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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 anal cancer uptake of F-18 fluorodeoxyglucose (FDG) measured as the maximum standardized uptake value (SUV(max)) by positron emission tomography (PET) and its correlation with prognostic factors. The study population consisted of 77 patients with stages 0-IIIB anal cancer who underwent pre-treatment FDG-PET. Tumor histology included 65 squamous cell, 11 basaloid, and 1 small cell cancers. SUV(max) and sites of lymph node metastasis were recorded. We analyzed the association between SUV(max) and prognostic factors. The mean SUV(max) was 10.0 (range 1.0-43.1). The stage distribution included: 2 stage 0, 7 stage I, 49 stage II, 10 stage IIIA, 9 stage IIIB. SUV(max) and clinical tumor size were not associated (R(2)=0.338). Histology did not significantly influence SUV(max) (mean SUV(max) 10.0 for squamous versus 9.90 for basaloid). Higher SUV(max) was associated with an increased risk of nodal metastasis at diagnosis (p<0.0001). Higher SUV(max) was associated with worse disease-free survival (p=0.05). Patients with high anal tumor SUV(max) at diagnosis were at an increased risk of persistent or recurrent disease on post-therapy FDG-PET performed less than 4months after completing therapy (p=0.0402).\n\nQuestion:\nIs anal cancer maximum F-18 fluorodeoxyglucose uptake on positron emission tomography correlated with prognosis?\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:\nBronchioles are critical zones in cigarette smoke (CS)-induced lung inflammation. However, there have been few studies on the in vivo dynamics of cytokine gene expression in bronchiolar epithelial cells in response to CS. We subjected C57BL/6J mice to CS (whole body exposure, 90 min/day) for various periods, and used laser capture microdissection to isolate bronchiolar epithelial cells for analysis of mRNA by quantitative reverse transcription-polymerase chain reaction. We detected enhanced expression of keratinocyte-derived chemokine (KC), macrophage inflammatory protein-2 (MIP-2), tumor necrosis factor-alpha (TNF-alpha), and interleukin-1beta (IL-1beta) by bronchial epithelial cells after 10 consecutive days of CS exposure. This was mirrored by increases in neutrophils and KC, MIP-2, TNF-alpha, and IL-1beta proteins in the bronchoalveolar lavage (BAL) fluid. The initial inhalation of CS resulted in rapid and robust upregulation of KC and MIP-2 with concomitant DNA oxidation within 1 hr, followed by a return to control values within 3 hrs. In contrast, after CS exposure for 10 days, this initial surge was not observed. As the CS exposure was extended to 4, 12, 18 and 24 weeks, the bronchiolar KC and MIP-2 expression and their levels in BAL fluid were relatively dampened compared to those at 10 days. However, neutrophils in BAL fluid continuously increased up to 24 weeks, suggesting that neutrophil accumulation as a result of long-term CS exposure became independent of KC and MIP-2.\n\nQuestion:\nIs bronchiolar chemokine expression different after single versus repeated cigarette smoke exposure?\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:\nSoluble ST2 (sST2), a novel biomarker predictive for heart disease, has recently been shown associated with the progression of atherosclerotic disease in a mouse model. The present study was designed to assess sST2 plasma levels in patients scheduled for carotid endarterectomy and relate it with the occurrence of adverse cardiovascular events during follow-up. In addition, sST2 levels were associated to patient clinical data and atherosclerotic plaque characteristics. Plasma sST2 levels were measured in 391 patients who underwent carotid endarterectomy and were subsequently followed for 3 years. Primary composite endpoint was the occurrence of an adverse cardiovascular event. At baseline, no differences were observed in sST2 levels between asymptomatic (n = 75) and symptomatic (n = 316) patients (85 [49-122] versus 90 [58-137] pg/ml, p = 0.263). Soluble ST2 plasma levels did not differ between patients who experienced a secondary manifestation of cardiovascular disease and patients who remained free of symptoms (90 [60-129] versus 88 [46-140] pg/ml, p = 0.519). There was no association between sST2 levels and any of the following plaque characteristics: size of a lipid core, degree of calcification, number of macrophages or smooth muscle cells, amount of collagen and number of microvessels.\n\nQuestion:\nAre soluble ST2 levels associated with secondary cardiovascular events and vulnerable plaque phenotype in patients with carotid artery stenosis?\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:\nWhile microsatellite instability is associated with prognosis and distinct clinical phenotypes in colon cancer, the basis for this remains incompletely defined. Novel bioinformatic techniques enable a detailed interrogation of the relationship between gene expression profiles and tumor characteristics. We aimed to determine if microsatellite instability high (MSI-H) and microsatellite stable (MSS) tumors could be differentiated by gene expression profiles. We investigated the basis of this using a system and network based algorithmic approach. Microsatellite status was established using a polymerase chain reaction (PCR) panel and fragment length analysis. Gene expression was determined using Illumina© microarrays comprising 48,701 transcripts, and scaling normalization was conducted using Limma in R. Following filtration for non-significant changes a meta-gene was established and subjected to unsupervised hierarchical clustering using Chipster©. A supervised learning algorithm (PAM) was used to generate a gene-expression based clinical-outcome predictor that was further tested using an independent validation group. A network based linkage analysis was conducted using Ingenuity© focusing on canonical, functional pathways, and associated therapeutic modalities. MSI-H and MSS tumors clustered separately following an unsupervised hierarchical clustering analysis. A transcriptomic classifier (with 19 component genes) was generated that reliably and reproducibly predicted microsatellite status. MSI-H associated canonical pathways were predominantly immune or inflammation related converging on increased IL-1B and thymidylate synthase expression. The network linkage analysis identified canakinumab, IL-trap and MDX-1100 as the strongest therapeutic candidates that remain to be assessed in the colon cancer setting.\n\nQuestion:\nDo transcriptional profiles underpin microsatellite status and associated features in colon cancer?\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:\nRecent findings have shown that the intrauterine environment can negatively influence long-term insulin sensitivity in the offspring. Here we look at maternal voluntary exercise as an intervention to improve offspring insulin sensitivity and glucose homeostasis. Female Sprague-Dawley rats were split into sedentary and exercise groups with the exercise cohort having voluntary access to a running wheel in the cage before and during mating, pregnancy, and nursing. Female offspring were weaned into sedentary cages. Glucose tolerance tests and hyperinsulinemic-euglycemic clamp were performed in adult offspring to evaluate glucose regulation and insulin sensitivity. Adult female offspring born to exercised dams had enhanced glucose disposal during glucose tolerance testing (P < 0.05) as well as increased glucose infusion rates (P < 0.01) and whole body glucose turnover rates (P < 0.05) during hyperinsulinemic-euglycemic clamp testing compared with offspring from sedentary dams. Offspring from exercised dams also had decreased insulin levels (P < 0.01) and hepatic glucose production (P < 0.05) during the clamp procedure compared with offspring born to sedentary dams. Offspring from exercised dams had increased glucose uptake in skeletal muscle (P < 0.05) and decreased heart glucose uptake (P < 0.01) compared with offspring from sedentary dams in response to insulin infusion during the clamp procedure.\n\nQuestion:\nDoes maternal exercise improve insulin sensitivity in mature rat offspring?\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 Parkinson's disease (PD), commonly reported risk factors for malnutrition in other populations commonly occur. Few studies have explored which of these factors are of particular importance in malnutrition in PD. The aim was to identify the determinants of nutritional status in people with Parkinson's disease (PWP). Community-dwelling PWP (>18 years) were recruited (n = 125; 73M/52F; Mdn 70 years). Self-report assessments included Beck's Depression Inventory (BDI), Spielberger Trait Anxiety Inventory (STAI), Scales for Outcomes in Parkinson's disease-Autonomic (SCOPA-AUT), Modified Constipation Assessment Scale (MCAS) and Freezing of Gait Questionnaire (FOG-Q). Information about age, PD duration, medications, co-morbid conditions and living situation was obtained. Addenbrooke's Cognitive Examination (ACE-R), Unified Parkinson's Disease Rating Scale (UPDRS) II and UPDRS III were performed. Nutritional status was assessed using the Subjective Global Assessment (SGA) as part of the scored Patient-Generated Subjective Global Assessment (PG-SGA). Nineteen (15%) were malnourished (SGA-B). Median PG-SGA score was 3. More of the malnourished were elderly (84% vs. 71%) and had more severe disease (H&Y: 21% vs. 5%). UPDRS II and UPDRS III scores and levodopa equivalent daily dose (LEDD)/body weight (mg/kg) were significantly higher in the malnourished (Mdn 18 vs. 15; 20 vs. 15; 10.1 vs. 7.6 respectively). Regression analyses revealed older age at diagnosis, higher LEDD/body weight (mg/kg), greater UPDRS III score, lower STAI score and higher BDI score as significant predictors of malnutrition (SGA-B). Living alone and higher BDI and UPDRS III scores were significant predictors of a higher log-adjusted PG-SGA score.\n\nQuestion:\nAre markers of disease severity associated with malnutrition in Parkinson '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:\nTaxol is a microtubule stabilizing agent that arrests cells in mitosis leading to cell death. Taxol is widely used to treat breast cancer, but resistance occurs in 25-69% of patients and it is vital to understand how Taxol resistance develops to improve chemotherapy. The effects of chemotherapeutic agents are overcome by survival signals that cancer cells receive. We focused our studies on autotaxin, which is a secreted protein that increases tumor growth, aggressiveness, angiogenesis and metastasis. We discovered that autotaxin strongly antagonizes the Taxol-induced killing of breast cancer and melanoma cells by converting the abundant extra-cellular lipid, lysophosphatidylcholine, into lysophosphatidate. This lipid stimulates specific G-protein coupled receptors that activate survival signals. In this study we determined the basis of these antagonistic actions of lysophosphatidate towards Taxol-induced G2/M arrest and cell death using cultured breast cancer cells. Lysophosphatidate does not antagonize Taxol action in MCF-7 cells by increasing Taxol metabolism or its expulsion through multi-drug resistance transporters. Lysophosphatidate does not lower the percentage of cells accumulating in G2/M by decreasing exit from S-phase or selective stimulation of cell death in G2/M. Instead, LPA had an unexpected and remarkable action in enabling MCF-7 and MDA-MB-468 cells, which had been arrested in G2/M by Taxol, to normalize spindle structure and divide, thus avoiding cell death. This action involves displacement of Taxol from the tubulin polymer fraction, which based on inhibitor studies, depends on activation of LPA receptors and phosphatidylinositol 3-kinase.\n\nQuestion:\nDoes lysophosphatidate induce chemo-resistance by releasing breast cancer cells from taxol-induced mitotic arrest?\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 measure the populations of 36 fungi in the homes and sinuses of chronic rhinosinusitis (CRS) and non-CRS patients. Single-blind cross-sectional study. Populations of 36 fungi were measured in sinus samples and in the home vacuum cleaner dust of CRS (n = 73) and non-CRS patients (n = 16) using quantitative polymerase chain reaction. Etest strips containing amphotericin B, anidulafungin, caspofungin, fluconazole, and voriconazole were used to test the susceptibility of seven potentially relevant fungi. Seven fungi (Alternaria alternata, Cladosporium cladosporioides types 1 and 2, Cladosporium herbarum, Penicillium brevicompactum, Penicillium crustosum, and Penicillium chrysogenum type 2) were discovered at very high concentrations in some CRS patients. In vitro antifungal susceptibility testing of these seven fungi demonstrated species specific sensitivities. Four CRS patients with marked elevations of fungal populations in their sinus samples underwent endoscopic sinus surgery. After surgical treatment, the fungal populations were reduced by several orders of magnitude.\n\nQuestion:\nDo some chronic rhinosinusitis patients have elevated populations of fungi in their sinuses?\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 osteoarthritic (OA) cartilage type-II collagen is preferentially cleaved by the proinflammatory cytokine-induced matrix metalloproteinases-13 (MMP-13). Interferon-gamma (IFN-gamma) potently inhibits interleukin-1 (IL-1)-induced MMP-13 expression in healthy chondrocytes. Our goal was to study the previously unknown impact of IFN-gamma on MMP-13 in OA and compare the levels and functional activity of IFN-gamma receptor (IFN-gammaR1) in healthy and OA chondrocytes. Chondrocytes were obtained from OA patients and non-arthritic control subjects and treated with IL-1+ or- IFN-gamma. MMP-13 mRNA and protein expression were measured by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting. IFN-gammaR1 expression was assessed by flow cytometry, immunoprecipitation and immunohistochemistry with fluorescein-labeled antibody. IFN-gammaR1 was neutralized with its antibody and signal transducer and activator of transcription 1 (STAT1) phosphorylation analyzed by Western blotting. OA chondrocytes were also transfected with control and IFN-gammaR1 expression vectors. OA chondrocytes displayed a drastically impaired MMP-13 suppression by IFN-gamma compared to control cells. IFN-gammaR1 levels were significantly decreased in OA chondrocytes as assessed by flow cytometry, immunoprecipitation and immunohistochemistry. Consequently, IFN-gamma-stimulated STAT1 phosphorylation mediated by IFN-gammaR1 was also considerably reduced in OA patient chondrocytes. IFN-gammaR1 overexpression in OA cells restored MMP-13 suppression by IFN-gamma.\n\nQuestion:\nAre human osteoarthritic chondrocytes impaired in matrix metalloproteinase-13 inhibition by IFN-gamma due to reduced IFN-gamma receptor levels?\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 investigate the presence of oral bacterial DNAs in serum and synovial fluid (SF) of patients with active rheumatoid arthritis (RA) and psoriatic arthritis (PsA). Serum and SF samples from 16 RA patients, 14 PsA patients, and 9 osteoarthritis (controls) patients were extracted for oral bacterial DNA. This was used in a checkerboard DNA-DNA-hybridization set up, to identify 40 different bacteria. Mean number +/- standard deviation (SD) of oral bacterial species in sera were 6.2 (3.2) in the RA group (p = 0.004) and 5.4 (2.7) in the PsA group (p = 0.009) compared to 2.1 (1.7) in the controls. Periodontitis associated species Porphyromonas gingivalis and Prevotella nigrescens were exclusively detected in RA and PsA. Mean number (+/- SD) of oral bacterial species in SF were 14.0 (6.8) in the RA (p = 0.001) and 19.4 (7.1) in the PsA group (p < 0.001) compared to 4.0 (1.7) in controls. P. gingivalis, Tannerella forsythensis and Prevotella intermedia were exclusively identified in RA and PsA SF. Higher means of DNAs were found in RA SF compared to RA serum (p < 0.001), and in PsA SF compared to PsA serum (p < 0.001). Higher concentrations of bacterial DNAs were found in RA and PsA compared to controls.\n\nQuestion:\nDoes synovial inflammation in active rheumatoid arthritis and psoriatic arthritis facilitate trapping of a variety of oral bacterial DNAs?\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 aimed at assessing the quality and quantity of protein-leakage across the alveolar-capillary membrane and its influence on surfactant function during the early neonatal period in preterm infants compared to newborns both with respiratory failure. We therefore prospectively analyzed total protein, elastase-alpha1-proteinase inhibitor complex (E-alpha1-PI) and alpha2-macroglobulin concentrations in tracheal aspirates from 31 infants < or = 32 weeks gestational age (group 1 : 29.3 +/- 2 weeks, 1214 +/- 410 g [means +/- SEM]) and from 21 neonates > 32 weeks (group 2 : 37.5 +/- 3 weeks, 2890 +/- 600 g [means +/- SEM]) and measured their surface activity in the pulsating bubble surfactometer. Day 1 total protein and alpha2-macroglobulin levels indicated an initial high leakage that declined to day 3 in both groups (from 1652 +/- 241 to 708 +/- 227 mg/l; p < 0.05; resp. from 28 +/- 6 to 12 +/- 4 mg/l [means +/- SEM]). In group 2 E-alpha1-PI concentrations were significantly elevated at day 1 compared to group 1 (15 754 +/- 5766 versus 3320 +/- 1056 microg/l [means +/- SEM]). In both groups a high minimum surface tension (15 - 30 mN/m) was recorded from day 1 - 4.\n\nQuestion:\nDo protein content and biophysical properties of tracheal aspirates form neonates with respiratory failure?\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:\nB cell receptor (BCR) -mediated signals are enhanced when CD72 expression is deficient on B cells in autoimmune diseases. The significance of soluble CD72 (sCD72) has not been elucidated. Soluble CD72 was analyzed in the serum of 159 SLE patients, 40 rheumatoid arthritis (RA) patients, and 100 healthy individuals. Correlations between sCD72 and SLE disease activity (SLEDAI) were assessed. Soluble CD72 was found increased in SLE patients, when compared to both RA patients and healthy individuals (20.2 ± 1.2 ng/ml; 10.6 ± 4.6 ng/ml and 7.2 ± 3.3 ng/ml; p < 0.001). Soluble CD72 level was significantly higher in SLE patients with renal involvement than in patients without (31.8 ± 2.3 ng/ml vs 13.9 ± 0.9 ng/ml; p < 0.001) and also with the presence of auto-antibodies.\n\nQuestion:\nIs increased soluble CD72 in systemic lupus erythematosus in association with disease activity and lupus nephritis?\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:\nChemotherapy-induced diarrhea (CID) is a well recognized side effect of cancer treatment. However, the pathophysiology behind this debilitating side effect remains unclear. Irinotecan causes cholinergic and delayed onset diarrhea in patients, in which beta-glucuronidase produced by gut bacteria is thought to be involved. Diarrhea occurred, as expected, following irinotecan treatment. beta-glucuronidase expression increased in the jejunum and colon. Faecal flora changed quantitatively after treatment also, with increases in E. coli, Staphylococcus spp. and Clostridium spp. (all beta-glucuronidase producing) and decreases in Lactobacillus spp., Bifidobacterium spp. (both beneficial bacteria), and Bacteroides spp. (beta-glucuronidase producing, major component of intestinal flora). Rats were treated with 200 mg/kg irinotecan and killed at various time points up to 72 h. Rats were monitored for diarrhea. Sections were stained for beta-glucuronidase expression, and faecal DNA was analysed using real time PCR.\n\nQuestion:\nAre faecal microflora and beta-glucuronidase expression altered in an irinotecan-induced diarrhea model in rats?\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 examine change in health-related quality of life in association with clinical outcomes of neuropsychiatric events in systemic lupus erythematosus (SLE). An international study evaluated newly diagnosed SLE patients for neuropsychiatric events attributed to SLE and non-SLE causes. The outcome of events was determined by a physician-completed seven-point scale and compared with patient-completed Short Form 36 (SF-36) health survey questionnaires. Statistical analysis used linear mixed-effects regression models with patient-specific random effects. 274 patients (92% female; 68% Caucasian), from a cohort of 1400, had one or more neuropsychiatric event in which the interval between assessments was 12.3 ± 2 months. The overall difference in change between visits in mental component summary (MCS) scores of the SF-36 was significant (p<0.0001) following adjustments for gender, ethnicity, centre and previous score. A consistent improvement in neuropsychiatric status (N=295) was associated with an increase in the mean (SD) adjusted MCS score of 3.66 (0.89) in SF-36 scores. Between paired visits when the neuropsychiatric status consistently deteriorated (N=30), the adjusted MCS score decreased by 4.00 (1.96). For the physical component summary scores the corresponding changes were +1.73 (0.71) and -0.62 (1.58) (p<0.05), respectively. Changes in SF-36 subscales were in the same direction (p<0.05; with the exception of role physical). Sensitivity analyses confirmed these findings. Adjustment for age, education, medications, SLE disease activity, organ damage, disease duration, attribution and characteristics of neuropsychiatric events did not substantially alter the results.\n\nQuestion:\nAre sF-36 summary and subscale scores reliable outcomes of neuropsychiatric events in systemic lupus erythematosus?\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 purpose of this study was to assess the association of myocardial salvage by cardiac magnetic resonance (CMR) with left ventricular (LV) remodeling and early ST-segment resolution in patients with acute myocardial infarction (MI). Experimental studies revealed that MI size is strongly influenced by the extent of the area at risk (AAR), limiting its accuracy as a marker of reperfusion treatment efficacy in acute MI studies. Hence, an index correcting MI size for AAR extent is warranted. T2-weighted CMR and delayed-enhancement CMR, respectively, enable the determination of AAR and MI size, and the myocardial salvage index (MSI) is calculated by correcting MI size for AAR extent. Nevertheless, the clinical value of CMR-derived MSI has not been evaluated yet. In a prospective cohort of 137 consecutive patients with acutely reperfused ST-segment elevation MI, CMR was performed at 1 week and 4 months. T2-weighted CMR was used to quantify AAR, whereas MI size was detected by delayed-enhancement imaging. MSI was defined as AAR extent minus MI size divided by AAR extent. Adverse LV remodeling was defined as an increase in LV end-systolic volume of >or=15%. The degree of ST-segment resolution 1 h after reperfusion was also calculated. AAR extent was consistently larger than MI size (32+/-15% of LV vs. 18+/-13% of LV, p<0.0001), yielding an MSI of 0.46+/-0.24. MI size was closely related to AAR extent (r=0.81, p<0.0001). After correction for the main baseline characteristics by multivariate analyses, MSI was a major and independent determinant of adverse LV remodeling (odds ratio: 0.64; 95% confidence interval: 0.49 to 0.84, p=0.001) and was independently associated with early ST-segment resolution (B coefficient=0.61, p<0.0001).\n\nQuestion:\nDoes myocardial salvage by CMR correlate with LV remodeling and early ST-segment resolution in acute 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.
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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:\nMetabolic disorders with visceral obesity have become a major medical problem associated with the development of hypertension, type 2 diabetes, and dyslipidemia and, ultimately, life-threatening cardiovascular and renal diseases. Adipose tissue dysfunction has been proposed as the cause of visceral obesity-related metabolic disorders, moving the tissue toward a proinflammatory phenotype. Here we first report that adipose tissues from patients and mice with metabolic disorders exhibit decreased expression of ATRAP/Agtrap, which is a specific binding modulator of the angiotensin II type 1 receptor, despite its abundant expression in adipose tissues from normal human and control mice. Subsequently, to examine a functional role of ATRAP in the pathophysiology of metabolic disorders, we produced homozygous ATRAP deficient (Agtrap(-/-)) mice, which exhibited largely normal physiological phenotype at baseline. Under dietary high fat loading, Agtrap(-/-) mice displayed systemic metabolic dysfunction, characterized by an increased accumulation of pad fat, hypertension, dyslipidemia, and insulin resistance, along with adipose tissue inflammation. Conversely, subcutaneous transplantation of donor fat pads overexpressing ATRAP derived from Agtrap transgenic mice to Agtrap(-/-) recipient mice improved the systemic metabolic dysfunction.\n\nQuestion:\nDoes angiotensin receptor-binding protein ATRAP/Agtrap inhibit metabolic dysfunction with visceral obesity?\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:\nUS guidelines recommend at least annual HIV testing for those at risk. This analysis assessed frequency and correlates of infrequent HIV testing and late diagnosis among black men who have sex with men (BMSM). HIV testing history was collected at enrollment from participants in HPTN 061, an HIV prevention trial for at-risk US BMSM. Two definitions of late HIV diagnosis were assessed: CD4 cell count <200 cells per cubic millimeter or <350 cells per cubic millimeter at diagnosis. HPTN 061 enrolled 1553 BMSM. HIV testing questions were completed at enrollment by 1284 (98.7%) of 1301 participants with no previous HIV diagnosis; 272 (21.2%) reported no HIV test in previous 12 months (infrequent testing); 155 of whom (12.1% of the 1284 with testing data) reported never testing. Infrequent HIV testing was associated with: not seeing a medical provider in the previous 6 months (relative risk [RR]: 1.08, 95% confidence interval [CI]: 1.03 to 1.13), being unemployed (RR: 1.04, CI: 1.01 to 1.07), and having high internalized HIV stigma (RR: 1.03, CI: 1.0 to 1.05). New HIV diagnoses were more likely among infrequent testers compared with men tested in the previous year (18.4% vs. 4.4%; odds ratio: 4.8, 95% CI: 3.2 to 7.4). Among men with newly diagnosed HIV, 33 (39.3%) had a CD4 cell count <350 cells per cubic millimeter including 17 (20.2%) with CD4 <200 cells per cubic millimeter.\n\nQuestion:\nAre infrequent HIV testing and late HIV diagnosis common among a cohort of black men who have sex with men in 6 US cities?\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:\nTo validate the AUDIT test for identifying women with excess alcohol consumption and/or dependency syndrome (DS). Descriptive study to validate a test. Two primary care centres and a county drug-dependency centre. 414 women from 18 to 75 recruited at the clinic. Interventions. Social and personal details were obtained through personal interview, their alcohol consumption was quantified and the AUDIT and MALT questionnaires were filled in. Then the semi-structured SCAN interview was conducted (gold standard; DSM-IV and CIE-10 criteria), and analyses were requested (GGT, GOT, GPT, VCM). 186 patients were given a follow-up appointment three-four weeks later (retest). Intra-observer reliability was evaluated with the Kappa index, internal consistency with Cronbach s alpha, and the validity of criteria with indexes of sensitivity and specificity, predictive values and probability quotients. To evaluate the diagnostic performance of the test and the most effective cut-off point, a ROC analysis was run. 11.4% (95% CI, 8.98-13.81) were diagnosed with alcohol abuse (0.5%) or DS (10.9%). The Kappa coefficients of the AUDIT items ranged between 0.685 and 0.795 (P<.001). Internal reliability, with Cronbach s alpha, was 0.932 (95% CI, 0.921-0.941). Test sensitivity was 89.6% (95% CI,76.11-96.02) and specificity was 95.07% (95% CI, 92.18-96.97). The most effective cut-off point was at 6 points.\n\nQuestion:\nDo [ Validation of the AUDIT test for identifying risk consumption and alcohol use disorders in women ]?\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:\nSeveral prior studies have linked serum prealbumin (PA) as a predictor for perioperative infection. However, whether peripheral blood PA levels can be used as an indicator of stroke-associated infection (SAI) is still unclear. In this study, we attempt to find whether serum PA is a meaningful predictor in SAI after an ischemic stroke, so as to provide theoretical basis for clinical treatment. Consecutive patients with acute ischemic stroke who were admitted to our hospital were enrolled and serum PA was collected. A prospective study was conducted to observe the predictive value of PA in the SAI incident in ischemic stroke patients. Of 104 patients, 29 (27.9%) developed an SAI after 7 d of follow-up. The stroke with SAI group had significantly lower PA levels than the stroke without SAI group ( p < 0.05). The optimal cutoff value for predicting SAI was PA ≤ 191 mg/L, with sensitivity and specificity of 58.62% and 81.33%, respectively. Kaplan-Meier survival analysis showed that stroke patients with low serum PA level (PA ≤ 191 mg/L) had a higher SAI rates (log-rank test, χ\n\nQuestion:\nIs serum prealbumin a predictive biomarker for stroke-associated infection after an ischemic stroke?\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 objective of this study was to examine the role of protein kinase C zeta (PKCzeta) in interleukin (IL)-8-mediated activation of Mac-1 (CD11b/CD18) in human neutrophils. Neutrophils were stimulated with IL-8 in the presence or absence of pharmacologic inhibitors of PKC or a myristoylated PKCzeta pseudosubstrate. The resulting changes in Mac-1 surface expression, affinity, and avidity, as measured by clustering, were determined by using a combination of flow cytometry and immunofluorescence (IF). Colocalization of Mac-1 with PKCzeta was also probed using IE Finally, neutrophil adhesion to matrix proteins was examined under static conditions and adhesion to tumor necrosis factor-alpha-stimulated human umbilical vein endothelial cells was examined under flow conditions, using a parallel-plate flow chamber PKCzeta and Mac-1 colocalized following stimulation with IL-8. Blocking PKCzeta prevented IL-8-induced Mac-1 clustering while simultaneously increasing Mac-1 affinity. To determine the relative contribution of affinity versus avidity in neutrophil adhesion, we examined adhesion under both static and flow conditions, and found that blocking PKCzeta prevented neutrophil adhesion, despite increased affinity of Mac-1.\n\nQuestion:\nDoes the atypical zeta ( zeta ) isoform of protein kinase C regulate CD11b/CD18 activation in human neutrophils?\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:\nMetabolic syndrome (MetS) clusters risk factors for age-related conditions including cardiovascular disease and diabetes. Shorter telomere length (TL), a cellular marker for biological age, may predict an individual's deteriorating metabolic condition. We examined whether shorter baseline TL is associated with a worse metabolic profile and with less favorable trajectories of MetS components over a 6-year follow-up. PARTICIPANTS were part of The Netherlands Study of Depression and Anxiety, an ongoing prospective cohort study with 6-year follow-up. This study included 2848 participants age 18-65 years. Baseline TL from leukocytes was determined using qPCR and MetS components (waist circumference, triglycerides, high-density lipoprotein [HDL] cholesterol, systolic blood pressure, and fasting glucose) were determined at baseline, and after 2 and 6 years. Cross-sectional and longitudinal analyses were adjusted for relevant sociodemographic, lifestyle, and health factors. Shorter baseline TL was cross-sectionally associated with HDL (β = -0.016, SE = 0.008, P = .05), waist circumference (β = 0.647, SE = 0.238, P = .007), triglycerides (β = 0.038, SE = 0.009, P < .001), and fasting glucose (β = 0.011, SE = 0.003, P < .001), as well as with the total number of MetS components (β = 0.075, SE = 0.023, P = .001) and the presence of MetS (OR = 1.19; 95% CI, 1.07-1.33; P = .002). Although baseline differences progressively reduced over time, shorter baseline TL was still significantly associated with unfavorable scores of most MetS components at the 2- or 6-year follow-up.\n\nQuestion:\nIs telomere length as a marker of cellular aging associated with prevalence and progression of metabolic 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:\nTransketolase-like (TKTL) 1 is one of the key enzymes for anaerobic sugar degradation even in the presence of oxygen (aerobic glycolysis). Transketolase-dependent reactions supply malignant tumors with ribose and NADPH. Therefore, TKTL1 activity could be crucial for tumor proliferation and survival. The aim of the study was to evaluate the expression of TKTL1 in colorectal cancer (CRC) and its regulation under hypoxic conditions. We studied TKTL1 mRNA and protein expression in CRC cell lines and human CRC biopsies by quantitative real-time PCR, Western blotting and immunohistochemistry. Regulation of TKTL1 under oxygen depletion was analyzed by cultivating cells either in a three-dimensional spheroid model or in a hypoxia incubator chamber. TKTL1 mRNA was heterogeneously expressed in monolayers of cells with high levels in HT-29 and SW480. TKTL1 protein was also clearly detectable in HT-29 and SW480. Hypoxia-inducible factor (HIF)-1α protein expression correlated with TKTL1 protein expression in SW480 spheroids over time. On the one hand, induction of hypoxia in T84 spheroids did not induce TKTL1; on the other hand, hypoxia by incubation at 1% O₂ in a hypoxia incubator chamber clearly showed an upregulation of TKTL1. In 50% of CRC patients, TKTL1 protein expression was upregulated in tumor compared to non-tumor tissue. The immunohistochemical staining of TKTL1 in CRC patient samples resulted in 14 positive and 30 negative samples.\n\nQuestion:\nDoes hypoxia induce the expression of transketolase-like 1 in human colorectal 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 determine whether conjunctivochalasis (CCh) interferes with tear flow from the fornix to the tear meniscus and depletes the fornix tear reservoir. Comparative case series. The study group of 24 CCh patients (8 asymptomatic and 16 symptomatic), 9 of whom underwent operative correction, was compared with a control group of 13 normal subjects. After instilling a 5-μl fluorescein drop into the inferior fornix, the inferior tear meniscus was depleted using a capillary tube. The tear meniscus height, with and without blinking, was recorded and calculated by video meniscometer from sequential captured images. The recovery rate of the original meniscus height was compared among groups at each time point after maximal depletion. The recovery rate of the tear meniscus was significantly slower in symptomatic than asymptomatic CCh patients when compared with normal subjects. Blinking 5 times facilitated such recovery in normal subjects and in asymptomatic CCh patients to the same extent as the normal, but not in symptomatic CCh patients. Deepening of the inferior fornix by removing degenerated Tenon's and reconstruction by cryopreserved amniotic membrane improved the recovery rate in symptomatic CCh patients to the same extent as normal subjects.\n\nQuestion:\nDoes conjunctivochalasis interfere with tear flow from fornix to tear meniscus?\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:\nWide geographic variations in cardiac rehabilitation (CR) participation in the United States have been demonstrated but are not well understood. Socioeconomic factors such as educational attainment are robust predictors of many health-related behaviors, including smoking, obesity, physical activity, substance abuse, and cardiovascular disease. We investigated potential associations between state-level differences in educational attainment, other socioeconomic factors, CR program availability, and variations in CR participation. A retrospective database analysis was conducted using data from the US Census Bureau, the Centers for Disease Control and Prevention, and the 1997 Medicare database. The outcome of interest was CR participation rates by state, and predictors included state-level high school (HS) graduation rates (in 2001 and 1970), median household income, smoking rates, density of CR program (programs per square mile and per state population), sex and race ratios, and median age. The relationship between HS graduation rates and CR participation by state was significant for both 2001 and 1970 (r = 0.64 and 0.44, respectively, P < .01). Adding the density of CR programs (per population) and income contributed significantly with a cumulative r value of 0.74 and 0.71 for the models using 2001 and 1970, respectively (Ps < .01). The amount of variance accounted for by each of the 3 variables differed between the 2000 and 1970 graduation rates, but both models were unaltered by including additional variables.\n\nQuestion:\nAre state-by-state variations in cardiac rehabilitation participation associated with educational attainment , income , and program availability?\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:\nAmyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder leading to progressive motor neuron cell death. Etiopathogenesis is still imperfectly known and much effort have been undertaken to find a biological marker that could help in the early diagnosis and in the monitoring of disease progression. Cerebrospinal fluid (CSF) concentrations of tau, an axonal microtubule-associated protein, have been measured in ALS with levels found increased in some studies and unchanged in others. Total CSF tau level was assayed in a population of ALS patients (n = 57) and controls (n = 110) using a specific ELISA method. No significant differences in the median CSF tau levels between ALS cases and controls were found [ALS: 126 pg/ml (78-222); controls: 112 pg/ml (71-188), P = ns]. In the ALS group, the bulbar-onset patients showed increased CSF tau levels as compared with the spinal-onset cases. These differences might be related to the higher age of the bulbar-onset patients. Further, no correlations were found between CSF tau concentrations and the rate of progression of the disease.\n\nQuestion:\nIs cerebrospinal fluid tau protein a biological marker in amyotrophic lateral sclerosis?\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:\nIn pig-to-primate organ transplantation, hyperacute rejection can be prevented, but the organ is rejected within days by acute vascular rejection, in which induced high-affinity anti-Gal alpha1-3Gal (alphaGal) IgG and possibly antibodies directed against new porcine (non-alphaGal) antigenic determinants are considered to play a major role. We have explored the role of an anti-CD40L monoclonal antibody in modifying the humoral response to porcine hematopoietic cells in baboons pretreated with a nonmyeloablative regimen. Porcine peripheral blood mobilized progenitor cells obtained by leukapheresis from both major histocompatibility complex-inbred miniature swine (n=7) and human decay-accelerating factor pigs (n=3) were transplanted into baboons. Group 1 baboons (n=3) underwent whole body (300 cGy) and thymic (700 cGy) irradiation, T cell depletion with ATG, complement depletion with cobra venom factor, short courses of cyclosporine, mycophenolate mofetil, porcine hematopoietic growth factors, and anti-alphaGal antibody depletion by immunoadsorption before transplantation of high doses (2-4 x 10(10)/cells/kg) of peripheral blood mobilized progenitor cells. In group 2 (n=5), cyclosporine was replaced by eight doses of anti-CD40L monoclonal antibodies over 14 days. The group 3 baboons (n=2) received the group 1 regimen plus 2 doses of anti-CD40L monoclonal antibodies (on days 0 and 2). In group 1, sensitization to alphaGal (with increases in IgM and IgG of 3- to 6-fold and 100-fold, respectively) and the development of antibodies to new non-alphaGal porcine antigens occurred within 20 days. In group 2, no sensitization to alphaGal or non-alphaGal determinants was seen, but alphaGal-reactive antibodies did return to their pre- peripheral blood mobilized progenitor cells transplant levels. In group 3, attenuated sensitization to alphaGal antigens was seen after cessation of cyclosporine and mycophenolate mofetil therapy at 30 days (IgM 4-fold, IgG 8-30-fold), but no antibodies developed against new porcine determinants. In no baboon did anti-CD40L monoclonal antibodies prevent sensitization to its own murine antigens.\n\nQuestion:\nDoes high-dose porcine hematopoietic cell transplantation combined with CD40 ligand blockade in baboons prevent an induced anti-pig humoral response?\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:\nPhysical inactivity represents a major risk for cardiovascular disorders, such as hypertension, myocardial infarction or sudden death; however, underlying mechanisms are not clearly elucidated. Clinical and epidemiological investigations suggest, beyond molecular changes, the possibility of an induced impairment in autonomic cardiovascular regulation. However, this hypothesis has not been tested directly. Accordingly, we planned a study with noninvasive, minimally intrusive, techniques on healthy volunteers. Participants were maintained for 90 days strictly in bed, 24 h a day, in head-down (-6 degrees ) position (HDBR). Physical activity was thus virtually abolished for the entire period of HDBR. We examined efferent muscle sympathetic nerve activity, as a measure of vascular sympathetic control, baroreceptor reflex sensitivity, heart rate variability (assessing cardiovagal regulation), RR and systolic arterial pressure and low-frequency and high-frequency normalized components (as a window on central oscillatory regulation). Measures were obtained at rest and during simple maneuvers (moderate handgrip, lower body negative pressure and active standing) to assess potential changes in autonomic cardiovascular responsiveness to standard stimuli and the related oscillatory profiles. HDBR transiently reduced muscle sympathetic nerve activity, RR, heart rate variability and baroreceptor reflex sensitivity late during HDBR or early during the recovery phase. Conversely, oscillatory profiles of RR and systolic arterial pressure variability were maintained throughout. Responsiveness to test stimuli was also largely maintained.\n\nQuestion:\nDoes prolonged head down bed rest-induced inactivity impair tonic autonomic regulation while sparing oscillatory cardiovascular rhythms in healthy humans?\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 the association between CCR5 and CCR2b genotype and the clinical manifestation of first and subsequent AIDS-defining illnesses (ADIs). The distribution of ADIs was examined by CCR5 and CCR2b genotype in a subset of homosexual men enrolled in the Sydney AIDS Prospective Study. The expected number of ADIs was calculated from rates observed in the same tertiary hospital over the same period. Information on initial ADI was collected for 117 homosexual men diagnosed with AIDS before January 1998. Of these individuals, 17 were heterozygous for the CCR5-Delta32 mutation and 11 were heterozygous for CCR2b-64I. The number of observed cases of Pneumocystis carinii pneumonia (PCP), toxoplasmosis, Mycobacterium avium complex (MAC) and cryptosporidiosis reported as a first ADI was substantially fewer in people heterozygous for the CCR5-Delta32 mutation than for those without the mutation, despite similar age, CD4 T-cell count at AIDS diagnosis, year of AIDS diagnosis and receipt of antiretroviral treatment. In addition, among individuals heterozygous for CCR5-Delta32 there were fewer cases of PCP, toxoplasmosis, MAC, and cryptosporidiosis observed as subsequent ADIs compared to the number expected, based on rates measured in the same hospital during the same period (seven observed vs. 24 expected, RR = 0.3, 95% CI = 0.01-0.6). The distribution of first and subsequent ADIs did not differ from the number expected in individuals heterozygous for the CCR2b-64I mutation.\n\nQuestion:\nDoes heterozygosity for CCR5-Delta32 but not CCR2b-64I protect against certain intracellular pathogens?\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 15 (IL15) promotes activation and proliferation of CD8+ T cells and enhances the differentiation into Th2 cells. A previous study described five polymorphisms in the IL15 gene to be associated with asthma in a haplotype analysis. We selected HapMap tagging single nucleotide polymorphisms (SNPs) from IL15 to systematically investigate these IL15 associations in a large population-based sample. Genotyping of seven IL15 SNPs was performed using MALDI-TOF MS in a cross-sectional study population of 3099 children from Dresden or Munich (age 9-11 years). All children were phenotyped by standardized and validated protocols for atopic phenotypes. Effects of single SNPs and haplotypes were studied using sas 9.1.3 and haploview. Equivalence tests were performed to prove the significance of negative results. Neither single IL15 polymorphisms nor haplotype analyses showed associations with asthma or atopy after correction for multiple testing.\n\nQuestion:\nAre iL15 gene variants associated with asthma and atopy?\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 examine consistency (interrater reliability) of applying guidance for grading strength of evidence in systematic reviews for the Agency for Healthcare Research and Quality Evidence-based Practice Center program. Using data from two systematic reviews, authors tested the main components of the approach: (1) scoring evidence on the four required domains (risk of bias, consistency, directness, and precision) separately for randomized controlled trials (RCTs) and observational studies and (2) developing an overall strength of evidence grade, given the scores for each of these domains. Conclusions about overall strength of evidence reached by experienced systematic reviewers based on the same evidence can differ greatly, especially for complex bodies of evidence. Current instructions may be sufficient for straightforward quantitative evaluations that use meta-analysis for summarizing RCT findings. In contrast, agreement suffered when evaluations did not lend themselves to meta-analysis and reviewers needed to rely on their own qualitative judgment. Three areas raised particular concern: (1) evidence from a combination of RCTs and observational studies, (2) outcomes with differing measurement, and (3) evidence that appeared to show no differences in outcomes.\n\nQuestion:\nDoes interrater reliability of grading strength of evidence vary with the complexity of the evidence in systematic reviews?\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:\nH. pylori infection significantly attenuated the expression of HSP70 in gastric mucosal cells. However, the role of HSP70 cancellation in H. pylori-associated cell damages is largely unclear. Small interfering RNA (siRNA) was used to down-regulate HSP70 in gastric epithelial cell lines AGS. The transfected cells were then incubated with H. pylori and the functions of HSP70 suppression were observed by viability assay, cell cycle analyses and TUNEL assay. HSP70 target apoptotic proteins were further identified by Western blot. The inhibition of HSP70 has further increased the effect of growth arrest and apoptosis activation triggered by H. pylori in gastric epithelial cells. The anti-proliferation function of HSP70 depletion was at least by up-regulating p21 and cell cycle modulation with S-phase accumulation. An increase of apoptosis-inducing factor (AIF) and cytosolic cytochrome C contributes to the activation of apoptosis following down-regulation of intracellular HSP70. Extracellular HSP70 increased cellular resistance to apoptosis by suppression the release of AIF and cytochrome c from mitochondria, as well as inhibition of p21 expression.\n\nQuestion:\nDoes down-regulation of HSP70 sensitize gastric epithelial cells to apoptosis and growth retardation triggered by H. pylori?\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:\nCore2 1-6-N-glucosaminyltransferase-I (C2GlcNAcT-I) modification of adhesion molecules is required for optimal binding to target ligands. The objective of this study was to determine the role of C2GlcNAcT-I in the recruitment of Ly-6C(hi) monocytes to atherosclerotic lesions and in lesion formation in mice. In a whole-blood binding assay, Ly-6C(hi) monocytes and certain lymphocytes and natural killer cells from wild-type mice bound to P- and E-selectin. C2GlcNAcT-I deficiency abrogated leukocyte binding to P- and E-selectin in this assay as well as in an in vitro flow chamber assay. Moreover, C2GlcNAcT-I deficiency decreased Ly-6C(hi) monocyte interactions with atherosclerotic arteries under physiological flow conditions and also inhibited monocyte recruitment to the peritoneal cavity in mice challenged with thioglycollate. In apolipoprotein E-deficient (apoE(-/-)) mice, lack of C2GlcNAcT-I resulted in fewer and smaller atherosclerotic lesions in mouse aortas. Atherosclerosis was also suppressed in C2GlcNAcT-I(-/-)/apoE(-/-) chimeric mice transplanted with C2GlcNAcT-I(+/+) bone marrow cells.\n\nQuestion:\nIs core2 1-6-N-glucosaminyltransferase-I crucial for the formation of atherosclerotic lesions in apolipoprotein E-deficient mice?\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 Cqm1 α-glucosidase of Culex quinquefasciatus larvae acts as the midgut receptor for the binary toxin of the biolarvicide Lysinibacillus sphaericus. Mutations within the cqm1 gene can code for aberrant polypeptides that can no longer be properly expressed or bind to the toxin, leading to insect resistance. The cqm1 REC and cqm1 REC-2 alleles were identified in a laboratory selected colony and both displayed mutations that lead to equivalent phenotypes of refractoriness to L. sphaericus. cqm1 REC was first identified as the major resistance allele in this colony but it was subsequently replaced by cqm1 REC-2 , suggesting the better adaptive features of the second allele. The major aim of this study was to evaluate the occurrence of cqm1 REC-2 and track its origin in field populations where cqm1 REC was previously identified. The screening of the cqm1 REC-2 allele was based on more than 2000 C. quinquefasciatus larvae from five localities in the city of Recife, Brazil and used a multiplex PCR assay that is also able to identify cqm1 REC . Full-length sequencing of the cqm1 REC-2 and selected cqm1 samples was performed to identify further polymorphisms between these alleles. The cqm1 REC-2 allele was found in field samples, specifically in two heterozygous individuals from a single locality with an overall frequency and distribution much lower than that observed for cqm1 REC . The full-length sequences from these two cqm1 REC-2 copies were almost identical to the cqm1 REC-2 derived from the resistant colony but displayed more than 30 SNPs when compared with cqm1 and cqm1 REC . The cqm1 REC and cqm1 REC-2 resistant alleles were found to be associated with two distinct sets of wild-type cqm1 variants found in field populations.\n\nQuestion:\nIs a new allele conferring resistance to Lysinibacillus sphaericus detected in low frequency in Culex quinquefasciatus field populations?\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 assess the effectiveness of recombinant human thrombopoietin (rhTPO) in severe aplastic anemia (SAA) patients receiving immunosuppressive therapy (IST). Eighty-eight SAA patients receiving IST from January 2007 to December 2012 were included in this retrospective analysis. Of these, 40 subjects received rhTPO treatment (15000 U, subcutaneously, three times a week). rhTPO treatment was discontinued when the platelet count returned to normal range. Hematologic response, bone marrow megakaryocyte recovery, and time to transfusion independence were compared. Hematologic response was achieved in 42.5%, 62.5%, and 67.5% of patients receiving rhTPO and 22.9%, 41.6%, and 47.9% of patients not receiving rhTPO at 3, 6, and 9 months after treatment, respectively (P = 0.0665, P = 0.0579, and P = 0.0847, resp.). Subjects receiving rhTPO presented an elevated number of megakaryocytes at 3, 6, and 9 months when compared with those without treatment (P = 0.025, P = 0.021, and P = 0.011, resp.). The time to platelet and red blood cell transfusion independence was shorter in patients who received rhTPO than in those without rhTPO treatment. Overall survival rate presented no differences between the two groups.\n\nQuestion:\nDoes recombinant human thrombopoietin treatment promote hematopoiesis recovery in patients with severe aplastic anemia receiving immunosuppressive therapy?\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:\nPathological angiogenesis is an intrinsic component of chronic intestinal inflammation, which results in remodeling and expansion of the gut microvascular bed. Endoglin is essential for endothelial cell function and physiological angiogenesis. In this study we investigated its potential role in the regulation of inflammation by testing the response of Endoglin heterozygous (Eng(+/-)) mice to experimental colitis. C57BL/6 Eng(+/-) and littermate control mice drank water supplemented with 3% dextran sulfate sodium (DSS) for 5 days and were monitored for up to 26 days for clinical signs of colitis. Inflammation, crypt damage, and angiogenic index were scored on histological sections of distal colon. Levels of the vascular endothelial growth factor (VEGF) and angiopoietins were measured by real-time polymerase chain reaction, enzyme-linked immunosorbent assay, and/or Western blots. Vascular permeability was assessed using Evans Blue. Eng(+/-) and control mice developed acute colitis, which peaked at day 9. While control mice recovered by days 19-26, Eng(+/-) mice progressed to chronic colitis and showed numerous vascular protrusions penetrating into the serosa of the inflamed distal colon. Prior to DSS induction, VEGF levels and vascular permeability were higher in the distal colon of Eng(+/-) mice, while angiopoietin 1 and 2 levels were unchanged. In the chronic phase of colitis, VEGF levels were increased in both groups of mice and remained significantly higher in the Eng(+/-) mice.\n\nQuestion:\nDoes dextran sulfate sodium lead to chronic colitis and pathological angiogenesis in Endoglin heterozygous mice?\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 evaluate if placental histopathological changes of vascular insufficiency correlate with circulating angiogenic factors in patients with preeclampsia. Subjects were selected from a previous prospective cohort study of preeclampsia based on the availability of plasma anti-angiogenic factor (sFlt1) and pro-angiogenic factor (PlGF) measurements and placental histology specimens. Preeclamptic patients were divided into two groups based on plasma levels of these factors described as a ratio: anti-angiogenic preeclampsia with sFlt1/PlGF ratio ≥85 and normal angiogenic preeclampsia with sFlt1/PlGF < 85. The placental lesions of vascular insufficiency that were studied specifically included atherosis, infarcts, syncytial knots, acute and chronic abruption, hematoma, and fetal thrombosis. The data are shown as median (quartile 1 and quartile 3) or n (%) when appropriate. The anti-angiogenic preeclampsia group (N = 48) presented at an earlier gestational age (weeks) than the normal angiogenic group (N = 28); {32 (28, 34) versus 35 (32, 36), p = 0.002}, had higher systolic blood pressure (mmHg) {154 (147, 168) versus 147 (132, 158), p = 0.02}, delivered early (weeks) {(32 (29, 34) versus 36 (34, 37), p < 0.001} and had lower birth weight (grams) {(1550 (1055, 2060) versus 2655 (2285, 3343), p < 0.001}. Several pathologic lesions were found significantly more often in the anti-angiogenic preeclampsia group; atherosis {27.7% versus 3.6%, p < 0.05}, infarcts {58.3% versus 3.6%, p = 0.002}, and syncytial knots {81.3% versus 39.3%, p < 0.001}.\n\nQuestion:\nAre placental lesions of vascular insufficiency associated with anti-angiogenic state in women with preeclampsia?\n\nAnswer:",
"role": "user"
},
{
"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:\nThe compound, diazoxide (DZ), is known to induce preconditioning through its effect as a mitochondrial K(ATP) channel opener and succinate dehydrogenase inhibitor. Our team tested the hypothesis that pharmacological induction of ischemic preconditioning with DZ can offer cytoprotection and preserve vital tissues after hemorrhagic shock and stroke. Sprague-Dawley male rats received an intraperitoneal injection of sterile saline or 5 mg/kg DZ in saline 24 h prior to 1 h of hemorrhagic shock, by approximately 40% total blood loss volume (Shock Study), or a permanent unilateral common carotid ligation just before shock (Stroke + Shock Study). While remaining under isoflurane anesthesia, animals then received 81 mL/kg intravenous sterile saline over the next 45 min for recovery and survived for another 24 h. When DZ was administered 24 h prior to shock, it significantly reduced hyperglycemia, which in vehicle-treated animals persisted after resuscitation. DZ also attenuated hyperlactatemia during the 1-h shock period. With more severe trauma from combined stroke and shock, DZ also decreased hyperlactatemia and hyperglycemia levels but the reduction was only significant for hyperglycemia. The expression levels of heat shock proteins 25 (HSP25) and 70 (HSP70) were used as biomarkers for response of the kidney and liver to DZ and combined stroke and shock. Compared to vehicle-treated animals, DZ-treated rats subjected to shock and stroke exhibited increased HSP25 and HSP70 in kidney and liver tissue.\n\nQuestion:\nDoes diazoxide increase liver and kidney HSP25 and HSP70 after shock and stroke?\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 the efficacy of ciliary body endophotocoagulation during pars plana vitrectomy in eyes of pediatric patients with medically uncontrolled glaucoma. We compared preoperative and postoperative intraocular pressure and visual acuity in five eyes of five patients aged between 10 months and 14.5 years who had 180 degrees of ciliary body endophotocoagulation with pars plana vitrectomy. Preoperative intraocular pressure on medical therapy for glaucoma ranged from 30 to 55 mm Hg (median, 35 mm Hg). Postoperative follow-up ranged from 12 to 24 months, with a median of 16 months. Postoperative intraocular pressure on medical therapy ranged from 12 to 35 mm Hg (median, 25 mm Hg) at 6 weeks, from 12 to 33 mm Hg (median, 29 mm Hg) at 6 months, and from 12 to 29 mm Hg (median, 27 mm Hg) at 12 months. Twelve months after surgery, mean intraocular pressure reduction of 20 mm Hg was statistically significant (P = .020).\n\nQuestion:\nDo ciliary body endophotocoagulation during pars plana vitrectomy for pediatric patients with vitreoretinal disorders and glaucoma?\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 purpose of this study was to investigate the efficacy of an experimental dentin conditioner consisting of ascorbic acid (AA) and ferric chloride (Fe), in terms of micro-tensile bond strength (microTBS). Five experimental solutions were prepared and evaluated: 10% AA and 5% Fe (10AA-5Fe); 10% AA and 0% Fe (10AA-0Fe); 0% AA and 5% Fe (0AA-5Fe); 10% citric acid and 3% ferric chloride (10-3); and, 0% AA and 0% Fe (0AA-0Fe). Flattened dentin surfaces were treated with each of the experimental solutions. A composite material rod was bonded to the dentin surface with a self curing luting agent (4-META/MMA-TBB resin). The specimens were stressed to failure under tension after 24h of immersion in water. The 10AA-5Fe group showed significantly higher bond strength than the 10AA-0Fe, 0AA-5Fe, 10-3 and AA-0Fe groups.\n\nQuestion:\nDoes surface treatment with ascorbic acid and ferric chloride improve the micro-tensile bond strength of 4-META/MMA-TBB resin to dentin?\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 study the basal and ACTH stimulated production of corticosterone by adrenal cortex on one hand and the binding and degradation of corticosterone in the liver of adult rats which were treated with monosodium glutamate (MSG) during the neonatal period. Male offsprings of Sprague-Dawley rats were injected i.p. with MSG (4 mg/g of b.w. in saline) on alternated days for the first 10 days of life, their littermates being used as controls. On the 21st postnatal day they were weaned and used for the observation at the age of 65-75 days. After sacrifice the level of corticosterone in serum and the release of corticosterone from incubated adrenals under basal and ACTH stimulated conditions (ACTH in 6 concentrations from 1.25 to 80 mU/ml medium) were estimated. In addition, glucocorticoid binding to cytosol receptors in the liver and muscle tissues was determined. Corticosterone degradation rate was measured by decrease of corticosterone concentration added to the medium after the incubation with liver slices. Adult rats neonatally treated with MSG had reduced weight of adrenal glands, while plasma corticosterone levels and its basal production by adrenals in vitro were significantly higher than in controls. In MSG treated rats the stimulation of corticosterone production by ACTH was diminished. Glucocorticoid binding to liver cytosolic receptors was significantly decreased, while that in muscle tissue was only slightly elevated. Moreover, a decreased corticosterone degradation rate in liver slices was observed in rats treated neonatally with MSG.\n\nQuestion:\nDoes postnatal monosodium glutamate treatment result in attenuation of corticosterone metabolic rate in adult rats?\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:\nTo study the effects of suberoyl bis-hydroxamic acid (SBHA), an inhibitor of histone deacetylases, on the apoptosis of MCF-7 breast cancer cells. Apoptosis in MCF-7 cells induced by SBHA was demonstrated by flow cytometric analysis, morphological observation, and DNA ladder. Mitochondrial membrane potential (DeltaPsim) was measured using the fluorescent probe JC-1. The expressions of p53, p21, Bax, and PUMA were determined using RT-PCR or Western blotting analysis after the MCF-7 cells were treated with SBHA or p53 siRNA. SBHA induced apoptosis in MCF-7 cells. The expressions of p53, p21, Bax, and PUMA were induced, and DeltaPsim collapsed after treatment with SBHA. p53 siRNA abrogated the SBHA-induced apoptosis and the expressions of p53, p21, Bax, and PUMA.\n\nQuestion:\nDoes suberoyl bis-hydroxamic acid induce p53-dependent apoptosis of MCF-7 breast cancer 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:\nThin-skin grafts taken from the thigh or buttock take a long time to heal and leave permanent scars. The authors conducted a retrospective study based on their experience with 945 thin-skin grafts (0.2 mm) taken from the scalps of 757 adult patients between January of 1999 and December of 2003. Of the 757 patients, 89 had grafts taken repeatedly from the scalp. The mean healing time was 6.2 days for a single harvest and 10.2 days for repeated (same hospitalization) harvests. During follow-up, eight patients had microalopecia and three developed \"concrete scalp deformity.\" Of these 11 patients, eight had undergone repeated harvests. None of the other patients had any scarring; they were completely healed by day 15.\n\nQuestion:\nIs the scalp an advantageous donor site for thin-skin grafts : a report on 945 harvested samples?\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:\nSince the hepatic extracellular matrix is remodeled in liver regeneration, we investigated whether increased collagenase activity in the liver can induce hepatocyte proliferation in vivo. To increase hepatic collagenase activity, human matrix metalloproteinase-1 was delivered to the rat liver by the recombinant adenoviral vector Ad5MMP-1. Hepatic delivery of Ad5MMP-1 increased the 5-bromo-2-deoxyuridine labeling index and mitotic index in hepatocytes, causing an increase in the dry liver weight; control adenovirus, Ad5LacZ, had minimal effect. Hepatocyte proliferation started approximately 48 h after infection with Ad5MMP-1 and ended after about 2 weeks. The increase in the dry liver weight also returned to baseline after 2 weeks. Transient liver injury by Ad5MMP-1, reflected by increased aspartate and alanine aminotransferase levels, peaked around 1 week, and was associated with hepatocyte apoptosis. Collagenase-induced hepatocyte proliferation was accompanied by cytoplasmic accumulation of beta-catenin and a transient decrease in E-cadherin expression.\n\nQuestion:\nDoes increased expression of collagenase in the liver induce hepatocyte proliferation with cytoplasmic accumulation of beta-catenin in the rat?\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:\nIn utero hematopoietic stem-cell transplantation has been shown to induce donor-specific tolerance in small-animal models. However, tolerance has been difficult to achieve in large-animal studies. Outbred swine underwent in utero transplantation of fully major histocompatibility complex (MHC)-mismatched CD3-depleted bone marrow mixed with fresh bone marrow to achieve a final CD3 content of 1.5%. Transplantation was performed at 50 to 55 days' gestation and two animals survived long term and demonstrated multilineage peripheral blood hematopoietic chimerism. These two long-term survivors were analyzed for in vitro evidence of donor-specific tolerance by mixed leukocyte reaction (MLR), cell-mediated lysis (CML), and antibody testing and in vivo by kidney transplantation. Both animals demonstrated in vitro donor-specific unresponsiveness by MLR and CML and did not demonstrate anti-donor antibody production. Donor matched kidney transplants were performed without immunosuppression and functioned for more than 100 days, with no evidence for rejection.\n\nQuestion:\nDoes in utero bone marrow transplantation induce kidney allograft tolerance across a full major histocompatibility complex barrier in Swine?\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:\nTo investigate whether common variants across the LBP gene contribute to the development of severe sepsis. Sepsis is the leading cause of multiple system organ dysfunction and death in critically ill patients. The lipopolysaccharide-binding protein is an acute-phase protein that plays a dominant role in the genesis of sepsis by initiating signal transduction pathways leading to the activation of the inflammatory host response. Prospectively enrolled case-control study of adults with severe sepsis. A network of intensive care units. We enrolled 175 patients meeting international definition criteria for severe sepsis and 357 population-based controls for comparison. Genotyping of the LBP gene was performed and disease association was tested. Serum lipopolysaccharide-binding protein levels were measured in patients and related to genetic variants. A haplotype window analysis revealed that a common 4-SNP risk haplotype from the 5'-flanking region of the LBP gene, comprising positions -1978 to -763 from the transcription start site, was strongly associated with susceptibility to severe sepsis. Risk haplotype homozygous carriers had an increased risk for severe sepsis (odds ratio = 2.21; 95% confidence interval = 1.39-3.51; unadjusted p < .001; adjusted p < .025). Mean serum lipopolysaccharide-binding protein levels from inclusion to 7th day were significantly higher in homozygous carriers patients (130.1 [102.9-164.5] and 98.9 [79.7-122.8] microg/mL, respectively) than in noncarriers (101.6 [87.9-117.5] and 58.7 [51.4-67.2] microg/mL, respectively) (p = .046).\n\nQuestion:\nDoes a common haplotype of the LBP gene predispose to severe sepsis?\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:\nThe aim of the study was to investigate whether erythropoietin (EPO) could protect against white matter damage (WMD) in a preterm equivalent neonatal rat hypoxic-ischemia (HI) model. 113 two-day-old male rat pups were divided randomly into three groups: sham-treated, bilateral carotid artery occlusion (BCAO)-treated, BCAO + EPO-treated group. EPO (50 U/10 g body weight) or saline alone was administered intraperitoneally immediately after BCAO surgery. Body weight, brain weight, brain water content, and expression of myelin basic protein (MBP) were assessed at day 1, 3, 7, and 14 after HI insult. Morris water-maze (MWM) test was used to assess neurological behavior from day 31 to 35 after HI insult. Body weights of BCAO + EPO group were greater than those of BCAO group rats (P < 0.05). Specifically, at day 3 and 7 after HI, brain weights of BCAO + EPO-treated rats were higher than BCAO-treated animals (P < 0.05); at day 7 and 14 after HI, MBP of BCAO + EPO-treated rats were higher than BCAO-treated animals (P < 0.05). Similarly, the brain water content at day 3 after HI in BCAO + EPO-treated rats was lower than BCAO-treated animals (P < 0.05). The body weight, brain weight, brain water content, and MBP expression in BCAO + EPO-treated group were comparable to those in the sham-treated group. Spatial learning and memory of BCAO + EPO-treated rats was significantly improved over the BCAO-treated group and was comparable to the sham-operated animals.\n\nQuestion:\nDoes erythropoietin reduce white matter damage in two-day-old rats exposed to hypoxic/ischemia injury?\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:\nEven though anaemia has been shown to be a risk factor for adverse cardiovascular disease, there is scarce evidence of its relationship with angiographically proven coronary artery disease (CAD). The aim of this study was to evaluate the relationship between haemoglobin (Hb) levels and the extent of CAD. We measured Hb, mean corpuscular volume and red blood cell count in 2363 consecutive patients undergoing coronary angiography. Patients were divided into four groups according to quartile values of Hb (≤12.2 g/dl, group 1; 12.3-13.5 g/dl, group 2; 13.6-14.6 g/dl, group 3; >14.6 g/dl, group 4). Patients with lower Hb were older (P<0.001), there was a predominance of women (P<0.0001), and patients had diabetes (P<0.0001), hypertension (P=0.024), renal failure (P<0.0001), previous coronary artery bypass graft (P<0.0001), previous cerebrovascular accident (P=0.039) and platelet count (P<0.0001). In terms of angiographic features, low Hb levels were associated with a larger prevalence of calcified lesions (P<0.001), but a lower prevalence of thrombus-containing lesions (P<0.001). Hb was not associated with the prevalence of CAD [odds ratio (OR) (95% confidence interval (CI))=0.96 (0.89-1.04), P=0.35], whereas an association was observed with the severity of CAD [OR (95% CI)=0.92 (0.85-0.99), P=0.032] that was not confirmed after correction for baseline confounding factors [OR (95% CI)=0.98 (0.89-1.09), P=0.76]. Similar findings were observed for mean corpuscular volume and red blood cell count.\n\nQuestion:\nDo haemoglobin levels correlate with the extent of coronary artery disease : results from a large cohort study?\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:\nThe purpose of the study is to determine the effect of exogenous vascular endothelial growth factor (VEGF) on the primate retina and its vasculature. Ten eyes of five animals were studied. Physiologically relevant amounts of the 165 amino acid isoform of human recombinant VEGF were injected into the vitreous of six healthy cynomolgus monkey eyes. Inactivated human recombinant VEGF or vehicle was injected into four contralateral control subject eyes. Eyes were assessed by slit-lamp biomicroscopy, tonometry, fundus color photography, fundus fluorescein angiography, light microscopy, and immunostaining with antibodies against proliferating cell nuclear antigen and factor VIII antigen. All six bioactive VEGF-injected eyes developed dilated, tortuous retinal vessels that leaked fluorescein. Eyes receiving multiple injections of VEGF developed progressively dilated and tortuous vessels, venous beading, edema, microaneurysms, intraretinal hemorrhages and capillary closure with ischemia. The severity of the retinopathy correlated with the number of VEGF injections. None of the four control eyes exhibited any abnormal retinal vascular changes. The endothelial cells of retinal blood vessels were proliferating cell nuclear antigen positive only in the bioactive VEGF-injected eyes.\n\nQuestion:\nDo intravitreous injections of vascular endothelial growth factor produce retinal ischemia and microangiopathy in an adult primate?\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 Wave complex activates the Arp2/3 complex, inducing actin polymerization in lamellipodia and membrane ruffles. The Wave complex is composed of five subunits, the smallest of which, Brick1/Hspc300 (Brk1), is the least characterized. We previously reported that, unlike the other subunits, Brk1 also exists as a free form. Here we report that this free form of Brk1 is composed of homotrimers. Using a novel assay in which purified free Brk1 is electroporated into HeLa cells, we were able to follow its biochemical fate in cells and to show that free Brk1 becomes incorporated into the Wave complex. Importantly, incorporation of free Brk1 into the Wave complex was blocked upon inhibition of protein synthesis and incorporated Brk1 was found to associate preferentially with neosynthesized subunits. Brk1 depleted HeLa cells were found to bleb, as were Nap1, Wave2 or ARPC2 depleted cells, suggesting that this blebbing phenotype of Brk1 depleted cells is due to an impairment of the Wave complex function rather than a specific function of free Brk1. Blebs of Brk1 depleted cells were emitted at sites where lamellipodia and membrane ruffles were normally emitted. In Brk1 depleted cells, the electroporation of free Brk1 was sufficient to restore Wave complex assembly and to rescue the blebbing phenotype.\n\nQuestion:\nIs free Brick1 a trimeric precursor in the assembly of a functional wave complex?\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:\nIt has been suggested that overweight is negatively associated with cognitive functions. The aim of this study was to investigate whether a reduction in body weight by dietary interventions could improve episodic memory performance and alter associated functional brain responses in overweight and obese women. 20 overweight postmenopausal women were randomized to either a modified paleolithic diet or a standard diet adhering to the Nordic Nutrition Recommendations for 6 months. We used functional magnetic resonance imaging to examine brain function during an episodic memory task as well as anthropometric and biochemical data before and after the interventions. Episodic memory performance improved significantly (p = 0.010) after the dietary interventions. Concomitantly, brain activity increased in the anterior part of the right hippocampus during memory encoding, without differences between diets. This was associated with decreased levels of plasma free fatty acids (FFA). Brain activity increased in pre-frontal cortex and superior/middle temporal gyri. The magnitude of increase correlated with waist circumference reduction. During episodic retrieval, brain activity decreased in inferior and middle frontal gyri, and increased in middle/superior temporal gyri.\n\nQuestion:\nDoes diet-Induced Weight Loss alter Functional Brain Responses during an Episodic Memory Task?\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:\nInformational masking (IM) refers to the problem of understanding target speech in the simultaneous presence of a masking speech signal. The adverse effects are attributable to the additional information provided by the competing talker. Cochlear implant (CI) recipients are not able to understand speech satisfactorily in situations such as these. The aim of the present study is to examine the extent to which CI recipients are able to use differences between the speakers with respect to level (target-to-masker ratio, TMR) and fundamental frequency (f0) in order to improve speech intelligibility. Target (TS) and masker sentences (MS) were selected from the Oldenburg Sentence Test (OlSa) and were modified and superimposed. The TS were explicitly labelled using a keyword. The MS were changed with respect to TMR and f0. The TS intelligibility of different modifications was measured in six post-lingually deafened CI recipients and six normal listeners (NL). The NL revealed speech understanding close to 100% even for small differences in f0 of 40 Hz or level differences of 5 dB. In CI recipients, a significant change in intelligibility could only be demonstrated with increased TMR, but not with differences in f0.\n\nQuestion:\nDo [ Examining informational masking in cochlear implant users ]?\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 investigate intraocular pressure (IOP) and ocular blood flow (OBF) changes as well as the individual normal range of IOP in patients with age-related macular degeneration (AMD) with or without concomitant glaucoma after intravitreal anti-vascular endothelial growth factor (VEGF) therapy. Group 1 included 34 patients (34 eyes) with AMD and no glaucoma, group 2-34 patients (34 eyes) with both AMD and glaucoma. In all patients the IOP and OBF were measured (with Ocular Blood Flow Analyzer) and the individual normal range of lOP calculated before the treatment, on the third day after the injection and at the 1-month follow-up visit. Statistical analysis was performed by STATISTICA 10. In group 1 there were no significant changes in ocular blood flow at different times after ranibizumab injection. In group 2 a considerable decrease in OBF was detected 1 month after the injection (p<0.001). In group 1 the intraocular pressure was at the same level before and after the treatment. In group 2 the IOP significantly decreased on the third day after the anti-VEGF injection (p=0.03) but was back to the initial level in 1 month. The individual normal range of lOP, when calculated on the third day after the injection, appeared to be much lower than before due to a moderate decrease in both IOP and OBF. At the 1-month follow-up the individual normal range of IOP was back to initial values in non-glaucoma patients but remained low in the glaucoma group due to reduced OBF.\n\nQuestion:\nDoes [ Intraocular pressure and ocular blood flow feature intravitreal infection of anti-vascular endothelial growth factor agents ]?\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:\nDome liver lesions (those in segments VII or VIII) pose a challenge to standard laparoscopic resection. The use of additional intercostal and transthoracic trocars (ITTs) potentially facilitates resection over standard subcostal laparoscopic (SSL) techniques. A retrospective review of a prospectively collected liver resection database was performed, selecting all minor resections of segments VII and VIII using the ITT and SSL approaches. The techniques of intercostal transdiaphragmatic access are described and the surgical outcomes of the two groups compared. A total of 19 patients were analysed. The ITT group included 8 patients and the SSL group included 11. The groups were comparable in median lesion size (20 mm in the ITT group and 26 mm in the SSL group). Blood loss, operative times, morbidity and conversion rates were similar. There was no lung injury or postoperative clinical pneumothorax in any patient undergoing transdiaphragmatic access. Median hospital stay was significantly shorter in the ITT group (2 days) than in the SSL group (6 days) (P = 0.032).\n\nQuestion:\nDo intercostal and transthoracic trocars enable easier laparoscopic resection of dome liver lesions?\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:\nLittle is known about the clinical efficacy of co-therapy of enprostil, a prostaglandin E2 analogue, with a histamine H2-receptor antagonist. We aimed to assess the additive benefit of enprostil in combination with cimetidine for treating gastric ulcer in a prospective multicenter randomized controlled trial. In 43 hospitals 171 intention-to-treat (ITT) patients, diagnosed as having gastric ulcer by endoscopy, were randomly allocated to receive either enprostil 25microg b.i.d. and cimetidine 400mg b.i.d. (Group E=85), or cimetidine 400mg b.i.d. alone (Group C=86) for 8 weeks. Healing was examined by endoscopy at 4 and 8 weeks. Per protocol (PP) analysis comprised 166 patients (E=82, C=84). Despite no significant advantage at 4 weeks (E=55.3%, C=42.2%), the combination yielded higher healing rates at 8 weeks by ITT (E=89.4%, C=68.6%; p<0.001) and PP analysis (E=92.7%, C=70.2%; p<0.001). Symptom relief rates [E, C] at 2, 4, and 8 weeks were [80.2%, 68.3%] (not significant), [97.4%, 88.3%] (p<0.05), and [95.6%, 87.0%] (p<0.05), respectively. Significant advantage was observed in the patients aged 40 or older, with solitary ulcer (>5mm in diameter), and without smoking or drinking habits. No adverse effects were critical.\n\nQuestion:\nIs combination of enprostil and cimetidine more effective than cimetidine alone in treating gastric ulcer : prospective multicenter randomized controlled trial?\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 introduce a new method: small endoscopic sphincterotomy (ES) combined with endoscopic papillary large balloon dilation (SES + EPLBD) to treat patients with large biliary stones. Retrieval of large biliary stones was performed in 88 patients. Mean stone size was 14 +/- 3 mm and mean number of stones was 2.5 +/- 3.5. Firstly, ES with a small incision was performed. Next, endoscopic papillary dilation was performed with a large balloon to slowly match the size of the bile duct. Stones were then retrieved from the biliary duct with a balloon and a basket. Stone retrieval was successful in all cases except one cystic duct stone case without the need to crush large stones. Mean procedure time was 30 +/- 5 min. Dilating the papillary orifice with a large balloon made it possible to remove large stones smoothly without crushing them. After dilation with the large balloon, there were some instances of oozing, but no perforations. One instance of post-procedural pancreatitis (1%) occurred.\n\nQuestion:\nDoes small sphincterotomy combined with papillary dilation with large balloon permit retrieval of large stones without mechanical lithotripsy?\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:\nAssociations of IRS1 genetic variation with adiposity and metabolic profile in U.S. Hispanic/Latino individuals of diverse backgrounds were examined. Previously genome-wide association study-identified IRS1 variants (rs2943650, rs2972146, rs2943641, and rs2943634) as related to body fat percentage (BF%) and multiple metabolic traits were tested among up to 12,730 adults (5,232 men; 7,515 women) from the Hispanic Community Health Study/Study of Latinos. The C-allele (frequency = 26%) of rs2943650 was significantly associated with higher BF% overall (β = 0.34 ± 0.11% per allele; P = 0.002) and in women (β = 0.41 ± 0.14% per C-allele; P = 0.003), but not in men (β = 0.28 ± 0.18% per C-allele; P = 0.11), though there was no significant sex difference. Using the inverse normal-transformed data to compare effect sizes, it was found that the association with BF% was stronger in Hispanic/Latino women than that previously reported in European women (β = 0.054 ± 0.018SD vs. β = 0.008 ± 0.011SD per C-allele; P = 0.03). The BF%-increasing allele of rs2943650 was significantly associated with lower levels of fasting insulin, homeostatic model assessment of insulin resistance, hemoglobin A1c, and triglycerides and higher high-density lipoprotein cholesterol (P < 0.05).\n\nQuestion:\nIs genetic variation near IRS1 associated with adiposity and a favorable metabolic profile in U.S. Hispanics/Latinos?\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:\nInjury-mediated corneal epithelial wound healing in vivo is mediated through different cell signaling pathways depending on whether or not the basement membrane is removed. Given this dependence, we ascertained if c-jun N-terminal kinase (JNK/SAPK) mitogen-activated protein kinase (MAPK) cell signaling mediates this response in vivo and in vitro, irrespective of the presence or absence of the basement membrane. Furthermore, in vitro the relative contribution was determined by the JNK/SAPK pathway to that of its p38 and ERK MAPK counterparts in mediating injury-induced increases in cell migration. Corneal epithelial debridement was performed in C57BL/6 mice and their organ-cultured eyes without removal of the basement membrane. In rabbits, following basement membrane removal by keratectomy, fluorescein-staining monitored reepithelialization was performed as in the mice. Immunohistochemistry evaluated changes in JNK phosphorylation status and localization. JNK inhibitor I and its inactive analogue determined if JNK signaling activation contributes to wound healing. BrdU staining assessed cell proliferation. A scratch wound assay of healing rates in SV40-immortalized human corneal epithelial cell line (HCEC) evaluated the relative contributions by p38 and ERK and JNK MAPK signaling activation to wound healing. A TUNEL assay probed for apoptosis after wound closure of HCEC. MTT assay evaluated corneal epithelial viability. Two hours following mice corneal epithelial debridement, phospho-JNK was transiently upregulated in the nucleus, whereas total JNK was constitutively expressed. JNK inhibitor I suppressed epithelial spreading in organ-cultured mouse eyes and rabbit corneal blocks, irrespective of the presence or absence of basement membrane. No proliferation was detected at the wound edges. In HCEC, a p38 (SB203580) and a JNK pathway inhibitor (JNK inhibitor I) inhibited migration rates more than U0126-induced ERK, whereas the JNK inhibitor I inactive analogue had no effect. JNK pathway inhibition wound closure in this region was not associated with either any TUNEL or BrdU-positive cells. Cell viability was unaffected by any of these MAPK inhibitors.\n\nQuestion:\nDoes jNK MAPK signaling contribute in vivo to injury-induced corneal epithelial migration?\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 neurofunctional correlates of movement ideation, which should be distinguished from motor imagery, have not been fully investigated. This functional Magnetic Resonance Imaging (fMRI) experiment revealed the brain activation patterns associated with different motor processes, including ideation. Fifteen healthy participants underwent fMRI and performed three tasks using the right index finger: 1. execution of a simple prespecified movement; 2. execution of a simple voluntary movement; 3. ideation of a simple voluntary movement without execution. A number of t-test comparisons across conditions were carried out. The execution ofa simple prespecified finger movement activated the right inferior parietal cortex and substantia nigra, the left middle frontal gyrus, and thalamus, and bilaterally the post-central gyri, the superior parietal lobule and the cerebellum. Execution of a simple voluntary movement activated the left anterior cingulate cortex. The ideation of a voluntary simple movement activated the left inferior, middle and superior temporal gyri and the inferior frontal gyri bilaterally.\n\nQuestion:\nIs the ideation of movement supported by fronto-temporal cortical regions involved in the retrieval of semantic knowledge?\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 20-HETE production contributes to platelet derived growth factor (PDGF)-BB stimulated migration of VSMC in a cell culture model. Studies were performed with A10 cells which are a rat vascular smooth muscle derived cell line. Migration was determined using a Boyden chamber chemotactic assay. Pre-treatment of cells with two doses of 20-HETE (100 and 500 nM) significantly increased PDGF-BB stimulated VSMC migration by 34-58% of control; whereas, prior incubation of cells with inhibitors of 20-HETE production, 17-ODYA (1-25 M) or HET0016 (100 nM), significantly decreased PDGF-BB stimulated migration by 40-90%. 20-HETE mediated increase in PDGF-BB migration was completely prevented by the 20-HETE antagonist, WIT-002. In order to determine what second messenger pathways are involved in the 20-HETE mediated stimulation of VSM migration, experiments were performed with specific inhibitors of tyrosine kinase (tyrphostin 25, 10 microM), mitogen-activated extracellular signal-regulated kinase (MEK, PD98059, 20 microM and U0126, 10 microM), protein kinase C (Myr-PKC, 50 microM), and phosphoinositide 3-kinases (PI3Ks) (wortmannin, 50 nM). Blockade of MEK and PI3K all abolished the increase in 20-HETE mediated migration.\n\nQuestion:\nDoes 20-Hydroxyeicosatetraenoic acid ( 20-HETE ) stimulate migration of vascular smooth muscle 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:\nMycophenolate mofetil (MMF) has been shown to be effective for systemic treatment of psoriasis. MMF is the prodrug of mycophenolic acid (MPA), the pharmacologically active compound. The measurement of plasma MPA levels could be useful for optimizing therapeutic management using MMF. To investigate whether plasma trough levels of MPA correlate with the efficacy and safety of oral MMF in the treatment of patients with psoriasis. Six patients (four women and two men, mean age 58 years) with severe chronic plaque-type psoriasis were treated with oral MMF 1 g twice daily. The Psoriasis Area and Severity Index (PASI), routine laboratory examinations and plasma MPA trough levels, measured by an enzyme-multiplied immunoassay (EMIT), were determined at 2 weeks and 1, 3, 5 and 7 months. All the patients experienced a marked improvement within the first 15 days and continued to do so for 5-7 months. Two patients achieved complete remission. MMF was well tolerated. MPA levels showed a wide intra- and interindividual variability. There was no significant correlation between MPA trough levels and the reduction of the PASI or the presence of adverse effects, but a good correlation with therapeutic compliance.\n\nQuestion:\nDo plasma trough levels of mycophenolic acid correlate with efficacy and safety of mycophenolate mofetil in psoriasis?\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:\nSystemic chemotherapy is being used increasingly in patients with colorectal cancer. The effects of prior systemic adjuvant or palliative chemotherapy on morbidity following hepatic resection for metastases are not well defined. To assess the peri-operative impact of systemic chemotherapy on liver resection for colorectal cancer hepatic metastases. Ninety-six resections for colorectal cancer hepatic metastases performed from July 2001 to July 2003 (93% > or =2 segments) were reviewed. Pre-operative demographics, peri-operative features, and post-operative outcomes were collected prospectively. Type of chemotherapy and the temporal relationship of chemotherapy to the liver resection were analyzed. Fifty-three of 96 patients (55%) received a mean of 5.7 cycles (6.1 months) of systemic chemotherapy prior to hepatic resection, with a median interval of 12 months from end of chemotherapy to liver resection (range 1-75 months). Thirty-five received 5-fluorouracil/leucovorin (5-FU/LV) alone, nine had irinotecan (CPT-11) in addition to 5-FU/LV, and nine were not specified. Pre-operative age, sex, co-morbidities, ASA score, biochemical and liver enzyme profiles, tumor number, and extent and technique of hepatic resection were the same in the chemotherapy and non-chemotherapy cohorts. Mean tumor size was smaller (4.5 cm vs. 5.8 cm) and synchronous metastases were half as common (25% vs. 49%) in the chemotherapy group. Liver resection operative time was equivalent (270 min) in the two groups. Higher estimated blood loss (EBL) (1,000 ml vs. 850 ml), but fewer transfusions (23% vs. 15%) were associated with the chemotherapy group. Although not statistically significant, post-operative liver enzyme peaks were higher in the chemotherapy group (AST = 402 U/L vs. 302 U/L, P = 0.09 and ALT = 433 U/L vs. 312 U/L, P = 0.1). Peak changes in INR and serum bilirubin did not differ. Complications and length of stay (LOS) did not differ between the groups. The only post-operative death was in the non-chemotherapy group. Interestingly, hepatic steatosis was present in 28% of the non-chemotherapy cases and 57% of the chemotherapy resection specimens (P = 0.005) and was marked (>30%) in 7% and 10%, respectively. Further analysis of the chemotherapy group based on the interval between completion of chemotherapy and the hepatic resection (<6 months, 7-12 months, 1-2 years, and >2 years) revealed a trend towards worse outcomes in most categories for those in the >2 years cohort. When comparing the 5-FU/LV alone, to the CPT-11 group there were no significant differences except higher intra-operative blood loss in the group receiving 5-FU/LV alone (1,295 ml vs. 756 ml, P = 0.01).\n\nQuestion:\nDoes chemotherapy for colorectal cancer prior to liver resection for colorectal cancer hepatic metastases adversely affect peri-operative outcomes?\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 survey the expression of members of the S100 family of calcium-binding proteins in normal human tissues and common cancers using tissue microarrays. S100A6, S100A8, S100A9 and S100A11 have all been suggested to have potential roles in carcinogenesis and tumour progression but their expression has not been described in a wide range of human tissues and tumours. A custom-made tissue array, containing 291 tissue cores representing 28 tissue types and 21 tumour types, was used to produce sections that were immunostained for S100A2, S100A6, S100A8, S100A9, S100A11, calbindin 1, calbindin 2, S100B and parvalbumin. S100A6, S100A8 and S100A9 were expressed in 32%, 12% and 28% of breast cancers, respectively. There was a translocation of S100A11 expression from exclusively nuclear in normal tissues to cytoplasmic and nuclear in all common cancers.\n\nQuestion:\nAre expression of S100 proteins in normal human tissues and common cancers using tissue microarrays : S100A6 , S100A8 , S100A9 and S100A11 all overexpressed in common cancers?\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:\nNoninvasive in vivo imaging of biologic processes using PET is an important tool in preclinical studies. We observed significant differences in 3'-deoxy-3'-(18)F-fluorothymidine ((18)F-FLT) uptake in arthritic ankles and carcinomas between dynamic and static PET measurements when mice breathed oxygen. Thus, we suspected that air or oxygen breathing and the anesthesia protocol might influence (18)F-FLT tracer uptake. We injected arthritic, healthy, and CT26 colon carcinoma-bearing mice with (18)F-FLT before static or dynamic small-animal PET measurements. The spontaneously oxygen- or air-breathing mice were kept conscious or anesthetized with ketamine and xylazine during (18)F-FLT uptake before the 10-min static PET measurements. For dynamic PET scans, mice were anesthetized during the entire measurement. (18)F-FLT uptake was reported in percentage injected dose per cubed centimeter by drawing regions of interest around ankles, carcinomas, and muscle tissue. Additionally, venous blood samples were collected before (18)F-FLT injection and after PET measurement to analyze pH, carbon dioxide partial pressure (pCO(2)), and lactate values. A significantly reduced (18)F-FLT uptake was measured in arthritic ankles and in CT26 colon carcinomas when the mice breathed oxygen and were conscious during tracer uptake, compared with mice that were anesthetized during (18)F-FLT uptake. Breathing air completely abolished this phenomenon. Analysis of blood samples that were obtained from the mice before (18)F-FLT injection and after the PET scan implicated respiratory acidosis that was induced by oxygen breathing and consciousness during tracer uptake. Acidosis was found to be the primary factor responsible for the reduced (18)F-FLT uptake, as reflected by increased pCO(2) and reduced pH and lactate values.\n\nQuestion:\nDoes oxygen breathing affect 3'-deoxy-3'-18F-fluorothymidine uptake in mouse models of arthritis and 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:\nMechanisms regulating the transition from hormone responsive to hormone refractory prostate cancer (PCa) have remained unclear. We analyzed androgen and anti-androgen treatment on endogenous AR activity in primary human prostate epithelial (HPE) cells cultured directly from patient radical prostatectomy specimens utilizing a transiently infected gene reporter (TIGR) assay. Flutamide treatment exhibited agonist activities in HPE cells derived from tumor and non-tumor specimens which contained wild-type AR. After proteomic comparison of these cells to those where flutamide functioned normally as an antagonist, we identified DJ-1, a positive regulator of AR. DJ-1 expression increased in HPE and LNCaP cells during flutamide treatment as a result of DJ-1 protein stabilization.\n\nQuestion:\nDoes androgen and anti-androgen treatment modulate androgen receptor activity and DJ-1 stability?\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:\nHigh circulating levels of group IIA secretory phospholipase A2 (sPLA2-IIA) activity and mass are independent cardiovascular risk factors. Therefore, inhibition of sPLA2-IIA may be a target for the treatment of atherosclerotic cardiovascular disease. The present study evaluated the effects of sPLA2-IIA inhibition with varespladib acid in a novel mouse model, human apolipoprotein B (apoB)/human cholesteryl ester transfer protein (CETP)/human sPLA2-IIA triple transgenic mice (TTT) fed a Western-type diet. sPLA2-IIA expression increased atherosclerotic lesion formation in TTT compared with human apoB/human CETP double transgenic mice (P<0.01). Varespladib acid effectively inhibited plasma sPLA2-IIA activity. Surprisingly, however, administration of varespladib acid to TTT had no impact on atherosclerosis, which could be attributed to a proatherogenic plasma lipoprotein profile that appears in response to sPLA2-IIA inhibition because of increased plasma CETP activity. In the TTT model, sPLA2-IIA decreased CETP activity by reducing the acceptor properties of sPLA2-IIA-modified very low-density lipoproteins specifically because of a significantly lower apoE content. Increasing very low-density lipoprotein-apoE content by means of adenovirus-mediated gene transfer in sPLA2-IIA transgenic mice restored the acceptor properties for CETP.\n\nQuestion:\nDoes expression of type IIA secretory phospholipase A2 inhibit cholesteryl ester transfer protein activity in transgenic mice?\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 necrosis is an important phenomenon with implications for grading and prognostication in meningiomas, the alternate form of cell death, apoptosis, has not been extensively studied. In this series, we aimed to determine whether apoptosis in meningiomas correlated with histological types and grading. We also looked for a relationship between expression of apoptosis-related genes bcl-2, p53, c-myc and apoptosis meningiomas. Fifty-one meningiomas of diverse histological subtypes and grades were investigated with in situ end-labelling of DNA fragments as well as immunohistochemical analysis of three apoptosis-related genes: p53, bcl-2 and c-myc. Our results showed that the apoptosis index was significantly higher in high-grade meningiomas (0.12%, n = 12) in than the benign meningiomas (0.023%, n = 39) P = 0.001) but there was no difference among the different histological subtypes of the benign meningiomas (P = 0.125). There is no obvious relationship between p53, bcl-2 and c-myc staining and apoptosis index in this group of meningiomas.\n\nQuestion:\nIs apoptosis associated with atypical or malignant change in meningiomas . An in situ labelling and immunohistochemical study?\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:\nDiscovery of cancer drivers is a major goal of cancer research. Driver genes and pathways are often predicted using mutation frequency, assuming that statistically significant recurrence of specific somatic mutations across independent samples indicates their importance in cancer. However, many mutations, including known cancer drivers, are not observed at high frequency. Fortunately, abundant information is available about functional \"active sites\" in proteins that can be integrated with mutations to predict cancer driver genes, even based on low frequency mutations. Further, considering active site information predicts detailed biochemical mechanisms impacted by the mutations. Post-translational modifications (PTMs) are active sites that are regulatory switches in proteins and pathways. We analyzed acetylation and ubiquitination, two important PTM types often involved in chromatin organization and protein degradation, to find proteins that are significantly affected by tumor somatic mutations. We performed computational analyses of acetylation and ubiquitination sites in a pan-cancer dataset of 3200 tumor samples from The Cancer Genome Atlas (TCGA). These analyses were targeted at different levels of biological organization including individual genes, pathway annotated gene sets, and protein-protein interaction networks. Acetylation and ubiquitination site mutations are enriched in cancer with significantly stronger evolutionary conservation and accumulation in protein domains. Gene-focused analysis with the ActiveDriver method reveals significant co-occurrences of acetylation and ubiquitination PTMs and mutation hotspots in known oncoproteins (TP53, AKT1, IDH1) and highlights candidate cancer driver genes with PTM-related mechanisms (e.g. several histone proteins and the splicing factor SF3B1). Pathway analysis shows that PTM mutations in acetylation and ubiquitination sites accumulate in cancer-related processes such as cell cycle, apoptosis, chromatin regulation, and metabolism. Integrated mutation analysis of clinical information and protein interaction networks suggests that many PTM-specific mutations associate with decreased patient survival.\n\nQuestion:\nDo frequent mutations in acetylation and ubiquitination sites suggest novel driver mechanisms of 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:\nHistological evidence of primary tumor regression (RG) is observed in 35% or fewer patients with cutaneous melanoma. Some advocate a lower threshold for sentinel lymph node (SLN) biopsy when RG is present. We identified 1,349 patients presenting to our center with clinically localized cutaneous melanoma between 1995 and 2004. Of these, 344 demonstrated histological RG in their primary melanoma. A retrospective analysis of their medical records was performed to obtain clinical and pathological information. The median Breslow depth for the 344 patients with RG was 1.1 mm versus 1.5 mm for 1,005 patients with no regression (NRG) (P < 0.005). SLN biopsy was performed in 64% of patients with RG and 72% without. Positive SLN was more common in those with NRG than in those with RG (18% vs 10%, P = 0.005). Only one RG patient with thin melanoma (</=1 mm, Clark IV) had a positive SLN. When stratified by Breslow depth, patients with RG had lower rates of SLN positivity in all groups (</=1.0mm, >1.0 and </=2.0mm, >2 and </=4 mm, and >4.0 mm). Recurrence was more common in patients with NRG (21% vs 12%; P < 0.005). Both local and systemic recurrence occurred more commonly in patients with NRG (4% vs 1%, P = 0.002 and 8% vs 3%, P < 0.005, respectively)\n\nQuestion:\nDoes primary cutaneous melanoma with regression require a lower threshold for sentinel lymph node biopsy?\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:\nOmeprazole is less effective in healthy subjects than in patients with duodenal ulcers. The aim of this study was to determine whether Helicobacter pylori augments the pH-increasing effect of omeprazole in patients with duodenal ulcers. In 16 patients with duodenal ulcers, baseline intragastric acidity was measured before and 4-6 weeks after the cure of H. pylori infection. In 17 patients with duodenal ulcers, 24-hour pH metry was performed during treatment with 20 mg omeprazole once daily before as well as after eradication of H. pylori. Intragastric acidity was measured using a glass electrode placed 5 cm below the cardia. H. pylori infection was assessed by [13C] urea breath test, culture, histology, and rapid urease test. H. pylori eradication resulted in marked decrease of the pH-increasing effect of omeprazole (24-hour median gastric pH, 5.5 vs. 3.0; P<0.002) that was most pronounced during nighttime (median gastric pH, 6.4 vs. 2.1; P=0.001). On the other hand, baseline intragastric pH remained unchanged after eradication (median gastric pH, 1.0 vs. 1.1; P=0.5).\n\nQuestion:\nDoes helicobacter pylori augment the pH-increasing effect of omeprazole in patients with duodenal ulcer?\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:\nAdvances in endoscopic submucosal dissection (ESD) techniques have led to the development of expanded criteria for endoscopic resection of early gas-tric cancer (EGC). The aim of this study was to evaluate the short- and long-term outcomes for ESD using indication cri-teria. A total of 1,105 patients underwent ESD for EGC at six medical centers. The patients were classified into the following two groups based on the lesion size, presence of ulceration and pathological review an absolute criteria group (n=517) and an expanded criteria group (n=588). The curative resection rates (91.1% vs 91.3%, p=0.896) were similar in the absolute criteria group and the expanded criteria group. The en bloc resection rates (93.4% and 92.3%, respectively; p=0.488) and complete resection rates (98.3% and 97.4%, respectively; p=0.357) did not differ between the groups. The cumulative disease-free survival rates and the overall survival rates were similar between the groups (p=0.778 and p=0.654, respectively). Independent factors for the curative resection of EGC included tumor lo-cation (upper vs middle and lower, 2.632 [1.128-6.144] vs 3.497 [1.560-7.842], respectively) and en bloc resection rate 12.576 [7.442-21.250].\n\nQuestion:\nAre clinical outcomes of the endoscopic submucosal dissection of early gastric cancer comparable between absolute and new expanded criteria?\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:\nMammals must sense the amount of sugar available to them and respond appropriately. For many years attention has focused on intracellular glucose sensing derived from glucose metabolism. Here, we studied the detection of extracellular glucose concentrations in vivo by invalidating the transduction pathway downstream from the transporter-detector GLUT2 and measured the physiological impact of this pathway. We produced mice that ubiquitously express the largest cytoplasmic loop of GLUT2, blocking glucose-mediated gene expression in vitro without affecting glucose metabolism. Impairment of GLUT2-mediated sugar detection transiently protected transgenic mice against starvation and streptozotocin-induced diabetes, suggesting that both low- and high-glucose concentrations were not detected. Transgenic mice favored lipid oxidation, and oral glucose was slowly cleared from blood due to low insulin production, despite massive urinary glucose excretion. Kidney adaptation was characterized by a lower rate of glucose reabsorption, whereas pancreatic adaptation was associated with a larger number of small islets.\n\nQuestion:\nDoes loss of sugar detection by GLUT2 affect glucose homeostasis 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.
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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 aim of this study was to determine whether anastomotic leakage has an independent association with overall survival and cancer-specific survival. There are many known prognostic indicators following surgery for colorectal cancer (CRC). However, the impact of anastomotic leakage has not been adequately assessed. Consecutive patients undergoing resection between 1971 and 1999 were recorded prospectively in the Concord Hospital CRC database. Total anastomotic leakage was defined as any leak, whether local, general, or radiologically diagnosed. Patients were followed until death or to December 31, 2002. The association between anastomotic leakage and both overall survival and cancer-specific survival was examined by proportional hazards regression with adjustment for other patient and tumor characteristics influencing survival. Confidence intervals (CI) were set at the 95% level. From an initial 2980 patients, 1722 remained after exclusions. The total leak rate was 5.1% (CI 4.1-6.2%). In patients with a leak, the 5-year overall survival rate was 44.3% (CI 33.5-54.6%) compared to 64.0% (CI 61.5-66.3%) in those without leak. In proportional hazards regression-after adjustment for age, gender, urgent resection, site, size, stage, grade, venous invasion, apical node metastasis and serosal surface involvement-anastomotic leakage had an independent negative association with overall survival (hazard ratio [HR] 1.6, CI 1.2-2.0) and cancer-specific survival (HR 1.8, CI 1.2-2.6).\n\nQuestion:\nIs anastomotic leakage predictive of diminished survival after potentially curative resection for colorectal cancer?\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 efficacy of umbilical cord-derived mesenchymal stem cells (UC-MSCs) transplantation in the treatment of liver fibrosis. Cultured human UC-MSCs were isolated and transfused into rats with liver fibrosis induced by dimethylnitrosamine (DMN). The effects of UC-MSCs transfusion on liver fibrosis were then evaluated by histopathology; serum interleukin (IL)-4 and IL-10 levels were also measured. Furthermore, Kupffer cells (KCs) in fibrotic livers were isolated and cultured to analyze their phenotype. Moreover, UC-MSCs were co-cultured with KCs in vitro to assess the effects of UC-MSCs on KCs' phenotype, and IL-4 and IL-10 levels were measured in cell culture supernatants. Finally, UC-MSCs and KCs were cultured in the presence of IL-4 antibodies to block the effects of this cytokine, followed by phenotypical analysis of KCs. UC-MSCs transfused into rats were recruited by the injured liver and alleviated liver fibrosis, increasing serum IL-4 and IL-10 levels. Interestingly, UC-MSCs promoted mobilization of KCs not only in fibrotic livers, but also in vitro. Co-culture of UC-MSCs with KCs resulted in increased production of IL-4 and IL-10. The addition of IL-4 antibodies into the co-culture system resulted in decreased KC mobilization.\n\nQuestion:\nDo umbilical cord-derived mesenchymal stem cells alleviate liver fibrosis in rats?\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 purpose of the study was to compare the rate of secondary resurfacing in a consecutive series of five different total knee arthroplasty (TKA) systems. It was our hypothesis that different TKA design features such as sulcus angle or trochlear height influence the rate of secondary resurfacing. A retrospective study was performed on data from patients who underwent TKA without primary patellar resurfacing from 2004 to 2012 in an university-affiliated hospital. The study cohort included 784 TKA patients (m:f = 302:482, mean age at surgery ± SD 71 ± 10). Five different cruciate-retaining TKA systems were used consecutively (Group A, Triathlon, Stryker, Switzerland (n = 296), Group B, PFC Sigma, DepuySynthes, Switzerland (n = 215), Group C, LCS, DepuySynthes, Switzerland (n = 81), Group D, Balansys, Mathys, Switzerland (n = 128), Group E, Duracon, Stryker, Switzerland (n = 64)). Data were retrospectively obtained from hospital archives. Patients demographics, age at surgery, type of TKA were noted. In addition, TKA component position was assessed on radiographs with respect to \"The knee society total knee arthroplasty roentgenographic evaluation and scoring system\" (TKA-RESS). Pearson Chi-square test was used to compare differences between groups (p < 0.05). There were no significant differences between the groups in terms of age, gender, and radiological outcomes. Twenty-six of 784 patients (3.3 %) underwent secondary resurfacing due to patellofemoral pain. In group A 4/296 patients (1.4 %), in group B 15/215 patients (7 %), in group C 5/81 patients (6.2 %), in group D 1/128 patients (0.8 %), in group E 1/64 patients (1.6 %) underwent secondary patellar resurfacing during follow-up. Significantly higher rates of secondary patellar resurfacing were seen in groups B and C when compared to the others (p < 0.001). It was found that the trochlear height in these TKA was higher than in the others.\n\nQuestion:\nIs the need for secondary resurfacing affected by trochlear height in total knee arthroplasty?\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 aim of the study was to conduct a meta-analysis of epidemiological and case control studies to determine whether arterial hypertension is specifically associated with an increased risk of vascular dementia (VaD). Longitudinal and cross-sectional prospective studies using operationalised criteria to define VaD and hypertension, with a normal control comparison group were systematically reviewed. Cochrane Library, Embase, Medline, and PsycInfo data sources were searched along with reference lists of included articles and reviews. Original, prevalence or incidence studies were included if operationalised criteria for hypertension and VaD as well as number of cases with and without hypertension in VaD and non-demented groups were provided. Intervention studies and post-stroke and CADASIL studies were excluded. Eleven studies recruiting either volunteers or clinical patients, or which were population-based, examined a total of 768 people with VaD and 9857 control cases. A meta-analysis of the six longitudinal studies showed that hypertension was significantly associated with increased risk of incident VaD (odds ratio, OR: 1.59, CI: 1.29-1.95, p < 0.0001). A similar association between hypertension and the risk of prevalent VaD was found in the five cross-sectional studies (OR: 4.84, CI: 3.52-6.67, p < 0.00001).\n\nQuestion:\nIs hypertension a potential risk factor for vascular dementia : systematic review?\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 effects of intrapulmonary artery (i.p.a.) administration of dihydroergotamine mesylate (DHE) were evaluated. Conscious beagle dogs (n=4) were given DHE via the i.p.a. or i.v. route as two 0.014 mg kg(-1) doses and a 0.14 mg kg(-1) dose given 60 min apart. A recovery period of > or =45 h occurred before crossover to the alternative route. Physiological parameters were monitored by telemetry or direct measurement, and venous blood samples were collected for pharmacokinetic assessments. No meaningful differences between i.v. and i.p.a. treatments were observed for heart rate, systemic pressures and vascular pressures. Aortic resistance increased 8, 27 and 70%, respectively, following three doses of i.v. DHE compared with 11, 37 and 57%, respectively, with i.p.a. DHE. Carotid artery resistance increased 22, 40 and 87%, respectively, following three doses of i.v. DHE, compared with 17, 45 and 67%, respectively, following i.p.a. DHE. Increases in coronary artery resistance were of similar magnitude following i.v. and i.p.a. DHE administration. Increases in left ventricular systolic and diastolic pressures were seen following all doses of i.v. and i.p.a. DHE. Changes following DHE 0.014 mg kg(-1) were minimal and not clinically significant. With DHE 0.14 mg kg(-1) by either route, emesis was the most common adverse event.\n\nQuestion:\nDo intrapulmonary and intravenous administrations of dihydroergotamine mesylate have similar cardiovascular effects in the conscious dog?\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:\nIt is unclear whether and how elite athletes process physiological or psychological challenges differently than healthy comparison subjects. In general, individuals optimize exercise level as it relates to differences between expected and experienced exertion, which can be conceptualized as a body prediction error. The process of computing a body prediction error involves the insular cortex, which is important for interoception, i.e. the sense of the physiological condition of the body. Thus, optimal performance may be related to efficient minimization of the body prediction error. We examined the hypothesis that elite athletes, compared to control subjects, show attenuated insular cortex activation during an aversive interoceptive challenge. Elite adventure racers (n = 10) and healthy volunteers (n = 11) performed a continuous performance task with varying degrees of a non-hypercapnic breathing load while undergoing functional magnetic resonance imaging. The results indicate that (1) non-hypercapnic inspiratory breathing load is an aversive experience associated with a profound activation of a distributed set of brain areas including bilateral insula, dorsolateral prefrontal cortex and anterior cingulated; (2) adventure racers relative to comparison subjects show greater accuracy on the continuous performance task during the aversive interoceptive condition; and (3) adventure racers show an attenuated right insula cortex response during and following the aversive interoceptive condition of non-hypercapnic inspiratory breathing load.\n\nQuestion:\nDoes subjecting elite athletes to inspiratory breathing load reveal behavioral and neural signatures of optimal performers in extreme environments?\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 investigate whether RGD peptide-exposing long circulating polyethylene glycol (PEG) liposomes (RGD-PEG-L) targeted to alphavbeta3 integrins expressed on angiogenic vascular endothelial cells (VECs) are able to bind VECs at sites of inflammation and whether such liposomes containing dexamethasone phosphate (DEXP) can be used as carriers to interfere with the development of experimental arthritis. Binding and internalization of RGD-PEG-L were studied by fluorescence-activated cell sorting and confocal microscopy using fluorescently labeled liposomes. Radiolabeled liposomes were used to test in vivo pharmacokinetics and inflammation site targeting in lipopolysaccharide (LPS)-induced inflammation and adjuvant-induced arthritis (AIA) in rats. In vivo inflammation targeting was visualized by intravital microscopy using fluorescently labeled RGD-PEG-L. Therapeutic efficacy of DEXP-encapsulating RGD-PEG-L compared with nontargeted liposomes was evaluated in rats with AIA. RGD-PEG-L bound to and were taken up by proliferating human VECs in vitro. In vivo, increased targeting of radiolabeled RGD-PEG-L to areas of LPS-induced inflammation in rats was observed. Specific association with the blood vessel wall at the site of inflammation was confirmed by intravital microscopy. One single intravenous injection of DEXP encapsulated in RGD-PEG-L resulted in a strong and long-lasting antiarthritic effect in rat AIA.\n\nQuestion:\nDoes targeting of angiogenic endothelial cells at sites of inflammation by dexamethasone phosphate-containing RGD peptide liposomes inhibit experimental arthritis?\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 investigate the role of p38MAPK signaling pathway in interleukin (IL)-1beta induced transdifferentiation and its functional influences in human renal proximal tubular cell line HK-2 cells. Human renal proximal tubular cells, cell line HK-2, were cultured and then co-incubated with IL-1beta (10 ng/ml) for 24 hours. The expression and distribution of cytokeratin and alpha-smooth muscle actin (SMA), markers of transdifferentiation of renal proximal tubular cells, were detected by immunofluorescence staining and confocal microscopy. Western blot technique was used to detect the expression of alpha-SMA 2, 4, 6, 12, 24, and 48 hours after IL-1beta stimulation. The morphology of cells was monitored from the 1st to the 5th day. Expression of alpha-SMA, phosphorylation of p38MAPK was assayed by western blot. Specific p38MAPK inhibitor SB203580 was added into the culture of HK-2 cells, 24 hours later IL-1beta was added for 24 hours Cell-cell adhesion and migration assay were performed. Inverted microscopy was used to examine the morphology of cells after stimulation of IL-1beta for 24 hours. Western blot technique was used to detected total and phosphorylated p38MAPK after stimulation of IL-1beta for 2, 5, 15, 30, 60 and 120 min. The phosphorylation of p38MAPK was increased after treatment of IL-1beta, and reached the level of 1.7 times the basic level 5 - 30 minutes after stimulation (P < 0.05). Almost no expression of alpha-SMA was shown in the control group. Two hours after IL-1beta stimulation, the expression of alpha-SMA was increased a little followed by an up-regulated expression of alpha-SMA 6 to 48 hours after the stimulation. The expression of alpha-SMA was down-regulated by 40% in the SB203580 group in comparison with that in the control (P < 0.01) and by 50% in comparison with that in the IL-1beta group (P < 0.001). The cell number was not significantly different between the IL-1beta group and control group (P > 0.05). A decreased expression of cytokeratin and disordered distribution of alpha-SMA were shown in the cells 24 hours after stimulation of IL-1beta. The morphology of cells remained unchanged 1 to 5 days after IL-1beta stimulation. The cell-cell adhesion was almost identical in the groups with IL-1beta and/or SB203580 no in comparison with that in the control group (P > 0.05). The migration ability of HK-2 cells was 2.2 times that in the control group in the IL-1beta group (P < 0.05) and decreased by 35% in the SB203580 group (P < 0.01). SB203580 uppercased the IL-1beta-induced expression of alpha-SMA and the enhancement of cell migration ability were suppressed by 51% (P < 0.05).\n\nQuestion:\nIs [ Interleukin-1beta-induced transdifferentiation of renal proximal tubular cells mediated by p38 mitogen-activated protein kinase phosphorylation ]?\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:\nCouroupita guianensis Aublet, 'macacarecuia', 'abricó-de-macaco', 'castanha-de-macaco' and 'amêndoa-dos-andes', is found in tropical regions and is widely used in the treatment of tumors, pain, and inflammatory processes. Ethanol extract and hexane and ethyl acetate fractions were evaluated in models of inflammatory pain (formalin-induced licking) and acute inflammation (carrageenan-induced peritonitis). Ethanol extract, hexane and ethyl acetate fractions (10, 30 or 100 mg/kg, p.o.) and the reference drugs dexamethasone (5 mg/kg), morphine (5 mg/kg, s.c.), and acetylsalicylic acid (100 mg/kg, p.o.) were tested in formalin-induced licking response and carrageenan-induced peritonitis. All three doses from Couroupita guianensis fractions significantly reduced the time that the animal spent licking the formalin-injected paw in first and second phases. However, only higher doses (30 and 100 mg/kg) were able to inhibit the leukocyte migration into the peritoneal cavity after carrageenan injection. In this model, the 100 mg/kg dose almost abolished the cell migration. It was also observed that protein concentration resulted from extravasation to the peritoneum and nitric oxide (NO) productions were significantly reduced. Cytokines production was differently affected by the treatment. TNF-α production was reduced after ethanol extract and ethyl acetate fraction pre-treatment whereas hexane fraction had effect only with 100 mg/kg dose. IL-1β production was inhibited only after hexane fraction pre-treatment. The inhibitory effect observed was not due to a direct cytotoxic effect on cells nor to a NO-scavenger activity. The effect was due to a direct inhibition on NO production by the cells.\n\nQuestion:\nDoes anti-inflammatory activity of ethanol extract and fractions from Couroupita guianensis Aublet leave?\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 periodontal ligament (PDL) is continually exposed to mechanical loading caused by mastication or occlusion. Physiological loading is thus considered a key regulator of PDL tissue homeostasis; however, it remains unclear how this occurs. We recently reported that an appropriate magnitude of mechanical stretch can maintain PDL tissue homeostasis via the renin-angiotensin system. In the present study, we investigated the expression of interleukin-11 (IL-11) in human primary PDL cells (HPDLCs) exposed to stretch loading, the contribution of angiotensin II (Ang II) to this event and the effects of IL-11 on osteoblastic/cementoblastic differentiation of human PDL progenitor cells (cell line 1-17). Human primary PDL cells, derived from human tissues, with or without antagonists against the Ang II receptors AT1 or AT2, were subjected to cyclical stretch loading with 8% elongation for 1 h. Expression of IL-11 was measured by ELISA in these cultures and by immunohistochemistry in the sectioned maxillae of rats. The osteoblastic/cementoblastic potential of cell line 1-17 was determined using cell proliferation, gene expression and Alizarin Red staining. Positive staining for IL-11 was observed in the PDL of rat maxillae and in cultures of HPDLCs. In HPDLCs exposed to stretch, expression of the IL11 gene and the IL-11 protein were up-regulated, concomitant with an increase in Ang II and via AT2. Recombinant human IL-11 (rhIL-11) stimulated an increase in expression of mRNA for the cementoblast-specific marker, CP-23, and for the osteoblastic markers, osteopontin and bone sialoprotein, and promoted proliferation in cell line 1-17. In addition, rhIL-11 also increased the degree of mineralized nodule formation in cell line 1-17 cultures treated with CaCl2 .\n\nQuestion:\nDoes mechanical induction of interleukin-11 regulate osteoblastic/cementoblastic differentiation of human periodontal ligament stem/progenitor 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:\nAccumulation of the excitatory neurotransmitter glutamate in ischemic brain tissue contributes to neuronal cell death. Volatile anesthetics at clinically relevant concentrations are neuroprotective in in vivo models of brain ischemia and reduce glutamate release in vivo and in vitro, but they appear to have weaker neuroprotective effects than hypothermia. The purpose of this study was to determine whether isoflurane reduces glutamate release in hypoxic brain slices, how large this effect is compared to that of hypothermia, and if it is diminished by hyperthermia. Glutamate released from rat cortical brain slices during chemical anoxia (100 microM NaCN) was measured continuously with a fluorescence assay. The release rate was compared at three temperatures (28 degrees C, 37 degrees C, and 39 degrees C) with and without isoflurane at concentrations equipotent to 1 minimum alveolar concentration. At the same three temperatures, glutamate release rates before and after exposure to isoflurane were compared. Isoflurane reduced glutamate release from brain slices during chemical anoxia at 37 degrees C (19.6%, P < 0.01) and at 39 degrees C (25.4%, P < 0.01), but not at 28 degrees C. The reduction in glutamate release with hypothermia was similar to that with isoflurane. Hyperthermia (39 degrees C) caused greater glutamate release under basal and anoxic conditions than normo- and hypothermia. Isoflurane caused a slight increase in basal glutamate release rates, although this effect was smaller than the increase caused by hyperthermia.\n\nQuestion:\nDo hypothermia and isoflurane similarly inhibit glutamate release evoked by chemical anoxia in rat cortical brain slices?\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:\nNonsteroidal anti-inflammatory drugs (NSAIDs) have been shown to reduce the risk of colorectal cancer in cyclooxygenase-2 (COX-2) overexpressing colorectal cancers. The present study was designed to evaluate the inhibitory effects of the COX-2 inhibitor celecoxib on the growth of colorectal cancer liver metastases in a syngeneic rat model, CC531. The effects of celecoxib on cell viability in vitro were evaluated by treatment of CC531 tumor cell cultures with celecoxib. In vivo, Wag/Rij rats were inoculated with CC531 tumor cells at two sites in the liver and treated with celecoxib starting one week before, or directly after tumor inoculation. Control rats were inoculated without treatment. Three weeks after tumor inoculation rats were sacrificed. Tumor size, immune cell infiltration, caspase-3 activity, PGE(2) and celecoxib levels were determined. CC531 tumors did not show COX-2 expression. Tumor growth was significantly inhibited by celecoxib treatment in a dose dependent manner. Immune cell infiltration was decreased after celecoxib treatment, indicating that the immune system was not involved in preventing tumor growth. Tumor caspase-3 levels were only significantly increased if treatment was started before tumor inoculation. Celecoxib serum concentration starting at 0.84 microg/ml significantly inhibited the outgrowth of CC531 liver tumors. In contrast, in vitro concentrations of celecoxib of at least 12 microg/ml were needed to affect tumor cell viability.\n\nQuestion:\nDoes celecoxib inhibit growth of tumors in a syngeneic rat liver metastases model for colorectal cancer?\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 determine the morningness-eveningness (ME) distribution of emergency medicine (EM) residents. A voluntary, modified ME questionnaire was administered to all EM residents in the United States at the time of the 1995 American Board of Emergency Medicine's annual In-Training Examination. Seventy-eight percent (2,047/2,614) of the surveys were returned. ME scores ranged from 24 to 76, with a median score of 49 (interquartile range 44, 56). The scores were distributed differently from those of the normal population (p < 0.001), being skewed toward eveningness. There was a correlation (r = 0.13, p < 0.0001) between resident age and ME score, with older residents being more morning-oriented. Males were more morning-oriented than females (p = 0.005), and respondents with children living at home also were significantly more morning-oriented (p < 0.001). Stepwise logistic regression showed that the influence of age, gender, and children was cumulative (r = 0.19) but accounted for only 4% of the observed variability.\n\nQuestion:\nAre morningness-eveningness preferences of emergency medicine residents skewed toward eveningness?\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:\nTumor necrosis factor alpha (TNFalpha) is associated with trauma-induced hearing loss. Local treatment of cochleae of trauma-exposed animals with a glucocorticoid is effective in reducing the level of hearing loss that occurs post-trauma (e.g., electrode insertion trauma-induced hearing loss/dexamethasone treatment). Dexamethasone (Dex) protects auditory hair cells (AHCs) from trauma-induced loss by activating cellular signal pathways that promote cell survival. Organ of Corti explants challenged with an ototoxic level of TNFalpha was the trauma model with Dex the otoprotective drug. A series of inhibitors were used in combination with the Dex treatment of TNFalpha-exposed explants to investigate the signal molecules that participate in Dex-mediated otoprotection. The otoprotective capacity of Dex against TNFalpha ototoxicity was determined by hair cell counts obtained from fixed explants stained with FITC-phalloidin labeling with investigators blinded to specimen identity. The general caspase inhibitor Boc-d-fmk prevented TNFalpha-induced AHC death. There was a significant reduction (p<0.05) in the efficacy of Dex otoprotection against TNFalpha ototoxicity when the following cellular events were blocked: (1) glucocorticoid receptors (Mif); (2) PI3K (LY294002); (3) Akt/PKB (SH-6); and (4) NFkappaB (NFkappaB-I).\n\nQuestion:\nDoes dexamethasone protect auditory hair cells against TNFalpha-initiated apoptosis via activation of PI3K/Akt and NFkappaB signaling?\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:\nNeurofilaments (Nfs) are protein biomarkers of neurodegeneration in human disease. There is in vivo evidence of changes of the Nf stoichiometry in the cerebrospinal fluid (CSF) of patients. The protein-structural implications of these findings are not known but may be assessed indirectly using simulations studies. Monte Carlo simulations were performed using a coarse-grained model of a Nf brush. Based on the published in vivo CSF data the tested Nf stoichiometries (NfL:NfM:NfH) were 16:11:4 for multiple system atrophy (MSA), 24:5:2 for relapsing remitting multiple sclerosis (RRMS), and 30:0:1 for clinically isolated syndromes (CIS). Simulations were performed in a wide range of ionic strength (1 mM-100 mM) for dephosphorylated and phosphorylated NF isoforms. At lower ionic strengths (1 mM, 10 mM), NfM is the main determinant for the radius of gyration (R(g)) ranging from ≈15 nm in the dephosphorylated state at 10 mM ionic strength to ≈27 nm at 1mM ionic strength if fully phosphorylated. At high ionic strength (100mM) NfH becomes the main determinant with R(g) of 14.8±0.2 nm if dephosphorylated and 15±0.2 nm if phosphorylated. There was no significant difference in the structures of the three Nf sidearms for MSA, RRMS or CIS.\n\nQuestion:\nDo neurofilament stoichiometry simulations during neurodegeneration suggest a remarkable self-sufficient and stable in vivo protein structure?\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:\nAldosterone levels are high early after admission for ST elevation myocardial infarction (STEMI) concomitantly with high risk of sudden death and life-threatening ventricular arrhythmia. We assessed the hypothesis that early aldosterone blockade on admission for primary percutaneous coronary intervention (PCI) may be associated with a reduction of life-threatening ventricular arrhythmia in a prospective cohort-nested case (n=159) versus historical control (n=623) study. All cases were treated on admission by 200mg IV bolus of potassium canrenoate, followed by 25mg PO spironolactone daily during the coronary care unit stay. The primary endpoint--in-hospital composite of death, resuscitated cardiac arrest and ventricular tachycardia--was assessed by logistic regression models adjusted on major pre-specified variables and validated by a bootstrap procedure and propensity-score based analyses. Aldosterone blockade was associated with lower risks of the primary endpoint (adjusted ORs 0.26, 95% CI [0.13-0.57]), resuscitated cardiac arrest (adjusted OR 0.39, 95% CI [0.16-0.94]), ventricular tachycardia or fibrillation (adjusted ORs 0.23, 95% CI [0.12-0.45]), as well as ventricular arrhythmia requiring resuscitation or anti-arrhythmic therapy (adjusted OR 0.41, 95% CI [0.19-0.88]). All findings were confirmed by the bootstrap procedure. The benefit on death or resuscitated cardiac arrest seemed sustained at 6month follow-up.\n\nQuestion:\nIs early mineralocorticoid receptor blockade in primary percutaneous coronary intervention for ST-elevation myocardial infarction associated with a reduction of life-threatening ventricular arrhythmia?\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:\nAs an acute-phase protein synthesized in response to systemic inflammation, the C-reactive protein (CRP) has been shown to be an independent prognostic factor for patients with castration-resistant prostate cancer (CRPC). The aim of this study was to investigate the association between CRP and progression-free survival (PFS), overall survival (OS) and radiological response in CRPC patients treated with docetaxel. 115 histologically confirmed CRPC patients who were treated with docetaxel chemotherapy from 2008 to 2013 were selected. Univariable and multivariable Cox regression models were used to predict the association of CRP as a dichotomous variable with PFS and OS after chemotherapy initiation. None of the clinicopathological features were associated with the CRP. In Kaplan-Meier analysis, the median PFS (9.8 vs. 7.5 months, p < 0.001) and OS (26.5 vs. 13.5 months, p = 0.002) were higher in patients who did not have an elevated CRP than in those with an elevated CRP. In univariable analysis, the pretreatment CRP was significantly associated with PFS (p < 0.001) and OS (p = 0.003).In multivariable analysis, patients with a CRP > 8 mg/l were at significantly higher risk of tumor progress (hazard ratio (HR) 2.184; 95% confidence interval (CI) 1.401-3.403; p = 0.001) and death (HR 2.003; 95% CI 1.285-3.121; p = 0.002) than patients with a CRP ≤ 8 mg/l.\n\nQuestion:\nIs c-Reactive Protein a Prognostic Marker for Patients with Castration-Resistant 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:\nUse of fluoroscopy and bone landmarks to guide percutaneous common femoral artery (CFA) access has decreased access site complications compared with palpation alone. However, only limited case series have examined the benefits of ultrasound to guide CFA access during peripheral vascular intervention (PVI). We evaluated the effect of routine vs selective use of ultrasound guidance (UG) on groin hematoma rates after PVI. The Vascular Study Group of New England database (2010-2014) was queried to identify the complication of postprocedural groin hematoma after 7359 PVIs performed through CFA access. Hematoma (including pseudoaneurysms) was defined as minor (requiring compression or observation), moderate (requiring transfusion or thrombin injection), and major (requiring operation). Both procedure-level and interventionalist-level analyses were performed. Multivariable Poisson regression models were used to compare hematoma rates of interventionalists based on routine (≥80% of PVIs) and selective (<80%) utilization of UG in the adjusted overall sample and in multiple subgroups. The overall postprocedural groin hematoma rate after PVI was 4.5%, and the rate of combined moderate and major hematoma was 0.8%. Among 114 interventionalists with ≥10 PVI procedures, routine and selective UG was used by 31 (27%) and 83 (73%) interventionalists, respectively. Routine UG was protective against hematoma (rate ratio [RR], 0.62; 95% confidence interval [CI], 0.46-0.84; P < .01). Subgroup analysis revealed that routine UG was also protective against hematoma under the following circumstances: age >80 years (RR, 0.47; 95% CI, 0.27-0.85; P = .01), body mass index ≥30 (RR, 0.51; 95% CI, 0.29-0.90; P = .02), and sheath size >6F (RR, 0.43; 95% CI, 0.23-0.79; P < .01).\n\nQuestion:\nDoes routine use of ultrasound guidance in femoral arterial access for peripheral vascular intervention decrease groin hematoma rates?\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:\nCytochrome P450 monooxygenases (P450s) catalyze oxidation of various substrates using oxygen and NAD(P)H. Plant P450s are involved in the biosynthesis of primary and secondary metabolites performing diverse biological functions. The recent availability of the soybean genome sequence allows us to identify and analyze soybean putative P450s at a genome scale. Co-expression analysis using an available soybean microarray and Illumina sequencing data provides clues for functional annotation of these enzymes. This approach is based on the assumption that genes that have similar expression patterns across a set of conditions may have a functional relationship. We have identified a total number of 332 full-length P450 genes and 378 pseudogenes from the soybean genome. From the full-length sequences, 195 genes belong to A-type, which could be further divided into 20 families. The remaining 137 genes belong to non-A type P450s and are classified into 28 families. A total of 178 probe sets were found to correspond to P450 genes on the Affymetrix soybean array. Out of these probe sets, 108 represented single genes. Using the 28 publicly available microarray libraries that contain organ-specific information, some tissue-specific P450s were identified. Similarly, stress responsive soybean P450s were retrieved from 99 microarray soybean libraries. We also utilized Illumina transcriptome sequencing technology to analyze the expressions of all 332 soybean P450 genes. This dataset contains total RNAs isolated from nodules, roots, root tips, leaves, flowers, green pods, apical meristem, mock-inoculated and Bradyrhizobium japonicum-infected root hair cells. The tissue-specific expression patterns of these P450 genes were analyzed and the expression of a representative set of genes were confirmed by qRT-PCR. We performed the co-expression analysis on many of the 108 P450 genes on the Affymetrix arrays. First we confirmed that CYP93C5 (an isoflavone synthase gene) is co-expressed with several genes encoding isoflavonoid-related metabolic enzymes. We then focused on nodulation-induced P450s and found that CYP728H1 was co-expressed with the genes involved in phenylpropanoid metabolism. Similarly, CYP736A34 was highly co-expressed with lipoxygenase, lectin and CYP83D1, all of which are involved in root and nodule development.\n\nQuestion:\nDoes whole genome co-expression analysis of soybean cytochrome P450 genes identify nodulation-specific P450 monooxygenases?\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:\nDiabetes has adverse effects on the retinal microvasculature. The purpose of this study was to compare the effects of inhalation of hypoxic, hyperoxic and normoxic-hypercapnic gas mixtures on retinal vessel diameter in people with and without diabetes. Sixty-one participants (aged 24-50 years) 29 with (male : female ratio 2.6 : 1) and 32 without (male : female ratio 0.7 : 1) diabetes, inhaled hypoxic, hyperoxic and normoxic-hypercapnic gas mixtures for 3-5 mins. The diameters of arterioles and venules were measured using digital retinal images taken before and after gas inhalation. There was no significant difference in the diameters of arterioles and venules prior to gas inhalation in people with and without diabetes. Inhalation of the hyperoxic gas mixture caused a statistically significant decrease in arteriolar and venular diameters without altering mean arterial pressure significantly. Arteriolar vasoconstriction in response to the hyperoxic gas mixture was significantly reduced in people with diabetes (3.95% versus 7.75%; p = 0.04), but venular vasoconstriction did not differ significantly. A hypoxic gas mixture caused increased arteriolar and venular diameter and a normoxic-hypercapnic gas mixture had no significant effect on vessel diameter. Responses to hypoxic and normoxic-hypercapnic gas did not differ significantly between diabetes and non-diabetes subjects.\n\nQuestion:\nDo retinal arterioles have impaired reactivity to hyperoxia in type 1 diabetes?\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:\nSleep quality declines with age, with less time in deep or slow wave sleep (SWS) and reduced amplitude of the delta waves that characterize it. Age-related declines also occur in lean body mass, growth hormone (GH), and insulin-like growth factor 1 (IGF-1). These changes in sleep quality and anabolic status may be related, as administration of GH or growth hormone releasing hormone (GHRH) can enhance SWS and decrease awakenings in young men. Here we examine the relationship between plasma IGF levels and delta sleep quality in older men. The sleep EEG of 30 healthy elderly men (64 +/- 6 yrs; range 50-75) was recorded on the second of 2 consecutive nights. Plasma samples were drawn within 3 weeks of EEG recording, and IGF levels were assayed by RIA after acid extraction. IGF explained 28% (semi-partial correlation coefficient r = .53; p = .003) of the variance in average delta energy per epoch of SWS, after age-related variance was removed. Higher IGF was associated with higher average delta energy. Similar results were obtained for total delta energy during SWS (r = .37, p = .04) 4nd time spent in SWS (r = .42, p = .02). Other measures of sleep quality (e.g., wakefulness, REM sleep) were not correlated with IGF. The IGF delta relationship was minimally influenced by moderator variables such as thyroxine (T3, T4), and/or body mass index (BMI).\n\nQuestion:\nAre higher plasma IGF-1 levels associated with increased delta sleep in healthy older 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:\nNaïve and memory T cells can utilize unique regulatory pathways to promote protection but prevent self-reactivity. A bacterial superantigen SEB exploits unique TCR proximal signaling processes in memory CD4 T cells to induce clonal anergy. The aim of this study was to determine if SEB could antagonize memory CD4 T cells BALB/c mice were primed with TNP-RGG to elicit memory B cells and also immunized with an ovalbumin peptide to elicit memory helper T cells. Another group of TNP-RGG immunized mice were used as adoptive transfer recipients of exogenous DO11.10 memory T cells. Mice were challenged with TNP-OVA with or without prior administration of SEB. B cells secreting IgM or IgG TNP-specific Ab were enumerated by ELISPOT as indicators of primary versus secondary humoral immunity. Comparing the SEB and non-SEB-treated groups, the SEB-treated group failed to produce TNP-specific IgG in response to challenge with TNP-OVA, even if they were previously immunized with OVA. All groups produced IgM, indicating that the primary Ab responses and naïve helper T cells were not impacted by SEB. SEB had no negative impact when DO11.10 × Fyn\n\nQuestion:\nDoes staphylococcal Enterotoxin B ( SEB ) induce Memory CD4 T Cell?\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 investigated whether parental history of hypertension (FH+) enhances the impact of depressed mood, indexed by Beck Depression Inventory (BDI), on ambulatory blood pressure (ABP). Twenty-four-hour ABP, urinary norepinephrine (NE), and cortisol were obtained in 314 unmedicated normotensive and hypertensive men and women (age 18-64 years) who also completed the BDI. Subjects with a positive family history of hypertension (N = 177) exhibited significantly greater mean body mass index (BMI) and ABP compared with subjects without (N = 137). Importantly, when covarying for age, BMI, gender, and race, linear regressions revealed significant FH by BDI interactions. Higher BDI scores were significantly associated with higher 24-hour ABP in FH+ subjects, but not in FH- participants. Relationships were significantly stronger in those with two hypertensive parents vs. those with one vs. those with no hypertensive parents. Increases in BDI scores were significantly related to greater heart rate (HR) and 24-hour urinary NE in both FH+ and FH- groups, although no evidence of a mediational role for NE in the effect of BDI score on blood pressure (BP) or HR was seen.\n\nQuestion:\nAre depressive symptoms related to higher ambulatory blood pressure in people with a family history of hypertension?\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 compare the effect of totally thoracoscopic with conventional, open repair of atrial septal defect. Forty atrial septal defect cases were divided into two groups by surgical approach: totally thoracoscopic approach (group A, n = 20) and conventional open approach (group B, n = 20). In group A, surgical procedures were performed through three portal incisions in the right lateral chest wall under thoracoscopic vision without the aid of a computerized robotic surgical system. Notably, all operations were completed by one surgeon who had just begun using this technique. In group B, the atrial septal defects were repaired in conventional open fashion. Clinical outcomes and serum levels of tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), interleukin-10 (IL-10), intercellular adhesion molecule 1 (ICAM-1), and creatine kinase isoenzyme-myocardial band (CK-MB) for the two groups were evaluated and compared. All operations were performed successfully without serious complications. Durations of cardiopulmonary bypass (CPB), CPB setup, aortic cross-clamping, and operative procedure were significantly longer in group A than in group B (P < 0.05). The recovery times for body temperature and laboratory values of leukocytes were significantly shorter for group A than for group B (P < 0.05). There were no differences in durations of postoperative assisted ventilation or intensive care unit and hospital stays, volumes of blood transfused intraoperatively or thoracic drainage, or medical costs between the two groups. Serum levels of inflammatory factors (TNF-α, IL-6, IL-10, and ICAM-1) and CK-MB increased significantly in both groups after surgery. However, 6 h and 12 h after surgery, levels of these inflammatory factors and CK-MB were significantly lower in group A than in group B (P < 0.05).\n\nQuestion:\nDoes totally thoracoscopic repair of atrial septal defect reduce systemic inflammatory reaction and myocardial damage in initial 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:\nDecreased spinal excitability contributes to the immobilizing effects of halogenated ethers during general anaesthesia. Recurrent spinal responses such as F-waves reflect spinal excitability and are suppressed by volatile anaesthetics. To evaluate whether F-waves are suitable for monitoring immobility, the concentration-dependent effects of sevoflurane on F-waves were compared with effects on the Bispectral Index (BIS). The predictive power of all parameters for movement responses to noxious stimuli was tested. In addition, the effect of the noxious stimulus itself on F-waves was investigated. In 28 patients, F-waves were recorded during sevoflurane anaesthesia at a frequency of 0.2 Hz at the lower limb. To insert a laryngeal mask, the sevoflurane concentration was initially increased to approximately 4%, which caused a complete extinction of F-waves. The sevoflurane concentration was then reduced until the F-waves recovered. BIS and spectral edge frequency (SEF(95)) were recorded continuously. The t(1/2ke0) and EC(50) values of the F-wave persistence and amplitude were calculated using a standard pharmacokinetic-pharmacodynamic model. During decreasing sevoflurane concentration motor responses to tetanic electrical stimulation (50 Hz, 60 mA, 5 s, volar forearm) were tested in seven patients and MAC(tetanus) was calculated using logistic regression. Sevoflurane reduces the F-wave amplitude with an EC(50) of 0.79 vol% at a far lower concentration than the calculated MAC(tetanus) (1.5 vol%), whereas the F-wave persistence yields an EC(50) of 1.4 vol%. Spinal and EEG parameters predicted the motor responses to movement better than chance alone, but did not differ significantly from each other.\n\nQuestion:\nDoes concentration-dependent suppression of F-waves by sevoflurane predict immobility to painful stimuli in humans?\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:\nProstacyclin (PGI2) that is released from the vascular endothelium plays an important role in vasodilatation and thrombo-resistance, and it has long been suspected to protect cell survival. How it does so has never been clear. Recently, it has been shown that the NADPH oxidase 4 (Nox4) improves endothelial cell functions and promotes angiogenesis in vivo, but it was not known how to boost Nox4 therapeutically to exploit its protective functions in the vasculature. Here, we identified such a stimulus. The selective and stable prostacyclin receptor (IP-R) agonist cicaprost increases the expression of Nox4 in human endothelial cells of several types, including endothelial progenitor cells. The elevation of cellular cyclic-AMP increased Nox4 expression and H2O2 production and prevented endothelial cell apoptosis. We delineate the intracellular signaling that promotes cytoprotection: Cicaprost acts via the IP-R/protein kinase A (PKA)/cyclic adenosine monophosphate (cAMP) response element binding (CREB) protein pathway. Importantly, the up-regulation of Nox4 by cicaprost also enhanced endothelial cell proliferation, migration, and angiogenesis, with all effects being substantially decreased by Nox4 gene silencing. Finally, cicaprost enhanced the growth of blood vessels into subcutaneous sponges implanted in mice, an effect that was also blocked by Nox4 gene silencing. The prostacyclin analogue cicaprost induces Nox4 via IP receptor-cAMP/PKA/CREB pathway. The activation of this pathway protects endothelial cells and enhances pro-angiogenic activity both in vitro and in vivo.\n\nQuestion:\nDoes prostacyclin signaling boost NADPH oxidase 4 in the endothelium promoting cytoprotection and angiogenesis?\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 scarce data on glucose transporter expression of leukocytes are contradictory and nothing is known about changes accompanying physiological leukocytosis during pregnancy, which imposes acute metabolic demands on the cells. Cytospin preparations of intravascular leukocytes were searched immunocytochemically for the high affinity glucose transporters GLUT1, 3 and 4. Pregnancy-associated quantitative changes in transporter expression were assessed by flow cytometry. Granulocytes and monocytes stained for GLUT1, 3 and 4. Major changes in cell surface transporter expression during pregnancy were a 36% (P < 0.05) down-regulation of granulocyte GLUT1 at term, and an increase in monocyte GLUT3 levels to 137% (P < 0.05), paralleled by a 24% (P < 0.05) decrease in GLUT4 content in second trimester. Apart from a minor subpopulation, lymphocytes were negative for these carriers.\n\nQuestion:\nIs physiological leukocytosis during pregnancy associated with changes in glucose transporter expression of maternal peripheral blood granulocytes and monocytes?\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:\nResveratrol is a polyphenol present in red wine for which the capability of directly interfering with the hallmark of Alzheimer's disease (AD), i.e. toxic β-amyloid protein (Aβ) aggregation, has been shown recently. Since the stimulation of proteostasis could explain reduced Aβ-aggregation, we searched for proteostasis targets of resveratrol. The transgenic Caenorhabditis elegans strain CL2006, expressing Aβ1-42 under control of a muscle-specific promoter and responding to Aβ-toxicity with paralysis, was used as a model. Target identification was accomplished through specific knockdowns of proteostasis genes by RNA interference. Effects of resveratrol on protein aggregation were identified using ProteoStat(®) Detection Reagent, and activation of proteasomal degradation by resveratrol was finally proven using a specific fluorogenic peptide substrate. Resveratrol at a concentration of 100 µM caused a 40 % decrease in paralysis. UBL-5 involved in unfolded protein response (UPR) in mitochondria proved to be necessary for the prevention of Aβ-toxicity by resveratrol. Also XBP-1, which represents an endoplasmic reticulum-resident factor involved in UPR, was identified to be necessary for the effects of resveratrol. Regarding protein degradation pathways, the inhibition of macroautophagy and chaperone-mediated autophagy prevented resveratrol from reducing paralysis as did the inhibition of proteasomal degradation. Finally, resveratrol reduced the amount of lysosomes, suggesting increased flux of proteins through the autophagy pathways and activated proteasomal degradation.\n\nQuestion:\nDoes resveratrol reduce amyloid-beta ( Aβ₁₋₄₂ ) -induced paralysis through targeting proteostasis in an Alzheimer model of Caenorhabditis elegans?\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 pathology of two cases of human Hendra virus infection, one with no clinical encephalitis and one with relapsing encephalitis. Autopsy tissues were investigated by light microscopy, immunohistochemistry and in situ hybridization. In the patient with acute pulmonary syndrome but not clinical acute encephalitis, vasculitis was found in the brain, lung, heart and kidney. Occasionally, viral antigens were demonstrated in vascular walls but multinucleated endothelial syncytia were absent. In the lung, there was severe inflammation, necrosis and viral antigens in type II pneumocytes and macrophages. The rare kidney glomerulus showed inflammation and viral antigens in capillary walls and podocytes. Discrete necrotic/vacuolar plaques in the brain parenchyma were associated with antigens and viral RNA. Brain inflammation was mild although CD68(+) microglia/macrophages were significantly increased. Cytoplasmic viral inclusions and antigens and viral RNA in neurones and ependyma suggested viral replication. In the case of relapsing encephalitis, there was severe widespread meningoencephalitis characterized by neuronal loss, macrophages and other inflammatory cells, reactive blood vessels and perivascular cuffing. Antigens and viral RNA were mainly found in neurones. Vasculitis was absent in all the tissues examined.\n\nQuestion:\nDoes human Hendra virus infection cause acute and relapsing encephalitis?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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