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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:\nDuchenne muscular dystrophy (DMD) is a genetic muscle disease caused by the absence of dystrophin. An established animal model of DMD is the mdx mouse, which is unable to express dystrophin. Inflammation, particularly the proinflammatory cytokine tumor necrosis factor alpha (TNF-α), strongly contributes to necrosis in the dystrophin-deficient fibers of the mdx mice and in DMD. In this study we investigated whether the antioxidant N-acetylcysteine (NAC) decreases TNF-α levels and protects the diaphragm muscle of mdx mice against necrosis. Mdx mice (14 days old) received daily intraperitoneal injections of NAC for 14 days, followed by removal of the diaphragm muscle. Control mdx mice were injected with saline. NAC reduced TNF-α and 4-HNE-protein adducts levels, inflammation, creatine kinase levels, and myonecrosis in diaphragm muscle.\n\nQuestion:\nDoes n-acetylcysteine treatment reduce TNF-α levels and myonecrosis in diaphragm muscle of mdx mice?\n\nAnswer:",
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"content": "yes",
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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:\nThis study aimed to investigate the expression and significance of ATF-3 in laryngeal squamous cell carcinoma (LSCC). Expression of ATF-3 was examined using immunohistochemistry methods in samples from 83 cases of LSCC carcinoma. MTT assay was used to detect proliferation of Hep-2 cells after ATF-3 knocked down by siRNA lentivirus. A mouse model was used to investigate the inhibitive role of ATF-3 siRNA in LSCC xenografts. Realtime RCR was used to detect Cyclin D1 expression after ATF-3 downregulation in Hep-2 cells. The expression of ATF-3 was positively detected in all the 83 cases of LSCC cancer tissues while Only 4 cases of adjacent non-neoplastic tissues were detected with positive ATF-3 expression. The ATF-3 expression was statistically related with T stage, neck nodal metastasis, clinical stage and prognosis of LSCC. Both cell proliferation in vitro and tumor growth in vivo were suppressed after ATF-3 knockdown. Furthermore, the expression of Cyclin D1 was decreased after ATF-3 downregulation in Hep-2 cells.\n\nQuestion:\nIs upregulation of ATF-3 correlated with prognosis and proliferation of laryngeal cancer by regulating Cyclin D1 expression?\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 in articular cartilage whether degraded type II collagen is more abundant in Col11a1 mutant cho/+ than in age-matched +/+ mice and whether collagen degradation occurs in a generalized or localized fashion. Knee joints from cho/+ and +/+ mice at 6, 9, 12 and 15 months of age were dissected, fixed, cryosectioned, and stained with antibody COL2-3/4m against denatured type II collagen using a FITC-conjugated secondary antibody. Sections were viewed and photographed under a fluorescence microscope and areas of staining were quantified. Before 12 months of age, little degraded collagen staining was detectable in +/+ or cho/+ mice. By 15 months, however, cho/+ mice showed significantly more degraded type II collagen than age-matched controls. Degraded collagen staining was localized at the articular surface, not distributed generally throughout the articular cartilage.\n\nQuestion:\nDoes a type XI collagen mutation lead to increased degradation of type II collagen in articular cartilage?\n\nAnswer:",
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"content": "yes",
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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 success of bone marrow transplantation in leukemia depends on graft-versus-leukemia (GvL) effects, mediated by cytotoxic T lymphocytes (CTL) and natural killer (NK) cells. These act by CD95L or granule cytotoxins, such as granzyme B (GrB) whose only known inhibitor is proteinase inhibitor 9 (PI-9). Since PI-9 protects cells from CTL, PI-9 may counteract GvL in leukemias. Our aim was to establish methods to analyze the expression and function of PI-9. We screened the most common pediatric ALL subsets, i.e. pre-B, common, and cortical T-ALL, for PI-9 expression, using a reverse transcription polymerase chain reaction (RT-PCR) approach which was correlated to semiquantitative and functional methods established in cell lines and patient probes. In vitro, PI-9 mediated resistance towards CTL and inhibited GrB-induced clevage of caspase 3. In patient-derived ALL cells, PI-9 high and PI-9 low specimens were studied by flow cytometry, RT-PCR, in vitro GrB treatment and NK assay, demonstrating concordant results and PI-9-dependent target cell protection. Analysis of PI-9 in probes from ALL patients showed differential expression, but no correlation with immunotype.\n\nQuestion:\nIs the granzyme B inhibitor PI-9 differentially expressed in all main subtypes of pediatric acute lymphoblastic leukemias?\n\nAnswer:",
"role": "user"
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"content": "yes",
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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:\nA major goal of bladder exstrophy management is urinary continence, often using bladder neck reconstruction. We report our experience with bladder neck reconstruction after complete primary repair of exstrophy. Patient history, ultrasound, voiding cystourethrogram, examination using anesthesia and urodynamics were performed during a prospective evaluation. Continence was assessed using the International Children's Continence Society classification and the dry interval. Bladder capacity was measured by examination using anesthesia, voiding cystourethrogram and/or urodynamics. Urodynamics were also done to assess bladder compliance and detrusor muscle function. From 1994 to 2010 we treated 31 male and 15 female patients with bladder exstrophy after complete primary repair of exstrophy. Of patients 5 years old or older bladder neck reconstruction was performed after complete primary repair in 9 of 21 males (43%) and in 3 of 11 females (27%) at a mean age of 6.3 and 8.1 years, respectively. By the International Children's Continence Society classification 6 of 12 patients (50%) were continent less than 1.5 years after bladder neck reconstruction and 2 of 9 (23%) were evaluable 1.5 years or greater after reconstruction. Median bladder capacity was 100 ml before, 50 ml less than 1.5 years after and 123 ml 1.5 years or greater after bladder neck reconstruction. Three males and 2 females emptied via an appendicovesicostomy. Two boys underwent augmentation.\n\nQuestion:\nIs bladder neck reconstruction often necessary after complete primary repair of exstrophy?\n\nAnswer:",
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMany studies have investigated the importance of oxidative stress on the cardiovascular system. In this study we evaluated the effects of central catalase inhibition on cardiopulmonary reflex in conscious Wistar rats. Male Wistar rats were implanted with a stainless steel guide cannula in the fourth cerebral ventricle. The femoral artery and vein were cannulated for mean arterial pressure and heart rate measurement and for drug infusion, respectively. After basal mean arterial pressure and heart rate recordings, the cardiopulmonary reflex was tested with a dose of phenylbiguanide (PBG, 8 μg/kg, bolus). Cardiopulmonary reflex was evaluated before and μ l15 minutes after 1.0 μl 3-amino-1,2,4-triazole (ATZ, 0.01 g/100 μl)0.01 g/100 μl) injection into the fourth cerebral ventricle. Vehicle treatment did not change cardiopulmonary reflex responses. Central ATZ significantly increased hypotensive responses without influencing the bradycardic reflex.\n\nQuestion:\nDoes aTZ ( 3-amino-1,2,4-triazole ) injected into the fourth cerebral ventricle influence the Bezold-Jarisch reflex in conscious 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 chemerin receptor CMKLR1 is one type of G protein-coupled receptors abundant in monocyte-derived dendritic cells and macrophages, which plays a key role in the entry of a subset of immunodeficiency viruses including HIV/SIV into lymphocytes and macrophages. The aim of this work was to investigate how CMKLR1 was internalized and whether its internalization affected cell signaling in vitro. Rat basophilic leukemia RBL-2H3 cells, HEK 293 cells, and HeLa cells were used. CMKLR1 internalization was visualized by confocal microscopy imaging or using a FACScan flow cytometer. Six potential phosphorylation sites (Ser337, Ser343, Thr352, Ser344, Ser347, and Ser350) in CMKLR1 were substituted with alanine using site-directed mutagenesis. Heterologous expression of wild type and mutant CMKLR1 allowed for functional characterization of endocytosis, Ca(2+) flux and extracellular signal-regulated kinase (ERK) phosphorylation. Chemerin and the chemerin-derived nonapeptide (C9) induced dose-dependent loss of cell surface CMKLR1-GFP fusion protein and increased its intracellular accumulation in HEK 293 cells and RBL-2H3 cells stably expressing CMKLR1. Up to 90% of CMKLR1 was internalized after treatment with C9 (1 μmol/L). By using different agents, it was demonstrated that clathrin-independent mechanism was involved in CMKLR1 internalization. Mutations in Ser343 for G protein-coupled receptor kinase phosphorylation and in Ser347 for PKC phosphorylation abrogated CMKLR1 internalization. Loss of CMKLR1 internalization partially enhanced the receptor signaling, as shown by increased Ca(2+) flux and a shorter latency to peak level of ERK phosphorylation.\n\nQuestion:\nDoes chemerin C9 peptide induce receptor internalization through a clathrin-independent pathway?\n\nAnswer:",
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWhether heart rate upon discharge following hospitalization for heart failure is associated with long-term adverse outcomes and whether this association differs between patients with sinus rhythm (SR) and atrial fibrillation (AF) have not been well studied. We conducted a retrospective cohort study from clinical registry data linked to Medicare claims for 46 217 patients participating in Get With The Guidelines(®)-Heart Failure. Cox proportional-hazards models were used to estimate the association between discharge heart rate and all-cause mortality, all-cause readmission, and the composite outcome of mortality/readmission through 1 year. For SR and AF patients with heart rate ≥75, the association between heart rate and mortality (expressed as hazard ratio [HR] per 10 beats-per-minute increment) was significant at 0 to 30 days (SR: HR 1.30, 95% CI 1.22 to 1.39; AF: HR 1.23, 95% CI 1.16 to 1.29) and 31 to 365 days (SR: HR 1.15, 95% CI 1.12 to 1.20; AF: HR 1.05, 95% CI 1.01 to 1.08). Similar associations between heart rate and all-cause readmission and the composite outcome were obtained for SR and AF patients from 0 to 30 days but only in the composite outcome for SR patients over the longer term. The HR from 0 to 30 days exceeded that from 31 to 365 days for both SR and AF patients. At heart rates <75, an association was significant for mortality only for both SR and AF patients.\n\nQuestion:\nIs heart rate at hospital discharge in patients with heart failure associated with mortality and rehospitalization?\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 quantify the resistance to torque of different implant systems and their connection devices using in vitro torsion tests. Three internal connection systems, 1 conventional system with internal torque and 1 conventional system with a mounting device used as a control group were tested on 5 groups. Rupture torque (in newton meter): Biomet 3i Certain group 4 showed a statistically significant higher average (2.65 N·m), followed in order by Biomet 3i Osseotite group 5 (2.18 N·m), Bonelike group 2 (1.80 N·m). Angle deformation/rupture: all groups obtained similar values, without significant differences. Elastic limit (in newton meter): Bonelike group 2 (1.06 N·m) showed similar behavior to group 1 (1.39 N·m) (Nobel Biocare), without significant differences, whereas Bonelike group 3 showed a significantly lower value (0.93 N·m). Maximum torque (in newton meter): Biomet 3i Certain group 4 showed significantly higher values in relation to other groups (2.80 N·m).\n\nQuestion:\nDo biomechanical evaluation of resistance to insertion torque of different implant systems and insertion driver types?\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 compare the detection rates of prostate cancer (PCa) and complications of the transrectal ultrasonography (TRUS)-guided 24-core saturation scheme versus 14-core scheme for transperineal prostate biopsy in patients with total PSA < 20 microg/L. We performed TRUS-guided 24-core saturation transperineal biopsy for 136 patients suspected of PCa (24-core group) and 14-core biopsy for another 116 (14-core group). We compared the PCa detection rates and post-biopsy complications, such as gross hematuria, urinary system infection, and acute urinary retention between the two groups. The baseline characteristics of the two groups were comparable with regard to the mean age, prostate volume and PSA level (P>0.05). The positive rates of PCa detection were 48.53% (66/136) in the 24-core group and 17.24% (20/116) in the 14-core group (P<0.001), and the positive rates of samples were 8.09% and 2.83%, respectively (P=0.012). The detection rate of PCa in the apex zone was significantly higher in the former (11.76%) than in the latter (1.72%) (P<0.05). There were no statistically significant differences in such post-biopsy complications as gross hematuria, urinary system infection, and acute urinary retention between the two groups (P>0.05).\n\nQuestion:\nIs [ Ultrasound-guided transperineal 24-core saturation prostate biopsy superior to the 14-core scheme in detecting prostate cancer in patients with PSA < 20 microg/L ]?\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:\nGamma glutamyl transferase (GGT) is involved in the pathophysiologic process of coronary atherosclerosis. GGT activity plays a role in the catabolism of glutathione which is known as one of the major antioxidants. However, there is a lack of research on direct examination of relevance between serum GGT activity with systemic oxidative stress. We aimed to investigate the relationship between GGT activity with systemic oxidative stress markers and the extent and complexity of coronary artery disease (CAD) assessed with SYNTAX score in stable CAD. Measurements were obtained from 359 patients with stable CAD (Mean age = 57.7 ± 10.1 years). The patients were divided into two groups according to the median GGT level (GGT < median group < 22 and GGT > median group ≥ 22). Angiography was performed and SYNTAX score was calculated in all patients. Oxidative stress markers (total oxidant status [TOS], total antioxidant capacity [TAC] and oxidative stress index [OSI]) were measured in all patients. While SYNTAX score and oxidative stress markers such as TOS and OSI have been increased, TAC was decreased in GGT > median group compared with GGT < median group (p < 0.05, for all). GGT activity was independently associated with diabetes (β = 0.106, p = 0.015) and OSI (β = 0.556, p < 0.001) in multiple linear regression analysis. However, the independent association between GGT activity and SYNTAX score was not found in present study (β = 0.063, p = 0.238).\n\nQuestion:\nIs gamma glutamyl transferase activity independently associated with oxidative stress rather than SYNTAX score?\n\nAnswer:",
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPlasma soluble CD40 ligand (sCD40L) is increased during HIV-1 infection, but it is unknown whether it circulates in monomeric or multimeric forms, and whether the circulating forms have differential effects on myeloid dendritic cell function and adaptive regulation. sCD40L forms were measured in plasma samples from HIV-infected donors. The effects of sCD40L forms on dendritic cell function were measured in vitro. To delineate which forms of sCD40L are present in plasma from HIV-infected donors, immunoblots were performed following enrichment of plasma for medium and low-abundance proteins. Dendritic cells from seronegative donors were exposed to multiple forms of sCD40L prior to Toll-like receptor stimulation and dendritic cell function and adaptive regulation was assessed in vitro. Monomeric and multimeric forms of sCD40L were identified in plasma from antiretroviral therapy-treated HIV-infected donors. Although monomeric and multimeric forms of sCD40L had differential effects on dendritic cell activation when given alone, both strongly suppressed secretion of the Th1 skewing cytokine, interleukin-12, upon subsequent Toll-like receptor stimulation. Furthermore, dendritic cells exposed to both monomeric and multimeric sCD40L induced regulatory T-cell formation and T-cell anergy.\n\nQuestion:\nDoes soluble CD40 ligand contribute to dendritic cell-mediated T-cell dysfunction in HIV-1 infection?\n\nAnswer:",
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe sought to identify potentially modifiable determinants associated with variability in leptomeningeal collateral status in patients with acute ischemic stroke. Data are from the Keimyung Stroke Registry. Consecutive patients with M1 segment middle cerebral artery ± intracranial internal carotid artery occlusions on baseline computed tomographic angiography (CTA) from May 2004 to July 2009 were included. Baseline and follow-up imaging was analyzed blinded to all clinical information. Two raters assessed leptomeningeal collaterals on baseline CTA by consensus, using a previously validated regional leptomeningeal score (rLMC). Baseline characteristics (N = 206) were: mean age = 66.9 ± 11.6 years, median baseline National Institutes of Health Stroke Scale = 14 (interquartile range [IQR] = 11-20), and median time from stroke symptom onset to CTA = 166 minutes (IQR = 96-262). Poor collateral status at baseline (rLMC score = 0-10) was seen in 73 of 206 patients (35.4%). On univariate analyses, patients with poor collateral status at baseline were older; were hypertensive; had higher white blood cell count, blood glucose, D-dimer, and serum uric acid levels; and were more likely to have metabolic syndrome. Multivariate modeling identified metabolic syndrome (odds ratio [OR] = 3.22, 95% confidence interval [CI] = 1.69-6.15, p < 0.001), hyperuricemia (per 1mg/dl serum uric acid; OR = 1.35, 95% CI = 1.12-1.62, p < 0.01), and older age (per 10 years; OR = 1.34, 95% CI = 1.02-1.77, p = 0.03) as independent predictors of poor leptomeningeal collateral status at baseline.\n\nQuestion:\nAre leptomeningeal collaterals associated with modifiable metabolic risk factors?\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:\nES-62, a phosphorylcholine (PC)-containing immunomodulator secreted by the parasitic worm Acanthocheilonema viteae, protects against nephritis in the MRL/Lpr mouse model of systemic lupus erythematosus (SLE). However, ES-62 is not suitable for development as a therapy and thus we have designed drug-like small molecule analogues (SMAs) based around its active PC-moiety. To provide proof of concept that ES-62-based SMAs exhibit therapeutic potential in SLE, we have investigated the capacity of two SMAs to protect against nephritis when administered to MRL/Lpr mice after onset of kidney damage. SMAs 11a and 12b were evaluated for their ability to suppress antinuclear antibody (ANA) generation and consequent kidney pathology in MRL/Lpr mice when administered after the onset of proteinuria. SMAs 11a and 12b suppressed development of ANA and proteinuria. Protection reflected downregulation of MyD88 expression by kidney cells and this was associated with reduced production of IL-6, a cytokine that exhibits promise as a therapeutic target for this condition.\n\nQuestion:\nAre drug-like analogues of the parasitic worm-derived immunomodulator ES-62 therapeutic in the MRL/Lpr model of 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 interaction of nitric oxide with superoxide (O2-) is a major O2- scavenging mechanism that can minimize O2 (-)-mediated oxidative stress. Glomeruli produce both nitric oxide and O2- and generation of both radicals is increased in various forms of glomerular disease. O2- increases glomerular capillary permeability to albumin (P(alb)). The present studies tested the hypothesis that nitric oxide opposes this effect, thereby preserving the glomerular protein permeability barrier. P(alb) was determined in isolated rat glomeruli by measuring the change in glomerular volume in response to an experimental oncotic gradient. Changes in P(alb) in response to O2- generated by tumor necrosis factor-alpha (TNF-alpha) or xanthine/xanthine oxidase (X/XO) was assessed under conditions of nitric oxide depletion and repletion. Incubation of rat glomeruli with the nitric oxide synthase (NOS) inhibitor L-N(G)-monomethyl arginine (L-NMMA) increased P(alb.) This effect was reversed by the nitric oxide donor diethylenetriamine NONOate (DETA-NONOate) and by the superoxide dismutase (SOD) mimetic Tempol. O2- generated after incubation with TNF-alpha or X/XO increased P(alb). This effect was blocked by DETA-NONOate.\n\nQuestion:\nDoes nitric oxide preserve the glomerular protein permeability barrier by antagonizing superoxide?\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:\nGardening has been reported as being beneficial for mental well-being for vulnerable populations since 2000. However, little is known concerning its role in the general population. Therefore, the aim of the present study was to investigate the relationship of gardening and mental health in adults in a countrywide and population-based setting. Data was retrieved from and analysed in the Scottish Health Survey, 2012-2013. Information on demographics, lifestyle factors, gardening engagement, and adult mental health by General Health Questionnaire was obtained by household interview. Statistical analyses including chi-square test, t-test and survey-weighted logistic and multi-nominal regression modelling were performed. Of 9709 Scottish adults aged 16-99, 5 531 (57.0%) people did not do any gardening or building work in the last four weeks. A total of 888 (9.2%) people reported poor self-rated health. Gardening was associated with adult mental health in people both with or without heart conditions including ability to concentrate, feeling playing a useful part in things, feeling capable of making decisions, thinking of self as worthless, feeling reasonably happy, etc.\n\nQuestion:\nIs gardening beneficial for adult mental health : Scottish Health Survey , 2012-2013?\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:\nAntiphospholipid antibodies (aPL) interfere with several physiologic functions of human trophoblasts, including reducing their ability to migrate, decreasing their production of angiogenic factors, and inducing an inflammatory response. This may provide the underlying mechanism by which aPL responses lead to recurrent pregnancy loss or preeclampsia in women with obstetric antiphospholipid syndrome (APS). Although treatment with heparin may reduce the rate of recurrent pregnancy loss, the risk of preeclampsia remains high. Therefore, alternative treatments are needed for the management of pregnant patients with APS. Since aspirin-triggered lipoxins (ATLs) have immune and angiogenic modulatory properties, the objective of this study was to determine the effects of the ATL 15-epi-lipoxin A4 on the function of aPL-altered human trophoblasts in the first trimester of pregnancy. A first-trimester human trophoblast cell line (HTR8) was treated with mouse anti-human β2 -glycoprotein I monoclonal antibodies (aPL) in the presence or absence of the ATL 15-epi-lipoxin A4 . Trophoblast migration and interactions with endometrial endothelial cells were measured using Transwell and coculture assays. Trophoblast secretion of cytokines and angiogenic factors was measured by enzyme-linked immunosorbent assay. Treatment of HTR8 cells with ATL reversed the aPL-induced decrease in trophoblast migration, an effect that appeared to be regulated through restoration of interleukin-6 production. Using a model of spiral artery transformation, aPL and sera from APS patients with pregnancy morbidity disrupted trophoblast-endothelial cell interactions, and treatment with ATL restored the stability of the cocultures. In contrast, ATL treatment did not resolve the proinflammatory and antiangiogenic responses of trophoblasts induced by aPL.\n\nQuestion:\nDoes aspirin-triggered lipoxin prevent antiphospholipid antibody effects on human trophoblast migration and endothelial cell interactions?\n\nAnswer:",
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo study the role of FABP4 in the plasma of type 2 diabetic (T2D) subjects with and without metabolic syndrome (MS) and the impact of thiazolidinedione (TZD) treatment. FABP4 was analyzed in 274 individuals (169 T2D subjects and 105 controls). MS-T2D subjects had higher FABP4 levels than non-MS-T2D subjects and controls (53% and 76% increase, respectively, p<0.005). FABP4 levels in T2D subjects were positively correlated to the number of MS elements, obesity degree, adiponectin, triglycerides, lipoperoxides, C-reactive protein, age, systolic blood pressure and diabetes duration (p<0.05). Neither clinical or subclinical atherosclerosis, nor plasma levels of insulin, glucose or RBP4 were associated to FABP4. TZD-treated T2D subjects showed >30% higher FABP4 levels (p<0.05) than non-TZD-treated T2D. A subgroup study confirmed that TZD treatment prospectively increased FABP4 levels (p<0.05) along with an increase of peripheral blood mononuclear cell PPARgamma activity (p<0.05). Furthermore, in vitro studies showed that TZD treatment increased FABP4 mRNA, intracellular protein levels and extracellular secretion from human adipocytes.\n\nQuestion:\nIs fatty acid binding protein 4 increased in metabolic syndrome and with thiazolidinedione treatment in diabetic patients?\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:\nIntestinal intraepithelial lymphocytes that reside within the epithelium of the intestine form one of the main branches of the immune system. A majority of IELs express CD8α homodimer together with other molecules associated with immune regulation. Growing evidence points to the WNT signaling pathway as a pivotal piece in the immune balance and focuses on its direct regulation in intestinal epithelium. Therefore we decided to investigate its role in IELs' immune status determination. DSS colitis was induced in male C57BL mice. IELs were isolated from colon samples using mechanical dissociation followed by percoll gradient purification and Magnetic-activated cell sorting. Phenotype and cytokine production and condition with Wnts were analyzed by flow cytometry, real-time PCR or ELISA. Proliferation of lymphocytes were evaluated using CFSE dilution. Cell responses after WNT pathway interference were also evaluated. Non-canonical WNT pathway elements represented by FZD5, WNT5A and NFATc1 were remarkably elevated in colitis IELs. The non-canonical WNT5A skewed them into a pro-inflammatory category as measured by inhibitory cell surface marker LAG3, LY49E, NKG2A and activated marker CD69 and FASL. Gaining of a pro-inflammatory marker was correlated with increased IFN-γ production but not TNF whilst decreased TGF-β and IL-10. Both interrupting WNT5A/PKC pathway and adding canonical WNT stimulants could curtail its immune-activating effect.\n\nQuestion:\nDoes wNT5A transform intestinal CD8αα⁺ IELs into an unconventional phenotype with pro-inflammatory features?\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:\nDuring the last few years, a number of children of asylum applicants in Sweden developed an apathetic or unconscious state. The syndrome was perceived as new, and various explanations were advanced such as factitious disorder, intoxication, or stress. Considering a potential association between traumatic stress and regulation of steroids biosynthesis, this study explored whether changes in concentrations of endogenous steroids were associated with the above syndrome. Eleven children were recruited in the study. Concentrations of steroids in blood samples were determined using high sensitivity liquid chromatography tandem mass spectrometry methods. Symptoms were assessed with a clinical rating scale developed for the study. Steroid concentrations were measured at the entry into study and after recovery; and concentrations were evaluated for the association with the symptoms in apathetic children. Cortisol and cortisone concentrations at baseline were negatively associated with duration of the symptoms from entry into the study to clinical recovery. Higher concentrations of pregnanes (pregnenolone, 17-OH-pregnenolone, and dehydroepiandrosterone) were observed in the symptomatic state and the concentrations decreased after the recovery.\n\nQuestion:\nAre patterns of endogenous steroids in apathetic refugee children compatible with long-term stress?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nA deficiency of tetrahydrobiopterin (BH4), an essential cofactor for nitric oxide (NO) synthase, decreases NO synthesis and increases superoxide production. Supplementation of BH4 has been postulated to improve endothelial function in atherosclerotic patients. The purpose of this study was to determine whether BH4 restores endothelium-dependent vasodilation in patients with essential hypertension. We evaluated the effects of BH4 on forearm vascular responses to acetylcholine (ACh), an endothelium-dependent vasodilator, and isosorbide dinitrate (ISDN), an endothelium-independent vasodilator, both in patients with essential hypertension and in age- and sex-matched normal control subjects. Forearm blood flow (FBF) was measured using strain gauge plethysmography. The response of FBF to ACh was less in hypertensive patients (n = 8) than in normal control subjects (n = 8). There was no significant difference in FBF response to ISDN in the two groups. During coinfusion of BH4 (500 mg/min), the FBF response to ACh in hypertensive patients increased significantly (14.8 +/- 4.6 to 25.6 +/- 7.3 mL/min/100 mL tissue, P < .05) to the level of normal control subjects. In the control subjects, also, BH4 augmented the FBF response to ACh (27.8 +/- 8.7 to 36.1 +/- 9.6 mL/min/100 mL tissue, P < .05). The increase in FBF after ISDN was not altered by BH4 in either group (each group, n = 6).\n\nQuestion:\nDoes tetrahydrobiopterin enhance forearm vascular response to acetylcholine in both normotensive and hypertensive individuals?\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 protect effects of sodium ferulate (SF) on the daunormbicin(DNR-induced cardiotoxicity in juvenile rats. Forty male juvenile SD rats were randomly divided into control group (Control), daunorubicin group (DNR), sodium ferudate treatment group (DNR + SF), sodium ferudate group (SF) (n = 10) . Juvenile rats were intraperitoneally treated with DNR (2.5 mg/kg every week for a cumulative dose of 10 mg/kg) preparation immature myocardial injury model in presence with SF (60 mg/kg) oral treat- ment for 25 days. The left ventricular pressure and its response to isoproterenol were measured using left ventricular catheter. Rat myocardium myocardial pathology specimens and ultrastructure changes were also observed. The expression of cardiac Troponin I (cTNI) was detected by Western blot and RT-PCR. Results: SF treatment could inhibit the decreasing of heart rates induced by DNR damage (P < 0.05); it could increase the left ventrivular end diastolic pressure(LVEDP), heart rate, the maximal left ventrivular systolic speed(LVP + dp/dtmax) and the maximal left ventrivular diastolic speed (LVP-dp/dtmax) responding to isoproterenol stimulation(P < 0.01); SF also could improve the myocardial ultrastructure injuries and inhibit the decreasing of cTNI expression caused by DNR damages (P < 0.05).\n\nQuestion:\nDoes [ Sodium ferulate protect against daunorubicin-induced cardiotoxicity in juvenile rats ]?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo test the hypothesis that prenatal exposure to the Hong Kong flu, an influenza pandemic that haunted Europe during winter 1969 to 1970, was associated with reduced intelligence in adulthood. Data from the Medical Birth Register of Norway were linked with register data from the National Conscript Service. The sample comprised all registered boys born alive in single birth after 37 to 43 weeks' gestation during 1967 to 1973 (n = 205,634). Intelligence test scores, recorded at military conscription, were available for 182,913 individuals. The mean intelligence score increased from one birth year to another, except for a downturn in 1970. The birth year 1970 was inversely associated with intelligence score (-0.03 standard deviation [SD]; p < 0.001) after adjustments for birth characteristics, parental characteristics, and the trend of increasing scores over the 7 birth years. Analyses with the sample stratified by birth month showed that the inverse association between the birth year 1970 and intelligence score was significant only among men born in July (-0.04 SD; p = 0.049), August (-0.05 SD; p = 0.013), September (-0.09 SD; p < 0.001), and October (-0.06 SD; p = 0.008). Thus, the intelligence scores of the men born 6 to 9 months after the epidemic were lower than the mean values for the men born in the same months a few years before or after.\n\nQuestion:\nDo register data suggest lower intelligence in men born the year after flu pandemic?\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:\nBrain regions that mediate learning of a conditioned place preference (CPP) undergo significant development in pre and periadolescence. Consuming a high fat (HF) diet during this developmental period and into adulthood can lead to learning impairments in rodents. The present study tested whether HF diet intake, consumed only in pre and periadolescence, would be sufficient to cause impairments using a CPP procedure. Rats were randomly assigned to consume a HF or a low fat (LF) diet during postnatal days (PD) 21-40 and were then placed back on a standard lab chow diet. A 20-day CPP procedure, using HF Cheetos® as the unconditioned stimulus (US), began either the next day (PD 41) or 40 days later (PD 81). A separate group of adult rats were given the HF diet for 20 days beginning on PD 61, and then immediately underwent the 20-day CPP procedure beginning on PD 81. Pre and periadolescent exposure to a LF diet or adult exposure to a HF diet did not interfere with the development of a HF food-induced CPP, as these groups exhibited robust preferences for the HF Cheetos® food-paired compartment. However, pre and periadolescent exposure to the HF diet impaired the development of a HF food-induced CPP regardless of whether it was assessed immediately or 40 days after the exposure to the HF diet, and despite showing increased consumption of the HF Cheetos® in conditioning.\n\nQuestion:\nDoes high fat diet intake during pre and periadolescence impair learning of a conditioned place preference in adulthood?\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:\nVascular calcification accompanying chronic kidney disease increases the mortality and morbidity associated with cardiovascular disorders, but no effective therapy is available. We hypothesized that glycosaminoglycans may contribute to osteoblastic differentiation of vascular smooth muscle cells during vascular calcification. We used exostosin-like glycosyltranferase 2-deficient (EXTL2 knockout) mice expressing high levels of glycosaminoglycans in several organs including the aorta. We performed 5/6 subtotal nephrectomy and fed the mice a high-phosphate diet to induce chronic kidney disease. Overexpression of glycosaminoglycans in the aorta enhanced aortic calcification in chronic kidney disease in EXTL2 knockout mice. Ex vivo and in vitro, matrix mineralization in aortic rings and vascular smooth muscle cells of EXTL2 knockout mice was augmented. Furthermore, removal of glycosaminoglycans in EXTL2 knockout and wild-type mice-derived vascular smooth muscle cells effectively suppressed calcium deposition in a high-phosphate environment.\n\nQuestion:\nDoes glycosaminoglycan overproduction in the aorta increase aortic calcification in murine chronic kidney disease?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe amount of contrast media and renal atheroemboli are risk factors for acute kidney injury after percutaneous coronary intervention (PCI). However, the chronic kidney injury after PCI has not been fully characterized. The purpose of this study was to investigate factors affecting renal function in the late phase after PCI by measuring serum Cystatin C (CysC). In 143 consecutive patients who underwent elective PCI, CysC was evaluated at baseline and at 9 months after PCI, and the percent change in CysC (%CysC) was calculated. The association between %CysC and baseline characteristics, including medication use, was assessed. Of 143 patients, 86 had worsening renal function (WRF; %CysC ≥0), and 57 did not (non-WRF; %CysC <0). Only the use of angiotensin-converting enzyme inhibitor (ACEI) and baseline CysC were significantly different between WRF and non-WRF patients (15 vs. 40%, p=0.001 and 1.02±0.26 vs. 1.13±0.26 mg/L, p=0.015). In univariate analysis, the use of ACEI and CysC were negatively associated with WRF [Odds ratio (OR)=0.26, 95% confidence interval (CI)=0.12-0.57, p<0.001 and OR=0.20, 95% CI=0.05-0.73, p=0.015]. Furthermore, multivariate analysis revealed that the use of ACEI and CysC significantly correlated with WRF (OR=0.26, 95% CI=0.11-0.57, p<0.001 and OR=0.20, 95% CI=0.05-0.74, p=0.016). The %CysC in 36 patients with ACEI was significantly lower than that in 107 patients without ACEI [median: -3.8%; interquartile range (IQR), -11.0 to 4.2%; vs. median: 3.3%; IQR -2.9 to 11.0%, p=0.001].\n\nQuestion:\nDoes angiotensin-Converting Enzyme Inhibitor prevent the Worsening of Renal Function in the Late Phase after Percutaneous Coronary Intervention?\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:\nObstructive sleep apnea (OSA) is influenced by sleep architecture with rapid eye movement (REM) sleep having the most adverse influence, especially in women. There is little data defining the influence of slow-wave sleep (SWS) on OSA. We wished to study the influence of SWS on OSA and identify differences attributable to gender and/or age, if any. Retrospective study of polysomnography (PSG) records of adult patients referred for diagnostic PSG. Records were excluded if they underwent split night or positive airway pressure titration studies, had <180 min of total sleep time (TST) and/or <40% sleep efficiency, or had SWS <5 min and/or <1% of TST. The apnea-hypopnea index (AHI) recorded during SWS was compared with that measured during other non-rapid eye movement (NREM) sleep and during REM sleep. The REM-SWS difference in AHI was measured, and compared between genders. Records from 239 patients were included. The mean AHI in all subjects was 17.7 ± 22.6. The SWS AHI was 6.8 ± 18.9, compared to the REM AHI of 24.9 ± 25.8, and NREM AHI of 15.8 ± 22.8. Females had significantly higher SWS by percentage, and lower NREM AHI (P < 0.0001) and SWS AHI (P = 0.03). Among patients with OSA (AHI ≥5), the difference between REM AHI and SWS AHI was greater in women than in men (34.2 ± 27.4 vs. 21.6 ± 26.0, P = 0.006).\n\nQuestion:\nDo gender and age influence the effects of slow-wave sleep on respiration in patients with obstructive sleep apnea?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIn children with Prader-Labhart-Willi syndrome (PWS), the insulin secretion is reduced, despite obesity, being ascribed to the growth hormone (GH) deficiency of hypothalamic origin. Besides, an increased prevalence of diabetes mellitus was described in this syndrome. Hence, we addressed the questions of how body composition and insulin secretion are interrelated and what impact GH therapy has on the carbohydrate metabolism in PWS. We measured weight, lean and fat mass (by dual-energy X-ray absorptiometry), triglycerides, HbA(1c), and fasting insulin and glucose levels in 17 children (age range 1.5-14.6 years) with PWS to examine whether the carbohydrate metabolism is altered during 36 months of therapy with 8 mg GH/m(2) body surface/week. In a subgroup of 8 children, the insulin secretion was longitudinally assayed during oral glucose tolerance at 0 and 12 months of therapy. Before therapy, the insulin secretion was lower and markedly delayed as compared with reference data and did not rise during therapy. The glucose tolerance was impaired in 2 of 12 children examined by oral glucose tolerance test before therapy and normalized during therapy. Fasting insulin and insulin resistance being normal at the beginning, significantly increased at 12 months and returned to initial levels at 36 months of GH therapy. Fasting glucose as well as HbA(1c) and triglyceride levels were always normal. The fat mass before GH therapy was increased (39.5%) and dropped into the upper normal range (28.3%) during 3 years of therapy, being correlated with fasting insulin concentration and indices of insulin sensitivity before and after 1 year of therapy.\n\nQuestion:\nIs carbohydrate metabolism impaired after 3 years of growth hormone therapy in children with Prader-Willi syndrome?\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 compare the platelet to lymphocyte ratio (PLR) in normal people, benign prostatic hyperplasia (BPH) patients and prostate cancer (PCA) patients, and to explore the prognostic role of PLR in PCA. 155 normal people, 168 BPH patients and 103 PCA patients were enrolled. PCA patients were divided into PLR low value group (PLR<150) and PLR high value group (PLR≥150), and the difference of patients' clinical characteristics between high value group and low value group was comparative studied. The differences of PLR among normal people, BPH patients and PCA patients were statistically significant. In addition, platelet counts, neutrophil counts, PSA level, LDH level, AKP level, CRP level and alkaline phosphatase level were also significantly increased in PLR high value group, while the hemoglobin level was decreased. Besides, serious events such as coma during hospitalization were also more likely to appear in PLR high value group. PCA patients had an average follow-up of 3 years, and a total of 25 cases of patients died, including 11 (16.4%) cases in the PLR low value group, and 14 (38.9%) cases in PLR high value group with. Three years survival rate of patients in high value group was significantly reduced. Additionally, PLR was a possible risk factor associated with mortality, and an independent predictor of all-cause mortality during follow-up.\n\nQuestion:\nDoes platelet to lymphocyte ratio play an important role in prostate cancer 's diagnosis and prognosis?\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:\nObese leptin deficient (ob/ob) mice are a model of adiposity that displays increased levels of fat, glucose, and liver lipids. Our hypothesis is that HO-1 overexpression ameliorates fatty liver development. Obese mice were administered cobalt protoporphyrin (CoPP) and stannic mesoporphyrin (SnMP) for 6 weeks. Heme, HO-1, HO activity, PGC1α, FGF21, glycogen content, and lipogenesis were assessed. CoPP administration increased hepatic HO-1 protein levels and HO activity, decreased hepatic heme, body weight gain, glucose levels, and resulted in decreased steatosis. Increased levels of HO-1 produced a decrease in lipid droplet size, Fatty acid synthase (FAS) levels involving recruitment of FGF21, PPARα, and Glut 1. These beneficial effects were reversed by inhibition of HO activity.\n\nQuestion:\nDo increased HO-1 levels ameliorate fatty liver development through a reduction of heme and recruitment of FGF21?\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 association between myositis autoantibodies and clinical subsets of inflammatory myositis in Korean patients. Immunoprecipitation was performed using the sera of classic polymyositis (PM) (n = 11) and dermatomyositis (DM) (n = 38) patients who met the Bohan and Peter criteria for definite inflammatory myositis. A panel of defined myositis autoantibodies was surveyed to investigate the association between each autoantibody and clinical subsets of inflammatory myositis. Either MSAs, anti-p140, or anti-p155/140 antibodies were found in 63.3% (31/49) of the study subjects. Anti-140-kDa-polypeptide (anti-p140) (18.4%, 9/49) and anti-155/140-kDa polypeptide (anti-p155/140) (16.3%, 8/49) antibodies were the most common, followed by anti-Mi2 (14.3%, 7/49), anti-ARS (12.2%, 6/49) and anti-SRP (2.0%, 1/49) antibodies. All MSAs and anti-p140 and anti-p155/140 antibodies were mutually exclusive. Anti-p140 (23.7%, 9/38), anti-p155/140 (21.1%, 8/38), and anti-Mi2 (18.4%, 3/38) antibodies were found exclusively in DM patients. Anti-p140 antibody was associated with rapidly progressive interstitial lung disease (ILD) (p = 0.001), with a sensitivity of 100.0% (4/4) and a specificity of 85.3% (29/34) in DM patients. Anti-p155/140 antibody was associated with cancer-associated DM (p = 0.009), with a sensitivity of 55.6% (5/9) and a specificity of 89.7% (26/29). Cancer-associated survival was significantly worse when anti-p155/140 antibody was present (19.2 ± 7.6 vs. 65.0 ± 3.5 months, p = 0.032). Finally, anti-ARS antibodies were associated with stable or slowly progressive ILD in PM and DM patients (p = 0.005).\n\nQuestion:\nIs myositis autoantibodies in Korean patients with inflammatory myositis : anti-140-kDa polypeptide antibody primarily associated with rapidly progressive interstitial lung disease independent of clinically amyopathic dermatomyositis?\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:\nIn an effort to assess the role of plasminogen activator inhibitor-1 (PAI-1) in oral squamous cancer development and progression, two different carcinogen treatment protocols were conducted. Protocol I included mice from a PAI-1 transgenic (Tg) breed (n=56) and their wild-type (WT) counterparts (n=56), divided into one control group and two main experimental groups, treated with 7,12-dimethylbenz[a]anthracene (DMBA) for 8 and 16 weeks, respectively. Protocol II included the same number and types of animals and groups, which were similarly treated with 4-Nitroquinoline 1-oxide (4-NQO) in drinking water. Two drugs that affect plasma PAI-1 levels, enalapril and pravastatin, were administered to certain subgroups of animals in both protocols. None of the animals developed macroscopically-visible oral cancer lesions. Eleven animals under Protocol I and 52 animals under Protocol II died. Skin lesions were noted only in DMBA-treated animals (n=9). Almost all animals administered with 4-NQO developed alopecia and lost weight, while two of them developed stomach tumours, and one female mouse developed a large ovarian cyst.\n\nQuestion:\nIs oral carcinogenesis achieved in different carcinogen-treated PAI-1 transgenic and wild-type mouse models?\n\nAnswer:",
"role": "user"
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{
"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:\nAsbestos induces DNA and chromosomal damage, but the DNA repair pathways protecting human cells against its genotoxicity are largely unknown. Polymorphisms in XRCC1 have been associated with altered susceptibility to asbestos-related diseases. However, it is unclear whether oxidative DNA damage repaired by XRCC1 contributes to asbestos-induced chromosomal damage. We sought to examine the importance of XRCC1 in protection against genotoxic effects of crocidolite and Libby amphibole asbestos. We developed a genetic model of XRCC1 deficiency in human lung epithelial H460 cells and evaluated genotoxic responses to carcinogenic fibers (crocidolite asbestos, Libby amphibole) and nongenotoxic materials (wollastonite, titanium dioxide). XRCC1 knockdown sensitized cells to the clastogenic and cytotoxic effects of oxidants [hydrogen peroxide (H₂O₂), bleomycin] but not to the nonoxidant paclitaxel. XRCC1 knockdown strongly enhanced genotoxicity of amphibole fibers as evidenced by elevated formation of clastogenic micronuclei. Crocidolite induced primarily clastogenic micronuclei, whereas Libby amphibole induced both clastogenic and aneugenic micronuclei. Crocidolite and bleomycin were potent inducers of nuclear buds, which were enhanced by XRCC1 deficiency. Libby amphibole and H₂O₂ did not induce nuclear buds, irrespective of XRCC1 status. Crocidolite and Libby amphibole similarly activated the p53 pathway.\n\nQuestion:\nDoes xRCC1 deficiency sensitize human lung epithelial cells to genotoxicity by crocidolite asbestos and Libby amphibole?\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 identify the potential mutations in a Chinese pedigree with hypertrophic cardiomyopathy (HCM), and to analyze the genotype-phenotype relationship in this pedigree. Clinical history and physical examinations, electrocardiography (ECG), echocardiography (UCG), cardiac magnetic resonance (CMR) data were obtained from 10 members of a three-generation Chinese family with HCM. A total of 96 genes related to hereditary cardiomyopathy were detected by exon and boarding intron analyses in the proband using second-generation sequencing. Mutations identified in the proband were confirmed by bi-directional Sanger sequencing in the rest 9 family members and 300 healthy controls. Three mutations, including MYBPC3-P1208fs, ANK2-H556R and ANK2-P1974H, were identified in this pedigree. MYBPC3-P1208fs gene mutation was detected in 3 family members (proband, his mother and son), while this mutation was not detected in the rest family members. HCM was diagnosed in the proband and his mother by ECG, UCG and CMR. Son of the proband demonstrated early phenotype of HCM: although UCG and CMR were normal, ECG showed sinus bradycardia and paroxysmal supraventricular arrhythmias as well as ST segment changes. The onset age of HCM diagnosis of the proband and his mother was 42 and 50 years old, presented with palpitation and chest pain, and myocardial fibrosis sign in CMR. Furthermore, we found that left ventricular myocardial fibrosis is related to ECG changes (increasing r wave, ST segment change) in the proband and his mother. No HCM phenotype was evidenced in the 7 family members carrying ANK2-H556R and ANK2-P1974H mutations.\n\nQuestion:\nIs [ P1208fs mutation in the cardiac myosin binding protein C associated with hypertrophic cardiomyopathy in a Chinese pedigree ]?\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:\nActivation of the immune system has been demonstrated in atopy and functional gastrointestinal disorders (FGIDs). Previous data from our group have suggested a connection between immune dysregulation, FGIDs and mood disorders. To investigate if these data translate to clinical practice and examine connections from the perspective of FGIDs to determine whether atopy and FGIDs are connected via mood disorders. Evidence of irritable bowel syndrome (IBS), functional dyspepsia (FD) and constipation was sought from the medical records of 30,000 primary care records over a minimum 5 year period. The same records yielded diagnoses of four atopic conditions (asthma, eczema, allergic rhinitis/hay fever and conjunctivitis). Atopic conditions were found in excess among all FGID groups considered when compared with controls. In the groups with IBS alone (OR = 1.43, 1.29-1.58), FD alone (OR = 1.41, 1.26-1.58) and those with multiple FGIDs (OR = 1.92, 1.75-2.12) there was elevated prevalence of asthma compared with controls without a FGID. Across disorders the excess was generally highest among patients diagnosed with multiple FGIDs (rhinitis/hay fever OR = 3.74, 3.32-4.20; conjunctivitis OR = 3.00, 2.49-3.62) and was only partly explained by a common association between both FGIDs and atopic conditions with mood disorders, although not for every atopic/FGID combination (rhinitis/hay fever OR = 2.60, 2.29-2.96, conjunctivitis OR = 2.34, 1.90-2.87).\n\nQuestion:\nDo the overlap of atopy and functional gastrointestinal disorders among 23,471 patients in primary care?\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:\nAromatic (ar-) turmerone is a major bioactive compound of the herb Curcuma longa. It has been suggested that ar-turmerone inhibits microglia activation, a property that may be useful in treating neurodegenerative disease. Furthermore, the effects of ar-turmerone on neural stem cells (NSCs) remain to be investigated. We exposed primary fetal rat NSCs to various concentrations of ar-turmerone. Thereafter, cell proliferation and differentiation potential were assessed. In vivo, naïve rats were treated with a single intracerebroventricular (i.c.v.) injection of ar-turmerone. Proliferative activity of endogenous NSCs was assessed in vivo, by using noninvasive positron emission tomography (PET) imaging and the tracer [(18)F]-fluoro-L-thymidine ([(18)F]FLT), as well as ex vivo. In vitro, ar-turmerone increased dose-dependently the number of cultured NSCs, because of an increase in NSC proliferation (P < 0.01). Proliferation data were supported by qPCR-data for Ki-67 mRNA. In vitro as well as in vivo, ar-turmerone promoted neuronal differentiation of NSCs. In vivo, after i.c.v. injection of ar-turmerone, proliferating NSCs were mobilized from the subventricular zone (SVZ) and the hippocampus of adult rats, as demonstrated by both [(18)F]FLT-PET and histology (P < 0.05).\n\nQuestion:\nDoes aromatic-turmerone induce neural stem cell proliferation in vitro and in vivo?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\n2-Methoxystypandrone (2-MS) is a naphthoquinone isolated from Polygonum cuspidatum, a Chinese herb used to treat bone diseases. Here we have determined whether 2-MS antagonised osteoclast development and bone resorption. RAW264.7 cells were treated with receptor activator of nuclear factor kappaB (NF-kappaB) ligand (RANKL) to induce differentiation into osteoclasts. RT-PCR and Western blot were used to analyse osteoclast-associated gene expression and signalling pathways. The number of multinuclear osteoclasts, actin rings and resorption pit formation were markedly inhibited by 2-MS, targeting osteoclast differentiation at an early stage and without significant cytotoxicity. The anti-resorption effect of 2-MS was accompanied by decreasing dendritic cell-specific transmembrane protein and matrix metalloproteinase-9 (MMP-9) mRNA expression. RANKL-increased MMP-9 gelatinolytic activity was also attenuated by concurrent, but not by subsequent addition of 2-MS. 2-MS markedly inhibited not only the RANKL-triggered nuclear translocations of NF-kappaB, c-Fos and nuclear factor of activated T cells c1 (NFATc1), but also the subsequent NFATc1 induction. Degradation of IkappaB and phosphorylation of mitogen-activated protein kinases were also suppressed. RANKL facilitated the formation of signaling complexes of tumour necrosis factor receptor-associated factor 6 and transforming growth factor beta-activated kinase 1 (TRAF6-TAK1), important for osteoclastogenesis and formation of such signalling complexes was prevented by 2-MS.\n\nQuestion:\nDoes 2-Methoxystypandrone repress RANKL-mediated osteoclastogenesis by down-regulating formation of TRAF6-TAK1 signalling complexes?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo examine the lifestyle, mental health, and stress-related factors associated with various types of sexual problems among sexually active, heterosexual Hong Kong residents aged 18 to 59 years. An anonymous, cross-sectional, random telephone survey was conducted using a special, validated, computerized telephone interview method. A total of 1281 men and 2130 women completed the interview (response rate 50.6%). Sexual problems were determined according to the Diagnostic and Statistical Manual (of Mental Disorders) IV definitions. Among the men, multivariate analyses indicated that older age, poor spousal relationship, less exercise, high level of family stress, high level of financial-related stress, and past year substance use were significantly associated with sexual problems (odds ratio [OR] 1.41 to 3.83). Among the women, being married or cohabiting with a partner was positively associated with lubrication problems, lack of orgasm, lack of pleasure, lack of interest (OR 1.43 to 1.73) and negatively associated with pain during intercourse (OR 0.66) and anxiety (OR 0.62). A high level of financial stress and neuroses diagnoses were also associated with various female sexual problems (OR 1.40 to 2.66). Sexual satisfaction was associated with being married/cohabitating (OR 1.94) and negatively associated with a poor spousal relationship, low level of exercise, and a high level of work-related stress among men (OR 0.37 to 0.71). Among women, a poor spousal relationship and high levels of family stress and financial stress were associated with not being satisfied sexually (OR 0.24 to 0.71).\n\nQuestion:\nDoes mental health and lifestyle correlate of sexual problems and sexual satisfaction in heterosexual Hong Kong Chinese population?\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:\nMounting evidence suggests that tumor-infiltrating immune cells have prognostic value for patients with solid organ malignancies. Our aim was to investigate the prognostic significance of the immune microenvironment in patients with stage I lung adenocarcinoma (ADC). Using tissue microarray and immunohistochemistry, we investigated eight types of tumor-infiltrating immune cells in the tumor nest and tumor-associated stroma as well as tumor expression of five cytokines in a uniform cohort of 956 patients with stage I lung ADC (478 each in training and validation cohorts). Although a high density of stromal forkhead box P3 (FoxP3) -positive cells was associated with shorter recurrence-free probability (RFP; P = .043), the relative proportion of stromal FoxP3 to CD3 was a stronger predictor of recurrence (5-year RFP, 85% for high v 77% for low ratio; P = .004). High expression of tumor interleukin-12 receptor β2 (IL-12Rβ2) was associated with better outcome (5-year RFP, 90% for high v 80% for low expression; P = .026), whereas high expression of tumor IL-7R was associated with worse outcome (5-year RFP, 76% for high v 86% for low expression; P = .001). In multivariate analysis, these immune markers were independently associated with recurrence. Although IL-7R remained significant for poor overall survival, all the markers remained prognostic for recurrence in patients with stages IA and IB disease as well as for patients with tumors ≤ 2 cm.\n\nQuestion:\nAre clinical impact of immune microenvironment in stage I lung adenocarcinoma : tumor interleukin-12 receptor β2 ( IL-12Rβ2 ) , IL-7R , and stromal FoxP3/CD3 ratio independent predictors of recurrence?\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 is controlled by both circadian and homeostatic mechanisms. As the light-dark cycle is the most important time cue in humans, blind individuals may have circadian rhythm disorders including sleep. The aim of the study was to assess sleep with simultaneous measurement of an endogenous marker of the circadian clock, namely 6-sulphatoxymelatonin (aMT6s). 59 registered blind subjects were studied in their own homes. Subjects completed daily sleep and nap diaries for at least four weeks, wore activity monitors continuously, and collected urine samples over 48 hours each week for 3-5 weeks for assessment of aMT6s rhythms. The most sensitive indicator of a circadian rhythm disorder was day-time napping. Subjects with normally entrained (NE) aMT6s rhythms had fewer naps of a shorter duration than abnormally entrained (AE) or free-running (FR) subjects. The timing of these naps was not random; significantly more naps occurred within a five-hour range before and after the aMT6s acrophase (phi (phi)) than outside this range. Disorders in the timing and duration of night sleep in AE subjects manifested as either a permanent advance (advanced sleep phase syndrome, ASPS) or delay (delayed sleep phase syndrome, DSPS). In FR subjects there were transient advances and delays in sleep timing that paralleled aMT6s timing with increased night sleep duration and reduced number and duration of day-time naps associated with a normal aMT6s phase.\n\nQuestion:\nAre sleep and activity rhythms related to circadian phase in the blind?\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:\nCyclosporine-based immunosuppressive regimens (INN: ciclosporin) in human lung transplantation continue to result in a high incidence of acute cellular rejection. We investigated the use of sirolimus, a macrolide with structural similarity to tacrolimus, as monotherapy and in combination with cyclosporine in a rodent lung transplant model. Orthotopic left lung transplantation was performed in Lewis recipients from Brown-Norway donor rats with syngeneic Lewis-to-Lewis controls. Open biopsies were performed on postoperative day 7, and the severity of acute lung rejection was graded by a pathologist blinded to the protocol. All recipients survived despite the amount of acute rejection seen on examination of the biopsy tissue. Lewis-to-Lewis isografts demonstrated near normal pulmonary architecture. Allogeneic recipients receiving high-dose cyclosporine (25 mg/kg) monotherapy showed mild to moderate acute rejection with some perivascular focal interstitial infiltrates. Recipients receiving low-dose cyclosporine (5 mg/kg) monotherapy or low- or high-dose sirolimus (0.5 or 2.0 mg/kg, respectively) monotherapy demonstrated massive cellular infiltration leading to necrosis and infarction and could not be graded. However, the addition of low-dose sirolimus (0.5 mg/kg) to low-dose cyclosporine (5 mg/kg) demonstrated a significant potentiating immunosuppressive effect, and the addition of high-dose sirolimus (2.0 mg/kg) to low-dose cyclosporine (5.0 mg/kg) demonstrated an even greater effect, with rejection scores better than those obtained with high-dose cyclosporine monotherapy and similar to those obtained with isografts.\n\nQuestion:\nDoes sirolimus ( rapamycin ) potentiate cyclosporine in prevention of acute lung rejection?\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 epidemiological studies have documented the presence of a 'J' or 'U' association between total cholesterol levels and total mortality. Not only the mechanism underlying the association between increased mortality and low total cholesterol values is not completely clear, but the relationship itself also appears to be complex in the elderly. The aim of the study was to evaluate the possible association between some biohumoral markers of the acute phase, comorbidity, disability, and reduced levels of some lipoprotein parameters in a sample of hospitalized elderly subjects. 341 patients over 65 years of age (185 males, 156 females; mean age 76.2 years), consecutively admitted to our department from 1994 to 1995, were studied. Acute phase was defined as the simultaneous presence of: (1) increased alpha2-plasma protein on electrophoresis (>12%); (2) high fibrinogen concentration (>450 mg/dl), and (3) increased blood sedimentation rate (>15 and >20 mm 1 h in males and females, respectively). The prevalence of signs of acute phase was higher in males and in the youngest patients, but did not change with the level of comorbidity. Patients with signs of acute phase were characterized by lower total, low-density lipoprotein (LDL)- and high-density lipoprotein (HDL)-cholesterol levels compared to subjects without signs of acute phase; this difference was significant even after adjustment for indicators of comorbidity, disability, and nutritional status. Multivariate logistic regression analysis evidenced that the simultaneous presence of these three markers of acute phase was independently associated with low levels of total cholesterol [odds ratio (OR) 2.1, 95% confidence interval (CI) 1.1 - 3.9], and HDL-cholesterol (OR 2.3, 95% CI 1.2 - 4.2), considered as the sex-specific first quintile.\n\nQuestion:\nAre acute phase markers associated with reduced plasma lipid levels in a population of hospitalized elderly 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:\nConcentrations of quinolinic acid, an N-methyl-D-aspartate agonist, are often elevated for long periods of time in the cerebrospinal fluid (CSF) and brain tissue of patients with AIDS dementia complex (ADC). This study was designed to test the hypothesis that chronic exposure of human neurons to quinolinic acid levels equivalent to those in the CSF of ADC patients is neurotoxic. Human fetal brain 14-16 weeks post-menses was cultured in medium with no detectable levels of quinolinic acid. After 4 weeks, 350 or 1200 nmol/l quinolinic acid was added to the feeding medium for a further 5 weeks. Neurotoxicity was evaluated using immunohistochemistry, transmission and scanning electron microscopy, and image analysis. A total of 1200 nmol/l quinolinic acid caused altered cell associations, a decrease in cell density and decreased microtubule-associated protein (MAP)-2 immunoreactivity compared with cultures exposed to 350 nmol/l quinolinic acid or controls. Image analysis of neurons in randomly selected fields revealed significantly swollen cells (P < 0.0001) compared with those treated with 350 nmol/l quinolinic acid or controls. Dendritic varicosities and discontinuous microtubular arrays were present in neurons exposed to both quinolinic acid concentrations, but not in control cultures.\n\nQuestion:\nDoes chronic exposure of human neurons to quinolinic acid result in neuronal changes consistent with AIDS dementia complex?\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 surrogate markers of HIV/AIDS progression include CD4 T cell count and plasma viral load. But, their reliability has been questioned in patients on anti-retroviral therapy (ART). Five microRNAs (miRNAs) - miR-16, miR-146b-5p, miR-150, miR-191 and miR-223 in peripheral blood mononuclear cells (PBMCs) were earlier found to assign HIV/AIDS patients into groups with varying CD4 T cell counts and viral loads. In this pilot study, we profiled the expression of these five miRNAs in PBMCs, and two of these miRNAs (miR-146b-5p and miR-150) in the plasma of HIV/AIDS patients, including those on ART and those who developed ART resistance, to evaluate if these are biomarkers of disease progression and therapy. We quantified miRNA levels by quantitative reverse transcription polymerase chain reaction (qRT-PCR) using RNA isolated from PBMCs and plasma of healthy persons or HIV-infected patients who were (1) asymptomatic; (2) symptomatic and ART naïve; (3) on ART; and (4) failing ART. Our results show miR-150 (p<0.01) and to a lesser extent miR-146b-5p (p<0.05) levels in PBMCs to reliably distinguish between ART-naïve AIDS patients, those on ART, and those developing drug resistance and failing ART. The plasma levels of these two miRNAs also varied significantly between patients in these groups and between patients and healthy controls (p values <0.05).\n\nQuestion:\nIs microRNA-150 a potential biomarker of HIV/AIDS disease progression and 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:\nIn Gilles de la Tourette syndrome (GTS) an immunopathogenic influence of autoantibodies is suspected. In familial GTS a disruption of the contactin-associated protein 2 gene (CNTNAP2), coding for the contactin-associated protein 2 (CASPR2), has been reported. Autoantibodies against CASPR2 are associated with other movement disorders like Morvan's syndrome. In addition, positive oligoclonal bands (OCB) in cerebrospinal fluid (CSF) have been found in more than a third of GTS patients, indicating a pathological intrathecal immunoglobulin synthesis. These findings drove the hypothesis that CASPR2 antibodies are involved in GTS. In this cross sectional study, 51 patients with GTS were examined for CASPR2 and other autoantibodies. We used indirect immunofluorescence or enzyme-linked visualization in cell-based assays on tissue sections from cerebellum (rat and monkey), hippocampus (rat), and immunoblots for the detection of specific or any other autoantibodies. Serum samples from 51 GTS patients, mean age 35.0 ± 13.1 y, were analyzed. In none of the 51 GTS sera CASPR2 antibodies were detectable. Neither had we found any other specific autoantibodies (LGI1, NMDAR, AMPA1, AMPA/2 or GABAB1/B2). An anti-nuclear pattern of immunoreactivity was observed in 7/51 (14 %) samples. In these patients an immunoblot analysis was used to rule out antibodies directed against well-defined intracellular target antigens. A specific anti-neuronal binding pattern could not be seen in any of the tissue sections.\n\nQuestion:\nIs gilles de la Tourette syndrome linked to contactin-associated protein receptor 2 antibodies?\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:\nAlthough the renal microvasculature, including the glomerular capillaries, is generally considered to develop from the metanephric mesenchyme, this has not been unequivocally demonstrated. Using a murine metanephric mesenchymal cell line (MS7), we tested whether the metanephric mesenchyme expresses phenotypic characteristics of endothelial cells and differentiates into vascular endothelial cells in vitro. MS7 cells were examined for the mRNA expression of endothelial markers by reverse transcription (RT)-PCR. Moreover, we attempted to induce the appearance of new endothelial markers by stimulation with growth factors and exposure to hypoxia. Before induction, MS7 cells expressed mRNA of fetal liver kinase 1 (Flk1), fms-like tyrosine kinase (Flt1), tyrosine kinase with Ig and EGF homology domains 2 (Tie2), CD31, and podocalyxin. However, they did not express mRNA for vascular endothelial-cadherin (VE-cadherin) or von Willebrand factor (vWF), which are markers specific for endothelial cells and mature endothelial cells. In the immunocytochemical analysis, MS7 absorbed DiI-acetylated LDL virtually, but the results of staining with anti-VE-cadherin, vWF, or CD31 antibodies were negative. MS7 cells that were cultured for 14 days after reaching confluence began to express VE-cadherin and vWF mRNA. In addition, immunofluorescence showed abundant granules stained with anti-vWF antibody in the cytoplasm. Stimulation with vascular endothelial growth factor (VEGF), or basic fibroblast growth factor (bFGF), or exposure to a hypoxic condition did not influence their characteristic changes.\n\nQuestion:\nDoes murine metanephric mesenchyme possess characteristics of vascular endothelial cells in vitro?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nA growing body of evidence shows the cardiovascular benefits of fish oil ingredients, including eicosapentaenoic acid (EPA), in humans and experimental animals. However, the effects of EPA on endothelin (ET)-1-induced cardiomyocyte hypertrophy and the involved signaling cascade are largely unknown. A previous study has demonstrated that peroxisomal proliferator-activated receptor (PPAR)-α ligand (fenofibrate) prevents ET-1-induced cardiomyocyte hypertrophy. Although EPA is a ligand of PPAR-α, to date, no study has examined a relationship between EPA and PPAR-α in cardiomyocyte hypertrophy. Here, we investigated whether EPA can block ET-1-induced cardiomyocyte hypertrophy and the possible underlying mechanisms. At day 4 of culture, neonatal rat cardiomyocytes were divided into four groups: control, control cells treated with EPA (10 μM), ET-1 (0.1 nM) administered only and EPA-pre-treated ET-1 administered groups. Also, the cardiomyocytes were treated with PPAR-α siRNA in order to elucidate the mechanisms that may underlie suppression of hypertrophy via the EPA-PPAR system. Following ET-1 treatment, 2.12- and 1.92-fold increases in surface area and total protein synthesis rate in cardiomyocytes, respectively, were observed and these changes were greatly blocked by EPA pre-treatment. Further, the expression of PPAR-α increased in EPA-treated groups. PPAR-PPRE binding activity was suppressed in ET-1 administered cardiomyocyte and this suppression was improved by EPA treatment. Lastly, pre-treatment of cardiomyocytes with PPAR-α siRNA prior to EPA treatment attenuated the suppressing effects of EPA on cardiomyocyte hypertrophy.\n\nQuestion:\nDoes fish oil constituent eicosapentaenoic acid inhibit endothelin-induced cardiomyocyte hypertrophy via PPAR-α?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\n A disturbed balance between excitatory and inhibitory neurotransmission underlies epileptic activity, although reports concerning neurotransmitter systems involved remain controversial. We quantified densities of 15 receptors in neocortical biopsies from patients with pharmacoresistant focal temporal lobe epilepsy and autopsy controls, and searched for correlations between density alterations and clinical factors or the occurrence of spontaneous synaptic potentials in vitro. α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), kainate, N-methyl-d-aspartate (NMDA), peripheral benzodiazepine, muscarinic (M)(1) , M(2) , nicotinic, α(1) , α(2h) , serotonin (5-HT)(1A) , and adenosine (A)(1) receptor densities were significantly altered in biopsies. The epileptic cohort was subdivided based on clinical (febrile seizures, hippocampal sclerosis, neocortical pathologies, surgery outcome) or electrophysiologic (spontaneous field potentials) criteria, resulting in different patterns of significantly altered receptor types when comparing a given epileptic group with controls. Only AMPA, kainate, M(2) , and 5-HT(1A) receptors were always significantly altered. γ-Aminobutyric acid (GABA)(A) , GABA(B) , and 5-HT(2) receptor alterations were never significant. Correlation patterns between receptor alterations and illness duration or seizure frequency varied depending on whether the epileptic cohort was considered as a whole or subdivided.\n\nQuestion:\nDoes multireceptor analysis in human neocortex reveal complex alterations of receptor ligand binding in focal epilepsies?\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 incidence of necrotizing enterocolitis (NEC) is higher in formula-fed babies than in breast-fed babies, which may be caused by breast-feeding-induced gut maturation. The effect of breast-feeding on gut maturation has been widely studied in animal models. This study aimed to assess the effects of breast-feeding on intestinal maturation in prematurely born babies by evaluating postnatal changes in urinary intestinal fatty acid binding protein (I-FABP) levels, a specific enterocyte marker. Gut maturation in 40 premature babies (<37 weeks of gestation) without gastrointestinal morbidity was studied, of whom 21 were exclusively breast-fed and 19 were formula-fed infants. Urinary I-FABP levels as the measure of gut maturation were measured at 5, 12, 19, and 26 days after birth. In breast-fed infants, there was a significant increase in median urinary I-FABP levels between 5 and 12 days after birth (104 [78-340] pg/mL to 408 [173-1028] pg/mL, P = 0.002), whereas I-FABP concentration in formula-fed infants increased between 12 and 19 days after birth (105 [44-557] pg/mL, 723 [103-1670] pg/mL, P = 0.004). Breast-fed babies had significantly higher median urinary I-FABP levels at postnatal day 12 (P = 0.01).\n\nQuestion:\nDoes breast-feeding improve gut maturation compared with formula feeding in preterm babies?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIn patients with pulmonary embolism, thrombi resist fibrinolysis induced by plasminogen activators. Because the molecular basis of this thrombus resistance is poorly understood, we used a potent inhibitor to examine the potential role of alpha 2-antiplasmin (alpha 2AP) in experimental pulmonary embolism. Lysis of experimental pulmonary emboli was measured 4 hours after embolization in anesthetized ferrets. All animals received heparin (100 U/kg). Five experimental groups were studied: (1) no recombinant tissue plasminogen activator (rTPA); (2) rTPA at 1 mg/kg; (3) rTPA at 2 mg/kg; (4) rTPA at 1 mg/kg plus a control monoclonal antibody (MAb); and (5) rTPA at 1 mg/kg plus an alpha 2AP inhibitor (MAb 77A3). In comparison with ferrets receiving no rTPA (15.6 +/- 10.5% lysis, mean +/- SD), rTPA-treated groups showed significantly greater lysis (P < .01). Animals treated with rTPA and alpha 2AP inhibitor (56.2 +/- 4.7% lysis) showed significantly greater lysis than all other treatment groups, including ferrets treated with the same dose of rTPA alone (38.5 +/- 6.3%, P < .01), with twice the rTPA dose alone (45.0 +/- 6.5%, P < .05), or with a control MAb (35.2 +/- 4.6%, P < .01). The combination of rTPA treatment and alpha 2AP inhibition caused no consumption of fibrinogen.\n\nQuestion:\nDo alpha 2-antiplasmin causes thrombi to resist fibrinolysis induced by tissue plasminogen activator in experimental pulmonary embolism?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPrevious studies have shown that hormone receptor (HR) and human epidermal growth factor receptor 2 (HER2) status influence the outcome of locoregional treatments. However, the interrelationship of these factors with trastuzumab is unclear. In this study, the role of HR and HER2 status on the locoregional benefit of trastuzumab treatment was investigated in patients with nonmetastatic breast cancer. Locoregional outcomes of 5683 women treated at The University of Texas MD Anderson Cancer Center from 2000 to 2008 for invasive breast cancer were analyzed using Kaplan-Meier and Cox regression methods to compare 6 subgroups: HR-positive (HR+)/HER2-negative (HER2-), HR-/HER2- (triple-negative), HR+/HER2+ with or without trastuzumab, and HR-/HER2+ with or without trastuzumab. Overall, locoregional recurrence (LRR) was 5% at 5 years among patients with HER2+ disease. Patients with HR+/HER2+ disease treated with trastuzumab had half the rate of LRR as patients who did not receive trastuzumab, whereas patients with HR-/HER2+ disease had similar rates of LRR regardless of trastuzumab treatment. On Cox regression analysis comparing LRR risk to the cohort with HR+/HER2- disease, only the HR+/HER2+ cohort treated with trastuzumab had similar LRR risk (hazard ratio = 1.24, 95% confidence interval = 0.56-2.73, P = .591). All other subgroups, including the HR+/HER2+ cohort who did not receive trastuzumab, had significantly worse outcomes. LRR risk was highest among patients with triple-negative disease (hazard ratio = 4.73, 95% confidence interval = 3.42-6.54, P < .001).\n\nQuestion:\nDoes hormone receptor status influence the locoregional benefit of trastuzumab in patients with nonmetastatic breast 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 study real-life experiences of drug treatment discontinuations and safety in a well-defined cohort of patients with juvenile idiopathic arthritis (JIA), over an eleven-year period in Uppsala County, Sweden. Clinical charts of all incident and prevalent cases of juvenile arthritis were reviewed prospectively by an experienced paediatric rheumatologist. Each patient file was supplemented retrospectively regarding hereditary diseases, clinical data and aspects of pharmacological treatment. Severe adverse events from methotrexate or biological agents were rare, but 84 occasions of interrupted therapy due to adverse events or inefficacy were identified within 225 treatment periods (37.3%) in the 156 patients (108 girls and 48 boys) studied. The median observation period was 8.6 years after disease onset (minimum 1.33, maximum 17.5 years). Oral and subcutaneous methotrexate caused adverse events in 22.6% of the treatment periods and biological agents in 19.2% (p = 0.71). Discontinuation of treatment periods was equally common for methotrexate (38.7%) and biological agents (33.3%) (p = 0.53).\n\nQuestion:\nDo children with juvenile idiopathic arthritis frequently experience interruptions to their medical 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:\nAlthough beneficial effects of potassium intake on blood pressure (BP) are well established, little is known about genetic factors that underlie interindividual variability in BP response to dietary potassium. In a previous study, we reported the first evidence for significant heritabilities for BP response in a dietary intervention study in rural Chinese. In this report, we extend our genetic studies to examine associations with polymorphisms in genes in vascular endothelial pathways. We genotyped study participants for 23 single nucleotide polymorphisms (SNPs) in endothelin 1 (EDN1), nitric oxide synthase 3, and E selectin (SELE). We tested 17 of these SNPs for associations with BP response to potassium supplementation in 1843 participants. Association tests used population-based [generalized estimation equation (GEE)] and family-based (quantitative transmission disequilibrium test) methods, as well as tests for gene-by-gene (GxG) interaction (generalized multifactor dimensionalilty reduction and GEE). Single SNP analysis identified significant associations for several SNPs in EDN1 with multiple measures of BP response to potassium supplementation. The cumulative effects of the minor EDN1 alleles that showed significant associations were to reduce measures of BP response by 0.5-0.9 mmHg. We found significant evidence for effects of GxG interactions between EDN1 and SELE, even in the absence of individual associations with SELE variants.\n\nQuestion:\nIs blood pressure response to potassium supplementation associated with genetic variation in endothelin 1 and interactions with E selectin in rural Chinese?\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:\nInsulin-like growth factor 1 (IGF-I), IGF binding proteins (IGFBP) 1 to 7, and C-peptide have been postulated to predict survival in non-small cell lung cancer (NSCLC). Studying serum levels in NSCLC patients treated with surgical resection may provide information on the aggressiveness of tumors and be predictive of disease recurrence. Immunobead assays were used to measure pretreatment serum levels of IGF-I, IGFBP1 to IGFBP7, and C-peptide in 100 NSCLC patients. Of these, 59 had no metastatic progression (T1 to T4 N0 M0), whereas 41 had positive lymph nodes (T1 to T4 N1 to N3 M0). Data were analyzed using the Mann-Whitney two-sided rank sum test or Kaplan-Meier curves. Low serum IGFBP5 levels correlated strongly with a positive nodal status (p < 0.001) and any incidence of disease recurrence (p = 0.003). Low serum levels of IGFBP5 also predicted poor recurrence-free survivals in the overall cohort (p ≤ 0.001) and in patients with no nodal metastases (p = 0.027). Conversely, a high serum level of IGFBP7 correlated with positive nodal status (p = 0.008), but was not prognostic for recurrence-free survival. No significant correlations were found for IGFBP5 or IGFBP7 for sex, age, race, smoking history, tumor histology, or fasting state.\n\nQuestion:\nDo biomarkers of the insulin-like growth factor pathway predict progression and outcome in lung 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:\nThe development of effective frameworks that permit an accurate diagnosis of tumors, especially in their early stages, remains a grand challenge in the field of bioinformatics. Our approach uses statistical learning techniques applied to multiple antigen tumor antigen markers utilizing the immune system as a very sensitive marker of molecular pathological processes. For validation purposes we choose the intracranial meningioma tumors as model system since they occur very frequently, are mostly benign, and are genetically stable. A total of 183 blood samples from 93 meningioma patients (WHO stages I-III) and 90 healthy controls were screened for seroreactivity with a set of 57 meningioma-associated antigens. We tested several established statistical learning methods on the resulting reactivity patterns using 10-fold cross validation. The best performance was achieved by Naïve Bayes Classifiers. With this classification method, our framework, called Minimally Invasive Multiple Marker (MIMM) approach, yielded a specificity of 96.2%, a sensitivity of 84.5%, and an accuracy of 90.3%, the respective area under the ROC curve was 0.957. Detailed analysis revealed that prediction performs particularly well on low-grade (WHO I) tumors, consistent with our goal of early stage tumor detection. For these tumors the best classification result with a specificity of 97.5%, a sensitivity of 91.3%, an accuracy of 95.6%, and an area under the ROC curve of 0.971 was achieved using a set of 12 antigen markers only. This antigen set was detected by a subset selection method based on Mutual Information. Remarkably, our study proves that the inclusion of non-specific antigens, detected not only in tumor but also in normal sera, increases the performance significantly, since non-specific antigens contribute additional diagnostic information.\n\nQuestion:\nDoes a minimally invasive multiple marker approach allow highly efficient detection of meningioma tumors?\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:\nRed blood cell (RBC) transfusion is linked to poor functional recovery after surgery and trauma. To investigate one potential mechanism, we examined the association between RBC transfusion and muscle strength in a cohort of critically ill patients. We performed a secondary analysis of 124 critically ill, mechanically ventilated patients enrolled in 2 prospective cohort studies where muscle strength testing was performed at a median of 12 days after mechanical ventilation onset. We examined the association between RBC transfusion and dynamometry handgrip strength using multivariable linear regression, adjusting for study site, age, sex, Acute Physiology and Chronic Health Evaluation, Sequential Organ Failure Assessment score, days from hospital admission to examination, and steroid use. Secondary outcomes included systematic manual muscle strength and intensive care unit-acquired paresis. Among 124 subjects, 73 (59%) received RBC transfusion in the 30 days before examination. In adjusted analyses, RBC transfusion was significantly associated with weaker handgrip (adjusted mean difference, -9.9 kg; 95% confidence interval, -16.6 to -3.2; P < .01) and proximal manual muscle strength (adjusted mean difference in Medical Research Council score, -0.5; 95% confidence interval, -0.7 to -0.2; P < .01) but not intensive care unit-acquired paresis.\n\nQuestion:\nIs red blood cell transfusion associated with decreased in-hospital muscle strength among critically ill patients requiring mechanical ventilation?\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 nonclassical human leucocyte antigen (HLA)-G molecule has been well recognized as a tolerogenic molecule and few studies have evaluated the role of the molecule in inflammatory cutaneous autoimmune diseases. To evaluate the expression of HLA-G in skin specimens of patients with psoriasis and to analyse its correlation with epidemiological and clinical variables. Thirty untreated patients with psoriasis and 32 healthy individuals were enrolled. Immunohistochemistry was applied to identify HLA-G expression in formalin-fixed paraffin-embedded cutaneous skin biopsies. Soluble and membrane-bound HLA-G expression was detected in 30 (90%) of the skin specimens from patients presenting clinical and histopathological features of psoriasis. Although infiltrating lymphomononuclear cells of the dermis exhibited HLA-G expression, the epidermis was primarily targeted. HLA-G expression was also observed in 27% (three of 11) of the specimens that exhibited no clinical and histopathological features of psoriasis (nonaffected areas). In contrast, skin specimens obtained from healthy individuals exhibited no HLA-G expression (P < 0·0001). The intensity of HLA-G expression was not associated with type I/II psoriasis, Psoriasis Area and Severity Index score or clinical forms.\n\nQuestion:\nDoes expression of human leucocyte antigen-G primarily target affected skin of patients with psoriasis?\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:\nHemorrhagic shock is known to disrupt the gut barrier leading to end-organ dysfunction. The vagus nerve can inhibit detrimental immune responses that contribute to organ damage in hemorrhagic shock. Therefore, we explored whether stimulation of the vagus nerve can protect the gut and recover lung permeability in trauma-hemorrhagic shock (THS). Male Sprague-Dawley rats were subjected to left cervical vagus nerve stimulation at 5 V for 10 minutes. The right internal jugular and femoral artery were cannulated for blood withdrawal and blood pressure monitoring, respectively. Animals were then subjected to hemorrhagic shock to a mean arterial pressure between 30 mm Hg and 35 mm Hg for 90 minutes then reperfused with their own whole blood. After observation for 3 hours, gut permeability was assessed with fluorescein dextran 4 in vivo injections in a ligated portion of distal ileum followed by Evans blue dye injection to assess lung permeability. Pulmonary myeloperoxidase levels were measured and compared. Vagal nerve stimulation abrogated THS-induced lung injury (mean [SD], 8.46 [0.36] vs. 4.87 [0.78]; p < 0.05) and neutrophil sequestration (19.39 [1.01] vs. 12.83 [1.16]; p < 0.05). Likewise, THS gut permeability was reduced to sham levels.\n\nQuestion:\nDoes vagal nerve stimulation modulate gut injury and lung permeability in trauma-hemorrhagic shock?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSearches of Cochrane Central Register of Controlled Trials (CENTRAL), Medline, Embase, six thesis databases (Networked Digital Library of Theses and Dissertations, Proquest Digital Dissertations, OAIster, Index to Theses, Australian Digital Thesis program and Dissertation.com) and one conference report database (BIOSIS Previews) were undertaken. There were no language restrictions. Studies were included in which participants had a noncontributory medical history, presented with mature teeth and radiographic evidence of periapical bone loss (as an indication of pre-operative canal infection), whose selected root canals had not previously received any endodontic treatment, and who had undergone nonsurgical root canal treatment during the study in which calcium hydroxide had also been used to seal in the canals. In addition, it was required that microbiological sampling had been undertaken during the course of treatment, before canal preparation, after canal preparation and after canal medication. Aerobic and anaerobic culturing techniques were performed on all samples. The treatment outcomes were stated in terms of positive and negative canal cultures. All data were extracted in the same manner using a standardised data extraction sheet. Between-study heterogeneity was assessed using the standard chi-squared test or Q-statistic. The principal measure of treatment effect (antibacterial efficacy) was risk difference, which is normally defined as the risk in the experimental group minus risk in the control group. For the purpose of this study, it is given as the difference in the proportion of bacteria-positive cultures pre- and post-medication. Out of the eight studies (257 cases) included, one study used a small control group (in which canals were left empty, and no intracanal medicament was used between appointments). The other seven studies simply compared the frequency of positive cultures before and after calcium hydroxide medication. Six studies demonstrated a statistically significant difference between pre- and postmedicated canals, whereas two did not. There was considerable heterogeneity among studies. The pooled risk difference was 21% (95% confidence intervals, 6-47%. The difference in the proportion of cases positive for bacteria before and after treatment was not statistically significant (P = 0.12).\n\nQuestion:\nDoes calcium hydroxide have limited effectiveness in eliminating bacteria from human root canal?\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:\nInterstitial cells of Cajal, expressing the proto-oncogene c-kit, have been shown to regulate the spontaneous activity of the gastrointestinal tract. They have been described in the human internal anal sphincter; however, their function is still unclear. We examined the effects of the c-kit tyrosine kinase inhibitor imatinib mesylate on sphincter strips to investigate the function of the interstitial cells. This was a case series study. This was a single-center study conducted at the University of Oxford. Internal anal sphincter strips were collected from 10 patients undergoing abdominoperineal resection or proctectomy and mounted in organ bath. Responses to electrical field stimulation and chemical agents were monitored in the absence of drugs and after the administration of increasing doses of imatinib mesylate. Immunohistochemistry was performed to identify interstitial cells. The role of the interstitial cells in the internal anal sphincter was assessed. Imatinib mesylate significantly reduced the tone and the spontaneous activity of the strips. In the absence of drugs, the tone generated was 147.7 ± 33.0 mg/mg of tissue. Administration of ≥5 μM of imatinib mesylate caused a dose-dependent reduction in the tone. Strips exhibited spontaneous activity characterized by intermittent low-amplitude contractions superimposed on basal tone (135.6 ± 4.6 contractions in 10 minutes). Imatinib mesylate significantly reduced the number of contractions at concentration >5 μM. No differences were observed in the responses to electrical field stimulation, carbachol, or phenylephrine. Immunohistochemistry showed c-kit-positive cells.\n\nQuestion:\nDo interstitial cells of Cajal modulate the tone of the human internal anal sphincter in vitro?\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:\nHyperacute lung dysfunction, which is always associated with pulmonary pig-to-primate xenotransplantation is not well understood. The mechanisms associated with its occurrence seem to differ from mechanisms involved in hyperacute xenograft rejection seen in porcine hearts or kidneys transplanted into primates. To determine the contribution of anti-Gal alpha1-3Gal antibodies (alphaGAb) in such a process, we performed a set of orthotopic pig lung transplants into baboons depleted of alphaGAb and compared graft function and survival with those receiving only immunosuppression. Pigs expressing human membrane cofactor protein served as donors. All baboons received triple immunosuppressive therapy. Depletion of alphaGAb in the experimental group (n = 4) was done by way of immunoadsorption using immunoaffinity membranes. Controls (n = 4) did not undergo immunoadsorption. Orthotopic lung transplants were performed through a left thoracotomy. Main pulmonary artery blood flow and pressure, left pulmonary artery blood flow, and left atrial pressure were recorded. At 1 hour after reperfusion, pulmonary artery graft flows and pulmonary vascular resistances (PVR) were better in animals depleted of alphaGAb than in controls (605 +/- 325.2 mL/min versus 230 +/- 21 mL/min; 27.1 +/- 41.3 mmHg/L/min versus 63 +/- 1 mmHg/L/min). But at 3 hours after reperfusion average graft flows in baboons depleted of alphaGAb had decreased to 277.6 +/- 302.2 mL/min and PVRs had increased 58.3 +/- 42.0 mmHg/L/min. On the other hand, controls maintained stable flows and PVRs (223 +/- 23 mL/min; 61 +/- 3 mmHg/L/min). Survival was ultimately better in control baboons when compared with alphaGAb depleted ones (12.2 +/- 3.3 h versus 4.4 +/- 3.2 h).\n\nQuestion:\nAre non-anti-Gal alpha1-3Gal antibody mechanisms sufficient to cause hyperacute lung dysfunction in pulmonary xenotransplantation?\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 human Bcr gene was originally identified by its presence in the chimeric Bcr/Abl oncogene, which is causative for chronic myeloblastic leukemia. Because Bcr encodes a serine/threonine protein kinase, we studied its kinase activity and determined the role of Bcr in the PDGF signaling pathway to ERK1/2 activation and DNA synthesis in rat aortic smooth muscle cells (RASMCs). In RASMCs, platelet-derived growth factor-BB (PDGF) stimulated Bcr kinase activity, with a maximum at 1 minute. Because phosphatidylinositol 3'-kinase (PI3-K) is essential for Bcr/Abl leukemogenesis, we evaluated the role of mouse PDGF-beta-receptor binding sites for PI3-K (Y708, Y719) and for phospholipase C-gamma (Y977, Y989) in PDGF-mediated Bcr kinase activation. The mutant PDGF receptor Y708F/Y719F but not Y977F/Y989F showed significantly reduced Bcr kinase activity. To determine the role of Bcr in PDGF-mediated signal transduction events leading to ERK1/2 and its downstream Elk1 transcription activation, wild-type (WT) and kinase-negative (KN) Bcr were transiently expressed in RASMCs. Bcr WT enhanced, whereas Bcr KN inhibited, PDGF-stimulated ERK1/2 and Elk1 transcriptional activity. Overexpression of Bcr also enhanced PDGF-induced Ras/Raf-1 activity and DNA synthesis, but this regulation is independent of the kinase activity of Bcr. Finally, we found that Bcr expression was increased in the neointimal layer after balloon injury of rat carotid artery.\n\nQuestion:\nDoes p160 Bcr mediate platelet-derived growth factor activation of extracellular signal-regulated kinase in 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:\nBreath hold is increasingly used for cardiac sparing in left-sided breast cancer irradiation. We have developed a fast automated method to verify breath hold stability in each treatment fraction. We evaluated 504 patients treated with breath hold. Moderate deep inspiration breath hold was audio-guided. Medial and lateral large tangential field segments were delivered in a single breath hold and movieloops of these fields were acquired with an EPID. The thoracic wall position was automatically detected in each frame and the full range of thoracic wall motion (RTWM) was determined. If the RTWM >4mm more than 3 times, the patient was excluded from breath hold treatment if further coaching did not yield improvement. Unstable breath hold was observed in 2.8% of the patients. However, this frequency dropped from 9.5% in the first 6months to 1.6% in the subsequent 16months. The 97% of patients with proper breath hold showed excellent stability: the average RTWM was 0.9±0.5mm. The reproducibility of the breath hold depth was confirmed by (1) the small difference between the thoracic wall positions in the medial and lateral fields within one fraction and (2) the setup errors of breath hold patients showed no significant differences with those of right-sided breast patients.\n\nQuestion:\nDo automated daily breath hold stability measurements by real-time imaging in radiotherapy of breast 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:\nThe use of fentanyl as a potent analgesic is contradicted by marked respiratory depression among a subpopulation of patients. The commonly used approach of reversing fentanyl-induced respiratory depression with mu-opiate receptor antagonists such as naloxone has the undesirable effect of blocking analgesia. Here, the authors report a clinically feasible pharmacological solution for countering fentanyl-induced respiratory depression via a mechanism that does not interfere with analgesia. Specifically, to determine if the ampakine CX717, which has been proven metabolically stable and safe for human use, can prevent and rescue from severe fentanyl-induced apnea. Plethsymographic recordings were performed from young and adult rats. Varying doses of fentanyl were administered either intraperitoneally or intravenously to induce moderate to life-threatening apneas. CX717 was administered either before or after fentanyl administration. In addition, phrenic nerve recordings were performed from in situ working heart brainstem preparations from juvenile rats. Preadministration of CX717 markedly attenuated fentanyl-induced respiratory depression. Postadministration of CX717 rescued animals from a lethal dose of fentanyl. Significantly, CX717 countered fentanyl-induced depression of respiratory frequency without suppressing analgesia. The effective dose of CX717 was in the range deemed safe on the basis of clinical trials examining its efficacy for cognitive disorders. In situ, fentanyl-induced depression in respiratory frequency and amplitude was alleviated by CX717.\n\nQuestion:\nDoes ampakine CX717 protect against fentanyl-induced respiratory depression and lethal apnea in rats?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nEthanol causes significant teratogenicity in normal (MT+/+) but not metallothionein-null (MT-/-) fetuses. Impaired maternal fetal zinc (Zn) transfer is indicated, because ethanol significantly reduces plasma Zn concentrations in MT+/+ dams while increasing concentrations in MT-/- dams. In this study we examined maternal-fetal Zn homeostasis in response to ethanol in MT+/+ and MT-/- mice and the origins of the increase in plasma Zn in MT-/- mice. Mice were treated with saline or ethanol (0.015 ml/g intraperitoneally at 0 and 4 hr) on day 12 of gestation. An additional subcutaneous injection of 65Zn tracer was administered after the second ethanol injection before mice were killed 3 hr later. Maternal liver MT levels were not different between ethanol and saline MT+/+ mice. Both liver Zn and 65Zn levels were higher in MT+/+ mice. Plasma Zn concentrations were higher in MT-/- mice, with MT-/- ethanol-treated mice having levels greater than those of MT-/- saline-treated controls. MT+/+ ethanol-treated fetuses exhibited lower 65Zn transfer and whole Zn concentrations compared with MT+/+ and MT-/- saline and MT-/- ethanol fetuses. So we could examine changes in plasma Zn after ethanol treatment, MT+/+ and MT-/- mice were injected with 65Zn 3 days before they received ethanol treatment. Muscle and skin showed a decrease in 65Zn retention in both genotypes over 3 hr. There was a trend toward greater 65Zn release from skin and muscle at an earlier time in MT-/- mice: 24% vs. 2% decrease (MT-/- vs. MT+/+) for muscle and 28% vs. 15% decrease (MT-/- vs. MT+/+) for skin at 2 hr.\n\nQuestion:\nDoes ethanol decrease zinc transfer to the fetus in normal but not metallothionein-null 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 assess the need for routine nasogastric decompression after extensive resections in patients with gastric cancer. Prospective randomised study. University hospital, Korea. Over a 1-year period (July 1999-July 200), 136 patients with gastric cancer who underwent radical gastrectomy with D2 or more lymph node dissection. Randomised to have nasogastric decompression (n = 69) or not (n = 67). Postoperative course, morbidity, and mortality. Time to passage of first flatus, time to taking liquid diet, length of operation, and postoperative hospital stay were all significantly shorter in the no decompression group. Two patients in each group required subsequent nasogastric decompression. There were no significant differences between the two groups concerning the presence of postoperative fever, nausea, vomiting, anastomotic leaks, or pulmonary or wound complications. No patients died.\n\nQuestion:\nIs nasogastric decompression necessary in operations for gastric cancer : prospective randomised trial?\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:\nStimulation of nitric oxide (NO) synthesis similar to the application of NO donors could be of benefit in liver fibrosis. Many authors believe that activation of NO synthesis by pharmacological agents is promising in the treatment of liver fibrosis. However, there is considerable controversy in understanding the role of NO in fibrogenesis and fibrolysis. The aims of our study were to evaluate the effects of L-arginine, as an NO metabolic precursor, and those of NO synthase (NOS) inhibitors, L-nitroarginine methyl ester (L-NAME) and aminoguanidine (AG) in rats with thioacetamide (TAA)-induced liver fibrosis reversal. Male Wistar rats, 230-240 g, received TAA (200 mg kg(-1), intraperitoneally) twice a week for 3 months. Liver resolution was simulated by withdrawal of TAA administration. Thereafter the animals were subdivided into five groups and treated by intragastric intubation with: L-arginine (100 and 300 mg kg(-1)); L-NAME as an inhibitor of both constitutively expressed NOS (eNOS) and inducible NOS (iNOS) (20 mg kg(-1)), AG as a specific inhibitor of iNOS (100 mg kg(-1)) or placebo. The severity of liver fibrosis was assessed by morphometric evaluation of liver slides stained with Azan-Mallory, hydroxyproline (Hyp) determination and mRNA steady state levels of collagen I, transforming growth factor (TGF)-beta1, metalloproteinases (MMP)-13, -14, tissue inhibitor of MMP (TIMP)-1 and plasminogen activator inhibitor (PAI)-1 were quantified by real time PCR. The activities of serum marker enzyme, alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase, were measured. TAA treatment during 3 months induced micronodular liver fibrosis with a pronounced deposition of collagen fibres. L-Arginine did not affect this deposition nor did it affect both relative and total liver hydroxyproline content. Both NOS inhibitors significantly increased the square of the liver connective tissue stained by Azan-Mallory and the above parameters characterizing liver hydroxyproline content. Both NOS inhibitors up-regulated procollagen alpha1 (I), MMP-13, TIMP-1 and PAI-1 mRNA expression. The AG effects were more pronounced. than those of L-NAME. AG treatment also increased mRNA expression of TGF-beta1 and PAI-1.\n\nQuestion:\nDoes inhibition of inducible nitric oxide synthase activity prevent liver recovery in rat thioacetamide-induced fibrosis reversal?\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:\nBacteria engage cell surface receptors and intracellular signaling molecules to enter the cell. Unc119 is an adaptor protein, which interacts with receptors and tyrosine kinases. Its role in bacterial invasion of cells is unknown. We used biochemical, molecular and cell biology approaches to identify the binding partners of Unc119, and to study the effect of Unc119 on Abl family kinases and Shigella infection. We employed loss-of-function and gain-in-function approaches to study the effect of Unc119 in a mouse model of pulmonary shigellosis. Unc119 interacts with Abl family kinases and inhibits their kinase activity. As a consequence, it inhibits Crk phosphorylation, which is essential for Shigella infection. Unc119 co-localizes with Crk and Shigella in infected cells. Shigella infectivity increases in Unc119-deficient epithelial and macrophage cells. In a mouse model of shigellosis cell-permeable TAT-Unc119 inhibits Shigella infection. Conversely, Unc119 knockdown in vivo results in enhanced bacterial invasion and increased lethality. Unc119 is an inducible protein. Its expression is upregulated by probacteria and bacterial products such as lipopolysacharide and sodium butyrate. The latter inhibits Shigella infection in mouse lungs but is ineffective in Unc119 deficiency.\n\nQuestion:\nDoes unc119 protect from Shigella infection by inhibiting the Abl family kinases?\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:\nNOTES has changed the working environment of endoscopy, leading to new difficulties. The limitations of conventional endoscopes call for the development of new platforms. Robotics may be the answer. The authors compared human to robotized manipulation of a flexible endoscope into the abdominal cavity, in an animal model. Thirty-two participants were enrolled. Results were analyzed according to the clinical background of the participants: experienced endoscopists, experienced laparoscopists, and medical students. Two single-channel gastroscopes were used. Whereas one was not modified, the other had the handling wheels replaced by motors controlled through a computer and a joystick. A NOTES transgastric approach was used to access the peritoneal cavity. The time to touch previously positioned intra-abdominal numbered plastic targets was recorded 3 times with each endoscope. Mean time to complete the tasks was significantly shorter using the conventional endoscope (2.71 vs 6.96 minutes, P < .001). When the robotized endoscope was used, the mean times of endoscopists (7.42 minutes), laparoscopists (6.84 minutes), and students (6.77 minutes) were statistically identical. No differences were found between laparoscopists and students in both techniques.\n\nQuestion:\nAre joystick interfaces suitable for robotized endoscope applied to NOTES?\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 this study was to evaluate placental lesions found in women with preeclampsia compared with normotensive control subjects and to determine whether the presence of these lesions are related to gestational age at delivery. Placental disease of women with preeclampsia at 24 to 42 weeks of gestation was compared with the placental disease of normotensive gestational age-matched control subjects. The placental lesions that were studied specifically included decidual arteriolopathy, thrombi in the fetal circulation, central infarction, intervillous thrombi, and hypermaturity of villi. Data analysis involved the chi(2) test, the Student t test, and logistic regression; odds ratios and CIs were estimated. Placentas from women with preeclampsia (n=158) and normotensive control subjects (n=156) were evaluated. Among women with preeclampsia, 67% had severe disease. Placental lesions were studied according to gestational age at delivery: <28, 28 to 32, 33 to 36, and >or=37 weeks of gestation. Of the placental lesions that were studied, decidual arteriolopathy (odds ratio, 23.8, 95% CI 10.0-57.0), hypermaturity of villi (odds ratio, 12.4; 95% CI 5.3-29.2), intervillous thrombi (odds ratio, 1.95;95% CI 1.0-3.7), central infarction (odds ratio, 5.9; 95% CI 3.1-11.1), and thrombi in the fetal circulation (odds ratio, 2.8; 95% CI 1.2-6.6) were found to have significantly higher rates in the preeclamptic group. In contrast, the rate of chorioamnionitis was significantly lower in the preeclamptic group (odds ratio, 0.2; 95% CI 0.1-0.4). The rates of abruptio placentae and meconium staining were not different between the two groups. Within the preeclamptic group, the rates of decidual arteriolopathy (P<.0001), central infarction (P=.0001), and hypermaturity of villi (P<.0001) were higher the earlier the gestational age at delivery.\n\nQuestion:\nAre the frequency and severity of placental findings in women with preeclampsia gestational age dependent?\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 aim of this study was to evaluate ERK phosphorylation as a stromal biomarker for breast cancer prognosis and tamoxifen treatment prediction within a randomized tamoxifen trial. Tissue microarrays of two breast cancer cohorts including in total 743 invasive breast cancer samples were analyzed for ERK phosphorylation (pERK) and smooth muscle actin-alpha expression (SMAα) in cancer-associated fibroblasts (CAFs) and links to clinico-pathological data and treatment-predictive values were delineated. By analyzing a unique randomized tamoxifen trial including breast cancer patients receiving no adjuvant treatment we show for the first time that patients low in ERK phosphorylation in CAFs did not respond to tamoxifen treatment despite having estrogen-receptor alpha (ERα-positive tumors compared to patients with high pERK levels in CAFs (P = 0.015, multivariate Cox regression interaction analysis). In both clinical materials we further show a significant association between pERK and SMAα, a characteristic marker for activated fibroblasts. SMAα expression however was not linked to treatment-predictive information but instead had prognostic qualities.\n\nQuestion:\nIs low ERK phosphorylation in cancer-associated fibroblasts associated with tamoxifen resistance in pre-menopausal breast 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:\nWe recently demonstrated a high-dose antioxidant (AO) protocol was associated with reduction in mortality. The purpose of this study was to evaluate the impact of AO on organ dysfunction and infectious complications following injury. High-dose AO protocol: ascorbic acid 1000 mg q 8 h, alpha-tocopherol 1000 IU q 8 h, and selenium 200 mcg qd for 7-day course. Retrospective cohort study evaluating all patients admitted after protocol implementation (AO+), October 1, 2005 to September 30, 2006. Comparison cohort (AO-): all patients admitted in the year prior to implementation, October 1, 2004 to September 30, 2005. 2272 patients included in the AO+ group, 2022 patients in the AO- group. Demographics and injury severity were similar. Abdominal compartment syndrome (ACS) (2.9% vs. 0.7%, <0.001), surgical site infections (2.7% vs. 1.3%, p=0.002), pulmonary failure (27.6% vs. 17.4%, p<0.001), and ventilator-dependent respiratory failure (10.8% vs. 7.1%, p<0.001) were significantly less in the AO+ group. Multivariate regression showed 53% odds reduction in abdominal wall complications and 38% odds reduction in respiratory failure in the AO+ group.\n\nQuestion:\nIs high-dose antioxidant administration associated with a reduction in post-injury complications in critically ill trauma 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:\nTo elucidate the detailed mechanisms underlying the appreciable effects of JG3, a novel marine-derived oligosaccharide, on cell migration using a Chinese hamster ovary (CHO) cell line stably over-expressing heparanase. A retrovirus infection system was used to establish a CHO-K1 cell line stably transfected with heparanase. Immunocytochemistry was used to assess cell morphology. Flow cytometry was selected to analyze the activation of beta1-integrin, and Western blotting was used to analyze the downstream effects on the cell adhesion pathway. An affinity precipitation assay was used to determine activation of the small GTPases, Rac1, and RhoA. JG3 abolished heparanase-driven formation of focal adhesions and cell spreading. Although JG3 failed to block the heparanase-triggered activation of beta1-integrin or the phosphorylation of Src, the oligosaccharide caused a significant dephosphorylation of FAK and subsequent inactivation of Erk. Furthermore, JG3 was found to arrest the activation of Rac1.\n\nQuestion:\nDoes marine-derived oligosaccharide sulfate ( JG3 ) suppress heparanase-driven cell adhesion events in heparanase over-expressing CHO-K1 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:\nTriple-negative breast cancers (TNBC) are characterized by a wide spectrum of genomic alterations, some of which might be caused by defects in DNA repair processes such as homologous recombination (HR). Despite this understanding, associating particular patterns of genomic instability with response to therapy has been challenging. Here, we show that allelic-imbalanced copy-number aberrations (AiCNA) are more prevalent in TNBCs that respond to platinum-based chemotherapy, thus providing a candidate predictive biomarker for this disease. Furthermore, we show that a high level of AiCNA is linked with elevated expression of a meiosis-associated gene, HORMAD1. Elevated HORMAD1 expression suppresses RAD51-dependent HR and drives the use of alternative forms of DNA repair, the generation of AiCNAs, as well as sensitizing cancer cells to HR-targeting therapies. Our data therefore provide a mechanistic association between HORMAD1 expression, a specific pattern of genomic instability, and an association with response to platinum-based chemotherapy in TNBC.\n\nQuestion:\nDoes genomic Complexity Profiling reveal That HORMAD1 Overexpression Contributes to Homologous Recombination Deficiency in Triple-Negative Breast 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:\nThe human coagulation trigger tissue factor (TF) is overexpressed in several types of cancer and involved in tumor growth, vascularization, and metastasis. To explore the role of TF in biological processes of lung adenocarcinoma, we used RNA interference (RNAi) technology to silence TF in a lung adenocarcinoma cell line A549 with high-level expression of TF and evaluate its antitumor effects in vitro and in vivo. The specific small interfering RNA (siRNA) designed for targeting human TF was transfected into A549 cells. The expression of TF was detected by reverse transcription-PCR and Western blot. Cell proliferation was measured by MTT and clonogenic assays. Cell apoptosis was assessed by flow cytometry. The metastatic potential of A549 cells was determined by wound healing, the mobility and Matrigel invasion assays. Expressions of PI3K/Akt, Erk1/2, VEGF and MMP-2/-9 in transfected cells were detected by Western blot. In vivo, the effect of TF-siRNA on the growth of A549 lung adenocarcinoma xenografts in nude mice was investigated. TF -siRNA significantly reduced the expression of TF in the mRNA and protein levels. The down-regulation of TF in A549 cells resulted in the suppression of cell proliferation, invasion and metastasis and induced cell apoptosis in dose-dependent manner. Erk MAPK, PI3K/Akt pathways as well as VEGF and MMP-2/-9 expressions were inhibited in TF-siRNA transfected cells. Moreover, intratumoral injection of siRNA targeting TF suppressed the tumor growth of A549 cells in vivo model of lung adenocarcinoma.\n\nQuestion:\nDoes small interference RNA targeting tissue factor inhibit human lung adenocarcinoma growth in vitro and in vivo?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nImplantation of an additional pace/sense (P/S) lead is commonly used in patients with implantable cardioverter/defibrillators (ICDs) to overcome P/S defects of integrated defibrillation leads (HV-P/S leads). No information is available about the clinical outcome and the incidence of complications in these patients. Retrospective analysis was performed in 151 patients (125 male, age 54.9 +/- 13.6 years, LVEF 48.1 +/- 17.8%, CAD in 86 [57%], DCM in 24 [16%], ARVCM in 11 [7%]) who received an additional P/S lead between 1990 and 2002 (54 patients with abdominal and 97 patients with pectoral ICD system). Statistical analysis was done using Kaplan-Meier survival curves. The average follow-up (FU) after implantation of the additional P/S lead was 43 +/- 27 months. In total 117 patients [77.5%] remain implanted; 22 patients died due to cardiac-related reasons. After a FU of 23 +/- 23 months, 43 patients [28.5%] experienced lead-related problems after implantation of the additional P/S lead: oversensing in 23 [53.5%], insulation defect in 3 [7.0%], fracture in 1 [2.3%], system infection in 4 [9.3%], and defect of the HV-P/S lead in 6 [14.0%] patients. The event-free cumulative survival of the additional P/S lead after 1, 2, and 5 years was 87.0%, 79.8%, and 59.4%, respectively (for pectoral leads: 89.6%, 82.0%, and 60.0%, respectively).\n\nQuestion:\nDo incidence of complications in patients with implantable cardioverter/defibrillator who receive additional transvenous pace/sense leads?\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:\nElevated plasma homocysteine (Hcy) is considered to be a risk factor of coronary artery disease (CAD), although this is still controversially discussed. This study investigated the role of Hcy in young patients with CAD in southern China. A total of 146 consecutive patients (aged ≤ 55 years) with angiographically proven CAD were enrolled in the study and 138 age-matched non-CAD individuals were included as the control group. Hcy levels were measured by enzymatic assay. Hyperhomocysteinemia (HHcy) was defined as Hcy ≥ 15 µmol/l. A 10-year CAD risk was calculated using the Framingham risk score (FRS) modified according to the National Cholesterol Education Program Adult Treatment Panel III. There were significant differences between the CAD and control groups with regard to male sex (P < 0.01), smoking history (P < 0.05), and triglyceride levels (TG, P < 0.05), but no remarkable difference in other conventional risk factors (all P > 0.05). Hcy and high-sensitivity C-reactive protein (hs-CRP) levels were significantly higher in the CAD group than those in the control group (both P < 0.05). The FRS and estimated 10-year absolute CAD event risk were low in both groups and did not show a statistical difference. Multivariate logistic regression showed that male sex (odds ratio, OR, 3.68; 95 % confidence interval, 95 % CI, 1.54-10.01), smoking (OR, 2.54; 95 % CI, 1.15-5.36), TG (OR, 1.30; 95 % CI, 1.08-3.06), hs-CRP (OR, 3.74; 95 % CI, 1.72-12.21), and HHcy (OR, 2.03; 95 % CI, 1.26-5.83) were independently correlated with CAD in young patients.\n\nQuestion:\nIs hyperhomocysteinemia an independent risk factor in young patients with coronary artery disease in southern China?\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:\nRegulator of chromosome condensation 1 (RCC1) is a critical cell cycle regulator. We firstly identified RCC1 gene hypermethylation in gastric tumor tissues using the differential methylation hybridization (DMH) microarray, but the role of RCC1 in the pathogenesis of gastric carcinoma is largely unknown. Three gastric cancer cell lines (AGS, MKN45, and TSGH9201) were used to analyze RCC1 gene methylation, mRNA and protein expressions. Furthermore, 85 pairs of matched human gastric carcinoma samples in a tissue microarray were used to analyze RCC1 expression by immunohistochemistry staining. A differential methylation pattern was found in TSGH9201 (100%), MKN45 (87%), and AGS (62%) cell lines at the 9th CpG site of RCC1 exon 1. RCC1 mRNA and protein expressions in AGS cells were significantly higher than in TSGH9201 and MKN45 cell lines (P < 0.05). Tissue array data showed that RCC1 expression was detected in 21% (18/85) of gastric carcinoma tissues and in 80% (76/95) of adjacent non-tumor tissues. The expression of RCC1 in gastric carcinoma tissues was significantly lower than in adjacent non-tumor tissues (P < 0.001). Furthermore, an association between RCC1 expression and clinicopathological features showed that RCC1 expression was closely correlated with tumor differentiation and depth of invasion (P < 0.05).\n\nQuestion:\nIs methylation-silencing RCC1 expression associated with tumorigenesis and depth of invasion in gastric 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:\nSerum sodium may have prognostic value in addition to the model for end-stage liver disease (MELD) score for prediction of early mortality in patients listed for liver transplant. In patients with cirrhosis, over-hydration is a common feature but its prognostic value has not been evaluated. This study examines the independent prognostic significance of MELD, serum sodium and hydration status on long-term survival in patients with cirrhosis. Serum sodium and hydration (total body water as a percentage of fat-free mass) were measured in 227 consecutive cirrhotic patients (146 male, 81 female; median age 49 years, range 19-73 years; median MELD score 13, range 6-36). Patients with hepatocellular carcinoma or listed for liver transplantation at the time of initial assessment were excluded. A competing risks Cox proportional hazards analysis was performed to evaluate the influence of MELD, sodium and hydration on risk of death or transplant. Median follow-up was 52 (range 4-93) months. Serum sodium and hydration were each associated with reduction in time to death or transplant on univariate analysis (sodium: hazard ratio [HR] 0.90, 95% confidence interval [CI] 0.87-0.94, P < 0.0001; hydration: HR 1.20, 95% CI 1.10-1.30, P < 0.0001). On multivariate analysis, MELD, serum sodium and hydration were independently predictive of death or transplant (MELD: HR 1.12, 95% CI 1.06-1.19, P < 0.0001; sodium: HR 0.93, 95% CI 0.87-0.99, P = 0.04; hydration: HR 1.17, 95% CI 1.02-1.33, P = 0.02).\n\nQuestion:\nDo serum sodium and hydration status predict transplant-free survival independent of MELD score in patients with cirrhosis?\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 3-amino-5-hydroxybenzoic acid (AHBA) synthase is one of the essential and unique enzymes for AHBA biosynthesis. The possibility of screening for ansamycin or AHBA-related antibiotic-producing strains from Actinomycetes by targeting an AHBA synthase gene was explored. A pair of degenerated primers designed according to the conserved regions of five known AHBA synthases was used to detect AHBA synthase genes within the genomic DNA of Actinomycetes. PCR screening resulted in obtaining 33 AHBA synthase gene-positive strains from 2000 newly isolated Actinomycetes. Phylogenetic analysis of these gene fragments along with those involved in the biosynthesis of structurally determined ansamycins showed that the genes with close phylogenetic relationships might be involved in the biosynthesis of compounds with the same/similar structures. Four strains have been proved to be actual geldanamycin or rifamycin producers by chemical characterization of their fermentation products.\n\nQuestion:\nDoes pCR screening of 3-amino-5-hydroxybenzoic acid synthase gene lead to identification of ansamycins and AHBA-related antibiotic producers in Actinomycetes?\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:\nEnsuring adequate dietary intake during pregnancy has important implications for optimising maternal and fetal health. It is not known whether diet quality is altered over pregnancy and the post-partum period. The aim of this study was to perform a comprehensive assessment of diet quality in overweight and obese women during pregnancy and early post-partum. In a prospective cohort study, n=301 overweight or obese pregnant women completed a food frequency questionnaire at study entry (10-20 weeks gestation), 28 weeks gestation, 36 weeks gestation and 4 months post-partum for assessment of macronutrient and micronutrient intake and diet quality by the Healthy Eating Index (HEI). Energy, macronutrient and dietary sources of micronutrients did not alter across pregnancy or post-partum. The HEI was of below average quality in 31.0% of women at baseline. This decreased from week 28 (P<0.001) and was maintained at a lower level post-partum such that HEI levels were lower compared with study entry (53.3±12.7 versus 56.7±10.1, P<0.001). The HEI decrease occurred in association with decreases in the milk, meat and unsaturated oil components, and increases in the proportion of energy from solid fats, alcohol and added sugars (P<0.001), and was independently predicted by the socioeconomic index for areas score (β=-0.011, s.e.=0.011, P=0.031).\n\nQuestion:\nDoes a decrease in diet quality occur during pregnancy in overweight and obese women which is maintained post-partum?\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:\nDespite improvements in neonatal heart surgery, neurologic complications continue to occur from low-flow cardiopulmonary bypass (LF-CPB) and deep hypothermic circulatory arrest (DHCA). Desflurane confers neuroprotection against ischemia at normothermia and for DHCA. This study compared neurologic outcome of a desflurane-based with a fentanyl-based anesthetic for LF-CPB. Thirty piglets aged 1 week received either fentanyl-droperidol (F/D), desflurane 4.5% (Des4.5), or desflurane 9% (Des9) during surgical preparation and CPB. Arterial blood gases, glucose, heart rate, arterial pressure, brain temperature, and cerebral blood flow (laser Doppler flowmetry) were recorded. After CPB cooling (22 degrees C brain) using pH-stat strategy, LF-CPB was performed for 150 min followed by CPB rewarming, separation from CPB, and extubation. On postoperative day 2, functional and histologic outcomes were assessed. Cardiovascular variables were physiologically similar between groups before, during, and after LF-CPB. Cerebral blood flow during LF-CPB (13% of pre-CPB value) did not differ significantly between the groups. Functional disability was worse in F/D than in Des9 (P = 0.04) but not Des4.5 (P = 0.1). In neocortex, histopathologic damage was greater in F/D than in Des4.5 (P = 0.03) and Des9 (P = 0.009). In hippocampus, damage was worse in F/D than in Des9 (P = 0.01) but not Des4.5 (P = 0.08). The incidences of ventricular fibrillation during LF-CPB were 90, 60, and 10% for F/D, Des4.5 (P = 0.06), and Des9 (P = 0.0002), respectively.\n\nQuestion:\nDoes desflurane improve neurologic outcome after low-flow cardiopulmonary bypass in newborn pigs?\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:\nQiliqiangxin (QL), a traditional Chinese medicine, has long been used to treat chronic heart failure. Previous studies demonstrated that QL could prevent cardiac remodeling and hypertrophy in response to hypertensive or ischemic stress. However, little is known about whether QL could modulate cardiac hypertrophy in vitro, and (if so) whether it is through modulation of specific hypertrophy-related microRNA. The primary neonatal rat ventricular cardiomyocytes were isolated, cultured, and treated with phenylephrine (PE, 50 µmol/L, 48 h) to induce hypertrophy in vitro, in the presence or absence of pretreatment with QL (0.5 µg/ml, 48 h). The cell surface area was determined by immunofluorescent staining for α-actinin. The mRNA levels of hypertrophic markers including atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and β-myosin heavy chain (MYH7) were assayed by qRT-PCRs. The protein synthesis of cardiomyocytes was determined by the protein/DNA ratio. The miR-199a-5p expression level was quantified in PE-treated cardiomyocytes and heart samples from acute myocardial infarction (AMI) mouse model. MiR-199a-5p overexpression was used to determine its role in the anti-hypertrophic effect of QL on cardiomyocytes. PE induced obvious enlargement of cell surface in cardiomyocytes, paralleling with increased ANP, BNP, and MYH7 mRNA levels and elevated protein/DNA ratio. All these changes were reversed by the treatment with QL. Meanwhile, miR-199a-5p was increased in AMI mouse heart tissues. Of note, the increase of miR-199a-5p in PE-treated cardiomyocytes was reversed by the treatment with QL. Moreover, overexpression of miR-199a-5p abolished the anti-hypertrophic effect of QL on cardiomyocytes.\n\nQuestion:\nDoes qiliqiangxin attenuate Phenylephrine-Induced Cardiac Hypertrophy through Downregulation of MiR-199a-5p?\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 test whether the reduced fecundity in women who smoke cigarettes may be attributed to the accelerated development of diminished ovarian reserve. Retrospective evaluation of clomiphene citrate (CC) challenge tests in women from a general infertility population who did and did not smoke cigarettes (part 1) and retrospective evaluation of the impact of smoking on pregnancy rates (PRs) in IVF among women with normal ovarian reserve (part 2). Large military tertiary care center. Sixty-five women who smoked cigarettes and 145 women who did not smoke cigarettes in the general infertility population (part 1) and women undergoing IVF for strict tubal factor infertility with normal ovarian reserve who did (n = 29) and did not (n = 73) smoke (part 2). Clomiphene citrate challenge tests, composed of FSH levels on cycle days 3 and 10 with 100 mg of CC administered on cycle days 5 through 9. Comparison of the incidence of abnormal CC challenge test results between women who did and did not smoke, and comparison of peak E2 levels, number of mature follicles, number of mature oocytes retrieved, fertilization rates, and total and ongoing PRs. The incidence of diminished ovarian reserve was increased in women who smoked (8 of 65 [12.31%]) when compared with age-matched controls who did not smoke (7 of 145 [4.83%]). Among women with normal CC challenge tests who were undergoing IVF, there were no differences in peak E2 levels, the number of mature follicles, the number of mature oocytes retrieved, fertilization rates, or total and ongoing PRs.\n\nQuestion:\nDoes cigarette smoking accelerate the development of diminished ovarian reserve as evidenced by the clomiphene citrate challenge test?\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:\nHeterogeneity in cardiac repolarization (Delta APD) is known to be arrhythmic. In the dog model of chronic complete AV-block and acquired long QT syndrome, an increase in Delta MAPD (defined as left ventricular monophasic action potential duration (MAPD) minus right ventricular MAPD) is often associated with changes in T-wave morphology. The purpose of this study was to correlate known changes in Delta MAPD with the planimetric total area of the T-wave on the surface ECG (integral of J-T, mVx ms). The relationship between Delta MAPD and total area of the T-wave (i.e., JT-area) was assessed in four different protocols with different types of dispersion: (1) class III drugs followed by levcromakalim (n= 7), (2) LAD coronary artery occlusion and reperfusion (n = 6), (3) dronedarone i.v., an amiodarone like agent (n = 5) and (4) steady state pacing at cycle lengths of 1000 ms and 500 ms (n = 5). Class III drugs increased Delta MAPD (55 +/- 40 ms to 120 +/- 50 ms(#), P<0.05), which was correlated (r = 0.74, P < 0.001) with JT-area (50 +/- 40 mV. ms to 95 +/- 35 mV x ms(#)). Ischemia increased both Delta MAPD (30 +/- 25 ms to 90 +/- 40 ms(#)) and JT-area (60 +/- 55 mV x ms to 75 +/- 50 mV x ms(#)). Both levcromakalim and reperfusion reversed these conditions. Dronedarone had no effect on Delta MAPD or on JT-area while a faster frequency reduced both Delta MAPD and JT-area.\n\nQuestion:\nDoes the JT-area indicate dispersion of repolarization in dogs with atrioventricular block?\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:\nS-adenosyl-l-homocysteine hydrolase (SAHH) is the only eukaryotic enzyme capable of S-adenosyl-l-homocysteine (SAH) catabolism for the maintenance of cellular transmethylation potential. Recently, biochemical and genetic studies in herbaceous species have obtained important discoveries in the function of SAHH, and an extensive characterization of SAHH family in even one tree species is essential, but currently lacking. Here, we first identified the SAHH family from Populus tomentosa using molecular cloning method. Phylogenetic analyses of 28 SAHH proteins from dicotyledons, monocotyledons, and lower plants revealed that the sequences formed two monophyletic groups: the PtrSAHHA with PtoSAHHA and PtrSAHHB with PtoSAHHB. Examination of tissue-specific expression profiles of the PtoSAHH family revealed similar expression patterns; high levels of expression in xylem were found. Nucleotide diversity and linkage disequilibrium (LD) in the PtoSAHH family, sampled from P. tomentosa natural distribution, revealed that PtoSAHH harbors high single-nucleotide polymorphism (SNP) diversity (π = 0.01059 ± 0.00122 and 0.00930 ± 0.00079,respectively) and low LD (r2 > 0.1, within 800 bp and 2,200 bp, respectively). Using an LD-linkage analysis approach, two noncoding SNPs (PtoSAHHB_1065 and PtoSAHHA_2203) and the corresponding haplotypes were found to significantly associate with α-cellulose content, and a nonsynonymous SNP (PtoSAHHB_410) within the SAHH signature motifs showed significant association with fiber length, with an average of 3.14% of the phenotypic variance explained.\n\nQuestion:\nIs allelic variation within the S-adenosyl-L-homocysteine hydrolase gene family associated with wood properties in Chinese white poplar ( Populus tomentosa )?\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 vitamin D receptor (VDR) has been studied as a novel target for cancer therapy in many tissue types as VDR ligands decrease cell proliferation in vitro and decrease tumor growth in vivo in sensitive cells. The objective of this study was to analyze the response to VDR agonist therapy in a panel of validated thyroid cancer cells and assess genetic markers predicting sensitivity and resistance to calcitriol and the noncalcemic analog DP006. Thyroid cancer cell lines were analyzed for VDR and RXR protein by Western blot. Cell growth after VDR agonist treatment (calcitriol or DP006) was assessed after 6 days of treatment by viable cell assay. To investigate calcitriol/DP006 resistance in VDR-expressing cells, the VDR was sequenced and 1-α and 24-hydroxylase mRNA expression was assessed. VDR protein was variably expressed in the thyroid cancer cell lines and its presence was not sufficient for decreased viable cell count in response to calcitriol or DP006. The most sensitive cells (TPC1) have an ff FokI VDR polymorphism and the most resistant cells (HTh7 and 8505C) have an FF FokI VDR. This is a unique finding given that the balance of the literature of VDR polymorphisms describes an association of the ff FokI polymorphism with cancer risk and/or decreased VDR transactivation. 1-α and 24-hydroxylase mRNA expression before and after VDR agonist therapy was examined. 1-α-Hydroxylase levels did not change after calcitriol treatment. However, we found that higher baseline 24-hydroxylase levels and/or lower stimulation of 24-hydroxylase levels after calcitriol treatment were associated with relative resistance to calcitriol/DP006.\n\nQuestion:\nIs thyroid cancer resistance to vitamin D receptor activation associated with 24-hydroxylase levels but not the ff FokI polymorphism?\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:\nSurgical intensive care unit (SICU) patients are known to be at high risk for venous thromboembolism (VTE). The 2005 Caprini Risk Assessment Model (RAM) predicts VTE risk in surgical patients. However, a physician's ability to accurately complete this RAM and the effect that inaccurate RAM completion might have on VTE risk remain unknown. Between 2009 and 2012, physicians completed a 2005 Caprini score for all SICU admissions at our institution. For comparison, we used a previously validated, computer-generated score. Regression-based techniques examined the effect of inadequate risk stratification on inpatient VTE risk, when controlling for other confounders. Among 3,338 consecutive SICU admissions, 55.2% had computer-generated scores that were higher than the physician-reported score, and 20.6% of scores were equal. Computer-generated scores were higher than physician-reported scores for both median (6 vs 5) and interquartile range (5 to 8 vs 3 to 7). Inter-rater reliability between the 2 scores was poor (kappa = 0.238). Risk score underestimation by ≥2 points was significantly associated with inpatient VTE (7.67% vs 4.59%, p = 0.002). Regression analysis demonstrated that each additional day's delay in chemoprophylaxis (odds ratio [OR] 1.05, 95% CI 1.01 to 1.08, p = 0.011) and under-risk stratification by ≥2 points (OR 2.46, 95% CI 1.53 to 3.96, p < 0.001) were independent predictors of inpatient VTE, as were higher admission APACHE score, personal history of VTE, recent pneumonia, and younger age.\n\nQuestion:\nDoes inadequate venous thromboembolism risk stratification predict venous thromboembolic events in surgical intensive care unit patients?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTransplant recipients are at increased risk of malignancy; however, the influence of transplantation on cancer outcomes has not been rigorously defined. The purpose of this study was to examine the influence of transplantation on the outcomes of individual cancers. De novo nonsmall cell lung cancer, colon cancer, breast cancer, prostate cancer, bladder cancer, renal cell cancer (RCC), and malignant melanoma data in 635 adult (>18 years of age) transplant recipients (from the Israel Penn International Transplant Tumor Registry) were compared with data from 1,282,984 adults in the general population (from the Surveillance, Epidemiology, and End Results database). Compared with the general population, transplant patients were more likely to have early stage (AJCC stage 0-II) RCC, but more advanced (AJCC stage >II) colon cancer, breast cancer, bladder cancer, and malignant melanoma. Compared with the general population, disease-specific survival was worse in the transplant population for colon cancer (all stages), nonsmall cell lung cancer (stage II), breast cancer (stage III), prostate cancer (stage II, III, and IV), bladder cancer (stage III), and RCC (stage IV). Multivariate analyses demonstrated transplantation to be a negative risk factor for survival for each cancer studied, and transplantation and cancer stage at diagnosis to be the most profound negative survival predictors.\n\nQuestion:\nAre de novo cancers arising in organ transplant recipients associated with adverse outcomes compared with the general population?\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 aim of this study was to test the hypothesis that severely injured trauma patients would be hypercoagulable compared with controls measured by thromboelastography and that this hypercoagulability would persist over a broad range of temperatures. A prospective study evaluating the effects of temperature on coagulation in trauma patients with Injury Severity Scores ≥ 15 and controls was completed. Thromboelastography was performed 24 hours after admission at 4 temperatures ranging from 32°C to 38°C. Ninety-two subjects (46 patients) were analyzed. Patients had a median Injury Severity Score of 20 (interquartile range, 16–26). Time to clot formation increased (P < .001) and fibrin cross-linking decreased (P < .01) in both groups as temperature decreased. Between groups, time to clot formation, fibrin cross-linking, and clot strength were significantly different at each temperature (P < .01), with patients being more hypercoagulable. Time to clot formation and fibrin cross-linking were more affected by temperature in controls compared with patients (P < .02).\n\nQuestion:\nDoes trauma induce a hypercoagulable state that is resistant to hypothermia as measured by thrombelastogram?\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:\nSelf-expanding metal stents can be used as bridge to elective surgery for acute malignant colonic obstruction. However, the impact on long-term oncological outcome and the optimal timing of surgery are still unknown. This was a retrospective multicenter study performed at four colorectal centers. Patients undergoing stent placement as bridge to surgery, between January 2010 and December 2013, were included in the study. Primary outcomes were survival and recurrence rates along with location of the metastases. Additionally, we recorded time from stent placement to elective surgery. Secondary outcomes were postoperative complication rates. Complications were classified according to the Clavien-Dindo classification score. A logistic regression model was used to describe impact of delayed stent removal on risk of recurrence. This study included 112 patients, with a median follow-up of 43 months. Survival rate was 70%. We found a recurrence rate of 37%, primarily local recurrences (17%). Procedure-related complications at the stent placement were seen in 18%, and complications after subsequent elective surgery were seen in 39%. A significantly higher risk of recurrence with increased time from stent placement to elective surgery (OR 5.1 [1.6-15.8], p = 0.005) was found.\n\nQuestion:\nIs delay of surgery after stent placement for resectable malignant colorectal obstruction associated with higher risk of recurrence?\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:\nInduction or overexpression of the heme-degrading enzyme, heme oxygenase 1 (HO-1), has been shown to protect mice from liver damage induced by acute inflammation. We have investigated the effects of HO-1 induction in a mouse model of chronic liver inflammation and fibrogenesis with progression to hepatocellular carcinoma (HCC) (Mdr2ko; FVB.129P2-Abcb4(tm1Bor)). HO-1 was induced in vivo by treatment with cobalt protoporphyrin IX, starting at week 5 or 12 of mice lifespan, and continued for 7 weeks. Our results showed that HO-1 induction reduced liver damage and chronic inflammation by regulating immune cell infiltration or proliferation as well as tumor necrosis factor receptor signaling. Fibrosis progression was significantly reduced by HO-1 induction in mice with mild, as well as established, portal and lobular fibrosis. HO-1 induction significantly suppressed hepatic stellate cell activation. During established fibrosis, HO-1 induction was able to revert portal inflammation and fibrosis below levels observed at the start of treatment. Moreover, hepatocellular proliferation and signs of dysplasia were decreased after HO-1 induction.\n\nQuestion:\nDoes induction of heme oxygenase 1 prevent progression of liver fibrosis in Mdr2 knockout 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 investigate possible protective effects of lens epithelium-derived growth factor (LEDGF) against photoreceptor death in light-damaged, Royal College of Surgeons (RCS) and P23H rhodopsin transgenic rats. Twelve-week-old Sprague-Dawley (SD), 6-week-old RCS, and 10-day-old P23H (line 1, heterozygote) rats received an intravitreal injection of LEDGF fused with glutathione-S-transferase (GST-LEDGF). Fellow eyes received vehicle and served as control specimens. Two days after the injections, the SD rats were exposed to light of 2000 lux for 48 hours. Corneal Ganzfeld ERGs were recorded 10 days after light damage, at 10 weeks of age in RCS rats, and at 4 weeks of age in P23H rats. The eyes were then processed for histologic analysis. Heat shock protein (hsp) content in the sensory retina was analyzed quantitatively by protein immunoblot. In light-damaged rats, the ERG indicated retinal protection in GST-LEDGF-injected eyes, with b-wave and STR thresholds being 1.14 +/- 0.50 (mean +/- SD) and 0.60 +/- 0.26 log candela (cd)/m2 lower, respectively, than in vehicle-injected eyes (P < 0.01). The GST-LEDGF-treated eyes had maximum b-wave amplitudes that were significantly larger (P < 0.0005), had more than twice as many remaining photoreceptors, and had better organized outer segments than the control eyes. In RCS rats, the treated eyes had 2.76 +/- 0.73 and 0.83 +/- 0.09 log cd/m(2) lower thresholds for the b-wave and STR, respectively (P < 0.005), and had significantly larger maximum b-wave amplitude (P < 0.0005). GST-LEDGF-treated eyes of RCS rats also had more photoreceptors remaining (P < 0.005) and a thinner debris layer than control eyes. In P23H rats, GST-LEDGF treatment did not protect either retinal function or structure. The retinas from GST-LEDGF-treated eyes of SD and RCS rats had higher levels of hsp25 and alphaB-crystallin than vehicle-injected eyes.\n\nQuestion:\nDoes lens epithelium-derived growth factor promote photoreceptor survival in light-damaged and RCS rats?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe Bedside Chronic Kidney Disease in Children (CKiD) equation was developed using data from children with chronic kidney disease. Some institutions are using this equation in all pediatric patients, regardless of renal function, to adjust medications. No data have shown that the Bedside CKiD equation is equivalent or better than the Schwartz equation in estimating glomerular filtration rate (GFR) in pediatric patients with normal renal function. To compare GFR estimates using the Bedside CKiD and Schwartz equations and determine if either offers sufficient vancomycin dosing guidance in hospitalized pediatric patients. This retrospective review at a single-center, academic, pediatric hospital included patients 2 to 12 years old with a steady-state vancomycin trough collected between January 1, 2010 and December 31, 2011. Patients with acute kidney injury or lacking essential data (e.g., height and serum creatinine), were excluded. An estimated GFR (eGFR) was calculated using the Schwartz and Bedside CKiD equations. Pearson correlations and linear regressions compared the eGFR values and vancomycin troughs. A total of 50 vancomycin troughs were analyzed. There was a weak relationship between the eGFR and troughs for the Schwartz equation (r (2) = 0.028) and Bedside CKiD equation (r (2) = 0.028). A weak relationship between serum creatinine and troughs was observed (r (2) = 0.132). Limitations include small sample size and retrospective design.\n\nQuestion:\nDo glomerular filtration rate equations accurately predict vancomycin trough concentrations in pediatric patients?\n\nAnswer:",
"role": "user"
},
{
"content": "no",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo test our previously generated hypothesis that women with secondary recurrent miscarriages with a firstborn boy have a poorer pregnancy prognosis than those with a firstborn girl. A study of a retrospective and a prospective cohort. The Danish recurrent miscarriage clinic. Two cohorts of 175 and 130 consecutive patients with unexplained secondary recurrent miscarriage referred from 1986 to 1999 (cohort 1) and 2000 to 2005 (cohort 2), respectively. The odds ratio (OR) for a live birth in the first pregnancy after referral in those with a firstborn boy compared with a firstborn girl in each of the two cohorts. The corresponding OR for a live birth adjusted for relevant prognostic variables in the combined group of patients. The crude ORs for a live birth in those with a firstborn boy compared with a firstborn girl were very similar in cohorts 1 and 2 (OR = 0.35, 0.33). In the adjusted analysis only two of five included variables significantly predicted live birth: a firstborn boy and the number of previous miscarriages.\n\nQuestion:\nIs a firstborn boy suggestive of a strong prognostic factor in secondary recurrent miscarriage : a confirmatory 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:\nOne of the most important events leading to morbidity and mortality in patients with severe sepsis is the development of global tissue hypoperfusion and oxidative damage. Ischemia-modified albumin (IMA), an albumin generated under ischemic and oxidative conditions, is a marker of oxidative stress and hypoperfusion. Here, we investigated whether IMA level could predict short-term mortality with severe sepsis. A prospective cohort study was conducted from April 2014 to October 2014 in intensive care units in a tertiary hospital. At the onset of severe sepsis, serum IMA level was measured, and baseline and laboratory data, infection sources, and underlying diseases were recorded; Sequential Organ Failure Assessment and Acute Physiology and Chronic Health Evaluation II scores were calculated. Multivariate logistic regression and receiver operating characteristic curve analyses were used to evaluate predictors of mortality. Kaplan-Meier analysis was used to compare survival at day 28. A total of 117 patients with severe sepsis were included (overall 28-day mortality, 24.8%). The IMA level was higher in nonsurvivors than in survivors (P < .05). It was a strong predictor of 28-day mortality (area under the receiver operating characteristic curve, 0.742; P < .001), and the optimal cutoff for IMA level maximizing sensitivity and specificity was 110 U/mL. On multivariate logistic regression, Acute Physiology and Chronic Health Evaluation II score and IMA level were independent risk factors for death. Survival rate was reduced with very high IMA level (≥110 U/mL; P < .05).\n\nQuestion:\nIs ischemia-modified albumin a predictor of short-term mortality in patients with severe sepsis?\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 mouse intravenous challenge model of Candida albicans infection is widely used to determine aspects of host-fungus interaction. We investigated the production of cytokines in the kidneys and spleen of animals up to 48 h after challenge with virulent and attenuated isolates and related these responses to semi-quantitative estimations of histopathological changes in the kidney. Progression of Candida albicans infection of the kidney in response to highly virulent fungal strains was characterized by higher levels of host cellular infiltrate, higher lesion densities and greater quantities of fungal elements at 24 and 48 h, and by higher kidney concentrations of IL-1beta, MCP-1, KC, IL-6, G-CSF, TNF, MIP-2 and MIP-1beta, among the immune effectors measured. Levels of the chemokine KC as early as 12 h after challenge correlated significantly with all later measurements of lesion severity. Early renal IL-6 and MIP-1beta concentrations also correlated with subsequent damage levels, but less significantly than for KC. All chemokines tested appeared in kidney homogenates, while most of the cytokines were undetectable in kidney and spleen homogenates. GM-CSF and IL-10 showed inverse correlations with measures of lesion severity, suggesting these alone may have exerted a defensive role. Spleen levels of KC at all times showed significant associations with kidney lesion measurements.\n\nQuestion:\nDo early-expressed chemokines predict kidney immunopathology in experimental disseminated Candida albicans infections?\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 effect of acetylcholine (ACh) on horse deep dorsal penile vein and to characterize the muscarinic receptor subtypes involved in this response. Vein rings were mounted in an organ bath chamber, and the isometric tension was recorded. In phenylephrine-contracted veins, ACh (1 nM to 1 microM) induced endothelium-dependent relaxation. The muscarinic receptor antagonist, atropine, produced parallel rightward shifts of the ACh response curves (pA2 = 10.04; pK(B) = 9.98). Carbachol (10 nM to 100 microM) also evoked relaxation in the vein segments, but showed a lower potency and similar relaxation to that induced by ACh. Pirenzepine, the high, intermediate, and low-affinity antagonist for M1, M3, and M2 receptors, respectively, inhibited ACh and carbachol-induced relaxation, yielding pA2 values of 7.51 and 7.37, and pK(B) values of 7.38 and 7.28, respectively. Methoctramine, a high-affinity M2 antagonist, showed no significant effect on the response to ACh. However, a high-affinity M3 antagonist, pFHHSiD, potently blocked the relaxation induced by carbachol and ACh, yielding pA2 and pK(B) values of 7.72 and 7.70 for pFHHSiD against ACh, respectively, and of 7.77 and 7.65 against carbachol, respectively.\n\nQuestion:\nDo muscarinic receptor subtypes mediate vasorelaxation in isolated horse deep dorsal penile vein?\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:\nUsher syndrome (USH) combines sensorineural deafness with blindness. It is inherited in an autosomal recessive mode. Early diagnosis is critical for adapted educational and patient management choices, and for genetic counseling. To date, nine causative genes have been identified for the three clinical subtypes (USH1, USH2 and USH3). Current diagnostic strategies make use of a genotyping microarray that is based on the previously reported mutations. The purpose of this study was to design a more accurate molecular diagnosis tool. We sequenced the 366 coding exons and flanking regions of the nine known USH genes, in 54 USH patients (27 USH1, 21 USH2 and 6 USH3). Biallelic mutations were detected in 39 patients (72%) and monoallelic mutations in an additional 10 patients (18.5%). In addition to biallelic mutations in one of the USH genes, presumably pathogenic mutations in another USH gene were detected in seven patients (13%), and another patient carried monoallelic mutations in three different USH genes. Notably, none of the USH3 patients carried detectable mutations in the only known USH3 gene, whereas they all carried mutations in USH2 genes. Most importantly, the currently used microarray would have detected only 30 of the 81 different mutations that we found, of which 39 (48%) were novel.\n\nQuestion:\nDoes complete exon sequencing of all known Usher syndrome genes greatly improve molecular diagnosis?\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:\nVery early mobilization may be one of the most important factors contributing to the favorable outcome observed from a stroke unit in Trondheim, Norway. The aims of this study were to (1) describe and compare the pattern of physical activity of patients with stroke managed in a stroke unit with specified mobilization protocols (Trondheim) and those without in Melbourne, Australia; and (2) identify differences in activity according to stroke severity between the 2 sites. Melbourne patients were recruited from 5 metropolitan stroke units. Trondheim patients were recruited from the stroke unit at University Hospital, Trondheim. All patients <14 days poststroke were eligible for the study. Patients receiving palliative care were excluded. Consenting participants were observed at 10-minute intervals from 8:00 am to 5:00 pm over a single day. At each observation, patient location, activity, and the people present were recorded. Negative binomial regression analyses were undertaken to assess differences in physical activity patterns between stroke units in the 2 cities. Patients in Melbourne and Trondheim had similar baseline characteristics. Melbourne patients spent 21% more time in bed and only 12.2% undertook moderate/high activity (versus 23.2% in Trondheim, P<0.001). This difference was even more pronounced among patients with greater stroke severity. The incidence rate ratio for time spent doing standing and walking activities in Melbourne was 0.44 (95% CI: 0.32 to 0.62) when compared with Trondheim.\n\nQuestion:\nAre not all stroke units the same : a comparison of physical activity patterns in Melbourne , Australia , and Trondheim , Norway?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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