the rate of neuromuscular junction activation or the efficiency of synaptic transmission.\n[1] We developed a small-molecule fast-skeletal-troponin activator, CK-2017357, as a means to increase muscle strength by amplifying the response of muscle when neural input is otherwise diminished secondary to neuromuscular disease.\n[2] Binding selectively to the fast-skeletal-troponin complex, CK-2017357 slows the rate of calcium release from troponin C and sensitizes muscle to calcium.\n[3] As a consequence, the force-calcium relationship of muscle fibers shifts leftwards, as does the force-frequency relationship of a nerve-muscle pair, so that CK-2017357 increases the production of muscle force in situ at sub-maximal nerve stimulation rates.\n[4] Notably, we show that sensitization of the fast-skeletal-troponin complex to calcium improves muscle force and grip strength immediately after administration of single doses of CK-2017357 in a model of the neuromuscular disease myasthenia gravis.\n[5] Troponin activation may provide a new therapeutic approach to improve physical activity in diseases where neuromuscular function is compromised."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Binding selectively to the fast-skeletal-troponin complex, CK-2017357 slows the rate of calcium release from troponin C and sensitizes muscle to calcium.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1305, "doc_id": 12631697, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [12631697], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Toll-like receptor (TLR) signaling is involved in the pathogenesis of human MDS.\n\nDocument title: The NLRP3 inflammasome functions as a driver of the myelodysplastic syndrome phenotype.\n\nAbstract sentences:\n[0] Despite genetic heterogeneity, myelodysplastic syndromes (MDSs) share features of cytological dysplasia and ineffective hematopoiesis.\n[1] We report that a hallmark of MDSs is activation of the NLRP3 inflammasome, which drives clonal expansion and pyroptotic cell death.\n[2] Independent of genotype, MDS hematopoietic stem and progenitor cells (HSPCs) overexpress inflammasome proteins and manifest activated NLRP3 complexes that direct activation of caspase-1, generation of interleukin-1β (IL-1β) and IL-18, and pyroptotic cell death.\n[3] Mechanistically, pyroptosis is triggered by the alarmin S100A9 that is found in excess in MDS HSPCs and bone marrow plasma.\n[4] Further, like somatic gene mutations, S100A9-induced signaling activates NADPH oxidase (NOX), increasing levels of reactive oxygen species (ROS) that initiate cation influx, cell swelling, and β-catenin activation.\n[5] Notably, knockdown of NLRP3 or caspase-1, neutralization of S100A9, and pharmacologic inhibition of NLRP3 or NOX suppress pyroptosis, ROS generation, and nuclear β-catenin in MDSs and are sufficient to restore effective hematopoiesis.\n[6] Thus, alarmins and founder gene mutations in MDSs license a common redox-sensitive inflammasome circuit, which suggests new avenues for therapeutic intervention."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1306, "doc_id": 6000423, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [6000423, 5836], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Tonic signaling from the scFv induces constitutive stimulation.\n\nDocument title: 4-1BB Costimulation Ameliorates T Cell Exhaustion Induced by Tonic Signaling of Chimeric Antigen Receptors\n\nAbstract sentences:\n[0] Chimeric antigen receptors (CARs) targeting CD19 have mediated dramatic antitumor responses in hematologic malignancies, but tumor regression has rarely occurred using CARs targeting other antigens.\n[1] It remains unknown whether the impressive effects of CD19 CARs relate to greater susceptibility of hematologic malignancies to CAR therapies, or superior functionality of the CD19 CAR itself.\n[2] We show that tonic CAR CD3-ζ phosphorylation, triggered by antigen-independent clustering of CAR single-chain variable fragments, can induce early exhaustion of CAR T cells that limits antitumor efficacy.\n[3] Such activation is present to varying degrees in all CARs studied, except the highly effective CD19 CAR.\n[4] We further determine that CD28 costimulation augments, whereas 4-1BB costimulation reduces, exhaustion induced by persistent CAR signaling.\n[5] Our results provide biological explanations for the antitumor effects of CD19 CARs and for the observations that CD19 CAR T cells incorporating the 4-1BB costimulatory domain are more persistent than those incorporating CD28 in clinical trials."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1307, "doc_id": 18231807, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [18231807], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Tonic signaling from the scFv is amplified by MyD88/CD40.\n\nDocument title: 4-1BB Costimulation Ameliorates T Cell Exhaustion Induced by Tonic Signaling of Chimeric Antigen Receptors\n\nAbstract sentences:\n[0] Chimeric antigen receptors (CARs) targeting CD19 have mediated dramatic antitumor responses in hematologic malignancies, but tumor regression has rarely occurred using CARs targeting other antigens.\n[1] It remains unknown whether the impressive effects of CD19 CARs relate to greater susceptibility of hematologic malignancies to CAR therapies, or superior functionality of the CD19 CAR itself.\n[2] We show that tonic CAR CD3-ζ phosphorylation, triggered by antigen-independent clustering of CAR single-chain variable fragments, can induce early exhaustion of CAR T cells that limits antitumor efficacy.\n[3] Such activation is present to varying degrees in all CARs studied, except the highly effective CD19 CAR.\n[4] We further determine that CD28 costimulation augments, whereas 4-1BB costimulation reduces, exhaustion induced by persistent CAR signaling.\n[5] Our results provide biological explanations for the antitumor effects of CD19 CARs and for the observations that CD19 CAR T cells incorporating the 4-1BB costimulatory domain are more persistent than those incorporating CD28 in clinical trials."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1308, "doc_id": 18231807, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [18231807], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Tonic signaling from the scFv prevents constitutive stimulation.\n\nDocument title: 4-1BB Costimulation Ameliorates T Cell Exhaustion Induced by Tonic Signaling of Chimeric Antigen Receptors\n\nAbstract sentences:\n[0] Chimeric antigen receptors (CARs) targeting CD19 have mediated dramatic antitumor responses in hematologic malignancies, but tumor regression has rarely occurred using CARs targeting other antigens.\n[1] It remains unknown whether the impressive effects of CD19 CARs relate to greater susceptibility of hematologic malignancies to CAR therapies, or superior functionality of the CD19 CAR itself.\n[2] We show that tonic CAR CD3-ζ phosphorylation, triggered by antigen-independent clustering of CAR single-chain variable fragments, can induce early exhaustion of CAR T cells that limits antitumor efficacy.\n[3] Such activation is present to varying degrees in all CARs studied, except the highly effective CD19 CAR.\n[4] We further determine that CD28 costimulation augments, whereas 4-1BB costimulation reduces, exhaustion induced by persistent CAR signaling.\n[5] Our results provide biological explanations for the antitumor effects of CD19 CARs and for the observations that CD19 CAR T cells incorporating the 4-1BB costimulatory domain are more persistent than those incorporating CD28 in clinical trials."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1309, "doc_id": 18231807, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [18231807], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Traditional reviews are biased in their interpretations.\n\nDocument title: Systematic reviews from astronomy to zoology: myths and misconceptions.\n\nAbstract sentences:\n[0] Systematic literature reviews are widely used as an aid to evidence based decision making.\n[1] For example, reviews of randomised controlled trials are regularly used to answer questions about the effectiveness of healthcare interventions.\n[2] The high profile of systematic reviews as a cornerstone of evidence based medicine, however, has led to several misconceptions about their purpose and methods.\n[3] Among these is the belief that systematic reviews are applicable only to randomised controlled trials and that they are incapable of dealing with other forms of evidence, such as from non-randomised studies or qualitative research.\n[4] The systematic literature review is a method of locating, appraising, and synthesising evidence.\n[5] The value of regularly updated systematic reviews in the assessment of effectiveness of healthcare interventions was dramatically illustrated by Antman and colleagues, who showed that review articles failed to mention advances in treatment identified by an updated systematic review.1  It is nearly a quarter of a century since Gene Glass coined the term “meta-analysis” to refer to the quantitative synthesis of the results of primary studies.2 The importance of making explicit efforts to limit bias in the review of literature, however, has been emphasised by social scientists at least since the 1960s.3 In recent years systematic reviews have found an important role in health services research, and the growing interest in evidence based approaches to decision making makes it likely that their use will increase.\n[6] Not everybody accepts that systematic reviews are necessary or desirable, and as one moves further away from the clinical applications of systematic reviews cynicism about their utility grows.\n[7] Several arguments are commonly used to reject a wider role for systematic reviews, and these arguments are often based on major misconceptions about the history, purpose, methods, and uses of systematic reviews.\n[8] I have examined eight common myths about …"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1310, "doc_id": 8042158, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [8042158], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Trans-acting factors, such as lncRNAs, influence mRNA translation.\n\nDocument title: LincRNA-p21 suppresses target mRNA translation.\n\nAbstract sentences:\n[0] Mammalian long intergenic noncoding RNAs (lincRNAs) are best known for modulating transcription.\n[1] Here we report a posttranscriptional function for lincRNA-p21 as a modulator of translation.\n[2] Association of the RNA-binding protein HuR with lincRNA-p21 favored the recruitment of let-7/Ago2 to lincRNA-p21, leading to lower lincRNA-p21 stability.\n[3] Under reduced HuR levels, lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation.\n[4] With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and β-catenin translation and increased the levels of these proteins.\n[5] We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels.\n[6] Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Here we report a posttranscriptional function for lincRNA-p21 as a modulator of translation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1311, "doc_id": 13763195, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [13763195], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Trans-acting factors, such as lncRNAs, influence mRNA translation.\n\nDocument title: LincRNA-p21 suppresses target mRNA translation.\n\nAbstract sentences:\n[0] Mammalian long intergenic noncoding RNAs (lincRNAs) are best known for modulating transcription.\n[1] Here we report a posttranscriptional function for lincRNA-p21 as a modulator of translation.\n[2] Association of the RNA-binding protein HuR with lincRNA-p21 favored the recruitment of let-7/Ago2 to lincRNA-p21, leading to lower lincRNA-p21 stability.\n[3] Under reduced HuR levels, lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation.\n[4] With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and β-catenin translation and increased the levels of these proteins.\n[5] We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels.\n[6] Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Under reduced HuR levels, lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1311, "doc_id": 13763195, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [13763195], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Trans-acting factors, such as lncRNAs, influence mRNA translation.\n\nDocument title: LincRNA-p21 suppresses target mRNA translation.\n\nAbstract sentences:\n[0] Mammalian long intergenic noncoding RNAs (lincRNAs) are best known for modulating transcription.\n[1] Here we report a posttranscriptional function for lincRNA-p21 as a modulator of translation.\n[2] Association of the RNA-binding protein HuR with lincRNA-p21 favored the recruitment of let-7/Ago2 to lincRNA-p21, leading to lower lincRNA-p21 stability.\n[3] Under reduced HuR levels, lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation.\n[4] With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and β-catenin translation and increased the levels of these proteins.\n[5] We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels.\n[6] Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and β-catenin translation and increased the levels of these proteins.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1311, "doc_id": 13763195, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [13763195], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Trans-acting factors, such as lncRNAs, influence mRNA translation.\n\nDocument title: LincRNA-p21 suppresses target mRNA translation.\n\nAbstract sentences:\n[0] Mammalian long intergenic noncoding RNAs (lincRNAs) are best known for modulating transcription.\n[1] Here we report a posttranscriptional function for lincRNA-p21 as a modulator of translation.\n[2] Association of the RNA-binding protein HuR with lincRNA-p21 favored the recruitment of let-7/Ago2 to lincRNA-p21, leading to lower lincRNA-p21 stability.\n[3] Under reduced HuR levels, lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation.\n[4] With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and β-catenin translation and increased the levels of these proteins.\n[5] We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels.\n[6] Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1311, "doc_id": 13763195, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [13763195], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Trans-acting factors, such as lncRNAs, influence mRNA translation.\n\nDocument title: LincRNA-p21 suppresses target mRNA translation.\n\nAbstract sentences:\n[0] Mammalian long intergenic noncoding RNAs (lincRNAs) are best known for modulating transcription.\n[1] Here we report a posttranscriptional function for lincRNA-p21 as a modulator of translation.\n[2] Association of the RNA-binding protein HuR with lincRNA-p21 favored the recruitment of let-7/Ago2 to lincRNA-p21, leading to lower lincRNA-p21 stability.\n[3] Under reduced HuR levels, lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation.\n[4] With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and β-catenin translation and increased the levels of these proteins.\n[5] We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels.\n[6] Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1311, "doc_id": 13763195, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [13763195], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Transcription factor EB induces transcription of pro-inflammatory cytokines in macrophages infected with Staphylococcus aureus.\n\nDocument title: Innate host defense requires TFEB-mediated transcription of cytoprotective and antimicrobial genes.\n\nAbstract sentences:\n[0] Animal host defense against infection requires the expression of defense genes at the right place and the right time.\n[1] Understanding such tight control of host defense requires the elucidation of the transcription factors involved.\n[2] By using an unbiased approach in the model Caenorhabditis elegans, we discovered that HLH-30 (known as TFEB in mammals) is a key transcription factor for host defense.\n[3] HLH-30 was activated shortly after Staphylococcus aureus infection, and drove the expression of close to 80% of the host response, including antimicrobial and autophagy genes that were essential for host tolerance of infection.\n[4] TFEB was also rapidly activated in murine macrophages upon S. aureus infection and was required for proper transcriptional induction of several proinflammatory cytokines and chemokines.\n[5] Thus, our data suggest that TFEB is a previously unappreciated, evolutionarily ancient transcription factor in the host response to infection."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"TFEB was also rapidly activated in murine macrophages upon S. aureus infection and was required for proper transcriptional induction of several proinflammatory cytokines and chemokines.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1312, "doc_id": 24177706, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [24177706], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Transcription rates in S. cerevisiae range between 0.7 and 2 kb/min.\n\nDocument title: Distinction and relationship between elongation rate and processivity of RNA polymerase II in vivo.\n\nAbstract sentences:\n[0] A number of proteins and drugs have been implicated in the process of transcriptional elongation by RNA polymerase (Pol) II, but the factors that govern the elongation rate (nucleotide additions per min) and processivity (nucleotide additions per initiation event) in vivo are poorly understood.\n[1] Here, we show that a mutation in the Rpb2 subunit of Pol II reduces both the elongation rate and processivity in vivo.\n[2] In contrast, none of the putative elongation factors tested affect the elongation rate, although mutations in the THO complex and in Spt4 significantly reduce processivity.\n[3] The drugs 6-azauracil and mycophenolic acid reduce both the elongation rate and processivity, and this processivity defect is aggravated by mutations in Spt4, TFIIS, and CTDK-1.\n[4] Our results suggest that, in vivo, a reduced rate of Pol II elongation leads to premature dissociation along the chromatin template and that Pol II processivity can be uncoupled from elongation rate."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1314, "doc_id": 13072112, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [13072112, 16237005], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Transcription rates in S. cerevisiae range between 7 and 12 kb/min.\n\nDocument title: Distinction and relationship between elongation rate and processivity of RNA polymerase II in vivo.\n\nAbstract sentences:\n[0] A number of proteins and drugs have been implicated in the process of transcriptional elongation by RNA polymerase (Pol) II, but the factors that govern the elongation rate (nucleotide additions per min) and processivity (nucleotide additions per initiation event) in vivo are poorly understood.\n[1] Here, we show that a mutation in the Rpb2 subunit of Pol II reduces both the elongation rate and processivity in vivo.\n[2] In contrast, none of the putative elongation factors tested affect the elongation rate, although mutations in the THO complex and in Spt4 significantly reduce processivity.\n[3] The drugs 6-azauracil and mycophenolic acid reduce both the elongation rate and processivity, and this processivity defect is aggravated by mutations in Spt4, TFIIS, and CTDK-1.\n[4] Our results suggest that, in vivo, a reduced rate of Pol II elongation leads to premature dissociation along the chromatin template and that Pol II processivity can be uncoupled from elongation rate."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1315, "doc_id": 13072112, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [13072112, 16237005], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Transplanted human glial progenitor cells can mature in their host animal.\n\nDocument title: Forebrain engraftment by human glial progenitor cells enhances synaptic plasticity and learning in adult mice.\n\nAbstract sentences:\n[0] Human astrocytes are larger and more complex than those of infraprimate mammals, suggesting that their role in neural processing has expanded with evolution.\n[1] To assess the cell-autonomous and species-selective properties of human glia, we engrafted human glial progenitor cells (GPCs) into neonatal immunodeficient mice.\n[2] Upon maturation, the recipient brains exhibited large numbers and high proportions of both human glial progenitors and astrocytes.\n[3] The engrafted human glia were gap-junction-coupled to host astroglia, yet retained the size and pleomorphism of hominid astroglia, and propagated Ca2+ signals 3-fold faster than their hosts.\n[4] Long-term potentiation (LTP) was sharply enhanced in the human glial chimeric mice, as was their learning, as assessed by Barnes maze navigation, object-location memory, and both contextual and tone fear conditioning.\n[5] Mice allografted with murine GPCs showed no enhancement of either LTP or learning.\n[6] These findings indicate that human glia differentially enhance both activity-dependent plasticity and learning in mice."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Upon maturation, the recipient brains exhibited large numbers and high proportions of both human glial progenitors and astrocytes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1322, "doc_id": 16284655, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [16284655], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Treatment with a protein named FN impairs regenerative abilities of aged muscles.\n\nDocument title: Loss of fibronectin from the aged stem cell niche affects the regenerative capacity of skeletal muscle in mice\n\nAbstract sentences:\n[0] Age-related changes in the niche have long been postulated to impair the function of somatic stem cells.\n[1] Here we demonstrate that the aged stem cell niche in skeletal muscle contains substantially reduced levels of fibronectin (FN), leading to detrimental consequences for the function and maintenance of muscle stem cells (MuSCs).\n[2] Deletion of the gene encoding FN from young regenerating muscles replicates the aging phenotype and leads to a loss of MuSC numbers.\n[3] By using an extracellular matrix (ECM) library screen and pathway profiling, we characterize FN as a preferred adhesion substrate for MuSCs and demonstrate that integrin-mediated signaling through focal adhesion kinase and the p38 mitogen-activated protein kinase pathway is strongly de-regulated in MuSCs from aged mice because of insufficient attachment to the niche.\n[4] Reconstitution of FN levels in the aged niche remobilizes stem cells and restores youth-like muscle regeneration.\n[5] Taken together, we identify the loss of stem cell adhesion to FN in the niche ECM as a previously unknown aging mechanism."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Deletion of the gene encoding FN from young regenerating muscles replicates the aging phenotype and leads to a loss of MuSC numbers.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1323, "doc_id": 19912367, "label": "CONTRADICTS", "evidence_sentence_ids": [2], "cited_doc_ids": [19912367], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Treatment with a protein named FN impairs regenerative abilities of aged muscles.\n\nDocument title: Loss of fibronectin from the aged stem cell niche affects the regenerative capacity of skeletal muscle in mice\n\nAbstract sentences:\n[0] Age-related changes in the niche have long been postulated to impair the function of somatic stem cells.\n[1] Here we demonstrate that the aged stem cell niche in skeletal muscle contains substantially reduced levels of fibronectin (FN), leading to detrimental consequences for the function and maintenance of muscle stem cells (MuSCs).\n[2] Deletion of the gene encoding FN from young regenerating muscles replicates the aging phenotype and leads to a loss of MuSC numbers.\n[3] By using an extracellular matrix (ECM) library screen and pathway profiling, we characterize FN as a preferred adhesion substrate for MuSCs and demonstrate that integrin-mediated signaling through focal adhesion kinase and the p38 mitogen-activated protein kinase pathway is strongly de-regulated in MuSCs from aged mice because of insufficient attachment to the niche.\n[4] Reconstitution of FN levels in the aged niche remobilizes stem cells and restores youth-like muscle regeneration.\n[5] Taken together, we identify the loss of stem cell adhesion to FN in the niche ECM as a previously unknown aging mechanism."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Reconstitution of FN levels in the aged niche remobilizes stem cells and restores youth-like muscle regeneration.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1323, "doc_id": 19912367, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [19912367], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Treatment with a protein named FN restores regenerative abilities of aged muscles.\n\nDocument title: Loss of fibronectin from the aged stem cell niche affects the regenerative capacity of skeletal muscle in mice\n\nAbstract sentences:\n[0] Age-related changes in the niche have long been postulated to impair the function of somatic stem cells.\n[1] Here we demonstrate that the aged stem cell niche in skeletal muscle contains substantially reduced levels of fibronectin (FN), leading to detrimental consequences for the function and maintenance of muscle stem cells (MuSCs).\n[2] Deletion of the gene encoding FN from young regenerating muscles replicates the aging phenotype and leads to a loss of MuSC numbers.\n[3] By using an extracellular matrix (ECM) library screen and pathway profiling, we characterize FN as a preferred adhesion substrate for MuSCs and demonstrate that integrin-mediated signaling through focal adhesion kinase and the p38 mitogen-activated protein kinase pathway is strongly de-regulated in MuSCs from aged mice because of insufficient attachment to the niche.\n[4] Reconstitution of FN levels in the aged niche remobilizes stem cells and restores youth-like muscle regeneration.\n[5] Taken together, we identify the loss of stem cell adhesion to FN in the niche ECM as a previously unknown aging mechanism."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Deletion of the gene encoding FN from young regenerating muscles replicates the aging phenotype and leads to a loss of MuSC numbers.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1324, "doc_id": 19912367, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [19912367], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Treatment with a protein named FN restores regenerative abilities of aged muscles.\n\nDocument title: Loss of fibronectin from the aged stem cell niche affects the regenerative capacity of skeletal muscle in mice\n\nAbstract sentences:\n[0] Age-related changes in the niche have long been postulated to impair the function of somatic stem cells.\n[1] Here we demonstrate that the aged stem cell niche in skeletal muscle contains substantially reduced levels of fibronectin (FN), leading to detrimental consequences for the function and maintenance of muscle stem cells (MuSCs).\n[2] Deletion of the gene encoding FN from young regenerating muscles replicates the aging phenotype and leads to a loss of MuSC numbers.\n[3] By using an extracellular matrix (ECM) library screen and pathway profiling, we characterize FN as a preferred adhesion substrate for MuSCs and demonstrate that integrin-mediated signaling through focal adhesion kinase and the p38 mitogen-activated protein kinase pathway is strongly de-regulated in MuSCs from aged mice because of insufficient attachment to the niche.\n[4] Reconstitution of FN levels in the aged niche remobilizes stem cells and restores youth-like muscle regeneration.\n[5] Taken together, we identify the loss of stem cell adhesion to FN in the niche ECM as a previously unknown aging mechanism."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Reconstitution of FN levels in the aged niche remobilizes stem cells and restores youth-like muscle regeneration.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1324, "doc_id": 19912367, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [19912367], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Treatment with the EC uptake inhibitor AM404 resulted in a dose-dependent decrease in the expression of immobility.\n\nDocument title: Functional role of high-affinity anandamide transport, as revealed by selective inhibition.\n\nAbstract sentences:\n[0] Anandamide, an endogenous ligand for central cannabinoid receptors, is released from neurons on depolarization and rapidly inactivated.\n[1] Anandamide inactivation is not completely understood, but it may occur by transport into cells or by enzymatic hydrolysis.\n[2] The compound N-(4-hydroxyphenyl)arachidonylamide (AM404) was shown to inhibit high-affinity anandamide accumulation in rat neurons and astrocytes in vitro, an indication that this accumulation resulted from carrier-mediated transport.\n[3] Although AM404 did not activate cannabinoid receptors or inhibit anandamide hydrolysis, it enhanced receptor-mediated anandamide responses in vitro and in vivo.\n[4] The data indicate that carrier-mediated transport may be essential for termination of the biological effects of anandamide, and may represent a potential drug target."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1325, "doc_id": 40476126, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [40476126], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Tuberculosis incidence occurs at higher rates in more sparsely populated areas in the UK.\n\nDocument title: Ecological analysis of ethnic differences in relation between tuberculosis and poverty.\n\nAbstract sentences:\n[0] OBJECTIVE To examine the effect of ethnicity on the relation between tuberculosis and deprivation.\n[1] DESIGN Retrospective ecological study comparing incidence of tuberculosis in white and south Asian residents of the 39 electoral wards in Birmingham with ethnic specific indices of deprivation.\n[2] SETTING Birmingham, 1989-93.\n[3] SUBJECTS 1516 notified cases of tuberculosis.\n[4] MAIN OUTCOME MEASURES Rates of tuberculosis and measures of deprivation.\n[5] RESULTS Univariate analysis showed significant associations of tuberculosis rates for the whole population with several indices of deprivation (P<0.01) and with the proportion of the population of south Asian origin (P<0.01).\n[6] All deprivation covariates were positively associated with each other but on multiple regression, higher level of overcrowding was independently associated with tuberculosis rates.\n[7] For the white population, overcrowding was associated with tuberculosis rates independently of other variables (P=0.0036).\n[8] No relation with deprivation was found for the south Asian population in either single or multivariable analyses.\n[9] CONCLUSIONS Poverty is significantly associated with tuberculosis in the white population, but no such relation exists for those of Asian ethnicity.\n[10] These findings suggest that causal factors, and therefore potential interventions, will also differ by ethnic group."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"All deprivation covariates were positively associated with each other but on multiple regression, higher level of overcrowding was independently associated with tuberculosis rates.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1327, "doc_id": 24241932, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [24241932, 22194407], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Tuberculosis incidence occurs at higher rates in more sparsely populated areas in the UK.\n\nDocument title: Ecological analysis of ethnic differences in relation between tuberculosis and poverty.\n\nAbstract sentences:\n[0] OBJECTIVE To examine the effect of ethnicity on the relation between tuberculosis and deprivation.\n[1] DESIGN Retrospective ecological study comparing incidence of tuberculosis in white and south Asian residents of the 39 electoral wards in Birmingham with ethnic specific indices of deprivation.\n[2] SETTING Birmingham, 1989-93.\n[3] SUBJECTS 1516 notified cases of tuberculosis.\n[4] MAIN OUTCOME MEASURES Rates of tuberculosis and measures of deprivation.\n[5] RESULTS Univariate analysis showed significant associations of tuberculosis rates for the whole population with several indices of deprivation (P<0.01) and with the proportion of the population of south Asian origin (P<0.01).\n[6] All deprivation covariates were positively associated with each other but on multiple regression, higher level of overcrowding was independently associated with tuberculosis rates.\n[7] For the white population, overcrowding was associated with tuberculosis rates independently of other variables (P=0.0036).\n[8] No relation with deprivation was found for the south Asian population in either single or multivariable analyses.\n[9] CONCLUSIONS Poverty is significantly associated with tuberculosis in the white population, but no such relation exists for those of Asian ethnicity.\n[10] These findings suggest that causal factors, and therefore potential interventions, will also differ by ethnic group."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"For the white population, overcrowding was associated with tuberculosis rates independently of other variables (P=0.0036).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1327, "doc_id": 24241932, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [24241932, 22194407], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Tuberculosis incidence occurs at higher rates in more sparsely populated areas in the UK.\n\nDocument title: Tuberculosis mortality in England and Wales during 1982-1992: its association with poverty, ethnicity and AIDS.\n\nAbstract sentences:\n[0] This paper seeks to establish the strength of association between contemporary tuberculosis (TB) in England and Wales and several potential aetiological factors.\n[1] It presents an ecological analysis of standardised annual TB mortality rates for the 403 local authority districts between 1982 and 1992, disaggregated by age and sex.\n[2] Social, demographic and ethnicity measures from the 1981 and 1991 censuses and standardised annual AIDS-related mortality rates for young men are used to calculate Poisson regression models.\n[3] A strong association was found between all TB mortality groups and overcrowding at the household level.\n[4] For women, no other measures improved the explanatory power of the models.\n[5] In multiple regressions, both poverty and AIDS-related mortality explained additional variation in the model for younger men.\n[6] The link between ethnicity and tuberculosis notifications was not reflected in this analysis of mortality.\n[7] For all groups no evidence of a positive relationship with ethnicity was found, once overcrowding had been accounted for.\n[8] The significance of household as opposed to district level crowding suggests that prolonged contact is required for disease transmission.\n[9] Regression analysis indicates that it is the overcrowding and poverty among ethnic populations that is significant for their tuberculosis mortality.\n[10] The fact that the relationship between AIDS and TB is confined to the group most typical of AIDS patients provides evidence that AIDS has little influence on the level of tuberculosis mortality in the wider population.\n[11] Explanations for the observed relationship include preferential certification, migration for treatment and shortcomings in health care provision."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"A strong association was found between all TB mortality groups and overcrowding at the household level.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1327, "doc_id": 22194407, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [24241932, 22194407], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Tuberculosis incidence occurs at higher rates in more sparsely populated areas in the UK.\n\nDocument title: Tuberculosis mortality in England and Wales during 1982-1992: its association with poverty, ethnicity and AIDS.\n\nAbstract sentences:\n[0] This paper seeks to establish the strength of association between contemporary tuberculosis (TB) in England and Wales and several potential aetiological factors.\n[1] It presents an ecological analysis of standardised annual TB mortality rates for the 403 local authority districts between 1982 and 1992, disaggregated by age and sex.\n[2] Social, demographic and ethnicity measures from the 1981 and 1991 censuses and standardised annual AIDS-related mortality rates for young men are used to calculate Poisson regression models.\n[3] A strong association was found between all TB mortality groups and overcrowding at the household level.\n[4] For women, no other measures improved the explanatory power of the models.\n[5] In multiple regressions, both poverty and AIDS-related mortality explained additional variation in the model for younger men.\n[6] The link between ethnicity and tuberculosis notifications was not reflected in this analysis of mortality.\n[7] For all groups no evidence of a positive relationship with ethnicity was found, once overcrowding had been accounted for.\n[8] The significance of household as opposed to district level crowding suggests that prolonged contact is required for disease transmission.\n[9] Regression analysis indicates that it is the overcrowding and poverty among ethnic populations that is significant for their tuberculosis mortality.\n[10] The fact that the relationship between AIDS and TB is confined to the group most typical of AIDS patients provides evidence that AIDS has little influence on the level of tuberculosis mortality in the wider population.\n[11] Explanations for the observed relationship include preferential certification, migration for treatment and shortcomings in health care provision."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Regression analysis indicates that it is the overcrowding and poverty among ethnic populations that is significant for their tuberculosis mortality.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1327, "doc_id": 22194407, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [24241932, 22194407], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Tuberculosis-induced granulomas express different immune system protein signatures than the surrounding tissue.\n\nDocument title: Inflammatory signaling in human Tuberculosis granulomas is spatially organized\n\nAbstract sentences:\n[0] Granulomas are the pathological hallmark of tuberculosis (TB).\n[1] However, their function and mechanisms of formation remain poorly understood.\n[2] To understand the role of granulomas in TB, we analyzed the proteomes of granulomas from subjects with tuberculosis in an unbiased manner.\n[3] Using laser-capture microdissection, mass spectrometry and confocal microscopy, we generated detailed molecular maps of human granulomas.\n[4] We found that the centers of granulomas have a pro-inflammatory environment that is characterized by the presence of antimicrobial peptides, reactive oxygen species and pro-inflammatory eicosanoids.\n[5] Conversely, the tissue surrounding the caseum has a comparatively anti-inflammatory signature.\n[6] These findings are consistent across a set of six human subjects and in rabbits.\n[7] Although the balance between systemic pro- and anti-inflammatory signals is crucial to TB disease outcome, here we find that these signals are physically segregated within each granuloma.\n[8] From the protein and lipid snapshots of human and rabbit lesions analyzed here, we hypothesize that the pathologic response to TB is shaped by the precise anatomical localization of these inflammatory pathways during the development of the granuloma."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4, 5]\nExplanation: Evidence states: \"We found that the centers of granulomas have a pro-inflammatory environment that is characterized by the presence of antimicrobial peptides, reactive oxygen species and pro-inflammatory eicosanoids. Conversely, the tissue surrounding the caseum has a comparatively anti-inflammatory signature.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1328, "doc_id": 3475317, "label": "SUPPORTS", "evidence_sentence_ids": [4, 5], "cited_doc_ids": [3475317], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Tuberculosis-induced granulomas express different immune system protein signatures than the surrounding tissue.\n\nDocument title: Inflammatory signaling in human Tuberculosis granulomas is spatially organized\n\nAbstract sentences:\n[0] Granulomas are the pathological hallmark of tuberculosis (TB).\n[1] However, their function and mechanisms of formation remain poorly understood.\n[2] To understand the role of granulomas in TB, we analyzed the proteomes of granulomas from subjects with tuberculosis in an unbiased manner.\n[3] Using laser-capture microdissection, mass spectrometry and confocal microscopy, we generated detailed molecular maps of human granulomas.\n[4] We found that the centers of granulomas have a pro-inflammatory environment that is characterized by the presence of antimicrobial peptides, reactive oxygen species and pro-inflammatory eicosanoids.\n[5] Conversely, the tissue surrounding the caseum has a comparatively anti-inflammatory signature.\n[6] These findings are consistent across a set of six human subjects and in rabbits.\n[7] Although the balance between systemic pro- and anti-inflammatory signals is crucial to TB disease outcome, here we find that these signals are physically segregated within each granuloma.\n[8] From the protein and lipid snapshots of human and rabbit lesions analyzed here, we hypothesize that the pathologic response to TB is shaped by the precise anatomical localization of these inflammatory pathways during the development of the granuloma."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Although the balance between systemic pro- and anti-inflammatory signals is crucial to TB disease outcome, here we find that these signals are physically segregated within each granuloma.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1328, "doc_id": 3475317, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [3475317], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Tumor development occurs in conjunction with suppression of pro-inflammatory cytokines.\n\nDocument title: Paraneoplastic thrombocytosis: the secrets of tumor self-promotion.\n\nAbstract sentences:\n[0] Paraneoplastic thrombocytosis is associated with many solid tumors and often correlates with reduced survival.\n[1] Recent studies suggest that a pathogenic feed back loop may be operative between platelets and tumor cells, with reciprocal interactions between tumor growth/metastasis and thrombocytosis/platelet activation.\n[2] Specific molecular pathways have been identified in which tumors can stimulate platelet production and activation; activated platelets can, in turn, promote tumor growth and metastasis.\n[3] Taken together, these findings provide exciting new potential targets for therapeutic intervention."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1330, "doc_id": 14075252, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14075252], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Tumor development occurs in conjunction with upregulation of pro-inflammatory cytokines.\n\nDocument title: Paraneoplastic thrombocytosis: the secrets of tumor self-promotion.\n\nAbstract sentences:\n[0] Paraneoplastic thrombocytosis is associated with many solid tumors and often correlates with reduced survival.\n[1] Recent studies suggest that a pathogenic feed back loop may be operative between platelets and tumor cells, with reciprocal interactions between tumor growth/metastasis and thrombocytosis/platelet activation.\n[2] Specific molecular pathways have been identified in which tumors can stimulate platelet production and activation; activated platelets can, in turn, promote tumor growth and metastasis.\n[3] Taken together, these findings provide exciting new potential targets for therapeutic intervention."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1331, "doc_id": 14075252, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14075252], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Two variants of chromosome 6q21 are associated with radiation therapy-induced second malignancies in pediatric Hodgkin lymphoma patients.\n\nDocument title: Variants at 6q21 implicate PRDM1 in the etiology of therapy-induced second malignancies after Hodgkin's lymphoma\n\nAbstract sentences:\n[0] Survivors of pediatric Hodgkin's lymphoma are at risk for radiation therapy–induced second malignant neoplasms (SMNs).\n[1] We identified two variants at chromosome 6q21 associated with SMNs in survivors of Hodgkin's lymphoma treated with radiation therapy as children but not as adults.\n[2] The variants comprise a risk locus associated with decreased basal expression of PRDM1 (encoding PR domain containing 1, with ZNF domain) and impaired induction of the PRDM1 protein after radiation exposure.\n[3] These data suggest a new gene-exposure interaction that may implicate PRDM1 in the etiology of radiation therapy-induced SMNs."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"We identified two variants at chromosome 6q21 associated with SMNs in survivors of Hodgkin's lymphoma treated with radiation therapy as children but not as adults.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1333, "doc_id": 1649738, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [1649738], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Type 1 Diabetes is associated with subtle perturbations in T reg development.\n\nDocument title: Large-scale genetic fine mapping and genotype-phenotype associations implicate polymorphism in the IL2RA region in type 1 diabetes\n\nAbstract sentences:\n[0] Genome-wide association studies are now identifying disease-associated chromosome regions.\n[1] However, even after convincing replication, the localization of the causal variant(s) requires comprehensive resequencing, extensive genotyping and statistical analyses in large sample sets leading to targeted functional studies.\n[2] Here, we have localized the type 1 diabetes (T1D) association in the interleukin 2 receptor alpha (IL2RA) gene region to two independent groups of SNPs, spanning overlapping regions of 14 and 40 kb, encompassing IL2RA intron 1 and the 5′ regions of IL2RA and RBM17 (odds ratio = 2.04, 95% confidence interval = 1.70–2.45; P = 1.92 × 10−28; control frequency = 0.635).\n[3] Furthermore, we have associated IL2RA T1D susceptibility genotypes with lower circulating levels of the biomarker, soluble IL-2RA (P = 6.28 × 10−28), suggesting that an inherited lower immune responsiveness predisposes to T1D."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here, we have localized the type 1 diabetes (T1D) association in the interleukin 2 receptor alpha (IL2RA) gene region to two independent groups of SNPs, spanning overlapping regions of 14 and 40 kb, encompassing IL2RA intron 1 and the 5′ regions of IL2RA and RBM17 (odds ratio = 2.04, 95% confidence interval = 1.70–2.45; P = 1.92 × 10−28; control frequency = 0.635).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1334, "doc_id": 13940200, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [13923140, 13940200, 11899391], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Type 1 Diabetes is associated with subtle perturbations in T reg development.\n\nDocument title: Large-scale genetic fine mapping and genotype-phenotype associations implicate polymorphism in the IL2RA region in type 1 diabetes\n\nAbstract sentences:\n[0] Genome-wide association studies are now identifying disease-associated chromosome regions.\n[1] However, even after convincing replication, the localization of the causal variant(s) requires comprehensive resequencing, extensive genotyping and statistical analyses in large sample sets leading to targeted functional studies.\n[2] Here, we have localized the type 1 diabetes (T1D) association in the interleukin 2 receptor alpha (IL2RA) gene region to two independent groups of SNPs, spanning overlapping regions of 14 and 40 kb, encompassing IL2RA intron 1 and the 5′ regions of IL2RA and RBM17 (odds ratio = 2.04, 95% confidence interval = 1.70–2.45; P = 1.92 × 10−28; control frequency = 0.635).\n[3] Furthermore, we have associated IL2RA T1D susceptibility genotypes with lower circulating levels of the biomarker, soluble IL-2RA (P = 6.28 × 10−28), suggesting that an inherited lower immune responsiveness predisposes to T1D."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Furthermore, we have associated IL2RA T1D susceptibility genotypes with lower circulating levels of the biomarker, soluble IL-2RA (P = 6.28 × 10−28), suggesting that an inherited lower immune responsiveness predisposes to T1D.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1334, "doc_id": 13940200, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [13923140, 13940200, 11899391], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Type 1 Diabetes is associated with subtle perturbations in T reg development.\n\nDocument title: Type 1 diabetes-associated IL2RA variation lowers IL-2 signaling and contributes to diminished CD4+CD25+ regulatory T cell function.\n\nAbstract sentences:\n[0] Numerous reports have demonstrated that CD4(+)CD25(+) regulatory T cells (Tregs) from individuals with a range of human autoimmune diseases, including type 1 diabetes, are deficient in their ability to control autologous proinflammatory responses when compared with nondiseased, control individuals.\n[1] Treg dysfunction could be a primary, causal event or may result from perturbations in the immune system during disease development.\n[2] Polymorphisms in genes associated with Treg function, such as IL2RA, confer a higher risk of autoimmune disease.\n[3] Although this suggests a primary role for defective Tregs in autoimmunity, a link between IL2RA gene polymorphisms and Treg function has not been examined.\n[4] We addressed this by examining the impact of an IL2RA haplotype associated with type 1 diabetes on Treg fitness and suppressive function.\n[5] Studies were conducted using healthy human subjects to avoid any confounding effects of disease.\n[6] We demonstrated that the presence of an autoimmune disease-associated IL2RA haplotype correlates with diminished IL-2 responsiveness in Ag-experienced CD4(+) T cells, as measured by phosphorylation of STAT5a, and is associated with lower levels of FOXP3 expression by Tregs and a reduction in their ability to suppress proliferation of autologous effector T cells.\n[7] These data offer a rationale that contributes to the molecular and cellular mechanisms through which polymorphisms in the IL-2RA gene affect immune regulation, and consequently upon susceptibility to autoimmune and inflammatory diseases."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Numerous reports have demonstrated that CD4(+)CD25(+) regulatory T cells (Tregs) from individuals with a range of human autoimmune diseases, including type 1 diabetes, are deficient in their ability to control autologous proinflammatory responses when compared with nondiseased, control individuals.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1334, "doc_id": 11899391, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [13923140, 13940200, 11899391], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ultrasound guidance significantly reduces the number of needle insertion attempts necessary for a given procedure.\n\nDocument title: Ultrasound imaging for lumbar punctures and epidural catheterisations: systematic review and meta-analysis.\n\nAbstract sentences:\n[0] OBJECTIVE To determine whether ultrasound imaging can reduce the risk of failed lumbar punctures or epidural catheterisations, when compared with standard palpation methods, and whether ultrasound imaging can reduce traumatic procedures, insertion attempts, and needle redirections.\n[1] DESIGN Systematic review and meta-analysis of randomised controlled trials.\n[2] DATA SOURCES Ovid Medline, Embase, and Cochrane Central Register of Controlled Trials up to May 2012, without restriction by language or publication status.\n[3] REVIEW METHODS Randomised trials that compared ultrasound imaging with standard methods (no imaging) in the performance of a lumbar puncture or epidural catheterisation were identified.\n[4] RESULTS 14 studies with a total of 1334 patients were included (674 patients assigned to the ultrasound group, 660 to the control group).\n[5] Five studies evaluated lumbar punctures and nine evaluated epidural catheterisations.\n[6] Six of 624 procedures conducted in the ultrasound group failed; 44 of 610 procedures in the control group failed.\n[7] Ultrasound imaging reduced the risk of failed procedures (risk ratio 0.21 (95% confidence interval 0.10 to 0.43), P<0.001).\n[8] Risk reduction was similar when subgroup analysis was performed for lumbar punctures (risk ratio 0.19 (0.07 to 0.56), P=0.002) or epidural catheterisations (0.23 (0.09 to 0.60), P=0.003).\n[9] Ultrasound imaging also significantly reduced the risk of traumatic procedures (risk ratio 0.27 (0.11 to 0.67), P=0.005), the number of insertion attempts (mean difference -0.44 (-0.64 to -0.24), P<0.001), and the number of needle redirections (mean difference -1.00 (-1.24 to -0.75), P<0.001).\n[10] CONCLUSIONS Ultrasound imaging can reduce the risk of failed or traumatic lumbar punctures and epidural catheterisations, as well as the number of needle insertions and redirections.\n[11] Ultrasound may be a useful adjunct for these procedures."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Ultrasound imaging also significantly reduced the risk of traumatic procedures (risk ratio 0.27 (0.11 to 0.67), P=0.005), the number of insertion attempts (mean difference -0.44 (-0.64 to -0.24), P<0.001), and the number of needle redirections (mean difference -1.00 (-1.24 to -0.75), P<0.001).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1340, "doc_id": 15482274, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [15482274], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ultrasound guidance significantly reduces the number of needle insertion attempts necessary for a given procedure.\n\nDocument title: Ultrasound imaging for lumbar punctures and epidural catheterisations: systematic review and meta-analysis.\n\nAbstract sentences:\n[0] OBJECTIVE To determine whether ultrasound imaging can reduce the risk of failed lumbar punctures or epidural catheterisations, when compared with standard palpation methods, and whether ultrasound imaging can reduce traumatic procedures, insertion attempts, and needle redirections.\n[1] DESIGN Systematic review and meta-analysis of randomised controlled trials.\n[2] DATA SOURCES Ovid Medline, Embase, and Cochrane Central Register of Controlled Trials up to May 2012, without restriction by language or publication status.\n[3] REVIEW METHODS Randomised trials that compared ultrasound imaging with standard methods (no imaging) in the performance of a lumbar puncture or epidural catheterisation were identified.\n[4] RESULTS 14 studies with a total of 1334 patients were included (674 patients assigned to the ultrasound group, 660 to the control group).\n[5] Five studies evaluated lumbar punctures and nine evaluated epidural catheterisations.\n[6] Six of 624 procedures conducted in the ultrasound group failed; 44 of 610 procedures in the control group failed.\n[7] Ultrasound imaging reduced the risk of failed procedures (risk ratio 0.21 (95% confidence interval 0.10 to 0.43), P<0.001).\n[8] Risk reduction was similar when subgroup analysis was performed for lumbar punctures (risk ratio 0.19 (0.07 to 0.56), P=0.002) or epidural catheterisations (0.23 (0.09 to 0.60), P=0.003).\n[9] Ultrasound imaging also significantly reduced the risk of traumatic procedures (risk ratio 0.27 (0.11 to 0.67), P=0.005), the number of insertion attempts (mean difference -0.44 (-0.64 to -0.24), P<0.001), and the number of needle redirections (mean difference -1.00 (-1.24 to -0.75), P<0.001).\n[10] CONCLUSIONS Ultrasound imaging can reduce the risk of failed or traumatic lumbar punctures and epidural catheterisations, as well as the number of needle insertions and redirections.\n[11] Ultrasound may be a useful adjunct for these procedures."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"CONCLUSIONS Ultrasound imaging can reduce the risk of failed or traumatic lumbar punctures and epidural catheterisations, as well as the number of needle insertions and redirections.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1340, "doc_id": 15482274, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [15482274], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ultrasound guidance significantly reduces the number of traumatic procedures when attempting needle insertion.\n\nDocument title: Ultrasound imaging for lumbar punctures and epidural catheterisations: systematic review and meta-analysis.\n\nAbstract sentences:\n[0] OBJECTIVE To determine whether ultrasound imaging can reduce the risk of failed lumbar punctures or epidural catheterisations, when compared with standard palpation methods, and whether ultrasound imaging can reduce traumatic procedures, insertion attempts, and needle redirections.\n[1] DESIGN Systematic review and meta-analysis of randomised controlled trials.\n[2] DATA SOURCES Ovid Medline, Embase, and Cochrane Central Register of Controlled Trials up to May 2012, without restriction by language or publication status.\n[3] REVIEW METHODS Randomised trials that compared ultrasound imaging with standard methods (no imaging) in the performance of a lumbar puncture or epidural catheterisation were identified.\n[4] RESULTS 14 studies with a total of 1334 patients were included (674 patients assigned to the ultrasound group, 660 to the control group).\n[5] Five studies evaluated lumbar punctures and nine evaluated epidural catheterisations.\n[6] Six of 624 procedures conducted in the ultrasound group failed; 44 of 610 procedures in the control group failed.\n[7] Ultrasound imaging reduced the risk of failed procedures (risk ratio 0.21 (95% confidence interval 0.10 to 0.43), P<0.001).\n[8] Risk reduction was similar when subgroup analysis was performed for lumbar punctures (risk ratio 0.19 (0.07 to 0.56), P=0.002) or epidural catheterisations (0.23 (0.09 to 0.60), P=0.003).\n[9] Ultrasound imaging also significantly reduced the risk of traumatic procedures (risk ratio 0.27 (0.11 to 0.67), P=0.005), the number of insertion attempts (mean difference -0.44 (-0.64 to -0.24), P<0.001), and the number of needle redirections (mean difference -1.00 (-1.24 to -0.75), P<0.001).\n[10] CONCLUSIONS Ultrasound imaging can reduce the risk of failed or traumatic lumbar punctures and epidural catheterisations, as well as the number of needle insertions and redirections.\n[11] Ultrasound may be a useful adjunct for these procedures."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7, 8, 9]\nExplanation: Evidence states: \"Ultrasound imaging reduced the risk of failed procedures (risk ratio 0.21 (95% confidence interval 0.10 to 0.43), P<0.001). Risk reduction was similar when subgroup analysis was performed for lumbar punctures (risk ratio 0.19 (0.07 to 0.56), P=0.002) or epidural catheterisations (0.23 (0.09 to 0.60), P=0.003). Ultrasound imaging also significantly reduced the risk of traumatic procedures (risk ratio 0.27 (0.11 to 0.67), P=0.005), the number of insertion attempts (mean difference -0.44 (-0.64 to -0.24), P<0.001), and the number of needle redirections (mean difference -1.00 (-1.24 to -0.75), P<0.001).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1341, "doc_id": 15482274, "label": "SUPPORTS", "evidence_sentence_ids": [7, 8, 9], "cited_doc_ids": [15482274], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ultrasound guidance significantly reduces the number of traumatic procedures when attempting needle insertion.\n\nDocument title: Ultrasound imaging for lumbar punctures and epidural catheterisations: systematic review and meta-analysis.\n\nAbstract sentences:\n[0] OBJECTIVE To determine whether ultrasound imaging can reduce the risk of failed lumbar punctures or epidural catheterisations, when compared with standard palpation methods, and whether ultrasound imaging can reduce traumatic procedures, insertion attempts, and needle redirections.\n[1] DESIGN Systematic review and meta-analysis of randomised controlled trials.\n[2] DATA SOURCES Ovid Medline, Embase, and Cochrane Central Register of Controlled Trials up to May 2012, without restriction by language or publication status.\n[3] REVIEW METHODS Randomised trials that compared ultrasound imaging with standard methods (no imaging) in the performance of a lumbar puncture or epidural catheterisation were identified.\n[4] RESULTS 14 studies with a total of 1334 patients were included (674 patients assigned to the ultrasound group, 660 to the control group).\n[5] Five studies evaluated lumbar punctures and nine evaluated epidural catheterisations.\n[6] Six of 624 procedures conducted in the ultrasound group failed; 44 of 610 procedures in the control group failed.\n[7] Ultrasound imaging reduced the risk of failed procedures (risk ratio 0.21 (95% confidence interval 0.10 to 0.43), P<0.001).\n[8] Risk reduction was similar when subgroup analysis was performed for lumbar punctures (risk ratio 0.19 (0.07 to 0.56), P=0.002) or epidural catheterisations (0.23 (0.09 to 0.60), P=0.003).\n[9] Ultrasound imaging also significantly reduced the risk of traumatic procedures (risk ratio 0.27 (0.11 to 0.67), P=0.005), the number of insertion attempts (mean difference -0.44 (-0.64 to -0.24), P<0.001), and the number of needle redirections (mean difference -1.00 (-1.24 to -0.75), P<0.001).\n[10] CONCLUSIONS Ultrasound imaging can reduce the risk of failed or traumatic lumbar punctures and epidural catheterisations, as well as the number of needle insertions and redirections.\n[11] Ultrasound may be a useful adjunct for these procedures."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"CONCLUSIONS Ultrasound imaging can reduce the risk of failed or traumatic lumbar punctures and epidural catheterisations, as well as the number of needle insertions and redirections.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1341, "doc_id": 15482274, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [15482274], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Understanding epigenetic regulation of replication is essential for the reational design of episomally replicating vectors.\n\nDocument title: Global Reorganization of Replication Domains During Embryonic Stem Cell Differentiation\n\nAbstract sentences:\n[0] DNA replication in mammals is regulated via the coordinate firing of clusters of replicons that duplicate megabase-sized chromosome segments at specific times during S-phase.\n[1] Cytogenetic studies show that these \"replicon clusters\" coalesce as subchromosomal units that persist through multiple cell generations, but the molecular boundaries of such units have remained elusive.\n[2] Moreover, the extent to which changes in replication timing occur during differentiation and their relationship to transcription changes has not been rigorously investigated.\n[3] We have constructed high-resolution replication-timing profiles in mouse embryonic stem cells (mESCs) before and after differentiation to neural precursor cells.\n[4] We demonstrate that chromosomes can be segmented into multimegabase domains of coordinate replication, which we call \"replication domains,\" separated by transition regions whose replication kinetics are consistent with large originless segments.\n[5] The molecular boundaries of replication domains are remarkably well conserved between distantly related ESC lines and induced pluripotent stem cells.\n[6] Unexpectedly, ESC differentiation was accompanied by the consolidation of smaller differentially replicating domains into larger coordinately replicated units whose replication time was more aligned to isochore GC content and the density of LINE-1 transposable elements, but not gene density.\n[7] Replication-timing changes were coordinated with transcription changes for weak promoters more than strong promoters, and were accompanied by rearrangements in subnuclear position.\n[8] We conclude that replication profiles are cell-type specific, and changes in these profiles reveal chromosome segments that undergo large changes in organization during differentiation.\n[9] Moreover, smaller replication domains and a higher density of timing transition regions that interrupt isochore replication timing define a novel characteristic of the pluripotent state."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1342, "doc_id": 8148122, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [8148122], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Up-regulation of the p53 pathway and related molecular events speeds cancer progression.\n\nDocument title: Senescent Cells, Tumor Suppression, and Organismal Aging: Good Citizens, Bad Neighbors\n\nAbstract sentences:\n[0] Cells from organisms with renewable tissues can permanently withdraw from the cell cycle in response to diverse stress, including dysfunctional telomeres, DNA damage, strong mitogenic signals, and disrupted chromatin.\n[1] This response, termed cellular senescence, is controlled by the p53 and RB tumor suppressor proteins and constitutes a potent anticancer mechanism.\n[2] Nonetheless, senescent cells acquire phenotypic changes that may contribute to aging and certain age-related diseases, including late-life cancer.\n[3] Thus, the senescence response may be antagonistically pleiotropic, promoting early-life survival by curtailing the development of cancer but eventually limiting longevity as dysfunctional senescent cells accumulate."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1345, "doc_id": 9559146, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [9559146], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Upon developing tyrosine-kinase inhibitor resistance, new mutations in epidermal growth factor receptors emerge and cause treatment failure.\n\nDocument title: Acquired EGFR C797S mutation mediates resistance to AZD9291 in non–small cell lung cancer harboring EGFR T790M\n\nAbstract sentences:\n[0] Here we studied cell-free plasma DNA (cfDNA) collected from subjects with advanced lung cancer whose tumors had developed resistance to the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) AZD9291.\n[1] We first performed next-generation sequencing of cfDNA from seven subjects and detected an acquired EGFR C797S mutation in one; expression of this mutant EGFR construct in a cell line rendered it resistant to AZD9291.\n[2] We then performed droplet digital PCR on serial cfDNA specimens collected from 15 AZD9291-treated subjects.\n[3] All were positive for the T790M mutation before treatment, but upon developing AZD9291 resistance three molecular subtypes emerged: six cases acquired the C797S mutation, five cases maintained the T790M mutation but did not acquire the C797S mutation and four cases lost the T790M mutation despite the presence of the underlying EGFR activating mutation.\n[4] Our findings provide insight into the diversity of mechanisms through which tumors acquire resistance to AZD9291 and highlight the need for therapies that are able to overcome resistance mediated by the EGFR C797S mutation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"We first performed next-generation sequencing of cfDNA from seven subjects and detected an acquired EGFR C797S mutation in one; expression of this mutant EGFR construct in a cell line rendered it resistant to AZD9291.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1346, "doc_id": 9505402, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [9505402], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Upon developing tyrosine-kinase inhibitor resistance, new mutations in epidermal growth factor receptors emerge and cause treatment failure.\n\nDocument title: Acquired EGFR C797S mutation mediates resistance to AZD9291 in non–small cell lung cancer harboring EGFR T790M\n\nAbstract sentences:\n[0] Here we studied cell-free plasma DNA (cfDNA) collected from subjects with advanced lung cancer whose tumors had developed resistance to the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) AZD9291.\n[1] We first performed next-generation sequencing of cfDNA from seven subjects and detected an acquired EGFR C797S mutation in one; expression of this mutant EGFR construct in a cell line rendered it resistant to AZD9291.\n[2] We then performed droplet digital PCR on serial cfDNA specimens collected from 15 AZD9291-treated subjects.\n[3] All were positive for the T790M mutation before treatment, but upon developing AZD9291 resistance three molecular subtypes emerged: six cases acquired the C797S mutation, five cases maintained the T790M mutation but did not acquire the C797S mutation and four cases lost the T790M mutation despite the presence of the underlying EGFR activating mutation.\n[4] Our findings provide insight into the diversity of mechanisms through which tumors acquire resistance to AZD9291 and highlight the need for therapies that are able to overcome resistance mediated by the EGFR C797S mutation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"All were positive for the T790M mutation before treatment, but upon developing AZD9291 resistance three molecular subtypes emerged: six cases acquired the C797S mutation, five cases maintained the T790M mutation but did not acquire the C797S mutation and four cases lost the T790M mutation despite the presence of the underlying EGFR activating mutation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1346, "doc_id": 9505402, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [9505402], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Upon viral challenge, influenza-specific memory CD4+ T cells greatly diminish the early production of inflammatory chemokines in the lung.\n\nDocument title: Memory CD4+ T cells induce innate responses independently of pathogen\n\nAbstract sentences:\n[0] Inflammation induced by recognition of pathogen-associated molecular patterns markedly affects subsequent adaptive responses.\n[1] We asked whether the adaptive immune system can also affect the character and magnitude of innate inflammatory responses.\n[2] We found that the response of memory, but not naive, CD4+ T cells enhances production of multiple innate inflammatory cytokines and chemokines (IICs) in the lung and that, during influenza infection, this leads to early control of virus.\n[3] Memory CD4+ T cell–induced IICs and viral control require cognate antigen recognition and are optimal when memory cells are either T helper type 1 (TH1) or TH17 polarized but are independent of interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) production and do not require activation of conserved pathogen recognition pathways.\n[4] This represents a previously undescribed mechanism by which memory CD4+ T cells induce an early innate response that enhances immune protection against pathogens."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"We found that the response of memory, but not naive, CD4+ T cells enhances production of multiple innate inflammatory cytokines and chemokines (IICs) in the lung and that, during influenza infection, this leads to early control of virus.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1347, "doc_id": 19005293, "label": "CONTRADICTS", "evidence_sentence_ids": [2], "cited_doc_ids": [19005293], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Upon viral challenge, influenza-specific memory CD4+ T cells greatly enhance the early production of inflammatory chemokines in the lung.\n\nDocument title: Memory CD4+ T cells induce innate responses independently of pathogen\n\nAbstract sentences:\n[0] Inflammation induced by recognition of pathogen-associated molecular patterns markedly affects subsequent adaptive responses.\n[1] We asked whether the adaptive immune system can also affect the character and magnitude of innate inflammatory responses.\n[2] We found that the response of memory, but not naive, CD4+ T cells enhances production of multiple innate inflammatory cytokines and chemokines (IICs) in the lung and that, during influenza infection, this leads to early control of virus.\n[3] Memory CD4+ T cell–induced IICs and viral control require cognate antigen recognition and are optimal when memory cells are either T helper type 1 (TH1) or TH17 polarized but are independent of interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) production and do not require activation of conserved pathogen recognition pathways.\n[4] This represents a previously undescribed mechanism by which memory CD4+ T cells induce an early innate response that enhances immune protection against pathogens."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"We found that the response of memory, but not naive, CD4+ T cells enhances production of multiple innate inflammatory cytokines and chemokines (IICs) in the lung and that, during influenza infection, this leads to early control of virus.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1348, "doc_id": 19005293, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [19005293], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Upregulation of PD1 causes the downmodulation of Satb1.\n\nDocument title: SATB1 Expression Governs Epigenetic Repression of PD‐1 in Tumor‐Reactive T Cells\n\nAbstract sentences:\n[0] &NA; Despite the importance of programmed cell death‐1 (PD‐1) in inhibiting T cell effector activity, the mechanisms regulating its expression remain poorly defined.\n[1] We found that the chromatin organizer special AT‐rich sequence‐binding protein‐1 (Satb1) restrains PD‐1 expression induced upon T cell activation by recruiting a nucleosome remodeling deacetylase (NuRD) complex to Pdcd1 regulatory regions.\n[2] Satb1 deficienct T cells exhibited a 40‐fold increase in PD‐1 expression.\n[3] Tumor‐derived transforming growth factor &bgr; (Tgf‐&bgr;) decreased Satb1 expression through binding of Smad proteins to the Satb1 promoter.\n[4] Smad proteins also competed with the Satb1‐NuRD complex for binding to Pdcd1 enhancers, releasing Pdcd1 expression from Satb1‐mediated repression, Satb1‐deficient tumor‐reactive T cells lost effector activity more rapidly than wild‐type lymphocytes at tumor beds expressing PD‐1 ligand (CD274), and these differences were abrogated by sustained CD274 blockade.\n[5] Our findings suggest that Satb1 functions to prevent premature T cell exhaustion by regulating Pdcd1 expression upon T cell activation.\n[6] Dysregulation of this pathway in tumor‐infiltrating T cells results in diminished anti‐tumor immunity.\n[7] Graphical Abstract Figure.\n[8] No caption available.\n[9] HighlightsT cell activation increased the expression of Satb1 in mature CD8+ and CD4+ T cellsRecruitment of the NuRD repression complex by Satb1 inhibits expression of Pdcd1In tumors, TGF‐&bgr; inhibits Satb1 expression in T cells, increasing Pdcd1 expressionSatb1−/− T cells express high amounts of PD‐1 and have decreased anti‐tumor activity &NA; Stephen et al. show that the chromatin organizer Satb1 controls expression levels of PD‐1 upon T cell activation through the recruitment of a de‐acetylase complex to regulatory regions of the Pdcd1 gene.\n[10] Tumor‐derived TGF‐&bgr; dysregulates this pathway, unleashing PD‐1 expression in tumor‐infiltrating T cells and decreasing anti‐tumor immunity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1349, "doc_id": 5377642, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [5377642], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Upregulation of PD1 causes the upregulation of Satb1.\n\nDocument title: SATB1 Expression Governs Epigenetic Repression of PD‐1 in Tumor‐Reactive T Cells\n\nAbstract sentences:\n[0] &NA; Despite the importance of programmed cell death‐1 (PD‐1) in inhibiting T cell effector activity, the mechanisms regulating its expression remain poorly defined.\n[1] We found that the chromatin organizer special AT‐rich sequence‐binding protein‐1 (Satb1) restrains PD‐1 expression induced upon T cell activation by recruiting a nucleosome remodeling deacetylase (NuRD) complex to Pdcd1 regulatory regions.\n[2] Satb1 deficienct T cells exhibited a 40‐fold increase in PD‐1 expression.\n[3] Tumor‐derived transforming growth factor &bgr; (Tgf‐&bgr;) decreased Satb1 expression through binding of Smad proteins to the Satb1 promoter.\n[4] Smad proteins also competed with the Satb1‐NuRD complex for binding to Pdcd1 enhancers, releasing Pdcd1 expression from Satb1‐mediated repression, Satb1‐deficient tumor‐reactive T cells lost effector activity more rapidly than wild‐type lymphocytes at tumor beds expressing PD‐1 ligand (CD274), and these differences were abrogated by sustained CD274 blockade.\n[5] Our findings suggest that Satb1 functions to prevent premature T cell exhaustion by regulating Pdcd1 expression upon T cell activation.\n[6] Dysregulation of this pathway in tumor‐infiltrating T cells results in diminished anti‐tumor immunity.\n[7] Graphical Abstract Figure.\n[8] No caption available.\n[9] HighlightsT cell activation increased the expression of Satb1 in mature CD8+ and CD4+ T cellsRecruitment of the NuRD repression complex by Satb1 inhibits expression of Pdcd1In tumors, TGF‐&bgr; inhibits Satb1 expression in T cells, increasing Pdcd1 expressionSatb1−/− T cells express high amounts of PD‐1 and have decreased anti‐tumor activity &NA; Stephen et al. show that the chromatin organizer Satb1 controls expression levels of PD‐1 upon T cell activation through the recruitment of a de‐acetylase complex to regulatory regions of the Pdcd1 gene.\n[10] Tumor‐derived TGF‐&bgr; dysregulates this pathway, unleashing PD‐1 expression in tumor‐infiltrating T cells and decreasing anti‐tumor immunity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1350, "doc_id": 5377642, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [5377642], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Upregulation of dynein in Drosophila neurons increases the number of microtubule plus-ends growing toward the cell body of each neuron.\n\nDocument title: Dynein is required for polarized dendritic transport and uniform microtubule orientation in axons\n\nAbstract sentences:\n[0] Axons and dendrites differ in both microtubule organization and in the organelles and proteins they contain.\n[1] Here we show that the microtubule motor dynein has a crucial role in polarized transport and in controlling the orientation of axonal microtubules in Drosophila melanogaster dendritic arborization (da) neurons.\n[2] Changes in organelle distribution within the dendritic arbors of dynein mutant neurons correlate with a proximal shift in dendritic branch position.\n[3] Dynein is also necessary for the dendrite-specific localization of Golgi outposts and the ion channel Pickpocket.\n[4] Axonal microtubules are normally oriented uniformly plus-end-distal; however, without dynein, axons contain both plus- and minus-end distal microtubules.\n[5] These data suggest that dynein is required for the distinguishing properties of the axon and dendrites: without dynein, dendritic organelles and proteins enter the axon and the axonal microtubules are no longer uniform in polarity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Axonal microtubules are normally oriented uniformly plus-end-distal; however, without dynein, axons contain both plus- and minus-end distal microtubules.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1351, "doc_id": 28369117, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [28369117], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Urbanization is an important risk factor related to the transmission of dengue fever.\n\nDocument title: Spatial and Temporal Clustering of Dengue Virus Transmission in Thai Villages\n\nAbstract sentences:\n[0] BACKGROUND Transmission of dengue viruses (DENV), the leading cause of arboviral disease worldwide, is known to vary through time and space, likely owing to a combination of factors related to the human host, virus, mosquito vector, and environment.\n[1] An improved understanding of variation in transmission patterns is fundamental to conducting surveillance and implementing disease prevention strategies.\n[2] To test the hypothesis that DENV transmission is spatially and temporally focal, we compared geographic and temporal characteristics within Thai villages where DENV are and are not being actively transmitted.\n[3] METHODS AND FINDINGS Cluster investigations were conducted within 100 m of homes where febrile index children with (positive clusters) and without (negative clusters) acute dengue lived during two seasons of peak DENV transmission.\n[4] Data on human infection and mosquito infection/density were examined to precisely (1) define the spatial and temporal dimensions of DENV transmission, (2) correlate these factors with variation in DENV transmission, and (3) determine the burden of inapparent and symptomatic infections.\n[5] Among 556 village children enrolled as neighbors of 12 dengue-positive and 22 dengue-negative index cases, all 27 DENV infections (4.9% of enrollees) occurred in positive clusters (p < 0.01; attributable risk [AR] = 10.4 per 100; 95% confidence interval 1-19.8 per 100].\n[6] In positive clusters, 12.4% of enrollees became infected in a 15-d period and DENV infections were aggregated centrally near homes of index cases.\n[7] As only 1 of 217 pairs of serologic specimens tested in positive clusters revealed a recent DENV infection that occurred prior to cluster initiation, we attribute the observed DENV transmission subsequent to cluster investigation to recent DENV transmission activity.\n[8] Of the 1,022 female adult Ae.\n[9] aegypti collected, all eight (0.8%) dengue-infected mosquitoes came from houses in positive clusters; none from control clusters or schools.\n[10] Distinguishing features between positive and negative clusters were greater availability of piped water in negative clusters (p < 0.01) and greater number of Ae.\n[11] aegypti pupae per person in positive clusters (p = 0.04).\n[12] During primarily DENV-4 transmission seasons, the ratio of inapparent to symptomatic infections was nearly 1:1 among child enrollees.\n[13] Study limitations included inability to sample all children and mosquitoes within each cluster and our reliance on serologic rather than virologic evidence of interval infections in enrollees given restrictions on the frequency of blood collections in children.\n[14] CONCLUSIONS Our data reveal the remarkably focal nature of DENV transmission within a hyperendemic rural area of Thailand.\n[15] These data suggest that active school-based dengue case detection prompting local spraying could contain recent virus introductions and reduce the longitudinal risk of virus spread within rural areas.\n[16] Our results should prompt future cluster studies to explore how host immune and behavioral aspects may impact DENV transmission and prevention strategies.\n[17] Cluster methodology could serve as a useful research tool for investigation of other temporally and spatially clustered infectious diseases."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1353, "doc_id": 18816720, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [18816720], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: V-9302 inhibits antitumor responses by decreasing cell death and oxidative stress.\n\nDocument title: Pharmacological Blockade of ASCT2-dependent Glutamine Transport Leads To Anti-tumor Efficacy in Preclinical Models\n\nAbstract sentences:\n[0] The unique metabolic demands of cancer cells underscore potentially fruitful opportunities for drug discovery in the era of precision medicine.\n[1] However, therapeutic targeting of cancer metabolism has led to surprisingly few new drugs to date.\n[2] The neutral amino acid glutamine serves as a key intermediate in numerous metabolic processes leveraged by cancer cells, including biosynthesis, cell signaling, and oxidative protection.\n[3] Herein we report the preclinical development of V-9302, a competitive small molecule antagonist of transmembrane glutamine flux that selectively and potently targets the amino acid transporter ASCT2.\n[4] Pharmacological blockade of ASCT2 with V-9302 resulted in attenuated cancer cell growth and proliferation, increased cell death, and increased oxidative stress, which collectively contributed to antitumor responses in vitro and in vivo.\n[5] This is the first study, to our knowledge, to demonstrate the utility of a pharmacological inhibitor of glutamine transport in oncology, representing a new class of targeted therapy and laying a framework for paradigm-shifting therapies targeting cancer cell metabolism."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Pharmacological blockade of ASCT2 with V-9302 resulted in attenuated cancer cell growth and proliferation, increased cell death, and increased oxidative stress, which collectively contributed to antitumor responses in vitro and in vivo.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1355, "doc_id": 5256564, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [5256564], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Vaccinating the gastrointestinal tract induces protection of rectal and vaginal mucosa.\n\nDocument title: Large intestine-targeted nanoparticle-releasing oral vaccine to control genitorectal viral infection\n\nAbstract sentences:\n[0] Both rectal and vaginal mucosal surfaces serve as transmission routes for pathogenic microorganisms.\n[1] Vaccination through large intestinal mucosa, previously proven protective for both of these mucosal sites in animal studies, can be achieved successfully by direct intracolorectal (i.c.r.) administration, but this route is clinically impractical.\n[2] Oral vaccine delivery seems preferable but runs the risk of the vaccine's destruction in the upper gastrointestinal tract.\n[3] Therefore, we designed a large intestine-targeted oral delivery with pH-dependent microparticles containing vaccine nanoparticles, which induced colorectal immunity in mice comparably to colorectal vaccination and protected against rectal and vaginal viral challenge.\n[4] Conversely, vaccine targeted to the small intestine induced only small intestinal immunity and provided no rectal or vaginal protection, demonstrating functional compartmentalization within the gut mucosal immune system.\n[5] Therefore, using this oral vaccine delivery system to target the large intestine, but not the small intestine, may represent a feasible new strategy for immune protection of rectal and vaginal mucosa."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Vaccination through large intestinal mucosa, previously proven protective for both of these mucosal sites in animal studies, can be achieved successfully by direct intracolorectal (i.c.r.) administration, but this route is clinically impractical.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1356, "doc_id": 13764090, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [13764090], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Vaccinating the gastrointestinal tract induces protection of rectal and vaginal mucosa.\n\nDocument title: Large intestine-targeted nanoparticle-releasing oral vaccine to control genitorectal viral infection\n\nAbstract sentences:\n[0] Both rectal and vaginal mucosal surfaces serve as transmission routes for pathogenic microorganisms.\n[1] Vaccination through large intestinal mucosa, previously proven protective for both of these mucosal sites in animal studies, can be achieved successfully by direct intracolorectal (i.c.r.) administration, but this route is clinically impractical.\n[2] Oral vaccine delivery seems preferable but runs the risk of the vaccine's destruction in the upper gastrointestinal tract.\n[3] Therefore, we designed a large intestine-targeted oral delivery with pH-dependent microparticles containing vaccine nanoparticles, which induced colorectal immunity in mice comparably to colorectal vaccination and protected against rectal and vaginal viral challenge.\n[4] Conversely, vaccine targeted to the small intestine induced only small intestinal immunity and provided no rectal or vaginal protection, demonstrating functional compartmentalization within the gut mucosal immune system.\n[5] Therefore, using this oral vaccine delivery system to target the large intestine, but not the small intestine, may represent a feasible new strategy for immune protection of rectal and vaginal mucosa."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Therefore, we designed a large intestine-targeted oral delivery with pH-dependent microparticles containing vaccine nanoparticles, which induced colorectal immunity in mice comparably to colorectal vaccination and protected against rectal and vaginal viral challenge.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1356, "doc_id": 13764090, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [13764090], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Vaccinating the gastrointestinal tract induces protection of rectal and vaginal mucosa.\n\nDocument title: Large intestine-targeted nanoparticle-releasing oral vaccine to control genitorectal viral infection\n\nAbstract sentences:\n[0] Both rectal and vaginal mucosal surfaces serve as transmission routes for pathogenic microorganisms.\n[1] Vaccination through large intestinal mucosa, previously proven protective for both of these mucosal sites in animal studies, can be achieved successfully by direct intracolorectal (i.c.r.) administration, but this route is clinically impractical.\n[2] Oral vaccine delivery seems preferable but runs the risk of the vaccine's destruction in the upper gastrointestinal tract.\n[3] Therefore, we designed a large intestine-targeted oral delivery with pH-dependent microparticles containing vaccine nanoparticles, which induced colorectal immunity in mice comparably to colorectal vaccination and protected against rectal and vaginal viral challenge.\n[4] Conversely, vaccine targeted to the small intestine induced only small intestinal immunity and provided no rectal or vaginal protection, demonstrating functional compartmentalization within the gut mucosal immune system.\n[5] Therefore, using this oral vaccine delivery system to target the large intestine, but not the small intestine, may represent a feasible new strategy for immune protection of rectal and vaginal mucosa."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Therefore, using this oral vaccine delivery system to target the large intestine, but not the small intestine, may represent a feasible new strategy for immune protection of rectal and vaginal mucosa.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1356, "doc_id": 13764090, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [13764090], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Varenicline monotherapy is more effective after 26 weeks of treatment compared to combination nicotine replacement therapies with varenicline or bupropion.\n\nDocument title: Combination varenicline and bupropion SR for tobacco-dependence treatment in cigarette smokers: a randomized trial.\n\nAbstract sentences:\n[0] IMPORTANCE Combining pharmacotherapies for tobacco-dependence treatment may increase smoking abstinence.\n[1] OBJECTIVE To determine efficacy and safety of varenicline and bupropion sustained-release (SR; combination therapy) compared with varenicline (monotherapy) in cigarette smokers.\n[2] DESIGN, SETTING, AND PARTICIPANTS Randomized, blinded, placebo-controlled multicenter clinical trial with a 12-week treatment period and follow-up through week 52 conducted between October 2009 and April 2013 at 3 midwestern clinical research sites.\n[3] Five hundred six adult (≥18 years) cigarette smokers were randomly assigned and 315 (62%) completed the study.\n[4] INTERVENTIONS Twelve weeks of varenicline and bupropion SR or varenicline and placebo.\n[5] MAIN OUTCOMES AND MEASURES Primary outcome was abstinence rates at week 12, defined as prolonged (no smoking from 2 weeks after the target quit date) abstinence and 7-day point-prevalence (no smoking past 7 days) abstinence.\n[6] Secondary outcomes were prolonged and point-prevalence smoking abstinence rates at weeks 26 and 52.\n[7] Outcomes were biochemically confirmed.\n[8] RESULTS At 12 weeks, 53.0% of the combination therapy group achieved prolonged smoking abstinence and 56.2% achieved 7-day point-prevalence smoking abstinence compared with 43.2% and 48.6% in varenicline monotherapy (odds ratio [OR], 1.49; 95% CI, 1.05-2.12; P = .03 and OR, 1.36; 95% CI, 0.95-1.93; P = .09, respectively).\n[9] At 26 weeks, 36.6% of the combination therapy group achieved prolonged and 38.2% achieved 7-day point-prevalence smoking abstinence compared with 27.6% and 31.9% in varenicline monotherapy (OR, 1.52; 95% CI, 1.04-2.22; P = .03 and OR, 1.32; 95% CI, 0.91-1.91; P = .14, respectively).\n[10] At 52 weeks, 30.9% of the combination therapy group achieved prolonged and 36.6% achieved 7-day point-prevalence smoking abstinence compared with 24.5% and 29.2% in varenicline monotherapy (OR, 1.39; 95% CI, 0.93-2.07; P = .11 and OR, 1.40; 95% CI, 0.96-2.05; P = .08, respectively).\n[11] Participants receiving combination therapy reported more anxiety (7.2% vs 3.1%; P = .04) and depressive symptoms (3.6% vs 0.8%; P = .03).\n[12] CONCLUSIONS AND RELEVANCE Among cigarette smokers, combined use of varenicline and bupropion, compared with varenicline alone, increased prolonged abstinence but not 7-day point prevalence at 12 and 26 weeks.\n[13] Neither outcome was significantly different at 52 weeks.\n[14] Further research is required to determine the role of combination therapy in smoking cessation.\n[15] TRIAL REGISTRATION clinicaltrials.gov Identifier: http://clinicaltrials.gov/show/NCT00935818."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"At 26 weeks, 36.6% of the combination therapy group achieved prolonged and 38.2% achieved 7-day point-prevalence smoking abstinence compared with 27.6% and 31.9% in varenicline monotherapy (OR, 1.52; 95% CI, 1.04-2.22; P = .03 and OR, 1.32; 95% CI, 0.91-1.91; P = .14, respectively).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1360, "doc_id": 11614737, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [11614737], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Varying expression levels of EBI2 affect the positioning and migration of B cells.\n\nDocument title: Guidance of B cells by the orphan G protein-coupled receptor EBI2 shapes humoral immune responses.\n\nAbstract sentences:\n[0] Humoral immunity depends on both rapid and long-term antibody production against invading pathogens.\n[1] This is achieved by the generation of spatially distinct extrafollicular plasmablast and follicular germinal center (GC) B cell populations, but the signals that guide responding B cells to these alternative compartments have not been fully elucidated.\n[2] Here, we show that expression of the orphan G protein-coupled receptor Epstein-Barr virus-induced gene 2 (EBI2, also known as GPR183) by activated B cells was essential for their movement to extrafollicular sites and induction of early plasmablast responses.\n[3] Conversely, downregulation of EBI2 enabled B cells to access the center of follicles and promoted efficient GC formation.\n[4] EBI2 therefore provides a previously uncharacterized dimension to B cell migration that is crucial for coordinating rapid versus long-term antibody responses."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2, 3]\nExplanation: Evidence states: \"Here, we show that expression of the orphan G protein-coupled receptor Epstein-Barr virus-induced gene 2 (EBI2, also known as GPR183) by activated B cells was essential for their movement to extrafollicular sites and induction of early plasmablast responses. Conversely, downregulation of EBI2 enabled B cells to access the center of follicles and promoted efficient GC formation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1361, "doc_id": 15488881, "label": "SUPPORTS", "evidence_sentence_ids": [2, 3], "cited_doc_ids": [15488881, 15058155], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Varying expression levels of EBI2 affect the positioning and migration of B cells.\n\nDocument title: 7α, 25-dihydroxycholesterol-mediated activation of EBI2 in immune regulation and diseases\n\nAbstract sentences:\n[0] EBI2, aka GPR183, is a G-couple receptor originally identified in 1993 as one of main genes induced in Burkitt's lymphoma cell line BL41 by Epstein-Barr virus (EBV) infection.\n[1] After it was reported in 2009 that the receptor played a key role in regulating B cell migration and responses, we initiated an effort in looking for its endogenous ligand.\n[2] In 2011 we and another group reported the identification of 7α, 25-dihydroxyxcholesterol (7α, 25-OHC), an oxysterol, as the likely physiological ligand of EBI2.\n[3] A few subsequently published studies further elucidated how 7α, 25-OHC bound to EBI2, and how a gradient of 7α, 25-OHC could be generated in vivo and regulated migration, activation, and functions of B cells, T cells, dendritic cells (DCs), monocytes/macrophages, and astrocytes.\n[4] The identification of 7α, 25-OHC as a G protein-coupled receptor ligand revealed a previously unknown signaling system of oxysterols, a class of molecules which exert profound biological functions.\n[5] Dysregulation of the synthesis or functions of these molecules is believed to contribute to inflammation and autoimmune diseases, cardiovascular diseases, neurodegenerative diseases, cancer as well as metabolic diseases such as diabetes, obesity, and dyslipidemia.\n[6] Therefore EBI2 may represent a promising target for therapeutic interventions for human diseases."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"A few subsequently published studies further elucidated how 7α, 25-OHC bound to EBI2, and how a gradient of 7α, 25-OHC could be generated in vivo and regulated migration, activation, and functions of B cells, T cells, dendritic cells (DCs), monocytes/macrophages, and astrocytes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1361, "doc_id": 15058155, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [15488881, 15058155], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Venules have less significant tunica adventitia than arterioles.\n\nDocument title: Scaffold-based three-dimensional human fibroblast culture provides a structural matrix that supports angiogenesis in infarcted heart tissue.\n\nAbstract sentences:\n[0] BACKGROUND We have developed techniques to implant angiogenic patches onto the epicardium over regions of infarcted cardiac tissue to stimulate revascularization of the damaged tissue.\n[1] These experiments used a scaffold-based 3D human dermal fibroblast culture (3DFC) as an epicardial patch.\n[2] The 3DFC contains viable cells that secrete angiogenic growth factors and has previously been shown to stimulate angiogenic activity.\n[3] The hypothesis tested was that a viable 3DFC cardiac patch would stimulate an angiogenic response within an area of infarcted cardiac tissue.\n[4] METHODS AND RESULTS A coronary occlusion of a branch of the left anterior descending coronary artery was performed by thermal ligation in severe combined immunodeficient mice.\n[5] 3DFCs with or without viable cells were sized to the damaged area, implanted in replicate mice onto the epicardium at the site of tissue injury, and compared with animals that received infarct surgery but no implant.\n[6] Fourteen and 30 days after surgery, hearts were exposed and photographed, and tissue samples were prepared for histology and cytochemistry.\n[7] Fourteen and 30 days after surgery, the damaged myocardium receiving viable 3DFC exhibited a significantly greater angiogenic response (including arterioles, venules, and capillaries) than nonviable and untreated control groups.\n[8] CONCLUSIONS In this animal model, viable 3DFC stimulates angiogenesis within a region of cardiac infarction and can augment a repair response in damaged tissue.\n[9] Therefore, a potential use for 3DFC is the repair of myocardial tissue damaged by infarction."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1364, "doc_id": 8290953, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [8290953], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: VgrG (Tssl) protein punctures membranes by forming a spike at the tip of the tube apparatus.\n\nDocument title: PAAR-repeat proteins sharpen and diversify the Type VI secretion system spike\n\nAbstract sentences:\n[0] The bacterial type VI secretion system (T6SS) is a large multicomponent, dynamic macromolecular machine that has an important role in the ecology of many Gram-negative bacteria.\n[1] T6SS is responsible for translocation of a wide range of toxic effector molecules, allowing predatory cells to kill both prokaryotic as well as eukaryotic prey cells.\n[2] The T6SS organelle is functionally analogous to contractile tails of bacteriophages and is thought to attack cells by initially penetrating them with a trimeric protein complex called the VgrG spike.\n[3] Neither the exact protein composition of the T6SS organelle nor the mechanisms of effector selection and delivery are known.\n[4] Here we report that proteins from the PAAR (proline-alanine-alanine-arginine) repeat superfamily form a sharp conical extension on the VgrG spike, which is further involved in attaching effector domains to the spike.\n[5] The crystal structures of two PAAR-repeat proteins bound to VgrG-like partners show that these proteins sharpen the tip of the T6SS spike complex.\n[6] We demonstrate that PAAR proteins are essential for T6SS-mediated secretion and target cell killing by Vibrio cholerae and Acinetobacter baylyi.\n[7] Our results indicate a new model of the T6SS organelle in which the VgrG-PAAR spike complex is decorated with multiple effectors that are delivered simultaneously into target cells in a single contraction-driven translocation event."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2, 4]\nExplanation: Evidence states: \"The T6SS organelle is functionally analogous to contractile tails of bacteriophages and is thought to attack cells by initially penetrating them with a trimeric protein complex called the VgrG spike. Here we report that proteins from the PAAR (proline-alanine-alanine-arginine) repeat superfamily form a sharp conical extension on the VgrG spike, which is further involved in attaching effector domains to the spike.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1366, "doc_id": 4406819, "label": "SUPPORTS", "evidence_sentence_ids": [2, 4], "cited_doc_ids": [4406819], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Vitamin D deficiency effects birth weight.\n\nDocument title: Association between maternal serum 25-hydroxyvitamin D level and pregnancy and neonatal outcomes: systematic review and meta-analysis of observational studies.\n\nAbstract sentences:\n[0] OBJECTIVE To assess the effect of 25-hydroxyvitamin D (25-OHD) levels on pregnancy outcomes and birth variables.\n[1] DESIGN Systematic review and meta-analysis.\n[2] DATA SOURCES Medline (1966 to August 2012), PubMed (2008 to August 2012), Embase (1980 to August 2012), CINAHL (1981 to August 2012), the Cochrane database of systematic reviews, and the Cochrane database of registered clinical trials.\n[3] STUDY SELECTION Studies reporting on the association between serum 25-OHD levels during pregnancy and the outcomes of interest (pre-eclampsia, gestational diabetes, bacterial vaginosis, caesarean section, small for gestational age infants, birth weight, birth length, and head circumference).\n[4] DATA EXTRACTION Two authors independently extracted data from original research articles, including key indicators of study quality.\n[5] We pooled the most adjusted odds ratios and weighted mean differences.\n[6] Associations were tested in subgroups representing different patient characteristics and study quality.\n[7] RESULTS 3357 studies were identified and reviewed for eligibility.\n[8] 31 eligible studies were included in the final analysis.\n[9] Insufficient serum levels of 25-OHD were associated with gestational diabetes (pooled odds ratio 1.49, 95% confidence interval 1.18 to 1.89), pre-eclampsia (1.79, 1.25 to 2.58), and small for gestational age infants (1.85, 1.52 to 2.26).\n[10] Pregnant women with low serum 25-OHD levels had an increased risk of bacterial vaginosis and low birthweight infants but not delivery by caesarean section.\n[11] CONCLUSION Vitamin D insufficiency is associated with an increased risk of gestational diabetes, pre-eclampsia, and small for gestational age infants.\n[12] Pregnant women with low 25-OHD levels had an increased risk of bacterial vaginosis and lower birth weight infants, but not delivery by caesarean section."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Pregnant women with low serum 25-OHD levels had an increased risk of bacterial vaginosis and low birthweight infants but not delivery by caesarean section.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1367, "doc_id": 2425364, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [2425364], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Vitamin D deficiency effects birth weight.\n\nDocument title: Association between maternal serum 25-hydroxyvitamin D level and pregnancy and neonatal outcomes: systematic review and meta-analysis of observational studies.\n\nAbstract sentences:\n[0] OBJECTIVE To assess the effect of 25-hydroxyvitamin D (25-OHD) levels on pregnancy outcomes and birth variables.\n[1] DESIGN Systematic review and meta-analysis.\n[2] DATA SOURCES Medline (1966 to August 2012), PubMed (2008 to August 2012), Embase (1980 to August 2012), CINAHL (1981 to August 2012), the Cochrane database of systematic reviews, and the Cochrane database of registered clinical trials.\n[3] STUDY SELECTION Studies reporting on the association between serum 25-OHD levels during pregnancy and the outcomes of interest (pre-eclampsia, gestational diabetes, bacterial vaginosis, caesarean section, small for gestational age infants, birth weight, birth length, and head circumference).\n[4] DATA EXTRACTION Two authors independently extracted data from original research articles, including key indicators of study quality.\n[5] We pooled the most adjusted odds ratios and weighted mean differences.\n[6] Associations were tested in subgroups representing different patient characteristics and study quality.\n[7] RESULTS 3357 studies were identified and reviewed for eligibility.\n[8] 31 eligible studies were included in the final analysis.\n[9] Insufficient serum levels of 25-OHD were associated with gestational diabetes (pooled odds ratio 1.49, 95% confidence interval 1.18 to 1.89), pre-eclampsia (1.79, 1.25 to 2.58), and small for gestational age infants (1.85, 1.52 to 2.26).\n[10] Pregnant women with low serum 25-OHD levels had an increased risk of bacterial vaginosis and low birthweight infants but not delivery by caesarean section.\n[11] CONCLUSION Vitamin D insufficiency is associated with an increased risk of gestational diabetes, pre-eclampsia, and small for gestational age infants.\n[12] Pregnant women with low 25-OHD levels had an increased risk of bacterial vaginosis and lower birth weight infants, but not delivery by caesarean section."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"Pregnant women with low 25-OHD levels had an increased risk of bacterial vaginosis and lower birth weight infants, but not delivery by caesarean section.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1367, "doc_id": 2425364, "label": "SUPPORTS", "evidence_sentence_ids": [12], "cited_doc_ids": [2425364], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Vitamin D is an important factor in the relationship between calcium and parathyroid hormone.\n\nDocument title: Relationship between serum parathyroid hormone levels, vitamin D sufficiency, and calcium intake.\n\nAbstract sentences:\n[0] CONTEXT Adequate vitamin D status for optimum bone health has received increased recognition in recent years; however, the ideal intake is not known.\n[1] Serum 25-hydroxyvitamin D is the generally accepted indicator of vitamin D status, but no universal reference level has been reached.\n[2] OBJECTIVE To investigate the relative importance of high calcium intake and serum 25-hydroxyvitamin D for calcium homeostasis, as determined by serum intact parathyroid hormone (PTH).\n[3] DESIGN, SETTING, AND PARTICIPANTS Cross-sectional study of 2310 healthy Icelandic adults who were divided equally into 3 age groups (30-45 years, 50-65 years, or 70-85 years) and recruited from February 2001 to January 2003.\n[4] They were administered a semi-quantitative food frequency questionnaire, which assessed vitamin D and calcium intake.\n[5] Participants were further divided into groups according to calcium intake (<800 mg/d, 800-1200 mg/d, and >1200 mg/d) and serum 25-hydroxyvitamin D level (<10 ng/mL, 10-18 ng/mL, and >18 ng/mL).\n[6] MAIN OUTCOME MEASURE Serum intact PTH as determined by calcium intake and vitamin D.   RESULTS A total of 944 healthy participants completed all parts of the study.\n[7] After adjusting for relevant factors, serum PTH was lowest in the group with a serum 25-hydroxyvitamin D level of more than 18 ng/mL but highest in the group with a serum 25-hydroxyvitamin D level of less than 10 ng/mL. At the low serum 25-hydroxyvitamin D level (<10 ng/mL), calcium intake of less than 800 mg/d vs more than 1200 mg/d was significantly associated with higher serum PTH (P = .04); and at a calcium intake of more than 1200 mg/d, there was a significant difference between the lowest and highest vitamin D groups (P = .04).\n[8] CONCLUSIONS As long as vitamin D status is ensured, calcium intake levels of more than 800 mg/d may be unnecessary for maintaining calcium metabolism.\n[9] Vitamin D supplements are necessary for adequate vitamin D status in northern climates."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"After adjusting for relevant factors, serum PTH was lowest in the group with a serum 25-hydroxyvitamin D level of more than 18 ng/mL but highest in the group with a serum 25-hydroxyvitamin D level of less than 10 ng/mL. At the low serum 25-hydroxyvitamin D level (<10 ng/mL), calcium intake of less than 800 mg/d vs more than 1200 mg/d was significantly associated with higher serum PTH (P = .04); and at a calcium intake of more than 1200 mg/d, there was a significant difference between the lowest and highest vitamin D groups (P = .04).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1371, "doc_id": 16256507, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [16256507], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Vitamin D is an important factor in the relationship between calcium and parathyroid hormone.\n\nDocument title: Relationship between serum parathyroid hormone levels, vitamin D sufficiency, and calcium intake.\n\nAbstract sentences:\n[0] CONTEXT Adequate vitamin D status for optimum bone health has received increased recognition in recent years; however, the ideal intake is not known.\n[1] Serum 25-hydroxyvitamin D is the generally accepted indicator of vitamin D status, but no universal reference level has been reached.\n[2] OBJECTIVE To investigate the relative importance of high calcium intake and serum 25-hydroxyvitamin D for calcium homeostasis, as determined by serum intact parathyroid hormone (PTH).\n[3] DESIGN, SETTING, AND PARTICIPANTS Cross-sectional study of 2310 healthy Icelandic adults who were divided equally into 3 age groups (30-45 years, 50-65 years, or 70-85 years) and recruited from February 2001 to January 2003.\n[4] They were administered a semi-quantitative food frequency questionnaire, which assessed vitamin D and calcium intake.\n[5] Participants were further divided into groups according to calcium intake (<800 mg/d, 800-1200 mg/d, and >1200 mg/d) and serum 25-hydroxyvitamin D level (<10 ng/mL, 10-18 ng/mL, and >18 ng/mL).\n[6] MAIN OUTCOME MEASURE Serum intact PTH as determined by calcium intake and vitamin D.   RESULTS A total of 944 healthy participants completed all parts of the study.\n[7] After adjusting for relevant factors, serum PTH was lowest in the group with a serum 25-hydroxyvitamin D level of more than 18 ng/mL but highest in the group with a serum 25-hydroxyvitamin D level of less than 10 ng/mL. At the low serum 25-hydroxyvitamin D level (<10 ng/mL), calcium intake of less than 800 mg/d vs more than 1200 mg/d was significantly associated with higher serum PTH (P = .04); and at a calcium intake of more than 1200 mg/d, there was a significant difference between the lowest and highest vitamin D groups (P = .04).\n[8] CONCLUSIONS As long as vitamin D status is ensured, calcium intake levels of more than 800 mg/d may be unnecessary for maintaining calcium metabolism.\n[9] Vitamin D supplements are necessary for adequate vitamin D status in northern climates."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"CONCLUSIONS As long as vitamin D status is ensured, calcium intake levels of more than 800 mg/d may be unnecessary for maintaining calcium metabolism.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1371, "doc_id": 16256507, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [16256507], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Walking in traffic areas in London did not improve lung function in elderly adults.\n\nDocument title: Respiratory and cardiovascular responses to walking down a traffic-polluted road compared with walking in a traffic-free area in participants aged 60 years and older with chronic lung or heart disease and age-matched healthy controls: a randomised, crossover study\n\nAbstract sentences:\n[0] BACKGROUND Long-term exposure to pollution can lead to an increase in the rate of decline of lung function, especially in older individuals and in those with chronic obstructive pulmonary disease (COPD), whereas shorter-term exposure at higher pollution levels has been implicated in causing excess deaths from ischaemic heart disease and exacerbations of COPD.\n[1] We aimed to assess the effects on respiratory and cardiovascular responses of walking down a busy street with high levels of pollution compared with walking in a traffic-free area with lower pollution levels in older adults.\n[2] METHODS In this randomised, crossover study, we recruited men and women aged 60 years and older with angiographically proven stable ischaemic heart disease or stage 2 Global initiative for Obstructive Lung Disease (GOLD) COPD who had been clinically stable for 6 months, and age-matched healthy volunteers.\n[3] Individuals with ischaemic heart disease or COPD were recruited from existing databases or outpatient respiratory and cardiology clinics at the Royal Brompton & Harefield NHS Foundation Trust and age-matched healthy volunteers using advertising and existing databases.\n[4] All participants had abstained from smoking for at least 12 months and medications were taken as recommended by participants' doctors during the study.\n[5] Participants were randomly assigned by drawing numbered disks at random from a bag to do a 2 h walk either along a commercial street in London (Oxford Street) or in an urban park (Hyde Park).\n[6] Baseline measurements of participants were taken before the walk in the hospital laboratory.\n[7] During each walk session, black carbon, particulate matter (PM) concentrations, ultrafine particles, and nitrogen dioxide (NO2) concentrations were measured.\n[8] FINDINGS Between October, 2012, and June, 2014, we screened 135 participants, of whom 40 healthy volunteers, 40 individuals with COPD, and 39 with ischaemic heart disease were recruited.\n[9] Concentrations of black carbon, NO2, PM10, PM2.5, and ultrafine particles were higher on Oxford Street than in Hyde Park.\n[10] Participants with COPD reported more cough (odds ratio [OR] 1·95, 95% CI 0·96-3·95; p<0·1), sputum (3·15, 1·39-7·13; p<0·05), shortness of breath (1·86, 0·97-3·57; p<0·1), and wheeze (4·00, 1·52-10·50; p<0·05) after walking down Oxford Street compared with Hyde Park.\n[11] In all participants, irrespective of their disease status, walking in Hyde Park led to an increase in lung function (forced expiratory volume in the first second [FEV1] and forced vital capacity [FVC]) and a decrease in pulse wave velocity (PWV) and augmentation index up to 26 h after the walk.\n[12] By contrast, these beneficial responses were attenuated after walking on Oxford Street.\n[13] In participants with COPD, a reduction in FEV1 and FVC, and an increase in R5-20 were associated with an increase in during-walk exposure to NO2, ultrafine particles and PM2.5, and an increase in PWV and augmentation index with NO2 and ultrafine particles.\n[14] In healthy volunteers, PWV and augmentation index were associated both with black carbon and ultrafine particles.\n[15] INTERPRETATION Short-term exposure to traffic pollution prevents the beneficial cardiopulmonary effects of walking in people with COPD, ischaemic heart disease, and those free from chronic cardiopulmonary diseases.\n[16] Medication use might reduce the adverse effects of air pollution in individuals with ischaemic heart disease.\n[17] Policies should aim to control ambient levels of air pollution along busy streets in view of these negative health effects.\n[18] FUNDING British Heart Foundation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Participants with COPD reported more cough (odds ratio [OR] 1·95, 95% CI 0·96-3·95; p<0·1), sputum (3·15, 1·39-7·13; p<0·05), shortness of breath (1·86, 0·97-3·57; p<0·1), and wheeze (4·00, 1·52-10·50; p<0·05) after walking down Oxford Street compared with Hyde Park.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1372, "doc_id": 21003930, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [21003930], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Walking in traffic areas in London did not improve lung function in elderly adults.\n\nDocument title: Respiratory and cardiovascular responses to walking down a traffic-polluted road compared with walking in a traffic-free area in participants aged 60 years and older with chronic lung or heart disease and age-matched healthy controls: a randomised, crossover study\n\nAbstract sentences:\n[0] BACKGROUND Long-term exposure to pollution can lead to an increase in the rate of decline of lung function, especially in older individuals and in those with chronic obstructive pulmonary disease (COPD), whereas shorter-term exposure at higher pollution levels has been implicated in causing excess deaths from ischaemic heart disease and exacerbations of COPD.\n[1] We aimed to assess the effects on respiratory and cardiovascular responses of walking down a busy street with high levels of pollution compared with walking in a traffic-free area with lower pollution levels in older adults.\n[2] METHODS In this randomised, crossover study, we recruited men and women aged 60 years and older with angiographically proven stable ischaemic heart disease or stage 2 Global initiative for Obstructive Lung Disease (GOLD) COPD who had been clinically stable for 6 months, and age-matched healthy volunteers.\n[3] Individuals with ischaemic heart disease or COPD were recruited from existing databases or outpatient respiratory and cardiology clinics at the Royal Brompton & Harefield NHS Foundation Trust and age-matched healthy volunteers using advertising and existing databases.\n[4] All participants had abstained from smoking for at least 12 months and medications were taken as recommended by participants' doctors during the study.\n[5] Participants were randomly assigned by drawing numbered disks at random from a bag to do a 2 h walk either along a commercial street in London (Oxford Street) or in an urban park (Hyde Park).\n[6] Baseline measurements of participants were taken before the walk in the hospital laboratory.\n[7] During each walk session, black carbon, particulate matter (PM) concentrations, ultrafine particles, and nitrogen dioxide (NO2) concentrations were measured.\n[8] FINDINGS Between October, 2012, and June, 2014, we screened 135 participants, of whom 40 healthy volunteers, 40 individuals with COPD, and 39 with ischaemic heart disease were recruited.\n[9] Concentrations of black carbon, NO2, PM10, PM2.5, and ultrafine particles were higher on Oxford Street than in Hyde Park.\n[10] Participants with COPD reported more cough (odds ratio [OR] 1·95, 95% CI 0·96-3·95; p<0·1), sputum (3·15, 1·39-7·13; p<0·05), shortness of breath (1·86, 0·97-3·57; p<0·1), and wheeze (4·00, 1·52-10·50; p<0·05) after walking down Oxford Street compared with Hyde Park.\n[11] In all participants, irrespective of their disease status, walking in Hyde Park led to an increase in lung function (forced expiratory volume in the first second [FEV1] and forced vital capacity [FVC]) and a decrease in pulse wave velocity (PWV) and augmentation index up to 26 h after the walk.\n[12] By contrast, these beneficial responses were attenuated after walking on Oxford Street.\n[13] In participants with COPD, a reduction in FEV1 and FVC, and an increase in R5-20 were associated with an increase in during-walk exposure to NO2, ultrafine particles and PM2.5, and an increase in PWV and augmentation index with NO2 and ultrafine particles.\n[14] In healthy volunteers, PWV and augmentation index were associated both with black carbon and ultrafine particles.\n[15] INTERPRETATION Short-term exposure to traffic pollution prevents the beneficial cardiopulmonary effects of walking in people with COPD, ischaemic heart disease, and those free from chronic cardiopulmonary diseases.\n[16] Medication use might reduce the adverse effects of air pollution in individuals with ischaemic heart disease.\n[17] Policies should aim to control ambient levels of air pollution along busy streets in view of these negative health effects.\n[18] FUNDING British Heart Foundation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11, 12]\nExplanation: Evidence states: \"In all participants, irrespective of their disease status, walking in Hyde Park led to an increase in lung function (forced expiratory volume in the first second [FEV1] and forced vital capacity [FVC]) and a decrease in pulse wave velocity (PWV) and augmentation index up to 26 h after the walk. By contrast, these beneficial responses were attenuated after walking on Oxford Street.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1372, "doc_id": 21003930, "label": "SUPPORTS", "evidence_sentence_ids": [11, 12], "cited_doc_ids": [21003930], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Walking in traffic areas in London did not improve lung function in elderly adults.\n\nDocument title: Respiratory and cardiovascular responses to walking down a traffic-polluted road compared with walking in a traffic-free area in participants aged 60 years and older with chronic lung or heart disease and age-matched healthy controls: a randomised, crossover study\n\nAbstract sentences:\n[0] BACKGROUND Long-term exposure to pollution can lead to an increase in the rate of decline of lung function, especially in older individuals and in those with chronic obstructive pulmonary disease (COPD), whereas shorter-term exposure at higher pollution levels has been implicated in causing excess deaths from ischaemic heart disease and exacerbations of COPD.\n[1] We aimed to assess the effects on respiratory and cardiovascular responses of walking down a busy street with high levels of pollution compared with walking in a traffic-free area with lower pollution levels in older adults.\n[2] METHODS In this randomised, crossover study, we recruited men and women aged 60 years and older with angiographically proven stable ischaemic heart disease or stage 2 Global initiative for Obstructive Lung Disease (GOLD) COPD who had been clinically stable for 6 months, and age-matched healthy volunteers.\n[3] Individuals with ischaemic heart disease or COPD were recruited from existing databases or outpatient respiratory and cardiology clinics at the Royal Brompton & Harefield NHS Foundation Trust and age-matched healthy volunteers using advertising and existing databases.\n[4] All participants had abstained from smoking for at least 12 months and medications were taken as recommended by participants' doctors during the study.\n[5] Participants were randomly assigned by drawing numbered disks at random from a bag to do a 2 h walk either along a commercial street in London (Oxford Street) or in an urban park (Hyde Park).\n[6] Baseline measurements of participants were taken before the walk in the hospital laboratory.\n[7] During each walk session, black carbon, particulate matter (PM) concentrations, ultrafine particles, and nitrogen dioxide (NO2) concentrations were measured.\n[8] FINDINGS Between October, 2012, and June, 2014, we screened 135 participants, of whom 40 healthy volunteers, 40 individuals with COPD, and 39 with ischaemic heart disease were recruited.\n[9] Concentrations of black carbon, NO2, PM10, PM2.5, and ultrafine particles were higher on Oxford Street than in Hyde Park.\n[10] Participants with COPD reported more cough (odds ratio [OR] 1·95, 95% CI 0·96-3·95; p<0·1), sputum (3·15, 1·39-7·13; p<0·05), shortness of breath (1·86, 0·97-3·57; p<0·1), and wheeze (4·00, 1·52-10·50; p<0·05) after walking down Oxford Street compared with Hyde Park.\n[11] In all participants, irrespective of their disease status, walking in Hyde Park led to an increase in lung function (forced expiratory volume in the first second [FEV1] and forced vital capacity [FVC]) and a decrease in pulse wave velocity (PWV) and augmentation index up to 26 h after the walk.\n[12] By contrast, these beneficial responses were attenuated after walking on Oxford Street.\n[13] In participants with COPD, a reduction in FEV1 and FVC, and an increase in R5-20 were associated with an increase in during-walk exposure to NO2, ultrafine particles and PM2.5, and an increase in PWV and augmentation index with NO2 and ultrafine particles.\n[14] In healthy volunteers, PWV and augmentation index were associated both with black carbon and ultrafine particles.\n[15] INTERPRETATION Short-term exposure to traffic pollution prevents the beneficial cardiopulmonary effects of walking in people with COPD, ischaemic heart disease, and those free from chronic cardiopulmonary diseases.\n[16] Medication use might reduce the adverse effects of air pollution in individuals with ischaemic heart disease.\n[17] Policies should aim to control ambient levels of air pollution along busy streets in view of these negative health effects.\n[18] FUNDING British Heart Foundation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [15]\nExplanation: Evidence states: \"INTERPRETATION Short-term exposure to traffic pollution prevents the beneficial cardiopulmonary effects of walking in people with COPD, ischaemic heart disease, and those free from chronic cardiopulmonary diseases.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1372, "doc_id": 21003930, "label": "SUPPORTS", "evidence_sentence_ids": [15], "cited_doc_ids": [21003930], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Walking in traffic areas in London improves lung function in elderly adults.\n\nDocument title: Respiratory and cardiovascular responses to walking down a traffic-polluted road compared with walking in a traffic-free area in participants aged 60 years and older with chronic lung or heart disease and age-matched healthy controls: a randomised, crossover study\n\nAbstract sentences:\n[0] BACKGROUND Long-term exposure to pollution can lead to an increase in the rate of decline of lung function, especially in older individuals and in those with chronic obstructive pulmonary disease (COPD), whereas shorter-term exposure at higher pollution levels has been implicated in causing excess deaths from ischaemic heart disease and exacerbations of COPD.\n[1] We aimed to assess the effects on respiratory and cardiovascular responses of walking down a busy street with high levels of pollution compared with walking in a traffic-free area with lower pollution levels in older adults.\n[2] METHODS In this randomised, crossover study, we recruited men and women aged 60 years and older with angiographically proven stable ischaemic heart disease or stage 2 Global initiative for Obstructive Lung Disease (GOLD) COPD who had been clinically stable for 6 months, and age-matched healthy volunteers.\n[3] Individuals with ischaemic heart disease or COPD were recruited from existing databases or outpatient respiratory and cardiology clinics at the Royal Brompton & Harefield NHS Foundation Trust and age-matched healthy volunteers using advertising and existing databases.\n[4] All participants had abstained from smoking for at least 12 months and medications were taken as recommended by participants' doctors during the study.\n[5] Participants were randomly assigned by drawing numbered disks at random from a bag to do a 2 h walk either along a commercial street in London (Oxford Street) or in an urban park (Hyde Park).\n[6] Baseline measurements of participants were taken before the walk in the hospital laboratory.\n[7] During each walk session, black carbon, particulate matter (PM) concentrations, ultrafine particles, and nitrogen dioxide (NO2) concentrations were measured.\n[8] FINDINGS Between October, 2012, and June, 2014, we screened 135 participants, of whom 40 healthy volunteers, 40 individuals with COPD, and 39 with ischaemic heart disease were recruited.\n[9] Concentrations of black carbon, NO2, PM10, PM2.5, and ultrafine particles were higher on Oxford Street than in Hyde Park.\n[10] Participants with COPD reported more cough (odds ratio [OR] 1·95, 95% CI 0·96-3·95; p<0·1), sputum (3·15, 1·39-7·13; p<0·05), shortness of breath (1·86, 0·97-3·57; p<0·1), and wheeze (4·00, 1·52-10·50; p<0·05) after walking down Oxford Street compared with Hyde Park.\n[11] In all participants, irrespective of their disease status, walking in Hyde Park led to an increase in lung function (forced expiratory volume in the first second [FEV1] and forced vital capacity [FVC]) and a decrease in pulse wave velocity (PWV) and augmentation index up to 26 h after the walk.\n[12] By contrast, these beneficial responses were attenuated after walking on Oxford Street.\n[13] In participants with COPD, a reduction in FEV1 and FVC, and an increase in R5-20 were associated with an increase in during-walk exposure to NO2, ultrafine particles and PM2.5, and an increase in PWV and augmentation index with NO2 and ultrafine particles.\n[14] In healthy volunteers, PWV and augmentation index were associated both with black carbon and ultrafine particles.\n[15] INTERPRETATION Short-term exposure to traffic pollution prevents the beneficial cardiopulmonary effects of walking in people with COPD, ischaemic heart disease, and those free from chronic cardiopulmonary diseases.\n[16] Medication use might reduce the adverse effects of air pollution in individuals with ischaemic heart disease.\n[17] Policies should aim to control ambient levels of air pollution along busy streets in view of these negative health effects.\n[18] FUNDING British Heart Foundation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Participants with COPD reported more cough (odds ratio [OR] 1·95, 95% CI 0·96-3·95; p<0·1), sputum (3·15, 1·39-7·13; p<0·05), shortness of breath (1·86, 0·97-3·57; p<0·1), and wheeze (4·00, 1·52-10·50; p<0·05) after walking down Oxford Street compared with Hyde Park.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1373, "doc_id": 21003930, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [21003930], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Walking in traffic areas in London improves lung function in elderly adults.\n\nDocument title: Respiratory and cardiovascular responses to walking down a traffic-polluted road compared with walking in a traffic-free area in participants aged 60 years and older with chronic lung or heart disease and age-matched healthy controls: a randomised, crossover study\n\nAbstract sentences:\n[0] BACKGROUND Long-term exposure to pollution can lead to an increase in the rate of decline of lung function, especially in older individuals and in those with chronic obstructive pulmonary disease (COPD), whereas shorter-term exposure at higher pollution levels has been implicated in causing excess deaths from ischaemic heart disease and exacerbations of COPD.\n[1] We aimed to assess the effects on respiratory and cardiovascular responses of walking down a busy street with high levels of pollution compared with walking in a traffic-free area with lower pollution levels in older adults.\n[2] METHODS In this randomised, crossover study, we recruited men and women aged 60 years and older with angiographically proven stable ischaemic heart disease or stage 2 Global initiative for Obstructive Lung Disease (GOLD) COPD who had been clinically stable for 6 months, and age-matched healthy volunteers.\n[3] Individuals with ischaemic heart disease or COPD were recruited from existing databases or outpatient respiratory and cardiology clinics at the Royal Brompton & Harefield NHS Foundation Trust and age-matched healthy volunteers using advertising and existing databases.\n[4] All participants had abstained from smoking for at least 12 months and medications were taken as recommended by participants' doctors during the study.\n[5] Participants were randomly assigned by drawing numbered disks at random from a bag to do a 2 h walk either along a commercial street in London (Oxford Street) or in an urban park (Hyde Park).\n[6] Baseline measurements of participants were taken before the walk in the hospital laboratory.\n[7] During each walk session, black carbon, particulate matter (PM) concentrations, ultrafine particles, and nitrogen dioxide (NO2) concentrations were measured.\n[8] FINDINGS Between October, 2012, and June, 2014, we screened 135 participants, of whom 40 healthy volunteers, 40 individuals with COPD, and 39 with ischaemic heart disease were recruited.\n[9] Concentrations of black carbon, NO2, PM10, PM2.5, and ultrafine particles were higher on Oxford Street than in Hyde Park.\n[10] Participants with COPD reported more cough (odds ratio [OR] 1·95, 95% CI 0·96-3·95; p<0·1), sputum (3·15, 1·39-7·13; p<0·05), shortness of breath (1·86, 0·97-3·57; p<0·1), and wheeze (4·00, 1·52-10·50; p<0·05) after walking down Oxford Street compared with Hyde Park.\n[11] In all participants, irrespective of their disease status, walking in Hyde Park led to an increase in lung function (forced expiratory volume in the first second [FEV1] and forced vital capacity [FVC]) and a decrease in pulse wave velocity (PWV) and augmentation index up to 26 h after the walk.\n[12] By contrast, these beneficial responses were attenuated after walking on Oxford Street.\n[13] In participants with COPD, a reduction in FEV1 and FVC, and an increase in R5-20 were associated with an increase in during-walk exposure to NO2, ultrafine particles and PM2.5, and an increase in PWV and augmentation index with NO2 and ultrafine particles.\n[14] In healthy volunteers, PWV and augmentation index were associated both with black carbon and ultrafine particles.\n[15] INTERPRETATION Short-term exposure to traffic pollution prevents the beneficial cardiopulmonary effects of walking in people with COPD, ischaemic heart disease, and those free from chronic cardiopulmonary diseases.\n[16] Medication use might reduce the adverse effects of air pollution in individuals with ischaemic heart disease.\n[17] Policies should aim to control ambient levels of air pollution along busy streets in view of these negative health effects.\n[18] FUNDING British Heart Foundation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [11, 12]\nExplanation: Evidence states: \"In all participants, irrespective of their disease status, walking in Hyde Park led to an increase in lung function (forced expiratory volume in the first second [FEV1] and forced vital capacity [FVC]) and a decrease in pulse wave velocity (PWV) and augmentation index up to 26 h after the walk. By contrast, these beneficial responses were attenuated after walking on Oxford Street.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1373, "doc_id": 21003930, "label": "CONTRADICTS", "evidence_sentence_ids": [11, 12], "cited_doc_ids": [21003930], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Walking in traffic areas in London improves lung function in elderly adults.\n\nDocument title: Respiratory and cardiovascular responses to walking down a traffic-polluted road compared with walking in a traffic-free area in participants aged 60 years and older with chronic lung or heart disease and age-matched healthy controls: a randomised, crossover study\n\nAbstract sentences:\n[0] BACKGROUND Long-term exposure to pollution can lead to an increase in the rate of decline of lung function, especially in older individuals and in those with chronic obstructive pulmonary disease (COPD), whereas shorter-term exposure at higher pollution levels has been implicated in causing excess deaths from ischaemic heart disease and exacerbations of COPD.\n[1] We aimed to assess the effects on respiratory and cardiovascular responses of walking down a busy street with high levels of pollution compared with walking in a traffic-free area with lower pollution levels in older adults.\n[2] METHODS In this randomised, crossover study, we recruited men and women aged 60 years and older with angiographically proven stable ischaemic heart disease or stage 2 Global initiative for Obstructive Lung Disease (GOLD) COPD who had been clinically stable for 6 months, and age-matched healthy volunteers.\n[3] Individuals with ischaemic heart disease or COPD were recruited from existing databases or outpatient respiratory and cardiology clinics at the Royal Brompton & Harefield NHS Foundation Trust and age-matched healthy volunteers using advertising and existing databases.\n[4] All participants had abstained from smoking for at least 12 months and medications were taken as recommended by participants' doctors during the study.\n[5] Participants were randomly assigned by drawing numbered disks at random from a bag to do a 2 h walk either along a commercial street in London (Oxford Street) or in an urban park (Hyde Park).\n[6] Baseline measurements of participants were taken before the walk in the hospital laboratory.\n[7] During each walk session, black carbon, particulate matter (PM) concentrations, ultrafine particles, and nitrogen dioxide (NO2) concentrations were measured.\n[8] FINDINGS Between October, 2012, and June, 2014, we screened 135 participants, of whom 40 healthy volunteers, 40 individuals with COPD, and 39 with ischaemic heart disease were recruited.\n[9] Concentrations of black carbon, NO2, PM10, PM2.5, and ultrafine particles were higher on Oxford Street than in Hyde Park.\n[10] Participants with COPD reported more cough (odds ratio [OR] 1·95, 95% CI 0·96-3·95; p<0·1), sputum (3·15, 1·39-7·13; p<0·05), shortness of breath (1·86, 0·97-3·57; p<0·1), and wheeze (4·00, 1·52-10·50; p<0·05) after walking down Oxford Street compared with Hyde Park.\n[11] In all participants, irrespective of their disease status, walking in Hyde Park led to an increase in lung function (forced expiratory volume in the first second [FEV1] and forced vital capacity [FVC]) and a decrease in pulse wave velocity (PWV) and augmentation index up to 26 h after the walk.\n[12] By contrast, these beneficial responses were attenuated after walking on Oxford Street.\n[13] In participants with COPD, a reduction in FEV1 and FVC, and an increase in R5-20 were associated with an increase in during-walk exposure to NO2, ultrafine particles and PM2.5, and an increase in PWV and augmentation index with NO2 and ultrafine particles.\n[14] In healthy volunteers, PWV and augmentation index were associated both with black carbon and ultrafine particles.\n[15] INTERPRETATION Short-term exposure to traffic pollution prevents the beneficial cardiopulmonary effects of walking in people with COPD, ischaemic heart disease, and those free from chronic cardiopulmonary diseases.\n[16] Medication use might reduce the adverse effects of air pollution in individuals with ischaemic heart disease.\n[17] Policies should aim to control ambient levels of air pollution along busy streets in view of these negative health effects.\n[18] FUNDING British Heart Foundation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [15]\nExplanation: Evidence states: \"INTERPRETATION Short-term exposure to traffic pollution prevents the beneficial cardiopulmonary effects of walking in people with COPD, ischaemic heart disease, and those free from chronic cardiopulmonary diseases.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1373, "doc_id": 21003930, "label": "CONTRADICTS", "evidence_sentence_ids": [15], "cited_doc_ids": [21003930], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Weighed food records (WFR) result in high completion since they're cheap to run and impose low participant burden.\n\nDocument title: Accuracy of weighed dietary records in studies of diet and health.\n\nAbstract sentences:\n[0] OBJECTIVE To provide an independent evaluation of seven day weighed dietary records, which are currently accepted as the most accurate technique for assessing habitual dietary intake in studies investigating the links between diet and health.\n[1] DESIGN Subjects who had previously participated in the Northern Ireland diet and health study were reselected by stratified random sampling to represent the range of energy intakes in the study as assessed by the seven day weighed dietary record.\n[2] SETTING Northern Ireland.\n[3] SUBJECTS 31 Free living adults (16 men and 15 women).\n[4] MAIN OUTCOME MEASURES Energy intake as measured by the seven day weighed dietary record and total energy expenditure estimated concurrently by the doubly labelled water technique.\n[5] RESULTS Average recorded energy intakes were significantly lower than measured expenditure in the group overall (9.66 MJ/day v 12.15 MJ/day, 95% confidence interval 1.45 to 3.53 MJ/day).\n[6] Among those in the upper third of energy intakes the mean (SE) ratio of intake to expenditure was close to 1.0, indicating accurate records (men 1.01 (0.11), women 0.96 (0.08].\n[7] In the middle and lower thirds the ratios for men were only 0.74 (0.05) and 0.70 (0.07) respectively and for women 0.89 (0.07) and 0.61 (0.07).\n[8] CONCLUSIONS These results show a serious bias in reporting habitual energy intake.\n[9] If substantiated they may have wide implications for the interpretation of many nutritional studies."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1374, "doc_id": 21993510, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [21993510], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Weighed food records (WFR) result in poor completion since they're costly to run and impose high participant burden.\n\nDocument title: Accuracy of weighed dietary records in studies of diet and health.\n\nAbstract sentences:\n[0] OBJECTIVE To provide an independent evaluation of seven day weighed dietary records, which are currently accepted as the most accurate technique for assessing habitual dietary intake in studies investigating the links between diet and health.\n[1] DESIGN Subjects who had previously participated in the Northern Ireland diet and health study were reselected by stratified random sampling to represent the range of energy intakes in the study as assessed by the seven day weighed dietary record.\n[2] SETTING Northern Ireland.\n[3] SUBJECTS 31 Free living adults (16 men and 15 women).\n[4] MAIN OUTCOME MEASURES Energy intake as measured by the seven day weighed dietary record and total energy expenditure estimated concurrently by the doubly labelled water technique.\n[5] RESULTS Average recorded energy intakes were significantly lower than measured expenditure in the group overall (9.66 MJ/day v 12.15 MJ/day, 95% confidence interval 1.45 to 3.53 MJ/day).\n[6] Among those in the upper third of energy intakes the mean (SE) ratio of intake to expenditure was close to 1.0, indicating accurate records (men 1.01 (0.11), women 0.96 (0.08].\n[7] In the middle and lower thirds the ratios for men were only 0.74 (0.05) and 0.70 (0.07) respectively and for women 0.89 (0.07) and 0.61 (0.07).\n[8] CONCLUSIONS These results show a serious bias in reporting habitual energy intake.\n[9] If substantiated they may have wide implications for the interpretation of many nutritional studies."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1375, "doc_id": 21993510, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [21993510], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Whole brain radiotherapy increases the occurrence of new brain metastases.\n\nDocument title: Stereotactic radiosurgery plus whole-brain radiation therapy vs stereotactic radiosurgery alone for treatment of brain metastases: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT In patients with brain metastases, it is unclear whether adding up-front whole-brain radiation therapy (WBRT) to stereotactic radiosurgery (SRS) has beneficial effects on mortality or neurologic function compared with SRS alone.\n[1] OBJECTIVE To determine if WBRT combined with SRS results in improvements in survival, brain tumor control, functional preservation rate, and frequency of neurologic death.\n[2] DESIGN, SETTING, AND PATIENTS Randomized controlled trial of 132 patients with 1 to 4 brain metastases, each less than 3 cm in diameter, enrolled at 11 hospitals in Japan between October 1999 and December 2003.\n[3] INTERVENTIONS Patients were randomly assigned to receive WBRT plus SRS (65 patients) or SRS alone (67 patients).\n[4] MAIN OUTCOME MEASURES The primary end point was overall survival; secondary end points were brain tumor recurrence, salvage brain treatment, functional preservation, toxic effects of radiation, and cause of death.\n[5] RESULTS The median survival time and the 1-year actuarial survival rate were 7.5 months and 38.5% (95% confidence interval, 26.7%-50.3%) in the WBRT + SRS group and 8.0 months and 28.4% (95% confidence interval, 17.6%-39.2%) for SRS alone (P = .42).\n[6] The 12-month brain tumor recurrence rate was 46.8% in the WBRT + SRS group and 76.4% for SRS alone group (P<.001).\n[7] Salvage brain treatment was less frequently required in the WBRT + SRS group (n = 10) than with SRS alone (n = 29) (P<.001).\n[8] Death was attributed to neurologic causes in 22.8% of patients in the WBRT + SRS group and in 19.3% of those treated with SRS alone (P = .64).\n[9] There were no significant differences in systemic and neurologic functional preservation and toxic effects of radiation.\n[10] CONCLUSIONS Compared with SRS alone, the use of WBRT plus SRS did not improve survival for patients with 1 to 4 brain metastases, but intracranial relapse occurred considerably more frequently in those who did not receive WBRT.\n[11] Consequently, salvage treatment is frequently required when up-front WBRT is not used.\n[12] TRIAL REGISTRATION umin.ac.jp/ctr Identifier: C000000412."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"The 12-month brain tumor recurrence rate was 46.8% in the WBRT + SRS group and 76.4% for SRS alone group (P<.001).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1376, "doc_id": 3944632, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [3944632], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Whole brain radiotherapy increases the occurrence of new brain metastases.\n\nDocument title: Stereotactic radiosurgery plus whole-brain radiation therapy vs stereotactic radiosurgery alone for treatment of brain metastases: a randomized controlled trial.\n\nAbstract sentences:\n[0] CONTEXT In patients with brain metastases, it is unclear whether adding up-front whole-brain radiation therapy (WBRT) to stereotactic radiosurgery (SRS) has beneficial effects on mortality or neurologic function compared with SRS alone.\n[1] OBJECTIVE To determine if WBRT combined with SRS results in improvements in survival, brain tumor control, functional preservation rate, and frequency of neurologic death.\n[2] DESIGN, SETTING, AND PATIENTS Randomized controlled trial of 132 patients with 1 to 4 brain metastases, each less than 3 cm in diameter, enrolled at 11 hospitals in Japan between October 1999 and December 2003.\n[3] INTERVENTIONS Patients were randomly assigned to receive WBRT plus SRS (65 patients) or SRS alone (67 patients).\n[4] MAIN OUTCOME MEASURES The primary end point was overall survival; secondary end points were brain tumor recurrence, salvage brain treatment, functional preservation, toxic effects of radiation, and cause of death.\n[5] RESULTS The median survival time and the 1-year actuarial survival rate were 7.5 months and 38.5% (95% confidence interval, 26.7%-50.3%) in the WBRT + SRS group and 8.0 months and 28.4% (95% confidence interval, 17.6%-39.2%) for SRS alone (P = .42).\n[6] The 12-month brain tumor recurrence rate was 46.8% in the WBRT + SRS group and 76.4% for SRS alone group (P<.001).\n[7] Salvage brain treatment was less frequently required in the WBRT + SRS group (n = 10) than with SRS alone (n = 29) (P<.001).\n[8] Death was attributed to neurologic causes in 22.8% of patients in the WBRT + SRS group and in 19.3% of those treated with SRS alone (P = .64).\n[9] There were no significant differences in systemic and neurologic functional preservation and toxic effects of radiation.\n[10] CONCLUSIONS Compared with SRS alone, the use of WBRT plus SRS did not improve survival for patients with 1 to 4 brain metastases, but intracranial relapse occurred considerably more frequently in those who did not receive WBRT.\n[11] Consequently, salvage treatment is frequently required when up-front WBRT is not used.\n[12] TRIAL REGISTRATION umin.ac.jp/ctr Identifier: C000000412."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"CONCLUSIONS Compared with SRS alone, the use of WBRT plus SRS did not improve survival for patients with 1 to 4 brain metastases, but intracranial relapse occurred considerably more frequently in those who did not receive WBRT.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1376, "doc_id": 3944632, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [3944632], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Women are more susceptible to death due to pneumonia when compared to men.\n\nDocument title: Gender-dependent differences in outcome after the treatment of infection in hospitalized patients.\n\nAbstract sentences:\n[0] CONTEXT While it is established that management strategies and outcomes differ by gender for many diseases, its effect on infection has not been adequately studied.\n[1] OBJECTIVE To investigate the role of gender among hospitalized patients treated for infection.\n[2] DESIGN Observational cohort study conducted during a 26-month period from December 1996 through January 1999.\n[3] SETTING University-affiliated hospital.\n[4] PARTICIPANTS A total of 892 patients in the surgical units of the hospital with 1470 consecutive infectious episodes (782 in men and 688 in women).\n[5] MAIN OUTCOME MEASURES Mortality during hospitalization by gender for infection episodes overall and for specific infectious sites, including lung, peritoneum, bloodstream, catheter, urine, surgical site, and skin/soft tissue.\n[6] RESULTS Among all infections, there was no significant difference in mortality based on gender (men, 11.1% vs women, 14.2%; P = .07).\n[7] After logistic regression analysis, factors independently associated with mortality included higher APACHE (Acute Physiology and Chronic Health Evaluation) II score, older age, malignancy, blood transfusion, and diagnosis of infection more than 7 days after admission, but not gender (female odds ratio [OR] for death, 1.32; 95% confidence interval [CI], 0.90-1.94; P = .16).\n[8] Mortality was higher in women for lung (men, 18% vs women, 34%; P = .002) and soft tissue (men, 2% vs women, 10%; P < or = .05) infection; for other infectious sites, mortality did not differ by gender.\n[9] Factors associated with mortality due to pneumonia by logistic regression included higher APACHE II score, malignancy, diabetes mellitus, diagnosis of infection more than 7 days after admission, older age, transplantation, and female gender (OR for death, 2.25; 95% CI, 1.17-4.32; P = .02).\n[10] CONCLUSIONS Although gender may not be predictive of mortality among all infections, women appear to be at increased risk for death from hospital-acquired pneumonia, even after controlling for other comorbidities."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"CONCLUSIONS Although gender may not be predictive of mortality among all infections, women appear to be at increased risk for death from hospital-acquired pneumonia, even after controlling for other comorbidities.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1378, "doc_id": 2488880, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [2488880], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Women with a lower birth weight are more likely to develop breast cancer later in life.\n\nDocument title: Birth Size and Breast Cancer Risk: Re-analysis of Individual Participant Data from 32 Studies\n\nAbstract sentences:\n[0] BACKGROUND Birth size, perhaps a proxy for prenatal environment, might be a correlate of subsequent breast cancer risk, but findings from epidemiological studies have been inconsistent.\n[1] We re-analysed individual participant data from published and unpublished studies to obtain more precise estimates of the magnitude and shape of the birth size-breast cancer association.\n[2] METHODS AND FINDINGS Studies were identified through computer-assisted and manual searches, and personal communication with investigators.\n[3] Individual participant data from 32 studies, comprising 22,058 breast cancer cases, were obtained.\n[4] Random effect models were used, if appropriate, to combine study-specific estimates of effect.\n[5] Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003).\n[6] Relative to women who weighed 3.000-3.499 kg, the risk was 0.96 (CI 0.80-1.16) in those who weighed < 2.500 kg, and 1.12 (95% CI 1.00-1.25) in those who weighed > or = 4.000 kg (p for linear trend = 0.001) in birth record data.\n[7] Birth length and head circumference from birth records were also positively associated with breast cancer risk (pooled RR per one SD increment: 1.06 [95% CI 1.03-1.10] and 1.09 [95% CI 1.03-1.15], respectively).\n[8] Simultaneous adjustment for these three birth size variables showed that length was the strongest independent predictor of risk.\n[9] The birth size effects did not appear to be confounded or mediated by established breast cancer risk factors and were not modified by age or menopausal status.\n[10] The cumulative incidence of breast cancer per 100 women by age 80 y in the study populations was estimated to be 10.0, 10.0, 10.4, and 11.5 in those who were, respectively, in the bottom, second, third, and top fourths of the birth length distribution.\n[11] CONCLUSIONS This pooled analysis of individual participant data is consistent with birth size, and in particular birth length, being an independent correlate of breast cancer risk in adulthood."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1380, "doc_id": 16322674, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [16322674, 23557241, 17450673], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Women with a lower birth weight are more likely to develop breast cancer later in life.\n\nDocument title: Birth Size and Breast Cancer Risk: Re-analysis of Individual Participant Data from 32 Studies\n\nAbstract sentences:\n[0] BACKGROUND Birth size, perhaps a proxy for prenatal environment, might be a correlate of subsequent breast cancer risk, but findings from epidemiological studies have been inconsistent.\n[1] We re-analysed individual participant data from published and unpublished studies to obtain more precise estimates of the magnitude and shape of the birth size-breast cancer association.\n[2] METHODS AND FINDINGS Studies were identified through computer-assisted and manual searches, and personal communication with investigators.\n[3] Individual participant data from 32 studies, comprising 22,058 breast cancer cases, were obtained.\n[4] Random effect models were used, if appropriate, to combine study-specific estimates of effect.\n[5] Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003).\n[6] Relative to women who weighed 3.000-3.499 kg, the risk was 0.96 (CI 0.80-1.16) in those who weighed < 2.500 kg, and 1.12 (95% CI 1.00-1.25) in those who weighed > or = 4.000 kg (p for linear trend = 0.001) in birth record data.\n[7] Birth length and head circumference from birth records were also positively associated with breast cancer risk (pooled RR per one SD increment: 1.06 [95% CI 1.03-1.10] and 1.09 [95% CI 1.03-1.15], respectively).\n[8] Simultaneous adjustment for these three birth size variables showed that length was the strongest independent predictor of risk.\n[9] The birth size effects did not appear to be confounded or mediated by established breast cancer risk factors and were not modified by age or menopausal status.\n[10] The cumulative incidence of breast cancer per 100 women by age 80 y in the study populations was estimated to be 10.0, 10.0, 10.4, and 11.5 in those who were, respectively, in the bottom, second, third, and top fourths of the birth length distribution.\n[11] CONCLUSIONS This pooled analysis of individual participant data is consistent with birth size, and in particular birth length, being an independent correlate of breast cancer risk in adulthood."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Relative to women who weighed 3.000-3.499 kg, the risk was 0.96 (CI 0.80-1.16) in those who weighed < 2.500 kg, and 1.12 (95% CI 1.00-1.25) in those who weighed > or = 4.000 kg (p for linear trend = 0.001) in birth record data.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1380, "doc_id": 16322674, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [16322674, 23557241, 17450673], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Women with a lower birth weight are more likely to develop breast cancer later in life.\n\nDocument title: Intrauterine factors and risk of breast cancer: a systematic review and meta-analysis of current evidence.\n\nAbstract sentences:\n[0] BACKGROUND Emerging evidence suggests an association between female prenatal experience and her subsequent risk of developing breast cancer.\n[1] Potential underlying mechanisms include variation in amounts of maternal endogenous sex hormones and growth hormones, germ-cell mutations, formation of cancer stem-cells, and other genetic or epigenetic events.\n[2] We reviewed and summarised quantitatively the available data on intrauterine exposures and risk of breast cancer.\n[3] METHODS We systematically searched for studies that assessed association between perinatal factors and risk of breast cancer.\n[4] We reviewed separately each of the perinatal factors, including birthweight, birth length, parental age at delivery, gestational age, intrauterine exposure to diethylstilbestrol, twin membership, maternal pre-eclampsia or eclampsia, and other factors.\n[5] FINDINGS We identified 57 studies published between Oct 1, 1980, and June 21, 2007.\n[6] Increased risk of breast cancer was noted with increased birthweight (relative risk [RR] 1.15 [95% CI 1.09-1.21]), birth length (1.28 [1.11-1.48]), higher maternal age (1.13 [1.02-1.25]), and paternal age (1.12 [1.05-1.19]).\n[7] Decreased risk of breast cancer was noted for maternal pre-eclampsia and eclampsia (0.48 [0.30-0.78]) and twin membership (0.93 [0.87-1.00]).\n[8] No association was noted between risk of breast cancer and gestational age at birth (0.95 [0.71-1.26]) or maternal diethylstilbestrol treatment (1.40 [0.86-2.28]).\n[9] INTERPRETATION The intrauterine environment contributes to the predisposition of women to breast cancer in adulthood.\n[10] The in-utero mechanisms responsible for such predisposition need to be elucidated."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Increased risk of breast cancer was noted with increased birthweight (relative risk [RR] 1.15 [95% CI 1.09-1.21]), birth length (1.28 [1.11-1.48]), higher maternal age (1.13 [1.02-1.25]), and paternal age (1.12 [1.05-1.19]).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1380, "doc_id": 23557241, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [16322674, 23557241, 17450673], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Women with a lower birth weight are more likely to develop breast cancer later in life.\n\nDocument title: Intrauterine environments and breast cancer risk: meta-analysis and systematic review\n\nAbstract sentences:\n[0] INTRODUCTION Various perinatal factors, including birth weight, birth order, maternal age, gestational age, twin status, and parental smoking, have been postulated to affect breast cancer risk in daughters by altering the hormonal environment of the developing fetal mammary glands.\n[1] Despite ample biologic plausibility, epidemiologic studies to date have yielded conflicting results.\n[2] We investigated the associations between perinatal factors and subsequent breast cancer risk through meta-analyses.\n[3] METHODS We reviewed breast cancer studies published from January 1966 to February 2007 that included data on birth weight, birth order, maternal age, gestational age, twin status, and maternal or paternal smoking.\n[4] Meta-analyses using random effect models were employed to summarize the results.\n[5] RESULTS We found that heavier birth weights were associated with increased breast cancer risk, with studies involving five categories of birth weight identifying odds ratios (ORs) of 1.24 (95% confidence interval [CI] 1.04 to 1.48) for 4,000 g or more and 1.15 (95% CI 1.04 to 1.26) for 3,500 g to 3,999 g, relative to a birth weight of 2,500 to 2,599 g. These studies provided no support for a J-shaped relationship of birthweight to risk.\n[6] Support for an association with birthweight was also derived from studies based on three birth weight categories (OR 1.15 [95% CI 1.01 to 1.31] for > or =4,000 g relative to <3,000 g) and two birth weight categories (OR 1.09 [95% CI 1.02 to 1.18] for > or =3,000 g relative to <3,000 g).\n[7] Women born to older mothers and twins were also at some increased risk, but the results were heterogeneous across studies and publication years.\n[8] Birth order, prematurity, and maternal smoking were unrelated to breast cancer risk.\n[9] CONCLUSION Our findings provide some support for the hypothesis that in utero exposures reflective of higher endogenous hormone levels could affect risk for development of breast cancer in adulthood."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"RESULTS We found that heavier birth weights were associated with increased breast cancer risk, with studies involving five categories of birth weight identifying odds ratios (ORs) of 1.24 (95% confidence interval [CI] 1.04 to 1.48) for 4,000 g or more and 1.15 (95% CI 1.04 to 1.26) for 3,500 g to 3,999 g, relative to a birth weight of 2,500 to 2,599 g. These studies provided no support for a J-shaped relationship of birthweight to risk.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1380, "doc_id": 17450673, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [16322674, 23557241, 17450673], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: YAP/TAZ is required in intestinal regeneration in mouse models of ulcerative colitis.\n\nDocument title: YAP/TAZ-Dependent Reprogramming of Colonic Epithelium Links ECM Remodeling to Tissue Regeneration\n\nAbstract sentences:\n[0] Tissue regeneration requires dynamic cellular adaptation to the wound environment.\n[1] It is currently unclear how this is orchestrated at the cellular level and how cell fate is affected by severe tissue damage.\n[2] Here we dissect cell fate transitions during colonic regeneration in a mouse dextran sulfate sodium (DSS) colitis model, and we demonstrate that the epithelium is transiently reprogrammed into a primitive state.\n[3] This is characterized by de novo expression of fetal markers as well as suppression of markers for adult stem and differentiated cells.\n[4] The fate change is orchestrated by remodeling the extracellular matrix (ECM), increased FAK/Src signaling, and ultimately YAP/TAZ activation.\n[5] In a defined cell culture system recapitulating the extracellular matrix remodeling observed in vivo, we show that a collagen 3D matrix supplemented with Wnt ligands is sufficient to sustain endogenous YAP/TAZ and induce conversion of cell fate.\n[6] This provides a simple model for tissue regeneration, implicating cellular reprogramming as an essential element."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"The fate change is orchestrated by remodeling the extracellular matrix (ECM), increased FAK/Src signaling, and ultimately YAP/TAZ activation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1381, "doc_id": 13481880, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [13481880], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: YAP/TAZ is required in intestinal regeneration in mouse models of ulcerative colitis.\n\nDocument title: YAP/TAZ-Dependent Reprogramming of Colonic Epithelium Links ECM Remodeling to Tissue Regeneration\n\nAbstract sentences:\n[0] Tissue regeneration requires dynamic cellular adaptation to the wound environment.\n[1] It is currently unclear how this is orchestrated at the cellular level and how cell fate is affected by severe tissue damage.\n[2] Here we dissect cell fate transitions during colonic regeneration in a mouse dextran sulfate sodium (DSS) colitis model, and we demonstrate that the epithelium is transiently reprogrammed into a primitive state.\n[3] This is characterized by de novo expression of fetal markers as well as suppression of markers for adult stem and differentiated cells.\n[4] The fate change is orchestrated by remodeling the extracellular matrix (ECM), increased FAK/Src signaling, and ultimately YAP/TAZ activation.\n[5] In a defined cell culture system recapitulating the extracellular matrix remodeling observed in vivo, we show that a collagen 3D matrix supplemented with Wnt ligands is sufficient to sustain endogenous YAP/TAZ and induce conversion of cell fate.\n[6] This provides a simple model for tissue regeneration, implicating cellular reprogramming as an essential element."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"In a defined cell culture system recapitulating the extracellular matrix remodeling observed in vivo, we show that a collagen 3D matrix supplemented with Wnt ligands is sufficient to sustain endogenous YAP/TAZ and induce conversion of cell fate.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1381, "doc_id": 13481880, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [13481880], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: aPKCz causes tumour suppression by affecting glutamine metabolism.\n\nDocument title: Control of Nutrient Stress-Induced Metabolic Reprogramming by PKCζ in Tumorigenesis\n\nAbstract sentences:\n[0] Tumor cells have high-energetic and anabolic needs and are known to adapt their metabolism to be able to survive and keep proliferating under conditions of nutrient stress.\n[1] We show that PKCζ deficiency promotes the plasticity necessary for cancer cells to reprogram their metabolism to utilize glutamine through the serine biosynthetic pathway in the absence of glucose.\n[2] PKCζ represses the expression of two key enzymes of the pathway, PHGDH and PSAT1, and phosphorylates PHGDH at key residues to inhibit its enzymatic activity.\n[3] Interestingly, the loss of PKCζ in mice results in enhanced intestinal tumorigenesis and increased levels of these two metabolic enzymes, whereas patients with low levels of PKCζ have a poor prognosis.\n[4] Furthermore, PKCζ and caspase-3 activities are correlated with PHGDH levels in human intestinal tumors.\n[5] Taken together, this demonstrates that PKCζ is a critical metabolic tumor suppressor in mouse and human cancer."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Interestingly, the loss of PKCζ in mice results in enhanced intestinal tumorigenesis and increased levels of these two metabolic enzymes, whereas patients with low levels of PKCζ have a poor prognosis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1383, "doc_id": 17755060, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [17755060], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: aPKCz causes tumour suppression by affecting glutamine metabolism.\n\nDocument title: Control of Nutrient Stress-Induced Metabolic Reprogramming by PKCζ in Tumorigenesis\n\nAbstract sentences:\n[0] Tumor cells have high-energetic and anabolic needs and are known to adapt their metabolism to be able to survive and keep proliferating under conditions of nutrient stress.\n[1] We show that PKCζ deficiency promotes the plasticity necessary for cancer cells to reprogram their metabolism to utilize glutamine through the serine biosynthetic pathway in the absence of glucose.\n[2] PKCζ represses the expression of two key enzymes of the pathway, PHGDH and PSAT1, and phosphorylates PHGDH at key residues to inhibit its enzymatic activity.\n[3] Interestingly, the loss of PKCζ in mice results in enhanced intestinal tumorigenesis and increased levels of these two metabolic enzymes, whereas patients with low levels of PKCζ have a poor prognosis.\n[4] Furthermore, PKCζ and caspase-3 activities are correlated with PHGDH levels in human intestinal tumors.\n[5] Taken together, this demonstrates that PKCζ is a critical metabolic tumor suppressor in mouse and human cancer."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Taken together, this demonstrates that PKCζ is a critical metabolic tumor suppressor in mouse and human cancer.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1383, "doc_id": 17755060, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [17755060], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: cSMAC formation represses weak ligand signalling.\n\nDocument title: The stimulatory potency of T cell antigens is influenced by the formation of the immunological synapse.\n\nAbstract sentences:\n[0] T cell activation is predicated on the interaction between the T cell receptor and peptide-major histocompatibility (pMHC) ligands.\n[1] The factors that determine the stimulatory potency of a pMHC molecule remain unclear.\n[2] We describe results showing that a peptide exhibiting many hallmarks of a weak agonist stimulates T cells to proliferate more than the wild-type agonist ligand.\n[3] An in silico approach suggested that the inability to form the central supramolecular activation cluster (cSMAC) could underlie the increased proliferation.\n[4] This conclusion was supported by experiments that showed that enhancing cSMAC formation reduced stimulatory capacity of the weak peptide.\n[5] Our studies highlight the fact that a complex interplay of factors determines the quality of a T cell antigen."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"This conclusion was supported by experiments that showed that enhancing cSMAC formation reduced stimulatory capacity of the weak peptide.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1386, "doc_id": 306006, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [306006], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: eRNAs influence is linked to senescence, aging, and carcinogenesis.\n\nDocument title: eRNAs are required for p53-dependent enhancer activity and gene transcription.\n\nAbstract sentences:\n[0] Binding within or nearby target genes involved in cell proliferation and survival enables the p53 tumor suppressor gene to regulate their transcription and cell-cycle progression.\n[1] Using genome-wide chromatin-binding profiles, we describe binding of p53 also to regions located distantly from any known p53 target gene.\n[2] Interestingly, many of these regions possess conserved p53-binding sites and all known hallmarks of enhancer regions.\n[3] We demonstrate that these p53-bound enhancer regions (p53BERs) indeed contain enhancer activity and interact intrachromosomally with multiple neighboring genes to convey long-distance p53-dependent transcription regulation.\n[4] Furthermore, p53BERs produce, in a p53-dependent manner, enhancer RNAs (eRNAs) that are required for efficient transcriptional enhancement of interacting target genes and induction of a p53-dependent cell-cycle arrest.\n[5] Thus, our results ascribe transcription enhancement activity to p53 with the capacity to regulate multiple genes from a single genomic binding site.\n[6] Moreover, eRNA production from p53BERs is required for efficient p53 transcription enhancement."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1387, "doc_id": 9669099, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [9669099], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: mcm 5 s 2 U is required for proper decoding of NNR codons in eukaryotes.\n\nDocument title: Mechanistic characterization of the sulfur-relay system for eukaryotic 2-thiouridine biogenesis at tRNA wobble positions\n\nAbstract sentences:\n[0] The wobble modification in tRNAs, 5-methoxycarbonylmethyl-2-thiouridine (mcm(5)s(2)U), is required for the proper decoding of NNR codons in eukaryotes.\n[1] The 2-thio group confers conformational rigidity of mcm(5)s(2)U by largely fixing the C3'-endo ribose puckering, ensuring stable and accurate codon-anticodon pairing.\n[2] We have identified five genes in Saccharomyces cerevisiae, YIL008w (URM1), YHR111w (UBA4), YOR251c (TUM1), YNL119w (NCS2) and YGL211w (NCS6), that are required for 2-thiolation of mcm(5)s(2)U. An in vitro sulfur transfer experiment revealed that Tum1p stimulated the cysteine desulfurase of Nfs1p, and accepted persulfide sulfurs from Nfs1p.\n[3] URM1 is a ubiquitin-related modifier, and UBA4 is an E1-like enzyme involved in protein urmylation.\n[4] The carboxy-terminus of Urm1p was activated as an acyl-adenylate (-COAMP), then thiocarboxylated (-COSH) by Uba4p.\n[5] The activated thiocarboxylate can be utilized in the subsequent reactions for 2-thiouridine formation, mediated by Ncs2p/Ncs6p.\n[6] We could successfully reconstitute the 2-thiouridine formation in vitro using recombinant proteins.\n[7] This study revealed that 2-thiouridine formation shares a pathway and chemical reactions with protein urmylation.\n[8] The sulfur-flow of eukaryotic 2-thiouridine formation is distinct mechanism from the bacterial sulfur-relay system which is based on the persulfide chemistry."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"The wobble modification in tRNAs, 5-methoxycarbonylmethyl-2-thiouridine (mcm(5)s(2)U), is required for the proper decoding of NNR codons in eukaryotes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1390, "doc_id": 2890952, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [2890952], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: miR-142-5P is a known regulator of raised body temperature.\n\nDocument title: RBM3 regulates temperature sensitive miR-142–5p and miR-143 (thermomiRs), which target immune genes and control fever\n\nAbstract sentences:\n[0] Fever is commonly used to diagnose disease and is consistently associated with increased mortality in critically ill patients.\n[1] However, the molecular controls of elevated body temperature are poorly understood.\n[2] We discovered that the expression of RNA-binding motif protein 3 (RBM3), known to respond to cold stress and to modulate microRNA (miRNA) expression, was reduced in 30 patients with fever, and in THP-1-derived macrophages maintained at a fever-like temperature (40 °C).\n[3] Notably, RBM3 expression is reduced during fever whether or not infection is demonstrable.\n[4] Reduced RBM3 expression resulted in increased expression of RBM3-targeted temperature-sensitive miRNAs, we termed thermomiRs.\n[5] ThermomiRs such as miR-142-5p and miR-143 in turn target endogenous pyrogens including IL-6, IL6ST, TLR2, PGE2 and TNF to complete a negative feedback mechanism, which may be crucial to prevent pathological hyperthermia.\n[6] Using normal PBMCs that were exogenously exposed to fever-like temperature (40 °C), we further demonstrate the trend by which decreased levels of RBM3 were associated with increased levels of miR-142-5p and miR-143 and vice versa over a 24 h time course.\n[7] Collectively, our results indicate the existence of a negative feedback loop that regulates fever via reduced RBM3 levels and increased expression of miR-142-5p and miR-143."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"ThermomiRs such as miR-142-5p and miR-143 in turn target endogenous pyrogens including IL-6, IL6ST, TLR2, PGE2 and TNF to complete a negative feedback mechanism, which may be crucial to prevent pathological hyperthermia.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1391, "doc_id": 6766459, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [6766459], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: miR-142-5P is a temperature-sensitive microRNA (miRNA).\n\nDocument title: RBM3 regulates temperature sensitive miR-142–5p and miR-143 (thermomiRs), which target immune genes and control fever\n\nAbstract sentences:\n[0] Fever is commonly used to diagnose disease and is consistently associated with increased mortality in critically ill patients.\n[1] However, the molecular controls of elevated body temperature are poorly understood.\n[2] We discovered that the expression of RNA-binding motif protein 3 (RBM3), known to respond to cold stress and to modulate microRNA (miRNA) expression, was reduced in 30 patients with fever, and in THP-1-derived macrophages maintained at a fever-like temperature (40 °C).\n[3] Notably, RBM3 expression is reduced during fever whether or not infection is demonstrable.\n[4] Reduced RBM3 expression resulted in increased expression of RBM3-targeted temperature-sensitive miRNAs, we termed thermomiRs.\n[5] ThermomiRs such as miR-142-5p and miR-143 in turn target endogenous pyrogens including IL-6, IL6ST, TLR2, PGE2 and TNF to complete a negative feedback mechanism, which may be crucial to prevent pathological hyperthermia.\n[6] Using normal PBMCs that were exogenously exposed to fever-like temperature (40 °C), we further demonstrate the trend by which decreased levels of RBM3 were associated with increased levels of miR-142-5p and miR-143 and vice versa over a 24 h time course.\n[7] Collectively, our results indicate the existence of a negative feedback loop that regulates fever via reduced RBM3 levels and increased expression of miR-142-5p and miR-143."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4, 5]\nExplanation: Evidence states: \"Reduced RBM3 expression resulted in increased expression of RBM3-targeted temperature-sensitive miRNAs, we termed thermomiRs. ThermomiRs such as miR-142-5p and miR-143 in turn target endogenous pyrogens including IL-6, IL6ST, TLR2, PGE2 and TNF to complete a negative feedback mechanism, which may be crucial to prevent pathological hyperthermia.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1392, "doc_id": 6766459, "label": "SUPPORTS", "evidence_sentence_ids": [4, 5], "cited_doc_ids": [6766459], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: miRNAs enforce homeostasis by suppressing low-level ''leaky'' transcription.\n\nDocument title: Roles for MicroRNAs in Conferring Robustness to Biological Processes\n\nAbstract sentences:\n[0] Biological systems use a variety of mechanisms to maintain their functions in the face of environmental and genetic perturbations.\n[1] Increasing evidence suggests that, among their roles as posttranscriptional repressors of gene expression, microRNAs (miRNAs) help to confer robustness to biological processes by reinforcing transcriptional programs and attenuating aberrant transcripts, and they may in some network contexts help suppress random fluctuations in transcript copy number.\n[2] These activities have important consequences for normal development and physiology, disease, and evolution.\n[3] Here, we will discuss examples and principles of miRNAs that contribute to robustness in animal systems."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Increasing evidence suggests that, among their roles as posttranscriptional repressors of gene expression, microRNAs (miRNAs) help to confer robustness to biological processes by reinforcing transcriptional programs and attenuating aberrant transcripts, and they may in some network contexts help suppress random fluctuations in transcript copy number.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1393, "doc_id": 12440953, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [2000038, 12440953], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: miRNAs regulate a unique suite of mRNAs to maintain homeostasis in cells.\n\nDocument title: microRNAs: A Safeguard against Turmoil?\n\nAbstract sentences:\n[0] Emerging data suggest that microRNAs (miRNAs) are instrumental in a variety of stress responses in addition to their more recognized role in development.\n[1] Surprisingly, miRNAs, which normally suppress expression of target transcripts, may become activators of expression during stress.\n[2] This might be partially explained by new interactions of miRNA/Argonaute complexes with RNA-binding proteins that relocate from different subcellular compartments during stress."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1394, "doc_id": 2251426, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [2251426], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: p16INK4A degradation is  linked to an abnormal wound response caused by the microinvasive step of advanced Oral Potentially Malignant Lesions (OPMLs).\n\nDocument title: Monitoring Tumorigenesis and Senescence In Vivo with a p16INK4a-Luciferase Model\n\nAbstract sentences:\n[0] Monitoring cancer and aging in vivo remains experimentally challenging.\n[1] Here, we describe a luciferase knockin mouse (p16(LUC)), which faithfully reports expression of p16(INK4a), a tumor suppressor and aging biomarker.\n[2] Lifelong assessment of luminescence in p16(+/LUC) mice revealed an exponential increase with aging, which was highly variable in a cohort of contemporaneously housed, syngeneic mice.\n[3] Expression of p16(INK4a) with aging did not predict cancer development, suggesting that the accumulation of senescent cells is not a principal determinant of cancer-related death.\n[4] In 14 of 14 tested tumor models, expression of p16(LUC) was focally activated by early neoplastic events, enabling visualization of tumors with sensitivity exceeding other imaging modalities.\n[5] Activation of p16(INK4a) was noted in the emerging neoplasm and surrounding stromal cells.\n[6] This work suggests that p16(INK4a) activation is a characteristic of all emerging cancers, making the p16(LUC) allele a sensitive, unbiased reporter of neoplastic transformation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1397, "doc_id": 17717391, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [17717391], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: p16INK4A degradation is encoded by CDKN2A.\n\nDocument title: Monitoring Tumorigenesis and Senescence In Vivo with a p16INK4a-Luciferase Model\n\nAbstract sentences:\n[0] Monitoring cancer and aging in vivo remains experimentally challenging.\n[1] Here, we describe a luciferase knockin mouse (p16(LUC)), which faithfully reports expression of p16(INK4a), a tumor suppressor and aging biomarker.\n[2] Lifelong assessment of luminescence in p16(+/LUC) mice revealed an exponential increase with aging, which was highly variable in a cohort of contemporaneously housed, syngeneic mice.\n[3] Expression of p16(INK4a) with aging did not predict cancer development, suggesting that the accumulation of senescent cells is not a principal determinant of cancer-related death.\n[4] In 14 of 14 tested tumor models, expression of p16(LUC) was focally activated by early neoplastic events, enabling visualization of tumors with sensitivity exceeding other imaging modalities.\n[5] Activation of p16(INK4a) was noted in the emerging neoplasm and surrounding stromal cells.\n[6] This work suggests that p16(INK4a) activation is a characteristic of all emerging cancers, making the p16(LUC) allele a sensitive, unbiased reporter of neoplastic transformation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1398, "doc_id": 17717391, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [17717391], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: p75 NTR - associated cell death executor (NADE) interacts with the p75 NTR death domain\n\nDocument title: Gamma-Secretase Represents a Therapeutic Target for the Treatment of Invasive Glioma Mediated by the p75 Neurotrophin Receptor\n\nAbstract sentences:\n[0] The multifunctional signaling protein p75 neurotrophin receptor (p75(NTR)) is a central regulator and major contributor to the highly invasive nature of malignant gliomas.\n[1] Here, we show that neurotrophin-dependent regulated intramembrane proteolysis (RIP) of p75(NTR) is required for p75(NTR)-mediated glioma invasion, and identify a previously unnamed process for targeted glioma therapy.\n[2] Expression of cleavage-resistant chimeras of p75(NTR) or treatment of animals bearing p75(NTR)-positive intracranial tumors with clinically applicable gamma-secretase inhibitors resulted in dramatically decreased glioma invasion and prolonged survival.\n[3] Importantly, proteolytic processing of p75(NTR) was observed in p75(NTR)-positive patient tumor specimens and brain tumor initiating cells.\n[4] This work highlights the importance of p75(NTR) as a therapeutic target, suggesting that gamma-secretase inhibitors may have direct clinical application for the treatment of malignant glioma."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1400, "doc_id": 14706752, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14706752], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: qSOFA scores are associated with length of stay in emergency department patients.\n\nDocument title: Prognostic Accuracy of the SOFA Score, SIRS Criteria, and qSOFA Score for In-Hospital Mortality Among Adults With Suspected Infection Admitted to the Intensive Care Unit\n\nAbstract sentences:\n[0] Importance The Sepsis-3 Criteria emphasized the value of a change of 2 or more points in the Sequential [Sepsis-related] Organ Failure Assessment (SOFA) score, introduced quick SOFA (qSOFA), and removed the systemic inflammatory response syndrome (SIRS) criteria from the sepsis definition.\n[1] Objective Externally validate and assess the discriminatory capacities of an increase in SOFA score by 2 or more points, 2 or more SIRS criteria, or a qSOFA score of 2 or more points for outcomes among patients who are critically ill with suspected infection.\n[2] Design, Setting, and Participants Retrospective cohort analysis of 184 875 patients with an infection-related primary admission diagnosis in 182 Australian and New Zealand intensive care units (ICUs) from 2000 through 2015.\n[3] Exposures SOFA, qSOFA, and SIRS criteria applied to data collected within 24 hours of ICU admission.\n[4] Main Outcomes and Measures The primary outcome was in-hospital mortality.\n[5] In-hospital mortality or ICU length of stay (LOS) of 3 days or more was a composite secondary outcome.\n[6] Discrimination was assessed using the area under the receiver operating characteristic curve (AUROC).\n[7] Adjusted analyses were performed using a model of baseline risk determined using variables independent of the scoring systems.\n[8] Results Among 184 875 patients (mean age, 62.9 years [SD, 17.4]; women, 82 540 [44.6%]; most common diagnosis bacterial pneumonia, 32 634 [17.7%]), a total of 34 578 patients (18.7%) died in the hospital, and 102 976 patients (55.7%) died or experienced an ICU LOS of 3 days or more.\n[9] SOFA score increased by 2 or more points in 90.1%; 86.7% manifested 2 or more SIRS criteria, and 54.4% had a qSOFA score of 2 or more points.\n[10] SOFA demonstrated significantly greater discrimination for in-hospital mortality (crude AUROC, 0.753 [99% CI, 0.750-0.757]) than SIRS criteria (crude AUROC, 0.589 [99% CI, 0.585-0.593]) or qSOFA (crude AUROC, 0.607 [99% CI, 0.603-0.611]).\n[11] Incremental improvements were 0.164 (99% CI, 0.159-0.169) for SOFA vs SIRS criteria and 0.146 (99% CI, 0.142-0.151) for SOFA vs qSOFA (P <.001).\n[12] SOFA (AUROC, 0.736 [99% CI, 0.733-0.739]) outperformed the other scores for the secondary end point (SIRS criteria: AUROC, 0.609 [99% CI, 0.606-0.612]; qSOFA: AUROC, 0.606 [99% CI, 0.602-0.609]).\n[13] Incremental improvements were 0.127 (99% CI, 0.123-0.131) for SOFA vs SIRS criteria and 0.131 (99% CI, 0.127-0.134) for SOFA vs qSOFA (P <.001).\n[14] Findings were consistent for both outcomes in multiple sensitivity analyses.\n[15] Conclusions and Relevance Among adults with suspected infection admitted to an ICU, an increase in SOFA score of 2 or more had greater prognostic accuracy for in-hospital mortality than SIRS criteria or the qSOFA score.\n[16] These findings suggest that SIRS criteria and qSOFA may have limited utility for predicting mortality in an ICU setting."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1401, "doc_id": 5185871, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [5185871], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: r-protein chaperones are found in complexes with their r-protein binding partners.\n\nDocument title: Rational Extension of the Ribosome Biogenesis Pathway Using Network-Guided Genetics\n\nAbstract sentences:\n[0] Biogenesis of ribosomes is an essential cellular process conserved across all eukaryotes and is known to require >170 genes for the assembly, modification, and trafficking of ribosome components through multiple cellular compartments.\n[1] Despite intensive study, this pathway likely involves many additional genes.\n[2] Here, we employ network-guided genetics-an approach for associating candidate genes with biological processes that capitalizes on recent advances in functional genomic and proteomic studies-to computationally identify additional ribosomal biogenesis genes.\n[3] We experimentally evaluated >100 candidate yeast genes in a battery of assays, confirming involvement of at least 15 new genes, including previously uncharacterized genes (YDL063C, YIL091C, YOR287C, YOR006C/TSR3, YOL022C/TSR4).\n[4] We associate the new genes with specific aspects of ribosomal subunit maturation, ribosomal particle association, and ribosomal subunit nuclear export, and we identify genes specifically required for the processing of 5S, 7S, 20S, 27S, and 35S rRNAs.\n[5] These results reveal new connections between ribosome biogenesis and mRNA splicing and add >10% new genes-most with human orthologs-to the biogenesis pathway, significantly extending our understanding of a universally conserved eukaryotic process."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1402, "doc_id": 8126244, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [8126244], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: siRNA knockdown of A20 accelerates tumor progression in an in vivo murine xenograft model.\n\nDocument title: Targeting A20 Decreases Glioma Stem Cell Survival and Tumor Growth\n\nAbstract sentences:\n[0] Glioblastomas are deadly cancers that display a functional cellular hierarchy maintained by self-renewing glioblastoma stem cells (GSCs).\n[1] GSCs are regulated by molecular pathways distinct from the bulk tumor that may be useful therapeutic targets.\n[2] We determined that A20 (TNFAIP3), a regulator of cell survival and the NF-kappaB pathway, is overexpressed in GSCs relative to non-stem glioblastoma cells at both the mRNA and protein levels.\n[3] To determine the functional significance of A20 in GSCs, we targeted A20 expression with lentiviral-mediated delivery of short hairpin RNA (shRNA).\n[4] Inhibiting A20 expression decreased GSC growth and survival through mechanisms associated with decreased cell-cycle progression and decreased phosphorylation of p65/RelA. Elevated levels of A20 in GSCs contributed to apoptotic resistance: GSCs were less susceptible to TNFalpha-induced cell death than matched non-stem glioma cells, but A20 knockdown sensitized GSCs to TNFalpha-mediated apoptosis.\n[5] The decreased survival of GSCs upon A20 knockdown contributed to the reduced ability of these cells to self-renew in primary and secondary neurosphere formation assays.\n[6] The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts.\n[7] In silico analysis of a glioma patient genomic database indicates that A20 overexpression and amplification is inversely correlated with survival.\n[8] Together these data indicate that A20 contributes to glioma maintenance through effects on the glioma stem cell subpopulation.\n[9] Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through glioma genomic sequencing: in fact, our data suggest A20 may function as a tumor enhancer in glioma through promotion of GSC survival.\n[10] A20 anticancer therapies should therefore be viewed with caution as effects will likely differ depending on the tumor type."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1403, "doc_id": 33370, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [33370, 38355793], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: siRNA knockdown of A20 accelerates tumor progression in an in vivo murine xenograft model.\n\nDocument title: A20 is overexpressed in glioma cells and may serve as a potential therapeutic target.\n\nAbstract sentences:\n[0] OBJECTIVE A20 is a TNF-inducible primary response gene, which has been found to have antiapoptotic function in several cancer cells.\n[1] This study investigates A20 expression in human glioma tissues and four glioma cell lines, and its effect on tumorigenesis of glioma cells and a mouse tumor model.\n[2] METHODS Human glioma tissue samples and cells were subject to reverse transcription-PCR (RT-PCR), western blotting and immunohistochemistry.\n[3] Glioma cells was tested by flow cytometry.\n[4] A xenograft tumor model in mice was utilized to examine the knock-down effect of specific A20 siRNAs on tumorigenesis.\n[5] RESULTS A20 was overexpressed in clinical glioma tissue samples (63.9%) and correlated with clinical staging.\n[6] All four human glioma cell lines expressed A20, among which U87 displayed the strongest expression signals.\n[7] Inhibiting A20 expression by siRNAs in vitro reduced the growth rates of glioma cells and resulted in G1/S arrest and increased apoptosis.\n[8] In a mouse tumor model, local administration of siRNA significantly suppressed solid tumor growth.\n[9] CONCLUSIONS A20 was overexpressed both in human glioma tissues and cell lines, and inhibiting A20 expression greatly slowed tumor cell growth in culture and in mice.\n[10] These findings indicated that A20 is involved in tumorigenesis of human glioma, and may serve as a future therapeutic target."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Inhibiting A20 expression by siRNAs in vitro reduced the growth rates of glioma cells and resulted in G1/S arrest and increased apoptosis.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1403, "doc_id": 38355793, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [33370, 38355793], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: siRNA knockdown of A20 accelerates tumor progression in an in vivo murine xenograft model.\n\nDocument title: A20 is overexpressed in glioma cells and may serve as a potential therapeutic target.\n\nAbstract sentences:\n[0] OBJECTIVE A20 is a TNF-inducible primary response gene, which has been found to have antiapoptotic function in several cancer cells.\n[1] This study investigates A20 expression in human glioma tissues and four glioma cell lines, and its effect on tumorigenesis of glioma cells and a mouse tumor model.\n[2] METHODS Human glioma tissue samples and cells were subject to reverse transcription-PCR (RT-PCR), western blotting and immunohistochemistry.\n[3] Glioma cells was tested by flow cytometry.\n[4] A xenograft tumor model in mice was utilized to examine the knock-down effect of specific A20 siRNAs on tumorigenesis.\n[5] RESULTS A20 was overexpressed in clinical glioma tissue samples (63.9%) and correlated with clinical staging.\n[6] All four human glioma cell lines expressed A20, among which U87 displayed the strongest expression signals.\n[7] Inhibiting A20 expression by siRNAs in vitro reduced the growth rates of glioma cells and resulted in G1/S arrest and increased apoptosis.\n[8] In a mouse tumor model, local administration of siRNA significantly suppressed solid tumor growth.\n[9] CONCLUSIONS A20 was overexpressed both in human glioma tissues and cell lines, and inhibiting A20 expression greatly slowed tumor cell growth in culture and in mice.\n[10] These findings indicated that A20 is involved in tumorigenesis of human glioma, and may serve as a future therapeutic target."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"In a mouse tumor model, local administration of siRNA significantly suppressed solid tumor growth.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1403, "doc_id": 38355793, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [33370, 38355793], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: siRNA knockdown of A20 accelerates tumor progression in an in vivo murine xenograft model.\n\nDocument title: A20 is overexpressed in glioma cells and may serve as a potential therapeutic target.\n\nAbstract sentences:\n[0] OBJECTIVE A20 is a TNF-inducible primary response gene, which has been found to have antiapoptotic function in several cancer cells.\n[1] This study investigates A20 expression in human glioma tissues and four glioma cell lines, and its effect on tumorigenesis of glioma cells and a mouse tumor model.\n[2] METHODS Human glioma tissue samples and cells were subject to reverse transcription-PCR (RT-PCR), western blotting and immunohistochemistry.\n[3] Glioma cells was tested by flow cytometry.\n[4] A xenograft tumor model in mice was utilized to examine the knock-down effect of specific A20 siRNAs on tumorigenesis.\n[5] RESULTS A20 was overexpressed in clinical glioma tissue samples (63.9%) and correlated with clinical staging.\n[6] All four human glioma cell lines expressed A20, among which U87 displayed the strongest expression signals.\n[7] Inhibiting A20 expression by siRNAs in vitro reduced the growth rates of glioma cells and resulted in G1/S arrest and increased apoptosis.\n[8] In a mouse tumor model, local administration of siRNA significantly suppressed solid tumor growth.\n[9] CONCLUSIONS A20 was overexpressed both in human glioma tissues and cell lines, and inhibiting A20 expression greatly slowed tumor cell growth in culture and in mice.\n[10] These findings indicated that A20 is involved in tumorigenesis of human glioma, and may serve as a future therapeutic target."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"CONCLUSIONS A20 was overexpressed both in human glioma tissues and cell lines, and inhibiting A20 expression greatly slowed tumor cell growth in culture and in mice.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1403, "doc_id": 38355793, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [33370, 38355793], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: siRNA knockdown of A20 slows tumor progression in an in vivo murine xenograft model.\n\nDocument title: Targeting A20 Decreases Glioma Stem Cell Survival and Tumor Growth\n\nAbstract sentences:\n[0] Glioblastomas are deadly cancers that display a functional cellular hierarchy maintained by self-renewing glioblastoma stem cells (GSCs).\n[1] GSCs are regulated by molecular pathways distinct from the bulk tumor that may be useful therapeutic targets.\n[2] We determined that A20 (TNFAIP3), a regulator of cell survival and the NF-kappaB pathway, is overexpressed in GSCs relative to non-stem glioblastoma cells at both the mRNA and protein levels.\n[3] To determine the functional significance of A20 in GSCs, we targeted A20 expression with lentiviral-mediated delivery of short hairpin RNA (shRNA).\n[4] Inhibiting A20 expression decreased GSC growth and survival through mechanisms associated with decreased cell-cycle progression and decreased phosphorylation of p65/RelA. Elevated levels of A20 in GSCs contributed to apoptotic resistance: GSCs were less susceptible to TNFalpha-induced cell death than matched non-stem glioma cells, but A20 knockdown sensitized GSCs to TNFalpha-mediated apoptosis.\n[5] The decreased survival of GSCs upon A20 knockdown contributed to the reduced ability of these cells to self-renew in primary and secondary neurosphere formation assays.\n[6] The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts.\n[7] In silico analysis of a glioma patient genomic database indicates that A20 overexpression and amplification is inversely correlated with survival.\n[8] Together these data indicate that A20 contributes to glioma maintenance through effects on the glioma stem cell subpopulation.\n[9] Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through glioma genomic sequencing: in fact, our data suggest A20 may function as a tumor enhancer in glioma through promotion of GSC survival.\n[10] A20 anticancer therapies should therefore be viewed with caution as effects will likely differ depending on the tumor type."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1404, "doc_id": 33370, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [33370, 38355793], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: siRNA knockdown of A20 slows tumor progression in an in vivo murine xenograft model.\n\nDocument title: A20 is overexpressed in glioma cells and may serve as a potential therapeutic target.\n\nAbstract sentences:\n[0] OBJECTIVE A20 is a TNF-inducible primary response gene, which has been found to have antiapoptotic function in several cancer cells.\n[1] This study investigates A20 expression in human glioma tissues and four glioma cell lines, and its effect on tumorigenesis of glioma cells and a mouse tumor model.\n[2] METHODS Human glioma tissue samples and cells were subject to reverse transcription-PCR (RT-PCR), western blotting and immunohistochemistry.\n[3] Glioma cells was tested by flow cytometry.\n[4] A xenograft tumor model in mice was utilized to examine the knock-down effect of specific A20 siRNAs on tumorigenesis.\n[5] RESULTS A20 was overexpressed in clinical glioma tissue samples (63.9%) and correlated with clinical staging.\n[6] All four human glioma cell lines expressed A20, among which U87 displayed the strongest expression signals.\n[7] Inhibiting A20 expression by siRNAs in vitro reduced the growth rates of glioma cells and resulted in G1/S arrest and increased apoptosis.\n[8] In a mouse tumor model, local administration of siRNA significantly suppressed solid tumor growth.\n[9] CONCLUSIONS A20 was overexpressed both in human glioma tissues and cell lines, and inhibiting A20 expression greatly slowed tumor cell growth in culture and in mice.\n[10] These findings indicated that A20 is involved in tumorigenesis of human glioma, and may serve as a future therapeutic target."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Inhibiting A20 expression by siRNAs in vitro reduced the growth rates of glioma cells and resulted in G1/S arrest and increased apoptosis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1404, "doc_id": 38355793, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [33370, 38355793], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: siRNA knockdown of A20 slows tumor progression in an in vivo murine xenograft model.\n\nDocument title: A20 is overexpressed in glioma cells and may serve as a potential therapeutic target.\n\nAbstract sentences:\n[0] OBJECTIVE A20 is a TNF-inducible primary response gene, which has been found to have antiapoptotic function in several cancer cells.\n[1] This study investigates A20 expression in human glioma tissues and four glioma cell lines, and its effect on tumorigenesis of glioma cells and a mouse tumor model.\n[2] METHODS Human glioma tissue samples and cells were subject to reverse transcription-PCR (RT-PCR), western blotting and immunohistochemistry.\n[3] Glioma cells was tested by flow cytometry.\n[4] A xenograft tumor model in mice was utilized to examine the knock-down effect of specific A20 siRNAs on tumorigenesis.\n[5] RESULTS A20 was overexpressed in clinical glioma tissue samples (63.9%) and correlated with clinical staging.\n[6] All four human glioma cell lines expressed A20, among which U87 displayed the strongest expression signals.\n[7] Inhibiting A20 expression by siRNAs in vitro reduced the growth rates of glioma cells and resulted in G1/S arrest and increased apoptosis.\n[8] In a mouse tumor model, local administration of siRNA significantly suppressed solid tumor growth.\n[9] CONCLUSIONS A20 was overexpressed both in human glioma tissues and cell lines, and inhibiting A20 expression greatly slowed tumor cell growth in culture and in mice.\n[10] These findings indicated that A20 is involved in tumorigenesis of human glioma, and may serve as a future therapeutic target."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"In a mouse tumor model, local administration of siRNA significantly suppressed solid tumor growth.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1404, "doc_id": 38355793, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [33370, 38355793], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: siRNA knockdown of A20 slows tumor progression in an in vivo murine xenograft model.\n\nDocument title: A20 is overexpressed in glioma cells and may serve as a potential therapeutic target.\n\nAbstract sentences:\n[0] OBJECTIVE A20 is a TNF-inducible primary response gene, which has been found to have antiapoptotic function in several cancer cells.\n[1] This study investigates A20 expression in human glioma tissues and four glioma cell lines, and its effect on tumorigenesis of glioma cells and a mouse tumor model.\n[2] METHODS Human glioma tissue samples and cells were subject to reverse transcription-PCR (RT-PCR), western blotting and immunohistochemistry.\n[3] Glioma cells was tested by flow cytometry.\n[4] A xenograft tumor model in mice was utilized to examine the knock-down effect of specific A20 siRNAs on tumorigenesis.\n[5] RESULTS A20 was overexpressed in clinical glioma tissue samples (63.9%) and correlated with clinical staging.\n[6] All four human glioma cell lines expressed A20, among which U87 displayed the strongest expression signals.\n[7] Inhibiting A20 expression by siRNAs in vitro reduced the growth rates of glioma cells and resulted in G1/S arrest and increased apoptosis.\n[8] In a mouse tumor model, local administration of siRNA significantly suppressed solid tumor growth.\n[9] CONCLUSIONS A20 was overexpressed both in human glioma tissues and cell lines, and inhibiting A20 expression greatly slowed tumor cell growth in culture and in mice.\n[10] These findings indicated that A20 is involved in tumorigenesis of human glioma, and may serve as a future therapeutic target."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"CONCLUSIONS A20 was overexpressed both in human glioma tissues and cell lines, and inhibiting A20 expression greatly slowed tumor cell growth in culture and in mice.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1404, "doc_id": 38355793, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [33370, 38355793], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: taa1 tar1 tar2 triple mutants in Arabidopsis do not make root meristem during embryogenesis.\n\nDocument title: TAA1-Mediated Auxin Biosynthesis Is Essential for Hormone Crosstalk and Plant Development\n\nAbstract sentences:\n[0] Plants have evolved a tremendous ability to respond to environmental changes by adapting their growth and development.\n[1] The interaction between hormonal and developmental signals is a critical mechanism in the generation of this enormous plasticity.\n[2] A good example is the response to the hormone ethylene that depends on tissue type, developmental stage, and environmental conditions.\n[3] By characterizing the Arabidopsis wei8 mutant, we have found that a small family of genes mediates tissue-specific responses to ethylene.\n[4] Biochemical studies revealed that WEI8 encodes a long-anticipated tryptophan aminotransferase, TAA1, in the essential, yet genetically uncharacterized, indole-3-pyruvic acid (IPA) branch of the auxin biosynthetic pathway.\n[5] Analysis of TAA1 and its paralogues revealed a link between local auxin production, tissue-specific ethylene effects, and organ development.\n[6] Thus, the IPA route of auxin production is key to generating robust auxin gradients in response to environmental and developmental cues."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1405, "doc_id": 10504681, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [10504681], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: β-sheet opening occurs during pleurotolysin pore formation.\n\nDocument title: Conformational Changes during Pore Formation by the Perforin-Related Protein Pleurotolysin\n\nAbstract sentences:\n[0] Membrane attack complex/perforin-like (MACPF) proteins comprise the largest superfamily of pore-forming proteins, playing crucial roles in immunity and pathogenesis.\n[1] Soluble monomers assemble into large transmembrane pores via conformational transitions that remain to be structurally and mechanistically characterised.\n[2] Here we present an 11 Å resolution cryo-electron microscopy (cryo-EM) structure of the two-part, fungal toxin Pleurotolysin (Ply), together with crystal structures of both components (the lipid binding PlyA protein and the pore-forming MACPF component PlyB).\n[3] These data reveal a 13-fold pore 80 Å in diameter and 100 Å in height, with each subunit comprised of a PlyB molecule atop a membrane bound dimer of PlyA. The resolution of the EM map, together with biophysical and computational experiments, allowed confident assignment of subdomains in a MACPF pore assembly.\n[4] The major conformational changes in PlyB are a ∼70° opening of the bent and distorted central β-sheet of the MACPF domain, accompanied by extrusion and refolding of two α-helical regions into transmembrane β-hairpins (TMH1 and TMH2).\n[5] We determined the structures of three different disulphide bond-trapped prepore intermediates.\n[6] Analysis of these data by molecular modelling and flexible fitting allows us to generate a potential trajectory of β-sheet unbending.\n[7] The results suggest that MACPF conformational change is triggered through disruption of the interface between a conserved helix-turn-helix motif and the top of TMH2.\n[8] Following their release we propose that the transmembrane regions assemble into β-hairpins via top down zippering of backbone hydrogen bonds to form the membrane-inserted β-barrel.\n[9] The intermediate structures of the MACPF domain during refolding into the β-barrel pore establish a structural paradigm for the transition from soluble monomer to pore, which may be conserved across the whole superfamily.\n[10] The TMH2 region is critical for the release of both TMH clusters, suggesting why this region is targeted by endogenous inhibitors of MACPF function."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"The major conformational changes in PlyB are a ∼70° opening of the bent and distorted central β-sheet of the MACPF domain, accompanied by extrusion and refolding of two α-helical regions into transmembrane β-hairpins (TMH1 and TMH2).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1406, "doc_id": 2617858, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [2617858], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: β1/Ketel is able to bind microtubules.\n\nDocument title: A Microtubule Interactome: Complexes with Roles in Cell Cycle and Mitosis\n\nAbstract sentences:\n[0] The microtubule (MT) cytoskeleton is required for many aspects of cell function, including the transport of intracellular materials, the maintenance of cell polarity, and the regulation of mitosis.\n[1] These functions are coordinated by MT-associated proteins (MAPs), which work in concert with each other, binding MTs and altering their properties.\n[2] We have used a MT cosedimentation assay, combined with 1D and 2D PAGE and mass spectrometry, to identify over 250 MAPs from early Drosophila embryos.\n[3] We have taken two complementary approaches to analyse the cellular function of novel MAPs isolated using this approach.\n[4] First, we have carried out an RNA interference (RNAi) screen, identifying 21 previously uncharacterised genes involved in MT organisation.\n[5] Second, we have undertaken a bioinformatics analysis based on binary protein interaction data to produce putative interaction networks of MAPs.\n[6] By combining both approaches, we have identified and validated MAP complexes with potentially important roles in cell cycle regulation and mitosis.\n[7] This study therefore demonstrates that biologically relevant data can be harvested using such a multidisciplinary approach, and identifies new MAPs, many of which appear to be important in cell division."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "train", "claim_id": 1407, "doc_id": 8087082, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [8087082, 29863668], "variant": "nei_with_cited_abstract"}}