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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.
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"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:\nAtrial fibrillation (AF) is the most common arrhythmia in women and is associated with higher rates of stroke and death. Rates of AF are lower in African American subjects compared with European Americans, suggesting European ancestry could contribute to AF risk. The Women's Health Initiative (WHI) Observational Study (OS) followed up 93,676 women since the mid 1990s for various cardiovascular outcomes including AF. Multivariate Cox hazard regression analysis was used to measure the association between African American race and incident AF. A total of 8,119 African American women from the WHI randomized clinical trials and OS were genotyped on the Affymetrix Human SNP Array 6.0. Genome-wide ancestry and previously reported single nucleotide polymorphisms associated with AF in European cohorts were tested for association with AF using multivariate logistic regression analyses. Self-reported African American race was associated with lower rates of AF (hazard ratio 0.43, 95% CI 0.32-0.60) in the OS, independent of demographic and clinical risk factors. In the genotyped cohort, there were 558 women with AF. By contrast, genome-wide European ancestry was not associated with AF. None of the single nucleotide polymorphisms previously associated with AF in European populations, including rs2200733, were associated with AF in the WHI African American cohort.\n\nQuestion:\nIs african American race but not genome-wide ancestry negatively associated with atrial fibrillation among postmenopausal women in the Women 's Health Initiative?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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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.
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{
"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:\nadverse outcomes and near misses are believed to share many characteristics in terms of clinical situations and care management problems. Little is documented concerning what prevents adverse outcomes from happening once the 'accident trajectory' begins. This two-stage pilot study set out to investigate midwives' understandings and recollections of clinical near misses. anonymous self-completion questionnaire and follow-up group interviews. clinically based midwives working in four maternity units in Scotland (questionnaire [n = 34]; interviews [n = 26]). despite a low response rate to the questionnaire, the cited examples seem to confirm that near misses and adverse outcomes follow essentially similar routes until the former are halted by a saving intervention. Dangerous situations are created by heavy workloads, and are aggravated by sub-optimal skill-mix, poor communication and individuals making mistakes or not following accepted procedures. Overwhelmingly, what prevents this situation from resulting in an adverse outcome is an intervention by another practitioner--often reported to be by chance and not design. In the interviews, these situations were discussed with reference to unit culture, the causes of errors and near misses, helping to prevent mistakes, the consequences of near misses and staff confiding in one another.\n\nQuestion:\nDoes an exploratory mixed-methods study of Scottish midwives ' understandings and perceptions of clinical near miss in maternity care?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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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.
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"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 the prognostic impact of the number of positive nodes and the lymph node ratio (LNR) of positive to excised nodes on survival in women diagnosed with nodal micrometastatic breast cancer before the era of widespread sentinel lymph node biopsy. Subjects were 62,551 women identified by the Surveillance Epidemiology and End Results database, diagnosed with pT1-2pN0-1 breast cancer between 1988 and 1997. Kaplan-Meier breast cancer-specific survival (BCSS) and overall survival (OS) were compared between three cohorts: node-negative (pN0, n=57,980) nodal micrometastasis all <or=2mm (pNmic, N=1818), and macroscopic nodal metastasis >2mm but <2 cm (pNmac, n=2753). Nodal subgroups were examined by the number of positive nodes (1-3 versus >or= 4) and the LNR (<or=0.25 versus >0.25). Median follow-up was 7.3 yr. Ten-year BCSS and OS in pNmic breast cancer were significantly lower compared to pN0 disease (BCSS 82.3% versus 91.9%, p<0.001 and OS 68.1% versus 75.7%, p<0.001). BCSS and OS with pNmic disease progressively declined with increasing number of positive nodes and increasing LNR. OS with pNmic was similar to pNmac disease when matched by the number of positive nodes and by the LNR. Both pN-based and LNR-based classifications were significantly prognostic of BCSS and OS on Cox regression multivariate analysis.\n\nQuestion:\nAre the number of positive nodes and the ratio of positive to excised nodes significant predictors of survival in women with micrometastatic node-positive breast cancer?\n\nAnswer:",
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"content": "yes",
"role": "assistant"
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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.
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"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 construct an eukaryotic expression vector for miRNA-1-2 that can be expressed in rat H9C2 cardiomyocytes. The precursor miRNA (pre-miRNA) DNA template for miRNA-1-2 was designed and generated by PCR amplification. The DNA template was inserted into the hairpin RNA expression vector pSilence-4.1-neo and identified by DNA sequencing analysis. The recombinant plasmid DNA was then transfected into H9C2 cells via Lipofectamine, and the green fluorescence protein expression vector pEGFP-N3 served as the transfection marker. Twenty-four hours after transfection, the total cellular RNA was extracted using TRIzol reagent, and thermoscript reverse transcriptase (RT)-PCR was performed to determine miRNA-1-2 precursor expression.\n\nQuestion:\nDoes [ Plasmid-mediated miRNA-1-2 specifically inhibit Hand2 protein expression in H9C2 cells ]?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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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.
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"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:\nShort chain fatty acids (SCFA) exert profound effects on the colonic mucosa. In particular, SCFA modulate mucosal immune functions. The antimicrobial cathelicidin LL-37 is expressed by colon epithelial cells. In the present study the effect of SCFA on LL-37 expression was investigated. LL-37 expression in vivo was assessed by immunohistochemistry. Real time quantitative reverse transcription-polymerase chain reaction was employed to determine LL-37 expression in colonocytes in vitro after treatment with various cytokines, SCFA, or flavone. LL-37 levels were correlated to cell differentiation which was determined by alkaline phosphatase (AP) activity. In addition, intracellular signalling pathways such as MEK-ERK (mitogen/extracellular signal protein kinase (MEK)/extracellular signal regulated protein kinase (ERK)) and p38/mitogen activated protein (MAP) kinase were explored. In vivo, LL-37 expression in healthy mucosa was restricted to differentiated epithelial cells in human colon and ileum. In colonocytes, increased LL-37 expression associated with cell differentiation was detected in vitro following treatment with butyrate, isobutyrate, propionate, and trichostatin A. Flavone induced LL-37 transcription but did not affect AP activity while cytokines had no effect. To dissect pathways mediating differentiation and LL-37 expression, specific inhibitors were applied. Inhibition of the protein kinase MEK enhanced butyrate induced AP activity while LL-37 expression in colon epithelial cells was blocked. In contrast, inhibition of p38/MAP kinase blocked cell differentiation without inhibiting LL-37 expression.\n\nQuestion:\nIs expression of the cathelicidin LL-37 modulated by short chain fatty acids in colonocytes : relevance of signalling pathways?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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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.
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"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 role of fundoplication in the prevention of esophageal adenocarcinoma is controversial. Development of cancer is associated with proliferation and anti-apoptosis, for which little data exist regarding their response to fundoplication. Ki-67 and Bcl-2 expression was assessed in the esophagogastric junction (EGJ) and the distal and proximal esophagus of 20 patients with gastroesophageal reflux disease (GERD) treated by fundoplication and in 7 controls. Endoscopy was performed preoperatively and 6 (20 patients) and 48 months (16 patients) postoperatively. There were positive correlations between Ki-67 and Bcl-2 levels in the EGJ (p > 0.001) and in the distal (p = 0.001) and proximal esophagus (p = 0.013). Compared to the preoperative level, Ki-67 expression was elevated in the distal (p = 0.012) and proximal (p = 0.007) esophagus at 48 months. In addition, compared to control values, Ki-67 expression was lower at the 6-month follow-up in the EGJ (p = 0.037) and the proximal esophagus (p = 0.003), and higher at the 48-month follow-up in the distal esophagus (p = 0.002). Compared to control values, Bcl-2 was lower at 6 months in the EGJ (p = 0.038).\n\nQuestion:\nIs proliferative and anti-apoptotic activity of esophageal mucosa in gastroesophageal reflux disease affected by fundoplication : a 4-year follow-up study?\n\nAnswer:",
"role": "user"
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{
"content": "no",
"role": "assistant"
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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.
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"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:\nLittle is known about how bacteria establish chronic infections of mucosal surfaces. Helicobacter pylori (H. pylori), a chronic pathogen that lives in the gastric mucosa of humans, interacts with the trefoil factor family (TFF) protein TFF1, which is found in gastric mucus. We aimed to characterize the interaction of H. pylori with TFF1 and to assess the role of this interaction in mediating colonization. Subcellular fractions of H. pylori were immobilized and then probed with TFF1, TFF2, or TFF3. The effect of glycosidases and preincubation with monosaccharides on the interaction and binding of TFF1 to a H. pylori adhesin was assessed. The interaction between H. pylori adhesin and TFF1 was characterized using surface plasmon resonance, flow cytometry, nondenaturing polyacrylamide gel electrophoresis, coimmunofluoresence, and incubation with tissue sections. The H. pylori core oligosaccharide portion (rough form) of lipopolysaccharide (RF-LPS) bound to TFF1 and to a lesser extent TFF3; this interaction was inhibited by incubation of RF-LPS with mannosidase, glucosidase, or mixed monosaccharides. TFF1 also bound to human serum albumin-conjugated mannose and glucose. The optimum pH for binding was 5.0-6.0 for TFF1 and 7.0 for TFF3. H. pylori bound TFF1 in gastric mucus ex vivo; binding of LPS-coated latex beads to human antral gastric tissue was inhibited by TFF1.\n\nQuestion:\nDoes helicobacter pylori lipopolysaccharide interact with TFF1 in a pH-dependent manner?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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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.
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"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:\nLittle is known about the effect of nonadherence among patients with coronary artery disease (CAD) on a broad spectrum of outcomes including cardiovascular mortality, cardiovascular hospitalizations, and revascularization procedures. This was a retrospective cohort study of 15,767 patients with CAD. Medication adherence was calculated as proportion of days covered for filled prescriptions of beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, and statin medications. Multivariable Cox regression assessed the association between medication nonadherence as a time-varying covariate and a broad range of outcomes, adjusting for demographics and clinical characteristics. Median follow-up was 4.1 years. Rates of medication nonadherence were 28.8% for beta-blockers, 21.6% for ACE inhibitors, and 26.0% for statins. In unadjusted analysis, nonadherence to each class of medication was associated with higher all-cause and cardiovascular mortality. In multivariable analysis, nonadherence remained significantly associated with increased all-cause mortality risk for beta-blockers (hazard ratio [HR] 1.50, 95% CI 1.33-1.71), ACE inhibitors (HR 1.74, 95% CI 1.52-1.98), and statins (HR 1.85, 95% CI 1.63-2.09). In addition, nonadherence remained significantly associated with higher risk of cardiovascular mortality for beta-blockers (HR 1.53, 95% CI 1.16-2.01), ACE inhibitors (HR 1.66, 95% CI 1.26-2.20), and statins (HR 1.62, 95% CI 1.124-2.13). The findings of increased risk associated with nonadherence were consistent for cardiovascular hospitalization and revascularization procedures.\n\nQuestion:\nIs medication nonadherence associated with a broad range of adverse outcomes in patients with coronary artery disease?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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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.
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{
"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:\nIn reaching the airways inhaled allergens pass through and contact with the oral mucosa. Although they are often responsible for initiating asthmatic attacks, it is unknown whether airborne allergens can also trigger chronic inflammation of gingival epithelial cells leading to chronic periodontitis. In this study, we investigated the inflammatory responses of human gingival epithelial cells (HGECs) to airborne allergens, particularly German cockroach extract (GCE) with a focus on calcium signaling. HGECs isolated from healthy donors were stimulated with GCE. Intracellular Ca(2+) concentration ([Ca(2+)]i) was measured with Fura-2-acetoxymethyl ester (Fura-2/AM) staining. Expression of inflammatory cytokines interleukin (IL)-8, IL-1β, IL-6, and NOD-like receptor family, pyridine domain-containing (NLRP) 3 was analyzed using reverse transcription-polymerase chain reaction (RT-PCR). GCE promoted increase in the [Ca(2+)]i in a dose-dependent manner. Depletion of endoplasmic reticulum (ER) Ca(2+) by the ER Ca(2+) ATPase inhibitor thapsigargin (Tg) but not the depletion of extracellular Ca(2+) abolished the GCE-induced increase in [Ca(2+)]i. Treatment of phospholipase C (PLC) inhibitor (U73122) or 1,4,5-trisinositolphosphate (IP3) receptor inhibitor (2-APB) also prevented GCE-induced increase in [Ca(2+)]i. Protease activated receptor (PAR)-2 activation mainly mediated the GCE-induced increase in [Ca(2+)]i and enhanced the expression of IL-8, NLRP3, IL-1β, and IL-6 in HGECs.\n\nQuestion:\nDo airborne allergens induce protease activated receptor-2-mediated production of inflammatory cytokines in human gingival epithelium?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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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.
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{
"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:\nWe examined the effect of oral vitamin B(12) treatment on fluctuations in plasma total cobalamin and its binding proteins transcobalamin (TC) and haptocorrin (HC). Patients (n = 88; age range, 38-80 years) undergoing coronary angiography (part of the homocysteine-lowering Western Norway B-Vitamin Intervention Trial) were allocated to daily oral treatment with (a) vitamin B(12) (0.4 mg), folic acid (0.8 mg), and vitamin B(6) (40 mg); (b) vitamin B(12) and folic acid; (c) vitamin B(6); or (d) placebo. EDTA blood was obtained before treatment and 3, 14, 28, and 84 days thereafter. The intraindividual variation for patients not treated with B(12) was approximately 10% for plasma total cobalamin, total TC, apo-TC, and apo-HC, and <20% for holo-TC and TC saturation. In B(12)-treated patients, the maximum change in concentrations was observed already after 3 days for total TC (-16%), holo-TC (+54%), and TC saturation (+82%). At this time holo-HC (+20%) and plasma total cobalamin (+28%) showed an initial burst, but had increased further at 84 days. All changes were highly significant compared with the control group (P <0.0001).\n\nQuestion:\nIs holo-transcobalamin an early marker of changes in cobalamin homeostasis . A randomized placebo-controlled study?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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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.
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{
"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:\nObese patients display an exaggerated morbidity during sepsis. Since consumption of a western-style diet (WD) is a major factor for obesity in the United States, the purpose of the present study was to examine the influence of chronic WD consumption on hepatic inflammation in mice made septic via cecal ligation and puncture (CLP). Feeding mice diets high in fat has been shown to enhance evidence of TLR signaling and this pathway also mediates the hepatic response to invading bacteria. Therefore, we hypothesized that the combined effects of sepsis and feeding WD on TRL-4 signaling would exacerbate hepatic inflammation. Male C57BL/6 mice were fed purified control diet (CD) or WD that was enriched in butter fat (34.4% of calories) for 3 weeks prior to CLP. Intravital microscopy was used to evaluate leukocyte adhesion in the hepatic microcirculation. To demonstrate the direct effect of saturated fatty acid on hepatocytes, C3A human hepatocytes were cultured in medium containing 100 μM palmitic acid (PA). Quantitative real-time PCR was used to assess mRNA expression of tumor necrosis factor-alpha (TNF-α, monocyte chemotactic protein-1 (MCP-1), intercellular adhesion molecule-1 (ICAM-1), toll-like receptor-4 (TLR-4) and interleukin-8 (IL-8). Feeding WD increased firm adhesion of leukocytes in the sinusoids and terminal hepatic venules by 8-fold six hours after CLP; the increase in platelet adhesion was similar to the response observed with leukocytes. Adhesion was accompanied by enhanced expression of TNF-α, MCP-1 and ICAM-1. Messenger RNA expression of TLR-4 was also exacerbated in the WD+CLP group. Exposure of C3A cells to PA up-regulated IL-8 and TLR-4 expression. In addition, PA stimulated the static adhesion of U937 monocytes to C3A cells, a phenomenon blocked by inclusion of an anti-TLR-4/MD2 antibody in the culture medium.\n\nQuestion:\nDoes western diet enhance hepatic inflammation in mice exposed to cecal ligation and puncture?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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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.
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{
"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:\nAntiangiogenic therapies could be limited by various escape mechanisms including bone marrow-derived myeloid cell-induced vasculogenesis. The recruitment of vascular accessory cells (VACs) to the tumor neovasculature is as a multistep process. However, the recruitment process of these cells during antiangiogenic treatment remains unknown. The aim of our study was to characterize the recruitment of VACs during antiangiogenic therapy using sunitinib. C6 glioma cells were implanted into dorsal skinfold chambers. Animals received antiangiogenic therapy intraperitoneally for 5 days prior to VAC application intra-arterially. Intravital microscopy was performed during VAC injection and 1 and 48 h after injection. Analyses included total (TVD) and functional vessel densities (FVD), the perfusion index (PI), microvascular permeability, blood flow rate (Q), microvascular diameter (D), red blood cell velocity (RBCV), wall shear rate (γ), wall shear stress (τ), first and firm adhesions of VACs, and accumulation in the perivascular niche. Antiangiogenic therapy resulted in a significant reduction in TVD (365 ± 47 cm/cm(2) vs. 183 ± 37 cm/cm(2)) and FVD (227 ± 65 cm/cm(2) vs. 147 ± 25 cm/cm(2)) and an increase in PI, Q, D, and RBCV. γ and τ remained unaltered. Initial adhesion and firm adhesion were unaffected by antiangiogenic therapy; however, the accumulation in the perivascular niche was significantly diminished in treated tumors (53.7 ± 8% vs. 24.0 ± 17%).\n\nQuestion:\nDoes antiangiogenic therapy inhibit the recruitment of vascular accessory cells to the perivascular niche in glioma angiogenesis?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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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.
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{
"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 update clinicians on the recent advances in the treatment of Adamantiades-Behçet's disease. Interferon-alpha-2a and infliximab have proved able to induce prompt remission in the vast majority of Adamantiades-Behçet's patients with DMARD-resistant uveoretinitis. Efficacy of interferon-alpha-2a has also been reported for mucocutaneous lesions, arthritis, and (more anecdotally) for neuro-Behçet, while results from small case series suggest that infliximab is beneficial for mucocutaneous lesions and (more anecdotally) for arthritis and gastro-intestinal manifestations. Two cases of neuro-Behçet treated with infliximab showed a complete resolution. Finally, in a randomized controlled trial of patients with mucocutaneous, arthritic manifestations, or both, etanercept effectively suppressed mucocutaneous lesions.A different approach is tolerization by oral administration of the 336-351 peptide of the human heat shock protein 60 (thought to have a pathogenic role in Adamantiades-Behçet's disease-associated uveitis), linked to recombinant cholera B-toxin B-subunit. Preliminary results have shown that tolerization is safe and effective in preventing relapses of uveitis.\n\nQuestion:\nDoes new approach in the treatment of Adamantiades-Behçet 's disease?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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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.
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{
"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:\nInflammation drives atherogenesis. Animal and human studies have implicated interleukin-1β (IL-1β) in this disease. Moderate hypoxia, a condition that prevails in the atherosclerotic plaque, may conspire with inflammation and contribute to the evolution and complications of atherosclerosis through mechanisms that remain incompletely understood. This study investigated the links between hypoxia and inflammation by testing the hypothesis that moderate hypoxia modulates IL-1β production in activated human macrophages. Our results demonstrated that hypoxia enhances pro-IL-1β protein, but not mRNA, expression in lipopolysaccharide-stimulated human macrophages. We show that hypoxia limits the selective targeting of pro-IL-1β to autophagic degradation, thus prolonging its half-life and promoting its intracellular accumulation. Furthermore, hypoxia increased the expression of NLRP3, a limiting factor in NLRP3 inflammasome function, and augmented caspase-1 activation in lipopolysaccharide-primed macrophages. Consequently, hypoxic human macrophages secreted higher amounts of mature IL-1β than did normoxic macrophages after treatment with crystalline cholesterol, an endogenous danger signal that contributes to atherogenesis. In human atherosclerotic plaques, IL-1β localizes predominantly to macrophage-rich regions that express activated caspase-1 and the hypoxia markers hypoxia-inducible factor 1α and hexokinase-2, as assessed by immunohistochemical staining of carotid endarterectomy specimens.\n\nQuestion:\nDoes moderate hypoxia potentiate interleukin-1β production in activated human macrophages?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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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.
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{
"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 most potent allergens in the Spermatophytae family exhibit significant homology with enzymes. Some of these are though to be involved in pectin metabolism, recognition of compatible stigma and delivery of sperm cells to the ovule. To test if glycohydrolase activities from some Mediterranean tree pollens could act as allergens in sensitized hosts. Freshly collected Cupressus and Olea pollens were investigated for their glycohydrolase activities by means of synthetic fluorogenic substrates and isoenzymes characterized by DEAE-cellulose ion-exchange chromatography. Binding of specific IgE was investigated by immunoblotting in 30 tree-sensitive subjects, as well as in 20 atopic non-tree-sensitive and 15 healthy controls. The enzymes were also adopted to stimulate proliferation of allergen-specific T cell clones. Finally, they were tested in vivo in a cutaneous immediate wheal and flare reaction. beta-Galactosidase (beta-GAL) is present with different isoenzymatic patterns on both pollen extracts, could be recognized by circulating IgE, as well as immunoprecipitated by sera from allergic subjects. The enzyme could stimulate the proliferation of T cells from allergic subjects, and favor the emergence of CD4+ T cell clones with specific in vitro reactivity to beta-GAL. Finally, the enzyme induced in vivo a cutaneous wheal and flare reaction in clinically sensitive subjects.\n\nQuestion:\nDoes biochemical and immunological characterization of pollen-derived beta-galactosidase reveal a new cross-reactive class of allergens among Mediterranean trees?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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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.
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{
"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:\nSome abnormalities in porphyrin metabolism have been described in erythrocytes from patients with end-stage renal failure. A peptidic fraction of 56.2 kD isolated from plasma of these patients was previously identified as an aminolevulinate dehydratase inhibitor. The aim of this study was to examine the in vitro effect of this peptide on heme synthesis in the erythroleukemia K562 cells. The 56.2-kD fraction was purified from uremic plasma by protein electroelution and, its action on the mitochondrial rate-limiting steps of heme synthesis, as well as the hemoglobin content during erythroid differentiation induced by sodium butyrate, was investigated in K562 cells. Two hours after addition of the 56.2-kD peptide, the activities of aminolevulinate acid synthase and aminolevulinate dehydratase were reduced while the activity of the ferrochelatase was enhanced, indicating that this peptide easily across the membranes. A 3-day incubation with this peptide enhanced approximately twofold the hemoglobin and porphyrin levels during erythroid differentiation of K562 cells without variation of cell growth.\n\nQuestion:\nIs hemoglobin content increased in the human erythroleukemia K562 cell line by a 56.2-kD peptide from uremic plasma?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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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.
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"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 papillomavirus (HPV) has been consistently implicated in causing several kinds of malignancies, and two HPV oncogenes, E6 and E7, represent two potential target antigens for cancer vaccines. We developed two fusion protein vaccines, PE(ΔIII)/E6 and PE(ΔIII)/E7 by targeting these two tumor antigens to test whether a combination of two fusion proteins can generate more potent anti-tumor effects than a single fusion protein. In vivo antitumor effects including preventive, therapeutic, and antibody depletion experiments were performed. In vitro assays including intracellular cytokine staining and ELISA for Ab responses were also performed. PE(ΔIII)/E6+PE(ΔIII)/E7 generated both stronger E6 and E7-specific immunity. Only 60% of the tumor protective effect was observed in the PE(ΔIII)/E6 group compared to 100% in the PE(ΔIII)/E7 and PE(ΔIII)/E6+PE(ΔIII)/E7 groups. Mice vaccinated with the PE(ΔIII)/E6+PE(ΔIII)/E7 fusion proteins had a smaller subcutaneous tumor size than those vaccinated with PE(ΔIII)/E6 or PE(ΔIII)/E7 fusion proteins alone.\n\nQuestion:\nDo fusion protein vaccines targeting two tumor antigens generate synergistic anti-tumor effects?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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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.
| [
{
"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:\nExtravasation of vesicant drugs such as vinca alkaloids causes severe injury, which may range from erythema to skin necrosis or ulceration. The skin necrosis may not be fully evident until several weeks or months after the initial damage, and may require surgical intervention. The main treatments for vincristine extravasation are hyaluronidase injection and topical warming, and the aim of treatment is to increase the clearance of the drug from the extravasation site. To investigate the effect of adrenomedullin, a potent vasodilatory peptide, in rats subjected to vincristine-induced extravasation. In total, 36 Wistar albino rats were given intradermal injection of vincristine and saline. The rats were assigned to one of three treatment groups (adrenomedullin, adrenomedullin + hyaluronidase, or hyaluronidase), a control group given vincristine only, or a sham group (saline). Tissue superoxide dismutase (SOD), glutathione peroxidase, malondialdehyde (MDA) and protein content were evaluated in skin biopsies taken on day 22. The ulcer size and histopathological grading scores were also recorded. SOD levels were significantly increased by adrenomedullin and increased by hyaluronidase. Glutathione peroxidase levels were significantly decreased in all four vincristine groups. Tissue MDA levels were highest in the adrenomedullin group. In all four vincristine groups, MDA levels were reduced, indicating preservation from tissue injury. Protein carbonyl (PCO) content levels in the adrenomedullin group were significantly greater than in the other three study groups (P < 0.05). In contrast, PCO levels in the hyaluronidase group were significantly lower than in the other three groups.\n\nQuestion:\nDoes adrenomedullin worsen skin necrosis in rats subjected to vincristine-induced extravasation?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nPurpose/aim of the study: Apolipoprotein E (APOE) has been implicated as one of the susceptibility genes for some subtypes of epilepsy and may be related to anti-epileptic drugs resistance. The purpose of this study was to investigate the possible association between APOE variants and the anti-epileptic drugs resistance in Chinese population. APOE gene rs429358 and rs7412 variants were genotyped for ϵ2, ϵ3, ϵ4 alleles using amplification refractory mutation system in 480 subjects including 207 anti-epileptic drugs-resistant patients and 273 drug-responsive patients. We found that the frequency of APOE gene rs429358 C allele in the drug resistant patients is higher than that in the drug-responsive patients (14.98% vs. 10.1%, OR = 1.25[1.02 - 1.52], p = 0.017). Moreover, according to the two variants, we analyzed the distributions of -ϵ4 and +ϵ4 alleles of APOE gene and found that there were higher frequencies of +ϵ4 allele in drug-resistant epileptic patients than that in drug-responsive patients (31.8% vs. 13.2%, OR = 1.15[1.05 - 1.25], p = 0.002).\n\nQuestion:\nAre common variants of APOE associated with anti-epileptic drugs resistance in Han Chinese patients?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nWhen using laser guidance for cone-beam computed tomography (CBCT)-guided needle interventions, planned needle paths are visualized to the operator without the need to switch between entry- and progress-view during needle placement. The current study assesses the effect of laser guidance during CBCT-guided biopsies on fluoroscopy and procedure times. Prospective data from 15 CBCT-guided biopsies of 8-65 mm thoracic and abdominal lesions assisted by a ceiling-mounted laser guidance technique were compared to retrospective data of 36 performed CBCT-guided biopsies of lesions >20 mm using the freehand technique. Fluoroscopy time, procedure time, and number of CBCT-scans were recorded. All data are presented as median (ranges). For biopsies using the freehand technique, more fluoroscopy time was necessary to guide the needle onto the target, 165 s (83-333 s) compared to 87 s (44-190 s) for laser guidance (p < 0.001). Procedure times were shorter for freehand-guided biopsies, 24 min versus 30 min for laser guidance (p < 0.001).\n\nQuestion:\nDoes the Use of Laser Guidance reduce Fluoroscopy Time for C-Arm Cone-Beam Computed Tomography-Guided Biopsies?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 the incidence of melanoma in the U.S. is rising faster than any other cancer, the FDA-approved chemotherapies lack efficacy for advanced disease, which results in poor overall survival. Lysophosphatidic acid (LPA), autotaxin (ATX), the enzyme that produces LPA, and the LPA receptors represent an emerging group of therapeutic targets in cancer, although it is not known which of these is most effective. Herein we demonstrate that thio-ccPA 18:1, a stabilized phosphonothionate analogue of carba cyclic phosphatidic acid, ATX inhibitor and LPA1/3 receptor antagonist, induced a marked reduction in the viability of B16F10 metastatic melanoma cells compared with PBS-treated control by 80-100%. Exogenous LPA 18:1 or D-sn-1-O-oleoyl-2-O-methylglyceryl-3-phosphothioate did not reverse the effect of thio-ccPA 18:1. The reduction in viability mediated by thio-ccPA 18:1 was also observed in A375 and MeWo melanoma cell lines, suggesting that the effects are generalizable. Interestingly, siRNA to LPA3 (siLPA3) but not other LPA receptors recapitulated the effects of thio-ccPA 18:1 on viability, suggesting that inhibition of the LPA3 receptor is an important dualistic function of the compound. In addition, siLPA3 reduced proliferation, plasma membrane integrity and altered morphology of A375 cells. Another experimental compound designed to antagonize the LPA1/3 receptors significantly reduced viability in MeWo cells, which predominantly express the LPA3 receptor.\n\nQuestion:\nDoes targeting melanoma growth and viability reveal dualistic functionality of the phosphonothionate analogue of carba cyclic phosphatidic acid?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 suppression of arthropod herbivores is the most common approach to plant protection. Insecticides, however, can cause unintended, adverse consequences for non-target organisms. Previous studies focused on the effects of pesticides on target and non-target pests, predatory arthropods, and concomitant ecological disruptions. Little research, however, has focused on the direct effects of insecticides on plants. Here we demonstrate that applications of neonicotinoid insecticides, one of the most important insecticide classes worldwide, suppress expression of important plant defense genes, alter levels of phytohormones involved in plant defense, and decrease plant resistance to unsusceptible herbivores, spider mites Tetranychus urticae (Acari: Tetranychidae), in multiple, distantly related crop plants. Using cotton (Gossypium hirsutum), corn (Zea mays) and tomato (Solanum lycopersicum) plants, we show that transcription of phenylalanine ammonia lyase, coenzyme A ligase, trypsin protease inhibitor and chitinase are suppressed and concentrations of the phytohormone OPDA and salicylic acid were altered by neonicotinoid insecticides. Consequently, the population growth of spider mites increased from 30% to over 100% on neonicotinoid-treated plants in the greenhouse and by nearly 200% in the field experiment.\n\nQuestion:\nDo neonicotinoid insecticides alter induced defenses and increase susceptibility to spider mites in distantly related crop plants?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 whether plateau pressure (Pplat) measurement is lowered and peak airway pressure (Pawpeak)-to-Plat gradient is increased by measurement on a decelerating compared with square gas delivery wave form. Prospective before and after study of mechanically ventilated injured and critically ill patients in an adult surgical intensive care unit. Pplat, Pawpeak, and Pawpeak-to-Pplat gradient were measured on decelerating and square gas delivery wave forms. Pplat and other routine ventilator parameters were measured in 82 (47 trauma, 35 emergency general surgery) consecutive convenience sampled adult intensive care unit patients on decelerating and then square gas delivery wave forms. Peak gas flow was fixed at 40 L/min; all other parameters (rate, tidal volume, positive end-expiratory pressure) were held constant. All patients were managed on assist control volume cycled ventilation using fentanyl and midazolam or propofol; no neuromuscular blockade was used. Patients with Pawpeak more than 35 cm H2O were excluded. Comparing decelerating with square gas delivery, mean Pawpeak was lower (25.1 ± 2.3 cm H2O vs. 33.1 ± 2.1 cm H2O; p < 0.0001) and mean Pplat was lower (21.3 ± 1.9 cm H2O vs. 24.8 ± 2.5 cm H2O; p < 0.0001), resulting in a decreased Pawpeak-to-Pplat gradient (3.8 ± 2.1 vs. 8.3 ± 2.3; p < 0.0001).\n\nQuestion:\nDoes ventilator gas delivery wave form substantially impact plateau pressure and peak-to-plateau pressure gradient determination?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 presents an automatic diagnostic method for the discrimination between persistent and long-standing atrial fibrillation (AF) based on the surface electrocardiogram (ECG). Standard 12-lead ECG recordings were acquired in 53 patients with either persistent (N= 20) or long-standing AF (N= 33), the latter including both long-standing persistent and permanent AF. A combined frequency analysis of multiple ECG leads followed by the computation of standard complexity measures provided a method for the quantification of spatiotemporal AF organization. All possible pairs of precordial ECG leads were analysed by this method and resulting organization measures were used for automatic classification of persistent and long-standing AF signals. Correct classification rates of 84.9% were obtained, with a predictive value for long-standing AF of 93.1%. Spatiotemporal organization as measured in lateral precordial leads V5 and V6 was shown to be significantly lower during long-standing AF than persistent AF, suggesting that time-related alterations in left atrial electrical activity can be detected in the ECG.\n\nQuestion:\nDo measures of spatiotemporal organization differentiate persistent from long-standing atrial fibrillation?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 molecular mechanisms that regulate hADSC differentiation toward osteogenic precursors and subsequent bone-forming osteoblasts is unknown. Using osteoblast precursors obtained from subcutaneous human adipose tissue, we observed that microRNA-26a modulated late osteoblasts differentiation by targeting the SMAD1 transcription factor. Elucidation of the molecular mechanisms guiding human adipose tissue-derived stem cells (hADSCs) differentiation is of extreme importance for improving the treatment of bone-related diseases such as osteoporosis. The aim of this study was to identify microRNA as a regulator of the osteogenic differentiation of hADSCs. Osteoblast differentiation of hADSCs was induced by treatment with dexamethasone, ascorbic acid, and beta-glycerol phosphate. The expression of osteoblastic phenotype was evaluated after the induction by simultaneous monitoring of alkaline phosphatase activity, the expression of genes involved in osteoblastic differentiation by real-time RT-PCR, and mineralization at the same time. MicroRNA expression was determined by Northern blot, and transfection of both antisense miR-RNA and sensor plasmids was done to validate the inhibitory role of microRNA during hADSC osteogenesis. Western blot was used to determine the expression levels of the SMAD1 protein. qRT-PCR analysis was used to compare the expression patterns of osteoblastic markers in transfected cells.\n\nQuestion:\nIs osteogenic differentiation of human adipose tissue-derived stem cells modulated by the miR-26a targeting of the SMAD1 transcription factor?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nOral submucous fibrosis (OSF), a chronic progressive scarring disease, has been considered as a precancerous condition of oral mucosa. In this study, we investigated the functional role of Twist, an epithelial-mesenchymal transition (EMT) transcriptional factor, in myofibroblastic differentiation activity of OSF. Arecoline, a major areca nut alkaloid, was used to explore whether expression of Twist could be changed dose-dependently in human primary buccal mucosal fibroblasts (BMFs). Collagen gel contraction and migration capability in arecoline-stimulated BMFs and primary oral submucous fibrosis-derived fibroblasts (OSFs) with Twist knockdown was presented. We observed that the treatment of arecoline dose-dependently increased Twist expression transcript and protein levels in BMFs. The myofibroblast activity including collagen gel contraction and migration capability also induced by arecoline, while knockdown of Twist reversed these phenomena. Importantly, inhibition of Twist led to the suppression collagen contraction and wound healing capability of primary cultivated OSFs. Clinically, Twist transcript and protein expression was higher in areca quid chewing-associated OSF tissues than in normal oral mucosa tissues.\n\nQuestion:\nDoes elevation of Twist expression by arecoline contribute to the pathogenesis of oral submucous fibrosis?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nGastrointestinal stromal tumors (GIST) exhibit an unpredictable clinical course and can rapidly progress to lethality. Predictions about the biological behavior of GIST are based on a number of canonical clinical and pathologic parameters whose validity in distinguishing between a benign and a malignant tumour is still imperfect. The aim of our study was to investigate the role of morphologic parameters and expression of cells cycle regulators as prognosticators in GIST. We performed an immunohistochemical analysis for Ki67, p27Kip1, Jab1, and Skp2, on a Tissue Microarray (TMA) containing 94 GIST. Expression of the above proteins was correlated to classically used prognosticators, as well as to risk groups. Clinical significance of histologic and immunohistochemical features were evaluated in 59 patients for whom follow-up information was available. Overexpression of Ki67 and Skp2, and p27Kip1 loss directly correlated with the high risk group (p = 0.03 for Ki67 and Skp2, p = 0.05 for p27Kip1). Jab1 expression did not exhibit correlation with risk. In 59 cases provided with clinical follow-up, high cellularity, presence of necrosis, and Ki67 overexpression were predictive of a reduced overall survival in a univariate model. The same parameters, as well as mitotic rate, tumour size, and p27Kip1 loss were indicative of a shortened relapse free survival interval. High cellularity, and high mitotic rate retained their prognostic significance by multivariate analysis.\n\nQuestion:\nIs skp2 expression associated with high risk and elevated Ki67 expression in gastrointestinal stromal tumours?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 clarify the role of activated Notch2 in the invasiveness of gastric cancer. To investigate the invasiveness of silencing Notch2 gene expression, we established a Notch2 small interfering RNA (siRNA) transfected cell line using the MKN-45 gastric cancer cell line. After the successful transfection confirmed by real-time reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting, migration and invasion assays were employed to evaluate the aggressiveness of the gastric cancer. RT-PCR and Western blottings were employed to confirm the down-regulation of Notch2 and to evaluate the expression of epithelial mesenchymal transition-related gene matrix metallopeptidase 9 (MMP9), Akt, p-Akt. To confirm the relationship between PI3K-Akt and MMP9, the PI3K inhibitor LY294002 was used to treat MKN-45 cells. Notch2 expression was dramatically decreased after Notch2 siRNA transfection (100.00% ± 9.74% vs 11.61% ± 3.85%, P < 0.01 by qRT-PCR). There was also a marked reduction of Notch target gene Hes1 (100.00% ± 4.74% vs 61.61% ± 3.58%, P < 0.05) at the mRNA, indicating an inhibition of Notch signaling. Inhibition of Notch signaling was also confirmed by the marked reduction of Notch2 intracellular domain at the protein levels (100.00% ± 9.74% vs 65.61% ± 7.58%, P < 0.05). Down-regulation of Notch2 by siRNA enhanced tumor cell invasion (100.00% ± 21.64% vs 162.22% ± 16.84%, P < 0.05) and expression of MMP9 (1.56 fold, P < 0.05), and activated the pro-MMP9 protein to its active form (1.48 fold, P < 0.05). There was no significant difference in the protein levels of Akt between the two groups (100.00% ± 10.87% vs 96.61% ± 7.33%, P > 0.05), while down-regulation of Notch2 elevated p-Akt expression (100.00% ± 9.87% vs 154.61% ± 13.10%, P < 0.05). Furthermore, p-Akt and MMP9 was down-regulated in response to the inhibitor LY294002 (p-Akt 100.00% ± 8.87% vs 58.27% ± 5.01%, P < 0.05; MMP9 100.00% ± 9.17% vs 50.03% ± 4.88%, P < 0.05).\n\nQuestion:\nDoes notch2 regulate matrix metallopeptidase 9 via PI3K/AKT signaling in human gastric carcinoma cell MKN-45?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 gastric tube is commonly used in thoracic esophageal reconstruction. When a gastric tube is not available, pedicled jejunum transfer and colonic interposition are alternative methods. Oral end of the reconstructed esophagus occasionally has poor blood flow and may result in partial necrosis of the oral segment. We performed additional microvascular blood flow augmentation, the \"supercharge\" technique, to improve a blood flow circulation in the oral segment of the reconstructed esophagus. A series of 86 esophageal reconstructions with microvascular blood flow augmentation using the \"supercharge\" technique were performed. Reconstructive methods included a gastric tube in five patients, a gastric tube combined with a free jejunual graft in one, an elongated gastric tube in eight, a pedicled colonic interposition in 22, and a pedicled jejunum in 50. Recipient vessels were used in neck or chest region. The color and blood flow of the transferred intestine appeared greatly improved after microvascular blood flow augmentation. Thrombosis was noticed in three patients during the surgery, and all thrombosies were salvaged by re-anastomosis. There were only three patients with partial graft necrosis of oral segment, two patients with anastomotic leakage, one anastomotic stricture.\n\nQuestion:\nDo variation of microvascular blood flow augmentation -- supercharge in esophageal and pharyngeal reconstruction?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nAneurysmal subarachnoid hemorrhage (aSAH) stands out from other subtypes of stroke because of the high early mortality and the risk of complications. Serum glial fibrillary acidic protein (s-GFAP) concentrations are increased after stroke. The aim of this study was to investigate whether s-GFAP could be used as a marker of brain damage and outcome after aSAH. Serum samples were obtained on a regular basis from 116 adults during a 2-week period after aSAH and analyzed using an enzyme-linked immunosorbent assay. The World Federation of Neurological Surgeons scale was used for neurological evaluation. Outcome was assessed after 1 year and categorized according to the Extended Glasgow Outcome Scale. Increased s-GFAP levels were seen in 81 of the 116 patients. Maximum s-GFAP correlated with World Federation of Neurological Surgeons scale on arrival and on days 10 to 15 (r=0.37, P<0.001 and r=0.47, P<0.001, respectively). Furthermore, maximum s-GFAP levels were increased in the patient group with radiological signs of focal lesions acute or at 1 year, compared with the group without focal lesions (P<0.001 in both comparisons). Patients with secondary events (re-bleeding or ischemia) reached maximum levels later in the series and both maximum and final s-GFAP levels increased compared with the levels in patients without secondary events (P<0.001 in all 3 comparisons). Finally, maximum s-GFAP correlated with outcome (r=-0.48, P<0.001) and s-GFAP was an independent predictor of dichotomized outcome.\n\nQuestion:\nIs serum glial fibrillary acidic protein related to focal brain injury and outcome after aneurysmal subarachnoid hemorrhage?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nLaparoscopic common bile duct (CBD) exploration is a well-established treatment option in dedicated centers. However, few data are available on the results in elderly patients. The outcome after laparoscopic CBD exploration in elderly patients (age <70 years) was compared with that in a concurrent control group of younger patients (age, <70 years). There were 77 elderly patients in group A and 207 younger patients in group B. American Society of Anesthesiology (ASA) III and IV patients and prior abdominal operations were more frequent in group A (p <0.001). Two patients from each group underwent conversion to open surgery. There was no significant difference frequency of use between the transcystic and choledochotomy approaches, although the latter tended to be more frequent in the group A because of larger stones, (group A 53.4%; group B, 37.6%). Minor and major morbidity (group A, 12%; group B, 13.6%), rate of recurrent stones (group A, 1.3%; group B, 1.9%), and mortality (group A, 1.3%; group B, 0%) were not significantly different between the two groups. The single death in group A involved a patient with acute toxic cholangitis who underwent emergency surgery after multiple failed attempts at endoscopic retrograde cholangiopancreatography/endoscopic sphincterotomy performed elsewhere. No CBD stenosis was observed at follow-up assessment.\n\nQuestion:\nAre laparoscopic cholecystectomy and common bile duct exploration safe for older patients?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nMeasles, mumps and rubella (MMR) vaccination is part of the Danish Childhood Vaccination Programme. It is known that children may react with anaphylaxis to MMR vaccines containing traces of egg protein. In Denmark, national clinical guidelines recommend that children with egg allergy be referred to vaccination at a paediatric ward despite changed recommendations in other countries. The purpose of this study was to determine whether children with egg allergy presented with anaphylactic/allergic reactions to MMR vaccination and to discuss whether Danish recommendations should be upheld. Data collected through evaluation of the histories of children referred to the Paediatric Ward at Hillerød Hospital from 01.01.2008 to 28.02.2011 and coded according to action diagnosis and/or supplementary diagnosis in International Classification of Diseases 10 (ICD-10) for food allergy, oedema angioneurotica and tentative diagnosis as well as the procedure code for oral food challenge. A total of 32 patients were included, all were both sensitized to egg and had been MMR vaccinated. The 32 patients had received a total of 41 doses of MMR vaccine. None of them had shown anaphylactic/allergic reactions to the MMR vaccines. 23% of the vaccines were given with considerable delay.\n\nQuestion:\nIs mMR vaccination of children with egg allergy safe?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 whether early enteral feeding in a septic intensive care unit (ICU) population, using a formula supplemented with arginine, mRNA, and omega-3 fatty acids from fish oil (Impact), improves clinical outcomes, when compared with a common use, high protein enteral feed without these nutrients. A prospective, randomized, multicentered trial. ICUs of six hospitals in Spain. One hundred eighty-one septic patients (122 males, 59 females) presenting for enteral nutrition in an ICU. Septic ICU patients with Acute Physiology and Chronic Health Evaluation (APACHE) II scores of > or =10 received either an enteral feed enriched with arginine, mRNA, and omega-3 fatty acids from fish oil (Impact), or a common use, high protein control feed (Precitene Hiperproteico). One hundred seventy-six (89 Impact patients, 87 control subjects) were eligible for intention-to-treat analysis. The mortality rate was reduced for the treatment group compared with the control group (17 of 89 vs. 28 of 87; p < .05). Bacteremias were reduced in the treatment group (7 of 89 vs. 19 of 87; p = .01) as well as the number of patients with more than one nosocomial infection (5 of 89 vs. 17 of 87; p = .01). The benefit in mortality rate for the treatment group was more pronounced for patients with APACHE II scores between 10 and 15 (1 of 26 vs. 8 of 29; p = .02).\n\nQuestion:\nDoes an immune-enhancing enteral diet reduce mortality rate and episodes of bacteremia in septic intensive care unit patients?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nWe tested the hypothesis that administration of the antioxidant tirilazad mesylate improves electrophysiological recovery and decreases infarct volume after transient focal cerebral ischemia in cats. Halothane-anesthetized cats underwent 90 minutes of left middle cerebral artery and bilateral common carotid artery occlusion followed by 180 minutes of reperfusion. Cats were assigned to receive tirilazad (1.5 mg/kg plus 0.2 mg/kg per hour IV infusion) either at the beginning (n = 9) or conclusion (n = 9) of ischemia. Control cats received an equal volume of diluent (citrate buffer, pH 3.0; n = 7) at the beginning and conclusion of ischemia in a blinded fashion. Infarct volume was measured by 2,3,5-triphenyltetrazolium chloride staining. Blood flow to the left temporoparietal cortex decreased to less than 10 mL/min per 100 g with ischemia but was minimally affected on the right side. Blood flow distribution during ischemia or reperfusion was not different in the tirilazad-treated groups. No group demonstrated postischemic hyperemia or delayed hypoperfusion. Somatosensory evoked potential recorded over the left cortex was ablated during ischemia and recovered to less than 15% of baseline amplitude at 180 minutes of reperfusion in all groups. There were no differences among groups in infarct volume of left hemisphere (pretreatment, 25 +/- 6% [mean +/- SE]; posttreatment, 33 +/- 5%; control, 28 +/- 8% of hemisphere) or caudate nucleus (pretreatment, 46 +/- 7%; posttreatment, 41 +/- 10%; control, 55 +/- 13% of hemisphere).\n\nQuestion:\nDoes tirilazad treatment decrease early brain injury after transient focal ischemia in cats?\n\nAnswer:",
"role": "user"
},
{
"content": "no",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nLysosomal acid lipase (LAL) hydrolyses cholesteryl esters and triacylglycerols (TG) within lysosomes to mobilise NEFA and cholesterol. Since LAL-deficient (Lal (-/-) ) mice suffer from progressive loss of adipose tissue and severe accumulation of lipids in hepatic lysosomes, we hypothesised that LAL deficiency triggers alternative energy pathway(s). We studied metabolic adaptations in Lal (-/-) mice. Despite loss of adipose tissue, Lal (-/-) mice show enhanced glucose clearance during insulin and glucose tolerance tests and have increased uptake of [(3)H]2-deoxy-D-glucose into skeletal muscle compared with wild-type mice. In agreement, fasted Lal (-/-) mice exhibit reduced glucose and glycogen levels in skeletal muscle. We observed 84% decreased plasma leptin levels and significantly reduced hepatic ATP, glucose, glycogen and glutamine concentrations in fed Lal (-/-) mice. Markedly reduced hepatic acyl-CoA concentrations decrease the expression of peroxisome proliferator-activated receptor α (PPARα) target genes. However, treatment of Lal (-/-) mice with the PPARα agonist fenofibrate further decreased plasma TG (and hepatic glucose and glycogen) concentrations in Lal (-/-) mice. Depletion of hepatic nuclear factor 4α and forkhead box protein a2 in fasted Lal (-/-) mice might be responsible for reduced expression of microsomal TG transfer protein, defective VLDL synthesis and drastically reduced plasma TG levels.\n\nQuestion:\nDoes lysosomal acid lipase regulate VLDL synthesis and insulin sensitivity in mice?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nCircular smooth muscle of the urethra generates spontaneous myogenic tone of relevance for the maintenance of continence. We tested if Rho guanosine triphosphatases (GTPases) and Rho-associated kinase (ROK) are involved in the generation of urethral tone. Small circular strips of female pig urethra were dissected out and mounted for recording isometric force. The effect of pharmacological agents known to modulate the activity of Rho GTPases or ROK was examined. The intracellular calcium concentration was measured using fura-2. Urethral tone was abolished by removing extracellular calcium or by adding the calcium antagonist felodipine. The decrease in force was closely related to a decrease in intracellular calcium concentration, indicating that tone depends on membrane associated mechanisms. Toxin B, which inactivates Rho GTPases, and Y 27632, which inhibits ROK, completely abolished tone in the female pig urethra. The latter effect occurred without any change in the intracellular calcium concentration.\n\nQuestion:\nIs female pig urethral tone dependent on Rho guanosine triphosphatases and Rho-associated kinase?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nActively growing post-embryonic sporophytes of desert mosses are restricted to the cooler, wetter months. However, most desert mosses have perennial gametophytes. It is hypothesized that these life history patterns are due in part to a reduced thermotolerance for sporophytes relative to gametophytes. Gametophytes with attached embryonic sporophytes of Microbryum starckeanum were exposed whilst desiccated to thermal episodes of 35 degrees C (1 hr), 55 degrees C (1 hr), 75 degrees C (1 hr) and 75 degrees C (3 hr), then moistened and allowed to recover for 35 d in a growth chamber. All of the gametophytes survived the thermal exposures and produced protonemata, with the majority also producing shoot buds. Symptoms of gametophytic stress (leaf burning and discoloration of entire shoots) were present in lower frequencies in the 55 degrees C exposure. Sporophyte resumption of growth and maturation to meiosis were significantly negatively affected by thermal treatment. Not a single sporophyte exposed to the two higher thermal treatments (75 degrees C for 1 h and 75 degrees C for 3 h) survived to meiosis, and those sporophytes exposed to 75 degrees C that survived to the post-embryonic phenophase took significantly longer to reach this phase. Furthermore, among the thermal treatments where some capsules reached maturity (35 degrees C and 55 degrees C), maternal shoots that produced a meiotic capsule took longer to regenerate through protonemata than maternal shoots aborting their sporophyte, suggestive of a resource trade-off between generations.\n\nQuestion:\nDo sporophyte and gametophyte generations differ in their thermotolerance response in the moss Microbryum?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 morphological studies had produced controversial results with regard to heart development in congenital diaphragmatic hernia (CDH), whereas a few publications investigated cardiac function and myocardial maturation. Myocardium maturation is associated with age-dependent increasing of gene expression of gap junction protein connexin 43 (Cx43), adenosine triphosphatase of the sarcoplasmic reticulum (SERCA2a), as well as switching of myosin heavy chains (MHCs) from beta to alpha isoforms. Our aim was to evaluate myocardium maturity in nitrofen-induced CDH rat model. Fetuses from dated pregnant Sprague-Dawley rats were assigned to 3 experimental groups: control, nitrofen (exposed to nitrofen, without CDH), and CDH (exposed to nitrofen, with CDH). Myocardial samples collected from left ventricle free wall were processed to (i) quantification of messenger RNA (mRNA) of Cx43, SERCA2a, alpha and beta MHC isoforms, as well as beta-actin (housekeeping gene); and (ii) separation of MHC isoforms (alpha and beta isoforms) by sodium dodecyl sulfate polyacrylamide gel electrophoresis silver stained. We demonstrated that there is no difference in myocardial gene expression of Cx43 (control, 1.0 +/- 0.1; nitrofen, 1.1 +/- 0.2; CDH, 1.3 +/- 0.2) and SERCA2a (control, 1.0 +/- 0.1; nitrofen, 0.9 +/- 0.1; CDH, 1.0 +/- 0.2). Myocardial gene expressions of alpha and beta mRNA of MHC isoforms were slightly decreased both in nitrofen and CDH fetuses when compared with control fetuses, but evaluation of the alpha-to-beta ratios of MHC isoforms at protein level revealed no significant differences between CDH and control (control, 16.9 +/- 2.5; CDH, 17.0 +/- 2.0).\n\nQuestion:\nAre myocardium expression of connexin 43 , SERCA2a , and myosin heavy chain isoforms preserved in nitrofen-induced congenital diaphragmatic hernia rat model?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 0 |
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.
| [
{
"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:\nStudies in population genetics suggest an important relationship between the eNOS G894T polymorphism and occurrence of acute myocardial infarction (AMI), with little known on its influence on the post-AMI period. To investigate the association of allelic variants produced by the G894T transversion in eNOS (rs1799983) with post-AMI variables. Cross-sectional analyses of anthropometric, clinical and laboratory assessments obtained within the first 24h and after 5 and 30 days of the AMI event across T carriers and G homozygotes of eNOS in 371 consecutive cases of AMI with ST-segment elevation admitted to a Brazilian emergency service in cardiology. Genotypes were determined by polymerase chain reaction followed by enzymatic restriction. Despite no difference between genotypic groups on aspects as Killip-Kimbal classification scores, extension of infarcted mass, lipid profile or pattern of medication use, an increase in serum nitric oxide from admission to day 5 was higher for T carriers (p<0.001). Thirty days post-AMI, peripheral blood flow reserve was larger among T carriers either by flow- (p=0.037) and nitrate-mediated (p=0.040) dilation testing.\n\nQuestion:\nDo endothelial nitric oxide synthase genotypes modulate peripheral vasodilatory properties after myocardial infarction?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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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.
| [
{
"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:\nRice is a major source of human food with a predominantly Asian production base. Domestication involved selection of traits that are desirable for agriculture and to human consumers. Wild relatives of crop plants are a source of useful variation which is of immense value for crop improvement. Australian wild rices have been isolated from the impacts of domestication in Asia and represents a source of novel diversity for global rice improvement. Oryza rufipogon is a perennial wild progenitor of cultivated rice. Oryza meridionalis is a related annual species in Australia. We have examined the sequence of the genomes of AA genome wild rices from Australia that are close relatives of cultivated rice through whole genome re-sequencing. Assembly of the resequencing data to the O. sativa ssp. japonica cv. Nipponbare shows that Australian wild rices possess 2.5 times more single nucleotide polymorphisms than in the Asian wild rice and cultivated O. sativa ssp. indica. Analysis of the genome of domesticated rice reveals regions of low diversity that show very little variation (polymorphism deserts). Both the perennial and annual wild rice from Australia show a high degree of conservation of sequence with that found in cultivated rice in the same 4.58 Mbp region on chromosome 5, which suggests that some of the 'polymorphism deserts' in this and other parts of the rice genome may have originated prior to domestication due to natural selection.\n\nQuestion:\nDoes australian wild rice reveal pre-domestication origin of polymorphism deserts in rice genome?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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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.
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{
"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:\nExpert consensus holds that post-market, systematic surveillance of ICD leads is essential to ensure confirmation of adequate lead performance. GALAXY (NCT00836589) and CELESTIAL (NCT00810264) are ongoing multicenter, prospective, non-randomized registries conducted to confirm the long-term safety and reliability of Biotronik leads. ICD and CRT-D patients are followed for Linox and Linox(smart) ICD lead performance and safety for 5 years post-implant. All procedural and system-related adverse events (AEs) were assessed at each follow-up, along with lead electrical parameters. An independent CEC of EPs adjudicated AEs to determine AE category and lead relatedness. The analysis used categories of lead observations per ISO 5841-2 (Third edition). A total of 3,933 leads were implanted in 3,840 patients (73.0% male, mean age 67.0 ± 12.2 years) at 146 US centers. The estimated cumulative survival probability was 96.3% at 5 years after implant for Linox leads and 96.6% at 4 years after implant for Linox(smart) leads. A comparison of the Linox and Linox(smart) survival functions did not find evidence of a difference (P = 0.2155). The most common AEs were oversensing (23, 0.58%), conductor fracture (14, 0.36%), failure to capture (13, 0.33%), lead dislodgement (12, 0.31%), insulation breach (10, 0.25%), and abnormal pacing impedance (8, 0.20%).\n\nQuestion:\nDoes long-Term Evaluation of Biotronik Linox and Linox ( smart ) Implantable Cardioverter Defibrillator lead?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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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.
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{
"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 type 2 diabetes mellitus (T2DM) have a high risk of fracture although they have slightly higher bone mineral density (BMD). There is no evidence that dipeptidyl peptidase-4 (DPP-4) is involved in the bone fragility of the patients. The aim of this study was to investigate the association between serum DPP-4 levels and vertebral fractures (VFs) in men with T2DM. We conducted a cross-sectional study and investigated the relationships between serum DPP-4 levels vs BMD at lumbar spine, femoral neck and radius, bone turnover markers and presence of VFs in 204 Japanese male patients. Multiple regression analyses adjusted for confounders such as age, duration of diabetes, body mass index, serum creatinine, HbA1c, serum albumin, log(alanine transaminase), and log(C-reactive protein) showed that serum DPP-4 was positively associated with bone formation markers (bone-specific alkaline phosphatase and osteocalcin) as well as a bone resorption marker [tartrate-resistant acid phosphatase 5b (TRACP-5b)] (β = 0·25, P < 0·01; β = 0·17, P < 0·05; and β = 0·30, P < 0·01, respectively), but not BMD at each site. Multivariate logistic regression analyses adjusted for the confounders described above revealed that serum DPP-4 levels were associated with the presence of multiple VFs (odds ratio 1·61, 95% confidential interval 1·05-2·49 per SD increase, P < 0·05). This association was still significant after additional adjustment for any sites of BMD or bone turnover markers except for TRACP-5b.\n\nQuestion:\nIs serum dipeptidyl peptidase-4 associated with multiple vertebral fractures in type 2 diabetes mellitus?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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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.
| [
{
"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:\nIkappaB kinase-beta is a critical regulator in the activation of nuclear factor-kappaB (NF-kappaB), a transcription factor related to the expression and regulation of proinflammatory cytokines. To evaluate if inhibition of IkappaB kinase-beta ameliorates pneumonitis and pulmonary fibrosis. We examined whether a novel IkappaB kinase-beta inhibitor, IMD-0354, attenuates bleomycin-induced pulmonary fibrosis in mice. Administration of IMD-0354 significantly improved the loss of body weight and survival of mice treated with bleomycin, whereas IMD-0354 alone did not cause any morphologic change in the lung. When mice were evaluated 28 d after bleomycin administration, IMD-0354 dose-dependently reduced the collagen content and fibrotic scores as shown by histologic examination. The findings in the bronchoalveolar lavage demonstrated that the proportions of neutrophils and lymphocytes were decreased in mice treated with IMD-0354 on Day 7 and 14, respectively. IMD-0354 treatment was confirmed to inhibit the activation of NF-kappaB, but not activator protein-1, in the lungs treated with bleomycin. The production of inflammatory cytokines tumor necrosis factor-alpha and interleukin-1beta was reduced in the lungs of mice treated with IMD-0354.\n\nQuestion:\nDoes a novel IkappaB kinase-beta inhibitor ameliorate bleomycin-induced pulmonary fibrosis in mice?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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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.
| [
{
"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:\nModified function of immune cells in nasal secretions may play a role in the enhanced susceptibility to respiratory viruses that is seen in smokers. Innate immune cells in nasal secretions have largely been characterized by cellular differentials using morphologic criteria alone, which have successfully identified neutrophils as a significant cell population within nasal lavage fluid (NLF) cells. However, flow cytometry may be a superior method to fully characterize NLF immune cells. We therefore characterized immune cells in NLF by flow cytometry, determined the effects of live attenuated influenza virus (LAIV) on NLF and peripheral blood immune cells, and compared responses in samples obtained from smokers and nonsmokers. In a prospective observational study, we characterized immune cells in NLF of nonsmokers at baseline using flow cytometry and immunohistochemistry. Nonsmokers and smokers were inoculated with LAIV on day 0 and serial nasal lavages were collected on days 1-4 and day 9 post-LAIV. LAIV-induced changes of NLF cells were characterized using flow cytometry. Cell-free NLF was analyzed for immune mediators by bioassay. Peripheral blood natural killer (NK) cells from nonsmokers and smokers at baseline were stimulated in vitro with LAIV followed by flow cytometric and mediator analyses. CD45(+)CD56(-)CD16(+) neutrophils and CD45(+)CD56(+) NK cells comprised median 4.62% (range 0.33-14.52) and 23.27% (18.29-33.97), respectively, of non-squamous NLF cells in nonsmokers at baseline. LAIV did not induce changes in total NK cell or neutrophil percentages in either nonsmokers or smokers. Following LAIV inoculation, CD16(+) NK cell percentages and granzyme B levels increased in nonsmokers, and these effects were suppressed in smokers. LAIV inoculation enhanced expression of activating receptor NKG2D and chemokine receptor CXCR3 on peripheral blood NK cells from both nonsmokers and smokers in vitro but did not induce changes in CD16(+) NK cells or granzyme B activity in either group.\n\nQuestion:\nIs nasal lavage natural killer cell function suppressed in smokers after live attenuated influenza virus?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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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.
| [
{
"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:\nNutritional depletion has been correlated with low plasma and mucosal glutamine concentrations and with increased intestinal permeability. Since nutritional depletion often is associated with (chronic) inflammatory stress, this study was designed to establish the influence of depletion and inflammation on glutamine concentrations and gut barrier function. Anthropometric parameters were calculated from 26 patients who required artificial nutrition. Glutamine concentrations in plasma and gut mucosa, gut permeability and mucosal morphology were assessed. For determination of the degree of inflammation erythrocyte sedimentation rates and (pre)albumin concentrations were measured. On the basis of these parameters patients were divided into two groups having significant inflammatory stress or not. Similarly, a depleted and a non-depleted group was formed based on percentage ideal body weight, fat-free mass index (FFMI) and percentage weight loss. Glutamine concentrations, gut permeability and villus morphology were compared between the groups. The presence of inflammatory activity had significant negative effects on glutamine concentrations in contrast to the presence or absence of nutritional depletion. Similarly, intestinal permeability increased during active inflammation but not in depleted patients. FFMI but not inflammation was related to villus height.\n\nQuestion:\nDoes inflammation rather than nutritional depletion determine glutamine concentrations and intestinal permeability?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 0 |
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.
| [
{
"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 the present study was to identify the mechanism by which genistein and 17β-estradiol inhibit proliferation of MDA-MB-231 breast cancer cells. The expression of cell signaling proteins involved in cell apoptosis, proliferation, and survival (BCL-2 associated X protein, BAX; B-cell lymphoma 2, BCL-2; extracellular signal regulated kinase, pERK1/2; and protein kinase B, pAKT) were examined by western blotting, and tested whether these effects correlated with cell proliferation and apoptosis. Compared to the control, 1 μM genistein plus 1 nM 17β-estradiol significantly increased apoptosis, and the BAX/BCL-2 ratio, with a concomitant decrease in ERK1/2 phosphorylation. High concentrations of genistein (100 μM) both in the presence and absence of 17β-estradiol also increased apoptosis; however, these changes were not correlated with the BAX/BCL-2 ratio or with phosphorylation of ERK1/2.\n\nQuestion:\nDo physiological concentrations of genistein and 17β-estradiol inhibit MDA-MB-231 breast cancer cell growth by increasing BAX/BCL-2 and reducing pERK1/2?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 was conducted to determine whether the major nasal airway ion transport abnormalities in cystic fibrosis (that is, defective cAMP regulated chloride secretion and basal sodium hyperabsorption) are related to the clinical expression of cystic fibrosis and/or to the genotype. Nasal potential difference was measured in 79 adult patients with cystic fibrosis for whom clinical status, respiratory function, and CFTR genotype were determined. In univariate and multivariate analysis, patients with pancreatic insufficiency were more likely to have low responses to low chloride (odds ratio (OR) 8.6 (95% CI 1.3 to 58.5), p = 0.03) and isoproterenol (OR 11.2 (95% CI 1.3 to 93.9), p = 0.03) solutions. Similarly, in univariate and multivariate analysis, patients with poor respiratory function (forced expiratory volume in 1 second <50% of predicted value) were more likely to have an enhanced response to amiloride solution (OR 3.7 (95% CI 1.3 to 11.0), p = 0.02). However, there was no significant relationship between nasal potential difference and the severity of the genotype.\n\nQuestion:\nIs nasal airway ion transport linked to the cystic fibrosis phenotype in adult patients?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nNoninvasive markers of liver fibrosis correlate with the stage of liver fibrosis, but have not been widely applied to predict liver-related mortality. We assessed the ability of two indices of liver fibrosis, aspartate aminotransferase (AST)-to-platelet ratio index (APRI) and Fib-4, and two markers of extracellular matrix metabolism, hyaluronic acid (HA) and YKL40, to predict liver mortality in a prospective cohort of hepatitis C virus (HCV)-infected individuals with and without HIV coinfection. These were compared with two established prognostic scores, the Child-Pugh-Turcotte (CPT) and model of end-stage liver disease (MELD) scores. A total of 303 subjects, of whom 207 were HIV positive at study entry, were followed up for a mean period of 3.1 years. There were 33 deaths due to liver disease. The ability of each test and score to predict 3-year liver mortality was expressed as the area under the receiver operator curve. The area under the receiver operator curve 95% confidence intervals were: HA 0.92 (0.86-0.96), CPT 0.91 (0.79-0.96), APRI 0.88 (0.80-0.93), Fib-4 0.87 (0.77-0.92), MELD 0.84 (71-0.91). In multivariate analyses HA, APRI, and fib-4 were independent predictors of mortality when included in models with MELD or CPT.\n\nQuestion:\nAre noninvasive markers of liver fibrosis highly predictive of liver-related death in a cohort of HCV-infected individuals with and without HIV infection?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 0 |
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.
| [
{
"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 genome-wide association study has identified three loci (five independent signals) that confer risk for polycystic ovary syndrome (PCOS) in Han Chinese women. Replication is necessary to determine whether the same variants confer risk for PCOS in women of European ancestry. The objective of the study was to test whether these PCOS risk variants in Han Chinese women confer risk for PCOS in women of European ancestry. This was a case-control study. The study was conducted at deCODE Genetics in Iceland and two academic medical centers in the United States. Cases were 376 Icelandic women and 565 and 203 women from Boston, MA, and Chicago, IL, respectively, all diagnosed with PCOS by the National Institutes of Health criteria. Controls were 16,947, 483, and 189 women not known to have PCOS from Iceland, Boston, and Chicago, respectively. There were no interventions. Main outcomes were allele frequencies for seven variants in PCOS cases and controls. Two strongly correlated Han Chinese PCOS risk variants on chromosome 9q33.3, rs10986105[C], and rs10818854[A], were replicated in samples of European ancestry with odds ratio of 1.68 (P = 0.00033) and odds ratio of 1.53 (P = 0.0019), respectively. Other risk variants at 2p16.3 (rs13405728), 2p21 (rs12468394, rs12478601, and rs13429458), and 9q33.3 (rs2479106), or variants correlated with them, did not associate with PCOS. The same allele of rs10986105 that increased the risk of PCOS also increased the risk of hyperandrogenism in women without PCOS from Iceland and demonstrated a stronger risk for PCOS defined by the National Institutes of Health criteria than the Rotterdam criteria.\n\nQuestion:\nAre variants in DENND1A associated with polycystic ovary syndrome in women of European ancestry?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 0 |
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.
| [
{
"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:\nConduit artery function in obese humans is frequently assessed at rest, but very little is known about resistance artery function in response to muscle contraction. We tested the hypothesis that obese adults will exhibit reduced contraction-induced rapid onset vasodilatation. Single and brief forearm contractions were used to isolate the local effects of muscle contraction on the forearm vasodilatory response, independent of systemic haemodynamic and sympathetic neural influence. We measured forearm blood flow (Doppler ultrasound), blood pressure (finger photoplethysmography) and heart rate (electrocardiogram) on a beat-by-beat basis in 14 obese (body mass index = 36.2 ± 1.7 kg m(-2)) and 14 lean (body mass index = 21.6 ± 0.7 kg m(-2)) young (18-40 years) adults. Percent changes from baseline in forearm vascular conductance (FVC(%) ) were calculated in response to single, brief forearm contractions performed in random order at 15, 20, 25, 30, 40 and 50% of maximal voluntary contraction (MVC). In both groups, each single contraction evoked a significant (P < 0.05), immediate (within one cardiac cycle) and graded FVC(%) increase from one up to six cardiac cycles post-contraction. Immediate (20-50% MVC), peak (15-50% MVC) and total (area under the curve, 20-50% MVC) vasodilatory responses were reduced with obesity. The degree of impaired vasodilatation increased with increasing workloads.\n\nQuestion:\nIs rapid onset vasodilatation blunted in obese humans?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nRisk factors for osteoporosis are prevalent in chronic heroin users who often start using opiates in their late teens. This study was the first to evaluate bone mineral density (BMD) in relatively young heroin-dependent patients on injectable heroin maintenance. Using cross-sectional design, BMD was assessed in a convenience sample of 19 patients (mean age ± SD = 33.9 ± 5.4; 13 men) prescribed injectable diacetylmorphine for heroin dependence. BMD of the lumbar spine and proximal femur was measured by dual-energy X-ray absorptiometry. Substance use and menstrual history, psychopathology and risk factors for low BMD were assessed by questionnaire-based interviews. According to World Health Organisation criteria almost three-quarters (74%) of the sample had osteopenia (n = 11) or osteoporosis (n = 3) at one or more sites of measurement. All patients showed multiple risk factors for bone loss, with pack-years of tobacco use and years of heroin use reaching marginally significant associations with spine Z-scores. Moreover, BMD Z-scores correlated significantly negatively with increasing age at all sites, indicating that the older the patient, the greater the BMD deviation from an age-controlled population.\n\nQuestion:\nDo patients on injectable diacetylmorphine maintenance have low bone mass?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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's access to food processing technology at the household level may have positive dietary benefits during the pre-harvest lean season when households are most stressed from food shortages and higher energy expenditures from agricultural work. This study in rural Gambia was conducted to determine if women's access to small manually operated oil presses (ram) for sesame oil extraction had any significant effects on seasonal fluctuations of household oil supply and on dietary intakes of women and children. Participants were 40 women and children with access to community-based motorized oil press expellers (Expeller-control), 37 women and children with access to village-based ram presses (Press-experiment), and 43 women and children with access to both ram press and motorized expeller (Combination). Dietary data were collected at baseline, at peak oil-pressing, at pre-harvest lean, and at the post-harvest seasons. Households in the Press-experiment and Combination groups consumed 37 and 51 percent more oil, respectively, than those in the Expeller-control group during the pre-harvest lean season. Women from the Press-experiment and Combination groups consumed more energy at the lean season than those in the Expeller-control group. Similarly, children from the Press-experiment and Combination groups consumed more protein at peak oil-processing season than those from the Expeller-control group. At the pre-harvest season children from these two groups also consumed more protein, however, only the consumption of the Combination children was statistically significant compared with that of the Expeller-control group (p < .05). Press-experiment children consumed more nutrient-dense weaning foods during the pre-harvest lean season than Expeller-control children.\n\nQuestion:\nIs women 's access to food-processing technology at the household level associated with improved diets at the pre-harvest lean season in The Gambia?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nAdipose tissue is infiltrated by an increasing number of macrophages during the development of obesity. These immune cells are suspected to be a major source of TNF-α that interferes with adipocyte function. Because lycopene possesses anti-inflammatory properties, we hypothesize that lycopene could reduce the production of TNF-α by macrophages and thus interfere in the cross-talk between macrophages and adipocytes. We demonstrated that physiological concentrations of lycopene were able to attenuate the lipopolysaccharide (LPS)-mediated induction of TNF-α in RAW 264.7 macrophages, at both the mRNA and protein levels. The molecular mechanism was studied. It appeared that the LPS-activation of both JNK and NF-κB signaling pathways was modulated by lycopene. The anti-inflammatory effects of lycopene on macrophages were accompanied by a decrease in LPS-stimulated macrophage migration in the presence of lycopene. Furthermore, lycopene decreased macrophage conditioned medium-induced proinflammatory cytokine, acute phase protein, and chemokine mRNA expression in 3T3-L1 adipocytes.\n\nQuestion:\nDoes lycopene attenuate LPS-induced TNF-α secretion in macrophages and inflammatory markers in adipocytes exposed to macrophage-conditioned media?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
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{
"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 influence of kinesiophobia on disability in patients with knee osteoarthritis is known, but its influence on functional recovery after total knee arthroplasty remains unexplored. To assess the influence of kinesiophobia on functional recovery following total knee arthroplasty (TKA) in patients with knee osteoarthritis and to investigate if kinesiophobia was more common in obese patients than in non-obese patients. Cohort study. Inpatients of the Physical Medicine and Rehabilitation unit of the Château-Renault hospital (France). The study included 89 consecutive patients (mean age = 72.6 years) hospitalized for postoperative rehabilitation after TKA. All patients completed the study. We evaluated functional outcome by testing maximum passive flexion, pain intensity, the duration of hospitalization, and performance in a six minute walk test. Kinesiophobia was assessed by the Tampa Scale for Kinesiophobia (TSK) score. Obesity was assessed by calculation of body mass index (BMI). A Stepwise multiple linear regression was used to determine significant independent predictors of the distance at the six minute walk test. During the six minute walk test, patients without kinesiophobia walked significantly farther than patients with kinesiophobia (309.5 [83.6] m vs. 264.8 [96.5] m, P=0.048). There were no significant differences in the duration of hospitalization, the maximum passive flexion, or pain intensity between the two groups. The best multivariate model of factors associated with the performance in the 6 minute walk test included the Lequesne's score before surgery, the degree of active extension of the knee at the beginning of hospitalization, the TSK scores (total score, classification with the TSK score, \"avoidance\" subscale score). The overall TSK score did not differ between the obese and non-obese groups.\n\nQuestion:\nDoes kinesiophobia negatively influence recovery of joint function following total knee arthroplasty?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 evaluated the effects of a structured nurse-led education programme that aimed to improve patient concordance and prevent venous leg ulcer recurrence. The design was quasi-experimental. Subjects (average age: 80) had venous leg ulceration that had healed within the previous two years, and were cared for at home by a district nurse. Data were available on 49 patients with 97 legs, 72 of which had had venous leg ulcers. Patients were divided into two groups: a control group, which received 'usual' care, and experimental group, which was exposed to the education programme. Recurrence rates, the effects of the education on patient behaviour and the effect on recurrence of having both ankle movement and general mobility were measured over one year. Patients in the experimental group experienced significantly less recurrence over the year (log rank test = 8.28, p = 0.004). To control for differences in mobility and ankle movement in the control and experimental groups at baseline, simultaneous logistic regression analysis was undertaken. This revealed a significant advantage for patients in the experimental group (p = 0.035; OR = 4.45, 95% CI = 1.11-17.74), who spent more time with their legs elevated each day. This difference was sustained throughout the 52 weeks (f = 2.88, p = 0.015). Those who had both full ankle movement (> 60 degrees) and full mobility (without aid) had significantly less recurrence (p = 0.042). Education had no significant effect on the amount of time patients wore compression hosiery (f = 2.1).\n\nQuestion:\nDoes nurse-led education set out to improve patient concordance and prevent recurrence of leg ulcers?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nReactive oxygen species (ROS), including H2O2, have been shown to induce hypersensitivity of vagal lung C-fibers (VLCFs) mainly through receptor potential ankyrin 1 (TRPA1) and P2X receptors. Cannabinoids (CBs) exert antinociceptive effects by binding to specific CB receptors, designated CB1 and CB2 (type 2) for type 1 and type 2, respectively. We investigated whether activation of CB receptors can suppress ROS-mediated VLCF hypersensitivity and, if so, what type(s) of CB receptors are involved. Aerosolized H2O2 (0.05%) was inhaled by anesthetized spontaneously breathing rats (n = 304) to sensitize VLCFs. Airway reflex reactivity to intravenous capsaicin, a VLCF stimulant, was measured. Perivagal pretreatments with various types of agonists and antagonists, a technique that can modulate VLCF sensitivity, were made to delineate the roles of the CB receptors. Aerosolized H2O2 induced an augmented apneic response to capsaicin, which was blocked by bilateral vagotomy or by perivagal capsaicin treatment, suggesting that the response is mediated through VLCFs. Perivagal treatment with HU210 (a nonselective CB agonist) or ACPA (a selective CB1 receptor agonist), but not JWH133 (a CB2 receptor agonist), attenuated this H2O2-induced VLCF hypersensitivity. The suppressive effects of HU210 and ACPA were prevented by an additional treatment with AM251 (a selective CB1 antagonist), but not with AM630 (a selective CB2 antagonist). Perivagal treatment with a combination of ACPA, HC030031 (a TRPA1 receptor antagonist), and iso-PPADS (a P2X receptor antagonist) further attenuated the H2O2-induced VLCF hypersensitivity, as compared with treatment with a combination of HC030031 and iso-PPADS.\n\nQuestion:\nDoes activation of cannabinoid CB1 receptors suppress the ROS-induced hypersensitivity of rat vagal lung C-fiber afferents?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nIrritant dermatitis, caused by genetic barrier dysfunction in atopic dermatitis or wet work in hand dermatitis, induces innate immune response that might predispose to allergic contact sensitization to less potent sensitizers. We sought to determine if positive patch test results to less potent allergens are more prevalent in patients with a history of childhood flexural dermatitis or current wet work. We examined our database of patients presenting to a contact dermatitis clinic tested to potential contact allergens as indicated by their history. Allergens from our most recent standard were studied if they could be classified as weak, moderate, or strong sensitizers based on published data from the local lymph node assay. Patients were stratified by a history of childhood-onset flexural dermatitis as a proxy for atopic dermatitis and by occupation. History of childhood-onset dermatitis predisposed to contact allergy to weak sensitizers and wet work to medium-potency sensitizers. Neither predisposed to contact allergy from strong sensitizers.\n\nQuestion:\nDoes inflamed skin predispose to sensitization to less potent allergens?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nOperative treatment is the standard for severely displaced proximal humerus fractures, but functional impairment can persist. Retaining of the implant can be a reason and in other fracture situations has proved to ameliorate patient satisfaction. The aim of this study was to analyse the functional outcome after locking plate removal in proximal humerus fractures. In a two-year period, all symptomatic patients with plate osteosynthesis for proximal humerus fracture and hardware removal were retrospectively evaluated clinically and radiologically pre- and post-implant removal. Evaluation included Constant score, height of plate position and possible impingement, as well as intraoperative complications. Twenty patients met the inclusion criteria. The mean age was 56 ± 12 years. The plates were placed 6.9 ± 3 mm distal to the greater tubercle. The operation was performed in 35 ± 10 min and no intraoperative complications were reported. The Constant score improved significantly after implant removal from 71 to 76 (p = 0.008).\n\nQuestion:\nDo elective implant removal in symptomatic patients after internal fixation of proximal humerus fractures improves clinical outcome?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nInterleukin 34 (IL-34) is a recently discovered cytokine that binds macrophage colony-stimulating factor (M-CSF) receptor. Rheumatoid arthritis (RA) is characterized by increased osteoclastogenesis. To identify the significance of IL-34 in RA, the IL-34 concentration was measured in serum and synovial fluid (SF). IL-34 concentrations were measured in serum from patients with RA (n = 113), patients with osteoarthritis (OA; n = 56), and controls (n = 36), and in SF isolated from patients with RA (n = 36) or OA (n = 24). Correlations between serum IL-34 levels and clinical features in RA were assessed. The levels of IL-1β, IL-6, IL-17α, interferon-γ-induced protein 10, receptor activator of nuclear factor κB ligand (RANKL), and Dickkopf-1 were also measured. Patients with RA had a higher mean serum level of IL-34 than did patients with OA and controls (188.0 ± 550.3, 36.6 ± 38.0, and 49.1 ± 78.5 pg/ml, respectively). Similarly, SF IL-34 concentration was higher in patients with RA than in those with OA. IL-34 levels were positively associated with IL-6 levels in serum from patients with RA and OA. SF IL-34 concentration correlated significantly with IL-6 and RANKL levels only in RA. The serum level of IL-34 was not correlated with systemic osteoporosis and radiographic joint damage in RA. IL-34 levels in the serum from patients with RA were positively correlated with rheumatoid factor and anticyclic citrullinated peptide antibody titers (r = 0.282 and 0.491, respectively).\n\nQuestion:\nAre increased levels of interleukin 34 in serum and synovial fluid associated with rheumatoid factor and anticyclic citrullinated peptide antibody titers in patients with rheumatoid arthritis?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nFrequent promoter hypermethylation of the inhibitors in either Rb or p53 pathways is associated with the hepatocellular carcinoma (HCC) development. To quantitatively assess the gradual changes of the promoter methylation of p14ARF, p15INK4b, p16INK4a and CCND2 genes in hepatitis B virus (HBV) infection-related HCC. A total of 118 pairs of tumour and their corresponding non-tumour tissues were collected from HCC patients with evidence of HBV infection. The promoter methylation status was analysed by combined DNA methylation-sensitive and methylation-dependent restriction endonuclease digestion, followed by subsequential quantitative PCR assay. Promoter hypermethylation frequencies were gradually increased from 6.25% in normal liver tissues to 21.19% in adjacent non-tumour and to 40.68% in tumour tissues for p16INK4a (P = 0.000), and from none to 10.20% and to 29.59% for CCND2 (P = 0.001). The hypermethylation intensities in HCC tissues were also significantly increased (P = 0.0018 for p16INK4a, P = 0.0001 for CCND2). Altogether, 48.93% cases were found with increased hypermethylation intensity of either p16INK4a and/or CCND2 promoter in tumour tissues, compared with their matched non-tumour tissues. In addition, tumour tissue p16INK4a promoter hypermethylation was significantly higher in male than that in female gender patients in frequency (P = 0.041) and was significantly increased in patients older than 50 years of age in intensity (P = 0.0021). No hypermethylation of p14ARF or p15INK4b was found.\n\nQuestion:\nDoes quantitative methylation analysis reveal gender and age differences in p16INK4a hypermethylation in hepatitis B virus-related hepatocellular carcinoma?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 evidence suggests that insulin-producing beta (beta)-cells arise in utero from duct-like structures of the fetal exocrine pancreas, and genetic lineage tracing studies indicate that they are maintained in the adult by self-renewal. These studies have not addressed the origin of the new beta-cells that arise in large numbers shortly after birth, and contradictory lineage tracing results have been published regarding the differentiation potential of duct cells in this period. We established an independent approach to address this question directly. We generated mice in which duct and acinar cells, comprising the exocrine pancreas, can be genetically marked by virtue of their expressing the mucin gene Muc1. Using these mice, we performed time-specific lineage tracing to determine if these cells undergo endocrine transdifferentiation in vivo. We find that Muc1+ cells do give rise to beta-cells and other islet cells in utero, providing formal proof that mature islets arise from embryonic duct structures. From birth onwards, Muc1 lineage-labeled cells are confined to the exocrine compartment, with no detectable contribution to islet cells.\n\nQuestion:\nIs exocrine-to-endocrine differentiation detectable only prior to birth in the uninjured mouse pancreas?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nArterial pulse pressure hypertension is associated with perioperative morbidity and mortality in cardiac surgery patients. However, its association with perioperative mortality in other high-risk surgical populations has not been determined. In this study, we tested the hypothesis that increased preoperative arterial pulse pressure is associated with 30-day and 1-year all-cause mortality after lower extremity arterial bypass surgery. A retrospective review of patients who had infrainguinal arterial bypass surgery at a single center over a 6-year period (January 2002 to January 2008) was performed (n = 556). Mean, systolic, and diastolic arterial blood pressure were determined from a single noninvasive oscillometric blood pressure cuff reading in the operating room before the administration of anesthetic drugs. Pulse pressure was calculated from this measurement in a retrospective manner by subtracting diastolic pressure from systolic pressure. Mortality for all subjects was determined using the social security death index. Comorbid conditions, preoperative medications, and anesthetic techniques were recorded. Univariate and multivariate analyses were performed to evaluate the association between arterial pulse pressure and the primary outcome variables, and all-cause 30-day and 1-year mortality. Of the 556 patients, a large percentage had elevated pulse pressure (44.9% had pulse pressure ≥80). Thirty-day mortality was 5.1% and 1-year mortality was 17.8%. There was no apparent association between preoperative pulse pressure and 30-day (P = 0.35) or 1-year (P = 0.14) all-cause mortality. Independent predictors of 30-day mortality were age ≥80 years (P = 0.02), ASA physical status ≥IV (P = 0.04), baseline creatinine >2.0 mg/dL (P < 0.0001), and emergency surgery (P = 0.009). The same variables were associated with 1-year mortality, as were the Lee's Revised Cardiac Risk Index score, female gender, and gangrene or ulcer as an indication for surgery.\n\nQuestion:\nDoes preoperative arterial pulse pressure have no apparent association with perioperative mortality after lower extremity arterial bypass?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nVitamin D can influence lipolysis and insulin secretion. A common genetic polymorphism of the vitamin D receptor (VDR), which has been found to be associated with bone mineral density, has been reported to be also associated with Type 2 diabetes mellitus (DM). To test the influence of the VDR polymorphism on fasting glucose in healthy young men before the onset of Type 2 DM, we studied a homogeneous population of aircrew members. A total of 1539 individuals were recruited during routine medical qualification for flying duty. Physical activity was assessed in all individuals and categorized into low physical activity (<or= 3 h per week) and high physical activity (> 3 h per week). The BsmI VDR polymorphism was analysed by polymerase chain reaction. On the day of blood testing the individuals were fasting for at least 8 h overnight. Serum glucose was measured within 60 min after sampling venous blood. In young males with low physical activity (n = 752) gene carriers with the VDR genotype BB (n = 137) have significantly (P < 0.001) higher levels of fasting glucose (5.61 +/- 0.49 mmol/l) than gene carriers with the genotype Bb (n = 370; 5.44 +/- 0.44 mmol/l) or bb (n = 245; 5.38 +/- 0.44 mmol/l). Of BB gene carriers, 47% had fasting glucose levels > 5.55 mmol/l compared with 36% of Bb gene carriers and 34% of bb gene carriers (P = 0.018). This effect is absent in gene carriers with high physical activity (n = 787).\n\nQuestion:\nDoes the vitamin D receptor gene variant and physical activity predict fasting glucose levels in healthy young men?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 vascular endothelial growth factor (VEGF) expression of podocyte is one of the well-known major factors in development of diabetic nephropathy. In this study, we investigated the effects of aldose reductase inhibitor, fidarestat on diabetic nephropathy, and renal VEGF expression in a type 1 diabetic rat model. Twenty four Sprague-Dawley male rats which were performed intraperitoneal injection of streptozotocin and normal six rats were divided into four groups including a normal control group, untreated diabetic control group, aldose reductase (AR) inhibitor (fidarestat, 16 mg kg(-1) day(-1)) treated diabetic group, and angiotensin receptor blocker (losartan, 20 mg kg(-1) day(-1)) treated diabetic group. We checked body weights and blood glucose levels monthly and measured urine albumin-creatinine ratio (ACR) at 8 and 32 weeks. We extracted the kidney to examine the renal morphology and VEGF expressions. The ACR decreased in fidarestat and losartan treated diabetic rat groups than in untreated diabetic group (24.79 +/- 11.12, 16.11 +/- 9.95, and 84.85 +/- 91.19, p < 0.05). The renal VEGF messenger RNA (mRNA) and protein expression were significantly decreased in the fidarestat and losartan treated diabetic rat groups than in the diabetic control group.\n\nQuestion:\nDoes aldose reductase inhibitor ameliorate renal vascular endothelial growth factor expression in streptozotocin-induced diabetic rats?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 study the prevalence of hand abnormalities in diabetic patients and to evaluate associations between the hand abnormalities and diabetic variables, ergonomic factors and smoking habits. Cross-sectional study of 100 patients selected at random. Setting. Out-patient clinic, Department of Internal Medicine, Orebro Medical Centre Hospital in Sweden. Presence and extent of carpal tunnel syndrome (CTS), Dupuytren's contracture (DC), flexor tenosynovitis (FTS), and limited joint mobility (LJM). Duration of diabetes, metabolic control, chronic diabetic complications, blood pressure, ergonomic factors and smoking habits. Carpal tunnel syndrome, DC, FTS and LJM were each present in about 20% of the patients. Hand abnormalities were observed in 50 patients and more than one abnormality was found in 26 of the patients. The hand abnormalities were associated with the duration of diabetes but not with the metabolic control or with other diabetic complications. However, the diabetic complications were associated with bad metabolic control and with the duration of diabetes. Hand abnormalities correlated with heavy manual work but not with smoking habits. Twenty-five of the 50 patients with hand syndromes were disabled to such an extent that surgery was recommended.\n\nQuestion:\nAre hand abnormalities strongly associated with the duration of diabetes mellitus?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nCigarette smoking is a major environmental contributor to COPD, but understanding its epigenetic regulation of oxidative genes involved in the pathogenesis of COPD remains elusive. We analyzed DNA methylation on glutamate-cysteine ligase catalytic subunit (GCLC), glutathione S-transferase M1 (GSTM1), glutathione S-transferase P1 (GSTP1), and superoxide dismutase 3 (SOD3) promoters in clinical samples from patients with COPD (current-smoker [CS-COPD]; ex-smoker [ES-COPD]) and subjects with normal pulmonary function (current-smoker [CS-NS]; ex-smoker [ES-NS]; never-smoker [NC]). Expression of GCLC messenger RNA (mRNA) and glutathione (GSH) synthesis in these clinical samples and human bronchial epithelial (BEAS-2B) cells stimulated by cigarette-smoke extract (CSE) was evaluated. GCLC mRNA and protein levels were measured to determine effects of demethylation and deacetylation agents on CSE-treated BEAS-2B cells. The DNA methylation level of the GCLC promoter was significantly increased in CS-COPD, CS-NS, and ES-COPD groups compared with ES-NS and NC groups. However, there were no significant differences in DNA methylation values of GSTM1, GSTP1, and SOD3 promoters among these groups. Expression of GCLC mRNA was downregulated in the lungs, and GSH levels decreased in plasma as a consequence of hypermethylation of the GCLC promoter. Similarly, CSE-treated BEAS-2B cells had hypermethylation of the GCLC gene, mRNA downregulation, and a decreased intracellular GSH level. GCLC expression in CSE-treated BEAS-2B cells was restored by the methylation inhibitor, 5-aza-2'-deoxycytidine, but not by the deacetylation agent, trichostatin A.\n\nQuestion:\nDoes cigarette Smoke-Induced Hypermethylation of the GCLC Gene be Associated With COPD?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nRadiofrequency atrial fibrillation ablation (AFA) is commonly performed in patients with atrial fibrillation. It is imperative to develop a strategy for the early detection of esophageal lesions secondary to AFA. The current protocol is to obtain cross-sectional imaging before and immediately after the procedure. If patients have evidence of esophageal inflammation, they undergo esophagogastroduodenoscopy (EGD). We hypothesized that esophageal abnormalities seen on imaging immediately post-ablation are a poor predictor of the damage seen during EGD. Patients referred for EGD following AFA from 1/2009 to 11/2010 were included. Two endoscopists reviewed and scored the EGD images. Two radiologists reviewed the post-AFA imaging studies. For computed tomography (CT) scans, esophageal inflammation was scored from 0 to 2. For T2 and delayed magnetic resonance imaging (MRI) pictures, esophageal enhancement was scored from 0 to 2, with the circumference involved as 0, <50%, or >50%, and the length of esophageal enhancement in mm. In total, 76 patients were included; 22 patients had only endoscopic images and 54 had both endoscopic and radiologic images for review. Of the post-AFA imaging studies, 16 were CTs and 60 were MRIs. The kappa score for the inter-rater agreement of esophageal inflammation on EGD was 0.4584 (moderate). For MRIs, the kappa scores for T2 images were 0.1980 and 0.2857 for edema and circumference, respectively. For delayed images, the kappa scores were 0.2687 and 0.3101 for edema and circumference, respectively. The kappa scores were negative between EGD score by T2 edema (-0.2104) and circumference (-0.2212), and between EGD score and delayed edema (-0.0588) and circumference (-0.0446). When measures were treated as dichotomous, the overall agreement between CT measures and EGD scores was kappa = 0, for T2 measures and EGD kappa = -0.2963, 95% confidence interval (CI) (-0.5643, -0.0282), and between delayed measures kappa = -0.0244, 95% CI (-0.1420, -0.0932).\n\nQuestion:\nDoes cross-sectional imaging obtained immediately following radiofrequency atrial fibrillation ablation predict endoscopic evidence of esophageal injury?\n\nAnswer:",
"role": "user"
},
{
"content": "no",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 if the concentration of interleukin-6 (IL-6) in the cerebrospinal fluid (CSF) is affected by perinatal asphyxia, and to examine the relation of IL-6 levels in the CSF to the severity of hypoxic-ischemic encephalopathy (HIE), to brain damage, and to the neurological outcome. Asphyxiated term neonates were included. Cerebrospinal fluid IL-6 was measured by a sensitive enzyme-linked immunosorbent assay. Twenty neonates were studied: 3 had no HIE, 5 had stage 1, 6 had stage 2, and 6 had stage 3. CSF IL-6 levels (8 to 90 hours of life) were higher in neonates with HIE stage 3 (range, 65 to 2250 pg/mL) when compared with neonates with HIE stage 0 to 2 (<2 pg/mL in 12 neonates, 10 pg/mL in 1). According to neuroimaging techniques and/or pathological examination, 14 neonates were normal, and 5 showed signs of brain damage; 1 was not classified. CSF IL-6 levels were significantly higher in neonates with signs of brain damage. Finally, 5 neonates had adverse outcomes (4 died, 1 had cerebral palsy), 2 had mild motor impairment, and 13 had normal outcomes. CSF IL-6 levels were higher in neonates with adverse outcomes (range, 65 to 2250 pg/mL) compared with neonates with favorable outcomes.\n\nQuestion:\nIs interleukin-6 in the cerebrospinal fluid after perinatal asphyxia related to early and late neurological manifestations?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 androgen deprivation therapy leads to weight gain within the first year in men with prostate cancer, longer term changes and the relationship to patient age are not well characterized. We examined long-term weight gain by age group in men on androgen deprivation therapy for up to 36 months. Three cohorts matched by age and education were recruited in this prospective study, including men in whom continuous androgen deprivation therapy was initiated, controls with prostate cancer and healthy controls. All patients with prostate cancer had nonmetastatic disease. We performed age stratified (less than 65 vs 65 years or greater) comparisons. Univariate and multivariable associations with weight change with time were evaluated using linear regression. We included 257 men with a mean age of 69.1 years. At baseline the cohorts were similar in age, education, body mass index, weight and comorbidity. Androgen deprivation therapy was associated with weight gain from baseline at 6, 12, 18, 24, 30 and 36 months compared to controls with prostate cancer and healthy controls (p = 0.006, 0.015, 0.028, 0.003, 0.014 and 0.0004, respectively). The proportion of men who gained weight was higher among androgen deprivation therapy users than controls with prostate cancer and healthy controls at most time points. Age stratified analyses showed that younger patients (age less than 65 years) on androgen deprivation therapy had significantly greater weight gain with time than older patients (4.7 vs 1.4 kg, p = 0.005). However, age did not appear to affect weight change with time in men not on androgen deprivation therapy (p = 0.37).\n\nQuestion:\nDoes impact of androgen deprivation therapy on weight gain differ by age in men with nonmetastatic prostate cancer?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 analyze the microvascular network in skeletal muscle biopsies from patients with dermatomyositis (DM) and systemic sclerosis (SSc) compared to polymyositis (PM) and systemic lupus erythematosus (SLE), and non-inflammatory myopathies, and to clarify whether reparative angiogenesis-related factors are expressed in parallel to blood vessel damage. Immunohistochemical staining of muscle biopsies (10 DM, 10 SSc, 10 PM, 10 SLE, and 10 non-inflammatory myopathies) with antibodies against von Willebrand factor (vWF), hypoxia-inducible factor-1beta (HIF-1beta), beta3 integrin subunit, and vascular endothelial growth factor receptor-1 (VEGFR-1). The TechMate staining robot and biotin-streptavidin protocol were used. DM and SSc muscles were characterized by endothelial damage and reduction of blood vessel network. Expression of angiogenesis-related factors (HIF-1beta, beta3, VEGFR-1) was also found in the same biopsies. In contrast, in PM and SLE muscles, vascular networks were apparently not affected and angiogenic stimuli were less expressed if at all.\n\nQuestion:\nDo disease-associated increased HIF-1 , alphavbeta3 integrin , and Flt-1 suffice to compensate the damage-inducing loss of blood vessels in inflammatory myopathies?\n\nAnswer:",
"role": "user"
},
{
"content": "no",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nNo guidelines comprise when or to what extent sinus surgery should be done in patients with cystic fibrosis (CF) or how a CT scan of the paranasal sinuses should influence the decision. Symptoms of rhinosinusitis and/or eradication of pathogenic bacteria from the sinuses are reasons for sinus surgery. In this observational cross sectional study, 55 CF cases had their preoperative CT scans scored according to the Lund Mackay- and the Nair-system. Correlations between the CT scans, symptoms, surgical findings and cultures obtained during sinus surgery were made. There was no significant correlation between the CT score and detection of pus, pathogenic bacteria or symptoms. Pus and pathogenic bacteria were found in several cases without sinus opacification on the CT scan. Non pathogenic and sterile cultures were also found in sinuses with opacification.\n\nQuestion:\nIs cT of the paranasal sinuses a valid indicator for sinus surgery in CF patients?\n\nAnswer:",
"role": "user"
},
{
"content": "no",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nCognitive/behavioral and environmental variables are significant predictors of patient adjustment in chronic pain. Using a biopsychosocial template and selecting several pain-relevant constructs from physical, cognitive/behavioral, and environmental predictors, outcomes of pain and disability in chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) were explored. Men (n = 253) from a North American multi-institutional NIH-funded Chronic Prostatitis Cohort Study in 6 US and 1 Canadian centers participated in a survey examining pain and disability. Measures included demographics, urinary symptoms, depression, pain, disability, catastrophizing, control over pain, pain-contingent rest, social support, and solicitous responses from a significant other. Regressions showed that urinary symptoms (beta = .20), depression (beta = .24), and helplessness catastrophizing (beta = .29) predicted overall pain. Further, affective pain was predicted by depression (beta = .39) and helplessness catastrophizing (beta = .44), whereas sensory pain was predicted by urinary symptoms (beta = .25) and helplessness catastrophizing (beta = .37). With regard to disability, urinary symptoms (beta = .17), pain (beta = .21), and pain-contingent rest (beta = .33) were the predictors. These results suggest cognitive/behavioral variables (ie, catastrophizing, pain-contingent rest) may have significant impact on patient adjustment in CP/CPPS. Findings support the need for greater research of such pain-related variables in CP/CPPS.\n\nQuestion:\nDo catastrophizing and pain-contingent rest predict patient adjustment in men with chronic prostatitis/chronic pelvic pain syndrome?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nIn controlled environments such as the operating room, bedside ultrasound (BUS) of the neck has shown high accuracy for distinguishing endotracheal (ETI) from esophageal intubations. We sought to determine the accuracy of BUS for endotracheal tube (ETT) position in the emergency department (ED) setting. We assessed the utility of BUS in a single-center observational study in an ED setting. BUS was performed either simultaneously with ED intubation (S/ED), within < 3 minutes of ED intubation (A/ED), or in < 3 minutes of patient's ED arrival after pre-hospital intubation (A/EMS). Trained ED providers performed BUS; intubators were blinded to ultrasound findings. We used Cormack and Lehane categories (CL) to classify intubation attempts as \"easy\" (CL-I/II), \"moderate\" (CL-III) and \"difficult\" (CL-IV). Additional data included the diagnostic accuracy of the sonographer and intubator compared to the clinical outcome, anatomy identified by sonography and time to diagnosis. During a 10-month period, 89 subjects with 115 intubation attempts were included in the study, and 86 patients/101 attempts with complete data were used in the study (63-easy, 19-moderate, 19-difficult). The sonographers achieved 100 % accuracy with respect to determining the correct ETT position utilizing an anterior neck approach, while the intubators' accuracy in assessing correct tube location was 97 % compared to the clinical outcome. A blinded review of sonography findings confirmed all BUS anatomical findings. A sonographically empty esophagus was 100 % specific for endotracheal intubation, and a \"double trachea sign\" was 100 % sensitive and 91 % specific for esophageal intubation. The sonographic time to diagnosis was significantly faster than the intubator time to diagnosis (\"easy\" p < 0.001; n = 47; \"moderate\" p = 0.001; n = 15; \"difficult\" p < 0.001; n = 19); Wilcoxon test; A/EMS cases excluded).\n\nQuestion:\nDoes bedside ultrasound of the neck confirm endotracheal tube position in emergency intubations?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 cell lines are often heterogeneous in their response to ionizing radiation. The tumorigenicity of some cells can be rapidly induced by gamma-radiation. The tumorigenicity of individual clones of C6 rat glioblastoma cells and the effect of gamma-radiation on their growth in vivo was studied by intracranial implantation into Wistar rats. A clone was found, C6#11, that was conditionally tumorigenic. It either did not form a tumor, or grew into a small encapsulated tumor, and did not cause death or neurological deficits in the animals. Gamma-irradiation of the animals (head only) with implanted C6#11 induced a fully developed invasive tumor that killed them within 25 days. Three grays of radiation of C6#11 cells two hours prior to implantation induced their tumorigenicity as well. The in vitro characteristics of the C6#11 cells as compared to a highly tumorigenic clone did not correlate with their behavior in vivo.\n\nQuestion:\nIs conditionally tumorigenic clone of C6 cells induced by gamma-irradiation?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nAsian sand dust (ASD) originating in the arid deserts of Mongolia and China causes annual severe air pollution events in the Asia-Pacific area, including Korea, Japan, and China. ASD is thought to impact public health by aggravating or inducing respiratory illness. Among the most common respiratory illnesses is the common cold caused by rhinovirus (RV) infection. To date, however, the impact of ASD on RV infection has not been studied. In this study, we investigated the effect of ASD on RV infection in human nasal epithelial cells. Primary human nasal epithelial cells grown at an air-liquid interface were treated with ASD and/or RV. After RV infections were confirmed using semi-nested reverse transcription-polymerase chain reaction (RT-PCR), mRNA expression and protein secretion of the inflammatory cytokines interferon-γ (IFN-γ), interleukin-1β (IL-1β),IL-6, and IL-8, indicators of the severity of RV-induced inflammation, were measured by real-time PCR and enzyme-linked immunosorbent assays. Viral titer was also assayed by culturing viruses to compare viral replication between RV-only and ASD-plus-RV groups. ASD significantly increased RV-induced IFN-γ, IL-1β, IL-6, and IL-8 mRNA levels and protein secretion in primary nasal epithelial cells. In addition, ASD caused a significant increase in RV replication.\n\nQuestion:\nDoes asian sand dust enhance rhinovirus-induced cytokine secretion and viral replication in human nasal epithelial cells?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 use of external banding during transcommissural external valvuloplasty has the theoretical advantage of increasing the durability of surgical procedure. The aim of this study was to assess the durability of this combined approach and compare its long-term results with those of external valvuloplasty procedure applied alone. We retrospectively reviewed data on 144 patients with combined superficial and deep venous reflux who underwent transcommissural external valvuloplasty procedure alone or transcommissural external valvuloplasty plus external banding procedure over a 7-year period from September 1998 to November 2005. The clinical study included only the patients who have completed at least 48 months of follow-up period. Seventy-six patients who have completed the necessary follow-up period were divided into 2 groups according to the surgical procedure performed. Group A consists of 40 patients in whom transcommissural external valvuloplasty was the procedure of choice and Group B consists of 36 patients in whom an external banding has been added to external valvuloplasty repair. The outcomes assessed are venous clinical severity scores of patients, ulcer recurrence and competency rates. In both groups, median preoperative Venous Clinical Severity Scores were 3. The severity scores improved in both groups during the postoperative follow-up period. However, although the scores of Group B patients at 12 and 24 months were lower than those of Group A, the difference was not statistically significantly at these time points; but, reached a statistical significance at the end of 36 months. Ulcer-freedom rates at 48 months for groups A and B were 72% and 96%, respectively. The cumulative competency rates of 40 Group A patients were 85% at 6 months, 77.5% at 12 months, 69% at 24 months, 58% at 36 months, 55% at 48 months, and 48.5% at 60 months. The cumulative competency rates of 36 patients in Group B were 88% at 6 months, 80% at 12 months, 75% at 24 months, 71.5% at 36 months, 69% at 48 months, and 69% at 60 months.\n\nQuestion:\nDoes the use of external banding increase the durability of transcommissural external deep venous valve repair?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nOesophageal adenocarcinoma (OAC) has a poor prognosis, and chemoprevention is an attractive option to reduce the burden of the disease. Hydroxyl-methyl-CoA reductase inhibitors (statins) have been shown to exert potentially useful anticancer effects against OAC cell lines, but there are only limited clinical data examining the effects of statins on the incidence of OAC. To examine the association between statin use and the incidence of OAC. We have carried out a case-control study comparing statin use between patients with an incident diagnosis of OAC and controls with nonprogressive Barrett's oesophagus. Eighty-five cancer cases were compared with 170 age-matched and sex-matched controls. Risk factors and drug exposure were established using standardized interviews. Logistic regression was used to compare statin exposure and correct for confounding factors. Regular statin use was associated with a significantly lower incidence of OAC [uncorrected odds ratio (OR) 0.45, 95% confidence intervals 0.24-0.84)]. After correction for confounding variables including aspirin and NSAID use, statin use was still associated with a reduced incidence of OAC (OR 0.57, 0.28-0.94). Longer duration of statin use and higher doses were both associated with a significantly greater reduction in OAC. The combination of regular statin and aspirin use was associated with a significantly further reduced incidence of OAC (OR 0.31, 0.04-0.69).\n\nQuestion:\nIs regular statin and aspirin use in patients with Barrett 's oesophagus associated with a reduced incidence of oesophageal adenocarcinoma?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nWe present our experience performing ureteroscopy in prepubertal children. We performed a retrospective cohort study of children 12 years or younger who underwent ureteroscopy at 2 institutions between 1993 and 2003. Patient demographics, indications for surgery, operative technique, surgical outcomes and complications were recorded. A total of 39 boys and 32 girls underwent 34 flexible and 47 rigid ureteroscopies. Retrograde access was obtained in 77 procedures, while 4 were performed via an antegrade approach. Mean age was 7.5 years (range 1 to 12) and mean followup was 2.2 years (0.5 to 10). Endoscopic lithotripsy was performed in 65 cases, with a success rate of 98%. A ureteral stent was placed postoperatively in 55 patients. Endoscopic incision was performed for a ureteral stricture in 3 patients and for ureteropelvic junction obstruction in 6. An obstructing fibroepithelial polyp was found in 2 patients, 1 underwent removal of a foreign body and 4 did not have intraluminal pathology. Dilation of the ureteral orifice was required in 23 cases (30%). There were no intraoperative ureteral injuries. One patient had development of a ureteral stricture (complication rate 1.3%) that was successfully treated endoscopically.\n\nQuestion:\nIs ureteroscopy safe and effective in prepubertal children?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nTelomerase is a reverse transcriptase that maintains the telomeres of linear chromosomes and preserves genomic integrity. The core components are a catalytic protein subunit, the telomerase reverse transcriptase (TERT), and an RNA subunit, the telomerase RNA (TR). Telomerase is unique in its ability to catalyze processive DNA synthesis, which is facilitated by telomere-specific DNA-binding domains in TERT called anchor sites. A conserved glutamine residue in the TERT N-terminus is important for anchor site interactions in lower eukaryotes. The significance of this residue in higher eukaryotes, however, has not been investigated. To understand the significance of this residue in higher eukaryotes, we performed site-directed mutagenesis on human TERT (hTERT) Q169 to create neutral (Q169A), conservative (Q169N), and non-conservative (Q169D) mutant proteins. We show that these mutations severely compromise telomerase activity in vitro and in vivo. The functional defects are not due to abrogated interactions with hTR or telomeric ssDNA. However, substitution of hTERT Q169 dramatically impaired the ability of telomerase to incorporate nucleotides at the second position of the template. Furthermore, Q169 mutagenesis altered the relative strength of hTERT-telomeric ssDNA interactions, which identifies Q169 as a novel residue in hTERT required for optimal primer binding. Proteolysis experiments indicate that Q169 substitution alters the protease-sensitivity of the hTERT N-terminus, indicating that a conformational change in this region of hTERT is likely critical for catalytic function.\n\nQuestion:\nIs human telomerase reverse transcriptase ( hTERT ) Q169 essential for telomerase function in vitro and in vivo?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 effect of moderate alcohol intake with a meal on glucose homeostasis in diabetic patients. Alcohol (1 g/kg, an aperitif before, wine during, and a drink after a meal) or an equal amount of mineral water was given during a dinner. Blood glucose and insulin concentrations were measured before, during, and after the meal until the next morning. This study was conducted at the Helsinki University Hospital Metabolic Ward and the Finnish Diabetes Association Education Center. The participants in the study included 10 type I diabetic patients treated with insulin and 16 type II diabetic patients treated with diet alone or with diet and oral drugs. In each subject, we examined hypoglycemic episodes or differences in blood glucose or serum insulin concentrations between alcohol and the control study. In type I diabetic patients, blood glucose and insulin concentrations were virtually identical in both studies. In type II diabetic patients, alcohol slightly enhanced the meal-induced insulin secretion resulting in lower blood glucose concentrations next morning. No hypoglycemic glucose concentrations were observed in either group after alcohol ingestion.\n\nQuestion:\nDoes alcohol with a meal have no adverse effects on postprandial glucose homeostasis in diabetic patients?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nDespite common disbelief that neutrophils are involved in atherosclerosis, evidence is accumulating for a causal role of neutrophils in atherosclerosis. CC chemokine ligand (CCL)3 is an inflammatory chemokine and its expression is significantly increased during atherosclerotic lesion formation in mice. It has recently been shown that under conditions of inflammation neutrophils can migrate along a CCL3 gradient. In this study, we aimed to elucidate the role of leukocyte-derived CCL3 in atherogenesis. Irradiated low density lipoprotein receptor(-/-) mice, reconstituted with CCL3(-/-) or littermate bone marrow showed markedly reduced CCL3 response to lipopolysaccharide treatment, establishing the critical relevance of leukocytes as source of CCL3. Hematopoietic deficiency of CCL3 significantly reduced aortic sinus lesion formation by 31% after 12 weeks of western-type diet. Interestingly, whereas plaque macrophage, collagen, and vascular smooth muscle cell content were unchanged, neutrophil adhesion to and presence in plaques was significantly attenuated in CCL3(-/-) chimeras. These mice had reduced circulating neutrophil numbers, which could be ascribed to an increased neutrophil turnover and CCL3(-/-) neutrophils were shown to be less responsive toward the neutrophil chemoattractant CXC chemokine ligand 1.\n\nQuestion:\nDoes leukocyte-specific CCL3 deficiency inhibit atherosclerotic lesion development by affecting neutrophil accumulation?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nIL-4 and IL-13 play a crucial role during allergic asthma. Both cytokines can be produced by T cells and a variety of cell types of the innate immune system. The relative contribution of T-cell-derived vs innate IL-4/IL-13 for allergic inflammation and airway hyperreactivity remains unclear. We compared the severity of OVA/alum-induced allergic lung inflammation in WT BALB/c mice to mice that lack expression of IL-4/IL-13 only in T cells (4-13Tko) or in all cell types (4-13ko). T-cell-derived IL-4/IL-13 was required for IgG1 and IgE production, recruitment of eosinophils and basophils to the lung, goblet cell hyperplasia, expression of Muc5ac, Clca3, and RELMβ, differentiation of alternatively activated macrophages, and airway hyperreactivity. Interestingly, ILC2 recruitment to the lung occurred independently of T-cell-derived IL-4/IL-13 but was diminished in the absence of IL-4/IL-13 from all cell types. Thus, the number of IL-4/IL-13-competent ILC2s did not correlate with the severity of lung pathology.\n\nQuestion:\nAre t cells the critical source of IL-4/IL-13 in a mouse model of allergic asthma?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 insulin-like growth factor-I (IGF-I) and vascular endothelial growth factor (VEGF) have been implicated in the pathogenesis of early renal dysfunction in diabetes. We investigated whether IGF-I affects VEGF gene expression and protein secretion in human mesangial cells. Furthermore, we studied the intracellular signaling pathway involved and the interaction of IGF-I with mechanical stretch, a known VEGF inducer. Human mesangial cells were exposed to IGF-I in the presence and in the absence of (1) anti-IGF-I type I receptor antibody (alpha IR3) (1 microg/mL), a monoclonal antibody blocking the IGF-I type I receptor; (2) wortmannin (600 nmol/L), a phosphatidylinositol 3-kinase (PI3K) inhibitor; (3) 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP2), a specific Src inhibitor (10 micromol/L); and (4) cyclic stretch (approximately 10% elongation). IGF-I induced a dose-dependent increase in VEGF protein levels (10(-11) mol/L, 5%; 10(-10) mol/L, 14%; 10(-9) mol/L, 46%; 10(-8) mol/L, 66%; 10(-7) mol/L, 68%; P < 0.001). IGF-I-induced VEGF production rose by 6 hours with a peak at 12 hours, and declined by 24 hours (52%, 72%, and 34%, respectively; P < 0.01 at 12 hours). A corresponding 50% increase in VEGF mRNA levels was seen at 6 hours (P < 0.01). IGF-I-induced VEGF protein secretion was not affected by the addition of wortmannin (IGF-I, 76% vs. IGF-I + wortmannin, 79% increase over control; P = NS), but was abolished by alpha IR3 (IGF-I, 69% vs. IGF-I +alpha IR3, 0%; P < 0.001) and significantly reduced by PP2 (IGF-I, 50% vs. IGF-I + PP2, 14%; P < 0.01). Simultaneous exposure of human mesangial cells to both IGF-I and stretch failed to further increase VEGF production (IGF-I, 1.49 +/- 0.05; stretch, 1.76 +/- 0.05; and IGF-I + stretch, 1.83 +/- 0.11).\n\nQuestion:\nDoes iGF-I induce vascular endothelial growth factor in human mesangial cells via a Src-dependent mechanism?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nTOR is a phosphatidylinositol kinase (PIK)-related kinase that controls cell growth and proliferation in response to nutritional cues. We describe a C. elegans TOR homolog (CeTOR) and phenotypes associated with CeTOR deficiency. These phenotypes are compared with the response to starvation and the inactivation of a variety of putative TOR targets. Whether caused by mutation or RNA interference, TOR deficiency results in developmental arrest at mid-to-late L3, which is accompanied by marked gonadal degeneration and a pronounced intestinal cell phenotype. A population of refractile, autofluorescent intestinal vesicles, which take up the lysosomal dye Neutral Red, increases dramatically in size, while the number of normal intestinal vesicles and the intestinal cytoplasmic volume decrease progressively. This is accompanied by an increase in the gut lumen size and a compromise in the intestine's ability to digest and absorb nutrients. CeTOR-deficient larvae exhibit no significant dauer characteristics, but share some features with starved L3 larvae. Notably, however, starved larvae do not have severe intestinal atrophy. Inactivation of C. elegans p70S6K or TAP42 homologs does not reproduce CeTOR deficiency phenotypes, nor does inactivation of C. elegans TIP41, a putative negative regulator of CeTOR function, rescue CeTOR deficiency. In contrast, inactivating the C. elegans eIF-4G homolog and eIF-2 subunits results in developmental arrest accompanied by the appearance of large, refractile intestinal vesicles and severe intestinal atrophy resembling that of CeTOR deficiency.\n\nQuestion:\nDoes tOR deficiency in C. elegans cause developmental arrest and intestinal atrophy by inhibition of mRNA translation?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 activity of the GH/IGF-I axis varies during life and is clearly reduced in the elderly. In fact, GH, IGF-I and IGFBP-3 levels in older people are clearly reduced and similar to those observed in patients with GH deficiency. The declining activity of the GH/IGF-I axis with advancing age may contribute to changes in body composition, structure, function and metabolism. In fact, treatment with pharmacological doses of rhGH restored plasma IGF-I levels, increased lean body mass and muscle strength while decreased adipose tissue mass in healthy elderly subjects. At present it is unclear whether peripheral GH sensitivity is preserved in aging. To clarify this point, we aimed to verify the effect of both single dose and short term treatment with very low rhGH doses on the IGF-I levels in normal elderly subjects. Normal young adults were studied as controls. We studied the IGF-I response to rhGH administration after single (20 micrograms/kg s.c.) or repeated administrations (5 micrograms/kg s.c. for 4 days) in two groups of young and elderly subjects. Twenty-seven healthy elderly (ES, 14 F and 13 M, age mean +/- SEM: 69.4 +/- 1.3 years, BMI: 23.9 +/- 0.5 kg/m2) and 21 young adult subjects (YS, 12 F and 9 M, 29.8 +/- 1.2 years, 23.8 +/- 0.5 kg/m2) were studied, divided into two groups. Group 1: blood samples for IGF-I and IGFBP-3 assay were drawn basally and 12 h after rhGH administration (20 micrograms/kg). Group 2: blood samples for IGF-I, IGFBP-3, glucose and insulin assays were drawn basally, 12 h after the first and the last rhGH administration (5 micrograms/kg). Free T3 (fT3), free T4 (fT4) and TSH levels were also assayed basally and after the last rhGH administration; oestradiol and testosterone levels were measured basally. Basal IGF-I levels were lower in ES (whole group) than in YS (whole group) (123.1 +/- 8.9 vs. 230.4 +/- 16.1 micrograms/l, P < 0.001) while IGFBP-3 levels in the two groups were similar (2.7 +/- 0.2 vs. 3.1 +/- 0.2 mg/l). No sex-related differences in IGF-I and IGFBP-3 levels were recorded in either group. Group 1: the single administration of 20 micrograms/kg rhGH induced a significant (P < 0.001) IGF-I rise both in YS (318.0 +/- 25.3 vs. 256.0 +/- 21.6 micrograms/l) and ES (187.2 +/- 16.8 vs. 100.4 +/- 9.5 micrograms/l). IGF-I levels after rhGH in ES persisted lower than those in YS (P < 0.001), but the percentage IGF-I increase after rhGH was higher (P < 0.001) in ES (91.6 +/- 12.9%) than in YS (23.9 +/- 5.0%) subjects. Both in YS and ES IGFBP-3 levels were significantly increased to the same extent by 20 micrograms/kg rhGH (3.0 +/- 0.2 vs. 2.3 +/- 0.2 mg/l; 2.9 +/- 0.2 vs. 2.6 +/- 0.2 mg/l, P < 0.001 vs. baseline). Group 2: basal glucose, insulin, fT3, fT4 and TSH levels in YS and ES were similar; testosterone levels in aged and young men were similar while oestradiol levels in aged women were lower (P < 0.01) than in the young ones. IGF-I levels were significantly increased 12 h after the first administration of 5 micrograms/kg rhGH both in ES (166.6 +/- 15.7 vs. 138.3 +/- 12.1 micrograms/l, P < 0.03) and YS (272.2 +/- 16.1 vs. 230.4 +/- 16.1 micrograms/l, P < 0.001). Twelve hours after the last rhGH administration IGF-I levels were further increased (P < 0.001) both in ES (208.7 +/- 21.1 micrograms/l) and YS (301.7 +/- 17.6 micrograms/l). IGF-I levels in ES persisted lower than those in YS at each time point (P < 0.001); however, the percentage IGF-I increase after rhGH in ES and YS was similar (after the first administration: 22.4 +/- 5.1 vs. 21.7 +/- 5.1%; after the last administration: 52.9 +/- 9.5 vs. 39.5 +/- 9.9%). No significant variation in IGFBP-3, glucose, insulin, fT3, fT4 or TSH levels was recorded in either ES or YS.\n\nQuestion:\nIs the IGF-I response to very low rhGH doses preserved in human ageing?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 still controversial whether carotid plaque is associated with cardiovascular events in patients with coronary artery disease (CAD). The aim of the present study is to evaluate the impact of carotid plaque on long term clinical outcomes especially in patients with CAD. The study population consisted of 1390 consecutive patients with angiographically proven CAD. All subjects underwent carotid scanning 1 day before or after coronary angiogram and were followed up for major adverse cardiovascular events (MACE; death, myocardial infarction, stroke, revascularization, restenosis and hospitalization for heart failure) during a mean of 54.2 ± 23.9 months. Patients with carotid plaque (n=433) were older, had higher prevalence of cardiovascular risk factors and acute coronary syndrome (34.2% vs. 24.6%, p<0.001) than those without carotid plaque (n=957). On univariate analysis, the presence of carotid plaque was a predictor of cardiac death, hard MACE (death, myocardial infarction and stroke) and total MACE, whereas carotid intima-media thickness (CIMT) was a predictor of total MACE. Multivariate analysis revealed that carotid plaque was associated with cardiac death (HR 6.99, 95% CI 1.88-25.95, p=0.004), hard MACE (HR 1.89, 95% CI 1.18-3.04, p=0.008) and total MACE (HR 1.47, 95% CI 1.13-1.90, p=0.004), whereas CIMT was associated only with total MACE (HR 1.39, 95% CI 1.06-1.81, p=0.017).\n\nQuestion:\nIs carotid plaque associated with increased cardiac mortality in patients with coronary artery disease?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nBone metastases often occur in the majority of patients with advanced cancer, such as prostate cancer, lung cancer and breast cancer. Serum tartrate-resistant acid phosphatase 5b (TRACP 5b), a novel bone resorption marker, has been used gradually in the clinics as a specific and sensitive marker of bone resorption for the early diagnosis of cancer patients with bone metastasis. Here, we reported that high concentrations of uric acid (UA) lead to decrease of TRACP 5b levels and determined whether TRACP 5b level was associated with UA in interference experiment. A total of 77 patients with high concentrations of UA and 77 healthy subjects were tested to evaluate the differences in their TRACP 5b levels. Serial dilutions of UA were respectively spiked with a known concentration of TRACP 5b standard sample, then Serum TRACP 5b was detected by using bone TRAP® Assay. A correction equation was set to eliminate UA-derived TRACP 5b false-decrease. The effect of this correction was evaluated in high-UA individuals. The average TRACP level of the high-UA individuals (1.47 ± 0.62 U/L) was significantly lower than that of the healthy subjects (2.62 ± 0.63 U/L) (t-test, p < 0.0001). The UA correction equation derived: ΔTRACP 5b = -1.9751lgΔUA + 3.7365 with an R2 = 0.98899. Application of the UA correction equation resulted in a statistically non-significant difference in TRACP 5b values between the healthy subjects and high-UA individuals (p = 0.24).\n\nQuestion:\nDoes high Uric Acid ( UA ) Negatively affect Serum Tartrate-Resistant Acid Phosphatase 5b ( TRACP 5b ) Immunoassay?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 whether levels of von Willebrand factor (vWF), fibrinogen and fibronectin are related to a parental history of type 2 diabetes and to determine possible explanatory factors for high versus low vWF and fibrinogen. Cross-sectional study. We compared vWF, fibrinogen and fibronectin in 88 nondiabetic offspring of type 2 diabetic subjects (relatives) and 103 offspring of nondiabetic subjects (controls). Other measurements included urinary albumin excretion rate, blood pressure, lipid profile and insulin resistance using homeostasis model assessment (HOMAIR). There were no significant differences in vWF (1.12 vs. 1.06 IU x mL(-1), P = 0.296), fibrinogen (3.2 vs. 3.1 g x L(-1); P = 0.263) or fibronectin (0.39 vs. 0.40 g x L(-1), P = 0.448) between relatives and controls. With multiple logistic regression we determined explanatory factors for high versus low vWF and fibrinogen. Age (P < 0.01), urinary albumin excretion rate (P < 0.05), ischaemic heart disease (IHD) (P < 0.05) were found to be significant explanatory factors for vWF above the median (1.10 IU x mL(-1)). Interaction between insulin resistance and sex was found. Odds ratio for high versus low insulin resistance was 18.39 (P < 0.001) for women and 1.92 (P = 0.32) for men. Body mass index (BMI) (P < 0.05), sex (P < 0.01), smoking status (P < 0.05) and IHD (P < 0.01) were significant explanatory factors for fibrinogen above the median (3.1 g x L(-1)).\n\nQuestion:\nIs insulin resistance accompanied by increased von Willebrand factor levels in nondiabetic women : a study of offspring of type 2 diabetic subjects compared to offspring of nondiabetic subjects?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nPeople who experience traumatic events have an increased risk of post-traumatic stress disorder (PTSD). However, PTSD-related pathological changes in the hippocampus and prefrontal cortex remain poorly understood. We investigated the effect of a PTSD-like animal model induced by severe stress. The experimental rats received 20 inescapable electric foot shocks in an enclosed box for a total of 6 times in 3 days. The physiological state (body weight and plasma corticosterone concentrations), emotion, cognitive behavior, brain morphology, apoptosis, and balance of gamma-aminobutyric acid (GABA) and glutamate in the hippocampus and prefrontal cortex were observed. Cell damages were examined with histological staining (HE, Nissl, and silver impregnation), while apoptosis was analyzed with flow cytometry using an Annexin V and propidium iodide (PI) binding and terminal deoxynucleotidyl transferase mediated-dUTP nick end labeling (TUNEL) method. In comparison with the sham litter-mates, the stressed rats showed decreased body weight, inhibition of hypothalamic-pituitary-adrenal (HPA) axis activation, increase in freezing response to trauma reminder, hypoactivity and anxiety-like behaviors in elevated plus maze and open field test, poor learning in Morris water maze, and shortened latency in hot-plate test. There were significant damages in the hippocampus but not in the prefrontal cortex. Imbalance between glutamate and GABA was more evident in the hippocampus than in the prefrontal cortex.\n\nQuestion:\nDoes glutamate and GABA imbalance promote neuronal apoptosis in hippocampus after stress?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nVirtually all living organisms have evolved a circadian (~24 hour) clock that controls physiological and behavioural processes with exquisite precision throughout the day/night cycle. The suprachiasmatic nucleus (SCN), which generates these ~24 h rhythms in mammals, consists of several thousand neurons. Each neuron contains a gene-regulatory network generating molecular oscillations, and the individual neuron oscillations are synchronised by intercellular coupling, presumably via neurotransmitters. Although this basic mechanism is currently accepted and has been recapitulated in mathematical models, several fundamental questions about the design principles of the SCN remain little understood. For example, a remarkable property of the SCN is that the phase of the SCN rhythm resets rapidly after a 'jet lag' type experiment, i.e. when the light/dark (LD) cycle is abruptly advanced or delayed by several hours. Here, we describe an extensive parameter optimization of a previously constructed simplified model of the SCN in order to further understand its design principles. By examining the top 50 solutions from the parameter optimization, we show that the neurotransmitters' role in generating the molecular circadian rhythms is extremely important. In addition, we show that when a neurotransmitter drives the rhythm of a system of coupled damped oscillators, it exhibits very robust synchronization and is much more easily entrained to light/dark cycles. We were also able to recreate in our simulations the fast rhythm resetting seen after a 'jet lag' type experiment.\n\nQuestion:\nDoes global parameter search reveal design principles of the mammalian circadian clock?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nWe studied the effect of thalidomide on NFκB-induced TNF-α in acute pancreatitis-associated lung injury in the rat. Rats were intragastrically administered thalidomide (100mg/kg) daily for 8 days and then acute pancreatitis was induced by retrograde infusion of 5% sodium taurocholate into the rat biliopancreatic duct. Serum amylase (AMY), blood oxygen partial pressure (PaO2), ratios of lung wet/dry weight, and cytoplasmic IκBα and TNF-α protein and nuclear NFκBp65 protein were measured. Also, lung NFκBp65 and TNF-α mRNA were measured. Compared with the model group, the pathological score of the pancreas and lung, serum AMY, ratios of lung wet/dry weight, and lung NFκBp65 and TNF-α mRNA and protein of rats given thalidomide were decreased significantly (P<0.01), but PaO2 and IκBα protein was elevated significantly (P<0.01).\n\nQuestion:\nDoes thalidomide alleviate acute pancreatitis-associated lung injury via down-regulation of NFκB induced TNF-α?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nHLA mismatch antigens are major targets of alloreactive T cells in HLA-incompatible stem-cell transplantation, which can trigger severe graft-versus-host disease and reduce survival in transplant recipients. Our objective was to identify T-cell subsets with reduced in vitro reactivity to allogeneic HLA antigens. We sorted CD4 and CD8 T-cell subsets from peripheral blood by flow cytometry according to their expression of naive and memory markers CD45RA, CD45RO, CD62L, and CCR7. Subsets were defined by a single marker to facilitate future establishment of a clinical-grade procedure for reducing alloreactive T-cell precursors and graft-versus-host disease. T cells were stimulated in mixed lymphocyte reactions against HLA-deficient K562 cells transfected with single HLA-A/-B/-C/-DR/-DQ mismatch alleles. Alloreactivity was measured by interferon-γ spot production and cell proliferation. We observed that allogeneic HLA-reactivity was preferentially derived from subsets enriched for naïve T cells rather than memory T cells in healthy donors, irrespective of the HLA mismatch allele. This separation was most efficient if CD45RA (versus other markers) was used for sorting. The numbers of allogeneic HLA-reactive effector cells were in median 7.2-fold and 16.6-fold lower in CD45RA(neg) memory CD8 and CD4 T cells than in entire CD8 and CD4 T cells, respectively. In contrast, proliferation of memory T cells in response to allogeneic HLA was more variably reduced (CD8) or equivalent (CD4) when compared to that of naïve T cells. We also demonstrated in HLA-matched donor-patient pairs that leukemia-reactive CD8 cytotoxic T-lymphocytes were mainly derived from subsets enriched for naïve T cells compared to memory T cells.\n\nQuestion:\nAre alloreactive and leukemia-reactive T cells preferentially derived from naive precursors in healthy donors : implications for immunotherapy with memory T cells?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nAny individualisation of incisional hernia repair requires a profound knowledge of risk factors for recurrence. A series of 160 patients underwent incisional hernia repair and were prospectively followed up at 3, 6, 12, and 24 months after surgery. We analysed the importance of various variables to predict recurrence. An overall recurrence rate of 11% ( n=17) was observed. The risk for recurrence was not significantly affected by any of the clinical variables except for obesity ( P=0.03). Even when controlling for the influence of age, gender, hernia size, and surgical technique, obesity remained a significant predictor with a rate ratio of 1.10 per unit BMI (95%-CI: 1.02-1.18; P=0.01).\n\nQuestion:\nIs obesity a risk factor for recurrence after incisional hernia repair?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 rhinosinusitis (CRS) is an important public health problem with substantial impact on patient quality of life and health care costs. We hypothesized that genetic variation may be one factor that affects this disease. Identification of genetic variation underlying susceptibility to CRS using linkage analysis in a founder population. We studied a religious isolate that practices a communal lifestyle and shares common environmental exposures. Using physical examination, medical interviews, and a review of medical records, we identified eight individuals with CRS of 291 screened. These eight individuals were related to each other in a single 60 member, nine generation pedigree. A genome-wide screen for loci influencing susceptibility to CRS using 1123 genome-wide markers was conducted. The largest linkage peak (P = .0023; 127.15 cM, equivalent to limit of detection = 2.01) was on chromosome 7q31.1-7q32.1, 7q31 (127.15 cM; 1-limit of detection support region: 115-135 cM) and included the CFTR locus. Genotyping of 38 mutations in the CFTR gene did not reveal variation accounting for this linkage signal.\n\nQuestion:\nDoes a genomewide screen for chronic rhinosinusitis genes identify a locus on chromosome 7q?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 sarcoplasmic reticulum (SR) Ca(2+) cycling and depressed contractility, a hallmark of human and experimental heart failure, has been partially attributed to increased protein phosphatase 1 (PP-1) activity, associated with down-regulation of its endogenous inhibitor-1. The levels and activity of inhibitor-1 are reduced in failing hearts, contributing to dephosphorylation and inactivation of key calcium cycling proteins. Therefore, we investigated the mechanisms that mediate decreases in inhibitor-1 by post-transcriptional modification. Bioinformatics revealed that 17 human microRNAs may serve as modulators of inhibitor-1. However, real-time PCR analysis identified only one of these microRNAs, miR-765, as being increased in human failing hearts concomitant with decreased inhibitor-1 levels. Expression of miR-765 in HEK293 cells or mouse ventricular myocytes confirmed suppression of inhibitor-1 levels through binding of this miR-765 to the 3'-untranslated region of inhibitor-1 mRNA. To determine the functional significance of miR-765 in Ca(2+) cycling, pri-miR-765 as well as a non-translated nucleotide sequence (miR-Ctrl) were expressed in adult mouse ventricular myocytes. The inhibitor-1 expression levels were decreased, accompanied by enhanced PP-1 activity in the miR-765 cardiomyocytes, and these reflected depressed contractile mechanics and Ca(2+) transients, compared with the miR-Ctrl group. The depressive effects were associated with decreases in the phosphorylation of phospholamban and SR Ca(2+) load. These miR-765 negative inotropic effects were abrogated in inhibitor-1-deficient cardiomyocytes, suggesting its apparent specificity for inhibitor-1.\n\nQuestion:\nIs up-regulation of micro-RNA765 in human failing hearts associated with post-transcriptional regulation of protein phosphatase inhibitor-1 and depressed contractility?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nThenar eminence tissue oxygen saturation (StO(2)) was developed to assess organ perfusion. However, mottling, a strong predictor of mortality in septic shock, develops preferentially around the knee. We aimed to evaluate the prognostic value of StO(2) measured around the knee in septic shock patients and compare it to thenar StO(2). This was a prospective observational study in a tertiary teaching hospital. All consecutive patients with septic shock were included. Parameters were recorded when vasopressors were started (H0) and every 6 h during 24 h. Their predictive value was assessed on 14-day mortality. Fifty-two patients were included. SOFA score was 11 (9-15) and SAPS II was 56 (40-72). At 6 h after ICU admission (H6), mean arterial pressure, cardiac index, and central venous pressure were not different between non-survivors and survivors; but non-survivors had higher arterial lactate level (8.8 ± 5.0 vs. 2.2 ± 1.5 mmol/l, P < 0.001), lower urinary output (0.22 ± 0.45 vs. 0.70 ± 0.50 ml/kg/h, P < 0.001) and ScvO(2) (62 ± 20 vs. 72 ± 9 %, P = 0.03). At H6, StO(2) was lower in non-survivors; this difference was not significant for thenar StO(2) (70 ± 15 vs. 77 ± 12 %, P = 0.10) but was very pronounced for knee StO(2) (39 ± 23 vs. 71 ± 12 %, P < 0.001). At H6, a low knee StO(2) was associated with a higher mottling score (P < 0.01), a higher lactate level (P < 0.002, R (2) = 0.2), and a lower urinary output (P = 0.02, R (2) = 0.12).\n\nQuestion:\nIs knee area tissue oxygen saturation predictive of 14-day mortality in septic shock?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 positive relationship between diversification (i.e., speciation) and nucleotide substitution rates is commonly reported for angiosperm clades. However, the underlying cause of this relationship is often unknown because multiple intrinsic and extrinsic factors can affect the relationship, and these have confounded previous attempts infer causation. Determining which factor drives this oft-reported correlation can lend insight into the macroevolutionary process. Using a new database of 13 time-calibrated angiosperm phylogenies based on internal transcribed spacer (ITS) sequences, and controlling for extrinsic variables of life history and habitat, I evaluated several potential intrinsic causes of this correlation. Speciation rates (lambda) and relative extinction rates (epsilon) were positively correlated with mean substitution rates, but were uncorrelated with substitution rate heterogeneity. It is unlikely that the positive diversification-substitution correlation is due to accelerated molecular evolution during speciation (e.g., via enhanced selection or drift), because punctuated increases in ITS rate (i.e., greater mean and variation in ITS rate for rapidly speciating clades) were not observed. Instead, fast molecular evolution likely increases speciation rate (via increased mutational variation as a substrate for selection and reproductive isolation) but also increases extinction (via mutational genetic load).\n\nQuestion:\nDo molecular evolutionary rates predict both extinction and speciation in temperate angiosperm lineages?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 CD44 levels in articular cartilage of knee osteoarthritis (OA) and the relationship between CD44 and severity of the disease. All 50 cartilage tissues included normal and OA cartilage, and were ascribed to the following four groups on the basis of modified Mankin score: normal, mild lesions, moderate lesions and severe lesions. CD44 levels in articular cartilage were assessed by immunohistochemical methods. CD44 levels were detected in all four groups. The difference in average gray value of CD44 expression showed statistical significance when compared between each group (P < 0.05). In addition, CD44 expression in each group correlated with disease severity, according to the modified Mankin score (ρ = -0.848, P < 0.01).\n\nQuestion:\nIs expression of CD44 in articular cartilage associated with disease severity in knee osteoarthritis?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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:\nKidney stone formation is a highly prevalent disease, affecting 8-10% of the human population worldwide. Proteins are the major constituents of human kidney stone's organic matrix and considered to play critical role in the pathogenesis of disease but their mechanism of modulation still needs to be explicated. Therefore, in this study we investigated the effect of human kidney stone matrix proteins on the calcium oxalate monohydrate (COM) mediated cellular injury. The renal epithelial cells (MDCK) were exposed to 200μg/ml COM crystals to induce injury. The effect of proteins isolated from human kidney stone was studied on COM injured cells. The alterations in cell-crystal interactions were examined by phase contrast, polarizing, fluorescence and scanning electron microscopy. Moreover, its effect on the extent of COM induced cell injury, was quantified by flow cytometric analysis. Our study indicated the antilithiatic potential of human kidney stone proteins on COM injured MDCK cells. Flow cytometric analysis and fluorescence imaging ascertained that matrix proteins decreased the extent of apoptotic injury caused by COM crystals on MDCK cells. Moreover, the electron microscopic studies of MDCK cells revealed that matrix proteins caused significant dissolution of COM crystals, indicating cytoprotection against the impact of calcium oxalate injury.\n\nQuestion:\nDo kidney stone matrix proteins ameliorate calcium oxalate monohydrate induced apoptotic injury to renal epithelial cells?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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.
| [
{
"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 goal of this study was to explore the role of NK cell alloreaction in predicting prognosis under unmanipulated HLA-haploidentical blood and marrow transplantation and examine whether the presence of any individual donor-activating KIR gene had an influence on the clinical outcome. We studied the HLA and KIR genotype of 64 donor-recipient pairs, who underwent transplantation. In contrast to Perugia's KIR ligand-ligand mismatch model or Handgretinger's KIR receptor-ligand mismatch model or Bignon's KIR gene-gene mismatch model between donor-recipient pairs, we found that the cumulative incidence of 3-yr disease-free survival (DFS), overall survival (OS), and transplantation-related mortality (TRM) were best predicted by the number of KIR ligands carried by patients (HR 0.355, 95% CI 0.186-0.678, P = 0.002 for DFS; HR 0.445, 95% CI 0.233-0.848, P = 0.014 for OS; HR 0.450, 95% CI 0.219-0.926, P = 0.030 for TRM). Moreover, an analysis of KIR ligand numbers was found to be correlative in patients with lymphoid malignancy. The KIR ligand-ligand mismatch model is a good predictor of acute graft vs. host disease (aGVHD; HR 3.812, 95% CI 1.667-8.720, P = 0.002). Meanwhile, the presence of donor-activating KIR2DS3 also contributed significantly to acute (HR 2.967, 95% CI 1.265-6.958, P = 0.012) and chronic GVHD (HR 2.541, 95% CI 1.127-5.730, P = 0.025).\n\nQuestion:\nIs prognosis after unmanipulated HLA-haploidentical blood and marrow transplantation correlated to the numbers of KIR ligands in recipients?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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