Datasets:

EllieS

/

pubmedqa_data

like 0

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe purpose of the present study was to examine the prevalence of celiac disease (CD) in children and adolescents with ADHD. In all, 102 participants between 4 and 18 years of age diagnosed with ADHD participated in the study (M = 12.8 years; 84 boys and 18 girls). CD was diagnosed according to the adapted guidelines of the European Society for Paediatric Gastroenterology, Hepatology and Nutrition (ESPHGAN). Among 102 tested children and teenagers with ADHD, we did not find anyone with suspected CD, so further diagnostic procedures for CD were not indicated.\n\nQuestion:\nIs prevalence of Celiac Disease Increased in ADHD Sample?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nmost fractures are preceded by falls. the aim of this study was to determine whether tests of physical performance are associated with fractures. a total of 10,998 men aged 65 years or above were recruited. questionnaires evaluated falls sustained 12 months before administration of the grip strength test, the timed stand test, the six-metre walk test and the twenty-centimetre narrow walk test. Means with 95% confidence interval (95% CI) are reported. P < 0.05 is a statistically significant difference. fallers with a fracture performed worse than non-fallers on all tests (all P < 0.001). Fallers with a fracture performed worse than fallers with no fractures both on the right-hand-grip strength test and on the six-metre walk test (P < 0.001). A score below -2 standard deviations in the right-hand-grip strength test was associated with an odds ratio of 3.9 (95% CI: 2.1-7.4) for having had a fall with a fracture compared with having had no fall and with an odds ratio of 2.6 (95% CI: 1.3-5.2) for having had a fall with a fracture compared with having had a fall with no fracture.\n\nQuestion:\nIs inferior physical performance test results of 10,998 men in the MrOS Study associated with high fracture risk?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIt is unclear whether primary writing tremor (PWT) is a tremulous form of dystonia or a tremor per se. Transcutaneous electrical nerve stimulation (TENS) at 50 Hz applied for 2 weeks was reported to improve the writing capabilities of patients with writer's cramp (WC). We explored whether such a beneficial effect can be obtained in patients with a PWT. In a cross-over, double-blinded randomized study we tested whether 2-week periods of 5, 25 or 50 Hz TENS applied to wrist flexor muscles, improved the score of the Fahn-Tolosa-Marin scale of nine patients with PWT. Excitability of neurons and of various intracortical circuits in the motor cortex were also tested before and after TENS by using transcranial magnetic stimulation. TENS at 5 and 25 Hz did not have any effect while TENS at 50 Hz worsened the clinical condition and the cortical excitability.\n\nQuestion:\nIs tENS harmful in primary writing tremor?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHistological examination of pre-transplant renal biopsy specimens can be used to select grafts from older donors after cardiac death (DCD) with a satisfactory transplant outcome. The aim was to determine whether such biopsy specimens can be reproducibly scored between pathologists and are representative of the whole kidney. In renal biopsy specimens from DCD aged >or=60 years (n = 44), globally sclerosed glomeruli, vascular narrowing, tubular atrophy and interstitial fibrosis were scored by three independent pathologists according to the Pirani scoring system. Interobserver agreement on the sum of scores improved considerably with the introduction of a combined tubulo-interstitial scoring system (intraclass correlation coefficient increased from 0.38 to 0.64). In small needle biopsy specimens (n = 144) obtained at autopsy, estimates of the proportion of globally sclerosed glomeruli were more precise with increasing sample size. Reasonably precise estimates may be obtained from specimens with at least seven glomeruli.\n\nQuestion:\nIs histological assessment of pre-transplant kidney biopsies reproducible and representative?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nInduction of allergen-specific IgG(4) antibodies is the most consistent immunological finding in immunotherapy trials. However, quantitative assessments of IgG(4) antibodies have not proven beneficial in evaluating clinical changes during or after immunotherapy. In the current study, we investigated the relationship between clinical outcome and allergen-specific IgG(4) titres or functional antibody responses following immunotherapy. We hypothesized that functional assays of serum IgG-associated inhibitory activity such as inhibition of IgE-allergen interactions (IgE-blocking factor) and inhibition of CD23-dependent IgE-facilitated allergen binding (IgE-FAB) correlate more closely with clinical outcome and may be biomarkers of clinical response. In an 8-month dose-response randomized double-blind placebo-controlled study, 221 polysensitized subjects with severe seasonal rhinitis received Alutard SQ, Phleum pratense 100,000 SQ-U, 10,000 SQ-U or placebo injections. Serum specimens were collected before treatment, after up-dosing, during the peak season and at the end of the study. Allergen-specific IgG(4) titres and IgG-associated inhibitory activity were evaluated. A time- and dose-dependent increase in serum inhibitory activity for both the IgE-blocking factor and IgE-FAB was observed, which paralleled increases in grass pollen-specific IgG(4) antibodies. A modest but significant inverse relationship was demonstrated between postimmunotherapy serum inhibitory activity and combined symptom-rescue medication scores (IgE-FAB: r = -0.25, P = 0.0002; IgE-blocking factor: r = -0.28, P < 0.0001), whereas this was not observed for immunoreactive IgG(4) levels (r = -0.11, P = 0.12).\n\nQuestion:\nDo functional rather than immunoreactive levels of IgG4 correlate closely with clinical response to grass pollen immunotherapy?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo evaluate whether anti-vascular endothelial growth factor (VEGF) neutralizing antibodies injected in the vitreous of rat eyes influence retinal microglia and macrophage activation. To dissociate the effect of anti-VEGF on microglia and macrophages subsequent to its antiangiogenic effect, we chose a model of acute intraocular inflammation. Lewis rats were challenged with systemic lipopolysaccharide (LPS) injection and concomitantly received 5 µl of rat anti-VEGF-neutralizing antibody (1.5 mg/ml) in the vitreous. Rat immunoglobulin G (IgG) isotype was used as the control. The effect of anti-VEGF was evaluated at 24 and 48 h clinically (uveitis scores), biologically (cytokine multiplex analysis in ocular media), and histologically (inflammatory cell counts on eye sections). Microglia and macrophages were immunodetected with ionized calcium-binding adaptor molecule 1 (IBA1) staining and counted based on their differential shapes (round amoeboid or ramified dendritiform) on sections and flatmounted retinas using confocal imaging and automatic quantification. Activation of microglia was also evaluated with inducible nitric oxide synthase (iNOS) and IBA1 coimmunostaining. Coimmunolocalization of VEGF receptor 1 and 2 (VEGF-R1 and R2) with IBA1 was performed on eye sections with or without anti-VEGF treatment. Neutralizing rat anti-VEGF antibodies significantly decreased ocular VEGF levels but did not decrease the endotoxin-induced uveitis (EIU) clinical score or the number of infiltrating cells and cytokines in ocular media (interleukin [IL]-1β, IL-6, tumor necrosis factor [TNF]-α, and monocyte chemoattractant protein [MCP]-1). Eyes treated with anti-VEGF showed a significantly decreased number of activated microglia and macrophages in the retina and the choroid and decreased iNOS-positive microglia. IBA1-positive cells expressed VEGF-R1 and R2 in the inflamed retina.\n\nQuestion:\nDoes anti-vascular endothelial growth factor act on retinal microglia/macrophage activation in a rat model of ocular inflammation?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe steroid ouabain is found in plasma and in many mammalian tissues, and is now considered as a hormone. In the immune system, ouabain regulates a number of lymphocyte functions, but little is known about its effects on monocyte function. Monocytes are important for adequate immune responses. The aim of this work was to analyze the effect of ouabain on mCD14 expression, a surface molecule involved in the response against Gram-negative bacteria and phagocytosis. Human peripheral blood mononuclear cells obtained from healthy donors were separated by density gradient centrifugation. Monocytes were separated by adherence and treated for 24 h with 100 nM ouabain. mCD14, CD1a and P-p38 expression was analyzed by flow cytometry. Inhibitors of cell-signaling pathways, i.e. SB202190, reduced glutathione, rottlerin, tyrphostin A23, genistein, chelerythrine chloride, PD98059, PP1 and Ly 294002, were used concomitantly with ouabain to observe their effect on mCD14 expression. Ouabain induced a significant decrease in mCD14 expression. This feature was not related to receptor endocytosis or cell death. Furthermore, mCD14 downregulation did not reflect a shift in differentiation into dendritic cells because this hormone failed to induce CD1a expression. Amongst several inhibitors of cell-signaling pathways triggered by ouabain, only epidermal growth factor receptor (EGFR) and p38 mitogen-activated protein kinase (MAPK) inhibitors (tyrphostin A23 and SB202109) significantly reverted the effect of ouabain on mCD14 expression. Accordingly, the levels of P-p38 were increased on monocytes after ouabain treatment. However, incubation with epidermal growth factor did not alter mCD14 expression.\n\nQuestion:\nIs mCD14 expression in human monocytes downregulated by ouabain via transactivation of epithelial growth factor receptor and activation of p38 mitogen-activated protein kinase?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo assess the recovery of various muscle fibre types in the posterior cricoarytenoid muscle after laryngeal reinnervation in the rat, and to determine the influence of tacrolimus on this process. Four groups of rats underwent resection and anastomosis of the left vagus nerve, and were administered either tacrolimus at a low dose or an immunosuppressive dose, or cyclosporin A at a low dose or an immunosuppressive dose. A fifth group received surgery alone, and a sixth group received neither surgery nor drug treatment (healthy group). Muscles were removed for immunohistochemical analysis 45 days after surgery. There was no difference in the proportion of types 1, 2a and 2b muscle fibres, comparing the immunosuppressive tacrolimus group and the healthy group, whereas there were fewer type 1 fibres in the group receiving surgery alone, compared with the healthy group (7 vs 12.1 per cent, respectively; p = 0.0303).\n\nQuestion:\nDoes tacrolimus enhance the recovery of normal laryngeal muscle fibre distribution after reinnervation?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSmoking and stress, pancreatic cancer (PanCa) risk factors, stimulate nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and catecholamines production respectively. NNK and catecholamine bind the β-adrenoceptors and induce PanCa cell proliferation; and we have previously suggested that β-adrenergic antagonists may suppress proliferation and invasion and stimulate apoptosis in PanCa. To clarify the mechanism of apoptosis induced by β2-adrenergic antagonist, we hypothesize that blockage of the β2-adrenoceptor could induce G1/S phase arrest and apoptosis and Ras may be a key player in PanCa cells. The β1 and β2-adrenoceptor proteins were detected on the cell surface of PanCa cells from pancreatic carcinoma specimen samples by immunohistochemistry. The β2-adrenergic antagonist ICI118,551 significantly induced G1/S phase arrest and apoptosis compared with the β1-adrenergic antagonist metoprolol, which was determined by the flow cytometry assay. β2-adrenergic antagonist therapy significantly suppressed the expression of extracellular signal-regulated kinase, Akt, Bcl-2, cyclin D1, and cyclin E and induced the activation of caspase-3, caspase-9 and Bax by Western blotting. Additionally, the β2-adrenergic antagonist reduced the activation of NFκB in vitro cultured PanCa cells.\n\nQuestion:\nDoes β2-adrenoceptor blockage induce G1/S phase arrest and apoptosis in pancreatic cancer cells via Ras/Akt/NFκB pathway?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCompensatory enlargement of the coronary arterial wall has been described in the early stages of native atherosclerosis. However, little is known about the specific effect of aging on this adaptive process in atherosclerosis. The purpose of the current study was to characterize the effects of advancing age on vascular remodeling and endothelium-dependent and -independent coronary vasodilation in patients without coronary artery disease risk factors. Twenty-six patients without coronary risk factors and with normal and mildly diseased coronary arteries were studied. Vessel, lumen and atherosclerotic plaque areas were evaluated by intravascular ultrasound and coronary flow response was assessed using papaverine and acetylcholine in the left anterior descending coronary artery. There was a weak but significant correlation between plaque area and age (r = 0.29, P<0.01). Vessel area was also weakly but significantly correlated with age (r = 0.22, P<0.05). However, lumen area had no correlation with age. Vessel area in the younger group (<50 years) and the older group (> or =50 years) increased 1.64 and 0.55 mm2 for every 1 mm2 increase in plaque area (r = 0.62, P<0.0001 and r = 0.39, P<0.05, respectively). With regard to vascular reactivity, there was an inverse correlation between the percentage increases in coronary blood flow (CBF) evoked by acetylcholine and aging (r = -0.49, P<0.05). The percentage increases in CBF evoked by papaverine also inversely correlated with aging (r=-0.53, P<0.01). However, the percentage changes in coronary artery diameter evoked with acetylcholine did not correlate with aging.\n\nQuestion:\nIs advancing age associated with diminished vascular remodeling and impaired vasodilation in resistance coronary arteries?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nintimal hyperplasia (IH) and constrictive remodelling are important causes of restenosis following endovascular interventions, such as percutaneous transluminal angioplasty. Photodynamic therapy (PDT) with 5-aminolaevulinic (ALA) may prevent restenosis by cellular depletion and the elimination of cholinergic innervation. rats (n=90) were subdivided into 4 main groups. In the experimental group (n=36: 3 replications x 4 doses x 3 examination time-points), ALA was administered (200mg/kg i.v.) 2-3h before balloon injury (BI) of the common iliac artery followed by endovascular illumination with 633nm at either 12.5, 25, 50 or 100J/cm diffuser length (dl BI+PDT group). As control groups served the BI+Light only (LO) group (n=36) that received no ALA, the BI only group (n=9) (BI), and a group (n=9) that received a Sham procedure (Sham group). planimetric analysis showed IH of 0.28+/-0.12mm(2) (BI), 0.27+/-0.12mm(2) (BI+LO at 100J/cmdl) in contrast to 0.02+/-0.02mm(2) after BI+PDT at 100J/cmdl at 16 weeks (p<0.05). In the BI+PDT groups, a light-dose increase of a factor 2 led to an IH decrease of 17% (p<0.05). In the BI and BI+LO groups constrictive remodelling was found, in contrast to BI+PDT treated groups at 16 weeks. The staining of cholinergic innervation of the tunic media of the blood vessel wall in BI+PDT showed no damage at the highest fluence.\n\nQuestion:\nDoes endovascular photodynamic therapy with aminolaevulinic acid prevent balloon induced intimal hyperplasia and constrictive remodelling?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPeripheral blood biomarkers are needed to identify and determine the extent of idiopathic pulmonary fibrosis (IPF). Current physiologic and radiographic prognostic indicators diagnose IPF too late in the course of disease. We hypothesize that peripheral blood biomarkers will identify disease in its early stages, and facilitate monitoring for disease progression. Gene expression profiles of peripheral blood RNA from 130 IPF patients were collected on Agilent microarrays. Significance analysis of microarrays (SAM) with a false discovery rate (FDR) of 1% was utilized to identify genes that were differentially-expressed in samples categorized based on percent predicted D(L)CO and FVC. At 1% FDR, 1428 genes were differentially-expressed in mild IPF (D(L)CO >65%) compared to controls and 2790 transcripts were differentially- expressed in severe IPF (D(L)CO >35%) compared to controls. When categorized by percent predicted D(L)CO, SAM demonstrated 13 differentially-expressed transcripts between mild and severe IPF (< 5% FDR). These include CAMP, CEACAM6, CTSG, DEFA3 and A4, OLFM4, HLTF, PACSIN1, GABBR1, IGHM, and 3 unknown genes. Principal component analysis (PCA) was performed to determine outliers based on severity of disease, and demonstrated 1 mild case to be clinically misclassified as a severe case of IPF. No differentially-expressed transcripts were identified between mild and severe IPF when categorized by percent predicted FVC.\n\nQuestion:\nDoes the peripheral blood transcriptome identify the presence and extent of disease in idiopathic pulmonary fibrosis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nOrnithine transcarbamylase (OTC) deficiency is the most common inborn error of urea metabolism that can lead to hyperammonemic crises and orotic aciduria. To date, a total of 341 causative mutations within the OTC gene have been described. However, in about 20% of the patients with enzymatically confirmed OTC deficiency no mutation can be detected when sequencing of genomic DNA analyzing exons and adjacent intronic segments of the OTC gene is performed. Standard genomic DNA analysis of the OTC gene in five consecutive patients from five families revealed no mutation. Hence, liver tissue was obtained by needle sampling or open biopsy and RNA extracted from liver was analyzed. Complex rearrangements of the OTC transcript (three insertions and two deletions) were found in all five patients.\n\nQuestion:\nDoes analysis of mRNA transcripts improve the success rate of molecular genetic testing in OTC deficiency?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nInterferon lambda 3 (IFN-λ3) is a newly identified cytokine with antiviral activity, and its single nucleotide polymorphisms are strongly associated with the treatment effectiveness and development of chronic hepatitis C virus infection. We thus examined the potential of IFN-λ3 to inhibit HIV replication and the possible mechanisms of the anti-HIV action by IFN-λ3 in human macrophages. Under different conditions (before, during, and after HIV infection), IFN-λ3 significantly inhibited viral replication in macrophages, which was associated with the induction of multiple antiviral cellular factors (ISG56, MxA, OAS-1, A3G/F and tetherin) and IFN regulatory factors (IRF-1, 3, 5, 7 and 9). This anti-HIV action of IFN-λ3 could be compromised by the JAK-STAT inhibitor. In addition, IFN-λ3 treatment of macrophages induced the expression of toll-like receptor 3 (TLR3) and two key adaptors (MyD88 and TRIF) in type I IFN pathway activation. However, HIV infection compromised IFN-λ3-mediated induction of the key elements in JAK-STAT signaling pathway.\n\nQuestion:\nDoes iFN-λ3 inhibit HIV infection of macrophages through the JAK-STAT pathway?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAsporin is a novel extracellular matrix protein (ECM) with an important role in the development of osteoarthritis (OA), because it has been reported that functional polymorphisms in the aspartic acid repeat (D) of the asporin gene (ASPN) are associated with susceptibility to OA. This study was planned to investigate the association of the ASPN polymorphism with primary OA of the knee in a Mexican population, including several countryside regions. We conducted a case-control study in which 93 cases with primary OA of the knee and 118 controls were included. Cases included patients > 40 years of age, with a body mass index (BMI) ≤ 27 and a radiologic score for OA of the knee of ≥ 2. Controls were subjects > 40 years of age with a radiologic score of < 2. The D repeat polymorphism was genotyped and logistic regression was developed to evaluate risk magnitude. The D14 allele was more common in our cases and was associated with an increased risk for developing OA, while the frequencies of the remaining alleles did not exhibit differences.\n\nQuestion:\nIs d14 repeat polymorphism of the asporin gene associated with primary osteoarthritis of the knee in a Mexican Mestizo population?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nOvarian cancer is the most lethal gynecological malignancy in North America. Although survival rates are high when the disease is diagnosed at an early stage, this decreases exponentially in late-stage diagnoses. As such, there is a need for novel early detection biomarkers. Through an integrated approach to ovarian cancer biomarker discovery that combines proteomics with transcriptomics and bioinformatics, our laboratory has identified folate-receptor 1 (FOLR1) and Dickkopf-related protein 3 (Dkk-3) as putative biomarkers. The objective of this study was to measure the levels of FOLR1 and Dkk-3 in the serum of patients with ovarian cancer, benign gynecological conditions and healthy women. FOLR1 and Dkk-3 were analyzed in serum of 100 ovarian cancer patients, 100 patients with benign gynecological conditions, and 100 healthy women using enzyme-linked immunosorbent assays (ELISAs). All specimens were analyzed in triplicate. FOLR1 was significantly elevated in the serum of ovarian cancer patients compared to serum of both healthy controls (P<0.0001) and patients with benign gynecological conditions (P<0.0001). Furthermore, FOLR1 was strongly correlated with CA125 as both were elevated in the serous histotype and in late-stage disease. FOLR1 did not outperform CA125 in receiver operating characteristic curve analysis and there was no significant complementarity between the two markers. Dkk-3 was not significantly different between the three serum cohorts and was not correlated with CA125.\n\nQuestion:\nIs folate-receptor 1 ( FOLR1 ) protein elevated in the serum of ovarian cancer patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCurrently, knowledge does not allow early prediction of which cases of dengue fever (DF) will progress to dengue hemorrhagic fever (DHF), to allow early intervention to prevent progression or to limit severity. The objective of this study is to investigate the hypothesis that some specific comorbidities increase the likelihood of a DF case progressing to DHF. A concurrent case-control study, conducted during dengue epidemics, from 2009 to 2012. Cases were patients with dengue fever that progressed to DHF, and controls were patients of dengue fever who did not progress to DHF. Logistic regression was used to estimate the association between DHF and comorbidities. There were 490 cases of DHF and 1,316 controls. Among adults, progression to DHF was associated with self-reported hypertension (OR = 1.6; 95% CI 1.1-2.1) and skin allergy (OR = 1.8; 95% CI 1.1-3.2) with DHF after adjusting for ethnicity and socio-economic variables. There was no statistically significant association between any chronic disease and progression to DHF in those younger than 15 years.\n\nQuestion:\nAre arterial hypertension and skin allergy risk factors for progression from dengue to dengue hemorrhagic fever : a case control study?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThere is increasing evidence that environmental exposures determining childhood illnesses operate early in life. Prenatal exposure to a farming environment through the mother might also play an important role. We sought to investigate the role of maternal exposures to environments rich in microbial compounds for the development of atopic sensitization, asthma, and corresponding alterations in the innate immune system in offspring. In the children of the cross-sectional Prevention of Allergy Risk Factors for Sensitization in Children Related to Farming and Anthroposophic Life Style study, asthma and atopy were assessed by means of standardized questionnaires (n = 8263) and serum IgE measurements (n = 2086). In a subsample (n = 322) gene expression of Toll-like receptors (TLR2 and TLR4) and CD14 was assessed. Maternal exposures were defined through questionnaire information. Both atopic sensitization (adjusted odds ratio, 0.58; 95% CI, 0.39-0.86) and the gene expression of receptors of innate immunity were strongly determined by maternal exposure to stables during pregnancy, whereas current exposures had much weaker or no effects. A dose-response relation was found between the extent of upregulation of these genes and the number of different farm animal species the mother had encountered in her pregnancy. Each additional farm animal species increased the expression of TLR2, TLR4, and CD14 by a factor of 1.16 (95% CI, 1.07-1.26), 1.12 (95% CI, 1.04-1.2), and 1.10 (95% CI, 1.03-1.23), respectively.\n\nQuestion:\nIs prenatal farm exposure related to the expression of receptors of the innate immunity and to atopic sensitization in school-age children?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHeat shock protein 27 (HSP27) is a cytoprotective chaperone, activated by stressful stimuli. HSP27 modulates aggregation and degradation of many proteins. Recent evidence suggests that HSP27 could be involved in the progression of tumor growth and in the development of resistance of various tumors to chemo- and radiotherapy. It has been reported that melatonin protects pancreatic cells and various tissues against inflammatory damage. Previous experimental studies have shown that melatonin stimulates pancreatic enzyme secretion and improves the outcome of experimental pancreatitis. To investigate whether melatonin could affect HSP27 protein level in human pancreatic carcinoma cells (PANC-1). PANC-1 cells were incubated in the standard medium DMEM supplemented with 10% fetal bovine serum at 37 degrees C with 5% CO2 and humidified atmosphere under basal conditions or in the presence of decreasing doses of melatonin (10(-6) - 10(-12)M). Control experiments were performed with the vehicle only (0,1% DMSO) without melatonin. After 24 h and 48 h the cells were harvested, the cytoplasmic and nuclear proteins were isolated for western blot and immunoblotting studies. Incubation of the PANC-1 cells with melatonin resulted in the stimulation both cytoplasmic and nuclear nonphosphorylated HSP27 protein levels after 24 h of incubation, however, above pools of nonphosphorylated chaperone protein levels were strongly diminished after subsequent 24 h. These changes were accompanied by marked rise of nuclear phosphorylated HSP27. The significant increase of this nuclear protein was observed after 48h of incubation.\n\nQuestion:\nDoes melatonin stimulate HSP27 phosphorylation in human pancreatic carcinoma cells ( PANC-1 )?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe endopeptidase dipeptidyl peptidase-IV (DPP-IV) has been shown to NH2-terminally truncate incretin hormones, glucose-dependent insulinotropic polypeptide, and glucagon-like peptide-1, thus ablating their ability to potentiate glucose-stimulated insulin secretion. Increasing the circulating levels of incretins through administration of DPP-IV inhibitors has therefore been introduced as a therapeutic approach for the treatment of type 2 diabetes. DPP-IV inhibitor treatment has also been shown to preserve islet mass in rodent models of type 1 diabetes. The current study was initiated to define the effects of the DPP-IV inhibitor sitagliptin (MK0431) on transplanted islet survival in nonobese diabetic (NOD) mice, an autoimmune type 1 diabetes model. Effects of MK0431 on islet graft survival in diabetic NOD mice were determined with metabolic studies and micropositron emission tomography imaging, and its underlying molecular mechanisms were assessed. Treatment of NOD mice with MK0431 before and after islet transplantation resulted in prolongation of islet graft survival, whereas treatment after transplantation alone resulted in small beneficial effects compared with nontreated controls. Subsequent studies demonstrated that MK0431 pretreatment resulted in decreased insulitis in diabetic NOD mice and reduced in vitro migration of isolated splenic CD4+ T-cells. Furthermore, in vitro treatment of splenic CD4+ T-cells with DPP-IV resulted in increased migration and activation of protein kinase A (PKA) and Rac1.\n\nQuestion:\nDoes dipeptidyl peptidase IV inhibition with MK0431 improve islet graft survival in diabetic NOD mice partially via T-cell modulation?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo investigate the rate of spontaneous passage of single and symptomatic common bile duct (CBD) stones ≤ 10 mm in diameter in 4 wk with or without a 2-wk course of anisodamine. A multicenter, randomized, placebo-controlled trial was undertaken. A total of 197 patients who met the inclusion criteria were enrolled. Ninety-seven patients were assigned randomly to the control group and the other 100 to the anisodamine group. The anisodamine group received intravenous infusions of anisodamine (10 mg every 8 h) for 2 wk. The control group received the same volume of 0.9% isotonic saline for 2 wk. Patients underwent imaging studies and liver-function tests every week for 4 wk. The rate of spontaneous passage of CBD stones was analyzed. The rate of spontaneous passage of CBD stones was significantly higher in the anisodamine group than that in the control group (47.0% vs 22.7%). Most (87.2%, 41/47) stone passages in the anisodamine group occurred in the first 2 wk, and passages in the control group occurred at a comparable rate each week. Factors significantly increasing the possibility of spontaneous passage by univariate logistic regression analyses were stone diameter (< 5 mm vs ≥ 5 mm and ≤ 10 mm) and anisodamine therapy. Multivariate logistic regression analyses revealed that these two factors were significantly associated with spontaneous passage.\n\nQuestion:\nDoes anisodamine accelerate spontaneous passage of single symptomatic bile duct stones ≤ 10 mm?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nUsing high resolution magnetic resonance imaging, we detected severely underdeveloped trabecular bone microarchitecture in the distal femur of children with cerebral palsy who can not ambulate independently vs. typically developing controls. Furthermore, very good short-term reliability of trabecular bone microarchitecture measurements was observed in both groups of children. Severe forms of cerebral palsy (CP) are associated with very low areal bone mineral density and a very high incidence of fracture in the distal femur; however, the state of trabecular bone microarchitecture has not been evaluated. Furthermore, the short-term reliability of trabecular bone microarchitecture assessment in children using high-resolution magnetic resonance imaging (MRI) has not been determined. Apparent bone volume to total volume (appBV/TV), trabecular number, (appTb.N), trabecular thickness (appTb.Th) and trabecular separation (appTb.Sp) were determined in the distal femur of non-ambulatory children with CP and typically developing children using MRI. Children with CP had a 30% lower appBV/TV, a 21% lower appTb.N, a 12% lower appTb.Th and a 48% higher appTb.Sp in the distal femur than controls (n = 10/group; P < 0.001). The short-term reliability of the trabecular bone microarchitecture measures was very good, with coefficients of variation ranging from 2.0 to 3.0% in children with CP (n = 6) and 1.8 to 3.5% in control children (n = 6).\n\nQuestion:\nIs underdeveloped trabecular bone microarchitecture detected in children with cerebral palsy using high-resolution magnetic resonance imaging?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nEndogenous hyperthyroidism is associated with altered coagulation. The aim of the present study is to investigate the effect of levothyroxine (LT(4)) suppression treatment for benign thyroid nodules on coagulation system. Prospective case-control study. Patients Thirty consecutive euthyroid pre-menopausal women with nodular goitre disease and 28 healthy controls were included in the study. Plasma fibrinogen, d-dimer, von Willebrand factor (vWF), tissue factor (TF), tissue plasminogen activator (tPA), plasminogen activator inhibitor (PAI-1) and tissue factor pathway inhibitor (TFPI) levels were measured at baseline and after LT(4) suppression therapy. Plasma levels of fibrinogen, d-dimer, vWF, TF and PAI-1 increased significantly after treatment with LT(4) for 1 year. Serum FT(4) was a significant predictor of increased fibrinogen, vWF and PAI-1 levels, when the data was controlled for age and BMI.\n\nQuestion:\nDoes levothyroxine ( LT4 ) suppression treatment for benign thyroid nodules alter coagulation?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIdiopathic pulmonary fibrosis (IPF) is a devastating disease characterized by epithelial phenotypic changes and fibroblast activation. Based on the temporal heterogeneity of IPF, we hypothesized that hyperplastic alveolar epithelial cells regulate the fibrotic response. To identify novel mediators of fibrosis comparing the transcriptional signature of hyperplastic epithelial cells and conserved epithelial cells in the same lung. Laser capture microscope and microarrays analysis were used to identify differentially expressed genes in IPF lungs. Bleomycin-induced lung fibrosis was evaluated in Mmp19-deficient and wild-type (WT) mice. The role of matrix metalloproteinase (MMP)-19 was additionally studied by transfecting the human MMP19 in alveolar epithelial cells. Laser capture microscope followed by microarray analysis revealed a novel mediator, MMP-19, in hyperplastic epithelial cells adjacent to fibrotic regions. Mmp19(-/-) mice showed a significantly increased lung fibrotic response to bleomycin compared with WT mice. A549 epithelial cells transfected with human MMP19 stimulated wound healing and cell migration, whereas silencing MMP19 had the opposite effect. Gene expression microarray of transfected A549 cells showed that PTGS2 (prostaglandin-endoperoxide synthase 2) was one of the highly induced genes. PTGS2 was overexpressed in IPF lungs and colocalized with MMP-19 in hyperplastic epithelial cells. In WT mice, PTGS2 was significantly increased in bronchoalveolar lavage and lung tissues after bleomycin-induced fibrosis, but not in Mmp19(-/-) mice. Inhibition of Mmp-19 by siRNA resulted in inhibition of Ptgs2 at mRNA and protein levels.\n\nQuestion:\nIs matrix metalloproteinase-19 a key regulator of lung fibrosis in mice and humans?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nInactivation of Shox2, a member of the short-stature homeobox gene family, leads to defective development of multiple organs and embryonic lethality as a result of cardiovascular defects, including bradycardia and severe hypoplastic sinoatrial node (SAN) and sinus valves, in mice. It has been demonstrated that Shox2 regulates a genetic network through the repression of Nkx2.5 to maintain the fate of the SAN cells. However, the functional mechanism of Shox2 protein as a transcriptional repressor on Nkx2.5 expression remains completely unknown. A specific interaction between the B56δ regulatory subunit of PP2A and Shox2a, the isoform that is expressed in the developing heart, was demonstrated by yeast 2-hybrid screen and coimmunoprecipitation. Western blotting and immunohistochemical assays further confirmed the presence of phosphorylated Shox2a (p-Shox2a) in cell culture as well as in the developing mouse and human SAN. Site-directed mutagenesis and in vitro kinase assays identified Ser92 and Ser110 as true phosphorylation sites and substrates of extracellular signal-regulated kinase 1 and 2. Despite that Shox2a and its phosphorylation mutants possessed similar transcriptional repressive activities in cell cultures when fused with Gal4 protein, the mutant forms exhibited a compromised repressive effect on the activity of the mouse Nkx2.5 promoter in cell cultures, indicating that phosphorylation is required for Shox2a to repress Nkx2.5 expression specifically. Transgenic expression of Shox2a, but not Shox2a-S92AS110A, mutant in the developing heart resulted in down-regulation of Nkx2.5 in wild-type mice and rescued the SAN defects in the Shox2 mutant background. Last, we demonstrated that elimination of both phosphorylation sites on Shox2a did not alter its nuclear location and dimerization, but depleted its capability to bind to the consensus sequences within the Nkx2.5 promoter region.\n\nQuestion:\nIs phosphorylation of Shox2 required for its function to control sinoatrial node formation?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nA major mechanism of resistance to methylating agents, including temozolomide, is the DNA repair protein O(6)-alkylguanine-DNA alkyltransferase (AGT). Preclinical data indicates that defective DNA mismatch repair (MMR) results in tolerance to temozolomide regardless of AGT activity. The purpose of this study was to determine the role of MMR deficiency in mediating resistance in samples from patients with both newly diagnosed malignant gliomas and those who have failed temozolomide therapy. The roles of AGT and MMR deficiency in mediating resistance in glioblastoma multiforme were assessed by immunohistochemistry and microsatellite instability (MSI), respectively. The mutation status of the MSH6 gene, a proposed correlate of temozolomide resistance, was determined by direct sequencing and compared with data from immunofluorescent detection of MSH6 protein and reverse transcription-PCR amplification of MSH6 RNA. Seventy percent of newly diagnosed and 78% of failed-therapy glioblastoma multiforme samples expressed nuclear AGT protein in > or = 20% of cells analyzed, suggesting alternate means of resistance in 20% to 30% of cases. Single loci MSI was observed in 3% of patient samples; no sample showed the presence of high MSI. MSI was not shown to correlate with MSH6 mutation or loss of MSH6 protein expression.\n\nQuestion:\nDoes mismatch repair deficiency mediate clinical resistance to temozolomide in malignant glioma?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nLaboratories traditionally culture toxoplasma tachyzoites in animals for testing and experimental use. This article considers why available cell culture methods are not used more often. To compare HeLa cell culture and animal culture for production of toxoplasma tachyzoites. In 2000 HeLa culture replaced animal culture for continuous production of toxoplasma tachyzoites in the Scottish Toxoplasma Reference Laboratory. The performance of animal culture (1994-1998) was compared with HeLa culture (2004-2008). A PubMed search was carried out for 1998 and 2008 to assess the culture methods used in laboratories. Animal culture was able to produce higher yields of tachyzoites (10(9) from a cotton rat peritoneal harvest compared to 10(7) from a 75 cm(2) cell culture flask) but significantly more HeLa cultures were successful (93% versus 84%; p=0.025). There was no difference in the quality of tachyzoites from animal and HeLa cultures as demonstrated by the high levels of success in the dye test. HeLa culture offered significant advantages in flexibility and control. A review of the literature showed no significant change in the method of culture used in laboratories between 1998 and 2008 (p=0.36).\n\nQuestion:\nAre toxoplasma tachyzoites from cell culture more appropriate in some situations?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe receptor for advanced glycation end products (RAGE) has been found to interact with amyloid β (Aβ). Although RAGE does not have any kinase motifs in its cytosolic domain, the interaction between RAGE and Aβ triggers multiple cellular signaling involved in Alzheimer's disease (AD). However, the mechanism of signal transduction by RAGE remains still unknown. Therefore, identifying binding proteins of RAGE may provide novel therapeutic targets for AD. In this study, we identified p38-regulated/activated protein kinase (PRAK) as a novel RAGE interacting molecule. To investigate the effect of Aβ on PRAK mediated RAGE signaling pathway, we treated SH-SY5Y cells with monomeric form of Aβ. We demonstrated that Aβ significantly increased the phosphorylation of PRAK as well as the interaction between PRAK and RAGE. We showed that knockdown of PRAK rescued mTORC1 inactivation induced by Aβ treatment and decreased the formation of Aβ-induced autophagosome.\n\nQuestion:\nIs the novel RAGE interactor PRAK associated with autophagy signaling in Alzheimer 's disease pathogenesis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe objective of this study was to increase the spatial and temporal resolution of dynamic 3-dimensional (3D) magnetic resonance imaging (MRI) of lung volumes and diaphragm motion. To achieve this goal, we evaluate the utility of the proposed blind compressed sensing (BCS) algorithm to recover data from highly undersampled measurements. We evaluated the performance of the BCS scheme to recover dynamic data sets from retrospectively and prospectively undersampled measurements. We also compared its performance against that of view-sharing, the nuclear norm minimization scheme, and the l1 Fourier sparsity regularization scheme. Quantitative experiments were performed on a healthy subject using a fully sampled 2D data set with uniform radial sampling, which was retrospectively undersampled with 16 radial spokes per frame to correspond to an undersampling factor of 8. The images obtained from the 4 reconstruction schemes were compared with the fully sampled data using mean square error and normalized high-frequency error metrics. The schemes were also compared using prospective 3D data acquired on a Siemens 3 T TIM TRIO MRI scanner on 8 healthy subjects during free breathing. Two expert cardiothoracic radiologists (R1 and R2) qualitatively evaluated the reconstructed 3D data sets using a 5-point scale (0-4) on the basis of spatial resolution, temporal resolution, and presence of aliasing artifacts. The BCS scheme gives better reconstructions (mean square error = 0.0232 and normalized high frequency = 0.133) than the other schemes in the 2D retrospective undersampling experiments, producing minimally distorted reconstructions up to an acceleration factor of 8 (16 radial spokes per frame). The prospective 3D experiments show that the BCS scheme provides visually improved reconstructions than the other schemes do. The BCS scheme provides improved qualitative scores over nuclear norm and l1 Fourier sparsity regularization schemes in the temporal blurring and spatial blurring categories. The qualitative scores for aliasing artifacts in the images reconstructed by nuclear norm scheme and BCS scheme are comparable.The comparisons of the tidal volume changes also show that the BCS scheme has less temporal blurring as compared with the nuclear norm minimization scheme and the l1 Fourier sparsity regularization scheme. The minute ventilation estimated by BCS for tidal breathing in supine position (4 L/min) and the measured supine inspiratory capacity (1.5 L) is in good correlation with the literature. The improved performance of BCS can be explained by its ability to efficiently adapt to the data, thus providing a richer representation of the signal.\n\nQuestion:\nDoes blind Compressed Sensing enable 3-Dimensional Dynamic Free Breathing Magnetic Resonance Imaging of Lung Volumes and Diaphragm Motion?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTargeting of KIT and platelet-derived growth factor receptor (PDGFR) tyrosine kinases by imatinib is an effective anticancer strategy. However, mutations of the gatekeeper residue (T670 in KIT and T681 in PDGFRbeta) render the two kinases resistant to imatinib. The aim of this study was to evaluate whether sorafenib (BAY 43-9006), a multitargeted ATP-competitive inhibitor of KIT and PDGFR, was active against imatinib-resistant KIT and PDGFRbeta kinases. We used in vitro kinase assays and immunoblot with phosphospecific antibodies to determine the activity of sorafenib on KIT and PDGFRbeta kinases. We also exploited reporter luciferase assays to measure the effects of sorafenib on KIT and PDGFRbeta downstream signaling events. The activity of sorafenib on interleukin-3-independent proliferation of Ba/F3 cells expressing oncogenic KIT or its imatinib-resistant T670I mutant was also tested. Sorafenib efficiently inhibited gatekeeper mutants of KIT and PDGFRbeta (IC(50) for KIT T670I, 60 nmol/L; IC(50) for PDGFRbeta T681I, 110 nmol/L). Instead, it was less active against activation loop mutants of the two receptors (IC(50) for KIT D816V, 3.8 micromol/L; IC(50) for PDGFRbeta D850V, 1.17 micromol/L) that are also imatinib-resistant. Sorafenib blocked receptor autophosphorylation and signaling of KIT and PDGFRbeta gatekeeper mutants in intact cells as well as activation of AP1-responsive and cyclin D1 gene promoters, respectively. Finally, the compound inhibited KIT-dependent proliferation of Ba/F3 cells expressing the oncogenic KIT mutant carrying the T670I mutation.\n\nQuestion:\nDoes sorafenib inhibit imatinib-resistant KIT and platelet-derived growth factor receptor beta gatekeeper mutants?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe presence of secondary hyperparathyroidism is very frequent in the elderly population living in geriatric institutions. It has been associated with an increased mortality rate in previous studies. To evaluate the association of secondary hyperparathyroidism with mortality or hospitalization or both (combined outcome) during a 6-month period in individuals living in geriatric institutions. A cohort of 100 individuals aged between 65 and 102 years living in geriatric institutions in the city of Porto Alegre, Brazil, was prospectively studied. Serum levels of 25-hydroxyvitamin D [25(OH)D], parathyroid hormone (PTH), albumin, total calcium, phosphorus, magnesium, creatinine and alkaline phosphatase were measured. The glomerular filtration rate (GFR) was calculated using the Cockcroft-Gault equation. Secondary hyperparathyroidism was defined as serum PTH levels higher than 48 pg/ml and normal or reduced serum calcium levels. The deaths were verified by means of death certificates and hospitalization by the discharge summaries provided by the Brazilian health system hospitals. Fifty-eight percent of the individuals had secondary hyperparathyroidism, defined as serum PTH >48 pg/ml and normal or low serum calcium. Mean serum 25(OH)D levels were 12.5 +/- 8 ng/ml. The odds ratio of an individual with secondary hyperparathyroidism to die, to be hospitalized or to have the combined outcome within 6 months was 6.6 [confidence interval (CI) 95% 0.8-54.6; p = 0.07], 10.7 (CI 95% 1.3-85.9; p = 0.007) and 5.20 (CI 95% 1.10-27.7; p = 0.04), respectively. Secondary hyperparathyroidism and body mass index were independently associated with the combined outcome, after correction for the GFR and 25(OH)D.\n\nQuestion:\nIs secondary hyperparathyroidism associated with increased risk of hospitalization or death in elderly adults living in a geriatric institution?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo verify the values and the time course of regional cerebral blood flow (rCBF) in the cortex located beneath an evacuated acute subdural hematoma (SDH) and their relationship with neurological outcome. rCBF levels were measured in multiple regions of interest, by means of a Xe-computed tomographic technique, in the cortex underlying an evacuated SDH and contralaterally in 20 patients with moderate or severe traumatic brain injury and an evacuated acute SDH. Twenty-three patients with moderate or severe traumatic brain injury and an evacuated extradural hematoma or diffuse injury served as the control group. Outcome was evaluated by means of the Glasgow Outcome Scale at 12 months. Values for the maximum (rCBFmax) and the mean of all rCBF levels in the cortex beneath the evacuated SDH were more frequently consistent with hyperemia. The side-to-side differences in the mean of all rCBF and rCBFmax levels between lesioned and nonlesioned hemispheres were greater in patients with evacuated SDH than in controls (P = 0.0013 and P = 0.0018, respectively). The side-to-side difference in the maximum rCBF value was higher in SDH patients with unfavorable outcomes than in controls at 24 to 96 hours and at 4 to 7 days and higher than in patients with favorable outcomes at 4 to 7 days. The widest side-to-side difference in rCBFmax value was more elevated in patients with an evacuated SDH with unfavorable outcome than in patients with a favorable outcome (P = 0.047), whereas no differences were found in controls. The SDH thickness and the associated midline shift were greater in patients with unfavorable outcomes than in those with favorable outcomes.\n\nQuestion:\nIs hyperemia beneath evacuated acute subdural hematoma frequent and prolonged in patients with an unfavorable outcome : a xe-computed tomographic study?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPhenethyl isothiocyanate (PEITC) is a cancer chemopreventive agent from cruciferous vegetables. Cholangiocarcinoma (CCA) is a chemo-resistant cancer with very poor prognosis. We evaluated the effects of PEITC on induction of apoptotic cell death in relation to cellular glutathione (GSH) and mitochondrial function of a CCA cell line, KKU-M214. Cytotoxic effects of PEITC on a CCA cell line, KKU-M214, and a reference cell line, Chang cells were evaluated. To delineate mechanisms of cell death, the following parameters were measured; GSH and superoxide levels as the oxidative status parameters, apoptosis related proteins levels using Western blotting. Cellular free calcium level and mitochondrial transmembrane potential were also measured. PEITC induced apoptotic cell death of both KKU-M214 and Chang cells. After PEITC treatment, both cells showed decrease of Bcl-xl and increase of Bax levels. While KKU-M214 cells released AIF, Chang cells released cytochrome c, with subsequent activation of caspase 3 and 9, upon PEITC treatment. PEITC induced superoxide formation in both cells, although it seemed not play a role in cell death. PEITC caused GSH redox stress in different ways in two cell types, because N-acetylcysteine (NAC) prevented redox stress in Chang but not in KKU-M214 cells. The loss of mitochondrial transmembrane potential was induced by PEITC concurrent with GSH stress, but was not a primary cause of cell death. The rapid increase of free calcium level in cytosol was associated with cell death in both cell lines. These events were prevented by NAC in Chang cells, but not in KKU-M214 cells.\n\nQuestion:\nDoes phenethyl isothiocyanate induce calcium mobilization and mitochondrial cell death pathway in cholangiocarcinoma KKU-M214 cells?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nGenetic manipulation of the allograft is an attractive approach to prevent the graft against chronic deterioration through stable expression of immunomodulatory or protective genes. However, the best strategy for prevention of chronic allograft deterioration remains unclear. The efficacies of adeno-associated viral vector-mediated stable expression of indoleamine 2,3-dioxygenase (IDO), cytotoxic T-lymphocyte associated antigen 4 with human immunoglobulin G(1) (CTLA4Ig) or interleukin-10 (IL-10) in the prevention of chronic allograft deterioration were compared in a rat heart transplantation model. Transduction of grafts with IL-10 significantly prolonged allograft survival, whereas transduction of grafts with IDO did not improve graft survival compared to controls. Analysis of long-term survived heart allografts showed that both CTLA4Ig and IL-10 could significantly reduced the T cells and macrophage infiltration. However, stable expression of CTLA4Ig failed to prevent the development of transplant arteriosclerosis. By contrast, IL-10 suppressed the development of transplant arteriosclerosis effectively. The suppressive effects of IL-10 in preventing the development of chronic allograft deterioration were associated with lower transcript levels of transforming tumor growth factor beta 1 and macrophage migration inhibitory factor in the graft. In addition, higher transcript levels of heme oxygenase-1 were found in IL-10-transduced allograft.\n\nQuestion:\nIs targeting of interleukin-10 superior to cytotoxic T-lymphocyte associated antigen 4 with human immunoglobulin G ( 1 ) for the prevention of chronic allograft deterioration in organ transplantation?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nA moderate intake of alcohol is associated with lower cardiovascular mortality, and the role of circulating progenitor cells in the beneficial effect of alcohol on atherosclerosis is unclear. The hypothesis of this study was that alcohol ameliorates atherosclerosis by modulating the circulating levels of stromal cell-derived growth factor (SDF)-1 and vascular progenitor cells. Atherosclerosis was induced by infusion of angiotensin II in apolipoprotein-E deficient mice, which were treated with high and low doses of ethanol for 28 days by intraperitoneal injection. Mice treated with low-dose ethanol had significantly less dilatation and fewer atheromatous lesions than mice receiving the high-dose ethanol. The number of circulating fibrocytes was significantly lower in mice treated with high-dose ethanol compared with mice with atherosclerosis untreated with ethanol. The plasma CXCL12/SDF-1 level was significantly increased in mice treated with low-dose ethanol compared with mice treated with a high dose, and the plasma concentration of transforming growth factor-β1 was significantly increased in mice treated with high-dose ethanol compared with control mice. Ethanol regulated the secretion of SDF-1 and vascular endothelial growth factor from fibroblasts in a dose-dependent and bimodal fashion.\n\nQuestion:\nIs atherosclerosis amelioration by moderate alcohol consumption associated with increased circulating levels of stromal cell-derived factor-1?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nOur aim was to investigate serum clusterin levels in preeclampsia and to determine whether any changes in clusterin levels are useful in distinguishing the presence of concomitant intrauterine growth restriction (IUGR) and in predicting adverse pregnancy outcomes. A prospective case-control study was carried out which included 86 pregnant women (47 patients with preeclampsia and 39 healthy controls). Maternal serum samples obtained from all participants and clusterin levels were determined by enzyme-linked immunosorbent assay (ELISA). Compared with controls, women with preeclampsia had significantly higher clusterin levels (mean 83.8±23.6 vs. 119.2±40.5, P<0.01). Further analysis revealed the highest clusterin levels were in patients with preeclampsia and IUGR (P<0.001). According to the receiver operating characteristic (ROC) analysis performed for the predictive value of clusterin levels for adverse maternal outcomes, the area under the curve (AUC) was 0.738 (95% CI: 0.616-0.859). The best clusterin cut-off value in predicting adverse maternal outcomes was 102.6 pg/mL with 75% sensitivity and 66% specifity. Multivariable logistic regression analysis revealed serum clusterin levels of >102.6 pg/mL was independently associated with preeclampsia (OR: 6.18, 95% CI: 2.41-15.9) and maternal adverse outcomes (OR: 5.13, 95% CI: 2.01-13.1) and also clusterin levels higher than 117.4 pg/mL were associated with adverse neonatal outcomes (OR: 5.02, 95% CI: 1.04-24.3).\n\nQuestion:\nIs increased levels of serum clusterin associated with intrauterine growth restriction and adverse pregnancy outcomes in preeclampsia?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nNeurons project their axons along specific pathways in order to establish appropriate connections with their target cells. The rate and direction of axonal growth is determined by interactions between the highly motile growth cone and environmental cues that can act in either an attractive or a repulsive manner. Locomotion is ultimately dependent upon the reorganisation of the actin cytoskeleton and an established role for the Rho family of small GTPases in regulating this process in non-neuronal cells identifies them as candidate signalling molecules in growth cones. An inactive form of Rac1 has recently been shown to inhibit the 'growth-cone collapse' response induced by chick Sema3A, a protein that has recently been established as an important guidance cue. The molecular basis for this inhibition remains unclear. We have made a series of overlapping peptides from the amino-terminal region of Rac1 and rendered them cell permeable by synthesis in tandem with an established internalisation vector. We report here that a peptide encompassing Rac1 amino acids 17-32 binds directly to the established Rac1-interacting molecules PAK, WASP, 3BP-1 and p85beta(P13K), but not to p67(Phox). Furthermore, the peptide can compete with activated Rac1 for target binding, and inhibits Sema3A-induced growth-cone collapse. We also synthesised cell-permeable peptides that correspond to the Cdc42/Rac1-binding (CRIB) motifs present in PAK and N-WASP. Our results show that a CRIB-containing peptide from PAK, but not that from N-WASP, inhibits growth-cone collapse and that the inhibitory activity correlates with binding to Rac1 and not to Cdc42.\n\nQuestion:\nIs sema3A-induced growth-cone collapse mediated by Rac1 amino acids 17-32?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWound healing depends on a well-balanced regulation of inflammation and angiogenesis. In chronic wounds the healing process is disturbed and inflammation persists. Regulation of wound closure is controlled by transmembrane and extracellular proteins, the folding and maturation of which occur in the endoplasmic reticulum (ER) by ER-resident chaperone machinery. To study the role of the ER-resident chaperones BiP/Grp78, its cochaperone Mdg1/ERdJ4, and Grp94 in chronic, nonhealing wounds. Immunohistochemical staining of these chaperones in individual human biopsies and investigation of the possible role of BiP and Mdg1 in endothelial cells, focusing on their inflammatory response and angiogenic potential. In all chronic wounds investigated, the levels of these ER-resident chaperones were elevated in endothelial cells and leucocytes. The proangiogenic role of BiP has been shown in tumour growth studies before and was confirmed in this study. Proangiogenic activity of the cochaperone Mdg1 has been postulated before but could not be confirmed in this study. The chemokine tumour necrosis factor (TNF)-α was shown to trigger the presentation of proinflammatory adhesion molecules and the release of proinflammatory cytokines. Here we show that TNF-α does not affect endogenous chaperone levels, but that the ER-resident chaperones BiP and Mdg1 modulate the cellular TNF-α-induced proinflammatory response.\n\nQuestion:\nDo endoplasmic reticulum-resident chaperones modulate the inflammatory and angiogenic responses of endothelial cells?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nDetermination of intracellular signalling pathways that mediate intestinal epithelial proliferation is fundamental to the understanding of the integrity and function of the intestinal tract under normal and diseased conditions. The phosphoinositide 3-kinase (PI3K)/Akt pathway transduces signals initiated by growth factors and is involved in cell proliferation and differentiation. In this study, we assessed the role of PI3K/Akt in transduction of proliferative signals in intestinal epithelial cells. A rat intestinal epithelial (RIE) cell line and human colorectal cancer HCA-7 and LS-174 cell lines served as in vitro models. The Balb/cJ mouse was the in vivo model. PI3K activation was critical for G1 cell cycle progression of intestinal epithelial cells. Ectopic expression of either active p110alpha or Akt-1 increased RIE cell proliferation. In vivo experiments demonstrated that PI3K activation was closely associated with the proliferative activity of intestinal mucosa. Treatment of mice with PI3K inhibitors blocked induction of PI3K activity and attenuated intestinal mucosal proliferation associated with oral intake. Epidermal growth factor and transforming growth factor alpha stimulated PI3K activation which was required for growth factor induced expression of cyclin D1.\n\nQuestion:\nDoes phosphatidylinositol 3-kinase mediate proliferative signals in intestinal epithelial cells?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSalvicine is a novel DNA topoisomerase II inhibitor with potent anticancer activity. In present study, the effect of salvicine against metastasis is evaluated using human breast carcinoma orthotopic metastasis model and its mechanism is further investigated both in animal and cellular levels. The MDA-MB-435 orthotopic xenograft model was applied to detect the antimetastatic effect of salvicine. Potential target candidates were detected and analyzed by microarray technology. Candidates were verified and explored by reverse transcription-PCR and Western blot. Salvicine activities on stress fiber formation, invasion, and membrane translocation were further investigated by immunofluorescence, invasion, and ultracentrifugal assays. Salvicine significantly reduced the lung metastatic foci of MDA-MB-435 orthotopic xenograft, without affecting primary tumor growth obviously. A comparison of gene expression profiles of primary tumors and lung metastatic focus between salvicine-treated and untreated groups using the CLOTECH Atlas human Cancer 1.2 cDNA microarray revealed that genes involved in tumor metastasis, particularly those closely related to cell adhesion and motility, were obviously down-regulated, including fibronectin, integrin alpha3, integrin beta3, integrin beta5, FAK, paxillin, and RhoC. Furthermore, salvicine significantly down-regulated RhoC at both mRNA and protein levels, greatly inhibited stress fiber formation and invasiveness of MDA-MB-435 cells, and markedly blocked translocation of both RhoA and RhoC from cytosol to membrane.\n\nQuestion:\nIs antimetastatic effect of salvicine on human breast cancer MDA-MB-435 orthotopic xenograft closely related to Rho-dependent pathway?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo assess the relationship between congenital uterine malformations and blood pressure in pregnancy. Twenty-four-hour automated ambulatory blood pressure monitoring (readings every 30 min) was performed in 16 normotensive, nonproteinuric, primigravidae with congenital uterine malformations (5 uterus septus, 9 uterus bicornis, 2 uterine didelphys) between 20 and 30 weeks. From the 24-hr blood pressure report, we calculated 24-hr mean, daytime and nighttime means. The results were compared with 16 primigravidae, matched for age and gestation, who were and remained normotensive throughout pregnancy, and tested for statistics with t-test; significance assessed at p < 0.001. Although they were within the normotensive range, all blood pressure measurements considered were significantly higher in pregnant women with congenital uterine malformations, compared to normal pregnant women. Namely, 24-hr, daytime, and nighttime systolic (mean +/- SD) were 121.1 +/- 8.4, 124.4 +/- 8.8, 114.0 +/- 7.7 mmHg, respectively, in women with uterine malformations and 108.0 +/- 7.4, 109.2 +/- 7.3, 102.1 +/- 8.5 mmHg, respectively, in normal pregnant women. Twenty-four-hour diastolic, daytime, and nighttime diastolic (mean +/- SD) 74.1 +/- 10.2, 77.1 +/- 10.6, 68.1 +/- 9.2 mmHg, in women with uterine malformations and 64.1 +/- 5.7, 66.0 +/- 5.7, 58.2 +/- 6.3 mmHg, in normal pregnant women (all differences p < 0.001). Fifteen of the fetuses from women with congenital uterine malformations showed intrauterine growth retardation. No differences were found 6 months after delivery.\n\nQuestion:\nAre congenital uterine malformations associated to increased blood pressure in pregnancy?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nFatty acids are important cellular constituents that may affect many metabolic processes relevant for the development of diabetes and its complications. We showed previously that vegetarian diet leads to greater increase in metabolic clearance rate of glucose (MCR) than conventional hypocaloric diet. The aim of this secondary analysis was to explore the role of changes in fatty acid composition of serum phospholipids in diet- and exercise-induced changes in MCR in subjects with type 2 diabetes (T2D). Subjects with T2D (n=74) were randomly assigned into a vegetarian group (VG, n=37) following vegetarian diet or a control group (CG, n=37) following a conventional diet. Both diets were calorie restricted (-500 kcal day(-1)). Participants were examined at baseline, 12 weeks of diet intervention and 24 weeks (subsequent 12 weeks of diet were combined with aerobic exercise). The fatty acid composition of serum phospholipids was measured by gas liquid chromatography. MCR was measured by hyperinsulinemic isoglycemic clamp. Visceral fat (VF) was measured by magnetic resonance imaging. Linoleic acid (LA; 18:2n6) increased in VG (P=0.04), whereas it decreased in CG (P=0.04) in response to dietary interventions. It did not change significantly after the addition of exercise in either group (group × time P<0.001). In VG, changes in 18:2n6 correlated positively with changes in MCR (r=+0.22; P=0.04) and negatively with changes in VF (r=-0.43; P=0.01). After adjustment for changes in body mass index, the association between 18:2n6 and MCR was no longer significant. The addition of exercise resulted in greater changes of phospholipid fatty acids composition in VG than in CG.\n\nQuestion:\nIs vegetarian diet-induced increase in linoleic acid in serum phospholipids associated with improved insulin sensitivity in subjects with type 2 diabetes?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis study aims to investigate the effect of 5(S), 6(R)-7-trihydroxymethyl heptanoate (BML-111) on the Wnt5a/frizzled-5 (FZD5)/calcium/calmodulin-dependent protein kinase II (CaMKII) signaling pathway in septic mice, and to explore whether this pathway mediates the effect of BML-111 on inflammatory response in lipopolysaccharide (LPS)-induced RAW 264.7 cells. The cecal ligation and puncture-induced mouse model of sepsis was constructed, and the mice were pretreated with BML-111. In vitro, LPS-induced RAW 264.7 cells were incubated with various concentrations of BML-111. Activation of Wnt5a/FZD5/CaMKII signaling pathway was achieved by transfection of the Wnt5a overexpression plasmid. The levels of interleukin-1 beta (IL-1β), IL-6 and IL-8 in the mouse serum and cell supernatant were determined by ELISA assay. The expression of Wnt5a, FZD5 and CaMKIIδ was examined by western blot analysis. The results from the in vivo studies revealed that BML-111 shows inhibitory effect on IL-1β, IL-6 and IL-8 expression in the serum of septic mice, and suppresses the expression of Wnt5a, FZD5 and CaMKIIδ protein. The in vitro studies demonstrated that BML-111 inhibits Wnt5a, FZD5 and CaMKIIδ proteins in a dose-dependent manner. BML-111 suppressed the levels of IL-1β, IL-6 and IL-8 in LPS-induced RAW 264.7 cells; however, this effect could be attenuated by transfection of the Wnt5a overexpression plasmid.\n\nQuestion:\nDoes wnt5a/FZD5/CaMKII signaling pathway mediate the effect of BML-111 on inflammatory reactions in sepsis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nUltrapure alginate gel is promising in terms of adhesion prevention. Because anti-adhesive barriers have been shown to disturb healing of bowel anastomoses, the effect of ultrapure alginate gel on the repair of colon anastomoses was studied. In 102 male Wistar rats, a 0.5-cm segment was resected from the descending colon and continuity was restored by an inverted single-layer end-to-end anastomosis. Animals were randomized into a control, an alginate gel, and a sodium hyaluronate carboxymethyl cellulose film group, each n = 34. Half of each group was sacrificed at day 3 and 7 postoperatively. Anastomotic strength was assessed by measuring both bursting pressure and breaking strength. Hydroxyproline content was measured and histologic analysis was performed. The incidence of adhesion and abscess formation was scored at sacrifice. No difference in either anastomotic-bursting pressure or breaking strength was found between experimental groups and the controls at any time point. Both the incidence of adhesion formation (35% versus 71%, P = 0.007) and the adhesion score (0.38 versus 0.79, P = 0.009) were significantly lower in the alginate gel group than in the controls. The abscess rate was higher (46% versus 18%, P = 0.030) in the hyaluronate carboxymethyl cellulose group than in the controls and unchanged in the alginate gel group.\n\nQuestion:\nDoes ultrapure alginate anti-adhesion gel impair colon anastomotic strength?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nUnderstanding the cellular mechanisms regulating axon degeneration and regeneration is crucial for developing treatments for nerve injury and neurodegenerative disease. In neurons, axon degeneration is distinct from cell body death and often precedes or is associated with the onset of disease symptoms. In the peripheral nervous system of both vertebrates and invertebrates, after degeneration of detached fragments, axons can often regenerate to restore function. Many studies of axonal degeneration and regeneration have used in vitro approaches, but the influence of extrinsic cell types on these processes can only be fully addressed in live animals. Because of its simplicity and superficial location, the larval zebrafish posterior lateral line (pLL) nerve is an ideal model system for live studies of axon degeneration and regeneration. We used laser axotomy and time-lapse imaging of pLL axons to characterize the roles of leukocytes, Schwann cells and target sensory hair cells in axon degeneration and regeneration in vivo. Immune cells were essential for efficient removal of axonal debris after axotomy. Schwann cells were required for proper fasciculation and pathfinding of regenerating axons to their target cells. Intact target hair cells were not themselves required for regeneration, but chemical ablation of neuromasts caused axons to transiently deviate from their normal paths.\n\nQuestion:\nDoes dynamics of degeneration and regeneration in developing zebrafish peripheral axons reveal a requirement for extrinsic cell types?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCochlear implant users still experience severe limitations regarding sound quality, music appreciation, and speech perception in adverse listening situation. To improve hearing in noisy environments, the incorporation of signal enhancement algorithms was initiated. The study group consisted of 13 postlingually deafened adults using HiRes 120. Participants were fitted with 2 versions of the noise reduction algorithm: a moderate and a strong setting. In an immediate session, the HSM sentence test in speech-shaped noise was administered using the clinical program as well as both noise reduction programs. Participants were asked to try all 3 programs in everyday listening situations at home and provide a rating of sound quality and speech perception via a questionnaire (Abbreviated Profile of Hearing Aid Benefit). During the fitting, no difficulties were encountered, and all participants accepted the noise reduction programs without any acclimatization. All participants achieved better results with both noise reduction programs in the HSM sentence test in noise compared with the clinical program. Group mean speech perception scores were highly significantly better for the ClearVoice settings compared with the clinical program score. The majority preferred one of the ClearVoice conditions, with 4 participants for the strong and 3 for the moderate setting.\n\nQuestion:\nDoes results of a pilot study with a signal enhancement algorithm for hire 120 cochlear implant users?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHepatocellular carcinoma (HCC) is one of the deadliest solid cancers and is the third leading cause of cancer-related death. There is a universal estimated male/female ratio of 2.5, but the reason for this is not well understood. The Sleeping Beauty (SB) transposon system was used to elucidate candidate oncogenic drivers of HCC in a forward genetics screening approach. Sex bias occurrence was conserved in our model, with male experimental mice developing liver tumors at reduced latency and higher tumor penetrance. In parallel, we explored sex differences regarding genomic aberrations in 235 HCC patients. Liver cancer candidate genes were identified from both sexes and genotypes. Interestingly, transposon insertions in the epidermal growth factor receptor (Egfr) gene were common in SB-induced liver tumors from male mice (10/10, 100%) but infrequent in female mice (2/9, 22%). Human single-nucleotide polymorphism data confirmed that polysomy of chromosome 7, locus of EGFR, was more frequent in males (26/62, 41%) than females (2/27, 7%) (P = 0.001). Gene expression-based Poly7 subclass patients were predominantly male (9/9) compared with 67% males (55/82) in other HCC subclasses (P = 0.02), and this subclass was accompanied by EGFR overexpression (P < 0.001).\n\nQuestion:\nIs sex bias occurrence of hepatocellular carcinoma in Poly7 molecular subclass associated with EGFR?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHigh SOCS3 expression in intestinal epithelial cells (IECs) of patients with ulcerative colitis (UC) in remission reflects the shorter time to relapse. We investigated whether high SOCS3 increased risk for relapse through violating STAT3-dependent protective effects of interleukin (IL)-22 during UC remission. Expression of IL-22 and c-Myc in UC remission mucosa was analyzed by immunohistochemistry. Effects of IL-22 on migration and proliferation of IEC cell lines with enforced SOCS3 expression were assessed with wounding assay and CCK-8 assay, respectively. Influence of STAT3 interference and SOCS3 overexpression on IL-22-regulated expression of antimicrobial peptide and proliferation-related molecules, including DMBT1, c-Myc, Survivin, Bcl-2, and Bcl-xL, were performed with quantitative real-time polymerase chain reaction or Western blot. Patients with UC in remission showed significantly more IL-22-positive immune cells, but no difference of epithelial c-Myc levels, in mucosa compared with healthy controls. Overexpression of SOCS3 nearly abolished IL-22-induced activation of STAT3. By inhibiting STAT3 signaling, SOCS3 influenced IL-22-induced expression of DMBT1, c-Myc, Survivin, and Bcl-2 as well as proliferation and migration processes in cultured IEC cell line.\n\nQuestion:\nDoes high suppressor of cytokine signaling-3 expression impair STAT3-dependent protective effects of interleukin-22 in ulcerative colitis in remission?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nRecent studies have identified signal transducer and activator of transcription 4 (STAT4) as a susceptibility gene for systemic lupus erythematosus (SLE) in different populations. In order to examine whether the allele distribution of the single nucleotide polymorphism (SNP) in gene STAT4 rs7574865 in patients with SLE is different from those of healthy controls in Chinese Northern Han population, we investigated whether the variants of STAT4 rs7574865 were associated with any specific clinical features of SLE. We genotyped SNPs in STAT4 rs7574865 in 252 patients with SLE and 497 healthy controls. All subjects were from the Northern part of Chinese Han population. The genotypes in rs7574865 were determined by polymerase chain reaction (PCR) and consequence direct sequencing of PCR products in the DNA samples. There was a significant difference in distribution of the SNPs in rs7574865 between the SLE patients and healthy controls. Compared with healthy controls, there was a significant correlation between TT genotypes in rs7574865 and the risk of SLE when GG genotype was used as a reference genotype after adjusting for gender and age. The frequency of T allele in the SLE patients was strongly significantly higher than that of healthy controls. Furthermore, there was a significant difference in the distribution of SNP in rs7574865 between male and female SLE patients, when compared with healthy controls. The frequency of T allele in rs7574865 in male patients was significantly higher than that of male healthy controls or female patients. There was no significant correlation between the frequencies of T allele in STAT4 rs7574865 and the clinical features of SLE.\n\nQuestion:\nIs variation in STAT4 associated with systemic lupus erythematosus in Chinese Northern Han population?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe lung is critical in surveillance and initial defense against pathogens. In humans, as in mice, individual genetic differences strongly modulate pulmonary responses to infectious agents, severity of lung disease, and potential allergic reactions. In a first step towards understanding genetic predisposition and pulmonary molecular networks that underlie individual differences in disease vulnerability, we performed a global analysis of normative lung gene expression levels in inbred mouse strains and a large family of BXD strains that are widely used for systems genetics. Our goal is to provide a key community resource on the genetics of the normative lung transcriptome that can serve as a foundation for experimental analysis and allow predicting genetic predisposition and response to pathogens, allergens, and xenobiotics. Steady-state polyA+ mRNA levels were assayed across a diverse and fully genotyped panel of 57 isogenic strains using the Affymetrix M430 2.0 array. Correlations of expression levels between genes were determined. Global expression QTL (eQTL) analysis and network covariance analysis was performed using tools and resources in GeneNetwork http://www.genenetwork.org. Expression values were highly variable across strains and in many cases exhibited a high heritability factor. Several genes which showed a restricted expression to lung tissue were identified. Using correlations between gene expression values across all strains, we defined and extended memberships of several important molecular networks in the lung. Furthermore, we were able to extract signatures of immune cell subpopulations and characterize co-variation and shared genetic modulation. Known QTL regions for respiratory infection susceptibility were investigated and several cis-eQTL genes were identified. Numerous cis- and trans-regulated transcripts and chromosomal intervals with strong regulatory activity were mapped. The Cyp1a1 P450 transcript had a strong trans-acting eQTL (LOD 11.8) on Chr 12 at 36 ± 1 Mb. This interval contains the transcription factor Ahr that has a critical mis-sense allele in the DBA/2J haplotype and evidently modulates transcriptional activation by AhR.\n\nQuestion:\nDoes genome-wide analysis of the mouse lung transcriptome reveal novel molecular gene interaction networks and cell-specific expression signatures?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nChronic stroke survivors with low hip bone density are particularly prone to fractures. This study shows that fear of falling is independently associated with falls in this population. Thus, fear of falling should not be overlooked in the prevention of fragility fractures in these patients. Chronic stroke survivors with low bone mineral density (BMD) are particularly prone to fragility fractures. The purpose of this study was to identify the determinants of balance, mobility and falls in this sub-group of stroke patients. Thirty-nine chronic stroke survivors with low hip BMD (T-score <-1.0) were studied. Each subject was evaluated for the following: balance, mobility, leg muscle strength, spasticity, and fall-related self-efficacy. Any falls in the past 12 months were also recorded. Multiple regression analysis was used to identify the determinants of balance and mobility performance, whereas logistic regression was used to identify the determinants of falls. Multiple regression analysis revealed that after adjusting for basic demographics, fall-related self-efficacy remained independently associated with balance/mobility performance (R2 = 0.494, P < 0.001). Logistic regression showed that fall-related self-efficacy, but not balance and mobility performance, was a significant determinant of falls (odds ratio: 0.18, P = 0.04).\n\nQuestion:\nIs fall-related self-efficacy , not balance and mobility performance , related to accidental falls in chronic stroke survivors with low bone mineral density?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo examine the influence of cloudy media on the slow double-stimulation multifocal electroretinogram (mfERG). Slow double-stimulation mfERG responses were measured from 26 subjects with normal ocular health under normal and light scattering conditions (induced using acrylic sheets) (Experiment 1) and another nine cataract patients before and after cataract surgery (Experiment 2). The amplitudes and implicit times of the first (M(1)) and second (M(2)) stimulation were compared under normal and light scattering conditions in Experiment 1 and they were compared under precataract and postcataract surgery in Experiment 2. Compared with control conditions (normal and postcataract surgery), the M(1) amplitude in the central region was significantly reduced in light scattering conditions (acrylic sheets and precataract surgery); the M(2) amplitude and both M(1) and M(2) implicit times of all regions examined were moderately affected in precataract surgery. The M(1):M(2) amplitude ratio and implicit time ratio were virtually unaffected in cloudy media for either central or mid-peripheral regions.\n\nQuestion:\nIs temporal interactive response resistant to cloudy ocular media in the slow double-stimulation multifocal electroretinogram?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nBoth multiple injection and single posterior cord injection techniques are associated with extensive anesthesia of the upper limb after an infraclavicular coracoid block (ICB). The main objective of this study was to directly compare the efficacy of both techniques in terms of the rates of completely anesthetizing cutaneous nerves below the elbow. Seventy patients undergoing surgery at or below the elbow were randomly assigned to receive an ICB after the elicitation of either a single radial nerve-type response (Radial group) or of two different main nerve-type responses of the upper limb, except for the radial nerve (Dual group). Forty milliliters of 1.5% mepivacaine was given in a single or a dual dose, according to group assignment. The sensory block was assessed in each of the cutaneous nerves at 10, 20 and 30 min. Block performance times and the rates of complete anesthesia below the elbow were also noted. Higher rates of sensory block of the radial nerve were found in the Radial group at 10, 20 and 30 min (P<0.05). The rates of sensory block of the ulnar nerve at 30 min were 97% and 75% in the Radial and in the Dual groups, respectively (P<0.05). The rate of complete anesthesia below the elbow was also higher in the Radial group at 30 min (P<0.05).\n\nQuestion:\nIs single stimulation of the posterior cord superior to dual nerve stimulation in a coracoid block?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe concern over rising antibiotic resistance necessitates exploration of alternative approaches in antimicrobial therapy. Bacterial communities use the auto-inducer 2 (AI-2) quorum sensing signal at a specific threshold level for intra- and interspecies communication in order to regulate virulence behaviour. AI-2 signal production occurs in bacteria that possess a luxS homologue. In this study, we investigate for the first time the association between AI-2 signalling and susceptibility to antibiotics. Streptococcus anginosus wild-type and its isogenic luxS mutant SA001 were exposed to erythromycin and ampicillin. Susceptibility to erythromycin and ampicillin was determined by measuring the cell density and viability. Complementation assays were conducted by exposing the mutant to wild-type supernatant or to the AI-2 precursor molecule dihydroxy-2,3-pentanedione (DPD). Disruption of luxS in S. anginosus resulted in a mutant with increased susceptibility to erythromycin and ampicillin. Supernatant from S. anginosus wild-type partially restored growth of SA001 in the presence of the two antibiotics. DPD restored growth of the luxS mutant in the presence of erythromycin and ampicillin to values similar to that of S. anginosus wild-type.\n\nQuestion:\nDoes aI-2 quorum sensing affect antibiotic susceptibility in Streptococcus anginosus?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCandida species are major causes of invasive mycoses in immunocompetent and immunocompromised hosts. Treatment options are limited in the setting of antifungal resistance and increased rates of echinocandin-resistant Candida glabrata have been reported. The novel arylamidine T-2307 demonstrates potent in vitro antifungal activity against Candida species. Our objective was to evaluate the in vitro and in vivo activity of T-2307 against resistant C. glabrata. In vitro activity was determined against 42 clinical C. glabrata isolates, including 17 echinocandin-resistant strains. Neutropenic ICR mice were inoculated intravenously with an echinocandin-resistant C. glabrata isolate (T-2307; caspofungin MICs ≤0.008 and 0.5 mg/L, respectively). Therapy with vehicle control, T-2307 (0.75, 1.5, 3 or 6 mg/kg subcutaneously once daily) or caspofungin (1 or 10 mg/kg intraperitoneally once daily) began 1 day post-challenge. Kidneys were collected on day 8 and fungal burden was assessed by counting cfu. T-2307 demonstrated potent in vitro activity against C. glabrata (geometric mean MIC 0.0135 mg/L), which was maintained against echinocandin-resistant isolates (geometric mean MIC 0.0083 mg/L). T-2307 also demonstrated in vivo efficacy in mice infected with echinocandin-resistant C. glabrata. Significant reductions in fungal burden were observed at each dosage level of T-2307 compared with control. Reductions in fungal burden were also observed with high-dose caspofungin.\n\nQuestion:\nDoes the novel arylamidine T-2307 demonstrate in vitro and in vivo activity against echinocandin-resistant Candida glabrata?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAn abnormal glucose tolerance (AGT) in coronary artery disease (CAD) patients could negatively influence recovery after an acute event but the question, relevant in the field of cardiac rehabilitation (CR), is still controversial. Prospective study, aiming to establish the prevalence of AGT and its possible influence on functional recovery in CAD patients without a previous diagnosis of diabetes mellitus (DM). An oral glucose tolerance test was performed on 230 CAD patients without known DM, submitted to a 2-week period of intensive exercise-based CR after a recent acute myocardial infarction or coronary artery bypass graft. Functional capacity was assessed by a cardiopulmonary exercise test (CPET) and by 6-minute walking tests (6MWT) performed both on admission and at discharge. The prevalence of AGT in our population was 53%. Exercise capacity was lower in AGT patients (maximum workload achieved at CPET 79.3 ± 29.9 vs. 91.8 ± 36.9 W, p = 0.01; peak-VO(2) 17.8 ± 4.7 vs. 19.8 ± 5.6 ml/kg/min, p = 0.01). In the subgroup of AGT patients characterized by an inferior walking capacity at baseline, the increment in the distance walked was less than in the controls (Δ6MWT: 81.9 ± 60.1 vs. 109.1 ± 72.1, p = 0.04). An independent, negative, association was observed between AGT and Δ6MWT in patients with lower baseline test, and between maximum workload and peak-VO(2) in the whole population.\n\nQuestion:\nDoes prediabetes influence cardiac rehabilitation in coronary artery disease patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPrevious reports on lymphocyte subpopulations in systemic sclerosis (SSc) are conflicting. Therefore, we aimed to investigate the lymphocyte subsets in SSc patients who were not on immunosuppressive therapy. Lymphocyte subsets were assessed in the peripheral blood of SSc patients (n = 29) and healthy controls (n = 29) using the four colour flow cytometry method. Correlation studies were also performed in order to assess the relationship between lymphocyte subsets and clinical parameters. The absolute count of lymphocytes (P = 0.0042), CD3+ (P = 0.0014), CD4+ (P = 0.0070), CD8+ (P = 0.021), and CD19+ cells (P = 0.024) was significantly decreased in SSc patients when compared to healthy controls. CD4+/CD8+ ratio and the absolute count of CD56+ cells observed in SSc patients did not significantly differ from controls (P=0.165; P = 0.632, respectively). There was no substantial relationship between the lymphocyte subset levels and clinical features (i.e., SSc subtype, autoantibody profiles, organ involvement), except for a significant inverse correlation of CD19+ cells and the modified Rodnan skin score (r = -0.43, P = 0.020).\n\nQuestion:\nIs absolute count of T and B lymphocyte subsets decreased in systemic sclerosis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo determine if docosahexaenoic acid (DHA) and arachidonic acid (ARA) supplementation influences growth or visual acuity of formula-fed premature infants. Double-blind, multi-center study of 194 premature infants given preterm formula with no DHA or ARA (control), 0.15% energy DHA, or 0.14% DHA + 0.27% ARA from single-cell triglycerides for at least 28 days and then fed term formula (no DHA or ARA) to 57 weeks postmenstrual age (PMA), with 90 breast-fed term infants as reference. Infants fed DHA+ARA formula gained weight significantly faster (post-hoc analysis) during preterm formula feeding than control infants (34.7 vs. 30.7 g/d) and had weights and weight:length ratios not different from term breast-fed infants at 48 and 57 weeks PMA. Infants fed control or DHA formula had lower body weights than term infants. Red blood cell phosphatidylethanolamine ARA was significantly correlated to weight gain during preterm formula feeding and to weight and length at 40, 48, and 57 weeks PMA (r = 0.19 to 0.24, P =.004-.02). Providing DHA or DHA+ARA during the preterm period had no effect on subsequent visual acuity or incidence of adverse events.\n\nQuestion:\nDo docosahexaenoic acid and arachidonic acid enhance growth with no adverse effects in preterm infants fed formula?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPatients with non-insulin-dependent diabetes mellitus (NIDDM) are at increased risk for stroke. Hyperuricemia is a common finding in NIDDM, but its significance as an independent risk factor for cardiovascular disease has remained uncertain. Therefore, we investigated serum urate as a predictor of stroke in NIDDM patients free of clinical nephropathy (ie, with a serum creatinine level of < or = 120 micromol/L). In this population-based study, cardiovascular risk factors were determined in 1017 patients (551 men and 466 women) with NIDDM, aged 45 to 64 years at baseline. The patients were followed up for 7 years with respect to stroke events. During the follow-up period, 31 NIDDM patients (12 men [2.2%] and 19 women [4.1%]) died from stroke and 114 NIDDM patients (55 men [10.0%] and 59 women [12.7%]) had a fatal or nonfatal stroke. The incidence of stroke increased significantly by quartiles of serum uric acid levels (P<.001). High uric acid level (above the median value of > 295 micromol/L) was significantly associated with the risk of fatal and nonfatal stroke by Cox regression analysis (hazard ratio, 1.93 [1.30 to 2.86]; P=.001). This association remained statistically significant even after adjustment for all cardiovascular risk factors (hazard ratio, 1.91 [1.24 to 2.94]; P=.003).\n\nQuestion:\nIs serum uric acid a strong predictor of stroke in patients with non-insulin-dependent diabetes mellitus?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWhile many studies show a correlation between chronological age and physiological indicators, the nature of this correlation is not fully understood. To perform a comprehensive analysis of the correlation between chronological age and age-related physiological indicators. Physiological aging scores were deduced using principal component analysis from a large dataset of 1,227 variables measured in a cohort of 4,796 human subjects, and the correlation between the physiological aging scores and chronological age was assessed. Physiological age does not progress linearly or exponentially with chronological age: a more rapid physiological change is observed around the age of 55 years, followed by a mild decline until around the age of 70 years.\n\nQuestion:\nDoes comprehensive Analysis of Large Sets of Age-Related Physiological Indicators reveal Rapid Aging around the Age of 55 Years?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nType 1 diabetes is the product of a complex interplay between genetic susceptibility and exposure to environmental factors. Existing bacterial profiling studies focus on people who are most at risk at the time of diagnosis; there are limited data on the gut microbiota of people with long-standing Type 1 diabetes. This study compared the gut microbiota of patients with Type 1 diabetes and good glycaemic control and high levels of physical-fitness with that of matched controls without diabetes. Ten males with Type 1 diabetes and ten matched controls without diabetes were recruited; groups were matched for gender, age, BMI, peak oxygen uptake (VO Faecalibacterium sp., Roseburia sp. and Bacteroides sp. were typically the most abundant members of the community in both patients with Type 1 diabetes and controls, and were present in every sample in the cohort. Each bacterial profile was relatively individual and no significant difference was reported between the bacterial profiles or the Shannon diversity indices of Type 1 diabetes compared with controls. The functional profiles were more conserved and the Type 1 diabetes group were comparable with the control group.\n\nQuestion:\nIs gut microbiota of Type 1 diabetes patients with good glycaemic control and high physical fitness similar to people without diabetes : an observational study?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nwomen of non-English speaking background who migrate by choice or seek refuge in developed countries such as Australia have notably poorer perinatal outcomes than local-born women. Using data collected in two consecutive population-based surveys conducted in 2000 and 2008, the objective of this paper is to compare the views and experiences of immigrant women of non-English speaking background (NESB) giving birth in Victoria, Australia with those of women who were born in Australia. consecutive population-based surveys of women giving birth in Victoria, Australia conducted in 2000 and 2008. Questionnaires were distributed to women giving birth in a two-week period in 2000 and a four-week period in 2008 by hospitals and home birth practitioners. Surveys were mailed to women at five to six months post partum. completed surveys were received from 67% of eligible women in 2000 (1616/2412), and 51.2% in 2008 (2900/5667). Compared to Australian-born women, immigrant women of NESB were more likely to report negative experiences of antenatal, intrapartum and postnatal care. In 2008, 47.1% of immigrant women expressed dissatisfaction antenatal care compared with 26.8% of Australian born women (Adj OR 2.17, 95% CI 1.7-2.7). Similarly, 40.5% of immigrant women were dissatisfied with intrapartum care compared with 25.5% of Australian born women (Adj OR 1.81, 95% CI 1.4-2.3), and 53.5% of immigrant women rated their postnatal care negatively compared with 41.0% of Australian born women (Adj OR 1.52, 95% CI 1.2-1.9). There was no evidence of improvement between the two surveys. Immigrant women were more likely than Australian-born women to say that health professionals did not always remember them between visits, make an effort to get to know the issues that were important to them, keep them informed about what was happening during labour or take their wishes into account.\n\nQuestion:\nAre maternity services meeting the needs of immigrant women of non-English speaking background : Results of two consecutive Australian population based studies?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCT angiography spot sign predicts hematoma expansion in patients with acute intracerebral hemorrhage (ICH). The spot sign may represent a site of active extravasation, a locus of arrested hemorrhage forming fibrin globes, or represent associated epiphenomena such as hypertensive microaneurysms. We sought to describe the evolution of spot signs over 60 seconds in acute ICH using dynamic CT angiography and determine whether they grow and diffuse into the hematoma as would be expected with active extravasation. We prospectively identified consecutive patients presenting with spontaneous ICH<6 hours from symptom onset that completed dynamic CT angiography imaging over a 60-second acquisition protocol. We determined spot positivity, quantified spot volumes, and then used repeated-measures ANOVA to assess changes in spot volume over time. We collected data on 35 patients; 13 of 35 (37%) patients were spot-positive. Spot-positive patients had larger median ICH volume compared with spot-negative patients (median 10.7 versus 49.2 mL; P=0.007). Maximal spot sign volumes ranged from 0.02 to 2.8 mL (median 0.17 mL). Spot sign volumes increased significantly with time (P<0.001) and seemed to disperse into the hematoma in all cases. Three of 13 (23%) spot-positive patients presented with 2 distinct spot signs, but the remaining patients either had only 1 spot sign or different contiguous components of an irregularly shaped spot sign.\n\nQuestion:\nIs evolution of computed tomography angiography spot sign consistent with a site of active hemorrhage in acute intracerebral hemorrhage?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe aim of this study was to investigate the linkage among ambulance transports, the number of death and air temperature in Takamatsu area, Japan. Monthly data of ambulance transports (total and acute disease) and the number of death from 2004 to 2012 were obtained from Fire Department Service in Takamatsu and Takamatsu city official website, Japan. Climate parameters for required period were also obtained from Japan Meteorological Agency. Population data in Takamatsu area were also used to adjust ambulance transports and the number of death. The linkage among ambulance transports, the number of death and climate parameters was evaluated by ecological analysis. Total ambulance transports (/a hundred thousand people/day) and ambulance transports due to acute disease (/a hundred thousand people/day) were 12.3 ± 0.9 and 6.8 ± 0.7, respectively. The number of death (/a hundred thousand people/day) was 2.5 ± 0.4. By quadratic curve, ambulance transports due to acute disease and the number of death were significantly correlated with the parameters of air temperature. However, the number of death was the highest in January and the lowest in August.\n\nQuestion:\nIs lower air temperature associated with ambulance transports and death in Takamatsu area , Japan?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nDiurnal preference towards eveningness among adults has been associated with unhealthy habits and a range of health hazards, such as sleeping problems and higher odds for depression. We wanted to analyse whether diurnal preference towards eveningness is associated with more severe symptoms regarding sleep problems and mental disorders among young adults. Our sample consists of 469 young adults, aged 18-29 years, from the Mental Health in Early Adulthood Study in Finland (MEAF) conducted in 2003-2005. Chronotype was based on the assessment of one question that was asked first in 2000-2001 and the second time in 2003-2005. Those 73 participants who changed their chronotype were excluded from the main analysis, but separate analyses were performed with this group. Concerning sleep, E-types reported higher dependency on alarm clocks (p < 0.001), and E-types and I-types had more problems in feeling refreshed after waking up (p < 0.0001 and p < 0.05 respectively) than M-types. Regarding mental health, E-types and I-types had lower odds for any lifetime DSM-IV Axis I disorder (p < 0.05 and p < 0.01 respectively) than M-types.\n\nQuestion:\nDoes eveningness relate to burnout and seasonal sleep and mood problems among young adults?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSonographic measurement of the inferior vena cava (IVC) caval index predicts central venous pressure in ED patients. Fluid responsiveness (FR) is a measure of preload dependence defined as an increase in cardiac output secondary to volume expansion. We sought to determine if the caval index is an accurate measurement of FR in ED patients. We conducted a prospective, observational trial at an urban, academic, adult ED with an annual census >105 000. Included patients were clinically suspected of eu- and hypovolemia. Excluded patients were <18 years old, pregnant, incarcerated, sustained significant trauma or unable to consent. Supine IVC diameter was measured by bedside ultrasonography (M-Turbo; Sonosite, Bothwell, WA, USA). Caval index = [(expiratory IVC diameter - inspiratory IVC diameter)/expiratory IVC diameter] × 100. FR was defined as an increase in the cardiac index by >10% by impedance cardiography (BioZ; Sonosite) following passive leg raise. The primary outcome was analysed using Spearman correlations for non-parametric data and the area under the receiver operating characteristics curve by Wilcoxon method. Thirty patients were enrolled; four were excluded because of incomplete data collection. Thirty-one per cent (95% CI 13-48) of the patients were FR. The mean initial caval and cardiac index were 15.8% (95% CI 9.5-22) and 2.9 L/min/m(2) (95% CI 2.6-3.2), respectively. Caval index did not predict FR (receiver operating curve = 0.46, 95% CI 0.21-0.71, P = 0.63).\n\nQuestion:\nIs bedside sonographic measurement of the inferior vena cava caval index a poor predictor of fluid responsiveness in emergency department patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nBecause of their regenerative and paracrine abilities, cardiac stem cells (CSCs) are the most appropriate, optimal and promising candidates for the development of cardiac regenerative medicine strategies. However, native and exogenous CSCs in ischemic hearts are exposed to various pro-apoptotic or cytotoxic factors preventing their regenerative and paracrine abilities. We examined the effects of H2O2 on mouse CSCs (mCSCs), and observed that hydrogen peroxide (H2O2) treatment induces mCSCs apoptosis via the caspase 3 pathway, in a dose-dependent manner. We then examined the effects of Wnt1 over-expression on H2O2-induced apoptosis in mCSCs and observed that Wnt1 significantly decreased H2O2-induced apoptosis in mCSCs. On the other hand, inhibition of the canonical Wnt pathway by the secreted frizzled related protein 2 (SFRP2) or knockdown of β-catenin in mCSCs reduced cells resistance to H2O2-induced apoptosis, suggesting that Wnt1 predominantly prevents H2O2-induced apoptosis through the canonical Wnt pathway.\n\nQuestion:\nDoes wnt1 inhibit hydrogen peroxide-induced apoptosis in mouse cardiac stem cells?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo directly examine the contribution of vitamin C to the antioxidant potential of fruits and vegetables, the antioxidant effect of orange juice consumption (8 and 16 fl. oz.) was compared to the antioxidant effect of supplemental vitamin C (dosage equivalent to that supplied by 8 fl. oz. of orange juice). Subjects (n = 11; 28.6 +/- 2.1 years) received each treatment in a 3 x 3 randomized crossover design, and each two-week treatment was preceded by a two-week washout. During the entire trial, subjects restricted fruit and vegetable consumption to < or =3 servings per day except the vitamin C-rich foods (items containing >20 mg/serving), which were restricted to < or =3 servings per week. A fasting blood sample was collected at the end of each washout and each treatment period. Following washouts, plasma vitamin C and lipid peroxidation (plasma TBARS) were similar by treatment group and averaged 25.4 +/- 3.6 micromol/L and 3.82 +/- 0.10 nmol/mL respectively. Plasma vitamin C concentrations were similar following each treatment period, 37.9 +/- 8.1, 45.8 +/- 9.4, and 38.3 +/- 12.4 micromol/L for the 8 and 16 fl. oz. orange juice treatments and the supplement treatment, respectively. All intervention treatments reduced plasma TBARS as compared to pretreatment values: -47% (p = 0.013), -40% (p = 0.083), and -46% (p = 0.015) for the 8 and 16 fl. oz. orange juice treatments and supplement treatment respectively.\n\nQuestion:\nAre orange juice ingestion and supplemental vitamin C equally effective at reducing plasma lipid peroxidation in healthy adult women?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe purpose of this study was to assess whether age, resting follicle number, intraovarian blood flow, and/or ovarian volume are predictive of follicular response and oocyte quality in patients with in vitro fertilization. A retrospective chart review was done on 90 in vitro fertilization cycles that were completed in a university setting. Multiple linear regression analysis was used to assess the predictive value of age, resting follicle number, pretreatment ovarian volume, and peak systolic velocity for response to gonadotropin stimulation. Age was predictive (P <.05) for the number of oocytes retrieved, the number that reached two pronuclei, and the number of embryos that reached > or = 4 cells by day 3 after insemination. Resting follicle number was also predictive of follicular response and subsequent embryonic development. Peak systolic velocity and ovarian volume were both found to be of no value.\n\nQuestion:\nDo age and resting follicle number predict response to gonadotropin stimulation in in vitro fertilization cycles?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHand-grip strength has been shown to be a reliable predictor of health outcomes. However, evidence supporting its use as an indicator of nutritional status is inconsistent. This study investigated its use in monitoring nutritional status in patients with head and neck cancer. A prospective audit of patients treated for head and neck cancer was undertaken at four centres over a three-month period in 2009. Nutritional outcomes were collected at 3, 6 and 12 months, and the data were statistically analysed. Data from 114 patients showed that mean weight, but not hand-grip strength, fell significantly at 3, 6 and 12 months post-treatment (p < 0.003 vs p < 0.126).\n\nQuestion:\nDoes hand-grip strength correlate with treatment-related weight loss in patients with head and neck cancer?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMicro ribonucleic acid (miR-101) can regulate the expression of cyclooxygenase-2 (COX-2) and participate in the pathogenesis of malignant tumors. This study investigates the effects of miRNA-101 and COX-2 in lung cancer and the impact of miR-101 on the proliferation and invasion of human lung cancer A549 cell line. The expression of miR-101 in 20 separate lung cancer tissues was detected by real time polymerase chain reaction; COX-2 expression was also detected. A549 cells were transfected with miR-101 or negative control oligonucleotide duplex mimic (miR-NC). In vivo tumorigenesis abilities were detected in localized human lung cancer xeno-transplant models in BALB/c nude mice. MiR-101 expression was significantly lower and the level of COX-2 significantly higher in lung cancer tissues than in adjacent parenchyma (2.918 ± 1.006 vs. 5.953 ± 1.976, P = 0.001; 0.887 ± 0.260 vs. 0.355 ± 0.156, P = 0.001, respectively). Correlation analysis revealed that miR-101 negatively correlated with COX-2 in lung cancer tissues (R = -0.596, P = 0.002). Compared with A549-miR-NC cells, the expression of COX-2 was significantly decreased in A549 cells transfected with miR-101 (P < 0.001). The proliferation of A549 cells was markedly inhibited after transfection of miR-101. The in vivo tumor growth of A549 cells transfected with miR-101 was significantly slower than wide type A549 cells.\n\nQuestion:\nDoes micro ribonucleic acid ( RNA ) -101 inhibit cell proliferation and invasion of lung cancer by regulating cyclooxygenase-2?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis study assessed the disparity in nutritional status of adolescents between public and private schools in urban Gambia. This is a school-based cross-sectional study in six private and six public upper basic schools in urban Gambia. This study recruited 491 students from public and 469 students from private schools (13-15 years of age). The prevalence of stunting (WHO height-for-age Z < -2SD) was 13.4 % for public school students and 4.5 % for private schools. After adjustment for children's sex, age, and family socioeconomic status, the differences in prevalence of stunting and underweight were significant between public and private schools. Private school students are more likely to be overweight/obese (WHO BMI-for-age Z > +1SD) (OR = 2.85, 95 % CI 1.55-5.22), but less likely to be thin (BMI-for-age Z < -2SD) (OR = 0.61 [0.39-0.96]), compared to public school students. Children from lower income families had lower odds for overweight/obese than normal weight, compared to those from higher income families (OR = 0.34 [0.15-0.76]).\n\nQuestion:\nDo stunting and weight statuses of adolescents differ between public and private schools in urban Gambia?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSurvivin was aberrantly expressed in most cancer tissues, suggesting that survivin plays an important role in carcinogenesis. This study was designed to investigate the function and mechanism of survivin mutants in tumor cells. The site-mutant and truncated survivin mutants were transfected into HeLa cells and selected using G418. Cell apoptosis was analyzed using flow cytometry. Protein level of cyclin D1 was detected by Western blot analysis. Survivin mutant plasmid expressed in the HeLa cells successfully. The expressed protein could be detected using related antibody. Colony formation ability significantly decreased in the HeLa cells with survivin mutants compared with that in the parental HeLa cells. The HeLa cells transfected instantly with survivin mutants could undergo apoptosis automatically. Meanwhile, survivin mutants could cause an increase of multinuclear HeLa cells. The effect of survivin-N showed more effective than that of survivin T34A. Survivin-N and survivin T34A could influence the expression of cyclin D1 and reduced its protein levels of 68% and 12%, respectively.\n\nQuestion:\nDo [ Survivin mutants reverse the malignancy of HeLa cells ]?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nVenous filling time (VFT90) is the time taken to reach 90% of the venous volume in the calf. It is recorded by air-plethysmography (APG(®)) and is assumed to measure global venous reflux duration. However, this has never been confirmed by duplex. The aim of the study was to compare VFT on APG to venous reflux time/duration (RT) measured simultaneously with duplex on the same patients. Twenty-six consecutive patients, M:F = 16:10, age (25-78), C1 = 1, C2 = 4, C3 = 8, C4a = 6, C4b = 4, C5 = 2, C6 = 1, underwent simultaneous APG with duplex. The venous filling index (VFI, mL/second), VFT90 (seconds), great saphenous vein (GSV) RT on duplex, averaged thigh GSV diameter and thigh length (length) between the APG sensor air-cuff and duplex transducer were recorded. The VFT100 was calculated by VFT90/0.9. The additional time taken to fill the thigh was achieved using the VFI, length and deep vein diameter (d), to determine the corrected reflux duration: CRD = VFT100 + (length × πd(2)/4 (1/VFI)). Twenty-five patients are presented. One patient with very mild reflux (VFT90 = 55.9 seconds) had an indeterminate endpoint on duplex and was excluded. The median (range) VFI and GSV diameter was 4.9(1.3-15.5) mL/second and 7(4-17) mm, respectively. The VFT90 and VFT100 both correlated with RT on duplex (Spearman, P < 0.0005) at: r = 0.933, r(2) linear = 0.72 and r = 0.933, r(2) linear = 0.68, respectively. The median (interquartile range) filling time with VFT90 was less than the duplex RT at 24 (16.9) versus 28 (20) seconds respectively, P < 0.0005 (Wilcoxon). The median percentage underestimation improved from 24% to 16% and then 4% using the VFT90, VFT100 and CRD, respectively.\n\nQuestion:\nDoes venous filling time using air-plethysmography correlate highly with great saphenous vein reflux time using duplex?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nA population-based study of 1363 older women showed that the 24% who achieved high physical activity and dietary calcium intakes had a 5.1% higher hip BMD than those who did not, supporting the concept that lifestyle factors play an important role in the maintenance of lower extremity bone mass in older women. Although there is general agreement that increased dietary calcium consumption and exercise can slow bone loss in older women, the amount required to have this effect in an older population remains uncertain. This study was devised to examine the effects of calcium consumption (CC) and physical activity (PA) (lifestyle management) on bone mass in an older female population. Using a cross-sectional study design, a population-based sample of older women (mean age, 75 +/- 3 years) had hip and heel bone mass measured using DXA (Hologic 4500A; n = 1076) and quantitative ultrasound (QUS, Lunar Achilles; n = 1363), respectively. CC and PA were measured by a validated habitual food frequency and activity questionnaire, respectively. Dose-response effects of PA and CC on bone mass were examined using ANOVA.\n\nQuestion:\nAre physical activity and calcium consumption important determinants of lower limb bone mass in older women?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIt is known that in vivo kinematics after total knee replacement is influenced by the design of the implant. The goal of this study was to show that the sagittal curvature of two different knee prostheses differing in geometric design predicts their in vivo motion behavior. Three-dimensional tibio-femoral displacements of two prosthesis designs (single radius vs. dual radius) were measured during knee extension under weight bearing conditions by in vivo video fluoroscopy. Finite helical axes were computed to represent the tibio-femoral motions. Angular deviation alpha and the spatial localization deviation delta were used to characterize the motions. Angular deviation is the angle between each incremental finite helical axis and the medio-lateral axis of the femoral component of the prosthesis. The spatial localization deviation is the distance between each finite helical axis and the center of the femoral component of the prosthesis. Statistical comparisons were performed using the median and the interquartile range of the angular deviation and the spatial localization deviation. The single-radius design showed finite helical axes concentrated at a single axis near to the medio-lateral axis of the femoral component. The angular and spatial localization deviation of the dual radius design were larger compared to the single radius design, exhibiting finite helical axes varying between two axes.\n\nQuestion:\nDoes sagittal curvature of total knee replacements predict in vivo kinematics?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWhether connexin43 gap junctions (Cx43 GJs) and spatial heterogeneity of conduction velocity (CV) restitutions are altered in hearts during moderate (MH; 33°C) and severe (SH; 30°C) hypothermia remains unclear. Using an optical mapping system, ventricular CV was evaluated by S₁ pacing in 29 Langendorff-perfused isolated rabbit hearts at baseline (37°C, n=9), 30-min MH (n=6), 30-min SH (n=9), and rewarming (R, 30-min SH followed by 30-min 37°C, n=5). After CV evaluation, myocardium was collected to measure the level and distribution of non-phosphorylated (NP-Cx43) and total (T-Cx43) Cx43 by immunoblotting and immunoconfocal microscopy. In 6 additional hearts, Cx43 GJ remodeling was evaluated at 30-min SH with (n=3) or without (n=3) pretreatment of a protein kinase C (PKC) inhibitor. CV slowing and spatial heterogeneities of CV restitutions were enhanced in MH and SH hearts. NP-Cx43 was downregulated in MH (P=0.002) and SH (P<0.001) hearts. NP-Cx43 levels among 4 different ventricular sites became inhomogeneous in MH (P=0.017) and SH (P=0.046) hearts. However, T-Cx43 levels were unchanged. The percentages of lateralized NP- and T-Cx43 were increased in MH, SH, and R hearts. Pretreatment of PKC inhibitor attenuated SH-induced NP-Cx43 lateralization (P=0.0495).\n\nQuestion:\nDoes short-duration therapeutic hypothermia cause prompt connexin43 gap junction remodeling in isolated rabbit hearts?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe rates of lumbar spinal fusion operations have increased dramatically over the past 2 decades, and several studies based on administrative databases such as the Nationwide Inpatient Sample (NIS) have suggested that the greatest rise is in the general categories of degenerative disc disease and disc herniation, neither of which is a well-accepted indication for lumbar fusion. The administrative databases classify cases with the International Classification of Disease, Ninth Revision, Clinical Modification (ICD-9-CM). The ICD-9-CM discharge codes are not generated by surgeons but rather are assigned by trained hospital medical coders. It is unclear how accurately they capture the surgeon's indication for fusion. The authors sought to compare the ICD-9-CM code(s) assigned by the medical coder to the surgeon's indication based on a review of the medical chart. A retrospective review was undertaken of all lumbar fusions performed at our institution by the department of neurosurgery between 8/1/2011 and 8/31/2013. Based on the authors' review, the indication for fusion for each case was categorized as spondylolisthesis, deformity, tumor, infection, nonpathological fracture, pseudarthrosis, adjacent-level degeneration, stenosis, degenerative disc pathology, or disc herniation. These surgeon diagnoses were compared with the primary ICD-9-CM codes that were submitted to administrative databases. There were 178 lumbar fusion operations performed for 170 hospital admissions. There were 44 hospitalizations in which fusion was performed for tumor, infection, or nonpathological fracture; the remaining 126 were for degenerative diagnoses. For these degenerative cases, the primary ICD-9-CM diagnosis matched the surgeon's diagnosis in only 61 of 126 degenerative cases (48.4%). When both the primary and all secondary ICD-9-CM diagnoses were considered, the indication for fusion was identified in 100 of 126 cases (79.4%).\n\nQuestion:\nDoes the Nationwide Inpatient Sample database accurately reflect surgical indications for fusion?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nImpaired microvascular function may contribute to organ complications in patients with systemic sclerosis (SSc). We investigated whether SSc patients with and without pulmonary arterial hypertension (PAH) show a graded impairment of microvascular function compared to healthy controls. Twenty-two patients with SSc and 22 controls were studied. All patients underwent right heart catheterization; 6 had no PAH (SSc-nonPAH) and 16 had PAH (SSc-PAH). Acetylcholine (ACh)-mediated endothelium-dependent vasodilatation and sodium nitroprusside (SNP)-mediated endothelium-independent vasodilatation were assessed by iontophoresis combined with laser Doppler flowmetry. Compared to sex- and age-matched controls, ACh-mediated vasodilatation was reduced in SSc-PAH (340.4% vs 79.5%, respectively; p < 0.01), but not in SSc-nonPAH (340.4% vs 397.9%; p = 0.90). No significant differences were present between the groups in SNP-mediated vasodilatation.\n\nQuestion:\nIs pulmonary arterial hypertension in systemic sclerosis associated with profound impairment of microvascular endothelium-dependent vasodilatation?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nExcess weight and type 2 diabetes lead to increased susceptibility to infections. Our aim was to investigate the role of diabetes-induced decreased arginine (Arg) availability and of a possible dysregulation of Arg metabolism in macrophages favoring inflammation and dysimmunity via altered nitric oxide (NO) and cytokine productions. Isolated peritoneal macrophages from Zucker Diabetic Fatty (ZDF) or lean rats were incubated with increasing Arg concentration (0-2 mM) and Arg metabolism and regulatory properties were studied. Inducible NO synthase (iNOS) expression did not vary with Arg concentration while NO production reached a maximum at 0.5 mM Arg, being significantly lower in macrophages from ZDF rats. Arginase I and II protein levels reached a maximum between 0.25 and 0.5 mM Arg in controls; in macrophages from ZDF rats arginase I was significantly lower and progressively increased up to 2 mM Arg while arginase II was not affected by Arg concentration. In parallel, Arg downregulated TNFα production in both groups and IL-6 only in control.\n\nQuestion:\nDoes arginine availability modulate arginine metabolism and TNFα production in peritoneal macrophages from Zucker Diabetic Fatty rats?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIndehiscent sporangia are reported for only a few of derived leptosporangiate ferns. Their evolution has been likely caused by conditions in which promotion of self-fertilization is an evolutionary advantageous strategy such as the colonization of isolated regions and responds to stressful habitat conditions. The Lepisorus clathratus complex provides the opportunity to test this hypothesis because these derived ferns include specimens with regular dehiscent and irregular indehiscent sporangia. The latter occurs preferably in well-defined regions in the Himalaya. Previous studies have shown evidence for multiple origins of indehiscent sporangia and the persistence of populations with indehiscent sporangia at extreme altitudinal ranges of the Qinghai-Tibetan Plateau (QTP). Independent phylogenetic relationships reconstructed using DNA sequences of the uniparentally inherited chloroplast genome and two low-copy nuclear genes confirmed the hypothesis of multiple origins of indehiscent sporangia and the restriction of particular haplotypes to indehiscent sporangia populations in the Lhasa and Nyingchi regions of the QTP. In contrast, the Hengduan Mountains were characterized by high haplotype diversity and the occurrence of accessions with and without indehiscent sporangia. Evidence was found for polyploidy and reticulate evolution in this complex. The putative case of chloroplast capture in the Nyingchi populations provided further evidence for the promotion of isolated but persistent populations by indehiscent sporangia.\n\nQuestion:\nDo indehiscent sporangia enable the accumulation of local fern diversity at the Qinghai-Tibetan Plateau?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCD133 is one of the most important cancer-initiating (stem) cell markers and was confirmed to be expressed in solid cancers such as colon cancer. However, no one has investigated the role of CD133 in intrahepatic cholangiocarcinoma (IHCC). The aim of this study was to clarify the clinical role of CD133 expression in IHCC. Twenty-nine patients with IHCC who underwent hepatic resection at our institution were enrolled in this study. Expression of CD133 was examined using anti-CD133 antibody. Staining was observed in the cytoplasm of cancer cells and CD133-positive cells distributed in the whole tumor. The patients were divided into two groups: the CD133-positive group (n = 14) and CD133-negative group (n = 15), in which no staining of CD133 was observed. Clinicopathological factors including hypoxia-inducible factor-1alpha expression were compared between the two groups. The prognostic factors were investigated by multivariate analysis using Cox's proportional hazard model. The 5-year survival rate in the CD133-positive group (8.0%) was worse than that in the CD133-negative group (57.0%). In the CD133-positive group, the incidence of intrahepatic metastasis and positive expression of hypoxia-inducible factor-1alpha tended to be higher than that in the CD133 negative group. The multivariate analysis revealed CD133 expression was an independent prognostic indicator in IHCC.\n\nQuestion:\nIs cD133 expression a potential prognostic indicator in intrahepatic cholangiocarcinoma?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis study investigated whether inducing central sensitization evokes segmental increases in trigger point pressure sensitivity. We evoked central sensitization at the C(5) segment and validated its presence via mechanical cutaneous sensitivity (brush allodynia) testing. Trigger point pressure sensitivity was quantified using the pain pressure threshold (PPT) value. A 50 cm(2) area of the C(5) dermatome at the right lateral elbow was pretreated with 45 degrees heat for 10 minutes. Test subjects (n = 20) then received topical capsaicin cream (0.075%; Medicis, Toronto, Canada) to the C(5) dermatome, whereas control subjects (n = 20) received a topical placebo cream (Biotherm Massage, Montreal, Canada). PPT readings were recorded from the infraspinatus (C(5,6)) and gluteus medius (L(4,5)S(1)) trigger points at zero (pre-intervention), 10, 20, and 30 minutes after intervention; all PPT readings were normalized to pre-intervention (baseline) values. The difference between the PPT readings at the 2 trigger point sites represents the direct influence of segmental mechanisms on the trigger point sensitivity at the infraspinatus site (PPT(seg)). Test subjects demonstrated statistically significant increases in Total Allodynia scores and significant decreases in PPT(seg) at 10, 20, and 30 minutes after application, when compared with control subjects. These results demonstrate that increases in central sensitization evoke increases in trigger point pressure sensitivity in segmentally related muscles.\n\nQuestion:\nDoes capsaicin-induced central sensitization evoke segmental increases in trigger point sensitivity in humans?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nChemical intolerance (CI) is characterised by negative health effects attributed to a heightened responsiveness to common airborne chemicals. This longitudinal study explored the hypothesised role of negative affect in the development and persistence of CI in a general population. A general population sample aged 19 to 72 years was examined in 2006-2008 and again in 2011-2012. Longitudinal data on CI were analysed with the purpose of examining baseline negative affect as a risk factor for having developed CI at 5-year follow-up and for reporting persistent CI. Participants were classified as reporting no signs of CI, having symptoms of CI and as being a likely CI case based on self-reported reactions to 11 common chemical exposures, symptoms related to chemical exposures and daily life adjustments attributed to reactions when exposed to chemicals. A total of 69.4% of the participants who had reported CI at baseline also reported CI at follow-up. In participants with no baseline CI, 15.5% reported CI at follow-up and 18.1% reported symptoms related to chemicals but no daily life adjustments. Baseline negative affect was positively and statistically significantly associated with both development and persistence of CI.\n\nQuestion:\nIs negative affect associated with development and persistence of chemical intolerance : a prospective population-based study?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPrestimulus EEG alpha activity in humans has been considered to reflect ongoing top-down preparation for the performance of subsequent tasks. Since theta oscillations may be related to poststimulus top-down processing, we investigated whether prestimulus EEG theta activity also reflects top-down cognitive preparation for a stimulus. We recorded EEG data from 15 healthy controls performing a color and shape discrimination task, and used the wavelet transformation to investigate the time course and power of oscillatory activity in the signals. We observed a relationship between both anterior theta and posterior alpha power in the prestimulus period and the type of subsequent task.\n\nQuestion:\nDoes task-related modulation of anterior theta and posterior alpha EEG reflect top-down preparation?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAltered extracellular matrix (ECM) remodeling and podocyte apoptosis are characteristic features of diabetic nephropathy (DN). Aliskiren (ALI) inhibits the renin-catalyzed conversion of angiotensinogen to angiotensin I. This study tested ALI's effect on podocyte ECM accretion and survival in a high-glucose environment in vitro. Conditionally immortalized mouse podocytes were incubated in normal glucose (NG; 5.5 mM) or high glucose (HG; 40 mM) for 24-48 h with and without ALI (20 nM). Real-time RT-PCR was performed for fibronectin (FN), collagen α5(type IV) (Cola5IV), matrix metalloproteinases 2 and 9 (MMP2 and MMP9), and tissue inhibitor of metalloproteinases 1 and 2 (TIMP1 and TIMP2). Western blots were performed for FN, Cola5IV, MMP2, MMP9, TIMP1 and cleaved (activated) caspase-3. ALI significantly reduced the mRNA and protein levels of FN, Cola5IV and TIMP1, and the mRNA of TIMP2 and cleaved caspase-3. ALI had no effect on MMP2 mRNA or protein or MMP9 mRNA tested under HG conditions. Under NG conditions, ALI had no effect on FN, Cola5IV, MMP2, MMP9 and activated caspase-3 proteins. ALI decreased the activated caspase-3 protein and evidence of apoptosis by TUNEL staining observed in podocytes cultured under HG conditions.\n\nQuestion:\nDoes the renin inhibitor aliskiren attenuate high-glucose induced extracellular matrix synthesis and prevents apoptosis in cultured podocytes?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe mechanism by which atheroma plaque becomes unstable is not completely understood to date but analysis of differentially expressed genes in stable versus unstable plaques may provide clues. This will be crucial toward disclosing the mechanistic basis of plaque instability, and may help to identify prognostic biomarkers for ischaemic events. The objective of our study was to identify differences in expression levels of 59 selected genes between symptomatic patients (unstable plaques) and asymptomatic patients (stable plaques). 80 carotid plaques obtained by carotid endarterectomy and classified as symptomatic (>70% stenosis) or asymptomatic (>80% stenosis) were used in this study. The expression levels of 59 genes were quantified by qPCR on RNA extracted from the carotid plaques obtained by endarterectomy and analyzed by means of various bioinformatic tools. Several genes associated with autophagy pathways displayed differential expression levels between asymptomatic and symptomatic (i.e. MAP1LC3B, RAB24, EVA1A). In particular, mRNA levels of MAP1LC3B, an autophagic marker, showed a 5-fold decrease in symptomatic samples, which was confirmed in protein blots. Immune system-related factors and endoplasmic reticulum-associated markers (i.e. ERP27, ITPR1, ERO1LB, TIMP1, IL12B) emerged as differently expressed genes between asymptomatic and symptomatic patients.\n\nQuestion:\nAre autophagic marker MAP1LC3B expression levels associated with carotid atherosclerosis symptomatology?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHuman milk contains immune molecules involved in the protection of newborns against infections. We analyzed the concentration of Deleted in Malignant Brain Tumors 1 (DMBT1), a protein with functions in innate immunity, in breast milk. DMBT1 was detected in breast milk by Western blotting and its concentration was quantified by ELISA in 95 breast milk samples collected from mothers of preterm and term neonates during the first four weeks after delivery. Possible effects of maternal or neonatal parameters were analyzed by different statistical tests. The mean DMBT1 concentration (± standard error of the mean) in the tested milk samples was 2.48 ± 0.26 μg/mL (range: 0.112 μg/mL to 17.984 μg/mL) and represented 0.0087% of the total protein content. The comparison between the newborns with infection and the newborns without infection revealed significantly higher DMBT1 concentrations in breast milk in the group with infection (6.72 ± 2.53 μg/mL versus 2.20 ± 0.35 μg/mL (P = 0.031)). Neither maternal nor neonatal parameters showed a correlation with the milk DMBT1 levels.\n\nQuestion:\nDo high DMBT1 concentrations in breast milk correlate with increased risk of infection in preterm and term neonates?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMMP2 and MMP9 are two gelatinolytic enzymes, which are key regulators of tumor invasion and metastasis. This study aimed to clarify the prognostic significance of MMP2 and MMP9 with particular regard to their transcript levels, enzymatic activities in renal cell carcinomas (RCCs). Through cDNA array, the differential expression of the MMP superfamily was evaluated in RCC. Various properties of MMP2 and MMP9 were quantified, in 178 patients with RCC, based on the Heidelberg classification. Of these, 145 cases including 16 fresh-frozen cases were available for MMP2 and MMP9 transcript level evaluation. In addition, gelatinolytic activity was assessed by zymography in 16 other fresh-frozen samples from new RCC cases. MMP2, 9, 11, 14, and 16 were upregulated in the conventional RCC in comparison with the chromophobe RCC, whereas MMP1, 11 and 16 were pronounced in papillary RCC. MMP9 transcript levels were strongly associated with the MMP9 enzymatic activity (p=0.001), and therefore, with disease-free survival (p=0.001) and metastasis (p=0.011). Gelatinolytic activity of MMP9 by zymography was strongly associated with MMP9 mRNA expression, which was more intense in 'conventional' RCC than in 'chromophobe' RCC (p=0.001), irrespective of tumor grade or stage. MMP9 was proven to be a significant prognostic predictor by multi-variate survival analysis (p=0.0054). MMP2 enzymatic activity disappeared in spite of its constant transcript expression in RCC.\n\nQuestion:\nDoes increased expression of matrix metalloproteinase 9 correlate with poor prognostic variables in renal cell carcinoma?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo ascertain if protective ventilation can attenuate the damaging postoperative pulmonary effects of cardiopulmonary bypass (increases in airway pressure, decreases in lung compliance, and increases in shunt). Prospective, randomized clinical trial. Single university hospital. Twenty-five patients undergoing elective coronary artery bypass graft procedure and early extubation. Thirteen patients received conventional mechanical ventilation (CV; respiratory rate, 8 breaths/min; tidal volume, 12 mL/kg; fraction of inspired oxygen [FIO2], 1.0; positive end-expiratory pressure [PEEP], +5), and 12 patients received protective mechanical ventilation (PV; respiratory rate, 16 breaths/min; tidal volume, 6 mL/kg; FIO2, 1.0; PEEP, +5). Perioperative anesthetic and surgical management were standardized. Various pulmonary parameters were determined twice perioperatively: 10 minutes after intubation and 60 minutes after arrival in the intensive care unit. The mean postoperative increase in peak airway pressure in group CV was significantly larger than the mean postoperative increase in peak airway pressure in group PV (7.1 v 2.4 cm H2O; p < 0.001). Group CV experienced significant postoperative increases in plateau airway pressure (p = 0.007), but group PV did not (p = 0.644). The mean postoperative decrease in dynamic lung compliance in group CV was significantly larger than the mean postoperative decrease in dynamic lung compliance in group PV (14.9 v 5.5 mL/cm H2O; p = 0.002). Group CV experienced significant postoperative decreases in static lung compliance (p = 0.014), but group PV did not (p = 0.645). Group CV experienced significant postoperative increases in shunt (15.5% to 21.4%; p = 0.021), but group PV did not (18.4% to 21.2%; p = 0.265).\n\nQuestion:\nDoes protective ventilation attenuate postoperative pulmonary dysfunction in patients undergoing cardiopulmonary bypass?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nComplex metacarpophalangeal (MCP) dislocations require open surgical reduction, but surgeons disagree about the best surgical approach. We hypothesized that a dorsal approach would require less operative time than would a volar approach and result in a decreased need for a secondary approach. We performed a retrospective chart review of all isolated irreducible dorsal MCP dislocations treated at 2 level 1 trauma centers between 2005 and 2015. We recorded the initial surgical approach (volar or dorsal), total operative time, and whether the surgeon used a second surgical approach. Operative times for initial volar approach versus initial dorsal approach, hand surgeon versus non-hand surgeon, and thumb versus other digits were compared using the 2-tailed Student t test. We used Fisher exact test to compare the need for a second approach between the volar and dorsal approach groups. A total of 21 patients (22 digits) with MCP dislocations required surgical reduction. Average operative time was longer for the 14 patients who underwent the initial volar approach (70 minutes) than for the 7 who underwent an initial dorsal approach (45 minutes). Six of the 14 MCP joints approached volarly (42%) required a second dorsal approach. None of the 7 patients in the dorsal group required a second approach.\n\nQuestion:\nDoes dorsal Approach decrease Operative Time for Complex Metacarpophalangeal Dislocations?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe purpose of this study was to examine the pattern of connections between coping strategies and indices of burn-related quality of life (BRQOL). Burn patients (n=83) were recruited from an outpatient burn clinic in the critical care hospital of a South Atlantic medical college. Participants completed measures of coping and BRQOL while in the waiting room before or after their medical appointment. A canonical correlation found that coping strategies and BRQOL were highly correlated with 47.6% overlapping variance. Within this canonical correlation, body image and dysfunctional coping had the largest loadings, suggesting that individuals with burn who exhibit negative perceptions of their body tend to engage in more dysfunctional coping styles. A multiple regression then found that a set of dysfunctional coping styles explained 39.2% of the variance in body image, with self-blame and self-distraction as independent predictors of negative perceptions of their body.\n\nQuestion:\nDo coping styles and quality of life in adults with burn?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMultiple sclerosis (MS) causes significant neurological disability. Experimental autoimmune encephalomyelitis (EAE) is an animal model of MS. Human bone marrow mesenchymal stem cells (hMSCs) possess anti-inflammatory and immunosuppressive effects. We studied whether hMSCs affect CD1d(high)CD5(+) regulatory B-cell activity in EAE. EAE was induced in C57BL/6N mice by immunization with MOG35-55 peptide. hMSCs were injected intravenously into EAE mice on day 3 and day 12 after first immunization. Mice were sacrificed on day 26. Immunohistochemistry of the spinal cord, serum cytokines levels, production of cytokines by cultured splenic cells, and flow cytometry for splenic Th17 and CD1d(high)CD5(+) regulatory B cells were studied. EAE mice with hMSC treatment on day 3 and day 12 had reduced EAE scores from day 14 to day 26 compared to EAE mice without hMSC treatment, and reduced infiltration of inflammatory cells and demyelination in the spinal cord. EAE mice with hMSC treatment on day 3 and day 12 had: (1) lower serum levels of IL-6, TNF-α (p < 0.0005), and IL-17 (p < 0.005 for day 3, p < 0.0005 for day 12); (2) reduced splenic cell production and secretion of IL-6, TNF-α (p < 0.05), and IL-17 (p < 0.05), and increased splenic production of IL-10; (3) reduced splenic Th17 cells (p < 0.05 for day 3, p < 0.005 for day 12), and (4) increased CD1d(high)CD5(+) regulatory B cells (p < 0.005) compared to EAE mice without hMSC treatment.\n\nQuestion:\nDo human mesenchymal stem cells upregulate CD1dCD5 ( + ) regulatory B cells in experimental autoimmune encephalomyelitis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe purpose of this study was to examine the heart rate reserve (HRR) at first and second ventilatory thresholds (VT's) in postmenopausal women and compare it with optimal intensity range recommended by the ACSM (40-84%HRR). An additional aim was to evaluate whether a higher aerobic power level corresponded to a higher HRR at VT's. Fifty-eight postmenopausal women participated in this study (aged 48-69). A graded 25 Wmin(-2) cycle ergometer (Monark E839) exercise protocol was performed in order to assess aerobic power. The heart rate and gas-exchange variables were measured continuously using a portable gas analyzer system (Cosmed K4b). The first (VT1) and the second (VT2) VT's were determined by the time course curves of ventilation and O2 and CO2 ventilatory equivalents. A K-means clustering analysis was used in order to identify VO2max groups (cut-off of 30.5 mlkg(-1)min(-1)) and differences were evaluated by an independent sample t-test. Bland-Altman plots were performed to illustrate the agreement between methods. The women's HRR values at VT1 were similar to 40% HRR in both VO2max groups. At VT2 both VO2max groups exhibited negative differences (P<0.01) for the predicted 84%HRR intensity (-14.46% in the lower VO2max group and -16.32% in the higher VO2max group).\n\nQuestion:\nIs the upper limit of the cardiorespiratory training zone ( 40-84 % HRR ) overestimated for postmenopausal women?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nObstructive sleep apnea (OSA) is associated with the cluster of clinical conditions that comprise the metabolic syndrome, including nonalcoholic fatty liver disease (NAFLD). Our primary purpose was to estimate the effect of OSA on serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Our secondary purpose was to investigate the potential influence of OSA on histological severity of NAFLD to explore whether chronic intermittent hypoxia is associated with inflammation and fibrosis. Our literature search identified 11 studies, from which we extracted information about numbers of control subjects and OSA patients, and ALT, AST, and NAFLD. From a total of 668 OSA patients and 404 controls, we found that the standardized difference in mean values of ALT and AST levels in patients with OSA was significantly different from that in the controls. Meta-regression showed that the association was independent of body mass index and type 2 diabetes. Fatty liver was associated with OSA in five studies with 400 subjects. OSA was significantly associated with liver fibrosis in 208 subjects, but not with lobular inflammation.\n\nQuestion:\nIs obstructive sleep apnea associated with fatty liver and abnormal liver enzymes : a meta-analysis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nEstablished prognostic factors are of limited value to predict long-term survival and benefit from metastasectomy in advanced melanoma. This study aimed to identify prognostic factors in patients with distant metastasis. We analysed overall survival of 855 institutional melanoma patients with distant metastasis by bivariate Kaplan-Meier survival probabilities and multivariate Cox hazard regression analysis. Serum lactate dehydrogenases (LDH), S100B, the interval between initial diagnosis and occurrence of distant metastasis, the site of distant metastases, and the number of involved distant sites were significant independent prognostic factors in both bivariate and multivariate analyses. Visceral metastases other than lung (hazard ratio (HR) 1.8), elevated S100B (HR 1.7) and elevated LDH (HR 1.6) had the highest negative impact on survival. Complete metastasectomy was likewise an independent prognostic factor in multivariate analysis. This treatment was associated with favourable survival for patients with normal LDH and S100B values (5-year survival, 37.2%).\n\nQuestion:\nDo serum markers lactate dehydrogenase and S100B predict independently disease outcome in melanoma patients with distant metastasis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSurvivin is known playing a role in drug resistance. However, its role in bortezomib-mediated inhibition of growth and induction of apoptosis is unclear. There are conflicting reports for the effect of bortezomib on survivin expression, which lacks of a plausible explanation. In this study, we tested cancer cells with both p53 wild type and mutant/null background for the relationship of bortezomib resistance with survivin expression and p53 status using MTT assay, flow cytometry, DNA fragmentation, caspase activation, western blots and RNAi technology. We found that cancer cells with wild type p53 show a low level expression of survivin and are sensitive to treatment with bortezomib, while cancer cells with a mutant or null p53 show a high level expression of survivin and are resistant to bortezomib-mediated apoptosis induction. However, silencing of survivin expression utilizing survivin mRNA-specific siRNA/shRNA in p53 mutant or null cells sensitized cancer cells to bortezomib mediated apoptosis induction, suggesting a role for survivin in bortezomib resistance. We further noted that modulation of survivin expression by bortezomib is dependent on p53 status but independent of cancer cell types. In cancer cells with mutated p53 or p53 null, bortezomib appears to induce survivin expression, while in cancer cells with wild type p53, bortezomib downregulates or shows no significant effect on survivin expression, which is dependent on the drug concentration, cell line and exposure time.\n\nQuestion:\nIs cancer cell sensitivity to bortezomib associated with survivin expression and p53 status but not cancer cell types?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAlthough increasing evidence has indicated that brain insulin dysfunction is a risk factor for Alzheimer disease (AD), the underlying mechanisms by which insulin deficiency may impact the development of AD are still obscure. Using a streptozotocin (STZ)-induced insulin deficient diabetic AD transgenic mouse model, we evaluated the effect of insulin deficiency on AD-like behavior and neuropathology. Our data showed that administration of STZ increased the level of blood glucose and reduced the level of serum insulin, and further decreased the phosphorylation levels of insulin receptors, and increased the activities of glycogen synthase kinase-3α/β and c-Jun N-terminal kinase in the APP/PS1 mouse brain. We further showed that STZ treatment promoted the processing of amyloid-β (Aβ) precursor protein resulting in increased Aβ generation, neuritic plaque formation, and spatial memory deficits in transgenic mice.\n\nQuestion:\nDoes insulin deficiency exacerbate cerebral amyloidosis and behavioral deficits in an Alzheimer transgenic mouse model?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo investigate the role of the sympathetic nervous system in the cardiovascular response to quiet standing in the postprandial state. Following a 30min pre-ingestion phase, 14 healthy young male subjects consumed a 600kcal carbohydrate-rich meal. Arterial blood pressure (BP) and heart rate (HR) were recorded for a further 120min. Measurements were obtained (Finometer) in both the supine (5min) and standing (5min) condition every 30min. Power spectral analysis of RR-interval and BP variability was calculated, and heart rate responses to the baroreceptor reflex were calculated to estimate spontaneous baroreflex sensitivity (sBRS). Derived stroke volume (SV) was measured to track changes to postural stress postprandially. Quiet standing increased RR-interval low frequency power, ratio of RR-interval low frequency power/high frequency power (ratio of RR LF/HF), and systolic BP low frequency power (SBP LF power), and decreased RR HF power and sBRS before, and after eating. After meal ingestion, SBP LF power increased and sBRS decreased in lying and standing conditions. During quiet standing postprandially, DBP and the mean arterial pressure increased (P<0.01). The increased BP is associated with increased SV (P<0.05) early postprandially, and increased SBP LF power (P<0.01) in the later postprandial phase. SBP LF power is inversely correlated with SV postprandially (P<0.001, R(2)=0.96).\n\nQuestion:\nDoes quiet standing after carbohydrate ingestion induce sympathoexcitatory and pressor responses in young healthy males?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHypoxia could lead to microglia activation and inflammatory mediators' overproduction. These inflammatory molecules could amplify the neuroinflammatory process and exacerbate neuronal injury. The aim of this study is to find out whether harpagoside could reduce hypoxia-induced microglia activation. In this study, primary microglia cells harvested from neonatal ICR mice were activated by exposure to hypoxia (1 % O2 for 3 h). Harpagoside had been shown to be no cytotoxicity on microglia cells by MTT assay. The scavenger effect of harpagoside on hypoxia-enhanced microglial cells proliferation, associated inflammatory genes expression (COX-II, IL-1β and IL-6 genes) and NO synthesis were also examined. Hypoxia enhances active proliferation of microglial cells, while harpagoside can scavenge this effect. We find that harpagoside could scavenge hypoxia-enhanced inflammatory genes expression (COX-2, IL-1β and IL-6 genes) and NO synthesis of microglial cells. Under 3 h' hypoxic stimulation, the nuclear contents of p65 and hypoxia inducible factor-1α (HIF-1α) significantly increase, while the cytosol IκB-α content decreases; these effects can be reversed by 1 h's pre-incubation of 10(-8) M harpagoside. Harpagoside could decrease IκB-α protein phosphorylation and inhibit p65 protein translocation from the cytosol to the nucleus, thus suppress NF-κB activation and reduce the HIF-1α generation.\n\nQuestion:\nDoes radix Scrophulariae extracts ( harpagoside ) suppress hypoxia-induced microglial activation and neurotoxicity?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]