{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 show 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": "validation", "claim_id": 1, "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: 1,000 genomes project enables mapping of genetic sequence variation consisting of rare variants with larger penetrance effects than common variants.\n\nDocument title: Rare Variants Create Synthetic Genome-Wide Associations\n\nAbstract sentences:\n[0] Genome-wide association studies (GWAS) have now identified at least 2,000 common variants that appear associated with common diseases or related traits (http://www.genome.gov/gwastudies), hundreds of which have been convincingly replicated.\n[1] It is generally thought that the associated markers reflect the effect of a nearby common (minor allele frequency >0.05) causal site, which is associated with the marker, leading to extensive resequencing efforts to find causal sites.\n[2] We propose as an alternative explanation that variants much less common than the associated one may create \"synthetic associations\" by occurring, stochastically, more often in association with one of the alleles at the common site versus the other allele.\n[3] Although synthetic associations are an obvious theoretical possibility, they have never been systematically explored as a possible explanation for GWAS findings.\n[4] Here, we use simple computer simulations to show the conditions under which such synthetic associations will arise and how they may be recognized.\n[5] We show that they are not only possible, but inevitable, and that under simple but reasonable genetic models, they are likely to account for or contribute to many of the recently identified signals reported in genome-wide association studies.\n[6] We also illustrate the behavior of synthetic associations in real datasets by showing that rare causal mutations responsible for both hearing loss and sickle cell anemia create genome-wide significant synthetic associations, in the latter case extending over a 2.5-Mb interval encompassing scores of \"blocks\" of associated variants.\n[7] In conclusion, uncommon or rare genetic variants can easily create synthetic associations that are credited to common variants, and this possibility requires careful consideration in the interpretation and follow up of GWAS signals."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2, 5]\nExplanation: Evidence states: \"We propose as an alternative explanation that variants much less common than the associated one may create \"synthetic associations\" by occurring, stochastically, more often in association with one of the alleles at the common site versus the other allele. We show that they are not only possible, but inevitable, and that under simple but reasonable genetic models, they are likely to account for or contribute to many of the recently identified signals reported in genome-wide association studies.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 3, "doc_id": 14717500, "label": "SUPPORTS", "evidence_sentence_ids": [2, 5], "cited_doc_ids": [14717500], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: 1,000 genomes project enables mapping of genetic sequence variation consisting of rare variants with larger penetrance effects than common variants.\n\nDocument title: Rare Variants Create Synthetic Genome-Wide Associations\n\nAbstract sentences:\n[0] Genome-wide association studies (GWAS) have now identified at least 2,000 common variants that appear associated with common diseases or related traits (http://www.genome.gov/gwastudies), hundreds of which have been convincingly replicated.\n[1] It is generally thought that the associated markers reflect the effect of a nearby common (minor allele frequency >0.05) causal site, which is associated with the marker, leading to extensive resequencing efforts to find causal sites.\n[2] We propose as an alternative explanation that variants much less common than the associated one may create \"synthetic associations\" by occurring, stochastically, more often in association with one of the alleles at the common site versus the other allele.\n[3] Although synthetic associations are an obvious theoretical possibility, they have never been systematically explored as a possible explanation for GWAS findings.\n[4] Here, we use simple computer simulations to show the conditions under which such synthetic associations will arise and how they may be recognized.\n[5] We show that they are not only possible, but inevitable, and that under simple but reasonable genetic models, they are likely to account for or contribute to many of the recently identified signals reported in genome-wide association studies.\n[6] We also illustrate the behavior of synthetic associations in real datasets by showing that rare causal mutations responsible for both hearing loss and sickle cell anemia create genome-wide significant synthetic associations, in the latter case extending over a 2.5-Mb interval encompassing scores of \"blocks\" of associated variants.\n[7] In conclusion, uncommon or rare genetic variants can easily create synthetic associations that are credited to common variants, and this possibility requires careful consideration in the interpretation and follow up of GWAS signals."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"In conclusion, uncommon or rare genetic variants can easily create synthetic associations that are credited to common variants, and this possibility requires careful consideration in the interpretation and follow up of GWAS signals.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 3, "doc_id": 14717500, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [14717500], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: 1/2000 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 5, "doc_id": 13734012, "label": "SUPPORTS", "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: 5% 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": "validation", "claim_id": 13, "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: A deficiency of vitamin B12 increases 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": "validation", "claim_id": 36, "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 high microerythrocyte count raises vulnerability to 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 42, "doc_id": 18174210, "label": "CONTRADICTS", "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 raises vulnerability to 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: 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": "validation", "claim_id": 42, "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: A total of 1,000 people in the UK are asymptomatic carriers of vCJD infection.\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": "validation", "claim_id": 48, "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: ADAR1 binds to Dicer to cleave pre-miRNA.\n\nDocument title: ADAR1 Forms a Complex with Dicer to Promote MicroRNA Processing and RNA-Induced Gene Silencing\n\nAbstract sentences:\n[0] Adenosine deaminases acting on RNA (ADARs) are involved in RNA editing that converts adenosine residues to inosine specifically in double-stranded RNAs.\n[1] In this study, we investigated the interaction of the RNA editing mechanism with the RNA interference (RNAi) machinery and found that ADAR1 forms a complex with Dicer through direct protein-protein interaction.\n[2] Most importantly, ADAR1 increases the maximum rate (Vmax) of pre-microRNA (miRNA) cleavage by Dicer and facilitates loading of miRNA onto RNA-induced silencing complexes, identifying a new role of ADAR1 in miRNA processing and RNAi mechanisms.\n[3] ADAR1 differentiates its functions in RNA editing and RNAi by the formation of either ADAR1/ADAR1 homodimer or Dicer/ADAR1 heterodimer complexes, respectively.\n[4] As expected, the expression of miRNAs is globally inhibited in ADAR1(-/-) mouse embryos, which, in turn, alters the expression of their target genes and might contribute to their embryonic lethal phenotype."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"In this study, we investigated the interaction of the RNA editing mechanism with the RNA interference (RNAi) machinery and found that ADAR1 forms a complex with Dicer through direct protein-protein interaction.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 49, "doc_id": 5953485, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [5953485], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: ADAR1 binds to Dicer to cleave pre-miRNA.\n\nDocument title: ADAR1 Forms a Complex with Dicer to Promote MicroRNA Processing and RNA-Induced Gene Silencing\n\nAbstract sentences:\n[0] Adenosine deaminases acting on RNA (ADARs) are involved in RNA editing that converts adenosine residues to inosine specifically in double-stranded RNAs.\n[1] In this study, we investigated the interaction of the RNA editing mechanism with the RNA interference (RNAi) machinery and found that ADAR1 forms a complex with Dicer through direct protein-protein interaction.\n[2] Most importantly, ADAR1 increases the maximum rate (Vmax) of pre-microRNA (miRNA) cleavage by Dicer and facilitates loading of miRNA onto RNA-induced silencing complexes, identifying a new role of ADAR1 in miRNA processing and RNAi mechanisms.\n[3] ADAR1 differentiates its functions in RNA editing and RNAi by the formation of either ADAR1/ADAR1 homodimer or Dicer/ADAR1 heterodimer complexes, respectively.\n[4] As expected, the expression of miRNAs is globally inhibited in ADAR1(-/-) mouse embryos, which, in turn, alters the expression of their target genes and might contribute to their embryonic lethal phenotype."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Most importantly, ADAR1 increases the maximum rate (Vmax) of pre-microRNA (miRNA) cleavage by Dicer and facilitates loading of miRNA onto RNA-induced silencing complexes, identifying a new role of ADAR1 in miRNA processing and RNAi mechanisms.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 49, "doc_id": 5953485, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [5953485], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: AIRE is expressed in some skin tumors.\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": "validation", "claim_id": 50, "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: ALDH1 expression is associated with better breast cancer outcomes.\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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 51, "doc_id": 45638119, "label": "CONTRADICTS", "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: ALDH1 expression is associated with poorer prognosis in breast cancer.\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": "validation", "claim_id": 53, "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 increases 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 54, "doc_id": 49556906, "label": "CONTRADICTS", "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 increases 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 54, "doc_id": 49556906, "label": "CONTRADICTS", "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 increases 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 54, "doc_id": 49556906, "label": "CONTRADICTS", "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 increases AlphaBeta production and tau phosphorylation causing GABA neuron degeneration.\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: [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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 56, "doc_id": 4709641, "label": "SUPPORTS", "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: APOE4 expression in iPSC-derived neurons increases AlphaBeta production and tau phosphorylation, delaying GABA neuron degeneration.\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": "validation", "claim_id": 57, "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: Activation of PPM1D suppresses 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 70, "doc_id": 5956380, "label": "SUPPORTS", "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 suppresses 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 70, "doc_id": 4414547, "label": "SUPPORTS", "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: Activator-inhibitor pairs are provided dorsally by Admpchordin.\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": "validation", "claim_id": 72, "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 that compromises two subunits, UreA and UreB.\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": "validation", "claim_id": 75, "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: Albendazole is used to treat lymphatic filariasis.\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": "validation", "claim_id": 94, "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: Alizarin 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": "validation", "claim_id": 99, "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: All hematopoietic stem cells segregate their chromosomes randomly.\n\nDocument title: Haematopoietic stem cells do not asymmetrically segregate chromosomes or retain BrdU\n\nAbstract sentences:\n[0] Stem cells are proposed to segregate chromosomes asymmetrically during self-renewing divisions so that older (‘immortal’) DNA strands are retained in daughter stem cells whereas newly synthesized strands segregate to differentiating cells.\n[1] Stem cells are also proposed to retain DNA labels, such as 5-bromo-2-deoxyuridine (BrdU), either because they segregate chromosomes asymmetrically or because they divide slowly.\n[2] However, the purity of stem cells among BrdU-label-retaining cells has not been documented in any tissue, and the ‘immortal strand hypothesis’ has not been tested in a system with definitive stem cell markers.\n[3] Here we tested these hypotheses in haematopoietic stem cells (HSCs), which can be highly purified using well characterized markers.\n[4] We administered BrdU to newborn mice, mice treated with cyclophosphamide and granulocyte colony-stimulating factor, and normal adult mice for 4 to 10 days, followed by 70 days without BrdU. In each case, less than 6% of HSCs retained BrdU and less than 0.5% of all BrdU-retaining haematopoietic cells were HSCs, revealing that BrdU has poor specificity and poor sensitivity as an HSC marker.\n[5] Sequential administration of 5-chloro-2-deoxyuridine and 5-iodo-2-deoxyuridine indicated that all HSCs segregate their chromosomes randomly.\n[6] Division of individual HSCs in culture revealed no asymmetric segregation of the label.\n[7] Thus, HSCs cannot be identified on the basis of BrdU-label retention and do not retain older DNA strands during division, indicating that these are not general properties of stem cells."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Sequential administration of 5-chloro-2-deoxyuridine and 5-iodo-2-deoxyuridine indicated that all HSCs segregate their chromosomes randomly.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 100, "doc_id": 4381486, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [4381486], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 increased 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 113, "doc_id": 6157837, "label": "SUPPORTS", "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 increased 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 113, "doc_id": 6157837, "label": "SUPPORTS", "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 can be disposed of easily after 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 115, "doc_id": 33872649, "label": "CONTRADICTS", "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: Antibiotic induced alterations in the gut microbiome reduce resistance against Clostridium difficile\n\nDocument title: Antibiotic-induced shifts in the mouse gut microbiome and metabolome increase susceptibility to Clostridium difficile infection\n\nAbstract sentences:\n[0] Antibiotics can have significant and long-lasting effects on the gastrointestinal tract microbiota, reducing colonization resistance against pathogens including Clostridium difficile.\n[1] Here we show that antibiotic treatment induces substantial changes in the gut microbial community and in the metabolome of mice susceptible to C. difficile infection.\n[2] Levels of secondary bile acids, glucose, free fatty acids and dipeptides decrease, whereas those of primary bile acids and sugar alcohols increase, reflecting the modified metabolic activity of the altered gut microbiome.\n[3] In vitro and ex vivo analyses demonstrate that C. difficile can exploit specific metabolites that become more abundant in the mouse gut after antibiotics, including the primary bile acid taurocholate for germination, and carbon sources such as mannitol, fructose, sorbitol, raffinose and stachyose for growth.\n[4] Our results indicate that antibiotic-mediated alteration of the gut microbiome converts the global metabolic profile to one that favours C. difficile germination and growth."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Antibiotics can have significant and long-lasting effects on the gastrointestinal tract microbiota, reducing colonization resistance against pathogens including Clostridium difficile.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 118, "doc_id": 6372244, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [6372244], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Antibiotic induced alterations in the gut microbiome reduce resistance against Clostridium difficile\n\nDocument title: Antibiotic-induced shifts in the mouse gut microbiome and metabolome increase susceptibility to Clostridium difficile infection\n\nAbstract sentences:\n[0] Antibiotics can have significant and long-lasting effects on the gastrointestinal tract microbiota, reducing colonization resistance against pathogens including Clostridium difficile.\n[1] Here we show that antibiotic treatment induces substantial changes in the gut microbial community and in the metabolome of mice susceptible to C. difficile infection.\n[2] Levels of secondary bile acids, glucose, free fatty acids and dipeptides decrease, whereas those of primary bile acids and sugar alcohols increase, reflecting the modified metabolic activity of the altered gut microbiome.\n[3] In vitro and ex vivo analyses demonstrate that C. difficile can exploit specific metabolites that become more abundant in the mouse gut after antibiotics, including the primary bile acid taurocholate for germination, and carbon sources such as mannitol, fructose, sorbitol, raffinose and stachyose for growth.\n[4] Our results indicate that antibiotic-mediated alteration of the gut microbiome converts the global metabolic profile to one that favours C. difficile germination and growth."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Our results indicate that antibiotic-mediated alteration of the gut microbiome converts the global metabolic profile to one that favours C. difficile germination and growth.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 118, "doc_id": 6372244, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [6372244], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 reduces 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 124, "doc_id": 4883040, "label": "SUPPORTS", "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 reduces 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 124, "doc_id": 4883040, "label": "SUPPORTS", "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: Arginine 90 in p150n is important for interaction with EB1.\n\nDocument title: Structural basis for the activation of microtubule assembly by the EB1 and p150Glued complex.\n\nAbstract sentences:\n[0] Plus-end tracking proteins, such as EB1 and the dynein/dynactin complex, regulate microtubule dynamics.\n[1] These proteins are thought to stabilize microtubules by forming a plus-end complex at microtubule growing ends with ill-defined mechanisms.\n[2] Here we report the crystal structure of two plus-end complex components, the carboxy-terminal dimerization domain of EB1 and the microtubule binding (CAP-Gly) domain of the dynactin subunit p150Glued.\n[3] Each molecule of the EB1 dimer contains two helices forming a conserved four-helix bundle, while also providing p150Glued binding sites in its flexible tail region.\n[4] Combining crystallography, NMR, and mutational analyses, our studies reveal the critical interacting elements of both EB1 and p150Glued, whose mutation alters microtubule polymerization activity.\n[5] Moreover, removal of the key flexible tail from EB1 activates microtubule assembly by EB1 alone, suggesting that the flexible tail negatively regulates EB1 activity.\n[6] We, therefore, propose that EB1 possesses an auto-inhibited conformation, which is relieved by p150Glued as an allosteric activator."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 127, "doc_id": 21598000, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [21598000], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Arterioles have a larger lumen diameter than venules.\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": "validation", "claim_id": 128, "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: Articles published in open access format are less likely to be cited than traditional journals.\n\nDocument title: Open Access Increases Citation Rate\n\nAbstract sentences:\n[0] PLoS Biology publishes today a research article by Gunther Eysenbach that is not about biology.\n[1] It is about citations.\n[2] It provides robust evidence that open-access articles (OA articles) are more immediately recognized and cited than non-OA articles.\n[3] As such, it adds objective support to the belief we have always held that open-access publication speeds up scientific dialog between researchers and, consequently, should be extended to the whole scientific literature as quickly as possible.\n[4] It is therefore fitting that we publish such a paper.\n[5] We have long argued that papers freely available in a journal will be more often read and cited than those behind a subscription barrier.\n[6] However, solid evidence to support or refute such a claim has been surprisingly hard to find.\n[7] Since most open-access journals are new, comparisons of the effects of open access with established subscription-based journals are easily confounded by age and reputation.\n[8] In the current study, Eysenbach compared citations compiled by Thomson Scientific (formerly Thomson ISI) to individual articles published between June 2004 and December 2004 in the same journal—namely, Proceedings of the National Academy of Sciences (PNAS), which announced its open-access option for authors on June 8 of that year, with an associated publication charge of US$1,000.\n[9] Non-OA articles in PNAS are subject to a six-month “toll-access” delay before the article becomes publicly available.\n[10] The results of this natural experiment are clear: in the 4 to 16 months following publication, OA articles gained a significant citation advantage over non-OA articles during the same period.\n[11] They are twice as likely to be cited 4 to 10 months after publication and almost three times as likely between 10 and 16 months.\n[12] Given that PNAS delays open access for only six months, the disparity between OA and non-OA articles in journals where the delay is longer or where articles remain “toll-access” is likely to be even greater.\n[13] Eysenbach also looked at the impact of self-archiving non-OA articles.\n[14] One route to open access, it is argued, is for authors to archive their published articles on their own Web sites or in institutional repositories, although this does not include an explicit business model to cover the cost of peer-review and publishing.\n[15] The analysis revealed that self-archived articles are also cited less often than OA articles from the same journal.\n[16] Yes, you're right; we do have a strong and vested interest in publishing results that so obviously endorse our existence.\n[17] Moreover, the author of the article is also an editor of an open-access journal.\n[18] But sometimes a potential conflict of interest can actually help to ensure rigor.\n[19] In this case, we have an acute interest in ensuring that the article meets the same, if not higher, standards as any other research article we publish.\n[20] Not only must the conclusions provide a significant advance for the field, but the study must be technically sound, with appropriate evidence to support those conclusions.\n[21] As with all our research articles, we consulted throughout the evaluation process with an academic editor with appropriate expertise—in this case, Carol Tenopir, professor of information sciences at the University of Tennessee (Knoxville, Tennessee, United States).\n[22] The article was reviewed by two experts in bibliometric analyses and information science, and an experienced research biologist with expertise in statistics.\n[23] They all enthusiastically supported publication, although one understandably questioned the suitability of PLoS Biology as the publication venue.\n[24] We have no intention of making PLoS Biology a regular home for bibliometric studies (even when about open access).\n[25] What makes this study worth publishing in PLoS Biology is not only the relative strength of evidence supporting the claim but also the extent to which many (especially other publishers) have anticipated such an analysis.\n[26] As far as we are aware, no other study has compared OA and non-OA articles from the same journal and controlled for so many potentially confounding factors.\n[27] Eysenbach's multivariate analysis took into account the number of days since publication, number of authors, article type, country of the corresponding author, funding type, subject area, submission track ( PNAS has three different ways that authors can submit a paper), and the previous citation record of the first and last authors.\n[28] He even administered a supplementary questionnaire to assess whether authors choosing the OA option in PNAS chose to do so for only their most important research (they didn't).\n[29] As Ian Rowlands from the Centre for Publishing at University College London—and one of the reviewers who agreed to be identified in this article—said at the start of his review:          “Many (most) of the papers and presentations I have read/seen on this topic have completely failed to address the kinds of confounding issues that are so convincingly tackled here.\n[30] For that reason alone, this paper deserves to be published and alerted to the widest possible audience.\n[31] ”          In addition to providing evidence for the immediate advantage of open access, Eysenbach's analysis also highlights several potential challenges to its long-term future.\n[32] Although a limited dataset, the citation history of the first and last authors differed between those who chose the open-access option and those who did not.\n[33] In the group that chose open access, last authors tended to have a “stronger” previous citation record, whereas this situation was reversed among the group that declined the open-access option—here, it was the first authors who tended to be stronger.\n[34] This may reflect varying attitudes of authors at different stages of their career, a stronger influence from the leader of a particular group, or an age- or career-related difference in the ability to pay the publication charge (e.g., [ 1]).\n[35] Indeed, access to appropriate funds may also be a reason why a lower proportion of authors from European countries tended to choose the open-access option.\n[36] In many of these countries, funds for page charges—and, by extension, open-access publication fees—are often not included within research grants.\n[37] PNAS was one of the first journals to offer an open-access option to its authors.\n[38] However, such hybrid journals are increasing: Blackwell, Springer, and Oxford University Press now provide this option as well.\n[39] This means that similar experiments can be replicated.\n[40] Moreover, although the evidence from the current analysis argues most strongly for a time advantage in citation for OA articles, a study over longer periods will reveal whether this translates into a sustained increase in the number of citations.\n[41] In the meantime, open-access advocates should be emboldened by tangible evidence for what has seemed obvious all along."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"It provides robust evidence that open-access articles (OA articles) are more immediately recognized and cited than non-OA articles.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 129, "doc_id": 27768226, "label": "CONTRADICTS", "evidence_sentence_ids": [2], "cited_doc_ids": [27768226], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Articles published in open access format are less likely to be cited than traditional journals.\n\nDocument title: Open Access Increases Citation Rate\n\nAbstract sentences:\n[0] PLoS Biology publishes today a research article by Gunther Eysenbach that is not about biology.\n[1] It is about citations.\n[2] It provides robust evidence that open-access articles (OA articles) are more immediately recognized and cited than non-OA articles.\n[3] As such, it adds objective support to the belief we have always held that open-access publication speeds up scientific dialog between researchers and, consequently, should be extended to the whole scientific literature as quickly as possible.\n[4] It is therefore fitting that we publish such a paper.\n[5] We have long argued that papers freely available in a journal will be more often read and cited than those behind a subscription barrier.\n[6] However, solid evidence to support or refute such a claim has been surprisingly hard to find.\n[7] Since most open-access journals are new, comparisons of the effects of open access with established subscription-based journals are easily confounded by age and reputation.\n[8] In the current study, Eysenbach compared citations compiled by Thomson Scientific (formerly Thomson ISI) to individual articles published between June 2004 and December 2004 in the same journal—namely, Proceedings of the National Academy of Sciences (PNAS), which announced its open-access option for authors on June 8 of that year, with an associated publication charge of US$1,000.\n[9] Non-OA articles in PNAS are subject to a six-month “toll-access” delay before the article becomes publicly available.\n[10] The results of this natural experiment are clear: in the 4 to 16 months following publication, OA articles gained a significant citation advantage over non-OA articles during the same period.\n[11] They are twice as likely to be cited 4 to 10 months after publication and almost three times as likely between 10 and 16 months.\n[12] Given that PNAS delays open access for only six months, the disparity between OA and non-OA articles in journals where the delay is longer or where articles remain “toll-access” is likely to be even greater.\n[13] Eysenbach also looked at the impact of self-archiving non-OA articles.\n[14] One route to open access, it is argued, is for authors to archive their published articles on their own Web sites or in institutional repositories, although this does not include an explicit business model to cover the cost of peer-review and publishing.\n[15] The analysis revealed that self-archived articles are also cited less often than OA articles from the same journal.\n[16] Yes, you're right; we do have a strong and vested interest in publishing results that so obviously endorse our existence.\n[17] Moreover, the author of the article is also an editor of an open-access journal.\n[18] But sometimes a potential conflict of interest can actually help to ensure rigor.\n[19] In this case, we have an acute interest in ensuring that the article meets the same, if not higher, standards as any other research article we publish.\n[20] Not only must the conclusions provide a significant advance for the field, but the study must be technically sound, with appropriate evidence to support those conclusions.\n[21] As with all our research articles, we consulted throughout the evaluation process with an academic editor with appropriate expertise—in this case, Carol Tenopir, professor of information sciences at the University of Tennessee (Knoxville, Tennessee, United States).\n[22] The article was reviewed by two experts in bibliometric analyses and information science, and an experienced research biologist with expertise in statistics.\n[23] They all enthusiastically supported publication, although one understandably questioned the suitability of PLoS Biology as the publication venue.\n[24] We have no intention of making PLoS Biology a regular home for bibliometric studies (even when about open access).\n[25] What makes this study worth publishing in PLoS Biology is not only the relative strength of evidence supporting the claim but also the extent to which many (especially other publishers) have anticipated such an analysis.\n[26] As far as we are aware, no other study has compared OA and non-OA articles from the same journal and controlled for so many potentially confounding factors.\n[27] Eysenbach's multivariate analysis took into account the number of days since publication, number of authors, article type, country of the corresponding author, funding type, subject area, submission track ( PNAS has three different ways that authors can submit a paper), and the previous citation record of the first and last authors.\n[28] He even administered a supplementary questionnaire to assess whether authors choosing the OA option in PNAS chose to do so for only their most important research (they didn't).\n[29] As Ian Rowlands from the Centre for Publishing at University College London—and one of the reviewers who agreed to be identified in this article—said at the start of his review:          “Many (most) of the papers and presentations I have read/seen on this topic have completely failed to address the kinds of confounding issues that are so convincingly tackled here.\n[30] For that reason alone, this paper deserves to be published and alerted to the widest possible audience.\n[31] ”          In addition to providing evidence for the immediate advantage of open access, Eysenbach's analysis also highlights several potential challenges to its long-term future.\n[32] Although a limited dataset, the citation history of the first and last authors differed between those who chose the open-access option and those who did not.\n[33] In the group that chose open access, last authors tended to have a “stronger” previous citation record, whereas this situation was reversed among the group that declined the open-access option—here, it was the first authors who tended to be stronger.\n[34] This may reflect varying attitudes of authors at different stages of their career, a stronger influence from the leader of a particular group, or an age- or career-related difference in the ability to pay the publication charge (e.g., [ 1]).\n[35] Indeed, access to appropriate funds may also be a reason why a lower proportion of authors from European countries tended to choose the open-access option.\n[36] In many of these countries, funds for page charges—and, by extension, open-access publication fees—are often not included within research grants.\n[37] PNAS was one of the first journals to offer an open-access option to its authors.\n[38] However, such hybrid journals are increasing: Blackwell, Springer, and Oxford University Press now provide this option as well.\n[39] This means that similar experiments can be replicated.\n[40] Moreover, although the evidence from the current analysis argues most strongly for a time advantage in citation for OA articles, a study over longer periods will reveal whether this translates into a sustained increase in the number of citations.\n[41] In the meantime, open-access advocates should be emboldened by tangible evidence for what has seemed obvious all along."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"The results of this natural experiment are clear: in the 4 to 16 months following publication, OA articles gained a significant citation advantage over non-OA articles during the same period.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 129, "doc_id": 27768226, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [27768226], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Articles published in open access format are less likely to be cited than traditional journals.\n\nDocument title: Open Access Increases Citation Rate\n\nAbstract sentences:\n[0] PLoS Biology publishes today a research article by Gunther Eysenbach that is not about biology.\n[1] It is about citations.\n[2] It provides robust evidence that open-access articles (OA articles) are more immediately recognized and cited than non-OA articles.\n[3] As such, it adds objective support to the belief we have always held that open-access publication speeds up scientific dialog between researchers and, consequently, should be extended to the whole scientific literature as quickly as possible.\n[4] It is therefore fitting that we publish such a paper.\n[5] We have long argued that papers freely available in a journal will be more often read and cited than those behind a subscription barrier.\n[6] However, solid evidence to support or refute such a claim has been surprisingly hard to find.\n[7] Since most open-access journals are new, comparisons of the effects of open access with established subscription-based journals are easily confounded by age and reputation.\n[8] In the current study, Eysenbach compared citations compiled by Thomson Scientific (formerly Thomson ISI) to individual articles published between June 2004 and December 2004 in the same journal—namely, Proceedings of the National Academy of Sciences (PNAS), which announced its open-access option for authors on June 8 of that year, with an associated publication charge of US$1,000.\n[9] Non-OA articles in PNAS are subject to a six-month “toll-access” delay before the article becomes publicly available.\n[10] The results of this natural experiment are clear: in the 4 to 16 months following publication, OA articles gained a significant citation advantage over non-OA articles during the same period.\n[11] They are twice as likely to be cited 4 to 10 months after publication and almost three times as likely between 10 and 16 months.\n[12] Given that PNAS delays open access for only six months, the disparity between OA and non-OA articles in journals where the delay is longer or where articles remain “toll-access” is likely to be even greater.\n[13] Eysenbach also looked at the impact of self-archiving non-OA articles.\n[14] One route to open access, it is argued, is for authors to archive their published articles on their own Web sites or in institutional repositories, although this does not include an explicit business model to cover the cost of peer-review and publishing.\n[15] The analysis revealed that self-archived articles are also cited less often than OA articles from the same journal.\n[16] Yes, you're right; we do have a strong and vested interest in publishing results that so obviously endorse our existence.\n[17] Moreover, the author of the article is also an editor of an open-access journal.\n[18] But sometimes a potential conflict of interest can actually help to ensure rigor.\n[19] In this case, we have an acute interest in ensuring that the article meets the same, if not higher, standards as any other research article we publish.\n[20] Not only must the conclusions provide a significant advance for the field, but the study must be technically sound, with appropriate evidence to support those conclusions.\n[21] As with all our research articles, we consulted throughout the evaluation process with an academic editor with appropriate expertise—in this case, Carol Tenopir, professor of information sciences at the University of Tennessee (Knoxville, Tennessee, United States).\n[22] The article was reviewed by two experts in bibliometric analyses and information science, and an experienced research biologist with expertise in statistics.\n[23] They all enthusiastically supported publication, although one understandably questioned the suitability of PLoS Biology as the publication venue.\n[24] We have no intention of making PLoS Biology a regular home for bibliometric studies (even when about open access).\n[25] What makes this study worth publishing in PLoS Biology is not only the relative strength of evidence supporting the claim but also the extent to which many (especially other publishers) have anticipated such an analysis.\n[26] As far as we are aware, no other study has compared OA and non-OA articles from the same journal and controlled for so many potentially confounding factors.\n[27] Eysenbach's multivariate analysis took into account the number of days since publication, number of authors, article type, country of the corresponding author, funding type, subject area, submission track ( PNAS has three different ways that authors can submit a paper), and the previous citation record of the first and last authors.\n[28] He even administered a supplementary questionnaire to assess whether authors choosing the OA option in PNAS chose to do so for only their most important research (they didn't).\n[29] As Ian Rowlands from the Centre for Publishing at University College London—and one of the reviewers who agreed to be identified in this article—said at the start of his review:          “Many (most) of the papers and presentations I have read/seen on this topic have completely failed to address the kinds of confounding issues that are so convincingly tackled here.\n[30] For that reason alone, this paper deserves to be published and alerted to the widest possible audience.\n[31] ”          In addition to providing evidence for the immediate advantage of open access, Eysenbach's analysis also highlights several potential challenges to its long-term future.\n[32] Although a limited dataset, the citation history of the first and last authors differed between those who chose the open-access option and those who did not.\n[33] In the group that chose open access, last authors tended to have a “stronger” previous citation record, whereas this situation was reversed among the group that declined the open-access option—here, it was the first authors who tended to be stronger.\n[34] This may reflect varying attitudes of authors at different stages of their career, a stronger influence from the leader of a particular group, or an age- or career-related difference in the ability to pay the publication charge (e.g., [ 1]).\n[35] Indeed, access to appropriate funds may also be a reason why a lower proportion of authors from European countries tended to choose the open-access option.\n[36] In many of these countries, funds for page charges—and, by extension, open-access publication fees—are often not included within research grants.\n[37] PNAS was one of the first journals to offer an open-access option to its authors.\n[38] However, such hybrid journals are increasing: Blackwell, Springer, and Oxford University Press now provide this option as well.\n[39] This means that similar experiments can be replicated.\n[40] Moreover, although the evidence from the current analysis argues most strongly for a time advantage in citation for OA articles, a study over longer periods will reveal whether this translates into a sustained increase in the number of citations.\n[41] In the meantime, open-access advocates should be emboldened by tangible evidence for what has seemed obvious all along."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"They are twice as likely to be cited 4 to 10 months after publication and almost three times as likely between 10 and 16 months.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 129, "doc_id": 27768226, "label": "CONTRADICTS", "evidence_sentence_ids": [11], "cited_doc_ids": [27768226], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Articles published in open access format are less likely to be cited than traditional journals.\n\nDocument title: Open Access Increases Citation Rate\n\nAbstract sentences:\n[0] PLoS Biology publishes today a research article by Gunther Eysenbach that is not about biology.\n[1] It is about citations.\n[2] It provides robust evidence that open-access articles (OA articles) are more immediately recognized and cited than non-OA articles.\n[3] As such, it adds objective support to the belief we have always held that open-access publication speeds up scientific dialog between researchers and, consequently, should be extended to the whole scientific literature as quickly as possible.\n[4] It is therefore fitting that we publish such a paper.\n[5] We have long argued that papers freely available in a journal will be more often read and cited than those behind a subscription barrier.\n[6] However, solid evidence to support or refute such a claim has been surprisingly hard to find.\n[7] Since most open-access journals are new, comparisons of the effects of open access with established subscription-based journals are easily confounded by age and reputation.\n[8] In the current study, Eysenbach compared citations compiled by Thomson Scientific (formerly Thomson ISI) to individual articles published between June 2004 and December 2004 in the same journal—namely, Proceedings of the National Academy of Sciences (PNAS), which announced its open-access option for authors on June 8 of that year, with an associated publication charge of US$1,000.\n[9] Non-OA articles in PNAS are subject to a six-month “toll-access” delay before the article becomes publicly available.\n[10] The results of this natural experiment are clear: in the 4 to 16 months following publication, OA articles gained a significant citation advantage over non-OA articles during the same period.\n[11] They are twice as likely to be cited 4 to 10 months after publication and almost three times as likely between 10 and 16 months.\n[12] Given that PNAS delays open access for only six months, the disparity between OA and non-OA articles in journals where the delay is longer or where articles remain “toll-access” is likely to be even greater.\n[13] Eysenbach also looked at the impact of self-archiving non-OA articles.\n[14] One route to open access, it is argued, is for authors to archive their published articles on their own Web sites or in institutional repositories, although this does not include an explicit business model to cover the cost of peer-review and publishing.\n[15] The analysis revealed that self-archived articles are also cited less often than OA articles from the same journal.\n[16] Yes, you're right; we do have a strong and vested interest in publishing results that so obviously endorse our existence.\n[17] Moreover, the author of the article is also an editor of an open-access journal.\n[18] But sometimes a potential conflict of interest can actually help to ensure rigor.\n[19] In this case, we have an acute interest in ensuring that the article meets the same, if not higher, standards as any other research article we publish.\n[20] Not only must the conclusions provide a significant advance for the field, but the study must be technically sound, with appropriate evidence to support those conclusions.\n[21] As with all our research articles, we consulted throughout the evaluation process with an academic editor with appropriate expertise—in this case, Carol Tenopir, professor of information sciences at the University of Tennessee (Knoxville, Tennessee, United States).\n[22] The article was reviewed by two experts in bibliometric analyses and information science, and an experienced research biologist with expertise in statistics.\n[23] They all enthusiastically supported publication, although one understandably questioned the suitability of PLoS Biology as the publication venue.\n[24] We have no intention of making PLoS Biology a regular home for bibliometric studies (even when about open access).\n[25] What makes this study worth publishing in PLoS Biology is not only the relative strength of evidence supporting the claim but also the extent to which many (especially other publishers) have anticipated such an analysis.\n[26] As far as we are aware, no other study has compared OA and non-OA articles from the same journal and controlled for so many potentially confounding factors.\n[27] Eysenbach's multivariate analysis took into account the number of days since publication, number of authors, article type, country of the corresponding author, funding type, subject area, submission track ( PNAS has three different ways that authors can submit a paper), and the previous citation record of the first and last authors.\n[28] He even administered a supplementary questionnaire to assess whether authors choosing the OA option in PNAS chose to do so for only their most important research (they didn't).\n[29] As Ian Rowlands from the Centre for Publishing at University College London—and one of the reviewers who agreed to be identified in this article—said at the start of his review:          “Many (most) of the papers and presentations I have read/seen on this topic have completely failed to address the kinds of confounding issues that are so convincingly tackled here.\n[30] For that reason alone, this paper deserves to be published and alerted to the widest possible audience.\n[31] ”          In addition to providing evidence for the immediate advantage of open access, Eysenbach's analysis also highlights several potential challenges to its long-term future.\n[32] Although a limited dataset, the citation history of the first and last authors differed between those who chose the open-access option and those who did not.\n[33] In the group that chose open access, last authors tended to have a “stronger” previous citation record, whereas this situation was reversed among the group that declined the open-access option—here, it was the first authors who tended to be stronger.\n[34] This may reflect varying attitudes of authors at different stages of their career, a stronger influence from the leader of a particular group, or an age- or career-related difference in the ability to pay the publication charge (e.g., [ 1]).\n[35] Indeed, access to appropriate funds may also be a reason why a lower proportion of authors from European countries tended to choose the open-access option.\n[36] In many of these countries, funds for page charges—and, by extension, open-access publication fees—are often not included within research grants.\n[37] PNAS was one of the first journals to offer an open-access option to its authors.\n[38] However, such hybrid journals are increasing: Blackwell, Springer, and Oxford University Press now provide this option as well.\n[39] This means that similar experiments can be replicated.\n[40] Moreover, although the evidence from the current analysis argues most strongly for a time advantage in citation for OA articles, a study over longer periods will reveal whether this translates into a sustained increase in the number of citations.\n[41] In the meantime, open-access advocates should be emboldened by tangible evidence for what has seemed obvious all along."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [40]\nExplanation: Evidence states: \"Moreover, although the evidence from the current analysis argues most strongly for a time advantage in citation for OA articles, a study over longer periods will reveal whether this translates into a sustained increase in the number of citations.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 129, "doc_id": 27768226, "label": "CONTRADICTS", "evidence_sentence_ids": [40], "cited_doc_ids": [27768226], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Articles published in open access format are more likely to be cited than traditional journals.\n\nDocument title: Open Access Increases Citation Rate\n\nAbstract sentences:\n[0] PLoS Biology publishes today a research article by Gunther Eysenbach that is not about biology.\n[1] It is about citations.\n[2] It provides robust evidence that open-access articles (OA articles) are more immediately recognized and cited than non-OA articles.\n[3] As such, it adds objective support to the belief we have always held that open-access publication speeds up scientific dialog between researchers and, consequently, should be extended to the whole scientific literature as quickly as possible.\n[4] It is therefore fitting that we publish such a paper.\n[5] We have long argued that papers freely available in a journal will be more often read and cited than those behind a subscription barrier.\n[6] However, solid evidence to support or refute such a claim has been surprisingly hard to find.\n[7] Since most open-access journals are new, comparisons of the effects of open access with established subscription-based journals are easily confounded by age and reputation.\n[8] In the current study, Eysenbach compared citations compiled by Thomson Scientific (formerly Thomson ISI) to individual articles published between June 2004 and December 2004 in the same journal—namely, Proceedings of the National Academy of Sciences (PNAS), which announced its open-access option for authors on June 8 of that year, with an associated publication charge of US$1,000.\n[9] Non-OA articles in PNAS are subject to a six-month “toll-access” delay before the article becomes publicly available.\n[10] The results of this natural experiment are clear: in the 4 to 16 months following publication, OA articles gained a significant citation advantage over non-OA articles during the same period.\n[11] They are twice as likely to be cited 4 to 10 months after publication and almost three times as likely between 10 and 16 months.\n[12] Given that PNAS delays open access for only six months, the disparity between OA and non-OA articles in journals where the delay is longer or where articles remain “toll-access” is likely to be even greater.\n[13] Eysenbach also looked at the impact of self-archiving non-OA articles.\n[14] One route to open access, it is argued, is for authors to archive their published articles on their own Web sites or in institutional repositories, although this does not include an explicit business model to cover the cost of peer-review and publishing.\n[15] The analysis revealed that self-archived articles are also cited less often than OA articles from the same journal.\n[16] Yes, you're right; we do have a strong and vested interest in publishing results that so obviously endorse our existence.\n[17] Moreover, the author of the article is also an editor of an open-access journal.\n[18] But sometimes a potential conflict of interest can actually help to ensure rigor.\n[19] In this case, we have an acute interest in ensuring that the article meets the same, if not higher, standards as any other research article we publish.\n[20] Not only must the conclusions provide a significant advance for the field, but the study must be technically sound, with appropriate evidence to support those conclusions.\n[21] As with all our research articles, we consulted throughout the evaluation process with an academic editor with appropriate expertise—in this case, Carol Tenopir, professor of information sciences at the University of Tennessee (Knoxville, Tennessee, United States).\n[22] The article was reviewed by two experts in bibliometric analyses and information science, and an experienced research biologist with expertise in statistics.\n[23] They all enthusiastically supported publication, although one understandably questioned the suitability of PLoS Biology as the publication venue.\n[24] We have no intention of making PLoS Biology a regular home for bibliometric studies (even when about open access).\n[25] What makes this study worth publishing in PLoS Biology is not only the relative strength of evidence supporting the claim but also the extent to which many (especially other publishers) have anticipated such an analysis.\n[26] As far as we are aware, no other study has compared OA and non-OA articles from the same journal and controlled for so many potentially confounding factors.\n[27] Eysenbach's multivariate analysis took into account the number of days since publication, number of authors, article type, country of the corresponding author, funding type, subject area, submission track ( PNAS has three different ways that authors can submit a paper), and the previous citation record of the first and last authors.\n[28] He even administered a supplementary questionnaire to assess whether authors choosing the OA option in PNAS chose to do so for only their most important research (they didn't).\n[29] As Ian Rowlands from the Centre for Publishing at University College London—and one of the reviewers who agreed to be identified in this article—said at the start of his review:          “Many (most) of the papers and presentations I have read/seen on this topic have completely failed to address the kinds of confounding issues that are so convincingly tackled here.\n[30] For that reason alone, this paper deserves to be published and alerted to the widest possible audience.\n[31] ”          In addition to providing evidence for the immediate advantage of open access, Eysenbach's analysis also highlights several potential challenges to its long-term future.\n[32] Although a limited dataset, the citation history of the first and last authors differed between those who chose the open-access option and those who did not.\n[33] In the group that chose open access, last authors tended to have a “stronger” previous citation record, whereas this situation was reversed among the group that declined the open-access option—here, it was the first authors who tended to be stronger.\n[34] This may reflect varying attitudes of authors at different stages of their career, a stronger influence from the leader of a particular group, or an age- or career-related difference in the ability to pay the publication charge (e.g., [ 1]).\n[35] Indeed, access to appropriate funds may also be a reason why a lower proportion of authors from European countries tended to choose the open-access option.\n[36] In many of these countries, funds for page charges—and, by extension, open-access publication fees—are often not included within research grants.\n[37] PNAS was one of the first journals to offer an open-access option to its authors.\n[38] However, such hybrid journals are increasing: Blackwell, Springer, and Oxford University Press now provide this option as well.\n[39] This means that similar experiments can be replicated.\n[40] Moreover, although the evidence from the current analysis argues most strongly for a time advantage in citation for OA articles, a study over longer periods will reveal whether this translates into a sustained increase in the number of citations.\n[41] In the meantime, open-access advocates should be emboldened by tangible evidence for what has seemed obvious all along."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"It provides robust evidence that open-access articles (OA articles) are more immediately recognized and cited than non-OA articles.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 130, "doc_id": 27768226, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [27768226], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Articles published in open access format are more likely to be cited than traditional journals.\n\nDocument title: Open Access Increases Citation Rate\n\nAbstract sentences:\n[0] PLoS Biology publishes today a research article by Gunther Eysenbach that is not about biology.\n[1] It is about citations.\n[2] It provides robust evidence that open-access articles (OA articles) are more immediately recognized and cited than non-OA articles.\n[3] As such, it adds objective support to the belief we have always held that open-access publication speeds up scientific dialog between researchers and, consequently, should be extended to the whole scientific literature as quickly as possible.\n[4] It is therefore fitting that we publish such a paper.\n[5] We have long argued that papers freely available in a journal will be more often read and cited than those behind a subscription barrier.\n[6] However, solid evidence to support or refute such a claim has been surprisingly hard to find.\n[7] Since most open-access journals are new, comparisons of the effects of open access with established subscription-based journals are easily confounded by age and reputation.\n[8] In the current study, Eysenbach compared citations compiled by Thomson Scientific (formerly Thomson ISI) to individual articles published between June 2004 and December 2004 in the same journal—namely, Proceedings of the National Academy of Sciences (PNAS), which announced its open-access option for authors on June 8 of that year, with an associated publication charge of US$1,000.\n[9] Non-OA articles in PNAS are subject to a six-month “toll-access” delay before the article becomes publicly available.\n[10] The results of this natural experiment are clear: in the 4 to 16 months following publication, OA articles gained a significant citation advantage over non-OA articles during the same period.\n[11] They are twice as likely to be cited 4 to 10 months after publication and almost three times as likely between 10 and 16 months.\n[12] Given that PNAS delays open access for only six months, the disparity between OA and non-OA articles in journals where the delay is longer or where articles remain “toll-access” is likely to be even greater.\n[13] Eysenbach also looked at the impact of self-archiving non-OA articles.\n[14] One route to open access, it is argued, is for authors to archive their published articles on their own Web sites or in institutional repositories, although this does not include an explicit business model to cover the cost of peer-review and publishing.\n[15] The analysis revealed that self-archived articles are also cited less often than OA articles from the same journal.\n[16] Yes, you're right; we do have a strong and vested interest in publishing results that so obviously endorse our existence.\n[17] Moreover, the author of the article is also an editor of an open-access journal.\n[18] But sometimes a potential conflict of interest can actually help to ensure rigor.\n[19] In this case, we have an acute interest in ensuring that the article meets the same, if not higher, standards as any other research article we publish.\n[20] Not only must the conclusions provide a significant advance for the field, but the study must be technically sound, with appropriate evidence to support those conclusions.\n[21] As with all our research articles, we consulted throughout the evaluation process with an academic editor with appropriate expertise—in this case, Carol Tenopir, professor of information sciences at the University of Tennessee (Knoxville, Tennessee, United States).\n[22] The article was reviewed by two experts in bibliometric analyses and information science, and an experienced research biologist with expertise in statistics.\n[23] They all enthusiastically supported publication, although one understandably questioned the suitability of PLoS Biology as the publication venue.\n[24] We have no intention of making PLoS Biology a regular home for bibliometric studies (even when about open access).\n[25] What makes this study worth publishing in PLoS Biology is not only the relative strength of evidence supporting the claim but also the extent to which many (especially other publishers) have anticipated such an analysis.\n[26] As far as we are aware, no other study has compared OA and non-OA articles from the same journal and controlled for so many potentially confounding factors.\n[27] Eysenbach's multivariate analysis took into account the number of days since publication, number of authors, article type, country of the corresponding author, funding type, subject area, submission track ( PNAS has three different ways that authors can submit a paper), and the previous citation record of the first and last authors.\n[28] He even administered a supplementary questionnaire to assess whether authors choosing the OA option in PNAS chose to do so for only their most important research (they didn't).\n[29] As Ian Rowlands from the Centre for Publishing at University College London—and one of the reviewers who agreed to be identified in this article—said at the start of his review:          “Many (most) of the papers and presentations I have read/seen on this topic have completely failed to address the kinds of confounding issues that are so convincingly tackled here.\n[30] For that reason alone, this paper deserves to be published and alerted to the widest possible audience.\n[31] ”          In addition to providing evidence for the immediate advantage of open access, Eysenbach's analysis also highlights several potential challenges to its long-term future.\n[32] Although a limited dataset, the citation history of the first and last authors differed between those who chose the open-access option and those who did not.\n[33] In the group that chose open access, last authors tended to have a “stronger” previous citation record, whereas this situation was reversed among the group that declined the open-access option—here, it was the first authors who tended to be stronger.\n[34] This may reflect varying attitudes of authors at different stages of their career, a stronger influence from the leader of a particular group, or an age- or career-related difference in the ability to pay the publication charge (e.g., [ 1]).\n[35] Indeed, access to appropriate funds may also be a reason why a lower proportion of authors from European countries tended to choose the open-access option.\n[36] In many of these countries, funds for page charges—and, by extension, open-access publication fees—are often not included within research grants.\n[37] PNAS was one of the first journals to offer an open-access option to its authors.\n[38] However, such hybrid journals are increasing: Blackwell, Springer, and Oxford University Press now provide this option as well.\n[39] This means that similar experiments can be replicated.\n[40] Moreover, although the evidence from the current analysis argues most strongly for a time advantage in citation for OA articles, a study over longer periods will reveal whether this translates into a sustained increase in the number of citations.\n[41] In the meantime, open-access advocates should be emboldened by tangible evidence for what has seemed obvious all along."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"The results of this natural experiment are clear: in the 4 to 16 months following publication, OA articles gained a significant citation advantage over non-OA articles during the same period.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 130, "doc_id": 27768226, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [27768226], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Articles published in open access format are more likely to be cited than traditional journals.\n\nDocument title: Open Access Increases Citation Rate\n\nAbstract sentences:\n[0] PLoS Biology publishes today a research article by Gunther Eysenbach that is not about biology.\n[1] It is about citations.\n[2] It provides robust evidence that open-access articles (OA articles) are more immediately recognized and cited than non-OA articles.\n[3] As such, it adds objective support to the belief we have always held that open-access publication speeds up scientific dialog between researchers and, consequently, should be extended to the whole scientific literature as quickly as possible.\n[4] It is therefore fitting that we publish such a paper.\n[5] We have long argued that papers freely available in a journal will be more often read and cited than those behind a subscription barrier.\n[6] However, solid evidence to support or refute such a claim has been surprisingly hard to find.\n[7] Since most open-access journals are new, comparisons of the effects of open access with established subscription-based journals are easily confounded by age and reputation.\n[8] In the current study, Eysenbach compared citations compiled by Thomson Scientific (formerly Thomson ISI) to individual articles published between June 2004 and December 2004 in the same journal—namely, Proceedings of the National Academy of Sciences (PNAS), which announced its open-access option for authors on June 8 of that year, with an associated publication charge of US$1,000.\n[9] Non-OA articles in PNAS are subject to a six-month “toll-access” delay before the article becomes publicly available.\n[10] The results of this natural experiment are clear: in the 4 to 16 months following publication, OA articles gained a significant citation advantage over non-OA articles during the same period.\n[11] They are twice as likely to be cited 4 to 10 months after publication and almost three times as likely between 10 and 16 months.\n[12] Given that PNAS delays open access for only six months, the disparity between OA and non-OA articles in journals where the delay is longer or where articles remain “toll-access” is likely to be even greater.\n[13] Eysenbach also looked at the impact of self-archiving non-OA articles.\n[14] One route to open access, it is argued, is for authors to archive their published articles on their own Web sites or in institutional repositories, although this does not include an explicit business model to cover the cost of peer-review and publishing.\n[15] The analysis revealed that self-archived articles are also cited less often than OA articles from the same journal.\n[16] Yes, you're right; we do have a strong and vested interest in publishing results that so obviously endorse our existence.\n[17] Moreover, the author of the article is also an editor of an open-access journal.\n[18] But sometimes a potential conflict of interest can actually help to ensure rigor.\n[19] In this case, we have an acute interest in ensuring that the article meets the same, if not higher, standards as any other research article we publish.\n[20] Not only must the conclusions provide a significant advance for the field, but the study must be technically sound, with appropriate evidence to support those conclusions.\n[21] As with all our research articles, we consulted throughout the evaluation process with an academic editor with appropriate expertise—in this case, Carol Tenopir, professor of information sciences at the University of Tennessee (Knoxville, Tennessee, United States).\n[22] The article was reviewed by two experts in bibliometric analyses and information science, and an experienced research biologist with expertise in statistics.\n[23] They all enthusiastically supported publication, although one understandably questioned the suitability of PLoS Biology as the publication venue.\n[24] We have no intention of making PLoS Biology a regular home for bibliometric studies (even when about open access).\n[25] What makes this study worth publishing in PLoS Biology is not only the relative strength of evidence supporting the claim but also the extent to which many (especially other publishers) have anticipated such an analysis.\n[26] As far as we are aware, no other study has compared OA and non-OA articles from the same journal and controlled for so many potentially confounding factors.\n[27] Eysenbach's multivariate analysis took into account the number of days since publication, number of authors, article type, country of the corresponding author, funding type, subject area, submission track ( PNAS has three different ways that authors can submit a paper), and the previous citation record of the first and last authors.\n[28] He even administered a supplementary questionnaire to assess whether authors choosing the OA option in PNAS chose to do so for only their most important research (they didn't).\n[29] As Ian Rowlands from the Centre for Publishing at University College London—and one of the reviewers who agreed to be identified in this article—said at the start of his review:          “Many (most) of the papers and presentations I have read/seen on this topic have completely failed to address the kinds of confounding issues that are so convincingly tackled here.\n[30] For that reason alone, this paper deserves to be published and alerted to the widest possible audience.\n[31] ”          In addition to providing evidence for the immediate advantage of open access, Eysenbach's analysis also highlights several potential challenges to its long-term future.\n[32] Although a limited dataset, the citation history of the first and last authors differed between those who chose the open-access option and those who did not.\n[33] In the group that chose open access, last authors tended to have a “stronger” previous citation record, whereas this situation was reversed among the group that declined the open-access option—here, it was the first authors who tended to be stronger.\n[34] This may reflect varying attitudes of authors at different stages of their career, a stronger influence from the leader of a particular group, or an age- or career-related difference in the ability to pay the publication charge (e.g., [ 1]).\n[35] Indeed, access to appropriate funds may also be a reason why a lower proportion of authors from European countries tended to choose the open-access option.\n[36] In many of these countries, funds for page charges—and, by extension, open-access publication fees—are often not included within research grants.\n[37] PNAS was one of the first journals to offer an open-access option to its authors.\n[38] However, such hybrid journals are increasing: Blackwell, Springer, and Oxford University Press now provide this option as well.\n[39] This means that similar experiments can be replicated.\n[40] Moreover, although the evidence from the current analysis argues most strongly for a time advantage in citation for OA articles, a study over longer periods will reveal whether this translates into a sustained increase in the number of citations.\n[41] In the meantime, open-access advocates should be emboldened by tangible evidence for what has seemed obvious all along."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"They are twice as likely to be cited 4 to 10 months after publication and almost three times as likely between 10 and 16 months.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 130, "doc_id": 27768226, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [27768226], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Articles published in open access format are more likely to be cited than traditional journals.\n\nDocument title: Open Access Increases Citation Rate\n\nAbstract sentences:\n[0] PLoS Biology publishes today a research article by Gunther Eysenbach that is not about biology.\n[1] It is about citations.\n[2] It provides robust evidence that open-access articles (OA articles) are more immediately recognized and cited than non-OA articles.\n[3] As such, it adds objective support to the belief we have always held that open-access publication speeds up scientific dialog between researchers and, consequently, should be extended to the whole scientific literature as quickly as possible.\n[4] It is therefore fitting that we publish such a paper.\n[5] We have long argued that papers freely available in a journal will be more often read and cited than those behind a subscription barrier.\n[6] However, solid evidence to support or refute such a claim has been surprisingly hard to find.\n[7] Since most open-access journals are new, comparisons of the effects of open access with established subscription-based journals are easily confounded by age and reputation.\n[8] In the current study, Eysenbach compared citations compiled by Thomson Scientific (formerly Thomson ISI) to individual articles published between June 2004 and December 2004 in the same journal—namely, Proceedings of the National Academy of Sciences (PNAS), which announced its open-access option for authors on June 8 of that year, with an associated publication charge of US$1,000.\n[9] Non-OA articles in PNAS are subject to a six-month “toll-access” delay before the article becomes publicly available.\n[10] The results of this natural experiment are clear: in the 4 to 16 months following publication, OA articles gained a significant citation advantage over non-OA articles during the same period.\n[11] They are twice as likely to be cited 4 to 10 months after publication and almost three times as likely between 10 and 16 months.\n[12] Given that PNAS delays open access for only six months, the disparity between OA and non-OA articles in journals where the delay is longer or where articles remain “toll-access” is likely to be even greater.\n[13] Eysenbach also looked at the impact of self-archiving non-OA articles.\n[14] One route to open access, it is argued, is for authors to archive their published articles on their own Web sites or in institutional repositories, although this does not include an explicit business model to cover the cost of peer-review and publishing.\n[15] The analysis revealed that self-archived articles are also cited less often than OA articles from the same journal.\n[16] Yes, you're right; we do have a strong and vested interest in publishing results that so obviously endorse our existence.\n[17] Moreover, the author of the article is also an editor of an open-access journal.\n[18] But sometimes a potential conflict of interest can actually help to ensure rigor.\n[19] In this case, we have an acute interest in ensuring that the article meets the same, if not higher, standards as any other research article we publish.\n[20] Not only must the conclusions provide a significant advance for the field, but the study must be technically sound, with appropriate evidence to support those conclusions.\n[21] As with all our research articles, we consulted throughout the evaluation process with an academic editor with appropriate expertise—in this case, Carol Tenopir, professor of information sciences at the University of Tennessee (Knoxville, Tennessee, United States).\n[22] The article was reviewed by two experts in bibliometric analyses and information science, and an experienced research biologist with expertise in statistics.\n[23] They all enthusiastically supported publication, although one understandably questioned the suitability of PLoS Biology as the publication venue.\n[24] We have no intention of making PLoS Biology a regular home for bibliometric studies (even when about open access).\n[25] What makes this study worth publishing in PLoS Biology is not only the relative strength of evidence supporting the claim but also the extent to which many (especially other publishers) have anticipated such an analysis.\n[26] As far as we are aware, no other study has compared OA and non-OA articles from the same journal and controlled for so many potentially confounding factors.\n[27] Eysenbach's multivariate analysis took into account the number of days since publication, number of authors, article type, country of the corresponding author, funding type, subject area, submission track ( PNAS has three different ways that authors can submit a paper), and the previous citation record of the first and last authors.\n[28] He even administered a supplementary questionnaire to assess whether authors choosing the OA option in PNAS chose to do so for only their most important research (they didn't).\n[29] As Ian Rowlands from the Centre for Publishing at University College London—and one of the reviewers who agreed to be identified in this article—said at the start of his review:          “Many (most) of the papers and presentations I have read/seen on this topic have completely failed to address the kinds of confounding issues that are so convincingly tackled here.\n[30] For that reason alone, this paper deserves to be published and alerted to the widest possible audience.\n[31] ”          In addition to providing evidence for the immediate advantage of open access, Eysenbach's analysis also highlights several potential challenges to its long-term future.\n[32] Although a limited dataset, the citation history of the first and last authors differed between those who chose the open-access option and those who did not.\n[33] In the group that chose open access, last authors tended to have a “stronger” previous citation record, whereas this situation was reversed among the group that declined the open-access option—here, it was the first authors who tended to be stronger.\n[34] This may reflect varying attitudes of authors at different stages of their career, a stronger influence from the leader of a particular group, or an age- or career-related difference in the ability to pay the publication charge (e.g., [ 1]).\n[35] Indeed, access to appropriate funds may also be a reason why a lower proportion of authors from European countries tended to choose the open-access option.\n[36] In many of these countries, funds for page charges—and, by extension, open-access publication fees—are often not included within research grants.\n[37] PNAS was one of the first journals to offer an open-access option to its authors.\n[38] However, such hybrid journals are increasing: Blackwell, Springer, and Oxford University Press now provide this option as well.\n[39] This means that similar experiments can be replicated.\n[40] Moreover, although the evidence from the current analysis argues most strongly for a time advantage in citation for OA articles, a study over longer periods will reveal whether this translates into a sustained increase in the number of citations.\n[41] In the meantime, open-access advocates should be emboldened by tangible evidence for what has seemed obvious all along."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [40]\nExplanation: Evidence states: \"Moreover, although the evidence from the current analysis argues most strongly for a time advantage in citation for OA articles, a study over longer periods will reveal whether this translates into a sustained increase in the number of citations.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 130, "doc_id": 27768226, "label": "SUPPORTS", "evidence_sentence_ids": [40], "cited_doc_ids": [27768226], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Aspirin inhibits the production of PGE2.\n\nDocument title: Cyclooxygenase-Dependent Tumor Growth through Evasion of Immunity\n\nAbstract sentences:\n[0] The mechanisms by which melanoma and other cancer cells evade anti-tumor immunity remain incompletely understood.\n[1] Here, we show that the growth of tumors formed by mutant Braf(V600E) mouse melanoma cells in an immunocompetent host requires their production of prostaglandin E2, which suppresses immunity and fuels tumor-promoting inflammation.\n[2] Genetic ablation of cyclooxygenases (COX) or prostaglandin E synthases in Braf(V600E) mouse melanoma cells, as well as in Nras(G12D) melanoma or in breast or colorectal cancer cells, renders them susceptible to immune control and provokes a shift in the tumor inflammatory profile toward classic anti-cancer immune pathways.\n[3] This mouse COX-dependent inflammatory signature is remarkably conserved in human cutaneous melanoma biopsies, arguing for COX activity as a driver of immune suppression across species.\n[4] Pre-clinical data demonstrate that inhibition of COX synergizes with anti-PD-1 blockade in inducing eradication of tumors, implying that COX inhibitors could be useful adjuvants for immune-based therapies in cancer 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": "validation", "claim_id": 132, "doc_id": 7975937, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [7975937], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Assembly of invadopodia is triggered by focal generation of phosphatidylinositol-3,4-biphosphate and the activation of the nonreceptor tyrosine kinase Src.\n\nDocument title: Sequential signals toward podosome formation in NIH-src cells\n\nAbstract sentences:\n[0] Podosomes (also termed invadopodia in cancer cells) are actin-rich adhesion structures with matrix degradation activity that develop in various cell types.\n[1] Despite their significant physiological importance, the molecular mechanism of podosome formation is largely unknown.\n[2] In this study, we investigated the molecular mechanisms of podosome formation.\n[3] The expression of various phosphoinositide-binding domains revealed that the podosomes in Src-transformed NIH3T3 (NIH-src) cells are enriched with PtdIns(3,4)P2, suggesting an important role of this phosphoinositide in podosome formation.\n[4] Live-cell imaging analysis revealed that Src-expression stimulated podosome formation at focal adhesions of NIH3T3 cells after PtdIns(3,4)P2 accumulation.\n[5] The adaptor protein Tks5/FISH, which is essential for podosome formation, was found to form a complex with Grb2 at adhesion sites in an Src-dependent manner.\n[6] Further, it was found that N-WASP bound all SH3 domains of Tks5/FISH, which facilitated circular podosome formation.\n[7] These results indicate that augmentation of the N-WASP-Arp2/3 signal was accomplished on the platform of Tks5/FISH-Grb2 complex at focal adhesions, which is stabilized by PtdIns(3,4)P2."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3, 4]\nExplanation: Evidence states: \"The expression of various phosphoinositide-binding domains revealed that the podosomes in Src-transformed NIH3T3 (NIH-src) cells are enriched with PtdIns(3,4)P2, suggesting an important role of this phosphoinositide in podosome formation. Live-cell imaging analysis revealed that Src-expression stimulated podosome formation at focal adhesions of NIH3T3 cells after PtdIns(3,4)P2 accumulation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 133, "doc_id": 16280642, "label": "SUPPORTS", "evidence_sentence_ids": [3, 4], "cited_doc_ids": [38485364, 6969753, 17934082, 16280642, 12640810], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 does not lead 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 137, "doc_id": 26016929, "label": "SUPPORTS", "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: Auditory entrainment is strengthened when people see congruent visual and auditory information.\n\nDocument title: Congruent Visual Speech Enhances Cortical Entrainment to Continuous Auditory Speech in Noise-Free Conditions.\n\nAbstract sentences:\n[0] UNLABELLED Congruent audiovisual speech enhances our ability to comprehend a speaker, even in noise-free conditions.\n[1] When incongruent auditory and visual information is presented concurrently, it can hinder a listener's perception and even cause him or her to perceive information that was not presented in either modality.\n[2] Efforts to investigate the neural basis of these effects have often focused on the special case of discrete audiovisual syllables that are spatially and temporally congruent, with less work done on the case of natural, continuous speech.\n[3] Recent electrophysiological studies have demonstrated that cortical response measures to continuous auditory speech can be easily obtained using multivariate analysis methods.\n[4] Here, we apply such methods to the case of audiovisual speech and, importantly, present a novel framework for indexing multisensory integration in the context of continuous speech.\n[5] Specifically, we examine how the temporal and contextual congruency of ongoing audiovisual speech affects the cortical encoding of the speech envelope in humans using electroencephalography.\n[6] We demonstrate that the cortical representation of the speech envelope is enhanced by the presentation of congruent audiovisual speech in noise-free conditions.\n[7] Furthermore, we show that this is likely attributable to the contribution of neural generators that are not particularly active during unimodal stimulation and that it is most prominent at the temporal scale corresponding to syllabic rate (2-6 Hz).\n[8] Finally, our data suggest that neural entrainment to the speech envelope is inhibited when the auditory and visual streams are incongruent both temporally and contextually.\n[9] SIGNIFICANCE STATEMENT Seeing a speaker's face as he or she talks can greatly help in understanding what the speaker is saying.\n[10] This is because the speaker's facial movements relay information about what the speaker is saying, but also, importantly, when the speaker is saying it.\n[11] Studying how the brain uses this timing relationship to combine information from continuous auditory and visual speech has traditionally been methodologically difficult.\n[12] Here we introduce a new approach for doing this using relatively inexpensive and noninvasive scalp recordings.\n[13] Specifically, we show that the brain's representation of auditory speech is enhanced when the accompanying visual speech signal shares the same timing.\n[14] Furthermore, we show that this enhancement is most pronounced at a time scale that corresponds to mean syllable length."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"UNLABELLED Congruent audiovisual speech enhances our ability to comprehend a speaker, even in noise-free conditions.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 141, "doc_id": 14437255, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [6955746, 14437255], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Auditory entrainment is strengthened when people see congruent visual and auditory information.\n\nDocument title: Congruent Visual Speech Enhances Cortical Entrainment to Continuous Auditory Speech in Noise-Free Conditions.\n\nAbstract sentences:\n[0] UNLABELLED Congruent audiovisual speech enhances our ability to comprehend a speaker, even in noise-free conditions.\n[1] When incongruent auditory and visual information is presented concurrently, it can hinder a listener's perception and even cause him or her to perceive information that was not presented in either modality.\n[2] Efforts to investigate the neural basis of these effects have often focused on the special case of discrete audiovisual syllables that are spatially and temporally congruent, with less work done on the case of natural, continuous speech.\n[3] Recent electrophysiological studies have demonstrated that cortical response measures to continuous auditory speech can be easily obtained using multivariate analysis methods.\n[4] Here, we apply such methods to the case of audiovisual speech and, importantly, present a novel framework for indexing multisensory integration in the context of continuous speech.\n[5] Specifically, we examine how the temporal and contextual congruency of ongoing audiovisual speech affects the cortical encoding of the speech envelope in humans using electroencephalography.\n[6] We demonstrate that the cortical representation of the speech envelope is enhanced by the presentation of congruent audiovisual speech in noise-free conditions.\n[7] Furthermore, we show that this is likely attributable to the contribution of neural generators that are not particularly active during unimodal stimulation and that it is most prominent at the temporal scale corresponding to syllabic rate (2-6 Hz).\n[8] Finally, our data suggest that neural entrainment to the speech envelope is inhibited when the auditory and visual streams are incongruent both temporally and contextually.\n[9] SIGNIFICANCE STATEMENT Seeing a speaker's face as he or she talks can greatly help in understanding what the speaker is saying.\n[10] This is because the speaker's facial movements relay information about what the speaker is saying, but also, importantly, when the speaker is saying it.\n[11] Studying how the brain uses this timing relationship to combine information from continuous auditory and visual speech has traditionally been methodologically difficult.\n[12] Here we introduce a new approach for doing this using relatively inexpensive and noninvasive scalp recordings.\n[13] Specifically, we show that the brain's representation of auditory speech is enhanced when the accompanying visual speech signal shares the same timing.\n[14] Furthermore, we show that this enhancement is most pronounced at a time scale that corresponds to mean syllable length."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"When incongruent auditory and visual information is presented concurrently, it can hinder a listener's perception and even cause him or her to perceive information that was not presented in either modality.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 141, "doc_id": 14437255, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [6955746, 14437255], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Auditory entrainment is strengthened when people see congruent visual and auditory information.\n\nDocument title: Congruent Visual Speech Enhances Cortical Entrainment to Continuous Auditory Speech in Noise-Free Conditions.\n\nAbstract sentences:\n[0] UNLABELLED Congruent audiovisual speech enhances our ability to comprehend a speaker, even in noise-free conditions.\n[1] When incongruent auditory and visual information is presented concurrently, it can hinder a listener's perception and even cause him or her to perceive information that was not presented in either modality.\n[2] Efforts to investigate the neural basis of these effects have often focused on the special case of discrete audiovisual syllables that are spatially and temporally congruent, with less work done on the case of natural, continuous speech.\n[3] Recent electrophysiological studies have demonstrated that cortical response measures to continuous auditory speech can be easily obtained using multivariate analysis methods.\n[4] Here, we apply such methods to the case of audiovisual speech and, importantly, present a novel framework for indexing multisensory integration in the context of continuous speech.\n[5] Specifically, we examine how the temporal and contextual congruency of ongoing audiovisual speech affects the cortical encoding of the speech envelope in humans using electroencephalography.\n[6] We demonstrate that the cortical representation of the speech envelope is enhanced by the presentation of congruent audiovisual speech in noise-free conditions.\n[7] Furthermore, we show that this is likely attributable to the contribution of neural generators that are not particularly active during unimodal stimulation and that it is most prominent at the temporal scale corresponding to syllabic rate (2-6 Hz).\n[8] Finally, our data suggest that neural entrainment to the speech envelope is inhibited when the auditory and visual streams are incongruent both temporally and contextually.\n[9] SIGNIFICANCE STATEMENT Seeing a speaker's face as he or she talks can greatly help in understanding what the speaker is saying.\n[10] This is because the speaker's facial movements relay information about what the speaker is saying, but also, importantly, when the speaker is saying it.\n[11] Studying how the brain uses this timing relationship to combine information from continuous auditory and visual speech has traditionally been methodologically difficult.\n[12] Here we introduce a new approach for doing this using relatively inexpensive and noninvasive scalp recordings.\n[13] Specifically, we show that the brain's representation of auditory speech is enhanced when the accompanying visual speech signal shares the same timing.\n[14] Furthermore, we show that this enhancement is most pronounced at a time scale that corresponds to mean syllable length."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"We demonstrate that the cortical representation of the speech envelope is enhanced by the presentation of congruent audiovisual speech in noise-free conditions.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 141, "doc_id": 14437255, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [6955746, 14437255], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Auditory entrainment is strengthened when people see congruent visual and auditory information.\n\nDocument title: Congruent Visual Speech Enhances Cortical Entrainment to Continuous Auditory Speech in Noise-Free Conditions.\n\nAbstract sentences:\n[0] UNLABELLED Congruent audiovisual speech enhances our ability to comprehend a speaker, even in noise-free conditions.\n[1] When incongruent auditory and visual information is presented concurrently, it can hinder a listener's perception and even cause him or her to perceive information that was not presented in either modality.\n[2] Efforts to investigate the neural basis of these effects have often focused on the special case of discrete audiovisual syllables that are spatially and temporally congruent, with less work done on the case of natural, continuous speech.\n[3] Recent electrophysiological studies have demonstrated that cortical response measures to continuous auditory speech can be easily obtained using multivariate analysis methods.\n[4] Here, we apply such methods to the case of audiovisual speech and, importantly, present a novel framework for indexing multisensory integration in the context of continuous speech.\n[5] Specifically, we examine how the temporal and contextual congruency of ongoing audiovisual speech affects the cortical encoding of the speech envelope in humans using electroencephalography.\n[6] We demonstrate that the cortical representation of the speech envelope is enhanced by the presentation of congruent audiovisual speech in noise-free conditions.\n[7] Furthermore, we show that this is likely attributable to the contribution of neural generators that are not particularly active during unimodal stimulation and that it is most prominent at the temporal scale corresponding to syllabic rate (2-6 Hz).\n[8] Finally, our data suggest that neural entrainment to the speech envelope is inhibited when the auditory and visual streams are incongruent both temporally and contextually.\n[9] SIGNIFICANCE STATEMENT Seeing a speaker's face as he or she talks can greatly help in understanding what the speaker is saying.\n[10] This is because the speaker's facial movements relay information about what the speaker is saying, but also, importantly, when the speaker is saying it.\n[11] Studying how the brain uses this timing relationship to combine information from continuous auditory and visual speech has traditionally been methodologically difficult.\n[12] Here we introduce a new approach for doing this using relatively inexpensive and noninvasive scalp recordings.\n[13] Specifically, we show that the brain's representation of auditory speech is enhanced when the accompanying visual speech signal shares the same timing.\n[14] Furthermore, we show that this enhancement is most pronounced at a time scale that corresponds to mean syllable length."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Finally, our data suggest that neural entrainment to the speech envelope is inhibited when the auditory and visual streams are incongruent both temporally and contextually.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 141, "doc_id": 14437255, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [6955746, 14437255], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Auditory entrainment is strengthened when people see congruent visual and auditory information.\n\nDocument title: Congruent Visual Speech Enhances Cortical Entrainment to Continuous Auditory Speech in Noise-Free Conditions.\n\nAbstract sentences:\n[0] UNLABELLED Congruent audiovisual speech enhances our ability to comprehend a speaker, even in noise-free conditions.\n[1] When incongruent auditory and visual information is presented concurrently, it can hinder a listener's perception and even cause him or her to perceive information that was not presented in either modality.\n[2] Efforts to investigate the neural basis of these effects have often focused on the special case of discrete audiovisual syllables that are spatially and temporally congruent, with less work done on the case of natural, continuous speech.\n[3] Recent electrophysiological studies have demonstrated that cortical response measures to continuous auditory speech can be easily obtained using multivariate analysis methods.\n[4] Here, we apply such methods to the case of audiovisual speech and, importantly, present a novel framework for indexing multisensory integration in the context of continuous speech.\n[5] Specifically, we examine how the temporal and contextual congruency of ongoing audiovisual speech affects the cortical encoding of the speech envelope in humans using electroencephalography.\n[6] We demonstrate that the cortical representation of the speech envelope is enhanced by the presentation of congruent audiovisual speech in noise-free conditions.\n[7] Furthermore, we show that this is likely attributable to the contribution of neural generators that are not particularly active during unimodal stimulation and that it is most prominent at the temporal scale corresponding to syllabic rate (2-6 Hz).\n[8] Finally, our data suggest that neural entrainment to the speech envelope is inhibited when the auditory and visual streams are incongruent both temporally and contextually.\n[9] SIGNIFICANCE STATEMENT Seeing a speaker's face as he or she talks can greatly help in understanding what the speaker is saying.\n[10] This is because the speaker's facial movements relay information about what the speaker is saying, but also, importantly, when the speaker is saying it.\n[11] Studying how the brain uses this timing relationship to combine information from continuous auditory and visual speech has traditionally been methodologically difficult.\n[12] Here we introduce a new approach for doing this using relatively inexpensive and noninvasive scalp recordings.\n[13] Specifically, we show that the brain's representation of auditory speech is enhanced when the accompanying visual speech signal shares the same timing.\n[14] Furthermore, we show that this enhancement is most pronounced at a time scale that corresponds to mean syllable length."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"SIGNIFICANCE STATEMENT Seeing a speaker's face as he or she talks can greatly help in understanding what the speaker is saying.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 141, "doc_id": 14437255, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [6955746, 14437255], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Auditory entrainment is strengthened when people see congruent visual and auditory information.\n\nDocument title: Congruent Visual Speech Enhances Cortical Entrainment to Continuous Auditory Speech in Noise-Free Conditions.\n\nAbstract sentences:\n[0] UNLABELLED Congruent audiovisual speech enhances our ability to comprehend a speaker, even in noise-free conditions.\n[1] When incongruent auditory and visual information is presented concurrently, it can hinder a listener's perception and even cause him or her to perceive information that was not presented in either modality.\n[2] Efforts to investigate the neural basis of these effects have often focused on the special case of discrete audiovisual syllables that are spatially and temporally congruent, with less work done on the case of natural, continuous speech.\n[3] Recent electrophysiological studies have demonstrated that cortical response measures to continuous auditory speech can be easily obtained using multivariate analysis methods.\n[4] Here, we apply such methods to the case of audiovisual speech and, importantly, present a novel framework for indexing multisensory integration in the context of continuous speech.\n[5] Specifically, we examine how the temporal and contextual congruency of ongoing audiovisual speech affects the cortical encoding of the speech envelope in humans using electroencephalography.\n[6] We demonstrate that the cortical representation of the speech envelope is enhanced by the presentation of congruent audiovisual speech in noise-free conditions.\n[7] Furthermore, we show that this is likely attributable to the contribution of neural generators that are not particularly active during unimodal stimulation and that it is most prominent at the temporal scale corresponding to syllabic rate (2-6 Hz).\n[8] Finally, our data suggest that neural entrainment to the speech envelope is inhibited when the auditory and visual streams are incongruent both temporally and contextually.\n[9] SIGNIFICANCE STATEMENT Seeing a speaker's face as he or she talks can greatly help in understanding what the speaker is saying.\n[10] This is because the speaker's facial movements relay information about what the speaker is saying, but also, importantly, when the speaker is saying it.\n[11] Studying how the brain uses this timing relationship to combine information from continuous auditory and visual speech has traditionally been methodologically difficult.\n[12] Here we introduce a new approach for doing this using relatively inexpensive and noninvasive scalp recordings.\n[13] Specifically, we show that the brain's representation of auditory speech is enhanced when the accompanying visual speech signal shares the same timing.\n[14] Furthermore, we show that this enhancement is most pronounced at a time scale that corresponds to mean syllable length."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"Specifically, we show that the brain's representation of auditory speech is enhanced when the accompanying visual speech signal shares the same timing.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 141, "doc_id": 14437255, "label": "SUPPORTS", "evidence_sentence_ids": [13], "cited_doc_ids": [6955746, 14437255], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 causes a higher rate of opportunistic infections 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 142, "doc_id": 10582939, "label": "CONTRADICTS", "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: Autologous transplantation of mesenchymal stem cells causes fewer opportunistic infections 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": "validation", "claim_id": 143, "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: Autologous transplantation of mesenchymal stem cells has lower rates of rejection 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": "validation", "claim_id": 146, "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 lower rates of rejection 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": "validation", "claim_id": 146, "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 declines in aged organisms.\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: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"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.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 148, "doc_id": 1084345, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [1084345], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 has a positive impact on 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": "validation", "claim_id": 163, "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 has a positive impact on 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": "validation", "claim_id": 163, "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: Basophils counteract 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": "validation", "claim_id": 171, "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: Basophils counteract 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": "validation", "claim_id": 171, "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: Basophils counteract 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": "validation", "claim_id": 171, "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: Birth-weight is positively 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 179, "doc_id": 16322674, "label": "SUPPORTS", "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 positively 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 179, "doc_id": 16322674, "label": "SUPPORTS", "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 positively 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 179, "doc_id": 16322674, "label": "SUPPORTS", "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 positively 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: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"The majority of studies identified a positive link between birthweight and premenopausal, but not postmenopausal, breast cancer.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 179, "doc_id": 27123743, "label": "SUPPORTS", "evidence_sentence_ids": [3], "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 positively 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 179, "doc_id": 27123743, "label": "SUPPORTS", "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 positively 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 179, "doc_id": 23557241, "label": "SUPPORTS", "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 positively 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 179, "doc_id": 17450673, "label": "SUPPORTS", "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 positively 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 179, "doc_id": 17450673, "label": "SUPPORTS", "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 leads to increased 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 180, "doc_id": 16966326, "label": "CONTRADICTS", "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 cells 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 183, "doc_id": 12827098, "label": "CONTRADICTS", "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: Breast cancer development is determined exclusively by genetic factors.\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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 185, "doc_id": 18340282, "label": "CONTRADICTS", "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: Breast cancer development is determined exclusively by genetic factors.\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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 185, "doc_id": 18340282, "label": "CONTRADICTS", "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: CCL19 is absent 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": "validation", "claim_id": 198, "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: CHEK2 is not associated with breast cancer.\n\nDocument title: Linkage Disequilibrium Mapping of       CHEK2: Common Variation and Breast Cancer Risk     \n\nAbstract sentences:\n[0] Background Checkpoint kinase 2 (CHEK2) averts cancer development by promoting cell cycle arrest and activating DNA repair in genetically damaged cells.\n[1] Previous investigation has established a role for the CHEK2 gene in breast cancer aetiology, but studies have largely been limited to the rare 1100delC mutation.\n[2] Whether common polymorphisms in this gene influence breast cancer risk remains unknown.\n[3] In this study, we aimed to assess the importance of common CHEK2 variants on population risk for breast cancer by capturing the majority of diversity in the gene using haplotype tagging single nucleotide polymorphisms (tagSNPs).\n[4] Methods and Findings We analyzed 14 common SNPs spanning 52 kilobases (kb) of the CHEK2 gene in 92 Swedish women.\n[5] Coverage evaluation indicated that these typed SNPs would efficiently convey association signal also from untyped SNPs in the same region.\n[6] Six of the 14 SNPs predicted well both the haplotypic and single SNP variations within CHEK2.\n[7] We genotyped these six tagSNPs in 1,577 postmenopausal breast cancer cases and 1,513 population controls, but found no convincing association between any common CHEK2 haplotype and breast cancer risk.\n[8] The 1100delC mutation was rare in our Swedish population—0.7% in cases and 0.4% in controls— with a corresponding odds ratio for carriers versus noncarriers of 2.26 (95% confidence interval, 0.99–5.15).\n[9] Estimates of the population frequency and the odds ratio of 1100delC indicate that our sample is representative of a Northern European population."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"We genotyped these six tagSNPs in 1,577 postmenopausal breast cancer cases and 1,513 population controls, but found no convincing association between any common CHEK2 haplotype and breast cancer risk.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 208, "doc_id": 13519661, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [13519661], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CR is associated with higher methylation age.\n\nDocument title: Caloric restriction delays age-related methylation drift\n\nAbstract sentences:\n[0] In mammals, caloric restriction consistently results in extended lifespan.\n[1] Epigenetic information encoded by DNA methylation is tightly regulated, but shows a striking drift associated with age that includes both gains and losses of DNA methylation at various sites.\n[2] Here, we report that epigenetic drift is conserved across species and the rate of drift correlates with lifespan when comparing mice, rhesus monkeys, and humans.\n[3] Twenty-two to 30-year-old rhesus monkeys exposed to 30% caloric restriction since 7-14 years of age showed attenuation of age-related methylation drift compared to ad libitum-fed controls such that their blood methylation age appeared 7 years younger than their chronologic age.\n[4] Even more pronounced effects were seen in 2.7-3.2-year-old mice exposed to 40% caloric restriction starting at 0.3 years of age.\n[5] The effects of caloric restriction on DNA methylation were detectable across different tissues and correlated with gene expression.\n[6] We propose that epigenetic drift is a determinant of lifespan in mammals.\n[7] Caloric restriction has been shown to increase lifespan in mammals.\n[8] Here, the authors provide evidence that age-related methylation drift correlates with lifespan and that caloric restriction in mice and rhesus monkeys results in attenuation of age-related methylation drift."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"Epigenetic information encoded by DNA methylation is tightly regulated, but shows a striking drift associated with age that includes both gains and losses of DNA methylation at various sites.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 212, "doc_id": 22038539, "label": "CONTRADICTS", "evidence_sentence_ids": [1], "cited_doc_ids": [22038539], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CR is associated with higher methylation age.\n\nDocument title: Caloric restriction delays age-related methylation drift\n\nAbstract sentences:\n[0] In mammals, caloric restriction consistently results in extended lifespan.\n[1] Epigenetic information encoded by DNA methylation is tightly regulated, but shows a striking drift associated with age that includes both gains and losses of DNA methylation at various sites.\n[2] Here, we report that epigenetic drift is conserved across species and the rate of drift correlates with lifespan when comparing mice, rhesus monkeys, and humans.\n[3] Twenty-two to 30-year-old rhesus monkeys exposed to 30% caloric restriction since 7-14 years of age showed attenuation of age-related methylation drift compared to ad libitum-fed controls such that their blood methylation age appeared 7 years younger than their chronologic age.\n[4] Even more pronounced effects were seen in 2.7-3.2-year-old mice exposed to 40% caloric restriction starting at 0.3 years of age.\n[5] The effects of caloric restriction on DNA methylation were detectable across different tissues and correlated with gene expression.\n[6] We propose that epigenetic drift is a determinant of lifespan in mammals.\n[7] Caloric restriction has been shown to increase lifespan in mammals.\n[8] Here, the authors provide evidence that age-related methylation drift correlates with lifespan and that caloric restriction in mice and rhesus monkeys results in attenuation of age-related methylation drift."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Twenty-two to 30-year-old rhesus monkeys exposed to 30% caloric restriction since 7-14 years of age showed attenuation of age-related methylation drift compared to ad libitum-fed controls such that their blood methylation age appeared 7 years younger than their chronologic age.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 212, "doc_id": 22038539, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [22038539], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CR is associated with higher methylation age.\n\nDocument title: Caloric restriction delays age-related methylation drift\n\nAbstract sentences:\n[0] In mammals, caloric restriction consistently results in extended lifespan.\n[1] Epigenetic information encoded by DNA methylation is tightly regulated, but shows a striking drift associated with age that includes both gains and losses of DNA methylation at various sites.\n[2] Here, we report that epigenetic drift is conserved across species and the rate of drift correlates with lifespan when comparing mice, rhesus monkeys, and humans.\n[3] Twenty-two to 30-year-old rhesus monkeys exposed to 30% caloric restriction since 7-14 years of age showed attenuation of age-related methylation drift compared to ad libitum-fed controls such that their blood methylation age appeared 7 years younger than their chronologic age.\n[4] Even more pronounced effects were seen in 2.7-3.2-year-old mice exposed to 40% caloric restriction starting at 0.3 years of age.\n[5] The effects of caloric restriction on DNA methylation were detectable across different tissues and correlated with gene expression.\n[6] We propose that epigenetic drift is a determinant of lifespan in mammals.\n[7] Caloric restriction has been shown to increase lifespan in mammals.\n[8] Here, the authors provide evidence that age-related methylation drift correlates with lifespan and that caloric restriction in mice and rhesus monkeys results in attenuation of age-related methylation drift."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Even more pronounced effects were seen in 2.7-3.2-year-old mice exposed to 40% caloric restriction starting at 0.3 years of age.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 212, "doc_id": 22038539, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [22038539], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CR is associated with higher methylation age.\n\nDocument title: Caloric restriction delays age-related methylation drift\n\nAbstract sentences:\n[0] In mammals, caloric restriction consistently results in extended lifespan.\n[1] Epigenetic information encoded by DNA methylation is tightly regulated, but shows a striking drift associated with age that includes both gains and losses of DNA methylation at various sites.\n[2] Here, we report that epigenetic drift is conserved across species and the rate of drift correlates with lifespan when comparing mice, rhesus monkeys, and humans.\n[3] Twenty-two to 30-year-old rhesus monkeys exposed to 30% caloric restriction since 7-14 years of age showed attenuation of age-related methylation drift compared to ad libitum-fed controls such that their blood methylation age appeared 7 years younger than their chronologic age.\n[4] Even more pronounced effects were seen in 2.7-3.2-year-old mice exposed to 40% caloric restriction starting at 0.3 years of age.\n[5] The effects of caloric restriction on DNA methylation were detectable across different tissues and correlated with gene expression.\n[6] We propose that epigenetic drift is a determinant of lifespan in mammals.\n[7] Caloric restriction has been shown to increase lifespan in mammals.\n[8] Here, the authors provide evidence that age-related methylation drift correlates with lifespan and that caloric restriction in mice and rhesus monkeys results in attenuation of age-related methylation drift."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Caloric restriction has been shown to increase lifespan in mammals.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 212, "doc_id": 22038539, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [22038539], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CR is associated with higher methylation age.\n\nDocument title: Caloric restriction delays age-related methylation drift\n\nAbstract sentences:\n[0] In mammals, caloric restriction consistently results in extended lifespan.\n[1] Epigenetic information encoded by DNA methylation is tightly regulated, but shows a striking drift associated with age that includes both gains and losses of DNA methylation at various sites.\n[2] Here, we report that epigenetic drift is conserved across species and the rate of drift correlates with lifespan when comparing mice, rhesus monkeys, and humans.\n[3] Twenty-two to 30-year-old rhesus monkeys exposed to 30% caloric restriction since 7-14 years of age showed attenuation of age-related methylation drift compared to ad libitum-fed controls such that their blood methylation age appeared 7 years younger than their chronologic age.\n[4] Even more pronounced effects were seen in 2.7-3.2-year-old mice exposed to 40% caloric restriction starting at 0.3 years of age.\n[5] The effects of caloric restriction on DNA methylation were detectable across different tissues and correlated with gene expression.\n[6] We propose that epigenetic drift is a determinant of lifespan in mammals.\n[7] Caloric restriction has been shown to increase lifespan in mammals.\n[8] Here, the authors provide evidence that age-related methylation drift correlates with lifespan and that caloric restriction in mice and rhesus monkeys results in attenuation of age-related methylation drift."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Here, the authors provide evidence that age-related methylation drift correlates with lifespan and that caloric restriction in mice and rhesus monkeys results in attenuation of age-related methylation drift.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 212, "doc_id": 22038539, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [22038539], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 not predictive of 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": "validation", "claim_id": 213, "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: CX3CR1 on the Th2 cells impairs T cell survival\n\nDocument title: CX3CR1 is required for airway inflammation by promoting T helper cell survival and maintenance in inflamed lung\n\nAbstract sentences:\n[0] Allergic asthma is a T helper type 2 (T(H)2)-dominated disease of the lung.\n[1] In people with asthma, a fraction of CD4(+) T cells express the CX3CL1 receptor, CX3CR1, and CX3CL1 expression is increased in airway smooth muscle, lung endothelium and epithelium upon allergen challenge.\n[2] Here we found that untreated CX3CR1-deficient mice or wild-type (WT) mice treated with CX3CR1-blocking reagents show reduced lung disease upon allergen sensitization and challenge.\n[3] Transfer of WT CD4(+) T cells into CX3CR1-deficient mice restored the cardinal features of asthma, and CX3CR1-blocking reagents prevented airway inflammation in CX3CR1-deficient recipients injected with WT T(H)2 cells.\n[4] We found that CX3CR1 signaling promoted T(H)2 survival in the inflamed lungs, and injection of B cell leukemia/lymphoma-2 protein (BCl-2)-transduced CX3CR1-deficient T(H)2 cells into CX3CR1-deficient mice restored asthma.\n[5] CX3CR1-induced survival was also observed for T(H)1 cells upon airway inflammation but not under homeostatic conditions or upon peripheral inflammation.\n[6] Therefore, CX3CR1 and CX3CL1 may represent attractive therapeutic targets in asthma."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"We found that CX3CR1 signaling promoted T(H)2 survival in the inflamed lungs, and injection of B cell leukemia/lymphoma-2 protein (BCl-2)-transduced CX3CR1-deficient T(H)2 cells into CX3CR1-deficient mice restored asthma.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 216, "doc_id": 21366394, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [21366394], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CX3CR1 on the Th2 cells promotes T cell survival\n\nDocument title: CX3CR1 is required for airway inflammation by promoting T helper cell survival and maintenance in inflamed lung\n\nAbstract sentences:\n[0] Allergic asthma is a T helper type 2 (T(H)2)-dominated disease of the lung.\n[1] In people with asthma, a fraction of CD4(+) T cells express the CX3CL1 receptor, CX3CR1, and CX3CL1 expression is increased in airway smooth muscle, lung endothelium and epithelium upon allergen challenge.\n[2] Here we found that untreated CX3CR1-deficient mice or wild-type (WT) mice treated with CX3CR1-blocking reagents show reduced lung disease upon allergen sensitization and challenge.\n[3] Transfer of WT CD4(+) T cells into CX3CR1-deficient mice restored the cardinal features of asthma, and CX3CR1-blocking reagents prevented airway inflammation in CX3CR1-deficient recipients injected with WT T(H)2 cells.\n[4] We found that CX3CR1 signaling promoted T(H)2 survival in the inflamed lungs, and injection of B cell leukemia/lymphoma-2 protein (BCl-2)-transduced CX3CR1-deficient T(H)2 cells into CX3CR1-deficient mice restored asthma.\n[5] CX3CR1-induced survival was also observed for T(H)1 cells upon airway inflammation but not under homeostatic conditions or upon peripheral inflammation.\n[6] Therefore, CX3CR1 and CX3CL1 may represent attractive therapeutic targets in asthma."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"We found that CX3CR1 signaling promoted T(H)2 survival in the inflamed lungs, and injection of B cell leukemia/lymphoma-2 protein (BCl-2)-transduced CX3CR1-deficient T(H)2 cells into CX3CR1-deficient mice restored asthma.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 217, "doc_id": 21366394, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [21366394], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CX3CR1 on the Th2 cells promotes airway inflammation.\n\nDocument title: CX3CR1 is required for airway inflammation by promoting T helper cell survival and maintenance in inflamed lung\n\nAbstract sentences:\n[0] Allergic asthma is a T helper type 2 (T(H)2)-dominated disease of the lung.\n[1] In people with asthma, a fraction of CD4(+) T cells express the CX3CL1 receptor, CX3CR1, and CX3CL1 expression is increased in airway smooth muscle, lung endothelium and epithelium upon allergen challenge.\n[2] Here we found that untreated CX3CR1-deficient mice or wild-type (WT) mice treated with CX3CR1-blocking reagents show reduced lung disease upon allergen sensitization and challenge.\n[3] Transfer of WT CD4(+) T cells into CX3CR1-deficient mice restored the cardinal features of asthma, and CX3CR1-blocking reagents prevented airway inflammation in CX3CR1-deficient recipients injected with WT T(H)2 cells.\n[4] We found that CX3CR1 signaling promoted T(H)2 survival in the inflamed lungs, and injection of B cell leukemia/lymphoma-2 protein (BCl-2)-transduced CX3CR1-deficient T(H)2 cells into CX3CR1-deficient mice restored asthma.\n[5] CX3CR1-induced survival was also observed for T(H)1 cells upon airway inflammation but not under homeostatic conditions or upon peripheral inflammation.\n[6] Therefore, CX3CR1 and CX3CL1 may represent attractive therapeutic targets in asthma."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here we found that untreated CX3CR1-deficient mice or wild-type (WT) mice treated with CX3CR1-blocking reagents show reduced lung disease upon allergen sensitization and challenge.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 218, "doc_id": 21366394, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [21366394], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CX3CR1 on the Th2 cells promotes airway inflammation.\n\nDocument title: CX3CR1 is required for airway inflammation by promoting T helper cell survival and maintenance in inflamed lung\n\nAbstract sentences:\n[0] Allergic asthma is a T helper type 2 (T(H)2)-dominated disease of the lung.\n[1] In people with asthma, a fraction of CD4(+) T cells express the CX3CL1 receptor, CX3CR1, and CX3CL1 expression is increased in airway smooth muscle, lung endothelium and epithelium upon allergen challenge.\n[2] Here we found that untreated CX3CR1-deficient mice or wild-type (WT) mice treated with CX3CR1-blocking reagents show reduced lung disease upon allergen sensitization and challenge.\n[3] Transfer of WT CD4(+) T cells into CX3CR1-deficient mice restored the cardinal features of asthma, and CX3CR1-blocking reagents prevented airway inflammation in CX3CR1-deficient recipients injected with WT T(H)2 cells.\n[4] We found that CX3CR1 signaling promoted T(H)2 survival in the inflamed lungs, and injection of B cell leukemia/lymphoma-2 protein (BCl-2)-transduced CX3CR1-deficient T(H)2 cells into CX3CR1-deficient mice restored asthma.\n[5] CX3CR1-induced survival was also observed for T(H)1 cells upon airway inflammation but not under homeostatic conditions or upon peripheral inflammation.\n[6] Therefore, CX3CR1 and CX3CL1 may represent attractive therapeutic targets in asthma."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Transfer of WT CD4(+) T cells into CX3CR1-deficient mice restored the cardinal features of asthma, and CX3CR1-blocking reagents prevented airway inflammation in CX3CR1-deficient recipients injected with WT T(H)2 cells.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 218, "doc_id": 21366394, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [21366394], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CX3CR1 on the Th2 cells promotes airway inflammation.\n\nDocument title: CX3CR1 is required for airway inflammation by promoting T helper cell survival and maintenance in inflamed lung\n\nAbstract sentences:\n[0] Allergic asthma is a T helper type 2 (T(H)2)-dominated disease of the lung.\n[1] In people with asthma, a fraction of CD4(+) T cells express the CX3CL1 receptor, CX3CR1, and CX3CL1 expression is increased in airway smooth muscle, lung endothelium and epithelium upon allergen challenge.\n[2] Here we found that untreated CX3CR1-deficient mice or wild-type (WT) mice treated with CX3CR1-blocking reagents show reduced lung disease upon allergen sensitization and challenge.\n[3] Transfer of WT CD4(+) T cells into CX3CR1-deficient mice restored the cardinal features of asthma, and CX3CR1-blocking reagents prevented airway inflammation in CX3CR1-deficient recipients injected with WT T(H)2 cells.\n[4] We found that CX3CR1 signaling promoted T(H)2 survival in the inflamed lungs, and injection of B cell leukemia/lymphoma-2 protein (BCl-2)-transduced CX3CR1-deficient T(H)2 cells into CX3CR1-deficient mice restored asthma.\n[5] CX3CR1-induced survival was also observed for T(H)1 cells upon airway inflammation but not under homeostatic conditions or upon peripheral inflammation.\n[6] Therefore, CX3CR1 and CX3CL1 may represent attractive therapeutic targets in asthma."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"CX3CR1-induced survival was also observed for T(H)1 cells upon airway inflammation but not under homeostatic conditions or upon peripheral inflammation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 218, "doc_id": 21366394, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [21366394], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CX3CR1 on the Th2 cells suppresses airway inflammation.\n\nDocument title: CX3CR1 is required for airway inflammation by promoting T helper cell survival and maintenance in inflamed lung\n\nAbstract sentences:\n[0] Allergic asthma is a T helper type 2 (T(H)2)-dominated disease of the lung.\n[1] In people with asthma, a fraction of CD4(+) T cells express the CX3CL1 receptor, CX3CR1, and CX3CL1 expression is increased in airway smooth muscle, lung endothelium and epithelium upon allergen challenge.\n[2] Here we found that untreated CX3CR1-deficient mice or wild-type (WT) mice treated with CX3CR1-blocking reagents show reduced lung disease upon allergen sensitization and challenge.\n[3] Transfer of WT CD4(+) T cells into CX3CR1-deficient mice restored the cardinal features of asthma, and CX3CR1-blocking reagents prevented airway inflammation in CX3CR1-deficient recipients injected with WT T(H)2 cells.\n[4] We found that CX3CR1 signaling promoted T(H)2 survival in the inflamed lungs, and injection of B cell leukemia/lymphoma-2 protein (BCl-2)-transduced CX3CR1-deficient T(H)2 cells into CX3CR1-deficient mice restored asthma.\n[5] CX3CR1-induced survival was also observed for T(H)1 cells upon airway inflammation but not under homeostatic conditions or upon peripheral inflammation.\n[6] Therefore, CX3CR1 and CX3CL1 may represent attractive therapeutic targets in asthma."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here we found that untreated CX3CR1-deficient mice or wild-type (WT) mice treated with CX3CR1-blocking reagents show reduced lung disease upon allergen sensitization and challenge.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 219, "doc_id": 21366394, "label": "CONTRADICTS", "evidence_sentence_ids": [2], "cited_doc_ids": [21366394], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: CX3CR1 on the Th2 cells suppresses airway inflammation.\n\nDocument title: CX3CR1 is required for airway inflammation by promoting T helper cell survival and maintenance in inflamed lung\n\nAbstract sentences:\n[0] Allergic asthma is a T helper type 2 (T(H)2)-dominated disease of the lung.\n[1] In people with asthma, a fraction of CD4(+) T cells express the CX3CL1 receptor, CX3CR1, and CX3CL1 expression is increased in airway smooth muscle, lung endothelium and epithelium upon allergen challenge.\n[2] Here we found that untreated CX3CR1-deficient mice or wild-type (WT) mice treated with CX3CR1-blocking reagents show reduced lung disease upon allergen sensitization and challenge.\n[3] Transfer of WT CD4(+) T cells into CX3CR1-deficient mice restored the cardinal features of asthma, and CX3CR1-blocking reagents prevented airway inflammation in CX3CR1-deficient recipients injected with WT T(H)2 cells.\n[4] We found that CX3CR1 signaling promoted T(H)2 survival in the inflamed lungs, and injection of B cell leukemia/lymphoma-2 protein (BCl-2)-transduced CX3CR1-deficient T(H)2 cells into CX3CR1-deficient mice restored asthma.\n[5] CX3CR1-induced survival was also observed for T(H)1 cells upon airway inflammation but not under homeostatic conditions or upon peripheral inflammation.\n[6] Therefore, CX3CR1 and CX3CL1 may represent attractive therapeutic targets in asthma."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Transfer of WT CD4(+) T cells into CX3CR1-deficient mice restored the cardinal features of asthma, and CX3CR1-blocking reagents prevented airway inflammation in CX3CR1-deficient recipients injected with WT T(H)2 cells.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 219, "doc_id": 21366394, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [21366394], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 the alcohol aldehyde dehydrogenase deficiency mutation drink less that non-carries.\n\nDocument title: Alcohol Intake and Blood Pressure: A Systematic Review Implementing a Mendelian Randomization Approach\n\nAbstract sentences:\n[0] BACKGROUND Alcohol has been reported to be a common and modifiable risk factor for hypertension.\n[1] However, observational studies are subject to confounding by other behavioural and sociodemographic factors, while clinical trials are difficult to implement and have limited follow-up time.\n[2] Mendelian randomization can provide robust evidence on the nature of this association by use of a common polymorphism in aldehyde dehydrogenase 2 (ALDH2) as a surrogate for measuring alcohol consumption.\n[3] ALDH2 encodes a major enzyme involved in alcohol metabolism.\n[4] Individuals homozygous for the null variant (*2*2) experience adverse symptoms when drinking alcohol and consequently drink considerably less alcohol than wild-type homozygotes (*1*1) or heterozygotes.\n[5] We hypothesise that this polymorphism may influence the risk of hypertension by affecting alcohol drinking behaviour.\n[6] METHODS AND FINDINGS We carried out fixed effect meta-analyses of the ALDH2 genotype with blood pressure (five studies, n = 7,658) and hypertension (three studies, n = 4,219) using studies identified via systematic review.\n[7] In males, we obtained an overall odds ratio of 2.42 (95% confidence interval [CI] 1.66-3.55, p = 4.8 x 10(-6)) for hypertension comparing *1*1 with *2*2 homozygotes and an odds ratio of 1.72 (95% CI 1.17-2.52, p = 0.006) comparing heterozygotes (surrogate for moderate drinkers) with *2*2 homozygotes.\n[8] Systolic blood pressure was 7.44 mmHg (95% CI 5.39-9.49, p = 1.1 x 10(-12)) greater among *1*1 than among *2*2 homozygotes, and 4.24 mmHg (95% CI 2.18-6.31, p = 0.00005) greater among heterozygotes than among *2*2 homozygotes.\n[9] CONCLUSIONS These findings support the hypothesis that alcohol intake has a marked effect on blood pressure and the risk of hypertension."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Individuals homozygous for the null variant (*2*2) experience adverse symptoms when drinking alcohol and consequently drink considerably less alcohol than wild-type homozygotes (*1*1) or heterozygotes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 230, "doc_id": 3067015, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [3067015], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cataract and trachoma are the primary cause of blindness in Southern Sudan.\n\nDocument title: Prevalence and Causes of Blindness and Low Vision in Southern Sudan \n\nAbstract sentences:\n[0] Background Blindness and low vision are thought to be common in southern Sudan.\n[1] However, the magnitude and geographical distribution are largely unknown.\n[2] We aimed to estimate the prevalence of blindness and low vision, identify the main causes of blindness and low vision, and estimate targets for blindness prevention programs in Mankien payam (district), southern Sudan."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 232, "doc_id": 10536636, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [10536636], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 does not occur 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 233, "doc_id": 4388470, "label": "CONTRADICTS", "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 does not occur 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 233, "doc_id": 4388470, "label": "CONTRADICTS", "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 does not occur 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 233, "doc_id": 4388470, "label": "CONTRADICTS", "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: Cell autonomous sex determination in somatic cells occurs in Passeriformes.\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": "validation", "claim_id": 236, "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 Passeriformes.\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": "validation", "claim_id": 236, "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 Passeriformes.\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": "validation", "claim_id": 236, "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: Cells lacking clpC have a defect in sporulation efficiency in Bacillus subtilis.\n\nDocument title: High-Throughput Genetic Screens Identify a Large and Diverse Collection of New Sporulation Genes in Bacillus subtilis\n\nAbstract sentences:\n[0] The differentiation of the bacterium Bacillus subtilis into a dormant spore is among the most well-characterized developmental pathways in biology.\n[1] Classical genetic screens performed over the past half century identified scores of factors involved in every step of this morphological process.\n[2] More recently, transcriptional profiling uncovered additional sporulation-induced genes required for successful spore development.\n[3] Here, we used transposon-sequencing (Tn-seq) to assess whether there were any sporulation genes left to be discovered.\n[4] Our screen identified 133 out of the 148 genes with known sporulation defects.\n[5] Surprisingly, we discovered 24 additional genes that had not been previously implicated in spore formation.\n[6] To investigate their functions, we used fluorescence microscopy to survey early, middle, and late stages of differentiation of null mutants from the B. subtilis ordered knockout collection.\n[7] This analysis identified mutants that are delayed in the initiation of sporulation, defective in membrane remodeling, and impaired in spore maturation.\n[8] Several mutants had novel sporulation phenotypes.\n[9] We performed in-depth characterization of two new factors that participate in cell-cell signaling pathways during sporulation.\n[10] One (SpoIIT) functions in the activation of σE in the mother cell; the other (SpoIIIL) is required for σG activity in the forespore.\n[11] Our analysis also revealed that as many as 36 sporulation-induced genes with no previously reported mutant phenotypes are required for timely spore maturation.\n[12] Finally, we discovered a large set of transposon insertions that trigger premature initiation of sporulation.\n[13] Our results highlight the power of Tn-seq for the discovery of new genes and novel pathways in sporulation and, combined with the recently completed null mutant collection, open the door for similar screens in other, less well-characterized processes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 237, "doc_id": 4942718, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4942718], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cells undergoing methionine restriction may activate miRNAs.\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": "validation", "claim_id": 238, "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: Cellular aging closely links to an older appearance.\n\nDocument title: Perceived age as clinically useful biomarker of ageing: cohort study.\n\nAbstract sentences:\n[0] OBJECTIVE To determine whether perceived age correlates with survival and important age related phenotypes.\n[1] DESIGN Follow-up study, with survival of twins determined up to January 2008, by which time 675 (37%) had died.\n[2] SETTING Population based twin cohort in Denmark.\n[3] PARTICIPANTS 20 nurses, 10 young men, and 11 older women (assessors); 1826 twins aged >or=70.\n[4] MAIN OUTCOME MEASURES Assessors: perceived age of twins from photographs.\n[5] Twins: physical and cognitive tests and molecular biomarker of ageing (leucocyte telomere length).\n[6] RESULTS For all three groups of assessors, perceived age was significantly associated with survival, even after adjustment for chronological age, sex, and rearing environment.\n[7] Perceived age was still significantly associated with survival after further adjustment for physical and cognitive functioning.\n[8] The likelihood that the older looking twin of the pair died first increased with increasing discordance in perceived age within the twin pair-that is, the bigger the difference in perceived age within the pair, the more likely that the older looking twin died first.\n[9] Twin analyses suggested that common genetic factors influence both perceived age and survival.\n[10] Perceived age, controlled for chronological age and sex, also correlated significantly with physical and cognitive functioning as well as with leucocyte telomere length.\n[11] CONCLUSION Perceived age-which is widely used by clinicians as a general indication of a patient's health-is a robust biomarker of ageing that predicts survival among those aged >or=70 and correlates with important functional and molecular ageing phenotypes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Perceived age, controlled for chronological age and sex, also correlated significantly with physical and cognitive functioning as well as with leucocyte telomere length.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 239, "doc_id": 14079881, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [14079881], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 aging closely links to an older appearance.\n\nDocument title: Perceived age as clinically useful biomarker of ageing: cohort study.\n\nAbstract sentences:\n[0] OBJECTIVE To determine whether perceived age correlates with survival and important age related phenotypes.\n[1] DESIGN Follow-up study, with survival of twins determined up to January 2008, by which time 675 (37%) had died.\n[2] SETTING Population based twin cohort in Denmark.\n[3] PARTICIPANTS 20 nurses, 10 young men, and 11 older women (assessors); 1826 twins aged >or=70.\n[4] MAIN OUTCOME MEASURES Assessors: perceived age of twins from photographs.\n[5] Twins: physical and cognitive tests and molecular biomarker of ageing (leucocyte telomere length).\n[6] RESULTS For all three groups of assessors, perceived age was significantly associated with survival, even after adjustment for chronological age, sex, and rearing environment.\n[7] Perceived age was still significantly associated with survival after further adjustment for physical and cognitive functioning.\n[8] The likelihood that the older looking twin of the pair died first increased with increasing discordance in perceived age within the twin pair-that is, the bigger the difference in perceived age within the pair, the more likely that the older looking twin died first.\n[9] Twin analyses suggested that common genetic factors influence both perceived age and survival.\n[10] Perceived age, controlled for chronological age and sex, also correlated significantly with physical and cognitive functioning as well as with leucocyte telomere length.\n[11] CONCLUSION Perceived age-which is widely used by clinicians as a general indication of a patient's health-is a robust biomarker of ageing that predicts survival among those aged >or=70 and correlates with important functional and molecular ageing phenotypes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"CONCLUSION Perceived age-which is widely used by clinicians as a general indication of a patient's health-is a robust biomarker of ageing that predicts survival among those aged >or=70 and correlates with important functional and molecular ageing phenotypes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 239, "doc_id": 14079881, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [14079881], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Chenodeosycholic acid treatment increases whole-body energy expenditure.\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: [1, 3]\nExplanation: Evidence states: \"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. Treatment of 12 healthy female subjects with CDCA for 2 days resulted in increased BAT activity.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 248, "doc_id": 1568684, "label": "SUPPORTS", "evidence_sentence_ids": [1, 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: Chenodeosycholic acid treatment increases whole-body energy expenditure.\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: [4]\nExplanation: Evidence states: \"Whole-body energy expenditure was also increased upon CDCA treatment.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 248, "doc_id": 1568684, "label": "SUPPORTS", "evidence_sentence_ids": [4], "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: Chenodeosycholic acid treatment reduces whole-body energy expenditure.\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: [1, 3]\nExplanation: Evidence states: \"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. Treatment of 12 healthy female subjects with CDCA for 2 days resulted in increased BAT activity.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 249, "doc_id": 1568684, "label": "CONTRADICTS", "evidence_sentence_ids": [1, 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: Chenodeosycholic acid treatment reduces whole-body energy expenditure.\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: [4]\nExplanation: Evidence states: \"Whole-body energy expenditure was also increased upon CDCA treatment.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 249, "doc_id": 1568684, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "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: Chronic aerobic exercise alters endothelial function, improving vasodilating mechanisms mediated by NO.\n\nDocument title: Endothelium-mediated relaxation of porcine collateral-dependent arterioles is improved by exercise training.\n\nAbstract sentences:\n[0] BACKGROUND Endothelium-dependent modulation of coronary tone is impaired in the collateral-dependent coronary microcirculation.\n[1] We used a porcine model of chronic coronary occlusion and collateral development to evaluate the hypothesis that exercise training enhances endothelium-mediated relaxation and increases endothelial nitric oxide synthase (ecNOS) mRNA levels of collateral-dependent microvasculature.\n[2] METHODS AND RESULTS Adult female miniature swine were subjected to chronic, progressive ameroid occlusion of the proximal left circumflex coronary artery (LCx); after 2 months, animals were randomly exposed to 16-week exercise-training (EX group; treadmill running) or sedentary (SED group; cage confinement) protocols.\n[3] After completion of EX or SED programs, coronary arterioles ( approximately 100 microm in diameter) were isolated from collateral-dependent LCx (distal to occlusion) and nonoccluded left anterior descending coronary artery (LAD) regions of each heart.\n[4] Arterioles were studied by in vitro videomicroscopy or frozen for ecNOS mRNA analysis (RT-PCR techniques).\n[5] Relaxation to the endothelium-dependent vasodilator bradykinin was decreased (P<0.05) in arterioles isolated from collateral-dependent LCx versus nonoccluded LAD regions of SED animals.\n[6] Bradykinin-mediated relaxation, however, was not different in LCx versus LAD arterioles isolated from EX animals.\n[7] Nitroprusside-induced relaxation was unaffected by either chronic occlusion or exercise.\n[8] Importantly, ecNOS mRNA expression was significantly decreased in arterioles isolated from LCx versus LAD regions of SED animals.\n[9] After training, ecNOS mRNA expression was not different between LAD and LCx arterioles.\n[10] CONCLUSIONS These data indicate that exercise training enhances bradykinin-mediated relaxation of collateral-dependent LCx arterioles isolated after chronic coronary occlusion, most likely because of effects on ecNOS mRNA expression and increased production of NO."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5, 10]\nExplanation: Evidence states: \"Relaxation to the endothelium-dependent vasodilator bradykinin was decreased (P<0.05) in arterioles isolated from collateral-dependent LCx versus nonoccluded LAD regions of SED animals. CONCLUSIONS These data indicate that exercise training enhances bradykinin-mediated relaxation of collateral-dependent LCx arterioles isolated after chronic coronary occlusion, most likely because of effects on ecNOS mRNA expression and increased production of NO.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 261, "doc_id": 1122279, "label": "SUPPORTS", "evidence_sentence_ids": [5, 10], "cited_doc_ids": [1122279, 10697096], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 aerobic exercise alters endothelial function, improving vasodilating mechanisms mediated by NO.\n\nDocument title: Vasodilator responses of coronary resistance arteries of exercise-trained pigs.\n\nAbstract sentences:\n[0] BACKGROUND The purpose of this study was to test the hypothesis that vasodilator responses of porcine coronary resistance arteries are increased by exercise training.\n[1] METHODS AND RESULTS Yucatan miniature swine were randomly divided into groups of exercise-trained (ET) and sedentary (SED) control pigs.\n[2] ET pigs were placed on a progressive treadmill training program lasting 16 to 20 weeks, and SED pigs remained inactive during the same time period.\n[3] Coronary resistance arteries 64 to 157 microns in diameter were isolated for in vitro evaluation of relaxation responses to the endothelium-independent dilators sodium nitroprusside (1 x 10(-10) to 1 x 10(-4) mol/L) and adenosine (1 x 10(-10) to 1 x 10(-5) mol/L) and to bradykinin (1 x 10(-13) to 3 x 10(-7) mol/L), an endothelium-dependent agent.\n[4] Relaxation responses to adenosine and sodium nitroprusside were not altered by exercise training.\n[5] Endothelium-dependent relaxation to bradykinin was enhanced in coronary resistance arteries from ET pigs (IC50: ET, 0.07 +/-\n[6] 0.02 nmol/L; SED, 1.59 +/-\n[7] 0.09 nmol/L).\n[8] To determine whether prostanoids and/or the nitric oxide synthase pathway were involved in the ET-induced changes in bradykinin-induced vasodilation, responses to bradykinin were examined in coronary resistance arteries from both ET and SED pigs in the presence of indomethacin and in the presence of nitro-monomethyl L-arginine (L-NMMA).\n[9] Both indomethacin and L-NMMA produced significant inhibition of the bradykinin-induced relaxation in vessels from both groups.\n[10] Despite decreased bradykinin-induced relaxation after indomethacin, bradykinin-induced vasodilation was still enhanced in vessels from the ET group.\n[11] L-NMMA caused greater inhibition of the bradykinin-induced relaxation in coronary resistance arteries from ET pigs relative to arteries from SED pigs and eliminated the training-induced enhancement of the bradykinin responses.\n[12] CONCLUSIONS These results suggest that exercise training enhances bradykinin-induced vasodilation through increased endothelium-derived relaxing factor/nitric oxide production by the L-arginine/nitric oxide synthase pathway."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"CONCLUSIONS These results suggest that exercise training enhances bradykinin-induced vasodilation through increased endothelium-derived relaxing factor/nitric oxide production by the L-arginine/nitric oxide synthase pathway.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 261, "doc_id": 10697096, "label": "SUPPORTS", "evidence_sentence_ids": [12], "cited_doc_ids": [1122279, 10697096], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cold exposure increases BAT recruitment.\n\nDocument title: Cold Exposure Promotes Atherosclerotic Plaque Growth and Instability via UCP1-Dependent Lipolysis\n\nAbstract sentences:\n[0] Molecular mechanisms underlying the cold-associated high cardiovascular risk remain unknown.\n[1] Here, we show that the cold-triggered food-intake-independent lipolysis significantly increased plasma levels of small low-density lipoprotein (LDL) remnants, leading to accelerated development of atherosclerotic lesions in mice.\n[2] In two genetic mouse knockout models (apolipoprotein E(-/-) [ApoE(-/-)] and LDL receptor(-/-) [Ldlr(-/-)] mice), persistent cold exposure stimulated atherosclerotic plaque growth by increasing lipid deposition.\n[3] Furthermore, marked increase of inflammatory cells and plaque-associated microvessels were detected in the cold-acclimated ApoE(-/-) and Ldlr(-/-) mice, leading to plaque instability.\n[4] Deletion of uncoupling protein 1 (UCP1), a key mitochondrial protein involved in thermogenesis in brown adipose tissue (BAT), in the ApoE(-/-) strain completely protected mice from the cold-induced atherosclerotic lesions.\n[5] Cold acclimation markedly reduced plasma levels of adiponectin, and systemic delivery of adiponectin protected ApoE(-/-) mice from plaque development.\n[6] These findings provide mechanistic insights on low-temperature-associated cardiovascular risks."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 268, "doc_id": 970012, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [970012], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Cold exposure reduces BAT recruitment.\n\nDocument title: Cold Exposure Promotes Atherosclerotic Plaque Growth and Instability via UCP1-Dependent Lipolysis\n\nAbstract sentences:\n[0] Molecular mechanisms underlying the cold-associated high cardiovascular risk remain unknown.\n[1] Here, we show that the cold-triggered food-intake-independent lipolysis significantly increased plasma levels of small low-density lipoprotein (LDL) remnants, leading to accelerated development of atherosclerotic lesions in mice.\n[2] In two genetic mouse knockout models (apolipoprotein E(-/-) [ApoE(-/-)] and LDL receptor(-/-) [Ldlr(-/-)] mice), persistent cold exposure stimulated atherosclerotic plaque growth by increasing lipid deposition.\n[3] Furthermore, marked increase of inflammatory cells and plaque-associated microvessels were detected in the cold-acclimated ApoE(-/-) and Ldlr(-/-) mice, leading to plaque instability.\n[4] Deletion of uncoupling protein 1 (UCP1), a key mitochondrial protein involved in thermogenesis in brown adipose tissue (BAT), in the ApoE(-/-) strain completely protected mice from the cold-induced atherosclerotic lesions.\n[5] Cold acclimation markedly reduced plasma levels of adiponectin, and systemic delivery of adiponectin protected ApoE(-/-) mice from plaque development.\n[6] These findings provide mechanistic insights on low-temperature-associated cardiovascular risks."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 269, "doc_id": 970012, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [970012], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 lead to significantly higher long-term abstinence rates at 52 weeks than 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: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"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).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 274, "doc_id": 11614737, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "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: Combination nicotine replacement therapies with varenicline or bupropion lead to significantly higher long-term abstinence rates at 52 weeks than 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: CONTRADICTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"Neither outcome was significantly different at 52 weeks.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 274, "doc_id": 11614737, "label": "CONTRADICTS", "evidence_sentence_ids": [13], "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: Combining phosphatidylinositide 3-kinase and MEK 1/2 inhibitors is effective at treating KRAS mutant tumors.\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": "validation", "claim_id": 275, "doc_id": 4961038, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [4961038, 14241418, 14819804], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Combining phosphatidylinositide 3-kinase and MEK 1/2 inhibitors is effective at treating KRAS mutant tumors.\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: [8]\nExplanation: Evidence states: \"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.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 275, "doc_id": 4961038, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [4961038, 14241418, 14819804], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Combining phosphatidylinositide 3-kinase and MEK 1/2 inhibitors is effective at treating KRAS mutant tumors.\n\nDocument title: NVP-BEZ235, a dual PI3K/mTOR inhibitor, prevents PI3K signaling and inhibits the growth of cancer cells with activating PI3K mutations.\n\nAbstract sentences:\n[0] Phosphatidylinositol-3-kinase (PI3K) pathway deregulation is a common event in human cancer, either through inactivation of the tumor suppressor phosphatase and tensin homologue deleted from chromosome 10 or activating mutations of p110-alpha.\n[1] These hotspot mutations result in oncogenic activity of the enzyme and contribute to therapeutic resistance to the anti-HER2 antibody trastuzumab.\n[2] The PI3K pathway is, therefore, an attractive target for cancer therapy.\n[3] We have studied NVP-BEZ235, a dual inhibitor of the PI3K and the downstream mammalian target of rapamycin (mTOR).\n[4] NVP-BEZ235 inhibited the activation of the downstream effectors Akt, S6 ribosomal protein, and 4EBP1 in breast cancer cells.\n[5] The antiproliferative activity of NVP-BEZ235 was superior to the allosteric selective mTOR complex inhibitor everolimus in a panel of 21 cancer cell lines of different origin and mutation status.\n[6] The described Akt activation due to mTOR inhibition was prevented by higher doses of NVP-BEZ235.\n[7] NVP-BEZ235 reversed the hyperactivation of the PI3K/mTOR pathway caused by the oncogenic mutations of p110-alpha, E545K, and H1047R, and inhibited the proliferation of HER2-amplified BT474 cells exogenously expressing these mutations that render them resistant to trastuzumab.\n[8] In trastuzumab-resistant BT474 H1047R breast cancer xenografts, NVP-BEZ235 inhibited PI3K signaling and had potent antitumor activity.\n[9] In treated animals, there was complete inhibition of PI3K signaling in the skin at pharmacologically active doses, suggesting that skin may serve as surrogate tissue for pharmacodynamic studies.\n[10] In summary, NVP-BEZ235 inhibits the PI3K/mTOR axis and results in antiproliferative and antitumoral activity in cancer cells with both wild-type and mutated p110-alpha."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"In summary, NVP-BEZ235 inhibits the PI3K/mTOR axis and results in antiproliferative and antitumoral activity in cancer cells with both wild-type and mutated p110-alpha.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 275, "doc_id": 14241418, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [4961038, 14241418, 14819804], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 7489 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: 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": "validation", "claim_id": 279, "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: Crossover hot spots are not 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": "validation", "claim_id": 294, "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: Crosstalk between dendritic cells (DCs) and innate lymphoid cells (ILCs) is important in the regulation of intestinal homeostasis.\n\nDocument title: The Transcription Factor T-bet Regulates Intestinal Inflammation Mediated by Interleukin-7 Receptor+ Innate Lymphoid Cells\n\nAbstract sentences:\n[0] Mice lacking the transcription factor T-bet in the innate immune system develop microbiota-dependent colitis.\n[1] Here, we show that interleukin-17A (IL-17A)-producing IL-7Rα(+) innate lymphoid cells (ILCs) were potent promoters of disease in Tbx21(-/-)Rag2(-/-) ulcerative colitis (TRUC) mice.\n[2] TNF-α produced by CD103(-)CD11b(+) dendritic cells synergized with IL-23 to drive IL-17A production by ILCs, demonstrating a previously unrecognized layer of cellular crosstalk between dendritic cells and ILCs.\n[3] We have identified Helicobacter typhlonius as a key disease trigger driving excess TNF-α production and promoting colitis in TRUC mice.\n[4] Crucially, T-bet also suppressed the expression of IL-7R, a key molecule involved in controlling intestinal ILC homeostasis.\n[5] The importance of IL-7R signaling in TRUC disease was highlighted by the dramatic reduction in intestinal ILCs and attenuated colitis following IL-7R blockade.\n[6] Taken together, these data demonstrate the mechanism by which T-bet regulates the complex interplay between mucosal dendritic cells, ILCs, and the intestinal microbiota."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2, 4]\nExplanation: Evidence states: \"TNF-α produced by CD103(-)CD11b(+) dendritic cells synergized with IL-23 to drive IL-17A production by ILCs, demonstrating a previously unrecognized layer of cellular crosstalk between dendritic cells and ILCs. Crucially, T-bet also suppressed the expression of IL-7R, a key molecule involved in controlling intestinal ILC homeostasis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 295, "doc_id": 20310709, "label": "SUPPORTS", "evidence_sentence_ids": [2, 4], "cited_doc_ids": [20310709], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Crosstalk between dendritic cells (DCs) and innate lymphoid cells (ILCs) is important in the regulation of intestinal homeostasis.\n\nDocument title: The Transcription Factor T-bet Regulates Intestinal Inflammation Mediated by Interleukin-7 Receptor+ Innate Lymphoid Cells\n\nAbstract sentences:\n[0] Mice lacking the transcription factor T-bet in the innate immune system develop microbiota-dependent colitis.\n[1] Here, we show that interleukin-17A (IL-17A)-producing IL-7Rα(+) innate lymphoid cells (ILCs) were potent promoters of disease in Tbx21(-/-)Rag2(-/-) ulcerative colitis (TRUC) mice.\n[2] TNF-α produced by CD103(-)CD11b(+) dendritic cells synergized with IL-23 to drive IL-17A production by ILCs, demonstrating a previously unrecognized layer of cellular crosstalk between dendritic cells and ILCs.\n[3] We have identified Helicobacter typhlonius as a key disease trigger driving excess TNF-α production and promoting colitis in TRUC mice.\n[4] Crucially, T-bet also suppressed the expression of IL-7R, a key molecule involved in controlling intestinal ILC homeostasis.\n[5] The importance of IL-7R signaling in TRUC disease was highlighted by the dramatic reduction in intestinal ILCs and attenuated colitis following IL-7R blockade.\n[6] Taken together, these data demonstrate the mechanism by which T-bet regulates the complex interplay between mucosal dendritic cells, ILCs, and the intestinal microbiota."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5, 6]\nExplanation: Evidence states: \"The importance of IL-7R signaling in TRUC disease was highlighted by the dramatic reduction in intestinal ILCs and attenuated colitis following IL-7R blockade. Taken together, these data demonstrate the mechanism by which T-bet regulates the complex interplay between mucosal dendritic cells, ILCs, and the intestinal microbiota.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 295, "doc_id": 20310709, "label": "SUPPORTS", "evidence_sentence_ids": [5, 6], "cited_doc_ids": [20310709], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 released from the mitochondrial intermembrane space to cytosol 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 298, "doc_id": 39381118, "label": "SUPPORTS", "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 DMT1. Cytosolic proteins bind to iron-responsive elements on mRNAs coding for proteins involved in iron uptake.\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": "validation", "claim_id": 300, "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: DMRT1 is a sex-determining gene that is epigenetically regulated by the MHM region.\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: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 303, "doc_id": 4388470, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4388470], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 more 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": "validation", "claim_id": 312, "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: Deamination of cytidine to uridine on the minus strand of viral DNA results in catastrophic G-to-A mutations in the viral genome.\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": "validation", "claim_id": 314, "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: Deleting Raptor reduces 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": "validation", "claim_id": 324, "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 αvβ8 does not result in a spontaneous inflammatory phenotype.\n\nDocument title: Integrin αvβ8-Mediated TGF-β Activation by Effector Regulatory T Cells Is Essential for Suppression of T-Cell-Mediated Inflammation\n\nAbstract sentences:\n[0] Regulatory T (Treg) cells play a pivotal role in suppressing self-harmful T cell responses, but how Treg cells mediate suppression to maintain immune homeostasis and limit responses during inflammation is unclear.\n[1] Here we show that effector Treg cells express high amounts of the integrin αvβ8, which enables them to activate latent transforming growth factor-β (TGF-β).\n[2] Treg-cell-specific deletion of integrin αvβ8 did not result in a spontaneous inflammatory phenotype, suggesting that this pathway is not important in Treg-cell-mediated maintenance of immune homeostasis.\n[3] However, Treg cells lacking expression of integrin αvβ8 were unable to suppress pathogenic T cell responses during active inflammation.\n[4] Thus, our results identify a mechanism by which Treg cells suppress exuberant immune responses, highlighting a key role for effector Treg-cell-mediated activation of latent TGF-β in suppression of self-harmful T cell responses during active inflammation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Treg-cell-specific deletion of integrin αvβ8 did not result in a spontaneous inflammatory phenotype, suggesting that this pathway is not important in Treg-cell-mediated maintenance of immune homeostasis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 327, "doc_id": 17997584, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [17997584], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 decreases 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 338, "doc_id": 23349986, "label": "CONTRADICTS", "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 decreases 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 338, "doc_id": 23349986, "label": "CONTRADICTS", "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 decreases 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 338, "doc_id": 23349986, "label": "CONTRADICTS", "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: Diabetic patients with acute coronary syndrome experience increased 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 343, "doc_id": 5884524, "label": "SUPPORTS", "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: Discrimination between the initiator and elongation tRNAs 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: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 350, "doc_id": 16927286, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [16927286], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Downregulation and mislocalization of Scribble prevents cell transformation and mammary tumorigenesis.\n\nDocument title: Deregulation of Scribble Promotes Mammary Tumorigenesis and Reveals a Role for Cell Polarity in Carcinoma\n\nAbstract sentences:\n[0] Loss of cell polarity proteins such as Scribble induces neoplasia in Drosophila by promoting uncontrolled proliferation.\n[1] In mammals, the role that polarity proteins play during tumorigenesis is not well understood.\n[2] Here, we demonstrate that depletion of Scribble in mammary epithelia disrupts cell polarity, blocks three-dimensional morphogenesis, inhibits apoptosis, and induces dysplasia in vivo that progress to tumors after long latency.\n[3] Loss of Scribble cooperates with oncogenes such as c-myc to transform epithelial cells and induce tumors in vivo by blocking activation of an apoptosis pathway.\n[4] Like depletion, mislocalization of Scribble from cell-cell junction was sufficient to promote cell transformation.\n[5] Interestingly, spontaneous mammary tumors in mice and humans possess both downregulated and mislocalized Scribble.\n[6] Thus, we demonstrate that scribble inhibits breast cancer formation and that deregulation of polarity pathways promotes dysplastic and neoplastic growth in mammals by disrupting morphogenesis and inhibiting cell death."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 354, "doc_id": 8774475, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [8774475], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 paracortical 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": "validation", "claim_id": 362, "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: Enhanced early production of inflammatory chemokines improves 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: 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": "validation", "claim_id": 380, "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: Epidemiological disease burden from noncommunicable diseases is more prevalent in low 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": "validation", "claim_id": 384, "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: Epigenetic modulating agents (EMAs) modulate antitumor immune response in a cancer model system.\n\nDocument title: Epigenetic Therapy Ties MYC Depletion to Reversing Immune Evasion and Treating Lung Cancer\n\nAbstract sentences:\n[0] Combining DNA-demethylating agents (DNA methyltransferase inhibitors [DNMTis]) with histone deacetylase inhibitors (HDACis) holds promise for enhancing cancer immune therapy.\n[1] Herein, pharmacologic and isoform specificity of HDACis are investigated to guide their addition to a DNMTi, thus devising a new, low-dose, sequential regimen that imparts a robust anti-tumor effect for non-small-cell lung cancer (NSCLC).\n[2] Using in-vitro-treated NSCLC cell lines, we elucidate an interferon α/β-based transcriptional program with accompanying upregulation of antigen presentation machinery, mediated in part through double-stranded RNA (dsRNA) induction.\n[3] This is accompanied by suppression of MYC signaling and an increase in the T cell chemoattractant CCL5.\n[4] Use of this combination treatment schema in mouse models of NSCLC reverses tumor immune evasion and modulates T cell exhaustion state towards memory and effector T cell phenotypes.\n[5] Key correlative science metrics emerge for an upcoming clinical trial, testing enhancement of immune checkpoint therapy for NSCLC."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Use of this combination treatment schema in mouse models of NSCLC reverses tumor immune evasion and modulates T cell exhaustion state towards memory and effector T cell phenotypes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 385, "doc_id": 9955779, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [9955779, 9767444], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Errors in peripheral IV drug administration are most common during bolus administration and multiple-step medicine preparations.\n\nDocument title: Ethnographic study of incidence and severity of intravenous drug errors.\n\nAbstract sentences:\n[0] OBJECTIVES To determine the incidence and clinical importance of errors in the preparation and administration of intravenous drugs and the stages of the process in which errors occur.\n[1] DESIGN Prospective ethnographic study using disguised observation.\n[2] PARTICIPANTS Nurses who prepared and administered intravenous drugs.\n[3] SETTING 10 wards in a teaching and non-teaching hospital in the United Kingdom.\n[4] MAIN OUTCOME MEASURES Number, type, and clinical importance of errors.\n[5] RESULTS 249 errors were identified.\n[6] At least one error occurred in 212 out of 430 intravenous drug doses (49%, 95% confidence interval 45% to 54%).\n[7] Three doses (1%) had potentially severe errors, 126 (29%) potentially moderate errors, and 83 (19%) potentially minor errors.\n[8] Most errors occurred when giving bolus doses or making up drugs that required multiple step preparation.\n[9] CONCLUSIONS The rate of intravenous drug errors was high.\n[10] Although most errors would cause only short term adverse effects, a few could have been serious.\n[11] A combination of reducing the amount of preparation on the ward, training, and technology to administer slow bolus doses would probably have the greatest effect on error rates."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Most errors occurred when giving bolus doses or making up drugs that required multiple step preparation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 386, "doc_id": 16495649, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [16495649], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Errors in peripheral IV drug administration are most common during bolus administration and multiple-step medicine preparations.\n\nDocument title: Ethnographic study of incidence and severity of intravenous drug errors.\n\nAbstract sentences:\n[0] OBJECTIVES To determine the incidence and clinical importance of errors in the preparation and administration of intravenous drugs and the stages of the process in which errors occur.\n[1] DESIGN Prospective ethnographic study using disguised observation.\n[2] PARTICIPANTS Nurses who prepared and administered intravenous drugs.\n[3] SETTING 10 wards in a teaching and non-teaching hospital in the United Kingdom.\n[4] MAIN OUTCOME MEASURES Number, type, and clinical importance of errors.\n[5] RESULTS 249 errors were identified.\n[6] At least one error occurred in 212 out of 430 intravenous drug doses (49%, 95% confidence interval 45% to 54%).\n[7] Three doses (1%) had potentially severe errors, 126 (29%) potentially moderate errors, and 83 (19%) potentially minor errors.\n[8] Most errors occurred when giving bolus doses or making up drugs that required multiple step preparation.\n[9] CONCLUSIONS The rate of intravenous drug errors was high.\n[10] Although most errors would cause only short term adverse effects, a few could have been serious.\n[11] A combination of reducing the amount of preparation on the ward, training, and technology to administer slow bolus doses would probably have the greatest effect on error rates."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"A combination of reducing the amount of preparation on the ward, training, and technology to administer slow bolus doses would probably have the greatest effect on error rates.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 386, "doc_id": 16495649, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [16495649], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 decreases 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": "validation", "claim_id": 388, "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: Exposure to fine particulate air pollution is relate 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 399, "doc_id": 791050, "label": "SUPPORTS", "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 relate 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 399, "doc_id": 791050, "label": "SUPPORTS", "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: Febrile seizures increase the threshold for development of epilepsy.\n\nDocument title: Febrile seizures in the developing brain result in persistent modification of neuronal excitability in limbic circuits\n\nAbstract sentences:\n[0] Febrile (fever-induced) seizures affect 3–5% of infants and young children.\n[1] Despite the high incidence of febrile seizures, their contribution to the development of epilepsy later in life has remained controversial.\n[2] Combining a new rat model of complex febrile seizures and patch clamp techniques, we determined that hyperthermia-induced seizures in the immature rat cause a selective presynaptic increase in inhibitory synaptic transmission in the hippocampus that lasts into adulthood.\n[3] The long-lasting nature of these potent alterations in synaptic communication after febrile seizures does not support the prevalent view of the 'benign' nature of early-life febrile convulsions."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 410, "doc_id": 14924526, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14924526], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Febrile seizures reduce the threshold for development of epilepsy.\n\nDocument title: Febrile seizures in the developing brain result in persistent modification of neuronal excitability in limbic circuits\n\nAbstract sentences:\n[0] Febrile (fever-induced) seizures affect 3–5% of infants and young children.\n[1] Despite the high incidence of febrile seizures, their contribution to the development of epilepsy later in life has remained controversial.\n[2] Combining a new rat model of complex febrile seizures and patch clamp techniques, we determined that hyperthermia-induced seizures in the immature rat cause a selective presynaptic increase in inhibitory synaptic transmission in the hippocampus that lasts into adulthood.\n[3] The long-lasting nature of these potent alterations in synaptic communication after febrile seizures does not support the prevalent view of the 'benign' nature of early-life febrile convulsions."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 411, "doc_id": 14924526, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14924526], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 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: 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": "validation", "claim_id": 415, "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: Flexible molecules experience greater 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": "validation", "claim_id": 421, "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: FoxO3a activation in neuronal death is mediated 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 431, "doc_id": 28937856, "label": "SUPPORTS", "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: Free histones are degraded by a Rad53-dependent mechanism once DNA has been replicated.\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: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"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.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 436, "doc_id": 14637235, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [14637235], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Free histones are degraded by a Rad53-dependent mechanism once DNA has been replicated.\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: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"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.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 436, "doc_id": 14637235, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [14637235], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Functional consequences of genomic alterations due to Myelodysplastic syndrome (MDS) are poorly understood due to the lack of an animal model.\n\nDocument title: Establishment of human iPSC-based models for the study and targeting of glioma initiating cells\n\nAbstract sentences:\n[0] Glioma tumour-initiating cells (GTICs) can originate upon the transformation of neural progenitor cells (NPCs).\n[1] Studies on GTICs have focused on primary tumours from which GTICs could be isolated and the use of human embryonic material.\n[2] Recently, the somatic genomic landscape of human gliomas has been reported.\n[3] RTK (receptor tyrosine kinase) and p53 signalling were found dysregulated in ∼90% and 86% of all primary tumours analysed, respectively.\n[4] Here we report on the use of human-induced pluripotent stem cells (hiPSCs) for modelling gliomagenesis.\n[5] Dysregulation of RTK and p53 signalling in hiPSC-derived NPCs (iNPCs) recapitulates GTIC properties in vitro.\n[6] In vivo transplantation of transformed iNPCs leads to highly aggressive tumours containing undifferentiated stem cells and their differentiated derivatives.\n[7] Metabolic modulation compromises GTIC viability.\n[8] Last, screening of 101 anti-cancer compounds identifies three molecules specifically targeting transformed iNPCs and primary GTICs.\n[9] Together, our results highlight the potential of hiPSCs for studying human tumourigenesis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 437, "doc_id": 18399038, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [18399038], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Fz/PCP-dependent Pk localizes to the anterior membrane of neuroectoderm cells during zebrafish neuralation\n\nDocument title: Planar cell polarity signalling couples cell division and morphogenesis during neurulation\n\nAbstract sentences:\n[0] Environmental and genetic aberrations lead to neural tube closure defects (NTDs) in 1 out of every 1,000 births.\n[1] Mouse and frog models for these birth defects have indicated that Van Gogh-like 2 (Vangl2, also known as Strabismus) and other components of planar cell polarity (PCP) signalling might control neurulation by promoting the convergence of neural progenitors to the midline.\n[2] Here we show a novel role for PCP signalling during neurulation in zebrafish.\n[3] We demonstrate that non-canonical Wnt/PCP signalling polarizes neural progenitors along the anteroposterior axis.\n[4] This polarity is transiently lost during cell division in the neural keel but is re-established as daughter cells reintegrate into the neuroepithelium.\n[5] Loss of zebrafish Vangl2 (in trilobite mutants) abolishes the polarization of neural keel cells, disrupts re-intercalation of daughter cells into the neuroepithelium, and results in ectopic neural progenitor accumulations and NTDs.\n[6] Remarkably, blocking cell division leads to rescue of trilobite neural tube morphogenesis despite persistent defects in convergence and extension.\n[7] These results reveal a function for PCP signalling in coupling cell division and morphogenesis at neurulation and indicate a previously unrecognized mechanism that might underlie NTDs."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 439, "doc_id": 4423559, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4423559], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Fz/PCP-dependent Pk localizes to the anterior membrane of notochord cells during zebrafish neuralation.\n\nDocument title: Planar cell polarity signalling couples cell division and morphogenesis during neurulation\n\nAbstract sentences:\n[0] Environmental and genetic aberrations lead to neural tube closure defects (NTDs) in 1 out of every 1,000 births.\n[1] Mouse and frog models for these birth defects have indicated that Van Gogh-like 2 (Vangl2, also known as Strabismus) and other components of planar cell polarity (PCP) signalling might control neurulation by promoting the convergence of neural progenitors to the midline.\n[2] Here we show a novel role for PCP signalling during neurulation in zebrafish.\n[3] We demonstrate that non-canonical Wnt/PCP signalling polarizes neural progenitors along the anteroposterior axis.\n[4] This polarity is transiently lost during cell division in the neural keel but is re-established as daughter cells reintegrate into the neuroepithelium.\n[5] Loss of zebrafish Vangl2 (in trilobite mutants) abolishes the polarization of neural keel cells, disrupts re-intercalation of daughter cells into the neuroepithelium, and results in ectopic neural progenitor accumulations and NTDs.\n[6] Remarkably, blocking cell division leads to rescue of trilobite neural tube morphogenesis despite persistent defects in convergence and extension.\n[7] These results reveal a function for PCP signalling in coupling cell division and morphogenesis at neurulation and indicate a previously unrecognized mechanism that might underlie NTDs."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 440, "doc_id": 4423559, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4423559], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: GATA-3 is important for hematopoietic stem cell (HSC) function.\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, 5, 6]\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. 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": "validation", "claim_id": 443, "doc_id": 10165258, "label": "SUPPORTS", "evidence_sentence_ids": [4, 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: Gene expression does not vary appreciably across genetically identical cells.\n\nDocument title: Nature, Nurture, or Chance: Stochastic Gene Expression and Its Consequences\n\nAbstract sentences:\n[0] Gene expression is a fundamentally stochastic process, with randomness in transcription and translation leading to cell-to-cell variations in mRNA and protein levels.\n[1] This variation appears in organisms ranging from microbes to metazoans, and its characteristics depend both on the biophysical parameters governing gene expression and on gene network structure.\n[2] Stochastic gene expression has important consequences for cellular function, being beneficial in some contexts and harmful in others.\n[3] These situations include the stress response, metabolism, development, the cell cycle, circadian rhythms, and aging."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Gene expression is a fundamentally stochastic process, with randomness in transcription and translation leading to cell-to-cell variations in mRNA and protein levels.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 452, "doc_id": 12804937, "label": "CONTRADICTS", "evidence_sentence_ids": [0], "cited_doc_ids": [12804937, 464511], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Gene expression does not vary appreciably across genetically identical cells.\n\nDocument title: Memory and Modularity in Cell-Fate Decision Making\n\nAbstract sentences:\n[0] Genetically identical cells sharing an environment can display markedly different phenotypes.\n[1] It is often unclear how much of this variation derives from chance, external signals, or attempts by individual cells to exert autonomous phenotypic programs.\n[2] By observing thousands of cells for hundreds of consecutive generations under constant conditions, we dissect the stochastic decision between a solitary, motile state and a chained, sessile state in Bacillus subtilis.\n[3] We show that the motile state is 'memoryless', exhibiting no autonomous control over the time spent in the state.\n[4] In contrast, the time spent as connected chains of cells is tightly controlled, enforcing coordination among related cells in the multicellular state.\n[5] We show that the three-protein regulatory circuit governing the decision is modular, as initiation and maintenance of chaining are genetically separable functions.\n[6] As stimulation of the same initiating pathway triggers biofilm formation, we argue that autonomous timing allows a trial commitment to multicellularity that external signals could extend."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Genetically identical cells sharing an environment can display markedly different phenotypes.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 452, "doc_id": 464511, "label": "CONTRADICTS", "evidence_sentence_ids": [0], "cited_doc_ids": [12804937, 464511], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Glycolysis 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: SUPPORTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"We demonstrate that glycolysis provides ATP for the FAT of vesicles.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 475, "doc_id": 18678095, "label": "SUPPORTS", "evidence_sentence_ids": [1], "cited_doc_ids": [18678095], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Golli-deficient T-cells prefer to differentiate into an anergic phenotype in the adaptive immune response when there are increased levels of Ca2+ in the cytosol.\n\nDocument title: Golli protein negatively regulates store depletion-induced calcium influx in T cells.\n\nAbstract sentences:\n[0] Calcium influx is crucial for T cell activation and differentiation.\n[1] The detailed regulation of this process remains unclear.\n[2] We report here that golli protein, an alternatively spliced product of the myelin basic protein gene, plays a critical role in regulating calcium influx in T cells.\n[3] Golli-deficient T cells were hyperproliferative and showed enhanced calcium entry upon T cell receptor stimulation.\n[4] We further found that golli regulates calcium influx in T cells through the inhibition of the store depletion-induced calcium influx.\n[5] Mutation of the myristoylation site on golli disrupted its association with the plasma membrane and reversed its inhibitory action on Ca2+ influx, indicating that membrane association of golli was essential for its inhibitory action.\n[6] These results indicate that golli functions in a unique way to regulate T cell activation through a mechanism involving the modulation of the calcium homeostasis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 478, "doc_id": 14767844, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [14767844], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 can cause diabetes in mutant carriers 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": "validation", "claim_id": 491, "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: Headaches are not 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: SUPPORTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"Evidence was lacking for cognitive impairment for any headache type with or without brain lesions.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 501, "doc_id": 17930286, "label": "SUPPORTS", "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: Healthcare delivery efficiency in crowded delivery centers is impaired by improving structural, logistical, and interpersonal elements.\n\nDocument title: The HIV Treatment Gap: Estimates of the Financial Resources Needed versus Available for Scale-Up of Antiretroviral Therapy in 97 Countries from 2015 to 2020\n\nAbstract sentences:\n[0] BACKGROUND The World Health Organization (WHO) released revised guidelines in 2015 recommending that all people living with HIV, regardless of CD4 count, initiate antiretroviral therapy (ART) upon diagnosis.\n[1] However, few studies have projected the global resources needed for rapid scale-up of ART.\n[2] Under the Health Policy Project, we conducted modeling analyses for 97 countries to estimate eligibility for and numbers on ART from 2015 to 2020, along with the facility-level financial resources required.\n[3] We compared the estimated financial requirements to estimated funding available.\n[4] METHODS AND FINDINGS Current coverage levels and future need for treatment were based on country-specific epidemiological and demographic data.\n[5] Simulated annual numbers of individuals on treatment were derived from three scenarios: (1) continuation of countries' current policies of eligibility for ART, (2) universal adoption of aspects of the WHO 2013 eligibility guidelines, and (3) expanded eligibility as per the WHO 2015 guidelines and meeting the Joint United Nations Programme on HIV/AIDS \"90-90-90\" ART targets.\n[6] We modeled uncertainty in the annual resource requirements for antiretroviral drugs, laboratory tests, and facility-level personnel and overhead.\n[7] We estimate that 25.7 (95% CI 25.5, 26.0) million adults and 1.57 (95% CI 1.55, 1.60) million children could receive ART by 2020 if countries maintain current eligibility plans and increase coverage based on historical rates, which may be ambitious.\n[8] If countries uniformly adopt aspects of the WHO 2013 guidelines, 26.5 (95% CI 26.0 27.0) million adults and 1.53 (95% CI 1.52, 1.55) million children could be on ART by 2020.\n[9] Under the 90-90-90 scenario, 30.4 (95% CI 30.1, 30.7) million adults and 1.68 (95% CI 1.63, 1.73) million children could receive treatment by 2020.\n[10] The facility-level financial resources needed for scaling up ART in these countries from 2015 to 2020 are estimated to be US$45.8 (95% CI 45.4, 46.2) billion under the current scenario, US$48.7 (95% CI 47.8, 49.6) billion under the WHO 2013 scenario, and US$52.5 (95% CI 51.4, 53.6) billion under the 90-90-90 scenario.\n[11] After projecting recent external and domestic funding trends, the estimated 6-y financing gap ranges from US$19.8 billion to US$25.0 billion, depending on the costing scenario and the U.S. President's Emergency Plan for AIDS Relief contribution level, with the gap for ART commodities alone ranging from US$14.0 to US$16.8 billion.\n[12] The study is limited by excluding above-facility and other costs essential to ART service delivery and by the availability and quality of country- and region-specific data.\n[13] CONCLUSIONS The projected number of people receiving ART across three scenarios suggests that countries are unlikely to meet the 90-90-90 treatment target (81% of people living with HIV on ART by 2020) unless they adopt a test-and-offer approach and increase ART coverage.\n[14] Our results suggest that future resource needs for ART scale-up are smaller than stated elsewhere but still significantly threaten the sustainability of the global HIV response without additional resource mobilization from domestic or innovative financing sources or efficiency gains.\n[15] As the world moves towards adopting the WHO 2015 guidelines, advances in technology, including the introduction of lower-cost, highly effective antiretroviral regimens, whose value are assessed here, may prove to be \"game changers\" that allow more people to be on ART with the resources available."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 502, "doc_id": 13071728, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [13071728], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 macrophages activated by IL-4 favor Mycobacterium tuberculosis replication.\n\nDocument title: T helper 2 cytokines inhibit autophagic control of intracellular Mycobacterium tuberculosis.\n\nAbstract sentences:\n[0] Autophagy is a recently recognized immune effector mechanism against intracellular pathogens.\n[1] The role of autophagy in innate immunity has been well established, but the extent of its regulation by the adaptive immune response is less well understood.\n[2] The T helper 1 (Th1) cell cytokine IFN-gamma induces autophagy in macrophages to eliminate Mycobacterium tuberculosis.\n[3] Here, we report that Th2 cytokines affect autophagy in macrophages and their ability to control intracellular M. tuberculosis.\n[4] IL-4 and IL-13 abrogated autophagy and autophagy-mediated killing of intracellular mycobacteria in murine and human macrophages.\n[5] Inhibition of starvation-induced autophagy by IL-4 and IL-13 was dependent on Akt signaling, whereas the inhibition of IFN-gamma-induced autophagy was Akt independent and signal transducer and activator of transcription 6 (STAT6) dependent.\n[6] These findings establish a mechanism through which Th1-Th2 polarization differentially affects the immune control of intracellular 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": "validation", "claim_id": 507, "doc_id": 30774694, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [30774694], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 rate of up to 50%.\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": "validation", "claim_id": 508, "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 cardiopulmonary fitness causes increased mortality rate.\n\nDocument title: Prevalence and cardiovascular disease correlates of low cardiorespiratory fitness in adolescents and adults.\n\nAbstract sentences:\n[0] CONTEXT Population surveys indicate that physical activity levels are low in the United States.\n[1] One consequence of inactivity, low cardiorespiratory fitness, is an established risk factor for cardiovascular disease (CVD) morbidity and mortality, but the prevalence of cardiorespiratory fitness has not been quantified in representative US population samples.\n[2] OBJECTIVES To describe the prevalence of low fitness in the US population aged 12 through 49 years and to relate low fitness to CVD risk factors in this population.\n[3] DESIGN, SETTING, AND PARTICIPANTS Inception cohort study using data from the cross-sectional nationally representative National Health and Nutrition Examination Survey 1999-2002.\n[4] Participants were adolescents (aged 12-19 years; n = 3110) and adults (aged 20-49 years; n = 2205) free from previously diagnosed CVD who underwent submaximal graded exercise treadmill testing to achieve at least 75% to 90% of their age-predicted maximum heart rate.\n[5] Maximal oxygen consumption (VO2max) was estimated by measuring the heart rate response to reference levels of submaximal work.\n[6] MAIN OUTCOME MEASURES Low fitness defined using percentile cut points of estimated VO2max from existing external referent populations; anthropometric and other CVD risk factors measured according to standard methods.\n[7] RESULTS Low fitness was identified in 33.6% of adolescents (approximately 7.5 million US adolescents) and 13.9% of adults (approximately 8.5 million US adults); the prevalence was similar in adolescent females (34.4%) and males (32.9%) (P = .40) but was higher in adult females (16.2%) than in males (11.8%) (P = .03).\n[8] Non-Hispanic blacks and Mexican Americans were less fit than non-Hispanic whites.\n[9] In all age-sex groups, body mass index and waist circumference were inversely associated with fitness; age- and race-adjusted odds ratios of overweight or obesity (body mass index > or =25) ranged from 2.1 to 3.7 (P<.01 for all), comparing persons with low fitness with those with moderate or high fitness.\n[10] Total cholesterol levels and systolic blood pressure were higher and levels of high-density lipoprotein cholesterol were lower among participants with low vs high fitness.\n[11] CONCLUSION Low fitness in adolescents and adults is common in the US population and is associated with an increased prevalence of CVD risk factors."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"CONCLUSION Low fitness in adolescents and adults is common in the US population and is associated with an increased prevalence of CVD risk factors.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 513, "doc_id": 13230773, "label": "CONTRADICTS", "evidence_sentence_ids": [11], "cited_doc_ids": [13230773], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 dietary calcium intakes are unnecessary for prevention of secondary hyperparathyroidism in subjects with 25(OH)D levels above 75 nmol/liter.\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: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 514, "doc_id": 16256507, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [16256507], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 reduces the 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 516, "doc_id": 29564505, "label": "CONTRADICTS", "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 reduces the 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 516, "doc_id": 29564505, "label": "CONTRADICTS", "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: High levels of copeptin decrease risk of 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: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 517, "doc_id": 15663829, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [15663829], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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-sensitivity cardiac troponin T (HSCT-T) dosage may not be diagnostic if the onset of symptoms occurs less than 3 hours before acute myocardial injury (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: SUPPORTS\nRationale sentence ids: [14]\nExplanation: Evidence states: \"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.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 521, "doc_id": 34873974, "label": "SUPPORTS", "evidence_sentence_ids": [14], "cited_doc_ids": [34873974], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Histone demethylase recruitment and a transient decrease in histone methylation is necessary for ligand-dependent induction of transcription by nuclear receptors.\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: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"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.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 525, "doc_id": 13639330, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [13639330], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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) prevents 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": "validation", "claim_id": 527, "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 T-lymphotropic virus type-I-associated myelopathy / tropical spastic paraparesis (HAM/TSP) patients produce Immunoglobulin G (IgG) antibodies which cross-react with an immunodominant epitope in Tax.\n\nDocument title: Autoimmunity due to molecular mimicry as a cause of neurological disease\n\nAbstract sentences:\n[0] One hypothesis that couples infection with autoimmune disease is molecular mimicry.\n[1] Molecular mimicry is characterized by an immune response to an environmental agent that cross-reacts with a host antigen, resulting in disease.\n[2] This hypothesis has been implicated in the pathogenesis of diabetes, lupus and multiple sclerosis (MS).\n[3] There is limited direct evidence linking causative agents with pathogenic immune reactions in these diseases.\n[4] Our study establishes a clear link between viral infection, autoimmunity and neurological disease in humans.\n[5] As a model for molecular mimicry, we studied patients with human T-lymphotropic virus type 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP), a disease that can be indistinguishable from MS (refs.\n[6] 5,6,7).\n[7] HAM/TSP patients develop antibodies to neurons.\n[8] We hypothesized these antibodies would identify a central nervous system (CNS) autoantigen.\n[9] Immunoglobulin G isolated from HAM/TSP patients identified heterogeneous nuclear ribonuclear protein-A1 (hnRNP-A1) as the autoantigen.\n[10] Antibodies to hnRNP-A1 cross-reacted with HTLV-1-tax, the immune response to which is associated with HAM/TSP (refs.\n[11] 5,9).\n[12] Immunoglobulin G specifically stained human Betz cells, whose axons are preferentially damaged.\n[13] Infusion of autoantibodies in brain sections inhibited neuronal firing, indicative of their pathogenic nature.\n[14] These data demonstrate the importance of molecular mimicry between an infecting agent and hnRNP-A1 in autoimmune disease of the CNS."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Antibodies to hnRNP-A1 cross-reacted with HTLV-1-tax, the immune response to which is associated with HAM/TSP (refs.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 528, "doc_id": 5476778, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [5476778], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Hyperfibrinogenemia decreases rates of femoropopliteal bypass thrombosis.\n\nDocument title: Influence of smoking and plasma factors on patency of femoropopliteal vein grafts.\n\nAbstract sentences:\n[0] OBJECTIVE To determine the effects of smoking, plasma lipids, lipoproteins, apolipoproteins, and fibrinogen on the patency of saphenous vein femoropopliteal bypass grafts at one year.\n[1] DESIGN Prospective study of patients with saphenous vein femoropopliteal bypass grafts entered into a multicentre trial.\n[2] SETTING Surgical wards, outpatient clinics, and home visits coordinated by two tertiary referral centres in London and Birmingham.\n[3] PATIENTS 157 Patients (mean age 66.6 (SD 8.2) years), 113 with patent grafts and 44 with occluded grafts one year after bypass.\n[4] MAIN OUTCOME MEASURE Cumulative percentage patency at one year.\n[5] RESULTS Markers for smoking (blood carboxyhaemoglobin concentration (p less than 0.05) and plasma thiocyanate concentration (p less than 0.01) and plasma concentrations of fibrinogen (p less than 0.001) and apolipoproteins AI (p less than 0.04) and (a) (p less than 0.05) were significantly higher in patients with occluded grafts.\n[6] Serum cholesterol concentrations were significantly higher in patients with grafts that remained patent one year after bypass (p less than 0.005).\n[7] Analysis of the smoking markers indicated that a quarter of patients (40) were untruthful in their claims to have stopped smoking.\n[8] Based on smoking markers, patency of grafts in smokers was significantly lower at one year by life table analysis than in non-smokers (63% v 84%, p less than 0.02).\n[9] Patency was significantly higher by life table analysis in patients with a plasma fibrinogen concentration below the median than in those with a concentration above (90% v 57%, p less than 0.0002).\n[10] Surprisingly, increased plasma low density lipoprotein cholesterol concentration was significantly associated with improved patency at one year (85%) at values above the median compared with patency (only 68%) at values in the lower half of the range (p less than 0.02).\n[11] CONCLUSIONS Plasma fibrinogen concentration was the most important variable predicting graft occlusion, followed by smoking markers.\n[12] A more forceful approach is needed to stop patients smoking; therapeutic measures to improve patency of vein grafts should focus on decreasing plasma fibrinogen concentration rather than serum cholesterol concentration."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"RESULTS Markers for smoking (blood carboxyhaemoglobin concentration (p less than 0.05) and plasma thiocyanate concentration (p less than 0.01) and plasma concentrations of fibrinogen (p less than 0.001) and apolipoproteins AI (p less than 0.04) and (a) (p less than 0.05) were significantly higher in patients with occluded grafts.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 532, "doc_id": 12991445, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [12991445], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Hyperfibrinogenemia decreases rates of femoropopliteal bypass thrombosis.\n\nDocument title: Influence of smoking and plasma factors on patency of femoropopliteal vein grafts.\n\nAbstract sentences:\n[0] OBJECTIVE To determine the effects of smoking, plasma lipids, lipoproteins, apolipoproteins, and fibrinogen on the patency of saphenous vein femoropopliteal bypass grafts at one year.\n[1] DESIGN Prospective study of patients with saphenous vein femoropopliteal bypass grafts entered into a multicentre trial.\n[2] SETTING Surgical wards, outpatient clinics, and home visits coordinated by two tertiary referral centres in London and Birmingham.\n[3] PATIENTS 157 Patients (mean age 66.6 (SD 8.2) years), 113 with patent grafts and 44 with occluded grafts one year after bypass.\n[4] MAIN OUTCOME MEASURE Cumulative percentage patency at one year.\n[5] RESULTS Markers for smoking (blood carboxyhaemoglobin concentration (p less than 0.05) and plasma thiocyanate concentration (p less than 0.01) and plasma concentrations of fibrinogen (p less than 0.001) and apolipoproteins AI (p less than 0.04) and (a) (p less than 0.05) were significantly higher in patients with occluded grafts.\n[6] Serum cholesterol concentrations were significantly higher in patients with grafts that remained patent one year after bypass (p less than 0.005).\n[7] Analysis of the smoking markers indicated that a quarter of patients (40) were untruthful in their claims to have stopped smoking.\n[8] Based on smoking markers, patency of grafts in smokers was significantly lower at one year by life table analysis than in non-smokers (63% v 84%, p less than 0.02).\n[9] Patency was significantly higher by life table analysis in patients with a plasma fibrinogen concentration below the median than in those with a concentration above (90% v 57%, p less than 0.0002).\n[10] Surprisingly, increased plasma low density lipoprotein cholesterol concentration was significantly associated with improved patency at one year (85%) at values above the median compared with patency (only 68%) at values in the lower half of the range (p less than 0.02).\n[11] CONCLUSIONS Plasma fibrinogen concentration was the most important variable predicting graft occlusion, followed by smoking markers.\n[12] A more forceful approach is needed to stop patients smoking; therapeutic measures to improve patency of vein grafts should focus on decreasing plasma fibrinogen concentration rather than serum cholesterol concentration."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Patency was significantly higher by life table analysis in patients with a plasma fibrinogen concentration below the median than in those with a concentration above (90% v 57%, p less than 0.0002).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 532, "doc_id": 12991445, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [12991445], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Hyperfibrinogenemia decreases rates of femoropopliteal bypass thrombosis.\n\nDocument title: Influence of smoking and plasma factors on patency of femoropopliteal vein grafts.\n\nAbstract sentences:\n[0] OBJECTIVE To determine the effects of smoking, plasma lipids, lipoproteins, apolipoproteins, and fibrinogen on the patency of saphenous vein femoropopliteal bypass grafts at one year.\n[1] DESIGN Prospective study of patients with saphenous vein femoropopliteal bypass grafts entered into a multicentre trial.\n[2] SETTING Surgical wards, outpatient clinics, and home visits coordinated by two tertiary referral centres in London and Birmingham.\n[3] PATIENTS 157 Patients (mean age 66.6 (SD 8.2) years), 113 with patent grafts and 44 with occluded grafts one year after bypass.\n[4] MAIN OUTCOME MEASURE Cumulative percentage patency at one year.\n[5] RESULTS Markers for smoking (blood carboxyhaemoglobin concentration (p less than 0.05) and plasma thiocyanate concentration (p less than 0.01) and plasma concentrations of fibrinogen (p less than 0.001) and apolipoproteins AI (p less than 0.04) and (a) (p less than 0.05) were significantly higher in patients with occluded grafts.\n[6] Serum cholesterol concentrations were significantly higher in patients with grafts that remained patent one year after bypass (p less than 0.005).\n[7] Analysis of the smoking markers indicated that a quarter of patients (40) were untruthful in their claims to have stopped smoking.\n[8] Based on smoking markers, patency of grafts in smokers was significantly lower at one year by life table analysis than in non-smokers (63% v 84%, p less than 0.02).\n[9] Patency was significantly higher by life table analysis in patients with a plasma fibrinogen concentration below the median than in those with a concentration above (90% v 57%, p less than 0.0002).\n[10] Surprisingly, increased plasma low density lipoprotein cholesterol concentration was significantly associated with improved patency at one year (85%) at values above the median compared with patency (only 68%) at values in the lower half of the range (p less than 0.02).\n[11] CONCLUSIONS Plasma fibrinogen concentration was the most important variable predicting graft occlusion, followed by smoking markers.\n[12] A more forceful approach is needed to stop patients smoking; therapeutic measures to improve patency of vein grafts should focus on decreasing plasma fibrinogen concentration rather than serum cholesterol concentration."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"CONCLUSIONS Plasma fibrinogen concentration was the most important variable predicting graft occlusion, followed by smoking markers.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 532, "doc_id": 12991445, "label": "CONTRADICTS", "evidence_sentence_ids": [11], "cited_doc_ids": [12991445], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Hyperfibrinogenemia decreases rates of femoropopliteal bypass thrombosis.\n\nDocument title: Influence of smoking and plasma factors on patency of femoropopliteal vein grafts.\n\nAbstract sentences:\n[0] OBJECTIVE To determine the effects of smoking, plasma lipids, lipoproteins, apolipoproteins, and fibrinogen on the patency of saphenous vein femoropopliteal bypass grafts at one year.\n[1] DESIGN Prospective study of patients with saphenous vein femoropopliteal bypass grafts entered into a multicentre trial.\n[2] SETTING Surgical wards, outpatient clinics, and home visits coordinated by two tertiary referral centres in London and Birmingham.\n[3] PATIENTS 157 Patients (mean age 66.6 (SD 8.2) years), 113 with patent grafts and 44 with occluded grafts one year after bypass.\n[4] MAIN OUTCOME MEASURE Cumulative percentage patency at one year.\n[5] RESULTS Markers for smoking (blood carboxyhaemoglobin concentration (p less than 0.05) and plasma thiocyanate concentration (p less than 0.01) and plasma concentrations of fibrinogen (p less than 0.001) and apolipoproteins AI (p less than 0.04) and (a) (p less than 0.05) were significantly higher in patients with occluded grafts.\n[6] Serum cholesterol concentrations were significantly higher in patients with grafts that remained patent one year after bypass (p less than 0.005).\n[7] Analysis of the smoking markers indicated that a quarter of patients (40) were untruthful in their claims to have stopped smoking.\n[8] Based on smoking markers, patency of grafts in smokers was significantly lower at one year by life table analysis than in non-smokers (63% v 84%, p less than 0.02).\n[9] Patency was significantly higher by life table analysis in patients with a plasma fibrinogen concentration below the median than in those with a concentration above (90% v 57%, p less than 0.0002).\n[10] Surprisingly, increased plasma low density lipoprotein cholesterol concentration was significantly associated with improved patency at one year (85%) at values above the median compared with patency (only 68%) at values in the lower half of the range (p less than 0.02).\n[11] CONCLUSIONS Plasma fibrinogen concentration was the most important variable predicting graft occlusion, followed by smoking markers.\n[12] A more forceful approach is needed to stop patients smoking; therapeutic measures to improve patency of vein grafts should focus on decreasing plasma fibrinogen concentration rather than serum cholesterol concentration."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"A more forceful approach is needed to stop patients smoking; therapeutic measures to improve patency of vein grafts should focus on decreasing plasma fibrinogen concentration rather than serum cholesterol concentration.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 532, "doc_id": 12991445, "label": "CONTRADICTS", "evidence_sentence_ids": [12], "cited_doc_ids": [12991445], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Hyperfibrinogenemia increases rates of femoropopliteal bypass thrombosis.\n\nDocument title: Influence of smoking and plasma factors on patency of femoropopliteal vein grafts.\n\nAbstract sentences:\n[0] OBJECTIVE To determine the effects of smoking, plasma lipids, lipoproteins, apolipoproteins, and fibrinogen on the patency of saphenous vein femoropopliteal bypass grafts at one year.\n[1] DESIGN Prospective study of patients with saphenous vein femoropopliteal bypass grafts entered into a multicentre trial.\n[2] SETTING Surgical wards, outpatient clinics, and home visits coordinated by two tertiary referral centres in London and Birmingham.\n[3] PATIENTS 157 Patients (mean age 66.6 (SD 8.2) years), 113 with patent grafts and 44 with occluded grafts one year after bypass.\n[4] MAIN OUTCOME MEASURE Cumulative percentage patency at one year.\n[5] RESULTS Markers for smoking (blood carboxyhaemoglobin concentration (p less than 0.05) and plasma thiocyanate concentration (p less than 0.01) and plasma concentrations of fibrinogen (p less than 0.001) and apolipoproteins AI (p less than 0.04) and (a) (p less than 0.05) were significantly higher in patients with occluded grafts.\n[6] Serum cholesterol concentrations were significantly higher in patients with grafts that remained patent one year after bypass (p less than 0.005).\n[7] Analysis of the smoking markers indicated that a quarter of patients (40) were untruthful in their claims to have stopped smoking.\n[8] Based on smoking markers, patency of grafts in smokers was significantly lower at one year by life table analysis than in non-smokers (63% v 84%, p less than 0.02).\n[9] Patency was significantly higher by life table analysis in patients with a plasma fibrinogen concentration below the median than in those with a concentration above (90% v 57%, p less than 0.0002).\n[10] Surprisingly, increased plasma low density lipoprotein cholesterol concentration was significantly associated with improved patency at one year (85%) at values above the median compared with patency (only 68%) at values in the lower half of the range (p less than 0.02).\n[11] CONCLUSIONS Plasma fibrinogen concentration was the most important variable predicting graft occlusion, followed by smoking markers.\n[12] A more forceful approach is needed to stop patients smoking; therapeutic measures to improve patency of vein grafts should focus on decreasing plasma fibrinogen concentration rather than serum cholesterol concentration."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"RESULTS Markers for smoking (blood carboxyhaemoglobin concentration (p less than 0.05) and plasma thiocyanate concentration (p less than 0.01) and plasma concentrations of fibrinogen (p less than 0.001) and apolipoproteins AI (p less than 0.04) and (a) (p less than 0.05) were significantly higher in patients with occluded grafts.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 533, "doc_id": 12991445, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [12991445], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Hyperfibrinogenemia increases rates of femoropopliteal bypass thrombosis.\n\nDocument title: Influence of smoking and plasma factors on patency of femoropopliteal vein grafts.\n\nAbstract sentences:\n[0] OBJECTIVE To determine the effects of smoking, plasma lipids, lipoproteins, apolipoproteins, and fibrinogen on the patency of saphenous vein femoropopliteal bypass grafts at one year.\n[1] DESIGN Prospective study of patients with saphenous vein femoropopliteal bypass grafts entered into a multicentre trial.\n[2] SETTING Surgical wards, outpatient clinics, and home visits coordinated by two tertiary referral centres in London and Birmingham.\n[3] PATIENTS 157 Patients (mean age 66.6 (SD 8.2) years), 113 with patent grafts and 44 with occluded grafts one year after bypass.\n[4] MAIN OUTCOME MEASURE Cumulative percentage patency at one year.\n[5] RESULTS Markers for smoking (blood carboxyhaemoglobin concentration (p less than 0.05) and plasma thiocyanate concentration (p less than 0.01) and plasma concentrations of fibrinogen (p less than 0.001) and apolipoproteins AI (p less than 0.04) and (a) (p less than 0.05) were significantly higher in patients with occluded grafts.\n[6] Serum cholesterol concentrations were significantly higher in patients with grafts that remained patent one year after bypass (p less than 0.005).\n[7] Analysis of the smoking markers indicated that a quarter of patients (40) were untruthful in their claims to have stopped smoking.\n[8] Based on smoking markers, patency of grafts in smokers was significantly lower at one year by life table analysis than in non-smokers (63% v 84%, p less than 0.02).\n[9] Patency was significantly higher by life table analysis in patients with a plasma fibrinogen concentration below the median than in those with a concentration above (90% v 57%, p less than 0.0002).\n[10] Surprisingly, increased plasma low density lipoprotein cholesterol concentration was significantly associated with improved patency at one year (85%) at values above the median compared with patency (only 68%) at values in the lower half of the range (p less than 0.02).\n[11] CONCLUSIONS Plasma fibrinogen concentration was the most important variable predicting graft occlusion, followed by smoking markers.\n[12] A more forceful approach is needed to stop patients smoking; therapeutic measures to improve patency of vein grafts should focus on decreasing plasma fibrinogen concentration rather than serum cholesterol concentration."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Patency was significantly higher by life table analysis in patients with a plasma fibrinogen concentration below the median than in those with a concentration above (90% v 57%, p less than 0.0002).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 533, "doc_id": 12991445, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [12991445], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Hyperfibrinogenemia increases rates of femoropopliteal bypass thrombosis.\n\nDocument title: Influence of smoking and plasma factors on patency of femoropopliteal vein grafts.\n\nAbstract sentences:\n[0] OBJECTIVE To determine the effects of smoking, plasma lipids, lipoproteins, apolipoproteins, and fibrinogen on the patency of saphenous vein femoropopliteal bypass grafts at one year.\n[1] DESIGN Prospective study of patients with saphenous vein femoropopliteal bypass grafts entered into a multicentre trial.\n[2] SETTING Surgical wards, outpatient clinics, and home visits coordinated by two tertiary referral centres in London and Birmingham.\n[3] PATIENTS 157 Patients (mean age 66.6 (SD 8.2) years), 113 with patent grafts and 44 with occluded grafts one year after bypass.\n[4] MAIN OUTCOME MEASURE Cumulative percentage patency at one year.\n[5] RESULTS Markers for smoking (blood carboxyhaemoglobin concentration (p less than 0.05) and plasma thiocyanate concentration (p less than 0.01) and plasma concentrations of fibrinogen (p less than 0.001) and apolipoproteins AI (p less than 0.04) and (a) (p less than 0.05) were significantly higher in patients with occluded grafts.\n[6] Serum cholesterol concentrations were significantly higher in patients with grafts that remained patent one year after bypass (p less than 0.005).\n[7] Analysis of the smoking markers indicated that a quarter of patients (40) were untruthful in their claims to have stopped smoking.\n[8] Based on smoking markers, patency of grafts in smokers was significantly lower at one year by life table analysis than in non-smokers (63% v 84%, p less than 0.02).\n[9] Patency was significantly higher by life table analysis in patients with a plasma fibrinogen concentration below the median than in those with a concentration above (90% v 57%, p less than 0.0002).\n[10] Surprisingly, increased plasma low density lipoprotein cholesterol concentration was significantly associated with improved patency at one year (85%) at values above the median compared with patency (only 68%) at values in the lower half of the range (p less than 0.02).\n[11] CONCLUSIONS Plasma fibrinogen concentration was the most important variable predicting graft occlusion, followed by smoking markers.\n[12] A more forceful approach is needed to stop patients smoking; therapeutic measures to improve patency of vein grafts should focus on decreasing plasma fibrinogen concentration rather than serum cholesterol concentration."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"CONCLUSIONS Plasma fibrinogen concentration was the most important variable predicting graft occlusion, followed by smoking markers.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 533, "doc_id": 12991445, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [12991445], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Hyperfibrinogenemia increases rates of femoropopliteal bypass thrombosis.\n\nDocument title: Influence of smoking and plasma factors on patency of femoropopliteal vein grafts.\n\nAbstract sentences:\n[0] OBJECTIVE To determine the effects of smoking, plasma lipids, lipoproteins, apolipoproteins, and fibrinogen on the patency of saphenous vein femoropopliteal bypass grafts at one year.\n[1] DESIGN Prospective study of patients with saphenous vein femoropopliteal bypass grafts entered into a multicentre trial.\n[2] SETTING Surgical wards, outpatient clinics, and home visits coordinated by two tertiary referral centres in London and Birmingham.\n[3] PATIENTS 157 Patients (mean age 66.6 (SD 8.2) years), 113 with patent grafts and 44 with occluded grafts one year after bypass.\n[4] MAIN OUTCOME MEASURE Cumulative percentage patency at one year.\n[5] RESULTS Markers for smoking (blood carboxyhaemoglobin concentration (p less than 0.05) and plasma thiocyanate concentration (p less than 0.01) and plasma concentrations of fibrinogen (p less than 0.001) and apolipoproteins AI (p less than 0.04) and (a) (p less than 0.05) were significantly higher in patients with occluded grafts.\n[6] Serum cholesterol concentrations were significantly higher in patients with grafts that remained patent one year after bypass (p less than 0.005).\n[7] Analysis of the smoking markers indicated that a quarter of patients (40) were untruthful in their claims to have stopped smoking.\n[8] Based on smoking markers, patency of grafts in smokers was significantly lower at one year by life table analysis than in non-smokers (63% v 84%, p less than 0.02).\n[9] Patency was significantly higher by life table analysis in patients with a plasma fibrinogen concentration below the median than in those with a concentration above (90% v 57%, p less than 0.0002).\n[10] Surprisingly, increased plasma low density lipoprotein cholesterol concentration was significantly associated with improved patency at one year (85%) at values above the median compared with patency (only 68%) at values in the lower half of the range (p less than 0.02).\n[11] CONCLUSIONS Plasma fibrinogen concentration was the most important variable predicting graft occlusion, followed by smoking markers.\n[12] A more forceful approach is needed to stop patients smoking; therapeutic measures to improve patency of vein grafts should focus on decreasing plasma fibrinogen concentration rather than serum cholesterol concentration."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"A more forceful approach is needed to stop patients smoking; therapeutic measures to improve patency of vein grafts should focus on decreasing plasma fibrinogen concentration rather than serum cholesterol concentration.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 533, "doc_id": 12991445, "label": "SUPPORTS", "evidence_sentence_ids": [12], "cited_doc_ids": [12991445], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Hypertension is frequently observed in type 1 diabetes patients.\n\nDocument title: Glucose tolerance and blood pressure: long term follow up in middle aged men.\n\nAbstract sentences:\n[0] OBJECTIVE to investigate the role of glucose tolerance in the development of hypertension.\n[1] DESIGN Retrospective analysis of the results of a health check up in a group of clinically healthy middle aged men in the late 1960s (median year 1968).\n[2] The subjects were invited to enter into a primary prevention trial for cardiovascular disease in 1974, when they underwent clinical examination for risk factors.\n[3] The trial was completed in 1979, when the men were re-examined.\n[4] Follow up was in 1986.\n[5] SETTING Institute of Occupational Health, Helsinki, Finland and second department of medicine, University of Helsinki.\n[6] SUBJECTS In all, 3490 men born during 1919-34 participated in a health check up in the late 1960s.\n[7] In 1974, 1815 of these men who were clinically healthy were entered into a primary prevention trial for cardiovascular disease.\n[8] On clinical examination 1222 of the men were considered at high risk of cardiovascular disease.\n[9] Of these, 612 received an intervention and were excluded from the study.\n[10] A total of 593 men were without risk factors.\n[11] The study comprised all of the men who did not have an intervention (n = 1203).\n[12] In 1979, 1120 men were re-examined, and in 1986 945 men attended follow up.\n[13] There were two groups for analysis: one comprising all subjects and the other comprising only men who were normotensive in 1968 and for whom complete information was available.\n[14] INTERVENTIONS By 1979, 103 men were taking antihypertensive drugs, and by 1986, 131 were taking antihypertensive drugs and 12 were taking drugs for hyperglycaemia.\n[15] MAIN OUTCOME MEASURES Blood glucose concentration one hour after a glucose load, blood pressure, and body weight were measured in 1968, 1974, and 1979.\n[16] In 1986 blood pressure and body weight were recorded.\n[17] RESULTS Men who were hypertensive in 1986 had significantly higher blood pressures (p less than 0.0001) and (after adjustment for body mass index and alcohol intake) significantly higher blood glucose concentrations one hour after a glucose load at all examinations than those who were normotensive in 1986.\n[18] Regression analysis showed that the higher the blood glucose concentration after a glucose load in 1968 the higher the blood pressure during the following years.\n[19] Those men between the second and third tertiles of blood glucose concentration in 1968 had a significantly higher risk of developing hypertension (odds ratio 1.71, 95% confidence interval 1.05 to 2.77) compared with those below the first tertile.\n[20] CONCLUSION In this study men who developed hypertension tended to have shown an increased intolerance to glucose up to 18 years before the clinical manifestation of their disorder.\n[21] Blood glucose concentration one hour after a glucose load was an independent predictor of future hypertension."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 535, "doc_id": 39368721, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [39368721], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 induce 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 536, "doc_id": 16056514, "label": "SUPPORTS", "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: Hypoglycemia increases the risk of dementia.\n\nDocument title: Hypoglycemic episodes and risk of dementia in older patients with type 2 diabetes mellitus.\n\nAbstract sentences:\n[0] CONTEXT Although acute hypoglycemia may be associated with cognitive impairment in children with type 1 diabetes, no studies to date have evaluated whether hypoglycemia is a risk factor for dementia in older patients with type 2 diabetes.\n[1] OBJECTIVE To determine if hypoglycemic episodes severe enough to require hospitalization are associated with an increased risk of dementia in a population of older patients with type 2 diabetes followed up for 27 years.\n[2] DESIGN, SETTING, AND PATIENTS A longitudinal cohort study from 1980-2007 of 16,667 patients with a mean age of 65 years and type 2 diabetes who are members of an integrated health care delivery system in northern California.\n[3] MAIN OUTCOME MEASURE Hypoglycemic events from 1980-2002 were collected and reviewed using hospital discharge and emergency department diagnoses.\n[4] Cohort members with no prior diagnoses of dementia, mild cognitive impairment, or general memory complaints as of January 1, 2003, were followed up for a dementia diagnosis through January 15, 2007.\n[5] Dementia risk was examined using Cox proportional hazard regression models, adjusted for age, sex, race/ethnicity, education, body mass index, duration of diabetes, 7-year mean glycated hemoglobin, diabetes treatment, duration of insulin use, hyperlipidemia, hypertension, cardiovascular disease, stroke, transient cerebral ischemia, and end-stage renal disease.\n[6] RESULTS At least 1 episode of hypoglycemia was diagnosed in 1465 patients (8.8%) and dementia was diagnosed in 1822 patients (11%) during follow-up; 250 patients had both dementia and at least 1 episode of hypoglycemia (16.95%).\n[7] Compared with patients with no hypoglycemia, patients with single or multiple episodes had a graded increase in risk with fully adjusted hazard ratios (HRs): for 1 episode (HR, 1.26; 95% confidence interval [CI], 1.10-1.49); 2 episodes (HR, 1.80; 95% CI, 1.37-2.36); and 3 or more episodes (HR, 1.94; 95% CI, 1.42-2.64).\n[8] The attributable risk of dementia between individuals with and without a history of hypoglycemia was 2.39% per year (95% CI, 1.72%-3.01%).\n[9] Results were not attenuated when medical utilization rates, length of health plan membership, or time since initial diabetes diagnosis were added to the model.\n[10] When examining emergency department admissions for hypoglycemia for association with risk of dementia (535 episodes), results were similar (compared with patients with 0 episodes) with fully adjusted HRs: for 1 episode (HR, 1.42; 95% CI, 1.12-1.78) and for 2 or more episodes (HR, 2.36; 95% CI, 1.57-3.55).\n[11] CONCLUSIONS Among older patients with type 2 diabetes, a history of severe hypoglycemic episodes was associated with a greater risk of dementia.\n[12] Whether minor hypoglycemic episodes increase risk of dementia is unknown."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Compared with patients with no hypoglycemia, patients with single or multiple episodes had a graded increase in risk with fully adjusted hazard ratios (HRs): for 1 episode (HR, 1.26; 95% confidence interval [CI], 1.10-1.49); 2 episodes (HR, 1.80; 95% CI, 1.37-2.36); and 3 or more episodes (HR, 1.94; 95% CI, 1.42-2.64).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 539, "doc_id": 13282296, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [13282296], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Hypoglycemia increases the risk of dementia.\n\nDocument title: Hypoglycemic episodes and risk of dementia in older patients with type 2 diabetes mellitus.\n\nAbstract sentences:\n[0] CONTEXT Although acute hypoglycemia may be associated with cognitive impairment in children with type 1 diabetes, no studies to date have evaluated whether hypoglycemia is a risk factor for dementia in older patients with type 2 diabetes.\n[1] OBJECTIVE To determine if hypoglycemic episodes severe enough to require hospitalization are associated with an increased risk of dementia in a population of older patients with type 2 diabetes followed up for 27 years.\n[2] DESIGN, SETTING, AND PATIENTS A longitudinal cohort study from 1980-2007 of 16,667 patients with a mean age of 65 years and type 2 diabetes who are members of an integrated health care delivery system in northern California.\n[3] MAIN OUTCOME MEASURE Hypoglycemic events from 1980-2002 were collected and reviewed using hospital discharge and emergency department diagnoses.\n[4] Cohort members with no prior diagnoses of dementia, mild cognitive impairment, or general memory complaints as of January 1, 2003, were followed up for a dementia diagnosis through January 15, 2007.\n[5] Dementia risk was examined using Cox proportional hazard regression models, adjusted for age, sex, race/ethnicity, education, body mass index, duration of diabetes, 7-year mean glycated hemoglobin, diabetes treatment, duration of insulin use, hyperlipidemia, hypertension, cardiovascular disease, stroke, transient cerebral ischemia, and end-stage renal disease.\n[6] RESULTS At least 1 episode of hypoglycemia was diagnosed in 1465 patients (8.8%) and dementia was diagnosed in 1822 patients (11%) during follow-up; 250 patients had both dementia and at least 1 episode of hypoglycemia (16.95%).\n[7] Compared with patients with no hypoglycemia, patients with single or multiple episodes had a graded increase in risk with fully adjusted hazard ratios (HRs): for 1 episode (HR, 1.26; 95% confidence interval [CI], 1.10-1.49); 2 episodes (HR, 1.80; 95% CI, 1.37-2.36); and 3 or more episodes (HR, 1.94; 95% CI, 1.42-2.64).\n[8] The attributable risk of dementia between individuals with and without a history of hypoglycemia was 2.39% per year (95% CI, 1.72%-3.01%).\n[9] Results were not attenuated when medical utilization rates, length of health plan membership, or time since initial diabetes diagnosis were added to the model.\n[10] When examining emergency department admissions for hypoglycemia for association with risk of dementia (535 episodes), results were similar (compared with patients with 0 episodes) with fully adjusted HRs: for 1 episode (HR, 1.42; 95% CI, 1.12-1.78) and for 2 or more episodes (HR, 2.36; 95% CI, 1.57-3.55).\n[11] CONCLUSIONS Among older patients with type 2 diabetes, a history of severe hypoglycemic episodes was associated with a greater risk of dementia.\n[12] Whether minor hypoglycemic episodes increase risk of dementia is unknown."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"CONCLUSIONS Among older patients with type 2 diabetes, a history of severe hypoglycemic episodes was associated with a greater risk of dementia.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 539, "doc_id": 13282296, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [13282296], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 crucial 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 540, "doc_id": 11886686, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [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: IFIT1 restricts viral replication by sequestrating 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": "validation", "claim_id": 544, "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: IRG1 has antiviral effects against neurotropic viruses.\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: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"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.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 549, "doc_id": 9433958, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [9433958], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 prevents 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": "validation", "claim_id": 551, "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 accumulate in the duodenal mucosa on commencement of a gluten-free diet.\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: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 552, "doc_id": 1471041, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [1471041], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 neutrophil protein HMGB1.\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": "validation", "claim_id": 554, "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 result in the development of inflammatory Th17 cells and anti-inflammatory iTregs.\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": "validation", "claim_id": 560, "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: In adult tissue, most T cells are memory T cells.\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": "validation", "claim_id": 569, "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 domesticated populations of Saccharomyces cerevisiae, whole chromosome aneuploidy is very uncommon.\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": "validation", "claim_id": 575, "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 mice, P. chabaudi parasites are able to proliferate faster early in infection when inoculated at lower numbers than when inoculated at high numbers.\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: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 577, "doc_id": 5289038, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [5289038], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 mouse models, the loss of CSF1R facilitates MOZ-TIF2-induced leuekmogenesis.\n\nDocument title: PU.1-mediated upregulation of CSF1R is crucial for leukemia stem cell potential induced by MOZ-TIF2\n\nAbstract sentences:\n[0] Leukemias and other cancers possess self-renewing stem cells that help to maintain the cancer.\n[1] Cancer stem cell eradication is thought to be crucial for successful anticancer therapy.\n[2] Using an acute myeloid leukemia (AML) model induced by the leukemia-associated monocytic leukemia zinc finger (MOZ)-TIF2 fusion protein, we show here that AML can be cured by the ablation of leukemia stem cells.\n[3] The MOZ fusion proteins MOZ-TIF2 and MOZ-CBP interacted with the transcription factor PU.1 to stimulate the expression of macrophage colony–stimulating factor receptor (CSF1R, also known as M-CSFR, c-FMS or CD115).\n[4] Studies using PU.1-deficient mice showed that PU.1 is essential for the ability of MOZ-TIF2 to establish and maintain AML stem cells.\n[5] Cells expressing high amounts of CSF1R (CSF1Rhigh cells), but not those expressing low amounts of CSF1R (CSF1Rlow cells), showed potent leukemia-initiating activity.\n[6] Using transgenic mice expressing a drug-inducible suicide gene controlled by the CSF1R promoter, we cured AML by ablation of CSF1Rhigh cells.\n[7] Moreover, induction of AML was suppressed in CSF1R-deficient mice and CSF1R inhibitors slowed the progression of MOZ-TIF2–induced leukemia.\n[8] Thus, in this subtype of AML, leukemia stem cells are contained within the CSF1Rhigh cell population, and we suggest that targeting of PU.1-mediated upregulation of CSF1R expression might be a useful therapeutic approach."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Cells expressing high amounts of CSF1R (CSF1Rhigh cells), but not those expressing low amounts of CSF1R (CSF1Rlow cells), showed potent leukemia-initiating activity.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 578, "doc_id": 8764879, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [8764879], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 mouse models, the loss of CSF1R facilitates MOZ-TIF2-induced leuekmogenesis.\n\nDocument title: PU.1-mediated upregulation of CSF1R is crucial for leukemia stem cell potential induced by MOZ-TIF2\n\nAbstract sentences:\n[0] Leukemias and other cancers possess self-renewing stem cells that help to maintain the cancer.\n[1] Cancer stem cell eradication is thought to be crucial for successful anticancer therapy.\n[2] Using an acute myeloid leukemia (AML) model induced by the leukemia-associated monocytic leukemia zinc finger (MOZ)-TIF2 fusion protein, we show here that AML can be cured by the ablation of leukemia stem cells.\n[3] The MOZ fusion proteins MOZ-TIF2 and MOZ-CBP interacted with the transcription factor PU.1 to stimulate the expression of macrophage colony–stimulating factor receptor (CSF1R, also known as M-CSFR, c-FMS or CD115).\n[4] Studies using PU.1-deficient mice showed that PU.1 is essential for the ability of MOZ-TIF2 to establish and maintain AML stem cells.\n[5] Cells expressing high amounts of CSF1R (CSF1Rhigh cells), but not those expressing low amounts of CSF1R (CSF1Rlow cells), showed potent leukemia-initiating activity.\n[6] Using transgenic mice expressing a drug-inducible suicide gene controlled by the CSF1R promoter, we cured AML by ablation of CSF1Rhigh cells.\n[7] Moreover, induction of AML was suppressed in CSF1R-deficient mice and CSF1R inhibitors slowed the progression of MOZ-TIF2–induced leukemia.\n[8] Thus, in this subtype of AML, leukemia stem cells are contained within the CSF1Rhigh cell population, and we suggest that targeting of PU.1-mediated upregulation of CSF1R expression might be a useful therapeutic approach."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Moreover, induction of AML was suppressed in CSF1R-deficient mice and CSF1R inhibitors slowed the progression of MOZ-TIF2–induced leukemia.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 578, "doc_id": 8764879, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [8764879], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 mouse models, the loss of CSF1R facilitates MOZ-TIF2-induced leuekmogenesis.\n\nDocument title: PU.1-mediated upregulation of CSF1R is crucial for leukemia stem cell potential induced by MOZ-TIF2\n\nAbstract sentences:\n[0] Leukemias and other cancers possess self-renewing stem cells that help to maintain the cancer.\n[1] Cancer stem cell eradication is thought to be crucial for successful anticancer therapy.\n[2] Using an acute myeloid leukemia (AML) model induced by the leukemia-associated monocytic leukemia zinc finger (MOZ)-TIF2 fusion protein, we show here that AML can be cured by the ablation of leukemia stem cells.\n[3] The MOZ fusion proteins MOZ-TIF2 and MOZ-CBP interacted with the transcription factor PU.1 to stimulate the expression of macrophage colony–stimulating factor receptor (CSF1R, also known as M-CSFR, c-FMS or CD115).\n[4] Studies using PU.1-deficient mice showed that PU.1 is essential for the ability of MOZ-TIF2 to establish and maintain AML stem cells.\n[5] Cells expressing high amounts of CSF1R (CSF1Rhigh cells), but not those expressing low amounts of CSF1R (CSF1Rlow cells), showed potent leukemia-initiating activity.\n[6] Using transgenic mice expressing a drug-inducible suicide gene controlled by the CSF1R promoter, we cured AML by ablation of CSF1Rhigh cells.\n[7] Moreover, induction of AML was suppressed in CSF1R-deficient mice and CSF1R inhibitors slowed the progression of MOZ-TIF2–induced leukemia.\n[8] Thus, in this subtype of AML, leukemia stem cells are contained within the CSF1Rhigh cell population, and we suggest that targeting of PU.1-mediated upregulation of CSF1R expression might be a useful therapeutic approach."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Thus, in this subtype of AML, leukemia stem cells are contained within the CSF1Rhigh cell population, and we suggest that targeting of PU.1-mediated upregulation of CSF1R expression might be a useful therapeutic approach.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 578, "doc_id": 8764879, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [8764879], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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, less than ten 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": "validation", "claim_id": 587, "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 do not 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 589, "doc_id": 10984005, "label": "SUPPORTS", "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 do not 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 589, "doc_id": 10984005, "label": "SUPPORTS", "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 heart failure decreased 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 593, "doc_id": 19675911, "label": "SUPPORTS", "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 rates of cervical cancer have decreased.\n\nDocument title: Effect of screening on cervical cancer mortality in England and Wales: analysis of trends with an age period cohort model.\n\nAbstract sentences:\n[0] The number of women dying from cervical cancer in 1997 was 7% lower than in 1996 and has fallen by over 25% since 1992.1 Such rapid change must be at least partly due to cervical screening, although strong cohort effects have caused large fluctuations in cervical mortality in the past.2 We modelled mortality data, taking into account the effects of age and year of birth and looking for trends in time within four age groups to estimate the beneficial effects of cervical screening.\n[1] We obtained mortality data, in 5 year age bands, from death registrations in England and Wales and calculated rates using mid-year population estimates.\n[2] Mortality since 1993 was adjusted upwards by 4% because of changes in classification of cause of death.3  We modelled the data assuming that the age specific mortality is the product of a smoothly varying age effect, birth cohort effect, and age dependent …"}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"The number of women dying from cervical cancer in 1997 was 7% lower than in 1996 and has fallen by over 25% since 1992.1 Such rapid change must be at least partly due to cervical screening, although strong cohort effects have caused large fluctuations in cervical mortality in the past.2 We modelled mortality data, taking into account the effects of age and year of birth and looking for trends in time within four age groups to estimate the beneficial effects of cervical screening.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 597, "doc_id": 12779444, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [12779444, 36355784, 25742130], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 rates of cervical cancer have decreased.\n\nDocument title: The effect of mass screening on incidence and mortality of squamous and adenocarcinoma of cervix uteri.\n\nAbstract sentences:\n[0] OBJECTIVE To describe the efficacy of the Finnish mass screening program for cervical squamous carcinoma and adenocarcinoma, as reflected by changes of incidence and mortality rate.\n[1] METHODS Cervical cancer incidence and mortality data were obtained from the Finnish Cancer Registry.\n[2] Data were available from the year 1953, when the registry was established.\n[3] The nationwide mass screening program in Finland was started in the mid-1960s.\n[4] A centralized organization administers this program.\n[5] Women age 30-60 years are notified for screening every 5 years.\n[6] RESULTS The mean incidence of cervical carcinoma in the early 1960s was 15.4 per 10(5) woman-years.\n[7] In 1991, it was only 2.7 per 10(5) woman-years.\n[8] The mortality rate has decreased in the same proportion since the mass screening program.\n[9] In the early 1960s, the mortality was 6.6 and in 1991 1.4 per 10(5) woman-years.\n[10] However, the decrease of the incidence is seen almost exclusively in squamous cell carcinomas.\n[11] The mortality caused by adenocarcinoma has decreased in screened birth cohorts, but the incidence rate has remained the same.\n[12] CONCLUSIONS The Finnish mass screening program has been effective and its continuation is of utmost importance.\n[13] In the future more attention should be given to glandular cell atypias in cervical smears.\n[14] Thus, it might be possible to decrease the incidence of cervical adenocarcinoma."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6, 7]\nExplanation: Evidence states: \"RESULTS The mean incidence of cervical carcinoma in the early 1960s was 15.4 per 10(5) woman-years. In 1991, it was only 2.7 per 10(5) woman-years.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 597, "doc_id": 36355784, "label": "SUPPORTS", "evidence_sentence_ids": [6, 7], "cited_doc_ids": [12779444, 36355784, 25742130], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 rates of cervical cancer have decreased.\n\nDocument title: Mass screening programmes and trends in cervical cancer in Finland and the Netherlands.\n\nAbstract sentences:\n[0] With respect to cervical cancer management, Finland and the Netherlands are comparable in relevant characteristics, e.g., fertility rate, age-of-mother at first birth and a national screening programme for several years.\n[1] The aim of this study is to compare trends in incidence of and mortality from cervical cancer in Finland and the Netherlands in relation to the introduction and intensity of the screening programmes.\n[2] Therefore, incidence and mortality rates were calculated using the Cancer Registries of Finland and the Netherlands.\n[3] Data on screening intensity were obtained from the Finnish Cancer Registry and the Dutch evaluation centre at ErasmusMC-Rotterdam.\n[4] Women aged 30-60 have been screened every 5 years, in Finland since 1992 and in the Netherlands since 1996.\n[5] Screening protocols for smear taking and referral to the gynaecologist are comparable.\n[6] Incidence and mortality rates have declined more in Finland.\n[7] In 2003, age-adjusted incidence and mortality in Finland were 4.0 and 0.9 and in the Netherlands 4.9 and 1.4 per 100,000 woman-years, respectively.\n[8] Excess smear use in the Netherlands was estimated to be 24 per 1,000 women during a 5-year interval compared to 121 in Finland.\n[9] The decline in mortality in Finland seems to be almost completely related to the screening programme whereas in the Netherlands it was initially considered to be a natural decline.\n[10] Differences in risk factors might also play a role: the Netherlands has higher population density and higher percentages of immigrants and (female) smokers.\n[11] The greater excess smear use in Finland might also have affected incidence."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Incidence and mortality rates have declined more in Finland.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 597, "doc_id": 25742130, "label": "SUPPORTS", "evidence_sentence_ids": [6], "cited_doc_ids": [12779444, 36355784, 25742130], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 rates of cervical cancer have increased due to nationwide screening programs based primarily on cytology to detect uterine cervical cancer.\n\nDocument title: Mass screening programmes and trends in cervical cancer in Finland and the Netherlands.\n\nAbstract sentences:\n[0] With respect to cervical cancer management, Finland and the Netherlands are comparable in relevant characteristics, e.g., fertility rate, age-of-mother at first birth and a national screening programme for several years.\n[1] The aim of this study is to compare trends in incidence of and mortality from cervical cancer in Finland and the Netherlands in relation to the introduction and intensity of the screening programmes.\n[2] Therefore, incidence and mortality rates were calculated using the Cancer Registries of Finland and the Netherlands.\n[3] Data on screening intensity were obtained from the Finnish Cancer Registry and the Dutch evaluation centre at ErasmusMC-Rotterdam.\n[4] Women aged 30-60 have been screened every 5 years, in Finland since 1992 and in the Netherlands since 1996.\n[5] Screening protocols for smear taking and referral to the gynaecologist are comparable.\n[6] Incidence and mortality rates have declined more in Finland.\n[7] In 2003, age-adjusted incidence and mortality in Finland were 4.0 and 0.9 and in the Netherlands 4.9 and 1.4 per 100,000 woman-years, respectively.\n[8] Excess smear use in the Netherlands was estimated to be 24 per 1,000 women during a 5-year interval compared to 121 in Finland.\n[9] The decline in mortality in Finland seems to be almost completely related to the screening programme whereas in the Netherlands it was initially considered to be a natural decline.\n[10] Differences in risk factors might also play a role: the Netherlands has higher population density and higher percentages of immigrants and (female) smokers.\n[11] The greater excess smear use in Finland might also have affected incidence."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"Incidence and mortality rates have declined more in Finland.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 598, "doc_id": 25742130, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [25742130], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 rates of cervical cancer have increased due to nationwide screening programs based primarily on cytology to detect uterine cervical cancer.\n\nDocument title: Mass screening programmes and trends in cervical cancer in Finland and the Netherlands.\n\nAbstract sentences:\n[0] With respect to cervical cancer management, Finland and the Netherlands are comparable in relevant characteristics, e.g., fertility rate, age-of-mother at first birth and a national screening programme for several years.\n[1] The aim of this study is to compare trends in incidence of and mortality from cervical cancer in Finland and the Netherlands in relation to the introduction and intensity of the screening programmes.\n[2] Therefore, incidence and mortality rates were calculated using the Cancer Registries of Finland and the Netherlands.\n[3] Data on screening intensity were obtained from the Finnish Cancer Registry and the Dutch evaluation centre at ErasmusMC-Rotterdam.\n[4] Women aged 30-60 have been screened every 5 years, in Finland since 1992 and in the Netherlands since 1996.\n[5] Screening protocols for smear taking and referral to the gynaecologist are comparable.\n[6] Incidence and mortality rates have declined more in Finland.\n[7] In 2003, age-adjusted incidence and mortality in Finland were 4.0 and 0.9 and in the Netherlands 4.9 and 1.4 per 100,000 woman-years, respectively.\n[8] Excess smear use in the Netherlands was estimated to be 24 per 1,000 women during a 5-year interval compared to 121 in Finland.\n[9] The decline in mortality in Finland seems to be almost completely related to the screening programme whereas in the Netherlands it was initially considered to be a natural decline.\n[10] Differences in risk factors might also play a role: the Netherlands has higher population density and higher percentages of immigrants and (female) smokers.\n[11] The greater excess smear use in Finland might also have affected incidence."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"The decline in mortality in Finland seems to be almost completely related to the screening programme whereas in the Netherlands it was initially considered to be a natural decline.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 598, "doc_id": 25742130, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [25742130], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 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: 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": "validation", "claim_id": 613, "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 vessel density along with a reduction in fibrosis decreases the efficacy of chemotherapy treatments.\n\nDocument title: Inhibition of Hedgehog signaling enhances delivery of chemotherapy in a mouse model of pancreatic cancer.\n\nAbstract sentences:\n[0] Pancreatic ductal adenocarcinoma (PDA) is among the most lethal human cancers in part because it is insensitive to many chemotherapeutic drugs.\n[1] Studying a mouse model of PDA that is refractory to the clinically used drug gemcitabine, we found that the tumors in this model were poorly perfused and poorly vascularized, properties that are shared with human PDA.\n[2] We tested whether the delivery and efficacy of gemcitabine in the mice could be improved by coadministration of IPI-926, a drug that depletes tumor-associated stromal tissue by inhibition of the Hedgehog cellular signaling pathway.\n[3] The combination therapy produced a transient increase in intratumoral vascular density and intratumoral concentration of gemcitabine, leading to transient stabilization of disease.\n[4] Thus, inefficient drug delivery may be an important contributor to chemoresistance in pancreatic cancer."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [2, 3]\nExplanation: Evidence states: \"We tested whether the delivery and efficacy of gemcitabine in the mice could be improved by coadministration of IPI-926, a drug that depletes tumor-associated stromal tissue by inhibition of the Hedgehog cellular signaling pathway. The combination therapy produced a transient increase in intratumoral vascular density and intratumoral concentration of gemcitabine, leading to transient stabilization of disease.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 619, "doc_id": 20888849, "label": "CONTRADICTS", "evidence_sentence_ids": [2, 3], "cited_doc_ids": [20888849, 2565138], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 increased 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": "validation", "claim_id": 623, "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: Infection of human T-cell lymphotropic virus type 1 is most frequent in individuals of African origin.\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": "validation", "claim_id": 628, "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: Inositol lipid 3-phosphatase PTEN converts Ptdlns(3,4)P 2 into phosphatidylinositol 4-phosphate.\n\nDocument title: PTEN Regulates PI(3,4)P2 Signaling Downstream of Class I PI3K\n\nAbstract sentences:\n[0] The PI3K signaling pathway regulates cell growth and movement and is heavily mutated in cancer.\n[1] Class I PI3Ks synthesize the lipid messenger PI(3,4,5)P3.\n[2] PI(3,4,5)P3 can be dephosphorylated by 3- or 5-phosphatases, the latter producing PI(3,4)P2.\n[3] The PTEN tumor suppressor is thought to function primarily as a PI(3,4,5)P3 3-phosphatase, limiting activation of this pathway.\n[4] Here we show that PTEN also functions as a PI(3,4)P2 3-phosphatase, both in vitro and in vivo.\n[5] PTEN is a major PI(3,4)P2 phosphatase in Mcf10a cytosol, and loss of PTEN and INPP4B, a known PI(3,4)P2 4-phosphatase, leads to synergistic accumulation of PI(3,4)P2, which correlated with increased invadopodia in epidermal growth factor (EGF)-stimulated cells.\n[6] PTEN deletion increased PI(3,4)P2 levels in a mouse model of prostate cancer, and it inversely correlated with PI(3,4)P2 levels across several EGF-stimulated prostate and breast cancer lines.\n[7] These results point to a role for PI(3,4)P2 in the phenotype caused by loss-of-function mutations or deletions in PTEN."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Here we show that PTEN also functions as a PI(3,4)P2 3-phosphatase, both in vitro and in vivo.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 636, "doc_id": 24294572, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [24294572], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 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": "validation", "claim_id": 637, "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: Insomnia can be effectively treated with cognitive behavioral therapy.\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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 641, "doc_id": 5912283, "label": "SUPPORTS", "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: Insomnia can be effectively treated with cognitive behavioral therapy.\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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 641, "doc_id": 5912283, "label": "SUPPORTS", "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: Insomnia can be effectively treated with cognitive behavioral therapy.\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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 641, "doc_id": 5912283, "label": "SUPPORTS", "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: Insomnia can be effectively treated with cognitive behavioral therapy.\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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 641, "doc_id": 5912283, "label": "SUPPORTS", "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: Insulin increases 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": "validation", "claim_id": 644, "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: Integrating classroom-based collaborative learning with Web-based collaborative learning leads to subpar 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": "validation", "claim_id": 649, "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: Ivermectin is used to treat lymphatic filariasis.\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": "validation", "claim_id": 659, "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: Ivermectin is used to treat onchocerciasis.\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": "validation", "claim_id": 660, "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: LDL cholesterol has no involvement 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: CONTRADICTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"BACKGROUND LDL cholesterol has a causal role in the development of cardiovascular disease.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 674, "doc_id": 2095573, "label": "CONTRADICTS", "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: Lack of clpC does not affect sporulation efficiency in Bacillus subtilis cells.\n\nDocument title: High-Throughput Genetic Screens Identify a Large and Diverse Collection of New Sporulation Genes in Bacillus subtilis\n\nAbstract sentences:\n[0] The differentiation of the bacterium Bacillus subtilis into a dormant spore is among the most well-characterized developmental pathways in biology.\n[1] Classical genetic screens performed over the past half century identified scores of factors involved in every step of this morphological process.\n[2] More recently, transcriptional profiling uncovered additional sporulation-induced genes required for successful spore development.\n[3] Here, we used transposon-sequencing (Tn-seq) to assess whether there were any sporulation genes left to be discovered.\n[4] Our screen identified 133 out of the 148 genes with known sporulation defects.\n[5] Surprisingly, we discovered 24 additional genes that had not been previously implicated in spore formation.\n[6] To investigate their functions, we used fluorescence microscopy to survey early, middle, and late stages of differentiation of null mutants from the B. subtilis ordered knockout collection.\n[7] This analysis identified mutants that are delayed in the initiation of sporulation, defective in membrane remodeling, and impaired in spore maturation.\n[8] Several mutants had novel sporulation phenotypes.\n[9] We performed in-depth characterization of two new factors that participate in cell-cell signaling pathways during sporulation.\n[10] One (SpoIIT) functions in the activation of σE in the mother cell; the other (SpoIIIL) is required for σG activity in the forespore.\n[11] Our analysis also revealed that as many as 36 sporulation-induced genes with no previously reported mutant phenotypes are required for timely spore maturation.\n[12] Finally, we discovered a large set of transposon insertions that trigger premature initiation of sporulation.\n[13] Our results highlight the power of Tn-seq for the discovery of new genes and novel pathways in sporulation and, combined with the recently completed null mutant collection, open the door for similar screens in other, less well-characterized processes."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 684, "doc_id": 4942718, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [4942718], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 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": "validation", "claim_id": 690, "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: Leukemia associated Rho guanine nucleotide-exchange factor represses RhoA in response to SRC activation.\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: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 691, "doc_id": 10991183, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [10991183], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Leuko-increased blood increases infectious complications in red blood cell transfusion.\n\nDocument title: Clinical outcomes following institution of the Canadian universal leukoreduction program for red blood cell transfusions.\n\nAbstract sentences:\n[0] CONTEXT A number of countries have implemented a policy of universal leukoreduction of their blood supply, but the potential role of leukoreduction in decreasing postoperative mortality and infection is unclear.\n[1] OBJECTIVE To evaluate clinical outcomes following adoption of a national universal prestorage leukoreduction program for blood transfusions.\n[2] DESIGN, SETTING, AND POPULATION Retrospective before-and-after cohort study conducted from August 1998 to August 2000 in 23 academic and community hospitals throughout Canada, enrolling 14 786 patients who received red blood cell transfusions following cardiac surgery or repair of hip fracture, or who required intensive care following a surgical intervention or multiple trauma.\n[3] INTERVENTION Universal prestorage leukoreduction program introduced by 2 Canadian blood agencies.\n[4] A total of 6982 patients were enrolled during the control period and 7804 patients were enrolled following prestorage leukoreduction.\n[5] MAIN OUTCOME MEASURES All-cause in-hospital mortality and serious nosocomial infections (pneumonia, bacteremia, septic shock, all surgical site infections) occurring after first transfusion and at least 2 days after index procedure or intensive care unit admission.\n[6] Secondary outcomes included rates of posttransfusion fever and antibiotic use.\n[7] RESULTS Unadjusted in-hospital mortality rates were significantly lower following the introduction of leukoreduction compared with the control period (6.19% vs 7.03%, respectively; P =.04).\n[8] Compared with the control period, the adjusted odds of death following leukoreduction were reduced (odds ratio [OR], 0.87; 95% confidence interval [CI], 0.75-0.99), but serious nosocomial infections did not decrease (adjusted OR, 0.97; 95% CI, 0.87-1.09).\n[9] The frequency of posttransfusion fevers decreased significantly following leukoreduction (adjusted OR, 0.86; 95% CI, 0.79-0.94), as did antibiotic use (adjusted OR, 0.90; 95% CI, 0.82-0.99).\n[10] CONCLUSION A national universal leukoreduction program is potentially associated with decreased mortality as well as decreased fever episodes and antibiotic use after red blood cell transfusion in high-risk patients."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Compared with the control period, the adjusted odds of death following leukoreduction were reduced (odds ratio [OR], 0.87; 95% confidence interval [CI], 0.75-0.99), but serious nosocomial infections did not decrease (adjusted OR, 0.97; 95% CI, 0.87-1.09).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 692, "doc_id": 24088502, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [24088502], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Leuko-increased blood increases infectious complications in red blood cell transfusion.\n\nDocument title: Clinical outcomes following institution of the Canadian universal leukoreduction program for red blood cell transfusions.\n\nAbstract sentences:\n[0] CONTEXT A number of countries have implemented a policy of universal leukoreduction of their blood supply, but the potential role of leukoreduction in decreasing postoperative mortality and infection is unclear.\n[1] OBJECTIVE To evaluate clinical outcomes following adoption of a national universal prestorage leukoreduction program for blood transfusions.\n[2] DESIGN, SETTING, AND POPULATION Retrospective before-and-after cohort study conducted from August 1998 to August 2000 in 23 academic and community hospitals throughout Canada, enrolling 14 786 patients who received red blood cell transfusions following cardiac surgery or repair of hip fracture, or who required intensive care following a surgical intervention or multiple trauma.\n[3] INTERVENTION Universal prestorage leukoreduction program introduced by 2 Canadian blood agencies.\n[4] A total of 6982 patients were enrolled during the control period and 7804 patients were enrolled following prestorage leukoreduction.\n[5] MAIN OUTCOME MEASURES All-cause in-hospital mortality and serious nosocomial infections (pneumonia, bacteremia, septic shock, all surgical site infections) occurring after first transfusion and at least 2 days after index procedure or intensive care unit admission.\n[6] Secondary outcomes included rates of posttransfusion fever and antibiotic use.\n[7] RESULTS Unadjusted in-hospital mortality rates were significantly lower following the introduction of leukoreduction compared with the control period (6.19% vs 7.03%, respectively; P =.04).\n[8] Compared with the control period, the adjusted odds of death following leukoreduction were reduced (odds ratio [OR], 0.87; 95% confidence interval [CI], 0.75-0.99), but serious nosocomial infections did not decrease (adjusted OR, 0.97; 95% CI, 0.87-1.09).\n[9] The frequency of posttransfusion fevers decreased significantly following leukoreduction (adjusted OR, 0.86; 95% CI, 0.79-0.94), as did antibiotic use (adjusted OR, 0.90; 95% CI, 0.82-0.99).\n[10] CONCLUSION A national universal leukoreduction program is potentially associated with decreased mortality as well as decreased fever episodes and antibiotic use after red blood cell transfusion in high-risk patients."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"The frequency of posttransfusion fevers decreased significantly following leukoreduction (adjusted OR, 0.86; 95% CI, 0.79-0.94), as did antibiotic use (adjusted OR, 0.90; 95% CI, 0.82-0.99).\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 692, "doc_id": 24088502, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [24088502], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Leuko-increased blood increases infectious complications in red blood cell transfusion.\n\nDocument title: Clinical outcomes following institution of the Canadian universal leukoreduction program for red blood cell transfusions.\n\nAbstract sentences:\n[0] CONTEXT A number of countries have implemented a policy of universal leukoreduction of their blood supply, but the potential role of leukoreduction in decreasing postoperative mortality and infection is unclear.\n[1] OBJECTIVE To evaluate clinical outcomes following adoption of a national universal prestorage leukoreduction program for blood transfusions.\n[2] DESIGN, SETTING, AND POPULATION Retrospective before-and-after cohort study conducted from August 1998 to August 2000 in 23 academic and community hospitals throughout Canada, enrolling 14 786 patients who received red blood cell transfusions following cardiac surgery or repair of hip fracture, or who required intensive care following a surgical intervention or multiple trauma.\n[3] INTERVENTION Universal prestorage leukoreduction program introduced by 2 Canadian blood agencies.\n[4] A total of 6982 patients were enrolled during the control period and 7804 patients were enrolled following prestorage leukoreduction.\n[5] MAIN OUTCOME MEASURES All-cause in-hospital mortality and serious nosocomial infections (pneumonia, bacteremia, septic shock, all surgical site infections) occurring after first transfusion and at least 2 days after index procedure or intensive care unit admission.\n[6] Secondary outcomes included rates of posttransfusion fever and antibiotic use.\n[7] RESULTS Unadjusted in-hospital mortality rates were significantly lower following the introduction of leukoreduction compared with the control period (6.19% vs 7.03%, respectively; P =.04).\n[8] Compared with the control period, the adjusted odds of death following leukoreduction were reduced (odds ratio [OR], 0.87; 95% confidence interval [CI], 0.75-0.99), but serious nosocomial infections did not decrease (adjusted OR, 0.97; 95% CI, 0.87-1.09).\n[9] The frequency of posttransfusion fevers decreased significantly following leukoreduction (adjusted OR, 0.86; 95% CI, 0.79-0.94), as did antibiotic use (adjusted OR, 0.90; 95% CI, 0.82-0.99).\n[10] CONCLUSION A national universal leukoreduction program is potentially associated with decreased mortality as well as decreased fever episodes and antibiotic use after red blood cell transfusion in high-risk patients."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"CONCLUSION A national universal leukoreduction program is potentially associated with decreased mortality as well as decreased fever episodes and antibiotic use after red blood cell transfusion in high-risk patients.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 692, "doc_id": 24088502, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [24088502], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Leuko-reduced blood reduces infectious complications in red blood cell transfusion.\n\nDocument title: Clinical outcomes following institution of the Canadian universal leukoreduction program for red blood cell transfusions.\n\nAbstract sentences:\n[0] CONTEXT A number of countries have implemented a policy of universal leukoreduction of their blood supply, but the potential role of leukoreduction in decreasing postoperative mortality and infection is unclear.\n[1] OBJECTIVE To evaluate clinical outcomes following adoption of a national universal prestorage leukoreduction program for blood transfusions.\n[2] DESIGN, SETTING, AND POPULATION Retrospective before-and-after cohort study conducted from August 1998 to August 2000 in 23 academic and community hospitals throughout Canada, enrolling 14 786 patients who received red blood cell transfusions following cardiac surgery or repair of hip fracture, or who required intensive care following a surgical intervention or multiple trauma.\n[3] INTERVENTION Universal prestorage leukoreduction program introduced by 2 Canadian blood agencies.\n[4] A total of 6982 patients were enrolled during the control period and 7804 patients were enrolled following prestorage leukoreduction.\n[5] MAIN OUTCOME MEASURES All-cause in-hospital mortality and serious nosocomial infections (pneumonia, bacteremia, septic shock, all surgical site infections) occurring after first transfusion and at least 2 days after index procedure or intensive care unit admission.\n[6] Secondary outcomes included rates of posttransfusion fever and antibiotic use.\n[7] RESULTS Unadjusted in-hospital mortality rates were significantly lower following the introduction of leukoreduction compared with the control period (6.19% vs 7.03%, respectively; P =.04).\n[8] Compared with the control period, the adjusted odds of death following leukoreduction were reduced (odds ratio [OR], 0.87; 95% confidence interval [CI], 0.75-0.99), but serious nosocomial infections did not decrease (adjusted OR, 0.97; 95% CI, 0.87-1.09).\n[9] The frequency of posttransfusion fevers decreased significantly following leukoreduction (adjusted OR, 0.86; 95% CI, 0.79-0.94), as did antibiotic use (adjusted OR, 0.90; 95% CI, 0.82-0.99).\n[10] CONCLUSION A national universal leukoreduction program is potentially associated with decreased mortality as well as decreased fever episodes and antibiotic use after red blood cell transfusion in high-risk patients."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Compared with the control period, the adjusted odds of death following leukoreduction were reduced (odds ratio [OR], 0.87; 95% confidence interval [CI], 0.75-0.99), but serious nosocomial infections did not decrease (adjusted OR, 0.97; 95% CI, 0.87-1.09).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 693, "doc_id": 24088502, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [24088502], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Leuko-reduced blood reduces infectious complications in red blood cell transfusion.\n\nDocument title: Clinical outcomes following institution of the Canadian universal leukoreduction program for red blood cell transfusions.\n\nAbstract sentences:\n[0] CONTEXT A number of countries have implemented a policy of universal leukoreduction of their blood supply, but the potential role of leukoreduction in decreasing postoperative mortality and infection is unclear.\n[1] OBJECTIVE To evaluate clinical outcomes following adoption of a national universal prestorage leukoreduction program for blood transfusions.\n[2] DESIGN, SETTING, AND POPULATION Retrospective before-and-after cohort study conducted from August 1998 to August 2000 in 23 academic and community hospitals throughout Canada, enrolling 14 786 patients who received red blood cell transfusions following cardiac surgery or repair of hip fracture, or who required intensive care following a surgical intervention or multiple trauma.\n[3] INTERVENTION Universal prestorage leukoreduction program introduced by 2 Canadian blood agencies.\n[4] A total of 6982 patients were enrolled during the control period and 7804 patients were enrolled following prestorage leukoreduction.\n[5] MAIN OUTCOME MEASURES All-cause in-hospital mortality and serious nosocomial infections (pneumonia, bacteremia, septic shock, all surgical site infections) occurring after first transfusion and at least 2 days after index procedure or intensive care unit admission.\n[6] Secondary outcomes included rates of posttransfusion fever and antibiotic use.\n[7] RESULTS Unadjusted in-hospital mortality rates were significantly lower following the introduction of leukoreduction compared with the control period (6.19% vs 7.03%, respectively; P =.04).\n[8] Compared with the control period, the adjusted odds of death following leukoreduction were reduced (odds ratio [OR], 0.87; 95% confidence interval [CI], 0.75-0.99), but serious nosocomial infections did not decrease (adjusted OR, 0.97; 95% CI, 0.87-1.09).\n[9] The frequency of posttransfusion fevers decreased significantly following leukoreduction (adjusted OR, 0.86; 95% CI, 0.79-0.94), as did antibiotic use (adjusted OR, 0.90; 95% CI, 0.82-0.99).\n[10] CONCLUSION A national universal leukoreduction program is potentially associated with decreased mortality as well as decreased fever episodes and antibiotic use after red blood cell transfusion in high-risk patients."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"The frequency of posttransfusion fevers decreased significantly following leukoreduction (adjusted OR, 0.86; 95% CI, 0.79-0.94), as did antibiotic use (adjusted OR, 0.90; 95% CI, 0.82-0.99).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 693, "doc_id": 24088502, "label": "SUPPORTS", "evidence_sentence_ids": [9], "cited_doc_ids": [24088502], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Leuko-reduced blood reduces infectious complications in red blood cell transfusion.\n\nDocument title: Clinical outcomes following institution of the Canadian universal leukoreduction program for red blood cell transfusions.\n\nAbstract sentences:\n[0] CONTEXT A number of countries have implemented a policy of universal leukoreduction of their blood supply, but the potential role of leukoreduction in decreasing postoperative mortality and infection is unclear.\n[1] OBJECTIVE To evaluate clinical outcomes following adoption of a national universal prestorage leukoreduction program for blood transfusions.\n[2] DESIGN, SETTING, AND POPULATION Retrospective before-and-after cohort study conducted from August 1998 to August 2000 in 23 academic and community hospitals throughout Canada, enrolling 14 786 patients who received red blood cell transfusions following cardiac surgery or repair of hip fracture, or who required intensive care following a surgical intervention or multiple trauma.\n[3] INTERVENTION Universal prestorage leukoreduction program introduced by 2 Canadian blood agencies.\n[4] A total of 6982 patients were enrolled during the control period and 7804 patients were enrolled following prestorage leukoreduction.\n[5] MAIN OUTCOME MEASURES All-cause in-hospital mortality and serious nosocomial infections (pneumonia, bacteremia, septic shock, all surgical site infections) occurring after first transfusion and at least 2 days after index procedure or intensive care unit admission.\n[6] Secondary outcomes included rates of posttransfusion fever and antibiotic use.\n[7] RESULTS Unadjusted in-hospital mortality rates were significantly lower following the introduction of leukoreduction compared with the control period (6.19% vs 7.03%, respectively; P =.04).\n[8] Compared with the control period, the adjusted odds of death following leukoreduction were reduced (odds ratio [OR], 0.87; 95% confidence interval [CI], 0.75-0.99), but serious nosocomial infections did not decrease (adjusted OR, 0.97; 95% CI, 0.87-1.09).\n[9] The frequency of posttransfusion fevers decreased significantly following leukoreduction (adjusted OR, 0.86; 95% CI, 0.79-0.94), as did antibiotic use (adjusted OR, 0.90; 95% CI, 0.82-0.99).\n[10] CONCLUSION A national universal leukoreduction program is potentially associated with decreased mortality as well as decreased fever episodes and antibiotic use after red blood cell transfusion in high-risk patients."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"CONCLUSION A national universal leukoreduction program is potentially associated with decreased mortality as well as decreased fever episodes and antibiotic use after red blood cell transfusion in high-risk patients.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 693, "doc_id": 24088502, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [24088502], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 Arabidopsis embryo does not require 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": "validation", "claim_id": 700, "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: Localization of PIN1 in the roots of Arabidopsis does not require 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": "validation", "claim_id": 702, "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: Low expression of miR7a does represses target genes and exerts 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": "validation", "claim_id": 715, "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 exerts 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": "validation", "claim_id": 716, "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 low 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: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Clustered methylation occurs at unprecedented densities and directly disfavors nucleosomes, contributing to nucleosome positioning between clusters.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 718, "doc_id": 17587795, "label": "CONTRADICTS", "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: Lupus-prone mice infected with curliproducing bacteria have higher autoantibody titers compared to controls.\n\nDocument title: Amyloid-DNA Composites of Bacterial Biofilms Stimulate Autoimmunity.\n\nAbstract sentences:\n[0] Research on the human microbiome has established that commensal and pathogenic bacteria can influence obesity, cancer, and autoimmunity through mechanisms mostly unknown.\n[1] We found that a component of bacterial biofilms, the amyloid protein curli, irreversibly formed fibers with bacterial DNA during biofilm formation.\n[2] This interaction accelerated amyloid polymerization and created potent immunogenic complexes that activated immune cells, including dendritic cells, to produce cytokines such as type I interferons, which are pathogenic in systemic lupus erythematosus (SLE).\n[3] When given systemically, curli-DNA composites triggered immune activation and production of autoantibodies in lupus-prone and wild-type mice.\n[4] We also found that the infection of lupus-prone mice with curli-producing bacteria triggered higher autoantibody titers compared to curli-deficient bacteria.\n[5] These data provide a mechanism by which the microbiome and biofilm-producing enteric infections may contribute to the progression of SLE and point to a potential molecular target for treatment of autoimmunity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"We also found that the infection of lupus-prone mice with curli-producing bacteria triggered higher autoantibody titers compared to curli-deficient bacteria.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 721, "doc_id": 1834762, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [1834762], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 migration to inflammation sites 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: [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": "validation", "claim_id": 723, "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: Ly49Q directs the organization of neutrophil migration to inflammation sites 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": "validation", "claim_id": 723, "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: Ly6C hi monocytes have a lower inflammatory capacity compared to their Ly6C lo counterparts.\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": "validation", "claim_id": 727, "doc_id": 7521113, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [7521113], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 lower 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 728, "doc_id": 36444198, "label": "CONTRADICTS", "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 lower 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: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"In addition, acute peritoneal inflammation recruited preferentially Ly-6C(med-high) monocytes.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 728, "doc_id": 36444198, "label": "CONTRADICTS", "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: Lymphadenopathy 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": "validation", "claim_id": 729, "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: Macrolides have no protective effect against myocardial infarction.\n\nDocument title: Antibiotics and risk of subsequent first-time acute myocardial infarction.\n\nAbstract sentences:\n[0] CONTEXT Increasing evidence supports the hypothesis of a causal association between certain bacterial infections and increased risk of developing acute myocardial infarction.\n[1] If such a causal association exists, subjects who used antibiotics active against the bacteria, regardless of indication, might be at lower risk of developing acute myocardial infarction than nonusers.\n[2] OBJECTIVE To determine whether previous use of antibiotics decreases the risk of developing a first-time acute myocardial infarction.\n[3] DESIGN Population-based case-control analysis.\n[4] SETTING The United Kingdom-based General Practice Research Database comprising 350 general practices.\n[5] PATIENTS A total of 3315 case patients aged 75 years or younger with a diagnosis of first-time acute myocardial infarction between 1992 and 1997 and 13139 controls without myocardial infarction matched to cases for age, sex, general practice attended, and calendar time.\n[6] MAIN OUTCOME MEASURES Use of antibiotics among those who did or did not have a first-time acute myocardial infarction.\n[7] RESULTS Cases were significantly less likely to have used tetracycline antibiotics (adjusted odds ratio [OR], 0.70; 95% confidence interval [CI], 0.55-0.90) or quinolones (adjusted OR, 0.45; 95% CI, 0.21-0.95).\n[8] No effect was found for previous use of macrolides (primarily erythromycin), sulfonamides, penicillins, or cephalosporins.\n[9] CONCLUSIONS The findings from this large case-control analysis provide further, albeit indirect, evidence for an association between bacterial infections with organisms susceptible to tetracycline or quinolone antibiotics and the risk of acute myocardial infarction.\n[10] These results of preliminary nature should stimulate more research to further explore the role of infections in the etiology of acute myocardial infarction."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"No effect was found for previous use of macrolides (primarily erythromycin), sulfonamides, penicillins, or cephalosporins.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 742, "doc_id": 32159283, "label": "SUPPORTS", "evidence_sentence_ids": [8], "cited_doc_ids": [32159283], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Macrolides protect against myocardial infarction.\n\nDocument title: Antibiotics and risk of subsequent first-time acute myocardial infarction.\n\nAbstract sentences:\n[0] CONTEXT Increasing evidence supports the hypothesis of a causal association between certain bacterial infections and increased risk of developing acute myocardial infarction.\n[1] If such a causal association exists, subjects who used antibiotics active against the bacteria, regardless of indication, might be at lower risk of developing acute myocardial infarction than nonusers.\n[2] OBJECTIVE To determine whether previous use of antibiotics decreases the risk of developing a first-time acute myocardial infarction.\n[3] DESIGN Population-based case-control analysis.\n[4] SETTING The United Kingdom-based General Practice Research Database comprising 350 general practices.\n[5] PATIENTS A total of 3315 case patients aged 75 years or younger with a diagnosis of first-time acute myocardial infarction between 1992 and 1997 and 13139 controls without myocardial infarction matched to cases for age, sex, general practice attended, and calendar time.\n[6] MAIN OUTCOME MEASURES Use of antibiotics among those who did or did not have a first-time acute myocardial infarction.\n[7] RESULTS Cases were significantly less likely to have used tetracycline antibiotics (adjusted odds ratio [OR], 0.70; 95% confidence interval [CI], 0.55-0.90) or quinolones (adjusted OR, 0.45; 95% CI, 0.21-0.95).\n[8] No effect was found for previous use of macrolides (primarily erythromycin), sulfonamides, penicillins, or cephalosporins.\n[9] CONCLUSIONS The findings from this large case-control analysis provide further, albeit indirect, evidence for an association between bacterial infections with organisms susceptible to tetracycline or quinolone antibiotics and the risk of acute myocardial infarction.\n[10] These results of preliminary nature should stimulate more research to further explore the role of infections in the etiology of acute myocardial infarction."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"No effect was found for previous use of macrolides (primarily erythromycin), sulfonamides, penicillins, or cephalosporins.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 743, "doc_id": 32159283, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [32159283], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Macropinocytosis contributes to a cell's supply of amino acids via the intracellular uptake of protein.\n\nDocument title: The Utilization of Extracellular Proteins as Nutrients Is Suppressed by mTORC1\n\nAbstract sentences:\n[0] Despite being surrounded by diverse nutrients, mammalian cells preferentially metabolize glucose and free amino acids.\n[1] Recently, Ras-induced macropinocytosis of extracellular proteins was shown to reduce a transformed cell's dependence on extracellular glutamine.\n[2] Here, we demonstrate that protein macropinocytosis can also serve as an essential amino acid source.\n[3] Lysosomal degradation of extracellular proteins can sustain cell survival and induce activation of mTORC1 but fails to elicit significant cell accumulation.\n[4] Unlike its growth-promoting activity under amino-acid-replete conditions, we discovered that mTORC1 activation suppresses proliferation when cells rely on extracellular proteins as an amino acid source.\n[5] Inhibiting mTORC1 results in increased catabolism of endocytosed proteins and enhances cell proliferation during nutrient-depleted conditions in vitro and within vascularly compromised tumors in vivo.\n[6] Thus, by preventing nutritional consumption of extracellular proteins, mTORC1 couples growth to availability of free amino acids.\n[7] These results may have important implications for the use of mTOR inhibitors as therapeutics."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here, we demonstrate that protein macropinocytosis can also serve as an essential amino acid source.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 744, "doc_id": 8460275, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [8460275], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 proteins in human cells can be post-translationally modified at lysine residues via acetylation.\n\nDocument title: Protein Lysine Acetylated/Deacetylated Enzymes and the Metabolism-Related Diseases\n\nAbstract sentences:\n[0] Lysine acetylation is a reversible posttranslational modifcation, an epigenetic phenomenon, referred to as transfer of an acetyl group from acetyl CoA to lysine e- amino group of targeted protein, which is modulated by acetyltransferases (histone/ lysine (K) acetyltransferases, HATs/KATs) and deacetylases (histone/lysine (K) deacetylases, HDACs/KDACs).\n[1] Lysine acetylation regulates various metabolic processes, such as fatty acid oxidation, Krebs cycle, oxidative phosphorylation, angiogenesis and so on.\n[2] Thus disorders of lysine acetylation may be correlated with obesity, diabetes and cardiovascular disease, which are termed as the metabolic complication.\n[3] With accumulating studies on proteomic acetylation, lysine acetylation also involves in cell immune status and degenerative diseases, for example, Alzheimer’s disease and Huntington’s disease.\n[4] This review primarily summarizes the current studies of lysine acetylation in metabolism modulation and in metabolism-related diseases, such as cardiovascular disease and fat metabolism disorder."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"Lysine acetylation is a reversible posttranslational modifcation, an epigenetic phenomenon, referred to as transfer of an acetyl group from acetyl CoA to lysine e- amino group of targeted protein, which is modulated by acetyltransferases (histone/ lysine (K) acetyltransferases, HATs/KATs) and deacetylases (histone/lysine (K) deacetylases, HDACs/KDACs).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 756, "doc_id": 2831620, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [2831620], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 a dramatic 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 759, "doc_id": 1805641, "label": "CONTRADICTS", "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: Mercaptopurine is anabolized into the inactive methylmercaptopurine by thiopurine methyltrasnferase (TPMT).\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": "validation", "claim_id": 768, "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: Metastatic colorectal cancer treated with a single agent fluoropyrimidines resulted in reduced efficacy and lower 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 770, "doc_id": 15476777, "label": "SUPPORTS", "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 defective for deoxyribonucleic acid (DNA) polymerase I (polI) 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": "validation", "claim_id": 775, "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 that lack Interferon-γ or its receptor exhibit high resistance 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 781, "doc_id": 24338780, "label": "CONTRADICTS", "evidence_sentence_ids": [2], "cited_doc_ids": [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 exhibit high resistance 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: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Although myocarditis subsided in wild-type mice after 3 weeks, IFN-gammaR(-/-) mice showed persistent disease.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 781, "doc_id": 24338780, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [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 exhibit high resistance 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 781, "doc_id": 24338780, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [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 resistant to EAM induced with α-MyHC/CFA.\n\nDocument title: Dual role of the IL-12/IFN-gamma axis in the development of autoimmune myocarditis: induction by IL-12 and protection by IFN-gamma.\n\nAbstract sentences:\n[0] IL-12 and IFN-gamma positively regulate each other and type 1 inflammatory responses, which are believed to cause tissue damage in autoimmune diseases.\n[1] We investigated the role of the IL-12/IFN-gamma (Th1) axis in the development of autoimmune myocarditis.\n[2] IL-12p40-deficient mice on a susceptible background resisted myocarditis.\n[3] In the absence of IL-12, autospecific CD4(+) T cells proliferated poorly and showed increased Th2 cytokine responses.\n[4] However, IFN-gamma-deficient mice developed fatal autoimmune disease, and blockade of IL-4R signaling did not confer susceptibility to myocarditis in IL-12p40-deficient mice, demonstrating that IL-12 triggers autoimmunity by a mechanism independent of the effector cytokines IFN-gamma and IL-4.\n[5] In conclusion, our results suggest that the IL-12/IFN-gamma axis is a double-edged sword for the development of autoimmune myocarditis.\n[6] Although IL-12 mediates disease by induction/expansion of Th1-type cells, IFN-gamma production from these cells limits disease 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": "validation", "claim_id": 783, "doc_id": 40632104, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [40632104], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: MicroRNA is involved in the regulation of Neural Stem Cell (NSC) differentiation and proliferation dynamic homeostasis\n\nDocument title: Epigenetic regulation of miR-184 by MBD1 governs neural stem cell proliferation and differentiation.\n\nAbstract sentences:\n[0] Methyl-CpG binding protein 1 (MBD1) regulates gene expression via a DNA methylation-mediated epigenetic mechanism.\n[1] We have previously demonstrated that MBD1 deficiency impairs adult neural stem/progenitor cell (aNSC) differentiation and neurogenesis, but the underlying mechanism was unclear.\n[2] Here, we show that MBD1 regulates the expression of several microRNAs in aNSCs and, specifically, that miR-184 is directly repressed by MBD1.\n[3] High levels of miR-184 promoted proliferation but inhibited differentiation of aNSCs, whereas inhibition of miR-184 rescued the phenotypes associated with MBD1 deficiency.\n[4] We further found that miR-184 regulates the expression of Numblike (Numbl), a known regulator of brain development, by binding to the 3'-UTR of Numbl mRNA and affecting its translation.\n[5] Expression of exogenous Numbl could rescue the aNSC defects that result from either miR-184 overexpression or MBD1 deficiency.\n[6] Therefore, MBD1, miR-184, and Numbl form a regulatory network that helps control the balance between proliferation and differentiation of aNSCs."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"High levels of miR-184 promoted proliferation but inhibited differentiation of aNSCs, whereas inhibition of miR-184 rescued the phenotypes associated with MBD1 deficiency.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 784, "doc_id": 2356950, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [2356950], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Microarray results from culture-amplified mixtures of serotypes correlate poorly with microarray results from uncultured mixtures.\n\nDocument title: The PneuCarriage Project: A Multi-Centre Comparative Study to Identify the Best Serotyping Methods for Examining Pneumococcal Carriage in Vaccine Evaluation Studies\n\nAbstract sentences:\n[0] BACKGROUND The pneumococcus is a diverse pathogen whose primary niche is the nasopharynx.\n[1] Over 90 different serotypes exist, and nasopharyngeal carriage of multiple serotypes is common.\n[2] Understanding pneumococcal carriage is essential for evaluating the impact of pneumococcal vaccines.\n[3] Traditional serotyping methods are cumbersome and insufficient for detecting multiple serotype carriage, and there are few data comparing the new methods that have been developed over the past decade.\n[4] We established the PneuCarriage project, a large, international multi-centre study dedicated to the identification of the best pneumococcal serotyping methods for carriage studies.\n[5] METHODS AND FINDINGS Reference sample sets were distributed to 15 research groups for blinded testing.\n[6] Twenty pneumococcal serotyping methods were used to test 81 laboratory-prepared (spiked) samples.\n[7] The five top-performing methods were used to test 260 nasopharyngeal (field) samples collected from children in six high-burden countries.\n[8] Sensitivity and positive predictive value (PPV) were determined for the test methods and the reference method (traditional serotyping of >100 colonies from each sample).\n[9] For the alternate serotyping methods, the overall sensitivity ranged from 1% to 99% (reference method 98%), and PPV from 8% to 100% (reference method 100%), when testing the spiked samples.\n[10] Fifteen methods had ≥70% sensitivity to detect the dominant (major) serotype, whilst only eight methods had ≥70% sensitivity to detect minor serotypes.\n[11] For the field samples, the overall sensitivity ranged from 74.2% to 95.8% (reference method 93.8%), and PPV from 82.2% to 96.4% (reference method 99.6%).\n[12] The microarray had the highest sensitivity (95.8%) and high PPV (93.7%).\n[13] The major limitation of this study is that not all of the available alternative serotyping methods were included.\n[14] CONCLUSIONS Most methods were able to detect the dominant serotype in a sample, but many performed poorly in detecting the minor serotype populations.\n[15] Microarray with a culture amplification step was the top-performing method.\n[16] Results from this comprehensive evaluation will inform future vaccine evaluation and impact studies, particularly in low-income settings, where pneumococcal disease burden remains high."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 785, "doc_id": 12471115, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [12471115], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 are uninvolved 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: 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": "validation", "claim_id": 793, "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: Modifying the epigenome in the brain affects the normal human aging process by affecting certain genes related to neurogenesis.\n\nDocument title: Epigenetic mechanisms in neurological disease\n\nAbstract sentences:\n[0] The exploration of brain epigenomes, which consist of various types of DNA methylation and covalent histone modifications, is providing new and unprecedented insights into the mechanisms of neural development, neurological disease and aging.\n[1] Traditionally, chromatin defects in the brain were considered static lesions of early development that occurred in the context of rare genetic syndromes, but it is now clear that mutations and maladaptations of the epigenetic machinery cover a much wider continuum that includes adult-onset neurodegenerative disease.\n[2] Here, we describe how recent advances in neuroepigenetics have contributed to an improved mechanistic understanding of developmental and degenerative brain disorders, and we discuss how they could influence the development of future therapies for these conditions."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 800, "doc_id": 22543403, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [22543403], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 805, "doc_id": 22180793, "label": "SUPPORTS", "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 inhibits 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: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Therapeutic targeting of this factor with monoclonal antibodies may have considerable clinical benefit.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 805, "doc_id": 22180793, "label": "SUPPORTS", "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: Most termination events in Okazaki fragments are sequence specific.\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: [1]\nExplanation: Evidence states: \"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.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 808, "doc_id": 36606083, "label": "SUPPORTS", "evidence_sentence_ids": [1], "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: Mutant mice lacking SVCT2 have greatly increased 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: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Ascorbic-acid levels were undetectable or markedly reduced in the blood and tissues of Slc23a1−/− mice.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 811, "doc_id": 19799455, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "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 greatly increased 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 811, "doc_id": 19799455, "label": "CONTRADICTS", "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 GNB2 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": "validation", "claim_id": 814, "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: N-terminal cleavage increases success identifying transcription start sites.\n\nDocument title: Identification and Functional Characterization of N-Terminally Acetylated Proteins in Drosophila melanogaster\n\nAbstract sentences:\n[0] Protein modifications play a major role for most biological processes in living organisms.\n[1] Amino-terminal acetylation of proteins is a common modification found throughout the tree of life: the N-terminus of a nascent polypeptide chain becomes co-translationally acetylated, often after the removal of the initiating methionine residue.\n[2] While the enzymes and protein complexes involved in these processes have been extensively studied, only little is known about the biological function of such N-terminal modification events.\n[3] To identify common principles of N-terminal acetylation, we analyzed the amino-terminal peptides from proteins extracted from Drosophila Kc167 cells.\n[4] We detected more than 1,200 mature protein N-termini and could show that N-terminal acetylation occurs in insects with a similar frequency as in humans.\n[5] As the sole true determinant for N-terminal acetylation we could extract the (X)PX rule that indicates the prevention of acetylation under all circumstances.\n[6] We could show that this rule can be used to genetically engineer a protein to study the biological relevance of the presence or absence of an acetyl group, thereby generating a generic assay to probe the functional importance of N-terminal acetylation.\n[7] We applied the assay by expressing mutated proteins as transgenes in cell lines and in flies.\n[8] Here, we present a straightforward strategy to systematically study the functional relevance of N-terminal acetylations in cells and whole organisms.\n[9] Since the (X)PX rule seems to be of general validity in lower as well as higher eukaryotes, we propose that it can be used to study the function of N-terminal acetylation in all species."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 820, "doc_id": 8646760, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [8646760], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: N-terminal cleavage reduces success identifying transcription start sites.\n\nDocument title: Identification and Functional Characterization of N-Terminally Acetylated Proteins in Drosophila melanogaster\n\nAbstract sentences:\n[0] Protein modifications play a major role for most biological processes in living organisms.\n[1] Amino-terminal acetylation of proteins is a common modification found throughout the tree of life: the N-terminus of a nascent polypeptide chain becomes co-translationally acetylated, often after the removal of the initiating methionine residue.\n[2] While the enzymes and protein complexes involved in these processes have been extensively studied, only little is known about the biological function of such N-terminal modification events.\n[3] To identify common principles of N-terminal acetylation, we analyzed the amino-terminal peptides from proteins extracted from Drosophila Kc167 cells.\n[4] We detected more than 1,200 mature protein N-termini and could show that N-terminal acetylation occurs in insects with a similar frequency as in humans.\n[5] As the sole true determinant for N-terminal acetylation we could extract the (X)PX rule that indicates the prevention of acetylation under all circumstances.\n[6] We could show that this rule can be used to genetically engineer a protein to study the biological relevance of the presence or absence of an acetyl group, thereby generating a generic assay to probe the functional importance of N-terminal acetylation.\n[7] We applied the assay by expressing mutated proteins as transgenes in cell lines and in flies.\n[8] Here, we present a straightforward strategy to systematically study the functional relevance of N-terminal acetylations in cells and whole organisms.\n[9] Since the (X)PX rule seems to be of general validity in lower as well as higher eukaryotes, we propose that it can be used to study the function of N-terminal acetylation in all species."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 821, "doc_id": 8646760, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [8646760], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 zidovudine (AZT).\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: [14]\nExplanation: Evidence states: \"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.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 823, "doc_id": 15319019, "label": "SUPPORTS", "evidence_sentence_ids": [14], "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: NF2 (Merlin) causes phosphorylation and subsequent cytoplasmic sequestration of YAP in Drosophila by activating LATS1/2 kinases.\n\nDocument title: A genetic screen identifies an LKB1–MARK signalling axis controlling the Hippo–YAP pathway\n\nAbstract sentences:\n[0] The Hippo–YAP pathway is an emerging signalling cascade involved in the regulation of stem cell activity and organ size.\n[1] To identify components of this pathway, we performed an RNAi-based kinome screen in human cells.\n[2] Our screen identified several kinases not previously associated with Hippo signalling that control multiple cellular processes.\n[3] One of the hits, LKB1, is a common tumour suppressor whose mechanism of action is only partially understood.\n[4] We demonstrate that LKB1 acts through its substrates of the microtubule affinity-regulating kinase family to regulate the localization of the polarity determinant Scribble and the activity of the core Hippo kinases.\n[5] Our data also indicate that YAP is functionally important for the tumour suppressive effects of LKB1.\n[6] Our results identify a signalling axis that links YAP activation with LKB1 mutations, and have implications for the treatment of LKB1-mutant human malignancies.\n[7] In addition, our findings provide insight into upstream signals of the Hippo–YAP signalling cascade."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 830, "doc_id": 1897324, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [1897324], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: NF2 (Merlin) prevents phosphorylation and subsequent cytoplasmic sequestration of YAP in Drosophila.\n\nDocument title: A genetic screen identifies an LKB1–MARK signalling axis controlling the Hippo–YAP pathway\n\nAbstract sentences:\n[0] The Hippo–YAP pathway is an emerging signalling cascade involved in the regulation of stem cell activity and organ size.\n[1] To identify components of this pathway, we performed an RNAi-based kinome screen in human cells.\n[2] Our screen identified several kinases not previously associated with Hippo signalling that control multiple cellular processes.\n[3] One of the hits, LKB1, is a common tumour suppressor whose mechanism of action is only partially understood.\n[4] We demonstrate that LKB1 acts through its substrates of the microtubule affinity-regulating kinase family to regulate the localization of the polarity determinant Scribble and the activity of the core Hippo kinases.\n[5] Our data also indicate that YAP is functionally important for the tumour suppressive effects of LKB1.\n[6] Our results identify a signalling axis that links YAP activation with LKB1 mutations, and have implications for the treatment of LKB1-mutant human malignancies.\n[7] In addition, our findings provide insight into upstream signals of the Hippo–YAP signalling cascade."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 831, "doc_id": 1897324, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [1897324], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: NFAT4 activation requires IP3R-mediated Ca2+ mobilization.\n\nDocument title: Control of NFAT Isoform Activation and NFAT-Dependent Gene Expression through Two Coincident and Spatially Segregated Intracellular Ca2+ Signals\n\nAbstract sentences:\n[0] Excitation-transcription coupling, linking stimulation at the cell surface to changes in nuclear gene expression, is conserved throughout eukaryotes.\n[1] How closely related coexpressed transcription factors are differentially activated remains unclear.\n[2] Here, we show that two Ca2+-dependent transcription factor isoforms, NFAT1 and NFAT4, require distinct sub-cellular InsP3 and Ca2+ signals for physiologically sustained activation.\n[3] NFAT1 is stimulated by sub-plasmalemmal Ca2+ microdomains, whereas NFAT4 additionally requires Ca2+ mobilization from the inner nuclear envelope by nuclear InsP3 receptors.\n[4] NFAT1 is rephosphorylated (deactivated) more slowly than NFAT4 in both cytoplasm and nucleus, enabling a more prolonged activation phase.\n[5] Oscillations in cytoplasmic Ca2+, long considered the physiological form of Ca2+ signaling, play no role in activating either NFAT protein.\n[6] Instead, effective sustained physiological activation of NFAT4 is tightly linked to oscillations in nuclear Ca2+.\n[7] Our results show how gene expression can be controlled by coincident yet geographically distinct Ca2+ signals, generated by a freely diffusible InsP3 message."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Here, we show that two Ca2+-dependent transcription factor isoforms, NFAT1 and NFAT4, require distinct sub-cellular InsP3 and Ca2+ signals for physiologically sustained activation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 832, "doc_id": 30303335, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [30303335], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: NFAT4 activation requires IP3R-mediated Ca2+ mobilization.\n\nDocument title: Control of NFAT Isoform Activation and NFAT-Dependent Gene Expression through Two Coincident and Spatially Segregated Intracellular Ca2+ Signals\n\nAbstract sentences:\n[0] Excitation-transcription coupling, linking stimulation at the cell surface to changes in nuclear gene expression, is conserved throughout eukaryotes.\n[1] How closely related coexpressed transcription factors are differentially activated remains unclear.\n[2] Here, we show that two Ca2+-dependent transcription factor isoforms, NFAT1 and NFAT4, require distinct sub-cellular InsP3 and Ca2+ signals for physiologically sustained activation.\n[3] NFAT1 is stimulated by sub-plasmalemmal Ca2+ microdomains, whereas NFAT4 additionally requires Ca2+ mobilization from the inner nuclear envelope by nuclear InsP3 receptors.\n[4] NFAT1 is rephosphorylated (deactivated) more slowly than NFAT4 in both cytoplasm and nucleus, enabling a more prolonged activation phase.\n[5] Oscillations in cytoplasmic Ca2+, long considered the physiological form of Ca2+ signaling, play no role in activating either NFAT protein.\n[6] Instead, effective sustained physiological activation of NFAT4 is tightly linked to oscillations in nuclear Ca2+.\n[7] Our results show how gene expression can be controlled by coincident yet geographically distinct Ca2+ signals, generated by a freely diffusible InsP3 message."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"NFAT1 is stimulated by sub-plasmalemmal Ca2+ microdomains, whereas NFAT4 additionally requires Ca2+ mobilization from the inner nuclear envelope by nuclear InsP3 receptors.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 832, "doc_id": 30303335, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [30303335], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: NFAT4 activation requires IP3R-mediated Ca2+ mobilization.\n\nDocument title: Control of NFAT Isoform Activation and NFAT-Dependent Gene Expression through Two Coincident and Spatially Segregated Intracellular Ca2+ Signals\n\nAbstract sentences:\n[0] Excitation-transcription coupling, linking stimulation at the cell surface to changes in nuclear gene expression, is conserved throughout eukaryotes.\n[1] How closely related coexpressed transcription factors are differentially activated remains unclear.\n[2] Here, we show that two Ca2+-dependent transcription factor isoforms, NFAT1 and NFAT4, require distinct sub-cellular InsP3 and Ca2+ signals for physiologically sustained activation.\n[3] NFAT1 is stimulated by sub-plasmalemmal Ca2+ microdomains, whereas NFAT4 additionally requires Ca2+ mobilization from the inner nuclear envelope by nuclear InsP3 receptors.\n[4] NFAT1 is rephosphorylated (deactivated) more slowly than NFAT4 in both cytoplasm and nucleus, enabling a more prolonged activation phase.\n[5] Oscillations in cytoplasmic Ca2+, long considered the physiological form of Ca2+ signaling, play no role in activating either NFAT protein.\n[6] Instead, effective sustained physiological activation of NFAT4 is tightly linked to oscillations in nuclear Ca2+.\n[7] Our results show how gene expression can be controlled by coincident yet geographically distinct Ca2+ signals, generated by a freely diffusible InsP3 message."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [6, 7]\nExplanation: Evidence states: \"Instead, effective sustained physiological activation of NFAT4 is tightly linked to oscillations in nuclear Ca2+. Our results show how gene expression can be controlled by coincident yet geographically distinct Ca2+ signals, generated by a freely diffusible InsP3 message.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 832, "doc_id": 30303335, "label": "SUPPORTS", "evidence_sentence_ids": [6, 7], "cited_doc_ids": [30303335], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: NOX2-independent pathways can generate peroxynitrite by reacting with nitrogen intermediates.\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: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 834, "doc_id": 5483793, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [5483793], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 837, "doc_id": 15928989, "label": "SUPPORTS", "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 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: SUPPORTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"These findings show that Lrh-1 is necessary for maintenance of the corpus luteum, for promotion of decidualization and for formation of the placenta.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 837, "doc_id": 15928989, "label": "SUPPORTS", "evidence_sentence_ids": [8], "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: Nanoparticles can be targeted against specific cell types by incorporating aptamers into lipid nanoparticles.\n\nDocument title: Aptamer-functionalized lipid nanoparticles targeting osteoblasts as a novel RNA interference–based bone anabolic strategy\n\nAbstract sentences:\n[0] Currently, major concerns about the safety and efficacy of RNA interference (RNAi)-based bone anabolic strategies still exist because of the lack of direct osteoblast-specific delivery systems for osteogenic siRNAs.\n[1] Here we screened the aptamer CH6 by cell-SELEX, specifically targeting both rat and human osteoblasts, and then we developed CH6 aptamer–functionalized lipid nanoparticles (LNPs) encapsulating osteogenic pleckstrin homology domain-containing family O member 1 (Plekho1) siRNA (CH6-LNPs-siRNA).\n[2] Our results showed that CH6 facilitated in vitro osteoblast-selective uptake of Plekho1 siRNA, mainly via macropinocytosis, and boosted in vivo osteoblast-specific Plekho1 gene silencing, which promoted bone formation, improved bone microarchitecture, increased bone mass and enhanced mechanical properties in both osteopenic and healthy rodents.\n[3] These results indicate that osteoblast-specific aptamer-functionalized LNPs could act as a new RNAi-based bone anabolic strategy, advancing the targeted delivery selectivity of osteogenic siRNAs from the tissue level to the cellular level."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Our results showed that CH6 facilitated in vitro osteoblast-selective uptake of Plekho1 siRNA, mainly via macropinocytosis, and boosted in vivo osteoblast-specific Plekho1 gene silencing, which promoted bone formation, improved bone microarchitecture, increased bone mass and enhanced mechanical properties in both osteopenic and healthy rodents.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 839, "doc_id": 1469751, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [1469751], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Nanoparticles can be targeted against specific cell types by incorporating aptamers into lipid nanoparticles.\n\nDocument title: Aptamer-functionalized lipid nanoparticles targeting osteoblasts as a novel RNA interference–based bone anabolic strategy\n\nAbstract sentences:\n[0] Currently, major concerns about the safety and efficacy of RNA interference (RNAi)-based bone anabolic strategies still exist because of the lack of direct osteoblast-specific delivery systems for osteogenic siRNAs.\n[1] Here we screened the aptamer CH6 by cell-SELEX, specifically targeting both rat and human osteoblasts, and then we developed CH6 aptamer–functionalized lipid nanoparticles (LNPs) encapsulating osteogenic pleckstrin homology domain-containing family O member 1 (Plekho1) siRNA (CH6-LNPs-siRNA).\n[2] Our results showed that CH6 facilitated in vitro osteoblast-selective uptake of Plekho1 siRNA, mainly via macropinocytosis, and boosted in vivo osteoblast-specific Plekho1 gene silencing, which promoted bone formation, improved bone microarchitecture, increased bone mass and enhanced mechanical properties in both osteopenic and healthy rodents.\n[3] These results indicate that osteoblast-specific aptamer-functionalized LNPs could act as a new RNAi-based bone anabolic strategy, advancing the targeted delivery selectivity of osteogenic siRNAs from the tissue level to the cellular level."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"These results indicate that osteoblast-specific aptamer-functionalized LNPs could act as a new RNAi-based bone anabolic strategy, advancing the targeted delivery selectivity of osteogenic siRNAs from the tissue level to the cellular level.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 839, "doc_id": 1469751, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [1469751], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 traps (NETs) are released by ANCA-stimulated neutrophils.\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": "validation", "claim_id": 845, "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: New drugs for tuberculosis often do not penetrate the necrotic portion of a tuberculosis lesion in high concentrations.\n\nDocument title: The association between sterilizing activity and drug distribution into tuberculosis lesions\n\nAbstract sentences:\n[0] Finding new treatment-shortening antibiotics to improve cure rates and curb the alarming emergence of drug resistance is the major objective of tuberculosis (TB) drug development.\n[1] Using a matrix-assisted laser desorption/ionization (MALDI) mass spectrometry imaging suite in a biosafety containment facility, we show that the key sterilizing drugs rifampicin and pyrazinamide efficiently penetrate the sites of TB infection in lung lesions.\n[2] Rifampicin even accumulates in necrotic caseum, a critical lesion site where persisting tubercle bacilli reside.\n[3] In contrast, moxifloxacin, which is active in vitro against a subpopulation of Mycobacterium tuberculosis that persists in specific niches under drug pressure and has achieved treatment shortening in mice, does not diffuse well in caseum, concordant with its failure to shorten therapy in recent clinical trials.\n[4] We suggest that such differential spatial distribution and kinetics of accumulation in lesions may create temporal and spatial windows of monotherapy in specific niches, allowing the gradual development of multidrug-resistant TB.\n[5] We propose an alternative working model to prioritize new antibiotic regimens based on quantitative and spatial distribution of TB drugs in the major lesion types found in human lungs.\n[6] The finding that lesion penetration may contribute to treatment outcome has wide implications for TB."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Rifampicin even accumulates in necrotic caseum, a critical lesion site where persisting tubercle bacilli reside.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 847, "doc_id": 16787954, "label": "CONTRADICTS", "evidence_sentence_ids": [2], "cited_doc_ids": [16787954], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Non-invasive ventilation use should be decreased if there is inadequate response to conventional treatment.\n\nDocument title: Cost effectiveness of ward based non-invasive ventilation for acute exacerbations of chronic obstructive pulmonary disease: economic analysis of randomised controlled trial.\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate the cost effectiveness of standard treatment with and without the addition of ward based non-invasive ventilation in patients admitted to hospital with an acute exacerbation of chronic obstructive pulmonary disease.\n[1] DESIGN Incremental cost effectiveness analysis of a randomised controlled trial.\n[2] SETTING Medical wards in 14 hospitals in the United Kingdom.\n[3] PARTICIPANTS The trial comprised 236 patients admitted to hospital with an acute exacerbation of chronic obstructive pulmonary disease and mild to moderate acidosis (pH 7.25-7.35) secondary to respiratory failure.\n[4] The economic analysis compared the costs of treatment that these patients received after randomisation.\n[5] MAIN OUTCOME MEASURE Incremental cost per in-hospital death.\n[6] RESULTS 24/118 died in the group receiving standard treatment and 12/118 in the group receiving non-invasive ventilation (P=0.05).\n[7] Allocation to the group receiving non-invasive ventilation was associated with a reduction in costs of 49362 pounds sterling (78741 dollars; 73109 euros), mainly through reduced use of intensive care units.\n[8] The incremental cost effectiveness ratio was -645 pounds sterling per death avoided (95% confidence interval -2310 pounds sterling to 386 pounds sterling), indicating a dominant (more effective and less costly) strategy.\n[9] Modelling of these data indicates that a typical UK hospital providing a non-invasive ventilation service will avoid six deaths and three to nine admissions to intensive care units per year, with an associated cost reduction of 12000-53000 pounds sterling per year.\n[10] CONCLUSIONS Non-invasive ventilation is a highly cost effective treatment that both reduced total costs and improved mortality in hospital."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [9]\nExplanation: Evidence states: \"Modelling of these data indicates that a typical UK hospital providing a non-invasive ventilation service will avoid six deaths and three to nine admissions to intensive care units per year, with an associated cost reduction of 12000-53000 pounds sterling per year.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 852, "doc_id": 13843341, "label": "CONTRADICTS", "evidence_sentence_ids": [9], "cited_doc_ids": [13843341], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Non-invasive ventilation use should be decreased if there is inadequate response to conventional treatment.\n\nDocument title: Cost effectiveness of ward based non-invasive ventilation for acute exacerbations of chronic obstructive pulmonary disease: economic analysis of randomised controlled trial.\n\nAbstract sentences:\n[0] OBJECTIVE To evaluate the cost effectiveness of standard treatment with and without the addition of ward based non-invasive ventilation in patients admitted to hospital with an acute exacerbation of chronic obstructive pulmonary disease.\n[1] DESIGN Incremental cost effectiveness analysis of a randomised controlled trial.\n[2] SETTING Medical wards in 14 hospitals in the United Kingdom.\n[3] PARTICIPANTS The trial comprised 236 patients admitted to hospital with an acute exacerbation of chronic obstructive pulmonary disease and mild to moderate acidosis (pH 7.25-7.35) secondary to respiratory failure.\n[4] The economic analysis compared the costs of treatment that these patients received after randomisation.\n[5] MAIN OUTCOME MEASURE Incremental cost per in-hospital death.\n[6] RESULTS 24/118 died in the group receiving standard treatment and 12/118 in the group receiving non-invasive ventilation (P=0.05).\n[7] Allocation to the group receiving non-invasive ventilation was associated with a reduction in costs of 49362 pounds sterling (78741 dollars; 73109 euros), mainly through reduced use of intensive care units.\n[8] The incremental cost effectiveness ratio was -645 pounds sterling per death avoided (95% confidence interval -2310 pounds sterling to 386 pounds sterling), indicating a dominant (more effective and less costly) strategy.\n[9] Modelling of these data indicates that a typical UK hospital providing a non-invasive ventilation service will avoid six deaths and three to nine admissions to intensive care units per year, with an associated cost reduction of 12000-53000 pounds sterling per year.\n[10] CONCLUSIONS Non-invasive ventilation is a highly cost effective treatment that both reduced total costs and improved mortality in hospital."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"CONCLUSIONS Non-invasive ventilation is a highly cost effective treatment that both reduced total costs and improved mortality in hospital.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 852, "doc_id": 13843341, "label": "CONTRADICTS", "evidence_sentence_ids": [10], "cited_doc_ids": [13843341], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 has tumor-promoting 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 859, "doc_id": 1982286, "label": "CONTRADICTS", "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: 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": "validation", "claim_id": 870, "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 is determined solely by environmental factors.\n\nDocument title: Genetics of obesity in adult adoptees and their biological siblings.\n\nAbstract sentences:\n[0] An adoption study of genetic effects on obesity in adulthood was carried out in which adoptees separated from their natural parents very early in life were compared with their biological full and half siblings reared by their natural parents.\n[1] The adoptees represented four groups who by sampling from a larger population were categorised as either thin, medium weight, overweight, or obese.\n[2] Weight and height were obtained for 115 full siblings of 57 adoptees and for 850 half siblings of 341 adoptees.\n[3] In full siblings body mass index (kg/m2) significantly increased with weight of the adoptees.\n[4] Body mass index of the half siblings showed a steady but weaker increase across the four weight groups of adoptees.\n[5] There were no significant interactions with sex of the adoptees, sex of the siblings, or (for the half siblings) sex of the common parent.\n[6] In contrast with the findings in half siblings and (previously) the natural parents there was a striking, significant increase in body mass index between full siblings of overweight and obese adoptees.\n[7] The degree of fatness in adults living in the same environment appears to be influenced by genetic factors independent of sex, which may include polygenic as well as major gene effects on obesity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3, 4]\nExplanation: Evidence states: \"In full siblings body mass index (kg/m2) significantly increased with weight of the adoptees. Body mass index of the half siblings showed a steady but weaker increase across the four weight groups of adoptees.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 873, "doc_id": 1180972, "label": "CONTRADICTS", "evidence_sentence_ids": [3, 4], "cited_doc_ids": [1180972, 19307912, 27393799, 29025270, 3315558], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 is determined solely by environmental factors.\n\nDocument title: Genetics of obesity in adult adoptees and their biological siblings.\n\nAbstract sentences:\n[0] An adoption study of genetic effects on obesity in adulthood was carried out in which adoptees separated from their natural parents very early in life were compared with their biological full and half siblings reared by their natural parents.\n[1] The adoptees represented four groups who by sampling from a larger population were categorised as either thin, medium weight, overweight, or obese.\n[2] Weight and height were obtained for 115 full siblings of 57 adoptees and for 850 half siblings of 341 adoptees.\n[3] In full siblings body mass index (kg/m2) significantly increased with weight of the adoptees.\n[4] Body mass index of the half siblings showed a steady but weaker increase across the four weight groups of adoptees.\n[5] There were no significant interactions with sex of the adoptees, sex of the siblings, or (for the half siblings) sex of the common parent.\n[6] In contrast with the findings in half siblings and (previously) the natural parents there was a striking, significant increase in body mass index between full siblings of overweight and obese adoptees.\n[7] The degree of fatness in adults living in the same environment appears to be influenced by genetic factors independent of sex, which may include polygenic as well as major gene effects on obesity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"In contrast with the findings in half siblings and (previously) the natural parents there was a striking, significant increase in body mass index between full siblings of overweight and obese adoptees.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 873, "doc_id": 1180972, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "cited_doc_ids": [1180972, 19307912, 27393799, 29025270, 3315558], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 is determined solely by environmental factors.\n\nDocument title: Genetics of obesity in adult adoptees and their biological siblings.\n\nAbstract sentences:\n[0] An adoption study of genetic effects on obesity in adulthood was carried out in which adoptees separated from their natural parents very early in life were compared with their biological full and half siblings reared by their natural parents.\n[1] The adoptees represented four groups who by sampling from a larger population were categorised as either thin, medium weight, overweight, or obese.\n[2] Weight and height were obtained for 115 full siblings of 57 adoptees and for 850 half siblings of 341 adoptees.\n[3] In full siblings body mass index (kg/m2) significantly increased with weight of the adoptees.\n[4] Body mass index of the half siblings showed a steady but weaker increase across the four weight groups of adoptees.\n[5] There were no significant interactions with sex of the adoptees, sex of the siblings, or (for the half siblings) sex of the common parent.\n[6] In contrast with the findings in half siblings and (previously) the natural parents there was a striking, significant increase in body mass index between full siblings of overweight and obese adoptees.\n[7] The degree of fatness in adults living in the same environment appears to be influenced by genetic factors independent of sex, which may include polygenic as well as major gene effects on obesity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"The degree of fatness in adults living in the same environment appears to be influenced by genetic factors independent of sex, which may include polygenic as well as major gene effects on obesity.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 873, "doc_id": 1180972, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [1180972, 19307912, 27393799, 29025270, 3315558], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 is determined solely by environmental factors.\n\nDocument title: Familial obesity and leanness.\n\nAbstract sentences:\n[0] Using the Princeton School District Family Study cohort, our specific aim was to estimate the prevalence of suspected familial ponderosity and leanness, to provide empirical risk estimates for the proportion of probands' first-degree relatives who were similarly affected, and to estimate the contributions of diseases, drugs and caloric intake to relative obesity and leanness.\n[1] We studied 379 probands, 125 whites and 52 blacks from a random recall group, 147 whites and 55 blacks from a hyperlipidemic recall group.\n[2] Suspected familial obesity and leanness were arbitrarily identified in those kindreds with at least two first-degree relatives in the same Quetelet index decile as the proband, top or bottom respectively.\n[3] Suspected familial obesity was observed in 2.4 percent and 6 percent respectively of random and hyperlipidemic recall group whites.\n[4] Suspected familial leanness was identified in 2.4 percent and 1.4 percent of random and hyperlipidemic recall whites and in 3.8 percent of randomly recalled blacks.\n[5] Approximately twice as many as expected white first-degree relatives of top Quetelet index decile probands themselves had top decile Quetelet indices; approximately three times as many as expected first-degree relatives of bottom decile Quetelet index probands themselves had bottom decile Quetelet indices.\n[6] Nineteen percent and 31 percent of top decile Quetelet index white probands from random and hyperlipidemic recall groups came from families where at least two other first-degree relatives were similarly obese; 18 percent and 20 percent of white random and hyperlipidemic recall group probands with bottom decile Quetelet indices had suspected familial leanness.\n[7] Nearly all subjects with familial obesity or leanness had no overt metabolic or pharmacological explanations for their body habitus.\n[8] Within-family clustering of hypertension was common in kindreds with suspected familial obesity and was absent in kindreds with suspected familial leanness.\n[9] Marked within-family clustering of both obesity and leanness is useful diagnostically; therapeutic intervention to reduce obesity, to be most effective, should be family-wide in the many kindreds which share familial obesity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Suspected familial obesity was observed in 2.4 percent and 6 percent respectively of random and hyperlipidemic recall group whites.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 873, "doc_id": 19307912, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [1180972, 19307912, 27393799, 29025270, 3315558], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 is determined solely by environmental factors.\n\nDocument title: Familial obesity and leanness.\n\nAbstract sentences:\n[0] Using the Princeton School District Family Study cohort, our specific aim was to estimate the prevalence of suspected familial ponderosity and leanness, to provide empirical risk estimates for the proportion of probands' first-degree relatives who were similarly affected, and to estimate the contributions of diseases, drugs and caloric intake to relative obesity and leanness.\n[1] We studied 379 probands, 125 whites and 52 blacks from a random recall group, 147 whites and 55 blacks from a hyperlipidemic recall group.\n[2] Suspected familial obesity and leanness were arbitrarily identified in those kindreds with at least two first-degree relatives in the same Quetelet index decile as the proband, top or bottom respectively.\n[3] Suspected familial obesity was observed in 2.4 percent and 6 percent respectively of random and hyperlipidemic recall group whites.\n[4] Suspected familial leanness was identified in 2.4 percent and 1.4 percent of random and hyperlipidemic recall whites and in 3.8 percent of randomly recalled blacks.\n[5] Approximately twice as many as expected white first-degree relatives of top Quetelet index decile probands themselves had top decile Quetelet indices; approximately three times as many as expected first-degree relatives of bottom decile Quetelet index probands themselves had bottom decile Quetelet indices.\n[6] Nineteen percent and 31 percent of top decile Quetelet index white probands from random and hyperlipidemic recall groups came from families where at least two other first-degree relatives were similarly obese; 18 percent and 20 percent of white random and hyperlipidemic recall group probands with bottom decile Quetelet indices had suspected familial leanness.\n[7] Nearly all subjects with familial obesity or leanness had no overt metabolic or pharmacological explanations for their body habitus.\n[8] Within-family clustering of hypertension was common in kindreds with suspected familial obesity and was absent in kindreds with suspected familial leanness.\n[9] Marked within-family clustering of both obesity and leanness is useful diagnostically; therapeutic intervention to reduce obesity, to be most effective, should be family-wide in the many kindreds which share familial obesity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Nearly all subjects with familial obesity or leanness had no overt metabolic or pharmacological explanations for their body habitus.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 873, "doc_id": 19307912, "label": "CONTRADICTS", "evidence_sentence_ids": [7], "cited_doc_ids": [1180972, 19307912, 27393799, 29025270, 3315558], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 is determined solely by environmental factors.\n\nDocument title: The body-mass index of twins who have been reared apart.\n\nAbstract sentences:\n[0] To assess the relative importance of genetic and environmental effects on the body-mass index (weight in kilograms divided by the square of the height in meters), we studied samples of identical and fraternal twins, reared apart or reared together.\n[1] The samples consisted of 93 pairs of identical twins reared apart, 154 pairs of identical twins reared together, 218 pairs of fraternal twins reared apart, and 208 pairs of fraternal twins reared together.\n[2] The intrapair correlation coefficients of the values for body-mass index of identical twins reared apart were 0.70 for men and 0.66 for women.\n[3] These are the most direct estimates of the relative importance of genetic influences (heritability) on the body-mass index, and they were only slightly lower than those for twins reared together in this and earlier studies.\n[4] Similar estimates were derived from maximum-likelihood model-fitting analyses--0.74 for men and 0.69 for women.\n[5] Nonadditive genetic variance made a significant contribution to the estimates of heritability, particularly among men.\n[6] Of the potential environmental influences, only those unique to the individual and not those shared by family members were important, contributing about 30 percent of the variance.\n[7] Sharing the same childhood environment did not contribute to the similarity of the body-mass index of twins later in life.\n[8] We conclude that genetic influences on body-mass index are substantial, whereas the childhood environment has little or no influence.\n[9] These findings corroborate and extend the results of earlier studies of twins and adoptees."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"We conclude that genetic influences on body-mass index are substantial, whereas the childhood environment has little or no influence.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 873, "doc_id": 27393799, "label": "CONTRADICTS", "evidence_sentence_ids": [8], "cited_doc_ids": [1180972, 19307912, 27393799, 29025270, 3315558], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 is determined solely by environmental factors.\n\nDocument title: An adoption study of human obesity.\n\nAbstract sentences:\n[0] We examined the contributions of genetic factors and the family environment to human fatness in a sample of 540 adult Danish adoptees who were selected from a population of 3580 and divided into four weight classes: thin, median weight, overweight, and obese.\n[1] There was a strong relation between the weight class of the adoptees and the body-mass index of their biologic parents - for the mothers, P less than 0.0001; for the fathers, P less than 0.02.\n[2] There was no relation between the weight class of the adoptees and the body-mass index of their adoptive parents.\n[3] Cumulative distributions of the body-mass index of parents showed similar results; there was a strong relation between the body-mass index of biologic parents and adoptee weight class and no relation between the index of adoptive parents and adoptee weight class.\n[4] Furthermore, the relation between biologic parents and adoptees was not confined to the obesity weight class, but was present across the whole range of body fatness - from very thin to very fat.\n[5] We conclude that genetic influences have an important role in determining human fatness in adults, whereas the family environment alone has no apparent effect."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [1]\nExplanation: Evidence states: \"There was a strong relation between the weight class of the adoptees and the body-mass index of their biologic parents - for the mothers, P less than 0.0001; for the fathers, P less than 0.02.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 873, "doc_id": 29025270, "label": "CONTRADICTS", "evidence_sentence_ids": [1], "cited_doc_ids": [1180972, 19307912, 27393799, 29025270, 3315558], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 is determined solely by environmental factors.\n\nDocument title: An adoption study of human obesity.\n\nAbstract sentences:\n[0] We examined the contributions of genetic factors and the family environment to human fatness in a sample of 540 adult Danish adoptees who were selected from a population of 3580 and divided into four weight classes: thin, median weight, overweight, and obese.\n[1] There was a strong relation between the weight class of the adoptees and the body-mass index of their biologic parents - for the mothers, P less than 0.0001; for the fathers, P less than 0.02.\n[2] There was no relation between the weight class of the adoptees and the body-mass index of their adoptive parents.\n[3] Cumulative distributions of the body-mass index of parents showed similar results; there was a strong relation between the body-mass index of biologic parents and adoptee weight class and no relation between the index of adoptive parents and adoptee weight class.\n[4] Furthermore, the relation between biologic parents and adoptees was not confined to the obesity weight class, but was present across the whole range of body fatness - from very thin to very fat.\n[5] We conclude that genetic influences have an important role in determining human fatness in adults, whereas the family environment alone has no apparent effect."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Cumulative distributions of the body-mass index of parents showed similar results; there was a strong relation between the body-mass index of biologic parents and adoptee weight class and no relation between the index of adoptive parents and adoptee weight class.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 873, "doc_id": 29025270, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [1180972, 19307912, 27393799, 29025270, 3315558], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 is determined solely by environmental factors.\n\nDocument title: An adoption study of human obesity.\n\nAbstract sentences:\n[0] We examined the contributions of genetic factors and the family environment to human fatness in a sample of 540 adult Danish adoptees who were selected from a population of 3580 and divided into four weight classes: thin, median weight, overweight, and obese.\n[1] There was a strong relation between the weight class of the adoptees and the body-mass index of their biologic parents - for the mothers, P less than 0.0001; for the fathers, P less than 0.02.\n[2] There was no relation between the weight class of the adoptees and the body-mass index of their adoptive parents.\n[3] Cumulative distributions of the body-mass index of parents showed similar results; there was a strong relation between the body-mass index of biologic parents and adoptee weight class and no relation between the index of adoptive parents and adoptee weight class.\n[4] Furthermore, the relation between biologic parents and adoptees was not confined to the obesity weight class, but was present across the whole range of body fatness - from very thin to very fat.\n[5] We conclude that genetic influences have an important role in determining human fatness in adults, whereas the family environment alone has no apparent effect."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"We conclude that genetic influences have an important role in determining human fatness in adults, whereas the family environment alone has no apparent effect.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 873, "doc_id": 29025270, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [1180972, 19307912, 27393799, 29025270, 3315558], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 is determined solely by environmental factors.\n\nDocument title: Genetic analysis of human obesity in an Italian sample.\n\nAbstract sentences:\n[0] An analysis of the genetic factors in obesity has been carried out on a sample of nuclear families from Aosta (N. Italy).\n[1] The families consisted of the parents and sibs of all elementary school children considered to be obese during a preliminary screening and a similar sample of non-obese children and their nuclear families.\n[2] The numbers of such families were 67 and 112, respectively.\n[3] Several tests were applied in order to examine the genetic contribution to obesity, and in particular to investigate the presence of a dominant major gene.\n[4] Our conclusions are that genetic factors are certainly present.\n[5] Several analyses suggest the presence of a dominant major gene with weak effect."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Our conclusions are that genetic factors are certainly present.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 873, "doc_id": 3315558, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [1180972, 19307912, 27393799, 29025270, 3315558], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 is determined solely by environmental factors.\n\nDocument title: Genetic analysis of human obesity in an Italian sample.\n\nAbstract sentences:\n[0] An analysis of the genetic factors in obesity has been carried out on a sample of nuclear families from Aosta (N. Italy).\n[1] The families consisted of the parents and sibs of all elementary school children considered to be obese during a preliminary screening and a similar sample of non-obese children and their nuclear families.\n[2] The numbers of such families were 67 and 112, respectively.\n[3] Several tests were applied in order to examine the genetic contribution to obesity, and in particular to investigate the presence of a dominant major gene.\n[4] Our conclusions are that genetic factors are certainly present.\n[5] Several analyses suggest the presence of a dominant major gene with weak effect."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Several analyses suggest the presence of a dominant major gene with weak effect.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 873, "doc_id": 3315558, "label": "CONTRADICTS", "evidence_sentence_ids": [5], "cited_doc_ids": [1180972, 19307912, 27393799, 29025270, 3315558], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Occupancy of ribosomes by IncRNAs do not make functional peptides.\n\nDocument title: Ribosome Profiling Provides Evidence that Large Noncoding RNAs Do Not Encode Proteins\n\nAbstract sentences:\n[0] Large noncoding RNAs are emerging as an important component in cellular regulation.\n[1] Considerable evidence indicates that these transcripts act directly as functional RNAs rather than through an encoded protein product.\n[2] However, a recent study of ribosome occupancy reported that many large intergenic ncRNAs (lincRNAs) are bound by ribosomes, raising the possibility that they are translated into proteins.\n[3] Here, we show that classical noncoding RNAs and 5' UTRs show the same ribosome occupancy as lincRNAs, demonstrating that ribosome occupancy alone is not sufficient to classify transcripts as coding or noncoding.\n[4] Instead, we define a metric based on the known property of translation whereby translating ribosomes are released upon encountering a bona fide stop codon.\n[5] We show that this metric accurately discriminates between protein-coding transcripts and all classes of known noncoding transcripts, including lincRNAs.\n[6] Taken together, these results argue that the large majority of lincRNAs do not function through encoded proteins."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Here, we show that classical noncoding RNAs and 5' UTRs show the same ribosome occupancy as lincRNAs, demonstrating that ribosome occupancy alone is not sufficient to classify transcripts as coding or noncoding.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 879, "doc_id": 8426046, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [8426046], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Occupancy of ribosomes by IncRNAs mirror 5 0-UTRs\n\nDocument title: Ribosome Profiling Provides Evidence that Large Noncoding RNAs Do Not Encode Proteins\n\nAbstract sentences:\n[0] Large noncoding RNAs are emerging as an important component in cellular regulation.\n[1] Considerable evidence indicates that these transcripts act directly as functional RNAs rather than through an encoded protein product.\n[2] However, a recent study of ribosome occupancy reported that many large intergenic ncRNAs (lincRNAs) are bound by ribosomes, raising the possibility that they are translated into proteins.\n[3] Here, we show that classical noncoding RNAs and 5' UTRs show the same ribosome occupancy as lincRNAs, demonstrating that ribosome occupancy alone is not sufficient to classify transcripts as coding or noncoding.\n[4] Instead, we define a metric based on the known property of translation whereby translating ribosomes are released upon encountering a bona fide stop codon.\n[5] We show that this metric accurately discriminates between protein-coding transcripts and all classes of known noncoding transcripts, including lincRNAs.\n[6] Taken together, these results argue that the large majority of lincRNAs do not function through encoded proteins."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Here, we show that classical noncoding RNAs and 5' UTRs show the same ribosome occupancy as lincRNAs, demonstrating that ribosome occupancy alone is not sufficient to classify transcripts as coding or noncoding.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 880, "doc_id": 8426046, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [8426046], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 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: 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": "validation", "claim_id": 882, "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: Only a minority of cells survive development after differentiation into stress-resistant spores.\n\nDocument title: Exploitative and Hierarchical Antagonism in a Cooperative Bacterium\n\nAbstract sentences:\n[0] Social organisms that cooperate with some members of their own species, such as close relatives, may fail to cooperate with other genotypes of the same species.\n[1] Such noncooperation may take the form of outright antagonism or social exploitation.\n[2] Myxococcus xanthus is a highly social prokaryote that cooperatively develops into spore-bearing, multicellular fruiting bodies in response to starvation.\n[3] Here we have characterized the nature of social interactions among nine developmentally proficient strains of M. xanthus isolated from spatially distant locations.\n[4] Strains were competed against one another in all possible pairwise combinations during starvation-induced development.\n[5] In most pairings, at least one competitor exhibited strong antagonism toward its partner and a majority of mixes showed bidirectional antagonism that decreased total spore production, even to the point of driving whole populations to extinction.\n[6] Differential response to mixing was the primary determinant of competitive superiority rather than the sporulation efficiencies of unmixed populations.\n[7] In some competitive pairings, the dominant partner sporulated more efficiently in mixed populations than in clonal isolation.\n[8] This finding represents a novel form of exploitation in bacteria carried out by socially competent genotypes and is the first documentation of social exploitation among natural bacterial isolates.\n[9] Patterns of antagonistic superiority among these strains form a highly linear dominance hierarchy.\n[10] At least some competition pairs construct chimeric, rather than segregated, fruiting bodies.\n[11] The cooperative prokaryote M. xanthus has diverged into a large number of distinct social types that cooperate with clone-mates but exhibit intense antagonism toward distinct social types of the same species.\n[12] Most lengthy migration events in nature may thus result in strong antagonism between migratory and resident populations, and this antagonism may have large effects on local population sizes and dynamics.\n[13] Intense mutual antagonism appears to be more prevalent in this prokaryotic social species than has been observed in the eukaryotic social slime mold Dictyostelium discoideum, which also exhibits multicellular development.\n[14] The finding of several cases of facultative social exploitation among these natural isolates suggests that such exploitation may occur frequently in nature in many prokaryotes with cooperative traits."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 887, "doc_id": 18855191, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [18855191], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 reduces 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 903, "doc_id": 10648422, "label": "CONTRADICTS", "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 reduces 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 903, "doc_id": 10648422, "label": "CONTRADICTS", "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: PDPN promotes efficient motility along stromal surfaces by activating the C-type lectin receptor to rearrange the actin cytoskeleton in dendritic cells.\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": "validation", "claim_id": 904, "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: PGE 2 promotes 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": "validation", "claim_id": 907, "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 plays an essential role in 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 911, "doc_id": 11254556, "label": "SUPPORTS", "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 plays an essential role in 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 911, "doc_id": 11254556, "label": "SUPPORTS", "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: PPAR-RXRs are inhibited by PPAR ligands.\n\nDocument title: Unique response pathways are established by allosteric interactions among nuclear hormone receptors\n\nAbstract sentences:\n[0] Heterodimerization is a common paradigm among eukaryotic transcription factors.\n[1] The 9-cis retinoic acid receptor (RXR) serves as a common heterodimerization partner for several nuclear receptors, including the thyroid hormone receptor (T3R) and retinoic acid receptor (RAR).\n[2] This raises the question as to whether these complexes possess dual hormonal responsiveness.\n[3] We devised a strategy to examine the transcriptional properties of each receptor individually or when tethered to a heterodimeric partner.\n[4] We find that the intrinsic binding properties of RXR are masked in T3R-RXR and RAR-RXR heterodimers.\n[5] In contrast, RXR is active as a non-DNA-binding cofactor with the NGFI-B/Nurr1 orphan receptors.\n[6] Heterodimerization of RXR with constitutively active NGFI-B/Nurr1 creates a novel hormone-dependent complex.\n[7] These findings suggest that allosteric interactions among heterodimers create complexes with unique properties.\n[8] We suggest that allostery is a critical feature underlying the generation of diversity in hormone response networks."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 913, "doc_id": 3203590, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [3203590], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: PPAR-RXRs can be activated by PPAR ligands.\n\nDocument title: Unique response pathways are established by allosteric interactions among nuclear hormone receptors\n\nAbstract sentences:\n[0] Heterodimerization is a common paradigm among eukaryotic transcription factors.\n[1] The 9-cis retinoic acid receptor (RXR) serves as a common heterodimerization partner for several nuclear receptors, including the thyroid hormone receptor (T3R) and retinoic acid receptor (RAR).\n[2] This raises the question as to whether these complexes possess dual hormonal responsiveness.\n[3] We devised a strategy to examine the transcriptional properties of each receptor individually or when tethered to a heterodimeric partner.\n[4] We find that the intrinsic binding properties of RXR are masked in T3R-RXR and RAR-RXR heterodimers.\n[5] In contrast, RXR is active as a non-DNA-binding cofactor with the NGFI-B/Nurr1 orphan receptors.\n[6] Heterodimerization of RXR with constitutively active NGFI-B/Nurr1 creates a novel hormone-dependent complex.\n[7] These findings suggest that allosteric interactions among heterodimers create complexes with unique properties.\n[8] We suggest that allostery is a critical feature underlying the generation of diversity in hormone response networks."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 914, "doc_id": 3203590, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [3203590], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Participating in six months of physical activity improves cognitive functioning.\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": "validation", "claim_id": 921, "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: Participating in six months of physical activity improves cognitive functioning.\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: [10]\nExplanation: Evidence states: \"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.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 921, "doc_id": 1642727, "label": "SUPPORTS", "evidence_sentence_ids": [10], "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: Participating in six months of physical activity improves cognitive functioning.\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": "validation", "claim_id": 921, "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: Patients in stable partnerships have a faster 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: 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": "validation", "claim_id": 922, "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 have a faster 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: 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": "validation", "claim_id": 922, "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: Peroxynitrite is required for nitration of TCR/CD8.\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]\nExplanation: Evidence states: \"Nitration of TCR-CD8 is induced by MDSCs through hyperproduction of reactive oxygen species and peroxynitrite during direct cell-cell contact.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 936, "doc_id": 5483793, "label": "SUPPORTS", "evidence_sentence_ids": [3], "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: Pleiotropic coupling of GLP-1R to intracellular effectors promotes distinct profiles of cellular signaling.\n\nDocument title: The Extracellular Surface of the GLP-1 Receptor Is a Molecular Trigger for Biased Agonism\n\nAbstract sentences:\n[0] Ligand-directed signal bias offers opportunities for sculpting molecular events, with the promise of better, safer therapeutics.\n[1] Critical to the exploitation of signal bias is an understanding of the molecular events coupling ligand binding to intracellular signaling.\n[2] Activation of class B G protein-coupled receptors is driven by interaction of the peptide N terminus with the receptor core.\n[3] To understand how this drives signaling, we have used advanced analytical methods that enable separation of effects on pathway-specific signaling from those that modify agonist affinity and mapped the functional consequence of receptor modification onto three-dimensional models of a receptor-ligand complex.\n[4] This yields molecular insights into the initiation of receptor activation and the mechanistic basis for biased agonism.\n[5] Our data reveal that peptide agonists can engage different elements of the receptor extracellular face to achieve effector coupling and biased signaling providing a foundation for rational design of biased agonists."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 956, "doc_id": 12956194, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [12956194], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Podocytes are motile and migrate in the presence of injury.\n\nDocument title: Tracking the fate of glomerular epithelial cells in vivo using serial multiphoton imaging in novel mouse models with fluorescent lineage tags\n\nAbstract sentences:\n[0] Podocytes are critical in the maintenance of a healthy glomerular filter; however, they have been difficult to study in the intact kidney because of technical limitations.\n[1] Here we report the development of serial multiphoton microscopy (MPM) of the same glomeruli over several days to visualize the motility of podocytes and parietal epithelial cells (PECs) in vivo.\n[2] In podocin-GFP mice, podocytes formed sporadic multicellular clusters after unilateral ureteral ligation and migrated into the parietal Bowman's capsule.\n[3] The tracking of single cells in podocin-confetti mice featuring cell-specific expression of CFP, GFP, YFP or RFP revealed the simultaneous migration of multiple podocytes.\n[4] In phosphoenolpyruvate carboxykinase (PEPCK)-GFP mice, serial MPM found PEC-to-podocyte migration and nanotubule connections.\n[5] Our data support a highly dynamic rather than a static nature of the glomerular environment and cellular composition.\n[6] Future application of this new approach should advance our understanding of the mechanisms of glomerular injury and regeneration."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"In podocin-GFP mice, podocytes formed sporadic multicellular clusters after unilateral ureteral ligation and migrated into the parietal Bowman's capsule.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 957, "doc_id": 123859, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [123859], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 reduces 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 960, "doc_id": 8780599, "label": "SUPPORTS", "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 reduces 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 960, "doc_id": 8780599, "label": "SUPPORTS", "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: Pretreatment with the Arp2/3 inhibitor CK-666 affects lamelliopodia formation.\n\nDocument title: Arp2/3 complex inhibition radically alters lamellipodial actin architecture, suspended cell shape, and the cell spreading process\n\nAbstract sentences:\n[0] Recent studies have investigated the dendritic actin cytoskeleton of the cell edge's lamellipodial (LP) region by experimentally decreasing the activity of the actin filament nucleator and branch former, the Arp2/3 complex.\n[1] Here we extend these studies via pharmacological inhibition of the Arp2/3 complex in sea urchin coelomocytes, cells that possess an unusually broad LP region and display correspondingly exaggerated centripetal flow.\n[2] Using light and electron microscopy, we demonstrate that Arp2/3 complex inhibition via the drug CK666 dramatically altered LP actin architecture, slowed centripetal flow, drove a lamellipodial-to-filopodial shape change in suspended cells, and induced a novel actin structural organization during cell spreading.\n[3] A general feature of the CK666 phenotype in coelomocytes was transverse actin arcs, and arc generation was arrested by a formin inhibitor.\n[4] We also demonstrate that CK666 treatment produces actin arcs in other cells with broad LP regions, namely fish keratocytes and Drosophila S2 cells.\n[5] We hypothesize that the actin arcs made visible by Arp2/3 complex inhibition in coelomocytes may represent an exaggerated manifestation of the elongate mother filaments that could possibly serve as the scaffold for the production of the dendritic actin network."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"Using light and electron microscopy, we demonstrate that Arp2/3 complex inhibition via the drug CK666 dramatically altered LP actin architecture, slowed centripetal flow, drove a lamellipodial-to-filopodial shape change in suspended cells, and induced a novel actin structural organization during cell spreading.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 967, "doc_id": 8997410, "label": "SUPPORTS", "evidence_sentence_ids": [2], "cited_doc_ids": [2119889, 8997410], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 higher 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 971, "doc_id": 46695481, "label": "SUPPORTS", "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 higher 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 971, "doc_id": 46695481, "label": "SUPPORTS", "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 higher 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: 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": "validation", "claim_id": 971, "doc_id": 27873158, "label": "SUPPORTS", "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 higher 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 971, "doc_id": 27873158, "label": "SUPPORTS", "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 higher 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: 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": "validation", "claim_id": 971, "doc_id": 27873158, "label": "SUPPORTS", "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 higher 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: 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": "validation", "claim_id": 971, "doc_id": 28617573, "label": "SUPPORTS", "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 higher 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: 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": "validation", "claim_id": 971, "doc_id": 9764256, "label": "SUPPORTS", "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 pro-inflammatory cytokines induce 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": "validation", "claim_id": 975, "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: Proteins synthesized at the growth cone are ubiquitinated at a higher rate than proteins from the cell body.\n\nDocument title: Coupled local translation and degradation regulate growth cone collapse\n\nAbstract sentences:\n[0] Local translation mediates axonal responses to Semaphorin3A (Sema3A) and other guidance cues.\n[1] However, only a subset of the axonal proteome is locally synthesized, whereas most proteins are trafficked from the soma.\n[2] The reason why only specific proteins are locally synthesized is unknown.\n[3] Here we show that local protein synthesis and degradation are linked events in growth cones.\n[4] We find that growth cones exhibit high levels of ubiquitination and that local signalling pathways trigger the ubiquitination and degradation of RhoA, a mediator of Sema3A-induced growth cone collapse.\n[5] Inhibition of RhoA degradation is sufficient to remove the protein-synthesis requirement for Sema3A-induced growth cone collapse.\n[6] In addition to RhoA, we find that locally translated proteins are the main targets of the ubiquitin-proteasome system in growth cones.\n[7] Thus, local protein degradation is a major feature of growth cones and creates a requirement for local translation to replenish proteins needed to maintain growth cone responses."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"We find that growth cones exhibit high levels of ubiquitination and that local signalling pathways trigger the ubiquitination and degradation of RhoA, a mediator of Sema3A-induced growth cone collapse.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 982, "doc_id": 2988714, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [2988714], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 regulates the expression of PTEN by functioning as an miRNA decoy.\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": "validation", "claim_id": 985, "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: Pyridostatin destabilizes 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: 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": "validation", "claim_id": 993, "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: Radioiodine treatment of non-toxic multinodular goitre reduces 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1012, "doc_id": 9745001, "label": "SUPPORTS", "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 reduces 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1012, "doc_id": 9745001, "label": "SUPPORTS", "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 decreases 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": "validation", "claim_id": 1014, "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 govern fidelity in two component systems\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: [7]\nExplanation: Evidence states: \"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.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1019, "doc_id": 11603066, "label": "SUPPORTS", "evidence_sentence_ids": [7], "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: Rapid up-regulation and higher basal expression of interferon-induced genes increase survival of granule cell neurons that are infected by West Nile virus.\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: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"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.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1020, "doc_id": 9433958, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [9433958], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 up-regulation and higher basal expression of interferon-induced genes reduce survival of granule cell neurons that are infected by West Nile virus.\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: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"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.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1021, "doc_id": 9433958, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [9433958], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Recurrent mutations occur frequently within CTCF anchor sites adjacent to oncogenes.\n\nDocument title: 3D Chromosome Regulatory Landscape of Human Pluripotent Cells.\n\nAbstract sentences:\n[0] In this study, we describe the 3D chromosome regulatory landscape of human naive and primed embryonic stem cells.\n[1] To devise this map, we identified transcriptional enhancers and insulators in these cells and placed them within the context of cohesin-associated CTCF-CTCF loops using cohesin ChIA-PET data.\n[2] The CTCF-CTCF loops we identified form a chromosomal framework of insulated neighborhoods, which in turn form topologically associating domains (TADs) that are largely preserved during the transition between the naive and primed states.\n[3] Regulatory changes in enhancer-promoter interactions occur within insulated neighborhoods during cell state transition.\n[4] The CTCF anchor regions we identified are conserved across species, influence gene expression, and are a frequent site of mutations in cancer cells, underscoring their functional importance in cellular regulation.\n[5] These 3D regulatory maps of human pluripotent cells therefore provide a foundation for future interrogation of the relationships between chromosome structure and gene control in development and disease."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"The CTCF anchor regions we identified are conserved across species, influence gene expression, and are a frequent site of mutations in cancer cells, underscoring their functional importance in cellular regulation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1024, "doc_id": 5373138, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [5373138], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 greater resistance to 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1029, "doc_id": 13923140, "label": "CONTRADICTS", "evidence_sentence_ids": [2, 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: Reduced responsiveness to interleukin-2 in regulatory T cells is associated with greater resistance to autoimmune diseases such as Type 1 Diabetes.\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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1029, "doc_id": 13940200, "label": "CONTRADICTS", "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: Reduced responsiveness to interleukin-2 in regulatory T cells is associated with greater resistance to 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1029, "doc_id": 11899391, "label": "CONTRADICTS", "evidence_sentence_ids": [6], "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: Replacement of histone H2A with H2A.Z slows gene activation in yeasts by stabilizing +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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1041, "doc_id": 25254425, "label": "CONTRADICTS", "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: Ribosomopathies have a low 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1049, "doc_id": 12486491, "label": "CONTRADICTS", "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: S-nitrosylated GAPDH physiologically transnitrosylates histone deacetylases.\n\nDocument title: GAPDH Mediates Nitrosylation of Nuclear Proteins\n\nAbstract sentences:\n[0] S-nitrosylation of proteins by nitric oxide is a major mode of signalling in cells.\n[1] S-nitrosylation can mediate the regulation of a range of proteins, including prominent nuclear proteins, such as HDAC2 (ref.\n[2] 2) and PARP1 (ref.\n[3] 3).\n[4] The high reactivity of the nitric oxide group with protein thiols, but the selective nature of nitrosylation within the cell, implies the existence of targeting mechanisms.\n[5] Specificity of nitric oxide signalling is often achieved by the binding of nitric oxide synthase (NOS) to target proteins, either directly or through scaffolding proteins such as PSD-95 (ref.\n[6] 5) and CAPON.\n[7] As the three principal isoforms of NOS--neuronal NOS (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS)--are primarily non-nuclear, the mechanisms by which nuclear proteins are selectively nitrosylated have been elusive.\n[8] Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is physiologically nitrosylated at its Cys 150 residue.\n[9] Nitrosylated GAPDH (SNO-GAPDH) binds to Siah1, which possesses a nuclear localization signal, and is transported to the nucleus.\n[10] Here, we show that SNO-GAPDH physiologically transnitrosylates nuclear proteins, including the deacetylating enzyme sirtuin-1 (SIRT1), histone deacetylase-2 (HDAC2) and DNA-activated protein kinase (DNA-PK).\n[11] Our findings reveal a novel mechanism for targeted nitrosylation of nuclear proteins and suggest that protein-protein transfer of nitric oxide groups may be a general mechanism in cellular signal transduction."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [10]\nExplanation: Evidence states: \"Here, we show that SNO-GAPDH physiologically transnitrosylates nuclear proteins, including the deacetylating enzyme sirtuin-1 (SIRT1), histone deacetylase-2 (HDAC2) and DNA-activated protein kinase (DNA-PK).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1062, "doc_id": 20381484, "label": "SUPPORTS", "evidence_sentence_ids": [10], "cited_doc_ids": [20381484], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 improves 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: SUPPORTS\nRationale sentence ids: [6]\nExplanation: Evidence states: \"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).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1086, "doc_id": 39281140, "label": "SUPPORTS", "evidence_sentence_ids": [6], "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 improves 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1086, "doc_id": 39281140, "label": "SUPPORTS", "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 improves 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1086, "doc_id": 39281140, "label": "SUPPORTS", "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: Silencing of Bcl2 is important for the maintenance and progression of tumors.\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": "validation", "claim_id": 1088, "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: Smc5/6 engagment drives 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1089, "doc_id": 17628888, "label": "SUPPORTS", "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: Statins decrease blood cholesterol.\n\nDocument title: A Century of Cholesterol and Coronaries: From Plaques to Genes to Statins\n\nAbstract sentences:\n[0] One-fourth of all deaths in industrialized countries result from coronary heart disease.\n[1] A century of research has revealed the essential causative agent: cholesterol-carrying low-density lipoprotein (LDL).\n[2] LDL is controlled by specific receptors (LDLRs) in liver that remove it from blood.\n[3] Mutations that eliminate LDLRs raise LDL and cause heart attacks in childhood, whereas mutations that raise LDLRs reduce LDL and diminish heart attacks.\n[4] If we are to eliminate coronary disease, lowering LDL should be the primary goal.\n[5] Effective means to achieve this goal are currently available.\n[6] The key questions are: who to treat, when to treat, and how long to treat."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1099, "doc_id": 7662206, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [7662206], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Statins increase blood cholesterol.\n\nDocument title: A Century of Cholesterol and Coronaries: From Plaques to Genes to Statins\n\nAbstract sentences:\n[0] One-fourth of all deaths in industrialized countries result from coronary heart disease.\n[1] A century of research has revealed the essential causative agent: cholesterol-carrying low-density lipoprotein (LDL).\n[2] LDL is controlled by specific receptors (LDLRs) in liver that remove it from blood.\n[3] Mutations that eliminate LDLRs raise LDL and cause heart attacks in childhood, whereas mutations that raise LDLRs reduce LDL and diminish heart attacks.\n[4] If we are to eliminate coronary disease, lowering LDL should be the primary goal.\n[5] Effective means to achieve this goal are currently available.\n[6] The key questions are: who to treat, when to treat, and how long to treat."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1100, "doc_id": 7662206, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [7662206], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 lower 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1104, "doc_id": 3898784, "label": "SUPPORTS", "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 lower 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1104, "doc_id": 3898784, "label": "SUPPORTS", "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 lower 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1104, "doc_id": 3898784, "label": "SUPPORTS", "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 lower 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1104, "doc_id": 3898784, "label": "SUPPORTS", "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: Subcutaneous fat depots undergo extensive browning processes after cold exposure.\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: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"During cold-induced 'browning' of subcutaneous fat, most 'beige' adipocytes stem from de novo–differentiated adipocytes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1107, "doc_id": 20532591, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [20532591], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 not predictive of chronic disease\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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1110, "doc_id": 13770184, "label": "CONTRADICTS", "evidence_sentence_ids": [13], "cited_doc_ids": [13770184], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Synaptic activity enhances local release of brain derived neurotrophic factor from postsynaptic dendrites.\n\nDocument title: Autocrine BDNF–TrkB signalling within a single dendritic spine\n\nAbstract sentences:\n[0] Brain-derived neurotrophic factor (BDNF) and its receptor TrkB are crucial for many forms of neuronal plasticity, including structural long-term potentiation (sLTP), which is a correlate of an animal’s learning.\n[1] However, it is unknown whether BDNF release and TrkB activation occur during sLTP, and if so, when and where.\n[2] Here, using a fluorescence resonance energy transfer-based sensor for TrkB and two-photon fluorescence lifetime imaging microscopy, we monitor TrkB activity in single dendritic spines of CA1 pyramidal neurons in cultured murine hippocampal slices.\n[3] In response to sLTP induction, we find fast (onset < 1 min) and sustained (>20 min) activation of TrkB in the stimulated spine that depends on NMDAR (N-methyl-d-aspartate receptor) and CaMKII signalling and on postsynaptically synthesized BDNF.\n[4] We confirm the presence of postsynaptic BDNF using electron microscopy to localize endogenous BDNF to dendrites and spines of hippocampal CA1 pyramidal neurons.\n[5] Consistent with these findings, we also show rapid, glutamate-uncaging-evoked, time-locked BDNF release from single dendritic spines using BDNF fused to superecliptic pHluorin.\n[6] We demonstrate that this postsynaptic BDNF–TrkB signalling pathway is necessary for both structural and functional LTP.\n[7] Together, these findings reveal a spine-autonomous, autocrine signalling mechanism involving NMDAR–CaMKII-dependent BDNF release from stimulated dendritic spines and subsequent TrkB activation on these same spines that is crucial for structural and functional plasticity."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"Together, these findings reveal a spine-autonomous, autocrine signalling mechanism involving NMDAR–CaMKII-dependent BDNF release from stimulated dendritic spines and subsequent TrkB activation on these same spines that is crucial for structural and functional plasticity.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1121, "doc_id": 4456756, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [4456756], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 regulatory cells (tTregs) lacking αvβ8 are more adept at suppressing pathogenic T-cell responses during active inflammation.\n\nDocument title: Integrin αvβ8-Mediated TGF-β Activation by Effector Regulatory T Cells Is Essential for Suppression of T-Cell-Mediated Inflammation\n\nAbstract sentences:\n[0] Regulatory T (Treg) cells play a pivotal role in suppressing self-harmful T cell responses, but how Treg cells mediate suppression to maintain immune homeostasis and limit responses during inflammation is unclear.\n[1] Here we show that effector Treg cells express high amounts of the integrin αvβ8, which enables them to activate latent transforming growth factor-β (TGF-β).\n[2] Treg-cell-specific deletion of integrin αvβ8 did not result in a spontaneous inflammatory phenotype, suggesting that this pathway is not important in Treg-cell-mediated maintenance of immune homeostasis.\n[3] However, Treg cells lacking expression of integrin αvβ8 were unable to suppress pathogenic T cell responses during active inflammation.\n[4] Thus, our results identify a mechanism by which Treg cells suppress exuberant immune responses, highlighting a key role for effector Treg-cell-mediated activation of latent TGF-β in suppression of self-harmful T cell responses during active inflammation."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"However, Treg cells lacking expression of integrin αvβ8 were unable to suppress pathogenic T cell responses during active inflammation.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1130, "doc_id": 17997584, "label": "CONTRADICTS", "evidence_sentence_ids": [3], "cited_doc_ids": [17997584], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: TCR/CD3 microdomains are a required to induce the immunologic synapse to activate T cells.\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: [3, 4]\nExplanation: Evidence states: \"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. This conformational change at CD3 reverts upon ligand dissociation and is required for T cell activation.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1132, "doc_id": 33499189, "label": "SUPPORTS", "evidence_sentence_ids": [3, 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: TNFAIP3 is a tumor suppressor 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: 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": "validation", "claim_id": 1137, "doc_id": 33370, "label": "CONTRADICTS", "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 suppressor 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: 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": "validation", "claim_id": 1137, "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: Taking 400mg of α-tocopheryl acetate helps to 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1140, "doc_id": 12009265, "label": "CONTRADICTS", "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 helps to 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: 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": "validation", "claim_id": 1140, "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: Taxation of sugar-sweetened beverages had no effect on 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1144, "doc_id": 10071552, "label": "CONTRADICTS", "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 had no effect on 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1144, "doc_id": 10071552, "label": "CONTRADICTS", "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 had no effect on 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1144, "doc_id": 10071552, "label": "CONTRADICTS", "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: Teaching hospitals do not provide better care than 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": "validation", "claim_id": 1146, "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: Teaching hospitals do not provide better care than 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: [12]\nExplanation: Evidence states: \"Other outcomes were diverse, but typically teaching healthcare structures did not do better than nonteaching ones.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1146, "doc_id": 13906581, "label": "SUPPORTS", "evidence_sentence_ids": [12], "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: Teaching hospitals do not provide better care than 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": "validation", "claim_id": 1146, "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: Tetraspanin-3 is a causative factor in the development of acute myelogenous leukemia\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: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"However, Tspan3 deletion impaired leukemia stem cell self-renewal and disease propagation and markedly improved survival in mouse models of AML.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1150, "doc_id": 11369420, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [11369420], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Tetraspanin-3 is a causative factor in the development of acute myelogenous leukemia\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: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"Additionally, Tspan3 inhibition blocked growth of AML patient samples, suggesting that Tspan3 is also important in human disease.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1150, "doc_id": 11369420, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [11369420], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Tetraspanin-3 is a causative factor in the development of acute myelogenous leukemia\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: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"These identify Tspan3 as an important regulator of aggressive leukemias and highlight a role for Tspan3 in oncogenesis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1150, "doc_id": 11369420, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [11369420], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 is an alternative SSB.\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: [5]\nExplanation: Evidence states: \"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.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1163, "doc_id": 15305881, "label": "SUPPORTS", "evidence_sentence_ids": [5], "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 PPR MDA5 has two 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": "validation", "claim_id": 1175, "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 PRR MDA5 has a central DExD/H RNA helices 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": "validation", "claim_id": 1179, "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 PRR MDA5 is a sensor of RNA virus infection.\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: SUPPORTS\nRationale sentence ids: [0]\nExplanation: Evidence states: \"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.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1180, "doc_id": 31272411, "label": "SUPPORTS", "evidence_sentence_ids": [0], "cited_doc_ids": [31272411], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 $750 million 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1185, "doc_id": 16737210, "label": "SUPPORTS", "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 YAP1 and TEAD complex tanslocates into the nucleus where it interacts with transcription factors and DNA-binding proteins that modulate target gene transcription.\n\nDocument title: Regulation of Hippo pathway transcription factor TEAD by p38 MAPK-induced cytoplasmic translocation\n\nAbstract sentences:\n[0] The Hippo pathway controls organ size and tissue homeostasis, with deregulation leading to cancer.\n[1] The core Hippo components in mammals are composed of the upstream serine/threonine kinases Mst1/2, MAPK4Ks and Lats1/2.\n[2] Inactivation of these upstream kinases leads to dephosphorylation, stabilization, nuclear translocation and thus activation of the major functional transducers of the Hippo pathway, YAP and its paralogue TAZ.\n[3] YAP/TAZ are transcription co-activators that regulate gene expression primarily through interaction with the TEA domain DNA-binding family of transcription factors (TEAD).\n[4] The current paradigm for regulation of this pathway centres on phosphorylation-dependent nucleocytoplasmic shuttling of YAP/TAZ through a complex network of upstream components.\n[5] However, unlike other transcription factors, such as SMAD, NF-κB, NFAT and STAT, the regulation of TEAD nucleocytoplasmic shuttling has been largely overlooked.\n[6] In the present study, we show that environmental stress promotes TEAD cytoplasmic translocation via p38 MAPK in a Hippo-independent manner.\n[7] Importantly, stress-induced TEAD inhibition predominates YAP-activating signals and selectively suppresses YAP-driven cancer cell growth.\n[8] Our data reveal a mechanism governing TEAD nucleocytoplasmic shuttling and show that TEAD localization is a critical determinant of Hippo signalling output."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"YAP/TAZ are transcription co-activators that regulate gene expression primarily through interaction with the TEA domain DNA-binding family of transcription factors (TEAD).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1187, "doc_id": 52873726, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [52873726], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 years.\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": "validation", "claim_id": 1191, "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 arm density of TatAd complexes is due to structural rearrangements within Class1 TatAd complexes such as the 'charge zipper mechanism'.\n\nDocument title: Folding and Self-Assembly of the TatA Translocation Pore Based on a Charge Zipper Mechanism\n\nAbstract sentences:\n[0] We propose a concept for the folding and self-assembly of the pore-forming TatA complex from the Twin-arginine translocase and of other membrane proteins based on electrostatic \"charge zippers.\n[1] \"\n[2] Each subunit of TatA consists of a transmembrane segment, an amphiphilic helix (APH), and a C-terminal densely charged region (DCR).\n[3] The sequence of charges in the DCR is complementary to the charge pattern on the APH, suggesting that the protein can be \"zipped up\" by a ladder of seven salt bridges.\n[4] The length of the resulting hairpin matches the lipid bilayer thickness, hence a transmembrane pore could self-assemble via intra- and intermolecular salt bridges.\n[5] The steric feasibility was rationalized by molecular dynamics simulations, and experimental evidence was obtained by monitoring the monomer-oligomer equilibrium of specific charge mutants.\n[6] Similar \"charge zippers\" are proposed for other membrane-associated proteins, e.g., the biofilm-inducing peptide TisB, the human antimicrobial peptide dermcidin, and the pestiviral E(RNS) protein."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1194, "doc_id": 11419230, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [11419230], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 availability of safe places to study 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": "validation", "claim_id": 1196, "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: The availability of safe places to study 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": "validation", "claim_id": 1197, "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: The benefits of colchicine were achieved with effective widespread use of secondary prevention strategies such as high-dose statins.\n\nDocument title: Comparative determinants of 4-year cardiovascular event rates in stable outpatients at risk of or with atherothrombosis.\n\nAbstract sentences:\n[0] CONTEXT Clinicians and trialists have difficulty with identifying which patients are highest risk for cardiovascular events.\n[1] Prior ischemic events, polyvascular disease, and diabetes mellitus have all been identified as predictors of ischemic events, but their comparative contributions to future risk remain unclear.\n[2] OBJECTIVE To categorize the risk of cardiovascular events in stable outpatients with various initial manifestations of atherothrombosis using simple clinical descriptors.\n[3] DESIGN, SETTING, AND PATIENTS Outpatients with coronary artery disease, cerebrovascular disease, or peripheral arterial disease or with multiple risk factors for atherothrombosis were enrolled in the global Reduction of Atherothrombosis for Continued Health (REACH) Registry and were followed up for as long as 4 years.\n[4] Patients from 3647 centers in 29 countries were enrolled between 2003 and 2004 and followed up until 2008.\n[5] Final database lock was in April 2009.\n[6] MAIN OUTCOME MEASURES Rates of cardiovascular death, myocardial infarction, and stroke.\n[7] RESULTS A total of 45,227 patients with baseline data were included in this 4-year analysis.\n[8] During the follow-up period, a total of 5481 patients experienced at least 1 event, including 2315 with cardiovascular death, 1228 with myocardial infarction, 1898 with stroke, and 40 with both a myocardial infarction and stroke on the same day.\n[9] Among patients with atherothrombosis, those with a prior history of ischemic events at baseline (n = 21,890) had the highest rate of subsequent ischemic events (18.3%; 95% confidence interval [CI], 17.4%-19.1%); patients with stable coronary, cerebrovascular, or peripheral artery disease (n = 15,264) had a lower risk (12.2%; 95% CI, 11.4%-12.9%); and patients without established atherothrombosis but with risk factors only (n = 8073) had the lowest risk (9.1%; 95% CI, 8.3%-9.9%) (P < .001 for all comparisons).\n[10] In addition, in multivariable modeling, the presence of diabetes (hazard ratio [HR], 1.44; 95% CI, 1.36-1.53; P < .001), an ischemic event in the previous year (HR, 1.71; 95% CI, 1.57-1.85; P < .001), and polyvascular disease (HR, 1.99; 95% CI, 1.78-2.24; P < .001) each were associated with a significantly higher risk of the primary end point.\n[11] CONCLUSION Clinical descriptors can assist clinicians in identifying high-risk patients within the broad range of risk for outpatients with atherothrombosis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1199, "doc_id": 16760369, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [16760369], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 binding orientation of the ML-SA1 activator at hTRPML2 is different from the binding orientation of the ML-SA1 activator at hTRPML1.\n\nDocument title: Human TRPML1 channel structures in open and closed conformations\n\nAbstract sentences:\n[0] Transient receptor potential mucolipin 1 (TRPML1) is a Ca2+-releasing cation channel that mediates the calcium signalling and homeostasis of lysosomes.\n[1] Mutations in TRPML1 lead to mucolipidosis type IV, a severe lysosomal storage disorder.\n[2] Here we report two electron cryo-microscopy structures of full-length human TRPML1: a 3.72-Å apo structure at pH 7.0 in the closed state, and a 3.49-Å agonist-bound structure at pH 6.0 in an open state.\n[3] Several aromatic and hydrophobic residues in pore helix 1, helices S5 and S6, and helix S6 of a neighbouring subunit, form a hydrophobic cavity to house the agonist, suggesting a distinct agonist-binding site from that found in TRPV1, a TRP channel from a different subfamily.\n[4] The opening of TRPML1 is associated with distinct dilations of its lower gate together with a slight structural movement of pore helix 1.\n[5] Our work reveals the regulatory mechanism of TRPML channels, facilitates better understanding of TRP channel activation, and provides insights into the molecular basis of mucolipidosis type IV 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": "validation", "claim_id": 1200, "doc_id": 3441524, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [3441524], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 center of the granuloma in an immune cell induces a pro-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: [4]\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.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1202, "doc_id": 3475317, "label": "SUPPORTS", "evidence_sentence_ids": [4], "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: The combination of H3K4me3 and H3K79me2 is found in quiescent hair follicle stem cells.\n\nDocument title: Genome-wide maps of histone modifications unwind in vivo chromatin states of the hair follicle lineage.\n\nAbstract sentences:\n[0] Using mouse skin, where bountiful reservoirs of synchronized hair follicle stem cells (HF-SCs) fuel cycles of regeneration, we explore how adult SCs remodel chromatin in response to activating cues.\n[1] By profiling global mRNA and chromatin changes in quiescent and activated HF-SCs and their committed, transit-amplifying (TA) progeny, we show that polycomb-group (PcG)-mediated H3K27-trimethylation features prominently in HF-lineage progression by mechanisms distinct from embryonic-SCs.\n[2] In HF-SCs, PcG represses nonskin lineages and HF differentiation.\n[3] In TA progeny, nonskin regulators remain PcG-repressed, HF-SC regulators acquire H3K27me3-marks, and HF-lineage regulators lose them.\n[4] Interestingly, genes poised in embryonic stem cells, active in HF-SCs, and PcG-repressed in TA progeny encode not only key transcription factors, but also signaling regulators.\n[5] We document their importance in balancing HF-SC quiescence, underscoring the power of chromatin mapping in dissecting SC behavior.\n[6] Our findings explain how HF-SCs cycle through quiescent and activated states without losing stemness and define roles for PcG-mediated repression in governing a fate switch irreversibly."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1204, "doc_id": 31141365, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [31141365], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 polarizable B isoform to the more homogenous A 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": "validation", "claim_id": 1207, "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 deregulated and prolonged activation of monocytes has deleterious effects in inflammatory diseases.\n\nDocument title: Myeloid-specific Krüppel-like factor 2 inactivation increases macrophage and neutrophil adhesion and promotes atherosclerosis.\n\nAbstract sentences:\n[0] RATIONALE Hemizygous deficiency of the transcription factor Krüppel-like factor 2 (KLF2) has been shown previously to augment atherosclerosis in hypercholesterolemic mice.\n[1] However, the cell type responsible for the increased atherosclerosis due to KLF2 deficiency has not been identified.\n[2] This study examined the consequence of myeloid cell-specific KLF2 inactivation in atherosclerosis.\n[3] METHODS AND RESULTS Cell-specific knockout mice were generated by Cre/loxP recombination.\n[4] Macrophages isolated from myeloid-specific Klf2 knockout (myeKlf2(-/-)) mice were similar to myeKlf2(+/+) macrophages in response to activation, polarization, and lipid accumulation.\n[5] However, in comparison to myeKlf2(+/+) macrophages, myeKlf2(-/-) macrophages adhered more robustly to endothelial cells.\n[6] Neutrophils from myeKlf2(-/-) mice also adhered more robustly to endothelial cells, and fewer myeKlf2(-/-) neutrophils survived in culture over a 24-hour period in comparison with myeKlf2(+/+) neutrophils.\n[7] When myeKlf2(-/-) mice were mated to Ldlr(-/-) mice and then fed a high fat and high cholesterol diet, significant increase in atherosclerosis was observed in the myeKlf2(-/-)Ldlr(-/-) mice compared with myeKlf2(+/+)Ldlr(-/-) littermates.\n[8] The increased atherosclerosis in myeKlf2(-/-)Ldlr(-/-) mice was associated with elevated presence of neutrophils and macrophages, with corresponding increase of myeloperoxidase as well as chlorinated and nitrosylated tyrosine epitopes in their lesion areas compared with myeKlf2(+/+)Ldlr(-/-) mice.\n[9] CONCLUSIONS This study documents a role for myeloid KLF2 expression in modulating atherosclerosis.\n[10] The increased neutrophil accumulation and atherosclerosis progression with myeloid-specific KLF2 deficiency also underscores the importance of neutrophils in promoting vascular oxidative stress and atherosclerosis.\n[11] Collectively, these results suggest that elevating KLF2 expression may be a novel strategy for prevention and treatment of atherosclerosis."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1213, "doc_id": 14407673, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [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 extracellular domain of TMEM27 is cleaved in human 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: [3]\nExplanation: Evidence states: \"Tmem27 forms dimers and its extracellular domain is glycosylated, cleaved and shed from the plasma membrane of beta cells.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1216, "doc_id": 24142891, "label": "SUPPORTS", "evidence_sentence_ids": [3], "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: The genomic aberrations found in matasteses are very similar to those found in the primary tumor.\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: CONTRADICTS\nRationale sentence ids: [2]\nExplanation: Evidence states: \"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.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1221, "doc_id": 19736671, "label": "CONTRADICTS", "evidence_sentence_ids": [2], "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: The locus rs647161 is associated with colorectal carcinoma.\n\nDocument title: Genome-wide association analyses in East Asians identify new susceptibility loci for colorectal cancer\n\nAbstract sentences:\n[0] To identify new genetic factors for colorectal cancer (CRC), we conducted a                 genome-wide association study in east Asians.\n[1] By analyzing genome-wide data in 2,098                 cases and 5,749 controls, we selected 64 promising SNPs for replication in an                 independent set of samples, including up to 5,358 cases and 5,922 controls.\n[2] We                 identified four SNPs with association P values of 8.58 ×                     10(-7) to 3.77 × 10(-10)                 in the combined analysis of all east Asian samples.\n[3] Three of the four were                 replicated in a study conducted in 26,060 individuals of European descent, with                 combined P values of 1.22 × 10(-10) for                 rs647161 (5q31.1), 6.64 × 10(-9) for rs2423279                 (20p12.3) and 3.06 × 10(-8) for rs10774214                 (12p13.32 near the CCND2 gene), derived from meta-analysis of data from both                 east Asian and European-ancestry populations.\n[4] This study identified three new CRC                 susceptibility loci and provides additional insight into the genetics and biology of                 CRC."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"Three of the four were                 replicated in a study conducted in 26,060 individuals of European descent, with                 combined P values of 1.22 × 10(-10) for                 rs647161 (5q31.1), 6.64 × 10(-9) for rs2423279                 (20p12.3) and 3.06 × 10(-8) for rs10774214                 (12p13.32 near the CCND2 gene), derived from meta-analysis of data from both                 east Asian and European-ancestry populations.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1225, "doc_id": 9650982, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [9650982], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 loss of the TET protein functions may have dire biological consequences, such as myeloid cancers.\n\nDocument title: Tet1 and Tet2 regulate 5-hydroxymethylcytosine production and cell lineage specification in mouse embryonic stem cells.\n\nAbstract sentences:\n[0] TET family enzymes convert 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) in DNA.\n[1] Here, we show that Tet1 and Tet2 are Oct4-regulated enzymes that together sustain 5hmC in mouse embryonic stem cells (ESCs) and are induced concomitantly with 5hmC during reprogramming of fibroblasts to induced pluripotent stem cells.\n[2] ESCs depleted of Tet1 by RNAi show diminished expression of the Nodal antagonist Lefty1 and display hyperactive Nodal signaling and skewed differentiation into the endoderm-mesoderm lineage in embryoid bodies in vitro.\n[3] In Fgf4- and heparin-supplemented culture conditions, Tet1-depleted ESCs activate the trophoblast stem cell lineage determinant Elf5 and can colonize the placenta in midgestation embryo chimeras.\n[4] Consistent with these findings, Tet1-depleted ESCs form aggressive hemorrhagic teratomas with increased endoderm, reduced neuroectoderm, and ectopic appearance of trophoblastic giant cells.\n[5] Thus, 5hmC is an epigenetic modification associated with the pluripotent state, and Tet1 functions to regulate the lineage differentiation potential of ESCs."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1226, "doc_id": 13777138, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [13777138], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 more 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1232, "doc_id": 13905670, "label": "CONTRADICTS", "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 myocardial lineage develops from cardiac progenitors of mesodermal 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: SUPPORTS\nRationale sentence ids: [0, 3, 4]\nExplanation: Evidence states: \"The functional heart is comprised of distinct mesoderm-derived lineages including cardiomyocytes, endothelial cells and vascular smooth muscle cells. 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. When plated in monolayer cultures, these KDRlow/C-KITneg cells differentiate to generate populations consisting of greater than 50% contracting cardiomyocytes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1241, "doc_id": 4427392, "label": "SUPPORTS", "evidence_sentence_ids": [0, 3, 4], "cited_doc_ids": [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 one-child policy has been successful in lowering population growth.\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: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1245, "doc_id": 7662395, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [7662395, 7662395], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 dependent on 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: 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": "validation", "claim_id": 1259, "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: The relationship between a breast cancer patient's capacity to metabolize tamoxifen and treatment outcome is dependent on 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: 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": "validation", "claim_id": 1259, "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: The relationship between a breast cancer patient's capacity to metabolize tamoxifen and treatment outcome is dependent on 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: 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": "validation", "claim_id": 1259, "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: The repair of Cas9-induced double strand breaks in human DNA is error-prone.\n\nDocument title: Kinetics and Fidelity of the Repair of Cas9-Induced Double-Strand DNA Breaks\n\nAbstract sentences:\n[0] The RNA-guided DNA endonuclease Cas9 is a powerful tool for genome editing.\n[1] Little is known about the kinetics and fidelity of the double-strand break (DSB) repair process that follows a Cas9 cutting event in living cells.\n[2] Here, we developed a strategy to measure the kinetics of DSB repair for single loci in human cells.\n[3] Quantitative modeling of repaired DNA in time series after Cas9 activation reveals variable and often slow repair rates, with half-life times up to ∼10 hr.\n[4] Furthermore, repair of the DSBs tends to be error prone.\n[5] Both classical and microhomology-mediated end joining pathways contribute to the erroneous repair.\n[6] Estimation of their individual rate constants indicates that the balance between these two pathways changes over time and can be altered by additional ionizing radiation.\n[7] Our approach provides quantitative insights into DSB repair kinetics and fidelity in single loci and indicates that Cas9-induced DSBs are repaired in an unusual manner."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Furthermore, repair of the DSBs tends to be error prone.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1262, "doc_id": 44172171, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [44172171], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 increases with placental weight of pregnancies, and this association is strongest for premenopausal breast cancer.\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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1266, "doc_id": 37480103, "label": "SUPPORTS", "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 increases with placental weight of pregnancies, and this association is strongest for premenopausal breast cancer.\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: SUPPORTS\nRationale sentence ids: [12]\nExplanation: Evidence states: \"CONCLUSIONS Placental weight is positively associated with maternal risk of breast cancer.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1266, "doc_id": 37480103, "label": "SUPPORTS", "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 male prisoners harming themselves is ten times that of female 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1270, "doc_id": 13900610, "label": "CONTRADICTS", "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 male prisoners harming themselves is ten times that of female 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: CONTRADICTS\nRationale sentence ids: [8]\nExplanation: Evidence states: \"Self-harm rates were more than ten times higher in female prisoners than in male inmates.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1270, "doc_id": 13900610, "label": "CONTRADICTS", "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 severity of cardiac involvement in amyloidosis can be described by the degree of transmurality of late gadolinium enhancement in MRI.\n\nDocument title: Prognostic Value of Late Gadolinium Enhancement Cardiovascular Magnetic Resonance in Cardiac Amyloidosis\n\nAbstract sentences:\n[0] BACKGROUND The prognosis and treatment of the 2 main types of cardiac amyloidosis, immunoglobulin light chain (AL) and transthyretin (ATTR) amyloidosis, are substantially influenced by cardiac involvement.\n[1] Cardiovascular magnetic resonance with late gadolinium enhancement (LGE) is a reference standard for the diagnosis of cardiac amyloidosis, but its potential for stratifying risk is unknown.\n[2] METHODS AND RESULTS Two hundred fifty prospectively recruited subjects, 122 patients with ATTR amyloid, 9 asymptomatic mutation carriers, and 119 patients with AL amyloidosis, underwent LGE cardiovascular magnetic resonance.\n[3] Subjects were followed up for a mean of 24±13 months.\n[4] LGE was performed with phase-sensitive inversion recovery (PSIR) and without (magnitude only).\n[5] These were compared with extracellular volume measured with T1 mapping.\n[6] PSIR was superior to magnitude-only inversion recovery LGE because PSIR always nulled the tissue (blood or myocardium) with the longest T1 (least gadolinium).\n[7] LGE was classified into 3 patterns: none, subendocardial, and transmural, which were associated with increasing amyloid burden as defined by extracellular volume (P<0.0001), with transitions from none to subendocardial LGE at an extracellular volume of 0.40 to 0.43 (AL) and 0.39 to 0.40 (ATTR) and to transmural at 0.48 to 0.55 (AL) and 0.47 to 0.59 (ATTR).\n[8] Sixty-seven patients (27%) died.\n[9] Transmural LGE predicted death (hazard ratio, 5.4; 95% confidence interval, 2.1-13.7; P<0.0001) and remained independent after adjustment for N-terminal pro-brain natriuretic peptide, ejection fraction, stroke volume index, E/E', and left ventricular mass index (hazard ratio, 4.1; 95% confidence interval, 1.3-13.1; P<0.05).\n[10] CONCLUSIONS There is a continuum of cardiac involvement in systemic AL and ATTR amyloidosis.\n[11] Transmural LGE is determined reliably by PSIR and represents advanced cardiac amyloidosis.\n[12] The PSIR technique provides incremental information on outcome even after adjustment for known prognostic factors."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [7]\nExplanation: Evidence states: \"LGE was classified into 3 patterns: none, subendocardial, and transmural, which were associated with increasing amyloid burden as defined by extracellular volume (P<0.0001), with transitions from none to subendocardial LGE at an extracellular volume of 0.40 to 0.43 (AL) and 0.39 to 0.40 (ATTR) and to transmural at 0.48 to 0.55 (AL) and 0.47 to 0.59 (ATTR).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1271, "doc_id": 13768432, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [13768432], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 severity of cardiac involvement in amyloidosis can be described by the degree of transmurality of late gadolinium enhancement in MRI.\n\nDocument title: Prognostic Value of Late Gadolinium Enhancement Cardiovascular Magnetic Resonance in Cardiac Amyloidosis\n\nAbstract sentences:\n[0] BACKGROUND The prognosis and treatment of the 2 main types of cardiac amyloidosis, immunoglobulin light chain (AL) and transthyretin (ATTR) amyloidosis, are substantially influenced by cardiac involvement.\n[1] Cardiovascular magnetic resonance with late gadolinium enhancement (LGE) is a reference standard for the diagnosis of cardiac amyloidosis, but its potential for stratifying risk is unknown.\n[2] METHODS AND RESULTS Two hundred fifty prospectively recruited subjects, 122 patients with ATTR amyloid, 9 asymptomatic mutation carriers, and 119 patients with AL amyloidosis, underwent LGE cardiovascular magnetic resonance.\n[3] Subjects were followed up for a mean of 24±13 months.\n[4] LGE was performed with phase-sensitive inversion recovery (PSIR) and without (magnitude only).\n[5] These were compared with extracellular volume measured with T1 mapping.\n[6] PSIR was superior to magnitude-only inversion recovery LGE because PSIR always nulled the tissue (blood or myocardium) with the longest T1 (least gadolinium).\n[7] LGE was classified into 3 patterns: none, subendocardial, and transmural, which were associated with increasing amyloid burden as defined by extracellular volume (P<0.0001), with transitions from none to subendocardial LGE at an extracellular volume of 0.40 to 0.43 (AL) and 0.39 to 0.40 (ATTR) and to transmural at 0.48 to 0.55 (AL) and 0.47 to 0.59 (ATTR).\n[8] Sixty-seven patients (27%) died.\n[9] Transmural LGE predicted death (hazard ratio, 5.4; 95% confidence interval, 2.1-13.7; P<0.0001) and remained independent after adjustment for N-terminal pro-brain natriuretic peptide, ejection fraction, stroke volume index, E/E', and left ventricular mass index (hazard ratio, 4.1; 95% confidence interval, 1.3-13.1; P<0.05).\n[10] CONCLUSIONS There is a continuum of cardiac involvement in systemic AL and ATTR amyloidosis.\n[11] Transmural LGE is determined reliably by PSIR and represents advanced cardiac amyloidosis.\n[12] The PSIR technique provides incremental information on outcome even after adjustment for known prognostic factors."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"Transmural LGE is determined reliably by PSIR and represents advanced cardiac amyloidosis.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1271, "doc_id": 13768432, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [13768432], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 single flash-evoked ERG b-wave is generated by activity of ON-bipolar cells.\n\nDocument title: Specific deficit of the ON response in visual transmission by targeted disruption of the mGIuR6 gene\n\nAbstract sentences:\n[0] Taking advantage of the restricted expression of metabotropic glutamate receptor subtype 6 (mGluR6) in retinal ON bipolar cells, we generated knockout mice lacking mGluR6 expression.\n[1] The homozygous mutant mice showed a loss of ON responses but unchanged OFF responses to light.\n[2] The mutant mice displayed no obvious changes in retinal cell organization nor in the projection of optic fibers to the brain.\n[3] Furthermore, the mGluR6-deficient mice showed visual behavioral responses to light stimulation as examined by shuttle box avoidance behavior experiments using light exposure as a conditioned stimulus.\n[4] The results demonstrate that mGluR6 is essential in synaptic transmission to the ON bipolar cell and that the OFF response provides an important means for transmitting visual information."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1272, "doc_id": 17081238, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [17081238], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 sliding activity of kinesin-8 protein Kip3 promotes bipolar spindle assembly.\n\nDocument title: Microtubule sliding activity of a kinesin-8 promotes spindle assembly and spindle length control\n\nAbstract sentences:\n[0] Molecular motors play critical roles in the formation of mitotic spindles, either through controlling the stability of individual microtubules, or by crosslinking and sliding microtubule arrays.\n[1] Kinesin-8 motors are best known for their regulatory roles in controlling microtubule dynamics.\n[2] They contain microtubule-destabilizing activities, and restrict spindle length in a wide variety of cell types and organisms.\n[3] Here, we report an antiparallel microtubule-sliding activity of the budding yeast kinesin-8, Kip3.\n[4] The in vivo importance of this sliding activity was established through the identification of complementary Kip3 mutants that separate the sliding activity and microtubule-destabilizing activity.\n[5] In conjunction with Cin8, a kinesin-5 family member, the sliding activity of Kip3 promotes bipolar spindle assembly and the maintenance of genome stability.\n[6] We propose a slide-disassemble model where the sliding and destabilizing activity of Kip3 balance during pre-anaphase.\n[7] This facilitates normal spindle assembly.\n[8] However, the destabilizing activity of Kip3 dominates in late anaphase, inhibiting spindle elongation and ultimately promoting spindle disassembly."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"In conjunction with Cin8, a kinesin-5 family member, the sliding activity of Kip3 promotes bipolar spindle assembly and the maintenance of genome stability.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1273, "doc_id": 11041152, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [11041152], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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) carries toxic effector proteins.\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: [4, 5]\nExplanation: Evidence states: \"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. 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.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1274, "doc_id": 4406819, "label": "SUPPORTS", "evidence_sentence_ids": [4, 5], "cited_doc_ids": [12428814, 27731651, 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: The tip of the inner tube of the toxic type VI secretion system (T6SS) antibacterial effector in Escherichia coli (E. coli) carries toxic effector proteins.\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: [7]\nExplanation: Evidence states: \"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.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1274, "doc_id": 4406819, "label": "SUPPORTS", "evidence_sentence_ids": [7], "cited_doc_ids": [12428814, 27731651, 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: The treatment of cancer patients with co-IR blockade does not cause any adverse autoimmune events.\n\nDocument title: Is autoimmunity the Achilles' heel of cancer immunotherapy?\n\nAbstract sentences:\n[0] The emergence of immuno-oncology as the first broadly successful strategy for metastatic cancer will require clinicians to integrate this new pillar of medicine with chemotherapy, radiation, and targeted small-molecule compounds.\n[1] Of equal importance is gaining an understanding of the limitations and toxicities of immunotherapy.\n[2] Immunotherapy was initially perceived to be a relatively less toxic approach to cancer treatment than other available therapies—and surely it is, when compared to those.\n[3] However, as the use of immunotherapy becomes more common, especially as first- and second-line treatments, immunotoxicity and autoimmunity are emerging as the Achilles' heel of immunotherapy.\n[4] In this Perspective, we discuss evidence that the occurrence of immunotoxicity bodes well for the patient, and describe mechanisms that might be related to the induction of autoimmunity.\n[5] We then explore approaches to limit immunotoxicity, and discuss the future directions of research and reporting that are needed to diminish it."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1278, "doc_id": 11335781, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [11335781], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 treatment of cancer patients with co-IR blockade precipitates adverse autoimmune events.\n\nDocument title: Is autoimmunity the Achilles' heel of cancer immunotherapy?\n\nAbstract sentences:\n[0] The emergence of immuno-oncology as the first broadly successful strategy for metastatic cancer will require clinicians to integrate this new pillar of medicine with chemotherapy, radiation, and targeted small-molecule compounds.\n[1] Of equal importance is gaining an understanding of the limitations and toxicities of immunotherapy.\n[2] Immunotherapy was initially perceived to be a relatively less toxic approach to cancer treatment than other available therapies—and surely it is, when compared to those.\n[3] However, as the use of immunotherapy becomes more common, especially as first- and second-line treatments, immunotoxicity and autoimmunity are emerging as the Achilles' heel of immunotherapy.\n[4] In this Perspective, we discuss evidence that the occurrence of immunotoxicity bodes well for the patient, and describe mechanisms that might be related to the induction of autoimmunity.\n[5] We then explore approaches to limit immunotoxicity, and discuss the future directions of research and reporting that are needed to diminish it."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1279, "doc_id": 11335781, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [11335781], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 ureABIEFGH gene cluster encodes urease maturation proteins : UreD/UreH, UreE, UreF, and UreG.\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": "validation", "claim_id": 1280, "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: The ureABIEFGH gene cluster is induced by nickel (II) ion.\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": "validation", "claim_id": 1281, "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: Therapeutic use of the drug Dapsone to treat pyoderma gangrenous is based on anecdotal evidence.\n\nDocument title: Clinical features and treatment of peristomal pyoderma gangrenosum.\n\nAbstract sentences:\n[0] CONTEXT Peristomal pyoderma gangrenosum (PPG), an unusual variant of pyoderma gangrenosum, has been reported almost exclusively in patients with inflammatory bowel disease (IBD) and is frequently misdiagnosed.\n[1] OBJECTIVE To better characterize the clinical manifestations, diagnosis, and management of PPG.\n[2] DESIGN, SETTING, AND PATIENTS Retrospective analysis of 7 patients with PPG observed in a university-affiliated community setting between 1988 and December 1999.\n[3] MAIN OUTCOME MEASURES Clinical and histopathologic features, associated disorders, and microbiologic findings.\n[4] RESULTS Two patients had Crohn disease, 2 had ulcerative colitis, and 3 had abdominal cancer.\n[5] Five patients had at least 1 relapse of PPG after initial healing.\n[6] Although 3 of 4 patients with IBD had active bowel disease, a parallel course with PPG occurred in only 1 patient.\n[7] Both patients whose stoma was relocated developed an ulcer at the new site.\n[8] Effective therapies included topical superpotent corticosteroids; intralesional injection of triamcinolone acetonide at the ulcer margin; topical cromolyn sodium; oral dapsone, prednisone, cyclosporine, mycophenolate mofetil; and intravenous infliximab.\n[9] CONCLUSION Our experiences demonstrate that although PPG has been most often reported in patients with IBD, it may occur in the absence of IBD.\n[10] Biopsy of the skin lesion is not diagnostic but excludes other causes.\n[11] Relocation of the stoma may be associated with a new ulceration and should be avoided.\n[12] Trauma to the skin of a predisposed patient may elicit the pustules or ulcerations associated with pathergy.\n[13] JAMA.\n[14] 2000;284:1546-1548."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1282, "doc_id": 23649163, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [23649163], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 an inverse relationship 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1290, "doc_id": 4687948, "label": "SUPPORTS", "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 an inverse relationship 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1290, "doc_id": 4687948, "label": "SUPPORTS", "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 an inverse relationship 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1290, "doc_id": 4687948, "label": "SUPPORTS", "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 an inverse relationship 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1290, "doc_id": 4687948, "label": "SUPPORTS", "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 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": "validation", "claim_id": 1292, "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: Thigh-length graduated compression stockings (GCS) did not reduce deep vein thrombosis in patients admitted to hospital who are immobile because of acute stroke.\n\nDocument title: Effectiveness of thigh-length graduated compression stockings to reduce the risk of deep vein thrombosis after stroke (CLOTS trial 1): a multicentre, randomised controlled trial\n\nAbstract sentences:\n[0] BACKGROUND Deep vein thrombosis (DVT) and pulmonary embolism are common after stroke.\n[1] In small trials of patients undergoing surgery, graduated compression stockings (GCS) reduce the risk of DVT.\n[2] National stroke guidelines extrapolating from these trials recommend their use in patients with stroke despite insufficient evidence.\n[3] We assessed the effectiveness of thigh-length GCS to reduce DVT after stroke.\n[4] METHODS In this outcome-blinded, randomised controlled trial, 2518 patients who were admitted to hospital within 1 week of an acute stroke and who were immobile were enrolled from 64 centres in the UK, Italy, and Australia.\n[5] Patients were allocated via a central randomisation system to routine care plus thigh-length GCS (n=1256) or to routine care plus avoidance of GCS (n=1262).\n[6] A technician who was blinded to treatment allocation undertook compression Doppler ultrasound of both legs at about 7-10 days and, when practical, again at 25-30 days after enrolment.\n[7] The primary outcome was the occurrence of symptomatic or asymptomatic DVT in the popliteal or femoral veins.\n[8] Analyses were by intention to treat.\n[9] This study is registered, number ISRCTN28163533.\n[10] FINDINGS All patients were included in the analyses.\n[11] The primary outcome occurred in 126 (10.0%) patients allocated to thigh-length GCS and in 133 (10.5%) allocated to avoid GCS, resulting in a non-significant absolute reduction in risk of 0.5% (95% CI -1.9% to 2.9%).\n[12] Skin breaks, ulcers, blisters, and skin necrosis were significantly more common in patients allocated to GCS than in those allocated to avoid their use (64 [5%] vs 16 [1%]; odds ratio 4.18, 95% CI 2.40-7.27).\n[13] INTERPRETATION These data do not lend support to the use of thigh-length GCS in patients admitted to hospital with acute stroke.\n[14] National guidelines for stroke might need to be revised on the basis of these results.\n[15] FUNDING Medical Research Council (UK), Chief Scientist Office of Scottish Government, Chest Heart and Stroke Scotland, Tyco Healthcare (Covidien) USA, and UK Stroke Research Network."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [11]\nExplanation: Evidence states: \"The primary outcome occurred in 126 (10.0%) patients allocated to thigh-length GCS and in 133 (10.5%) allocated to avoid GCS, resulting in a non-significant absolute reduction in risk of 0.5% (95% CI -1.9% to 2.9%).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1298, "doc_id": 11718220, "label": "SUPPORTS", "evidence_sentence_ids": [11], "cited_doc_ids": [11718220], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Thigh-length graduated compression stockings (GCS) did not reduce deep vein thrombosis in patients admitted to hospital who are immobile because of acute stroke.\n\nDocument title: Effectiveness of thigh-length graduated compression stockings to reduce the risk of deep vein thrombosis after stroke (CLOTS trial 1): a multicentre, randomised controlled trial\n\nAbstract sentences:\n[0] BACKGROUND Deep vein thrombosis (DVT) and pulmonary embolism are common after stroke.\n[1] In small trials of patients undergoing surgery, graduated compression stockings (GCS) reduce the risk of DVT.\n[2] National stroke guidelines extrapolating from these trials recommend their use in patients with stroke despite insufficient evidence.\n[3] We assessed the effectiveness of thigh-length GCS to reduce DVT after stroke.\n[4] METHODS In this outcome-blinded, randomised controlled trial, 2518 patients who were admitted to hospital within 1 week of an acute stroke and who were immobile were enrolled from 64 centres in the UK, Italy, and Australia.\n[5] Patients were allocated via a central randomisation system to routine care plus thigh-length GCS (n=1256) or to routine care plus avoidance of GCS (n=1262).\n[6] A technician who was blinded to treatment allocation undertook compression Doppler ultrasound of both legs at about 7-10 days and, when practical, again at 25-30 days after enrolment.\n[7] The primary outcome was the occurrence of symptomatic or asymptomatic DVT in the popliteal or femoral veins.\n[8] Analyses were by intention to treat.\n[9] This study is registered, number ISRCTN28163533.\n[10] FINDINGS All patients were included in the analyses.\n[11] The primary outcome occurred in 126 (10.0%) patients allocated to thigh-length GCS and in 133 (10.5%) allocated to avoid GCS, resulting in a non-significant absolute reduction in risk of 0.5% (95% CI -1.9% to 2.9%).\n[12] Skin breaks, ulcers, blisters, and skin necrosis were significantly more common in patients allocated to GCS than in those allocated to avoid their use (64 [5%] vs 16 [1%]; odds ratio 4.18, 95% CI 2.40-7.27).\n[13] INTERPRETATION These data do not lend support to the use of thigh-length GCS in patients admitted to hospital with acute stroke.\n[14] National guidelines for stroke might need to be revised on the basis of these results.\n[15] FUNDING Medical Research Council (UK), Chief Scientist Office of Scottish Government, Chest Heart and Stroke Scotland, Tyco Healthcare (Covidien) USA, and UK Stroke Research Network."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [13]\nExplanation: Evidence states: \"INTERPRETATION These data do not lend support to the use of thigh-length GCS in patients admitted to hospital with acute stroke.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1298, "doc_id": 11718220, "label": "SUPPORTS", "evidence_sentence_ids": [13], "cited_doc_ids": [11718220], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1303, "doc_id": 12631697, "label": "CONTRADICTS", "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 has no effect on 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1303, "doc_id": 12631697, "label": "CONTRADICTS", "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: Transferred UCB T cells acquire a memory-like phenotype in recipients.\n\nDocument title: Quantitative assessment of T-cell repertoire recovery after hematopoietic stem cell transplantation\n\nAbstract sentences:\n[0] Delayed T cell recovery and restricted T cell receptor (TCR) diversity after allogeneic hematopoietic stem cell transplantation (allo-HSCT) are associated with increased risks of infection and cancer relapse.\n[1] Technical challenges have limited faithful measurement of TCR diversity after allo-HSCT.\n[2] Here we combined 5' rapid amplification of complementary DNA ends PCR with deep sequencing to quantify TCR diversity in 28 recipients of allo-HSCT using a single oligonucleotide pair.\n[3] Analysis of duplicate blood samples confirmed that we accurately determined the frequency of individual TCRs.\n[4] After 6 months, cord blood-graft recipients approximated the TCR diversity of healthy individuals, whereas recipients of T cell-depleted peripheral-blood stem cell grafts had 28-fold and 14-fold lower CD4(+) and CD8(+) T cell diversities, respectively.\n[5] After 12 months, these deficiencies had improved for the CD4(+) but not the CD8(+) T cell compartment.\n[6] Overall, this method provides unprecedented views of T cell repertoire recovery after allo-HSCT and may identify patients at high risk of infection or relapse."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: NOT ENOUGH INFORMATION\nRationale sentence ids: []\nExplanation: The provided abstract does not contain direct evidence to support or contradict the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1316, "doc_id": 27910499, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [27910499], "variant": "nei_with_cited_abstract"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 cells can differentiate within the 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": "validation", "claim_id": 1319, "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: Transplanted human glial progenitor cells are incapable of forming a neural network with host animals' neurons.\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: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"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.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1320, "doc_id": 16284655, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "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: Tumor necrosis factor alpha (TNF-α) and interleukin-1 (IL-1) are pro-inflammatory cytokines that inhibit IL-6 and IL-10.\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": "validation", "claim_id": 1332, "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: UCB T cells maintain high TCR diversity after transplantation.\n\nDocument title: Quantitative assessment of T-cell repertoire recovery after hematopoietic stem cell transplantation\n\nAbstract sentences:\n[0] Delayed T cell recovery and restricted T cell receptor (TCR) diversity after allogeneic hematopoietic stem cell transplantation (allo-HSCT) are associated with increased risks of infection and cancer relapse.\n[1] Technical challenges have limited faithful measurement of TCR diversity after allo-HSCT.\n[2] Here we combined 5' rapid amplification of complementary DNA ends PCR with deep sequencing to quantify TCR diversity in 28 recipients of allo-HSCT using a single oligonucleotide pair.\n[3] Analysis of duplicate blood samples confirmed that we accurately determined the frequency of individual TCRs.\n[4] After 6 months, cord blood-graft recipients approximated the TCR diversity of healthy individuals, whereas recipients of T cell-depleted peripheral-blood stem cell grafts had 28-fold and 14-fold lower CD4(+) and CD8(+) T cell diversities, respectively.\n[5] After 12 months, these deficiencies had improved for the CD4(+) but not the CD8(+) T cell compartment.\n[6] Overall, this method provides unprecedented views of T cell repertoire recovery after allo-HSCT and may identify patients at high risk of infection or relapse."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"After 6 months, cord blood-graft recipients approximated the TCR diversity of healthy individuals, whereas recipients of T cell-depleted peripheral-blood stem cell grafts had 28-fold and 14-fold lower CD4(+) and CD8(+) T cell diversities, respectively.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1335, "doc_id": 27910499, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [27910499], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: UCB T cells reduce TCR diversity after transplantation.\n\nDocument title: Quantitative assessment of T-cell repertoire recovery after hematopoietic stem cell transplantation\n\nAbstract sentences:\n[0] Delayed T cell recovery and restricted T cell receptor (TCR) diversity after allogeneic hematopoietic stem cell transplantation (allo-HSCT) are associated with increased risks of infection and cancer relapse.\n[1] Technical challenges have limited faithful measurement of TCR diversity after allo-HSCT.\n[2] Here we combined 5' rapid amplification of complementary DNA ends PCR with deep sequencing to quantify TCR diversity in 28 recipients of allo-HSCT using a single oligonucleotide pair.\n[3] Analysis of duplicate blood samples confirmed that we accurately determined the frequency of individual TCRs.\n[4] After 6 months, cord blood-graft recipients approximated the TCR diversity of healthy individuals, whereas recipients of T cell-depleted peripheral-blood stem cell grafts had 28-fold and 14-fold lower CD4(+) and CD8(+) T cell diversities, respectively.\n[5] After 12 months, these deficiencies had improved for the CD4(+) but not the CD8(+) T cell compartment.\n[6] Overall, this method provides unprecedented views of T cell repertoire recovery after allo-HSCT and may identify patients at high risk of infection or relapse."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: CONTRADICTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"After 6 months, cord blood-graft recipients approximated the TCR diversity of healthy individuals, whereas recipients of T cell-depleted peripheral-blood stem cell grafts had 28-fold and 14-fold lower CD4(+) and CD8(+) T cell diversities, respectively.\". This contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1336, "doc_id": 27910499, "label": "CONTRADICTS", "evidence_sentence_ids": [4], "cited_doc_ids": [27910499], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine whether the claim is SUPPORTS, CONTRADICTS, or NOT ENOUGH INFORMATION based only on the provided abstract. Use sentence indices as rationale evidence.\n\nClaim: Ubiquitin ligase UBC13 generates a K63-linked polyubiquitin moiety at PCNA K164.\n\nDocument title: Replication Fork Slowing and Reversal upon DNA Damage Require PCNA Polyubiquitination and ZRANB3 DNA Translocase Activity\n\nAbstract sentences:\n[0] DNA damage tolerance during eukaryotic replication is orchestrated by PCNA ubiquitination.\n[1] While monoubiquitination activates mutagenic translesion synthesis, polyubiquitination activates an error-free pathway, elusive in mammals, enabling damage bypass by template switching.\n[2] Fork reversal is driven in vitro by multiple enzymes, including the DNA translocase ZRANB3, shown to bind polyubiquitinated PCNA.\n[3] However, whether this interaction promotes fork remodeling and template switching in vivo was unknown.\n[4] Here we show that damage-induced fork reversal in mammalian cells requires PCNA ubiquitination, UBC13, and K63-linked polyubiquitin chains, previously involved in error-free damage tolerance.\n[5] Fork reversal in vivo also requires ZRANB3 translocase activity and its interaction with polyubiquitinated PCNA, pinpointing ZRANB3 as a key effector of error-free DNA damage tolerance.\n[6] Mutations affecting fork reversal also induced unrestrained fork progression and chromosomal breakage, suggesting fork remodeling as a global fork slowing and protection mechanism.\n[7] Targeting these fork protection systems represents a promising strategy to potentiate cancer chemotherapy."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [4]\nExplanation: Evidence states: \"Here we show that damage-induced fork reversal in mammalian cells requires PCNA ubiquitination, UBC13, and K63-linked polyubiquitin chains, previously involved in error-free damage tolerance.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1337, "doc_id": 20231138, "label": "SUPPORTS", "evidence_sentence_ids": [4], "cited_doc_ids": [20231138], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 raises 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1339, "doc_id": 15482274, "label": "CONTRADICTS", "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 raises 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1339, "doc_id": 15482274, "label": "CONTRADICTS", "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: Up-regulation of the p53 pathway and related molecular events casues cancer resistance and results in a significantly shortened lifespan marked by senescent cells and accelerated organismal aging.\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": "validation", "claim_id": 1344, "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: Upregulation of mosGCTL-1 is induced upon infection with West Nile virus.\n\nDocument title: A C-Type Lectin Collaborates with a CD45 Phosphatase Homolog to Facilitate West Nile Virus Infection of Mosquitoes\n\nAbstract sentences:\n[0] West Nile virus (WNV) is the most common arthropod-borne flavivirus in the United States; however, the vector ligand(s) that participate in infection are not known.\n[1] We now show that an Aedes aegypti C-type lectin, mosGCTL-1, is induced by WNV, interacts with WNV in a calcium-dependent manner, and facilitates infection in vivo and in vitro.\n[2] A mosquito homolog of human CD45 in A. aegypti, designated mosPTP-1, recruits mosGCTL-1 to enable viral attachment to cells and to enhance viral entry.\n[3] In vivo experiments show that mosGCTL-1 and mosPTP-1 function as part of the same pathway and are critical for WNV infection of mosquitoes.\n[4] A similar phenomenon was also observed in Culex quinquefasciatus, a natural vector of WNV, further demonstrating that these genes participate in WNV infection.\n[5] During the mosquito blood-feeding process, WNV infection was blocked in vivo with mosGCTL-1 antibodies.\n[6] A molecular understanding of flaviviral-arthropod interactions may lead to strategies to control viral dissemination in nature."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"In vivo experiments show that mosGCTL-1 and mosPTP-1 function as part of the same pathway and are critical for WNV infection of mosquitoes.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1352, "doc_id": 12885341, "label": "SUPPORTS", "evidence_sentence_ids": [3], "cited_doc_ids": [12885341], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 mosGCTL-1 is induced upon infection with West Nile virus.\n\nDocument title: A C-Type Lectin Collaborates with a CD45 Phosphatase Homolog to Facilitate West Nile Virus Infection of Mosquitoes\n\nAbstract sentences:\n[0] West Nile virus (WNV) is the most common arthropod-borne flavivirus in the United States; however, the vector ligand(s) that participate in infection are not known.\n[1] We now show that an Aedes aegypti C-type lectin, mosGCTL-1, is induced by WNV, interacts with WNV in a calcium-dependent manner, and facilitates infection in vivo and in vitro.\n[2] A mosquito homolog of human CD45 in A. aegypti, designated mosPTP-1, recruits mosGCTL-1 to enable viral attachment to cells and to enhance viral entry.\n[3] In vivo experiments show that mosGCTL-1 and mosPTP-1 function as part of the same pathway and are critical for WNV infection of mosquitoes.\n[4] A similar phenomenon was also observed in Culex quinquefasciatus, a natural vector of WNV, further demonstrating that these genes participate in WNV infection.\n[5] During the mosquito blood-feeding process, WNV infection was blocked in vivo with mosGCTL-1 antibodies.\n[6] A molecular understanding of flaviviral-arthropod interactions may lead to strategies to control viral dissemination in nature."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [5]\nExplanation: Evidence states: \"During the mosquito blood-feeding process, WNV infection was blocked in vivo with mosGCTL-1 antibodies.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1352, "doc_id": 12885341, "label": "SUPPORTS", "evidence_sentence_ids": [5], "cited_doc_ids": [12885341], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 12 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: [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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1359, "doc_id": 11614737, "label": "CONTRADICTS", "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: Venules have a larger lumen diameter 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": "validation", "claim_id": 1362, "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: Venules have a thinner or absent smooth layer compared to 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": "validation", "claim_id": 1363, "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: Vitamin D deficiency effects the term of delivery.\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: [9]\nExplanation: Evidence states: \"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).\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1368, "doc_id": 2425364, "label": "SUPPORTS", "evidence_sentence_ids": [9], "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 the term of delivery.\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": "validation", "claim_id": 1368, "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 the term of delivery.\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: [11]\nExplanation: Evidence states: \"CONCLUSION Vitamin D insufficiency is associated with an increased risk of gestational diabetes, pre-eclampsia, and small for gestational age infants.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1368, "doc_id": 2425364, "label": "SUPPORTS", "evidence_sentence_ids": [11], "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 the term of delivery.\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": "validation", "claim_id": 1368, "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 deficiency is unrelated to 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1370, "doc_id": 2425364, "label": "CONTRADICTS", "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 is unrelated to 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1370, "doc_id": 2425364, "label": "CONTRADICTS", "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: Women with a higher 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1379, "doc_id": 16322674, "label": "SUPPORTS", "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: Women with a higher 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1379, "doc_id": 16322674, "label": "SUPPORTS", "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: Women with a higher birth weight are more likely to develop breast cancer later in life.\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: SUPPORTS\nRationale sentence ids: [3]\nExplanation: Evidence states: \"The majority of studies identified a positive link between birthweight and premenopausal, but not postmenopausal, breast cancer.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1379, "doc_id": 27123743, "label": "SUPPORTS", "evidence_sentence_ids": [3], "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: Women with a higher birth weight are more likely to develop breast cancer later in life.\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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1379, "doc_id": 27123743, "label": "SUPPORTS", "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: Women with a higher 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1379, "doc_id": 23557241, "label": "SUPPORTS", "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: Women with a higher 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1379, "doc_id": 17450673, "label": "SUPPORTS", "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: aPKCz causes tumour enhancement 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1382, "doc_id": 17755060, "label": "CONTRADICTS", "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 enhancement 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: CONTRADICTS\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 contradicts the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1382, "doc_id": 17755060, "label": "CONTRADICTS", "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 enhances 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: SUPPORTS\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 supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1385, "doc_id": 306006, "label": "SUPPORTS", "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: mTORC2 regulates intracellular cysteine levels through xCT inhibition.\n\nDocument title: mTORC2 Regulates Amino Acid Metabolism in Cancer by Phosphorylation of the Cystine-Glutamate Antiporter xCT.\n\nAbstract sentences:\n[0] Mutations in cancer reprogram amino acid metabolism to drive tumor growth, but the molecular mechanisms are not well understood.\n[1] Using an unbiased proteomic screen, we identified mTORC2 as a critical regulator of amino acid metabolism in cancer via phosphorylation of the cystine-glutamate antiporter xCT.\n[2] mTORC2 phosphorylates serine 26 at the cytosolic N terminus of xCT, inhibiting its activity.\n[3] Genetic inhibition of mTORC2, or pharmacologic inhibition of the mammalian target of rapamycin (mTOR) kinase, promotes glutamate secretion, cystine uptake, and incorporation into glutathione, linking growth factor receptor signaling with amino acid uptake and utilization.\n[4] These results identify an unanticipated mechanism regulating amino acid metabolism in cancer, enabling tumor cells to adapt to changing environmental conditions."}]}, {"role": "assistant", "content": [{"type": "text", "text": "Label: SUPPORTS\nRationale sentence ids: [2, 3]\nExplanation: Evidence states: \"mTORC2 phosphorylates serine 26 at the cytosolic N terminus of xCT, inhibiting its activity. Genetic inhibition of mTORC2, or pharmacologic inhibition of the mammalian target of rapamycin (mTOR) kinase, promotes glutamate secretion, cystine uptake, and incorporation into glutathione, linking growth factor receptor signaling with amino acid uptake and utilization.\". This supports the claim."}]}], "meta": {"dataset": "scifact", "split": "validation", "claim_id": 1389, "doc_id": 23895668, "label": "SUPPORTS", "evidence_sentence_ids": [2, 3], "cited_doc_ids": [23895668], "variant": "evidence_rationale"}}
{"messages": [{"role": "user", "content": [{"type": "text", "text": "Determine 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 accumulation 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": "validation", "claim_id": 1395, "doc_id": 17717391, "label": "NOT ENOUGH INFORMATION", "evidence_sentence_ids": [], "cited_doc_ids": [17717391], "variant": "nei_with_cited_abstract"}}