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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:\nDietary fish oil potentiates the susceptibility of cellular membranes to lipid peroxidation, although it is also known to have beneficial effects on the development of cardiovascular diseases. The effects of dietary fish oil against doxorubicin-induced cardiomyopathy, in which free radicals and lipid peroxidation are involved, were investigated in rats. Sprague-Dawley rats (100 g) were fed a standard diet or a high fish oil diet (containing 10% fish oil) throughout the experimental period. Four weeks after starting each diet, experimental rats were treated with doxorubicin (cumulative dose 15 mg/kg) or vehicle (0.28 M dextrose solution). After three weeks of doxorubicin treatment, the cardiac performance, myocardial lipid peroxidation and myocardial vitamin E level were assessed. Compared with control rats, doxorubicin-treated rats showed a significantly increased mortality rate (P<0.05), and significantly decreased systolic blood pressure and left ventricular fractional shortening (P<0.01). The myocardial thiobarbituric acid-reactive substance level was significantly higher in doxorubicin-treated rats than in control rats (P<0.01), while the myocardial vitamin E level was significantly lower (P<0.05). Dietary fish oil enhanced the myocardial lipid peroxidation caused by doxorubicin, which was associated with a further decrease in myocardial vitamin E level. As a result, the rats treated with both doxorubicin and the high fish oil diet showed the highest mortality rate and the lowest cardiac performance of all the experimental groups.\n\nQuestion:\nDoes dietary fish oil prevent doxorubicin-induced cardiomyopathy in rats?\n\nAnswer:",
"role": "user"
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{
"content": "no",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nUltrasound is a potential therapeutic tool for dental tissue repair, but its biological effects on odontoblasts have not been well characterized. In this study, the effects of low-intensity low-frequency ultrasound on the viability, proliferation, and differentiation of odontoblast-like cells were investigated. Cell viability and proliferation were assessed after the treatment of adherent clonal MDPC-23 odontoblast-like cells with a 25-mW/cm(2) 45-kHz ultrasound. An in vitro scratch wound healing assay was used to investigate the ultrasound effects on cell migration. Long-term cultures were used to study odontogenic differentiation and extracellular mineralization. Ultrasound exposure for up to 30 minutes did not significantly affect odontoblast-like cell viability but significantly increased cell numbers after 2 days in culture. Ultrasound did not influence the scratch wound closure rate in the absence or presence of the mitogen inhibitor mitomycin C, indicating that ultrasound did not influence cellular migration. Single and consecutive exposures to ultrasound resulted in the enhancement of in vitro mineralization after 14 days in culture with an osteogenic differentiation medium. This coincided with the up-regulation of gene expression of collagen type I, osteoadherin, dentine matrix protein 1, and osteocalcin as well as the expression of cell markers alkaline phosphatase and nestin.\n\nQuestion:\nDoes low-intensity low-frequency ultrasound promote proliferation and differentiation of odontoblast-like cells?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nChemerin is a novel adipokine that is correlated with adipocyte differentiation, glucose metabolism, and inflammation. We aimed to investigate the relation between serum chemerin level and subclinical atherosclerosis markers as exemplified by brachial artery pulse wave velocity (baPWV), carotid intima-media thickness (CIMT), epicardial fat thickness (EFT), and carotid plaque presence in diabetes and prediabetes. Age-, body mass index (BMI)-, and gender-matched patients with type 2 DM (n=30), prediabetes (n=25), and normal glucose tolerance (n=25) were included in this cross-sectional study. Serum chemerin level, lipid parameters, glucose metabolism marker, baPWV, CIMT, EFT, and anthropometric were recorded. The independent risk factors for atherosclerosis markers were determined by linear and/or multiple logistic regression analysis. baPWV and carotid plaque presence were higher in the diabetes group than in prediabetes and control groups (p=0.039 and p=0.035 respectively), whereas serum chemerin levels were similar among groups (p=0.338). Chemerin levels were not correlated with PWV, CIMT, and epicardial fat thickness overall or in the subgroups. Overall and in the diabetes group, chemerin levels were positively correlated with the key components of metabolic syndrome as BMI, total body fat percentage, waist circumference, triglyceride, and systolic and diastolic blood pressure (BP). After adjusting for age, gender, and BMI, only the association between chemerin and systolic BP remained significant. Chemerin was not found as an independent risk factor for predicting atherosclerosis in diabetes and prediabetes.\n\nQuestion:\nIs chemerin associated with subclinical atherosclerosis markers in prediabetes and diabetes?\n\nAnswer:",
"role": "user"
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"content": "no",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPigment epithelium-derived factor (PEDF), a serine protease inhibitor, is secreted from the adipose tissue and circulates at high concentrations. A recent study found that PEDF played a causal role in obesity-induced insulin resistance and metabolic dysfunctions in mice. Here we investigated whether circulating PEDF levels predicted the development of the metabolic syndrome (MetS) in a 10-yr prospective study. Baseline plasma PEDF levels were measured with an ELISA in 520 nondiabetic subjects, recruited from the Hong Kong Cardiovascular Risk Factor Prevalence Study cohort. Multiple logistic regression was used to analyze whether PEDF was an independent factor related to the MetS at baseline. The role of PEDF in predicting the development of the MetS over 10 yr was analyzed using Cox regression analysis. Plasma levels of PEDF were significantly higher in men than women. At baseline, sex-adjusted PEDF levels were significantly higher in subjects with MetS (P < 0.001), and the association remained significant (odds ratio: 1.17, P = 0.015), even after adjustment for covariates. Among the components of the MetS, PEDF was independently associated with hypertriglyceridemia (P = 0.026) and hypertension (P = 0.005). Of the 396 subjects without the MetS at baseline, a total of 80 had developed the MetS over 10 yr. High baseline sex-adjusted PEDF was an independent predictor of the development of the MetS in men (hazard ratio: 1.25, P = 0.034) but not in women.\n\nQuestion:\nIs plasma level of pigment epithelium-derived factor independently associated with the development of the metabolic syndrome in Chinese men : a 10-year prospective study?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIntraocular pressure is increased during laparoscopic surgeries performed in a steep Trendelenburg position. This study compared the effects of propofol with those of sevoflurane on intraocular pressure in patients undergoing robot-assisted laparoscopic radical prostatectomy in a 30° Trendelenburg position. Sixty-six patients were randomly allocated to a maintenance anesthetic consisting of remifentanil and sevoflurane (Sevoflurane Group) or remifentanil and propofol (Propofol Group). Intraocular pressure (IOP) was measured at nine predefined time points, including baseline (T0), five minutes after establishing pneumoperitoneum (T2), 30 min after establishing the Trendelenburg position with pneumoperitoneum (T3), five minutes after returning to the horizontal position (T4), and immediately after tracheal extubation (T6). The primary outcome was the change in intraocular pressure from T0 to T3. The results of linear mixed model analysis showed that intraocular pressure differed between the two groups (P = 0.0039). At T3, the mean (SD) IOP was greater in the Sevoflurane Group [23.5 (4.3) mmHg] than in the Propofol Group [19.9 (3.8) mmHg] (P = 0.0019). At T2 and T6, IOP was also greater in the Sevoflurane Group than in the Propofol Group (P = 0.038 and P = 0.009, respectively). There was a statistically significant increase in intraocular pressure from baseline to T3 (pneumoperitoneum and steep Trendelenberg) in the Sevoflurane Group [6.0 (5.0) mmHg; P < 0.001] but not in the Propofol Group [2.1 (5.1) mmHg; P = 0.136]. None of the patients experienced ocular complications.\n\nQuestion:\nIs increase in intraocular pressure less with propofol than with sevoflurane during laparoscopic surgery in the steep Trendelenburg position?\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:\nGlucocorticoid-induced leucine zipper (GILZ) represents an anti-inflammatory mediator, whose downregulation has been described in various inflammatory processes. Aim of our study was to decipher the regulation of GILZ in vascular inflammation. Degenerated aortocoronary saphenous vein bypass grafts (n = 15), which exhibited inflammatory cell activation as determined by enhanced monocyte chemoattractrant protein 1 (MCP-1, CCL2) and Toll-like receptor 2 (TLR2) expression, showed significantly diminished GILZ protein and mRNA levels compared to healthy veins (n = 23). GILZ was also downregulated in human umbilical vein endothelial cells (HUVEC) and macrophages upon treatment with the inflammatory cytokine TNF-α in a tristetraprolin (ZFP36, TTP)- and p38 MAPK-dependent manner. To assess the functional implications of decreased GILZ expression, we determined NF-κB activation after GILZ knockdown by siRNA and found that NF-κB activity and inflammatory gene expression were significantly enhanced. Importantly, ZFP36 is induced in TNF-α-activated HUVEC as well as in degenerated vein bypasses. When atheroprotective laminar shear stress was employed, GILZ levels in HUVEC increased on mRNA and protein level. Laminar flow also counteracted TNF-α-induced ZFP36 expression and GILZ downregulation. MAP kinase phosphatase 1 (MKP-1, DUSP1), a negative regulator of ZFP36 expression, was distinctly upregulated under laminar shear stress conditions and downregulated in degenerated vein bypasses.\n\nQuestion:\nDoes downregulation of the glucocorticoid-induced leucine zipper ( GILZ ) promote vascular inflammation?\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:\nConstraint-based reconstruction and analysis (COBRA) is used for modeling genome-scale metabolic networks (MNs). In a COBRA model, extreme pathways (ExPas) are the edges of its conical solution space, which is formed by all viable steady-state flux distributions. ExPa analysis has been successfully applied to MNs to reveal their phenotypic capabilities and properties. Recently, the COBRA framework has been extended to transcriptional regulatory networks (TRNs) and transcriptional and translational networks (TTNs), so efforts are needed to determine whether ExPa analysis is also effective on these two types of networks. In this paper, the ExPas resulting from the COBRA models of E.coli's MN, TRN and TTN were horizontally compared from 5 aspects: (1) Total number and the ratio of their amount to reaction amount; (2) Length distribution; (3) Reaction participation; (4) Correlated reaction sets (CoSets); (5) interconnectivity degree. Significant discrepancies in above properties were observed during the comparison, which reveals the biological natures of different biological processes. Besides, by demonstrating the application of ExPa analysis on E.coli, we provide a practical guidance of an improved approach to compute ExPas on COBRA models of TRNs.\n\nQuestion:\nDoes comparison on extreme pathways reveal nature of different biological processes?\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 explore the protective effects of N-acetylcysteine (NAC) on cochlear damage occurring in irradiated guinea pigs. Seventy-two guinea pigs were randomly divided into 4 groups (n = 18 each). Control group received neither NAC nor irradiation, irradiation group received total cranium irradiation of 70 Gy, irradiation & saline group cranium irradiation of 70 Gy and saline solution through a round window and NAC group cranium irradiation of 70 Gy and NAC through a round window. The right ear received radiation. The animals were sacrificed at Day 14 post-irradiation. The specimens were dehydrated, embeded in paraffin and serially cut into 5-µm slices. Sections were stained with immunohistochemistry and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL). The cochlear basal membranes were observed for malondialdehyde (MDA) and superoxide dismutase (SOD) with scanning electron microscope. The cilium of hair cells had no clear loss and apoptotic number of spiral ganglion cells decreased in NAC group. The average optical density value of Caspase 3 in spiral ganglion in NAC group significantly decreased versus the irradiation group (0.08 ± 0.02 vs 0.10 ± 0.01, P < 0.01). The level of MDA of NAC group also decreased versus the irradiation group (0.33 ± 0.05 vs 0.84 ± 0.13, P < 0.05). The level of SOD in the NAC group increased versus the irradiation group (10.7 ± 3.0 vs 8.7 ± 1.3, P < 0.05). The ratio of apoptotic cell in SGC in the NAC group at Day 14 (7.8% ± 1.8%) decreased versus the irradiation group (32.0% ± 8.7%) at Day 14.\n\nQuestion:\nDo [ Protective effects of N-acetylcysteine on cochlear damage occur in guinea pigs exposed to irradiation ]?\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:\nAnxiety is a common non-motor symptom among patients with Parkinson's disease (PD). Although the etiology of anxiety in PD is likely to be multifactorial, a dysfunction in the dopaminergic system might be implicated in its pathogenesis. The aim of our study was to investigate a possible dopaminergic mechanism involved in anxiety in newly diagnosed never-medicated PD patients using SPECT and ¹²³I-FP-CIT as the dopamine transporter ligand. Thirty-four newly diagnosed, untreated PD patients with asymmetric motor symptoms were included in the study: 17 patients with right- and 17 with left-motor onset, matched for age, disease duration and motor disability constituted the group. They were all evaluated for anxiety and depression and underwent an SPECT with ¹²³I-FP-CIT. Dopamine transporter (DAT) availability values for right and left caudate and putamen were calculated and compared between patients with and without anxiety. Regression analyses were also performed in order to correlate DAT availability with the severity of the anxiety symptoms. Comparison between PD patients with and those without anxiety revealed significant differences of DAT availability in all the examined regions except the right putamen. In the group of patients considered as a whole, a significant correlation was found between increased anxiety severity and decreased DAT availability in right caudate.\n\nQuestion:\nIs anxiety associated with striatal dopamine transporter availability in newly diagnosed untreated Parkinson 's disease 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:\nVascular stiffening, a risk factor for cardiovascular disease, is accelerated, particularly in women with obesity and type 2 diabetes. Preclinical evidence suggests that dipeptidylpeptidase-4 (DPP-4) inhibitors may have cardiovascular benefits independent of glycemic lowering effects. Recent studies show that consumption of a western diet (WD) high in fat and simple sugars induces aortic stiffening in female C57BL/6J mice in advance of increasing blood pressure. The aims of this study were to determine whether administration of the DPP-4 inhibitor, linagliptin (LGT), prevents the development of aortic and endothelial stiffness induced by a WD in female mice. C56Bl6/J female mice were fed a WD for 4 months. Aortic stiffness and ex vivo endothelial stiffness were evaluated by Doppler pulse wave velocity (PWV) and atomic force microscopy (AFM), respectively. In addition, we examined aortic vasomotor responses and remodeling markers via immunohistochemistry. Results were analyzed via 2-way ANOVA, p < 0.05 was considered as statistically significant. Compared to mice fed a control diet (CD), WD-fed mice exhibited a 24 % increase in aortic PWV, a five-fold increase in aortic endothelial stiffness, and impaired endothelium-dependent vasodilation. In aorta, these findings were accompanied by medial wall thickening, adventitial fibrosis, increased fibroblast growth factor 23 (FGF-23), decreased Klotho, enhanced oxidative stress, and endothelial cell ultrastructural changes, all of which were prevented with administration of LGT.\n\nQuestion:\nDoes dipeptidyl peptidase-4 inhibition with linagliptin prevent western diet-induced vascular abnormalities in female mice?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTumor volume is an important prognosticator for predicting prostate cancer recurrence following radical prostatectomy (RP). We assessed the ability of the visual estimate of the percent of carcinoma (VEPC) to predict recurrence. As performed by 1 surgeon (MSS), 1,114 men underwent radical prostatectomy between 1992 and February 2002. Patients who had less than 12 months of followup, who underwent salvage RP or in whom VEPC was not assessed in the pathology specimen were excluded. VEPC and other clinical variables were analyzed. We performed univariate analysis using the Kaplan-Meier log rank test. Multivariate analysis using Cox proportional hazards regression was performed. A total of 692 patients with a mean age of 61 +/- 7 years met the criteria for this analysis. Mean followup was 52 +/- 30 months. Of the patients 17% had biochemical recurrence. Mean VEPC was 25% and 13% in those with and without recurrence, respectively. On univariate analysis all variables were significant predictors of recurrence. However, multivariate analysis showed that the only significant predictors of recurrence were patient age, initial prostate specific antigen 10 ng/ml or greater, RP Gleason 8 to 10, extraprostatic extension, seminal vesicle involvement and VEPC. Based on disease-free survival curves patients were stratified into 3 broad groups, namely low, intermediate and high volume. The HR for biochemical recurrence was 2.1 for the intermediate VEPC group (9.1% to 20%) and 2.7 for the high VEPC group (greater than 20%). In the reference group it was less than 9% (low volume).\n\nQuestion:\nDoes visual estimate of percent of carcinoma predict recurrence after radical prostatectomy?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe purpose of our study is to evaluate imaging features suggestive of a conjoined nerve root on routine axial MRI. Two radiologists and two surgeons retrospectively reviewed the MRI of three cases in which a conjoined nerve root was discovered during operation and found three suggestive signs on routine axial MR images: \"corner\" (asymmetric morphology of the anterolateral corner of the dural sac), \"fat crescent\" (intervening extradural fat between the asymmetric dura and the nerve root), and \"parallel\" signs (visualization of the entire parallel course of the nerve root at the disc level). Two radiologists prospectively found these signs during routine MRI interpretation sessions over a period of 6 months. If one or a combination of signs were noted on axial MR images, contiguous axial scans were additionally obtained. Three cases that were previously found during operations were also included. Prevalence and confidence scores for each sign were assessed on axial T1- and T2-weighted images. Twelve patients showed one or a combination of the three signs, 9 had contiguous axial MR scans. Five cases were confirmed by operation. The prevalence of the corner, fat crescent, and parallel signs were 12 out of 12 (100%), 6 out of 12 (50%), and 8 out of 12 (67.7%) on axial T1-weighted images. The overall diagnostic confidence was higher on T1- than on T2-weighted images (P<0.05).\n\nQuestion:\nDoes imaging feature suggestive of a conjoined nerve root on routine axial MRI?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe studied three different injection techniques of sciatic nerve block in terms of block onset time and efficacy with 0.75% ropivacaine. A total of 75 patients undergoing foot surgery were randomly allocated to receive sciatic nerve blockade by means of the classic posterior approach (group classic; n = 25), a modified subgluteus posterior approach (group subgluteus; n = 25), or a lateral popliteal approach (group popliteal; n = 25). All blocks were performed with the use of a nerve stimulator (stimulation frequency, 2 Hz; intensity, 2-0.5 mA) and 30 mL of 0.75% ropivacaine. Onset of nerve block was defined as complete loss of pinprick sensation in the sciatic nerve distribution with concomitant inability to perform plantar or dorsal flexion of the foot. In the three groups, an appropriate sciatic stimulation was elicited at <0.5 mA. The failure rate was similar in the three groups (group popliteal: 4% versus group classic: 4% versus group subgluteus: 8%). The onset of nerve block was slower in group popliteal (25 +/- 5 min) compared with group classic (16 +/- 4 min) and group subgluteus (17 +/- 4 min; P < 0.001). There was no significant difference in the onset of nerve block between group classic and group subgluteus. No differences in the degree of pain measured at the first postoperative administration of pain medication were observed among the three groups. We conclude that the three approaches resulted in clinically acceptable anesthesia in the distribution of the sciatic nerve. The subgluteus and classic posterior approaches generated a significantly faster onset of anesthesia than the lateral popliteal approach.\n\nQuestion:\nDoes the effects of three different approaches on the onset time of sciatic nerve block with 0.75 % ropivacaine?\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:\nWhile ischemic preconditioning confers significant protection against subsequent prolonged periods of ischemia, the mechanisms triggering protection remain speculative. We hypothesize that a sub-lethal oxidative stress during ischemic preconditioning induces defense mechanisms preventing subsequent lethal injury. We used mouse models of partial and total hepatic ischemia for 75 min. Ischemic preconditioning consisted of 10-min ischemia and 15-min reperfusion prior to the prolonged ischemic insult. Tissue levels of peroxides increased about three times after 10 min of ischemia and normalized within 15 min of reperfusion. This limited oxidative stress during ischemic preconditioning prevented the negative effects of subsequent prolonged ischemia as assessed by AST-levels, TUNEL-staining of hepatocytes and animal survival. N-Acetylcysteine inhibited the mild oxidative burst of ischemic preconditioning, and fully reversed the protective effects of preconditioning. The protective role of a sub-lethal oxidative stress was supported by the benefit of delivery of an H2O2-analog through the portal vein prior to a long ischemic insult. This challenge conferred similar protection as ischemic preconditioning.\n\nQuestion:\nDoes sub-lethal oxidative stress trigger the protective effects of ischemic preconditioning in the mouse liver?\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:\nComa is associated with poor outcome in patients with basilar artery occlusion. We sought to assess whether the posterior circulation Acute Stroke Prognosis Early CT Score and the Pons-Midbrain Index applied to CT angiography source images predict the outcome of comatose patients in the Basilar Artery International Cooperation Study. Basilar Artery International Cooperation Study was a prospective, observational registry of patients with acute basilar artery occlusion with 48 recruiting centers worldwide. We applied posterior circulation Acute Stroke Prognosis Early CT Score and Pons-Midbrain Index to CT angiography source images of Basilar Artery International Cooperation Study patients who presented with coma. We calculated adjusted risk ratios to assess the association of dichotomized posterior circulation Acute Stroke Prognosis Early CT Score (≥8 vs. <8) and Pons-Midbrain Index (<3 vs. ≥3) with mortality and favourable outcome (modified Rankin Scale score 0-3) at one month. Of 619 patients in the Basilar Artery International Cooperation Study registry, CT angiography source images were available for review in 158 patients. Among these, 78 patients (49%) presented with coma. Compared to non-comatose patients, comatose patients were more likely to die (risk ratios 2.34; CI 95% 1.56-3.52) and less likely to have a favourable outcome (risk ratios 0.44; CI 95% 0.24-0.80). Among comatose patients, a Pons-Midbrain Index < 3 was related to reduced mortality (adjusted RR 0.66; 95% CI 0.46-0.96), but not to favourable outcome (adjusted RR 1.19; 95% CI 0.39-3.62). Posterior circulation Acute Stroke Prognosis Early CT Score dichotomized at ≥ 8 vs. <8 was not significantly associated with death (adjusted RR 0.70; 95% CI 0.46-1.05).\n\nQuestion:\nDo cT-angiography source images indicate less fatal outcome despite coma of patients in the Basilar Artery International Cooperation Study?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo report the clinical findings and management of a case of endogenous endophthalmitis in a patient with bacterial endocarditis presenting with a septic metastasis to the iris. Observational case report. Review of clinical findings and treatment. A 37-year-old intravenous drug user hospitalized with bacterial endocarditis secondary to methicillin-sensitive Staphylococcus aureus bacteremia presented with a painful red left eye, hypopyon, and iris abscess. Roth spots were noted in the fundus of the right eye. Aqueous culture was positive for methicillin-sensitive S aureus. The patient was treated with intravitreal, topical, and intravenous antibiotics. The hypopyon and iris abscess resolved within 2 weeks, and the patient achieved a final visual acuity of 20/25 in the left eye.\n\nQuestion:\nDoes iris abscess as an unusual presentation of endogenous endophthalmitis in a patient with bacterial endocarditis?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo investigate the role of miR-181c in glycolysis of cancer-associated fibroblasts (CAFs) and explore the mechanism. Human lung CAFs and normal fibroblasts (NFs), isolated from fresh human lung adenocarcinoma tissue specimens by primary culture of tissue explants, were transfected with a miR -181c mimics, a miR-181c inhibitor, a siRNA siRNA-HK2 or the vector HK2-vector via Lipofectamine(TM) 2000. Quantitative real-time PCR was used to analyze the changes in miR-125b expression in the transfected cells; hexokinase-2 (HK2) protein expression in the cells was detected using Western blotting, and the cellular glucose uptake was assessed with 2-NBDG. Lactate production in the cells was examined and expression of HK2 mRNA was detected with dual luciferase reporter gene assay. No obvious difference was found in the cell morphology between CAFs and NFs. Compared with the NFs, the CAFs showed obviously increased glucose uptake, lactate production and HK2 protein expression with decreased expressions of the miR-181 family (P<0.05). Transfection with the miR-181 inhibito- rsignificantly increased glucose uptake, lactate production and HK2 protein expression in the NFs. In CAFs, transfection with the miR-181 mimics caused significantly lowered glucose uptake, lactate production and HK2 protein expression of. Knockdown of endogenous HK2 by siRNA abolished miR-181 mimics-mediated decrease of glucose uptake and lactate production in CAFs, while transfection with miR-181 mimics suppressed HK2 overexpression-induced enhancement of glucose uptake and lactate production in NFs.\n\nQuestion:\nDoes [ miR-181c inhibit glycolysis by targeting hexokinase 2 in cancer-associated fibroblasts ]?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
}
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo evaluate whether infliction of peritoneal trauma would promote tumor cell adherence to damaged peritoneal surfaces; to investigate whether peritoneal damage could promote tumor growth of extraperitoneal tumors; and to evaluate whether the amount of trauma correlated with the degree of tumor cell adherence and local and distant tumor growth. After potentially curative resection of colorectal carcinoma, the most common site for recurrence is locoregional. We previously demonstrated that surgical trauma induces a cascade of events leading to adhesion formation. The same mechanisms may be responsible for improved tumor cell adherence and growth facilitation in early local recurrence. A reproducible rat model was used in which peritoneal damage was inflicted by standardized rubbing of the peritoneum with surgical gauzes of different texture. In the first experiment, tumor cell adherence and growth at traumatized and nontraumatized peritoneal sites were assessed semiquantitatively 3 weeks after perioperative intra-abdominal injection of CC-531 tumor cells. In the second experiment, the effect of peritoneal trauma on ectopic tumor growth was investigated (CC-531 implanted under the renal capsule). In the final experiment, we evaluated how soon after peritoneal traumatization tumor cell adhesion and growth-promoting factors were active and whether they could be passively transferred to naïve nontraumatized abdominal cavities. A significant correlation between the amount of peritoneal trauma and the degree of tumor take at damaged peritoneal surfaces was found (p < or = 0.018). Tumor take at remote peritoneal sites not directly traumatized was also significantly higher after severe trauma than after moderate trauma of the peritoneum (p < or = 0.005). In addition, a significant correlation between the degree of peritoneal trauma and the growth of ectopic tumors under the renal capsule was observed (p < or = 0.009). The final experiment demonstrated that within a few hours after infliction of peritoneal trauma, tumor growth-promoting effects could be passively transferred to naïve recipients.\n\nQuestion:\nDoes reduction of peritoneal trauma by using nonsurgical gauze lead to less implantation metastasis of spilled tumor 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:\nRegression of left ventricular hypertrophy (LVH) after surgical correction for aortic stenosis is not fully understood on the molecular level. The aim of this study was to examine whether there is an association between LVH regression and extracellular matrix (ECM) gene expression. A standard model of controlled LVH induction by supracoronary banding (A=baseline) was applied in 44 growing sheep (age, 6 to 8 months). Surgical correction to release the pressure gradient was performed 8.3+/-1 months later (B). The animals were killed after another 10.1+/-2 months (C). At all time points, hemodynamic evaluations and quantitative analysis of mRNA and protein expression for matrix metalloproteinases (MMP) and their tissue inhibitors (TIMP) was performed. Left ventricular mass index was 82+/-21 (A) versus 150+/-33 (B), P<0.01, and 78+/-18 g/m(2) (C), P<0.01. Left ventricular function and cardiac index remained stable. Myocardial fiber diameter index was 9.1+/-1.2 (A) versus 12.3+/-1.4 (B), P<0.01, and 8.4+/-1.3 micrometer/m(2) (C), P<0.01. In parallel to the development of LVH at B, gene expression was increased significantly for MMP-1, MMP-2, MMP-3, and MMP-9 and for TIMP-1 and TIMP-2 and decreased significantly for TIMP-3. After surgical correction (C), there was a complete regression of gene expression to baseline measures.\n\nQuestion:\nIs regression of left ventricular hypertrophy after surgical therapy for aortic stenosis associated with changes in extracellular matrix gene expression?\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 investigate the expression of receptor for advanced glycation end products (RAGE) on the surface of circulating endothelial cells (CECs) in patients with Kawasaki disease (KD). The positive rate of RAGE on the surface of CECs (CECs-RAGE/CECs) and the fluorescence intensity of RAGE on the surface of CECs (FI-RAGE-CECs) were evaluated in 89 patients with KD in the acute stage (A-KD), subacute stage (SA-KD), or convalescent stage (C-KD). CECs-RAGE/CECs and the FI-RAGE-CECs increased significantly in patients with KD. The CECs-RAGE/CECs was significantly higher in C-KD patients with coronary artery lesions (CALs) than in those without CALs. The FI-RAGE-CECs level was significantly higher in SA-KD and C-KD patients with CALs than in A-KD patients. In SA-KD and C-KD patients, the CECs-RAGE/CECs and FI-RAGE-CECs levels decreased in intravenous immunoglobulin (IVIG)-respondent patients but increased progressively in IVIG-resistant patients and were significantly higher in IVIG-resistant patients than in IVIG-respondent patients.\n\nQuestion:\nIs expression of receptor for advanced glycation end products ( RAGE ) on the surface of circulating endothelial cells upregulated in Kawasaki 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:\nVarious studies examined the relationship between the expression of phosphatase and tensin homolog (PTEN) with the clinical outcome in patients with lung cancer, but yielded conflicting results. Electronic databases updated to January 2016 were searched to find relevant studies. A meta-analysis was conducted with eligible studies which quantitatively evaluated the relationship between the expression of PTEN and clinical outcomes of patients with lung cancer. Subgroup and sensitivity analysis were conducted. A total of 13 studies were included. When compared with high PTEN expression group, the lung cancer patients with reduced PTEN expression exhibited shorter overall survival (hazard ratio=0.40, 95%CI=0.32~0.52, P<0.001) and shorter progression-free survival (hazard ratio=0.53, 95%CI=0.38~0.74, P<0.001). In subgroup analysis, among lung cancer patients whose treatments including EGFR TKIs, we observed significant benefits of OS in high PTEN expression group.\n\nQuestion:\nIs pTEN expression associated with the outcome of lung cancer : evidence from a meta-analysis?\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 endoscopic fibrin glue or platelet-rich fibrin glue (PRFG) injection is an easy, safe and effective technique for the fistula. So far, the use of fibrin glue has been limited to selected cases. Our case is a three years old male child with a neck trauma resulting in a Esophago-Cutaneous fistula after a 3 month period of follow up we decided to use PRFG for this lesion after fine debridement of the fistula tract, and the surrounding fibrosed tissue twice with a one week interval. Our visit after two weeks showed complete recovery and normal general condition. A contrast study revealed complete disappearance of the lesion.\n\nQuestion:\nDo lateral Traumatic Esophago-Cutaneous fistula in a Child ; Platelet-Rich Fibrin Glue Challenge?\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:\nVascular smooth muscle (SM) cell phenotypic modulation plays an important role in arterial stiffening associated with aging. Serum response factor (SRF) is a major transcription factor regulating SM genes involved in maintenance of the contractile state of vascular SM cells. We investigated whether SRF and its target genes regulate intrinsic SM tone and thereby arterial stiffness. The SRF gene was inactivated SM-specific knockout of SRF (SRF(SMKO)) specifically in vascular SM cells by injection of tamoxifen into adult transgenic mice. Fifteen days later, arterial pressure and carotid thickness were lower in SRF(SMKO) than in control mice. The carotid distensibility/pressure and elastic modulus/wall stress curves showed a greater arterial elasticity in SRF(SMKO) without modification in collagen/elastin ratio. In SRF(SMKO), vasodilation was decreased in aorta and carotid arteries, whereas a decrease in contractile response was found in mesenteric arteries. By contrast, in mice with inducible SRF overexpression, the in vitro contractile response was significantly increased in all arteries. Without endothelium, the contraction was reduced in SRF(SMKO) compared with control aortic rings owing to impairment of the NO pathway. Contractile components (SM-actin and myosin light chain), regulators of the contractile response (myosin light chain kinase, myosin phosphatase target subunit 1, and protein kinase C-potentiated myosin phosphatase inhibitor) and integrins were reduced in SRF(SMKO).\n\nQuestion:\nDoes inactivation of serum response factor contribute to decrease vascular muscular tone and arterial stiffness in 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:\nLevels of serum thyroid-stimulating hormone (TSH) indicate thyroid function, because thyroid hormone negatively controls TSH release. Genetic variants in the vascular endothelial growth factor A (VEGFA) gene are associated with TSH levels. The aim of this study was to characterise the association of VEGFA variants with TSH in a Danish cohort and to identify and characterise functional variants. We performed an association study of the VEGFA locus for circulating TSH levels in 8445 Danish individuals. Lead variants were tested for allele-specific effects in vitro using luciferase reporter and gel-shift assays. Four SNPs in VEGFA were associated with circulating TSH (rs9472138, rs881858, rs943080 and rs4711751). For rs881858, the presence of each G-allele was associated with a corresponding decrease in TSH levels of 2.3% (p=8.4×10\n\nQuestion:\nAre carriers of a VEGFA enhancer polymorphism selectively binding CHOP/DDIT3 predisposed to increased circulating levels of thyroid-stimulating hormone?\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 inability to make profitable long-term decisions has been implicated in several psychiatric disorders. There is emerging evidence to support a role for dopamine (DA) in decision making, but our understanding of the role of noradrenaline (NA) and serotonin (5-HT) in decision making, and of possible interactions between the three monoamines, is limited. Moreover, impulsivity has been associated with aberrant decision making, but the underlying mechanisms are incompletely understood. The purpose of this study is to improve our understanding of the neuropharmacological mechanisms of decision making and impulse control. We investigated the effects of amphetamine (0.25-1.0 mg/kg) and selective reuptake inhibitors of DA (GBR12909; 2.5-10 mg/kg), NA (atomoxetine; 0.3-3.0 mg/kg), and 5-HT (citalopram; 0.3-3.0 mg/kg) in a rat gambling task (rGT). Since the rGT allows for detection of impulsive action, i.e., premature responding, we also assessed the relationship between decision making and impulsivity. In the rGT, rats developed an optimal choice strategy from the first session onwards. Elevation of endogenous DA or NA levels increased and decreased impulsivity, respectively, but did not alter decision making. However, simultaneous blockade of DA and NA disrupted decision making, reflected by a relative decrease in choice for the advantageous choice options. Increasing 5-HT neurotransmission did not affect decision making or impulsivity.\n\nQuestion:\nDoes simultaneous blockade of dopamine and noradrenaline reuptake promote disadvantageous decision making in a rat gambling task?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSeveral reports have indicated that the measurement of parathyroid gland size assists the management of patients with secondary hyperparathyroidism. This study examined whether parathyroid gland enlargement influenced the response of secondary hyperparathyroidism to cinacalcet. Clinically stable hemodialysis patients with secondary hyperparathyroidism that was resistant to conventional treatment received cinacalcet for 6 months. Based on the parathyroid gland size measured by ultrasonography, the patients were divided into group S (gland <500 mm(3)) and group L (gland >or=500 mm(3)). Serum levels of intact parathyroid hormone (intact PTH), bone-specific alkaline phosphatase, osteocalcin, and cross-linked N-terminal telopeptide of type 1 collagen were measured over time. Twenty-four patients completed the study. In group S, all markers of bone metabolism and intact PTH were significantly decreased after 3 months of cinacalcet treatment. In contrast, there were no significant changes of these parameters, except for intact PTH, after 3 months in group L. After 6 months of cinacalcet treatment, however, all of the markers of bone metabolism were significantly decreased in both groups.\n\nQuestion:\nDoes response of secondary hyperparathyroidism to cinacalcet depend on parathyroid size?\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 evaluated the use of continuous infusion of ketamine to reduce intraoperative remifentanil side effects, such as bradycardia and hypotension, and to improve postoperative analgesia from balanced anesthesia with remifentanil. Forty patients undergoing spine surgery under remifentanil-based anesthesia were randomly assigned to intraoperative ketamine group and saline (control) group. Balanced anesthesia was maintained with infusion of propofol (2-4 mg x kg(-1) x hr(-1)), remifentanil (6-8 microg x kg(-1) hr(-1)) and vecuronium (60-80 microg x kg(-1) x hr(-1)) with nitrous oxide (60%) and with or without ketamine (300-400 microg x kg(-1) x hr(-)). All patients were given scheduled NSAIDs by their own doctor at the end of surgery. Intraoperative bradycardia (HR <50) and hypotension (SBP <80), and postoperative additional NSAIDs request were recorded. Adverse events, such as bradycardia and hypotension, were less frequent in the ketamine group (P < 0.05). Less additional NSAIDs was required in the ketamine than in the control group (P < 0.05). Emergence time from anesthesia was within 5 min in both groups.\n\nQuestion:\nDoes [ Balanced anesthesia with continuous ketamine reduce adverse effects of remifentanil ]?\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:\nAlcoholism is characterized by impaired decision-making (i.e., choosing intoxication in the face of mounting negative consequences). This impairment may involve a reduced brain response to the negative consequences of behavior, which supports an inclination to engage in risky behaviors. The feedback error-related negativity (F-ERN) is hypothesized to reflect the valence attached to the negative consequences of behavior. Performance on the Balloon Analogue Risk Task (BART) measures risk-taking propensity. We recorded F-ERNs during the BART and during a BART simulation, where individuals observed the rewards and consequences of (someone else's) BART performance. EEGs were recorded on 22 actively drinking, treatment-naïve alcoholics during the BART and BART simulation. F-ERNs were measured and their association with psychological and alcohol use measures was examined. F-ERNs over fronto-central electrode sites were observed to balloon pops in the BART and BART simulation. F-ERNs during the BART were more than twice the amplitude of F-ERNs during the BART simulation. Smaller F-ERN amplitudes from the BART (but not the BART simulation) were associated with a greater family history density of alcohol problems.\n\nQuestion:\nAre smaller feedback ERN amplitudes during the BART associated with a greater family history density of alcohol problems in treatment-naïve alcoholics?\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:\nPeriodontal ligament (PL) width is precisely maintained throughout the lifetime of adult mammals, but the biological mechanisms that regulate the spatial locations of the cell populations for bone, cementum, and PL are unknown. As bisphosphonates induce ankylosis in mouse molar teeth, we used ethane-1-hydroxy-1, 1-bisphosphonate-(HEBP, Etidronate; Didronel) in combination with a periodontal window wound model to identify those cell populations involved in the regulation of PL width during the reformation of cellular domains after wounding. Four groups of Wistar rats were wounded by drilling through the alveolar bone and extirpation of the PL. Rats were administered HEBP for 1 week and then sacrificed or allowed to recover for an additional week prior to sacrifice. Control rats were sacrificed after 1 or 2 weeks. One hour prior to sacrifice, rats were injected with 3H-thymidine to label proliferating cells. Tissue sections were immunohistochemically stained for osteopontin (OPN) or bone sialoprotein (BSP) or were prepared for in situ hybridization (BSP) to identify extra- and intracellular expression of these non-collagenous bone proteins associated with periodontal healing. HEBP treatment for 1 week induced a twofold increase in the thickness of the alveolar bone matrix in which weak immuno-staining for OPN and BSP mRNA signal was seen. During the recovery phase the increased bone width was reduced but was still considerably thicker than in control (P < 0.001). OPN staining as well as the BSP mRNA signal were much more intense than at 1 week. HEBP induced a > 40% reduction of PL width which returned to normal dimensions following the recovery phase. HEBP also modulated PL cell proliferation and differentiation: PL cell counts and labelling indices were reduced fivefold after 1 week of HEBP but returned to control values after the recovery phase. In controls, PL cells did not express OPN and BSP, but after HEBP treatment, and particularly after the recovery phase, PL cells expressed both of these markers intensely. In contrast, gingival and pulp connective tissues that were contiguous with the PL were not stained for OPN and did not express BSP mRNA after HEBP treatment.\n\nQuestion:\nDoes bisphosphonate modulate proliferation and differentiation of rat periodontal ligament cells during wound healing?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo investigate potential antitumor effects of rAd-p53 by determining if it enhanced sensitivity of gastric cancer cells to chemotherapy. Three gastric cancer cell lines with distinct levels of differentiation were treated with various doses of rAd-p53 alone, oxaliplatin (OXA) alone, or a combination of both. Cell growth was assessed with an 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-diphenytetrazoliumromide assay and the expression levels of p53, Bax and Bcl-2 were determined by immunohistochemistry. The presence of apoptosis and the expression of caspase-3 were determined using flow cytometry. Treatment with rAd-p53 or OXA alone inhibited gastric cancer cell growth in a time- and dose-dependent manner; moreover, significant synergistic effects were observed when these treatments were combined. Immunohistochemical analysis demonstrated that treatment with rAd-p53 alone, OXA alone or combined treatment led to decreased Bcl-2 expression and increased Bax expression in gastric cancer cells. Furthermore, flow cytometry showed that rAd-p53 alone, OXA alone or combination treatment induced apoptosis of gastric cancer cells, which was accompanied by increased expression of caspase-3.\n\nQuestion:\nDoes rAd-p53 enhance the sensitivity of human gastric cancer cells to chemotherapy?\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:\nB cells positively contribute to immunity by antigen presentation to CD4(+) T cells, cytokine production, and differentiation into antibody secreting plasma cells. Accumulating evidence implies that B cells also possess immunoregulatory functions closely linked to their capability of IL-10 secretion. Colitis development was followed in CD4(+) CD25(-) T cell transplanted SCID mice co-transferred with B cells exposed to an enterobacterial extract (ebx-B cells). B and T cell cytokine expression was measured by flow cytometry and enzyme-linked immunosorbent assay (ELISA). We demonstrate that splenic B cells exposed to ebx produce large amounts of IL-10 in vitro and express CD1d and CD5 previously known to be associated with regulatory B cells. In SCID mice transplanted with colitogenic CD4(+) CD25(-) T cells, co-transfer of ebx-B cells significantly suppressed development of colitis. Suppression was dependent on B cell-derived IL-10, as co-transfer of IL-10 knockout ebx-B cells failed to suppress colitis. Ebx-B cell-mediated suppression of colitis was associated with a decrease in interferon gamma (IFN-γ)-producing T(H) 1 cells and increased frequencies of Foxp3-expressing T cells.\n\nQuestion:\nDo b cells exposed to enterobacterial components suppress development of experimental colitis?\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:\nDesign of effective vaccines against the human immunodeficiency virus (HIV-1) continues to present formidable challenges. However, individuals who are exposed HIV-1 but do not get infected may reveal correlates of protection that may inform on effective vaccine design. A preliminary gene expression analysis of HIV resistant female sex workers (HIV-R) suggested a high expression CD26/DPPIV gene. Previous studies have indicated an anti-HIV effect of high CD26/DPPIV expressing cells in vitro. Similarly, high CD26/DPPIV protein levels in vivo have been shown to be a risk factor for type 2 diabetes. We carried out a study to confirm if the high CD26/DPPIV gene expression among the HIV-R were concordant with high blood protein levels and its correlation with clinical type 2 diabetes and other perturbations in the insulin signaling pathway. A quantitative CD26/DPPIV plasma analysis from 100 HIV-R, 100 HIV infected (HIV +) and 100 HIV negative controls (HIV Neg) showed a significantly elevated CD26/DPPIV concentration among the HIV-R group (mean 1315 ng/ml) than the HIV Neg (910 ng/ml) and HIV + (870 ng/ml, p < 0.001). Similarly a FACs analysis of cell associated DPPIV (CD26) revealed a higher CD26/DPPIV expression on CD4+ T-cells derived from HIV-R than from the HIV+ (90.30% vs 80.90 p = 0.002) and HIV Neg controls (90.30% vs 82.30 p < 0.001) respectively. A further comparison of the mean fluorescent intensity (MFI) of CD26/DPPIV expression showed a higher DPP4 MFI on HIV-R CD4+ T cells (median 118 vs 91 for HIV-Neg, p = 0.0003). An evaluation for hyperglycemia, did not confirm Type 2 diabetes but an impaired fasting glucose condition (5.775 mmol/L). A follow-up quantitative PCR analysis of the insulin signaling pathway genes showed a down expression of NFκB, a central mediator of the immune response and activator of HIV-1 transcription.\n\nQuestion:\nIs cD26/dipeptidyl peptidase IV ( CD26/DPPIV ) highly expressed in peripheral blood of HIV-1 exposed uninfected female sex workers?\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:\nToll-like receptors (TLRs) are involved in a variety of cardiovascular disorders, including septic cardiomyopathy, ischemia/reperfusion, heart failure, and cardiac hypertrophy. Previous research revealed that TLR4 promotes cardiac hypertrophy in vivo. Therefore, we investigated whether TLR2 is also involved in the development of cardiac hypertrophy. Tlr2 deficient and wild type mice were subjected to transverse aortic constriction (TAC) or sham operation procedure. Left ventricular, heart and lung weights as well as hemodynamic parameters were determined after 3, 14 or 28 days. Real-time RT PCR was used to evaluate left ventricular gene expression. Protein content was determined via ELISA. TAC increased systolic left ventricular pressure, contraction and relaxations velocities as well as the heart weight in both genotypes. Tlr2 deficiency significantly enhanced cardiac hypertrophy after 14 and 28 days of TAC. Left ventricular end-diastolic pressure and heart rate increased in Tlr2(-/-) TAC mice only. Fourteen days of TAC led to a significant elevation of ANP, BNP, TGFβ and TLR4 mRNA levels in Tlr2(-/-) left ventricular tissue.\n\nQuestion:\nDoes tlr2 deficiency limit the development of left ventricular hypertrophy in a model of transverse aortic constriction induced pressure overload?\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:\nDetection of smear-positive pulmonary tuberculosis (PTB) cases is vital for tuberculosis (TB) control. Methods to augment sputum collection are available, but their additional benefit is uncertain in resource-limited settings. To compare the diagnostic yields using five methods to obtain sputum from adults diagnosed with smear-negative PTB in Malawi. Self-expectorated sputum was collected under supervision for microscopy and mycobacterial culture in the study laboratory. Confirmed smear-negative patients provided physiotherapy-assisted sputum and induced sputum, followed the next morning by gastric washing and bronchoalveolar lavage (BAL) samples. A total of 150 patients diagnosed with smear-negative PTB by the hospital service were screened; 39 (26%) were smear-positive from supervised self-expectorated sputum examined in the study laboratory. The remaining 111 confirmed smear-negative patients were enrolled in the study; 89% were human immunodeficiency virus positive. Seven additional smear-positive cases were diagnosed using the augmented sputum collection techniques. No differences were observed in the numbers of cases detected using the different methods. Of the 46 smear-positive cases, 44 (95.6%) could be detected from self-expectorated and physiotherapy-assisted samples.\n\nQuestion:\nAre simple measures as effective as invasive techniques in the diagnosis of pulmonary tuberculosis in Malawi?\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:\nEpidemiologic studies implicate air pollutant exposure during pregnancy as a risk factor for wheezing in offspring. Ozone exposure is linked to exacerbations of wheezing in children. To determine if maternal pulmonary exposure to traffic-related particles during pregnancy augments ozone-induced airway hyperresponsiveness in offspring. C57BL6 time-mated mice were given NIST SRM#1648 (particulate matter [PM]) 0.48 mg, saline vehicle, or no treatment by tracheal insufflation twice weekly for 3 weeks. PM exposure augmented maternal lung inflammation and placental TNF-alpha, Keratinocyte-derived cytokine (KC), and IL-6 (measured at gestation Day 18). After parturition, dams and litters were exposed to air or ozone 1 ppm 3 h/d, every other day, thrice weekly for 4 weeks. Respiratory system resistance in pups was measured at baseline and after administration of nebulized methacholine. Ozone increased airway hyperresponsiveness, but the increase was greatest in pups born to PM-treated dams. Whole-lung TNF-alpha, IL-1beta, KC, IL-6, and MCP-1 were increased in ozone-treated pups, with the greatest increase in pups born to dams given PM. Airway epithelial mucous metaplasia estimated by periodic acid-Schiff Alcian blue staining was increased in ozone-exposed pups born to PM-treated dams. Alveolar development, determined by morphometry, and airway smooth muscle bulk, estimated using alpha-actin histochemistry, were unaffected by prenatal or postnatal treatment.\n\nQuestion:\nDoes maternal exposure to particulate matter increase postnatal ozone-induced airway hyperreactivity in juvenile mice?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSoy isoflavones have numerous biological properties that suggest that they may protect against colorectal cancer. Colorectal epithelial cell proliferation has been used extensively as an intermediate endpoint biomarker for colorectal neoplasia. We tested the hypothesis that supplementation with soy protein containing isoflavones decreases colorectal epithelial cell proliferation. A 12-mo randomized intervention was conducted in men and women aged 50-80 y with recently diagnosed adenomatous polyps. One hundred fifty participants were enrolled and randomly assigned to an active treatment group (58 g protein powder/d containing 83 mg isoflavones/d; +ISO) or a control group (ethanol-extracted soy-protein powder containing 3 mg isoflavones; -ISO). Biopsy specimens from the cecum, sigmoid colon, and rectum were collected at baseline and at the 12-mo follow-up. Ki-67 antibody immunohistostaining was used to detect cell proliferation. One hundred twenty-five participants completed the study, and proliferation was measured in the first 91 who completed the study. In the sigmoid colon, cell proliferation increased by 0.9 (95% CI: 0.09, 1.9) labeled nuclei per crypt more (11%) in the +ISO group than in the -ISO group over the 12-mo intervention, which was opposite the direction predicted. The number of labeled nuclei per 100 mum crypt height also increased more in the +ISO than in the -ISO group. In the cecum and sigmoid colon, but not in the rectum, the proliferation count increased as the serum genistein concentration increased. Proliferation distribution and crypt height were not changed by treatment at any site.\n\nQuestion:\nDoes soy protein containing isoflavones decrease colorectal epithelial cell proliferation in a randomized controlled 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:\nCryptococcus neoformans is the most common cause of fungal meningitis among individuals with HIV/AIDS, which is uniformly fatal without proper treatment. The underlying mechanism of disease development in the brain that leads to cryptococcal meningoencephalitis remains incompletely understood. We have previously demonstrated that inositol transporters (ITR) are required for Cryptococcus virulence. The itr1aΔ itr3cΔ double mutant of C. neoformans was attenuated for virulence in a murine model of intra-cerebral infection; demonstrating that Itr1a and Itr3c are required for full virulence during brain infection, despite a similar growth rate between the mutant and wild type strains in the infected brain. To understand the immune pathology associated with infection by the itr1aΔ itr3cΔ double mutant, we investigated the molecular correlates of host immune response during mouse brain infection. We used genome-wide transcriptome shotgun sequencing (RNA-Seq) and quantitative real-time PCR (qRT-PCR) methods to examine the host gene expression profile in the infected brain. Our results show that compared to the wild type, infection of mouse brains by the mutant leads to significant activation of cellular networks/pathways associated with host protective immunity. Most of the significantly differentially expressed genes (SDEG) are part of immune cell networks such as tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ) regulon, indicating that infection by the mutant mounts a stronger host immune response compared to the wild type. Interestingly, a significant reduction in glucuronoxylomannan (GXM) secretion was observed in the itr1aΔ itr3cΔ mutant cells, indicating that inositol utilization pathways play a role in capsule production.\n\nQuestion:\nDoes cryptococcus inositol utilization modulate the host protective immune response during brain infection?\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 purpose of this study was to assess whether the addition of intravenous magnesium sulphate (Mg) at the induction of anaesthesia to a balanced anaesthetic protocol including wound infiltration, paracetamol and tramadol resulted in improved analgesic efficiency after radical prostatectomy. We conducted a randomized, double-blind, controlled study. Thirty ASA I or II males scheduled to undergo radical retropubic prostatectomy with general anaesthesia were prospectively assigned to one of the two groups (n = 15 each). The Mg group (Gr Mg) received 50 mg kg-1 of MgSO4 in 100 mL of isotonic saline over 20 min immediately after induction of anaesthesia and before skin incision. The patients in the control group (Gr C) received the same volume of saline over the same period. At the time of abdominal closure, wound infiltration with 190 mg (40 mL) of ropivacaine was performed in both groups. Pain was assessed by a 10-point visual analogue scale in the recovery room starting from the time of tracheal extubation. Standardized postoperative analgesia included paracetamol and tramadol administered via a patient-controlled analgesia device. In the postoperative period, both groups experienced an identical pain course evolution. Cumulative mean tramadol dose after 24 h was 226 mg in the magnesium group and 446 mg in the control group (P < 0.001). Postoperative nausea occurred in two patients in each group. Two vs. eight patients required analgesic rescue in magnesium and control groups, respectively (P = 0.053).\n\nQuestion:\nDoes intravenous magnesium sulphate decrease postoperative tramadol requirement after radical prostatectomy?\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:\nHistologic grade, completeness of resection, and presence of metastases are traditionally regarded as the primary factors in predicting survival for retroperitoneal soft tissue sarcoma (RPSTS). We sought to examine the importance of histologic type as a prognostic factor among patients with RPSTS. We identified 2337 cases of RPSTS in the Surveillance, Epidemiology, and End Results (SEER) database from 1988 to 2004. After excluding 273 cases of age <18, identification by autopsy only, or absence of histologic confirmation, we arrived at a final study cohort of 2064 patients. Overall survival (OS) and disease-specific survival (DSS) were estimated using the Kaplan-Meier method. Multivariate analysis was performed using a Cox proportional hazards model, adjusting for age, gender, race, histologic type, histologic grade, tumor size, extent of resection, and SEER summary stage. Among 33 histologic types, leiomyosarcoma (28.7%), well-differentiated/dedifferentiated liposarcoma (20.3%), liposarcoma not otherwise specified (NOS) (11.9%), malignant fibrous histiocytoma (MFH-11.0%), and sarcoma NOS (10.7%) were the most prevalent. Grade distribution was low, 24.2%; intermediate, 16%; high 34.3%, and unknown, 25.5%. Surgery was performed in 85.8%, and radiotherapy was administered to 22.8%. With a median follow-up of 38 mo, median OS was 78, 35, 25, 18, and 10 mo for liposarcoma, leiomyosarcoma, other histologies, MFH, and sarcoma NOS, respectively (P < 0.0001). Median DSS was 120, 53, not reached, 30, and 13 mo for liposarcoma, leiomyosarcoma, other histologies, MFH, and sarcoma NOS, respectively (P < 0.0001). On multivariate analysis, histologic type was associated with statistically significant differences in both OS and DSS.\n\nQuestion:\nDoes histologic type predict survival in patients with retroperitoneal soft tissue sarcoma?\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 adults, binding of mucosal addressin cell adhesion molecule 1 (MAdCAM-1) to lymphocyte alpha4beta7 integrin directs cell trafficking to gut, whereas interaction of peripheral node addressins (PNAd) with lymphocyte L-selectin targets immune cells to peripheral lymph nodes (PLNs). Because nothing is known about these addressins during human development, we studied the expression and function of MAdCAM-1 (and PNAd for comparison) in fetuses and children. Series of human tissue samples obtained from fetuses (7-40 weeks), children (2 months-7 years), and adults were immunostained with monoclonal antibodies. The function of the addressins and their lymphocyte counter-receptors was tested in in vitro binding assays on fetal and adult tissues. Unlike in adults, MAdCAM-1 is widely expressed from embryonic week 7 onwards, and it only gradually becomes polarized to mucosal vessels after birth. In utero MAdCAM-1 functionally governs lymphocyte adhesion to vessels both in the gut and PLNs by binding to alpha4beta7 integrin. The later induction of PNAd gradually starts to dominate the binding of lymphocytes to PLNs during childhood.\n\nQuestion:\nIs immune cell trafficking in uterus and early life dominated by the mucosal addressin MAdCAM-1 in humans?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPulmonary metastases are common in patients with primary colorectal cancer (CRC). Heat-shock protein 27 (Hsp27) is upregulated in activated fibroblasts during wound healing and systemically elevated in various diseases. Cancer-associated fibroblasts (CAFs) are also thought to play a role as prognostic and predictive markers in various malignancies including CRC. Surprisingly, the expression of Hsp27 has never been assessed in CAFs. Therefore we aimed to investigate the expression level of Hsp27 in CAFs and its clinical implications in patients with CRC lung metastases. FFPE tissue samples from 51 pulmonary metastases (PMs) and 33 paired primary tumors were evaluated for alpha-SMA, CD31, Hsp27 and vimentin expression by immunohistochemistry and correlated with clinicopathological variables. 25 liver metastases served as control group. Moreover, serum samples (n=10) before and after pulmonary metastasectomy were assessed for circulating phospho-Hsp27 and total Hsp27 by ELISA. Stromal expression of Hsp27 was observed in all PM and showed strong correlation with alpha-SMA (P<0.001) and vimentin (P<0.001). Strong stromal Hsp27 was associated with higher microvessel density in primary CRC and PM. Moreover, high stromal Hsp27 and αSMA expression were associated with decreased recurrence-free survival after pulmonary metastasectomy (P=0.018 and P=0.008, respectively) and overall survival (P=0.031 and P=0.017, respectively). Serum levels of phospho- and total Hsp27 dropped after metastasectomy to levels comparable to healthy controls.\n\nQuestion:\nIs stromal expression of heat-shock protein 27 associated with worse clinical outcome in patients with colorectal cancer lung metastases?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis study evaluated the involvement of tumour necrosis factor α (TNF-α) in orofacial thermal and mechanical hyperalgesia induced by an inflammatory stimulus or by chronic constriction of the infraorbital nerve (CION) using etanercept (Eta), a TNF-receptor fusion protein that inhibits TNF-α action. Animals were treated with Eta (0.5 and 5.0 mg/kg, s.c.) or dexamethasone (Dex, 0.5, 1.0 and 2.0 mg/kg, s.c.) and orofacial thermal (cold and heat) and mechanical hyperalgesia induced by an inflammatory stimulus (carrageenan, Cg 50 and 100 μg/lip) or by chronic CION, a model of neuropathic pain in the orofacial region was evaluated. Treatments with Dex or Eta were carried out before Cg or before or after CION. Eta or Dex abolished inflammatory thermal and mechanical hyperalgesia. Also, each drug, when given at the day of the surgery and the subsequent day, was effective to abolish thermal and mechanical hyperalgesia induced by CION, assessed on day 4 and on day 13 after the surgery, respectively. However, Eta, but not Dex, given after the CION, abolished thermal and mechanical hyperalgesia and reduced TNF-α level in the trigeminal ganglion.\n\nQuestion:\nDoes etanercept reduce thermal and mechanical orofacial hyperalgesia following inflammation and neuropathic injury?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nP. gingivalis is a gram-negative anaerobic bacterium and a major periodontal pathogen. LPS produced by P. gingivalis promotes osteoclast formation. TECK is a CC chemokine whose expression is increased in gingival epithelial cells exposed to P. gingivalis LPS. In this study, we investigated the effect of TECK in osteoclastogenesis induced by P. gingivalis LPS. Real time reverse transcriptase polymerase chain reaction (RTPCR) analysis and western blotting were performed to confirm TECK in MG63, human osteoblast cell line and primary murine osteoblasts and CCR9 in RAW 264.7 cells and murine bone marrow macrophages (BMMs) as osteoclast precursors. P. gingivalis LPS-treated BMMs and Raw 264.7 cells were cultured with or without TECK or TECK antibody to examine the effect of TECK on osteoclast formation. Cocultures with murine osteoblasts and bone marrow cells were also treated with or without TECK or TECK antibody. Luciferase assay and western blotting were used to determine whether TECK-CCR9 induced osteoclastogenesis was mediated through NFATc1 or NF-kB signaling. TECK was shown to be expressed by osteoblasts, and its receptor, CCR9, by osteoclast precursors. TECK increased P. gingivalis LPS-induced osteoclast numbers in an in vitro osteoclast formation assay using osteoclast precursors. The enhanced osteoclast formation by TECK was mediated by NFATc1, but not by NF-kB signaling.\n\nQuestion:\nDoes thymus-expressed chemokine enhance Porphyromonas gingivalis LPS-induced osteoclast formation via NFATc1 activation?\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:\nATM is an important protein that protects the genome from double-stranded DNA breaks. Mutations and polymorphisms in the ATM gene have been associated with an increased risk of certain types of malignancies, especially breast cancer. We analyzed tissue from 98 white patients with prostate cancer for the presence of IVS62+60G>A polymorphism in the ATM gene. The frequency of the homozygous IVS62+60G/G, heterozygous IVS62+60G/A, and homozygous IVS62+60A/A was 18.37% (18 of 98), 30.61% (30 of 98), and 51.02% (50 of 98), respectively. Using Fisher's exact test, we found the polymorphism IVS62+60G>A was not significantly related to age, tumor grade, prostate-specific antigen level, or clinical stage (P >0.05). No difference was found in relapse-free survival between patients with IVS62+60G/G and those with IVS62+60G/A or IVS62+60A/A (P = 0.4533).\n\nQuestion:\nDoes aTM polymorphism IVS62+60G > A is not associate with disease aggressiveness in prostate cancer?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nDarbepoetin, a long-acting erythropoietin derivative, attenuates cardiomyocyte apoptosis and improves short-term (3 days) cardiac function, but the mechanisms responsible are unknown. We investigated potential mechanisms by which darbepoetin exerts cardioprotection following myocardial infarction in mice and the significance of the erythropoietin receptor (EPOR)-common beta-chain (c-beta-chain) heteroreceptor. Mice underwent 60 min coronary occlusion followed by treatment with vehicle or a single dose of darbepoetin. Effects on gene expression, apoptosis and neutrophil accumulation in infarcted left ventricle were assessed 24 h later. Cardiac function, effects on vascularization and fibrosis were assessed 28 days later. The significance of EPOR-c-beta-chain heteroreceptor was examined 28 days after infarction using mice deficient in c-beta-chain. Twenty-four hours after darbepoetin, mRNAs encoding haeme oxygenase-1 (HO-1), iNOS and brain natriuretic peptide (BNP) were markedly elevated only in infarcted regions, and the frequency of apoptotic cells attenuated. Inflammation was also attenuated with reductions in neutrophil numbers. Darbepoetin also elevated mRNAs encoding angiogenic factors: placental growth factor, monocyte chemoattractant protein-1 and interleukin-1beta. Twenty-eight days after treatment, CD31+ vessels in the infarct zone doubled and fibrosis reduced. Cardiac haemodynamics were improved. Darbepoetin also improved cardiac haemodynamics in c-beta-chain-deficient mice, increased HO-1 and iNOS expression and vessel numbers and attenuated fibrosis.\n\nQuestion:\nDoes darbepoetin-mediated cardioprotection after myocardial infarction involve multiple mechanisms independent of erythropoietin receptor-common beta-chain heteroreceptor?\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:\nLinker histone H1 has been studied in vivo and using reconstituted chromatin, but there have been few systematic studies of the effects of the cellular environment on its function. Due to the presence of many other chromatin factors and specific chaperones such as RanBP7/importin beta that regulate histone H1, linker histones likely function differently in vivo than in purified systems. We have directly compared H1 binding to sperm nuclei in buffer versus Xenopus egg extract cytoplasm, and monitored the effects of adding nuclear import chaperones. In buffer, RanBP7 decondenses sperm nuclei, while H1 binds tightly to the chromatin and rescues RanBP7-mediated decondensation. H1 binding is reduced in cytoplasm, and H1 exhibits rapid FRAP dynamics in cytoplasm but not in buffer. RanBP7 decreases H1 binding to chromatin in both buffer and extract but does not significantly affect H1 dynamics in either condition. Importin beta has a lesser effect than RanBP7 on sperm chromatin decondensation and H1 binding, while a combination of RanBP7/importin beta is no more effective than RanBP7 alone. In extracts supplemented with RanBP7, H1 localizes to chromosomal foci, which increase after DNA damage. Unlike somatic H1, the embryonic linker histone H1M binds equally well to chromatin in cytoplasm compared to buffer. Amino-globular and carboxyl terminal domains of H1M bind chromatin comparably to the full-length protein in buffer, but are inhibited ∼10-fold in cytoplasm. High levels of H1 or its truncations distort mitotic chromosomes and block their segregation during anaphase.\n\nQuestion:\nDo xenopus egg extracts increase dynamics of histone H1 on sperm chromatin?\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 analyzed 9 cases by immunohistochemical studies in order to elucidate the mechanisms of cartilage destruction in relapsing polychondritis (RP), which often involves the external auricle and respiratory tract through immunological disorder. Cartilage tissues were obtained during surgical operations. Cell species in the granulation tissues, especially near the cartilage, were identified by cell-surface markers [CD3, CD4, CD8, CD20, CD45 (LCA), and CD68]. The proteolytic enzymes expressed in the cells in the perichondral granulation and in chondrocytes themselves were analyzed by immunohistochemical studies using anti-matrix metalloproteinase (MMP) -1, -3, -8, -9, and -13, and cathepsin D, K, L, and elastase antibodies. Apoptosis and nitric oxide (NO), an apoptosis-related factor, were also examined using ApopTag and antinitrotyrosine antibody, respectively. Among cell species that infiltrated in perichondral granulation, LCA, CD68 (monocytes/macrophages), and CD4 cells were dominant in number; MMP-8, MMP-9, and elastase were expressed only in the perichondral granulation; whereas MMP-3 and cathepsin K and L were detected in both chondrocytes and granulations. Out of 9 cases examined, 6 revealed apoptotic cells in excess of 50% of chondrocytes. There was a strong correlation between the number of apoptotic cells and the number of MMP-3-positive (r = 0.83) and cathepsin K-positive cells (r = 0.92). Abundant NO-expressing cells were observed in the chondrocytes in degenerated cartilage, similar to apoptosis.\n\nQuestion:\nIs cartilage destruction partly induced by the internal proteolytic enzymes and apoptotic phenomenon of chondrocytes in relapsing polychondritis?\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:\nTumor cells can metastasize by entering existing vessels or new vessels actively recruited into the primary tumor. Invasion of the lymphatics and blood vessels in the periphery of the tumor seems to be a prerequisite step in the metastatic process. The aim of this study was to correlate peripheral lymphatic vessel infiltration (PLI) and peripheral blood vessel infiltration (PVI) in a cohort of patients with invasive ductal carcinoma of the breast with various other prognostic parameters and outcome. The study population consisted of 236 female patients with invasive ductal breast carcinomas, who had been operated between 2011 and 2013. The registered data included age at diagnosis, histological subtype, tumor size, TNM stage, histological grade, estrogen (ER) and progesterone receptors (PR), HER-2, p53, and PLI and PVI. Pathological examination revealed that 22.5% of the patients had PVI and 37.3% had PLI at the tumor front. PVI correlated with younger age (p<0.05), higher histologic grade (p<0.05), advanced TNM stage (p<0.05), higher T stage (p<0.05), higher N stage (p<0.05) and positive Ki67 expression (p<0.05). Similarly, PLI correlated with higher histologic grade (p<0.05), advanced TNM stage (p<0.05), higher T stage (p<0.05) and higher N stage (p<0.05). Statistical analysis did not reveal significant correlation between the presence of tumor blood and lymphatic vessels with infiltration in overall (OS) and disease-free survival (DFS).\n\nQuestion:\nIs lymphovascular infiltration in the tumor bed a useful marker of biological behavior in 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:\nBurn and trauma patients present a clinical challenge due to metabolic derangements and hypermetabolism that result in a prolonged catabolic state with impaired healing and secondary complications, including ventilator dependence. Previous work has shown that circulating levels of growth hormone (GH) are predictive of mortality in critically ill adults, but few studies have examined the prognostic potential of GH levels in adult trauma patients. To investigate the utility of GH and other endocrine responses in the prediction of outcomes, we conducted a prospective, observational study of adult burn and trauma patients. We evaluated the serum concentration of GH, insulin-like growth factor 1 (IGF-1), IGF binding protein 3 (IGFBP-3), and glucagon-like peptide-2 (GLP-2) weekly for up to 6 weeks in 36 adult burn and trauma patients admitted between 2010 and 2013. Non-survivors had significantly higher levels of GH and GLP-2 on admission than survivors.\n\nQuestion:\nAre elevations in growth hormone and glucagon-like peptide-2 levels on admission associated with increased mortality in 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 determine the antiplatelet effect of cilostazol (Pletal) and its interaction with dipyridamole in in vitro and in vivo rabbit models, and to see if it can be dissociated from bleeding time prolongation. In vitro collagen-induced platelet aggregation was measured by an impedance-based aggregometer. The in vivo antithrombotic effect was evaluated in a rabbit carotid artery cyclic flow reduction (CFR) model, in which repetitive thrombosis was induced by mechanical injuries of the artery and stenosis. Template bleeding time was determined in rabbit ear arterioles and hindlimb nail cuticles. In vitro platelet aggregation was slightly inhibited by 4 microM cilostazol (22 +/- 6%), and modestly by 13 microM (57 +/- 3% of aggregation). While dipyridamole itself up to 13 microM had no significant inhibition, it potentiated the effect from cilostazol: in the presence of 4 microM dipyridamole, 4 microM cilostazol inhibited aggregation by 47 +/- 6%. Dipyridamole also potentiated the CFR reducing effect of cilostazol: combination of dipyridamole (no effect by itself) and cilostazol at 1 microM decreased CFRs to levels achieved by 3-4 microM cilostazol alone. Bleeding times were similar in controls and animals treated with cilostazol, or with cilostazol and dipyridamole. In contrast, aspirin (4 mg/kg), while reducing CFRs, significantly increased bleeding time.\n\nQuestion:\nIs antiplatelet and antithrombotic activity of cilostazol potentiated by dipyridamole in rabbits and dissociated from bleeding time prolongation?\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:\nVentilator-associated pneumonia (VAP) is one of the leading causes of morbidity in critically ill surgical patients. Certain pathogens (e.g., methicillin-resistant Staphylococcus aureus, Pseudomonas aeruginosa) have been associated with an excess mortality rate from sepsis in several studies, but not in the surgical setting specifically or when protocol-driven antibiotic therapy is administered. We sought to determine which factors and, in particular, whether the individual pathogen affected the mortality rate in our surgical intensive care unit (ICU), where a rotational antibiotic system has been employed continuously since 1997. We hypothesized that the type of pathogen and illness severity were the primary influences on the mortality rate of patients with VAP. A total of 198 consecutive patients from a university surgical ICU, with clinical signs of VAP confirmed by quantified isolation of significant numbers of a pathogen (> or =10(4) colony-forming units [cfu]/mL) from bronchoalveolar (BAL) fluid obtained by fiberoptic bronchoscopy, were identified prospectively from January 2001 to November 2004. The data collected were age, sex, Acute Physiology and Chronic Health Evaluation (APACHE) III score, multiple organ dysfunction score, unit day of diagnosis, time (h) to antibiotic administration (TTA), appropriateness of initial therapy (AIT), unit and hospital length of stay, and mortality rate. Pathogens were classified as non-lactose-fermenting gram-negative bacilli (NGNB), lactose-fermenting gram-negative bacilli (LGNB), methicillin-sensitive Staphylococcus aureus, methicillin-resistant S. aureus, yeast, community-acquired pneumonia (e.g., Streptococcus pneumoniae), or other pathogens. Patients with a polymicrobial isolate were placed in the \"other\" category. The overall mortality rate was 32.3% vs. 55% as predicted by APACHE III normative data. The overall AIT was 92%. The mortality rate for NGNB infections was 35.6% vs. 29.4% for LGNB infections (p = NS). By logistic regression, neither TTA, AIT, nor pathogen influenced the mortality rate.\n\nQuestion:\nDoes the pathogen of ventilator-associated pneumonia influence the mortality rate of surgical intensive care unit patients treated with a rotational antibiotic system?\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 the hypothesis that children enrolled in Medicaid managed care health plans that provide asthma-specific communication to providers would be more likely to have adequate asthma medication filling. We conducted a historical cohort study of 4498 children (2-17 years old) with moderate-severe asthma in Washington State and Tennessee Medicaid managed care programs from 2000 to 2002. Interviews with health plans were conducted to identify communication strategies health plans used to improve asthma care by providers in the plan. The main outcome measure was guideline-recommended filling of asthma preventer medications. Children in plans that provided specific feedback to providers about asthma quality and notified providers when children had an asthma-related event had the highest mean days plus or minus SE of filling in the 365-day follow-up period (164.6 +/- 13 days) compared with children in plans with neither (135.3 +/- 10.8 days; P < .05). In children with the greatest asthma severity, enrollment in a plan with both features was associated with 27.1 additional days of filling (95% CI, 0.7-53.4 days) during the follow-up period.\n\nQuestion:\nIs health plan notification and feedback to providers associated with increased filling of preventer medications for children with asthma enrolled in Medicaid?\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 longterm results after liver resection for hepatocellular carcinoma with macroscopic tumor thrombus of the portal vein are unclear. The records of 47 HCC patients with tumor thrombus in the segmental portal branch (n = 33) and the first portal branch or portal vein trunk (n = 14) were reviewed in this study. Survival rates of the patients were calculated with regard to 14 dinicopathologic variables. A log-rank analysis was performed to identify which variables predicted the prognosis. Overall 1-, 3-, and 5-year survival rates were 53.9%, 33.2%, and 23.9%, respectively. The indicators of a favorable prognosis included curative liver resection, tumor size less than 10 cm in diameter, and absence of intrahepatic metastases.\n\nQuestion:\nDoes surgical result for hepatocellular carcinoma with macroscopic portal vein tumor thrombosis?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo evaluate the accuracy and precision of \"deep-forehead\" temperature with rectal, esophageal, and tympanic membrane temperatures, compared with blood temperature. We studied 41 ASA physical status 1 or 2 patients undergoing abdominal and thoracic surgery scheduled to require at least three hours. \"Deep-forehead\" temperature was measured using a Coretemp thermometer (Terumo, Tokyo, Japan). Blood temperature was measured with a thermistor of a pulmonary artery. Rectal, tympanic membrane, and distal esophageal temperatures were measured with thermocouples. All temperatures were recorded at 20 min intervals after the induction of anesthesia. We considered blood temperature as the reference value. Temperatures at the other four sites were compared with blood temperature using correlation, regression, and Bland and Altman analyses. We determined accuracy (mean difference between reference and test temperatures) and precision (standard deviation of the difference) of 0.5 degrees C to be clinically acceptable. \"Deep-forehead\" temperature correlated well with blood temperature as well as other temperatures, the determination coefficients (r2) being 0.85 in each case. The bias for the \"deep-forehead\" temperature was 0.0 degrees C, which was the same as tympanic membrane temperature and was smaller than rectal and esophageal temperatures. The standard deviation of the differences for the \"deep-forehead\" temperature was 0.3 degrees C, which was the same as rectal temperature.\n\nQuestion:\nDoes `` Deep-forehead '' temperature correlate well with blood temperature?\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 analyze the difficulty of discriminating Japanese nonsense monosyllables in each of several grades of high-frequency hearing loss and to evaluate the limitations of amplification. We collected retrospective data on the discrimination of Japanese nonsense monosyllables by patients with three grades of high-frequency hearing loss who fulfilled or nearly fulfilled the Japanese criteria for EAS. Discrimination of the twenty monosyllables included in the 67-S speech audiometric test, which is approved by the Japan Audiological Society, was evaluated under quiet conditions. One hundred and five ears of ninety-one adults with high-frequency hearing loss were tested. We classified the ears according to hearing threshold at 1000 Hz; Group 1: <45 dB; Group 2: ≥45 dB and <70 dB; Group 3: ≥70 dB. Under the best conditions, the best speech discrimination scores were 72.3 ± 18.6% (mean ± SD, N=11), 56.9 ± 19.9% (N=57) and 38.1 ± 22.6% (N=37) in Group 1, Group 2 and Group 3, respectively. For most of the monosyllables, discrimination score declined gradually as high-frequency hearing loss became more severe. The high incidence in the Japanese language of [k], an easy consonant to distinguish, may be an advantage for patients with high-frequency hearing loss who use hearing aids. By employing a new confusion matrix that displays consonants and the following vowels separately, we were able to reveal the interactions of those two components. We observed that discrimination of preceding nasal consonants and that of the following vowels were not independent in patients with high-frequency hearing loss.\n\nQuestion:\nDo discrimination of Japanese monosyllables in patients with high-frequency hearing loss?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nRemission is the ultimate goal in systemic lupus erythematosus (SLE). In this study, we applied four definitions of remission agreed on by an international collaboration (Definitions of Remission in SLE, DORIS) to a large clinical cohort to estimate rates and predictors of remission. We applied the DORIS definitions of Clinical Remission, Complete Remission (requiring negative serologies), Clinical Remission on treatment (ROT) and Complete ROT. 2307 patients entered the cohort from 1987 to 2014 and were seen at least quarterly. Patients not in remission at cohort entry were followed prospectively. We used the Kaplan-Meier approach to estimate the time to remission and the time from remission to relapse. Cox regression was used to identify baseline factors associated with time to remission, adjusting for baseline disease activity and baseline treatment. The median time to remission was 8.7, 11.0, 1.8 and 3.1 years for Clinical Remission, Complete Remission, Clinical ROT and Complete ROT, respectively. High baseline treatment was the major predictor of a longer time to remission, followed by high baseline activity. The median duration of remission for all definitions was 3 months. African-American ethnicity, baseline low C3 and baseline haematological activity were associated with longer time to remission for all definitions. Baseline anti-dsDNA and baseline low C4 were associated with longer time to Complete Remission and Complete ROT. Baseline low C4 was also negatively associated with Clinical Remission.\n\nQuestion:\nIs remission in systemic lupus erythematosus : durable remission rare?\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:\nOxidative stress is implicated in the pathogenesis of atherosclerosis, and Nrf2 is the transcriptional factor central in cellular antioxidant responses. In the present study, we investigate the effect of a dihydrolipoic acid derivative lipoicmethylenedioxyphenol (LMDP) on the progression of atherosclerosis and test whether its effect on atherosclerosis is mediated by Nrf2. Both magnetic resonance imaging (MRI) scanning and en face analysis reveal that 14 weeks of treatment with LMDP markedly reduced atherosclerotic burden in a rabbit balloon vascular injury model. Myograph analyses show decreased aortic contractile response to phenylephrine and increased aortic response to acetylcholine and insulin in LMDP-treated animals, suggesting that LMDP inhibits atherosclerosis through improving vascular function. A role of Nrf2 signaling in mediating the amelioration of vascular function by LMDP was supported by increased Nrf2 translocation into nuclear and increased expression of Nrf2 target genes. Furthermore, chemotaxis analysis with Boydem chamber shows that leukocytes isolated from LMDP-treated rabbits had reduced chemotaxis, and knock-down of Nrf2 significantly reduced the effect of LMDP on the chemotaxis of mouse macrophages.\n\nQuestion:\nDoes lipoicmethylenedioxyphenol reduce Experimental Atherosclerosis through Activation of Nrf2 Signaling?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe aim of the present study was to examine the effects of onion as functional ingredient on the oxidative status, lipoprotein levels (total cholesterol-TC, HDL-C, LDL-C), triacylglycerides (TAG) and vascular reactivity of mesenteric arteries in hypercholesterolemic Wistar rats. Twenty-four animals were fed with three different diets [control, high-cholesterol diet (HC) and high-cholesterol enriched with onion diet (HCO)]. After seven weeks of experimental feeding the rats were euthanized for blood and tissues collection. TC, HDL-C, LDL-C and TAG were measured, and 2,2'-azinobis-(3-ethylbenzothiazoline-6-sulfonic acid) radical cation (ABTS(•+)) scavenging capacity and ferric reducing antioxidant power (FRAP) were determined in plasma. Superoxide dismutase (SOD) and glutathione peroxidase (GPx) enzyme activities were assayed in erythrocyte lysates. Endothelium-dependent vasodilation to acetylcholine was evaluated in mesenteric arterial segments. NADPH oxidase (NOX) was also measured by lucigenin-derived chemiluminiscence. The dietary cholesterol content significantly affected plasma lipoprotein levels, increased superoxide generation from NOX, and caused impaired endothelium-dependent vasodilation in the rat mesenteric arteries. Onion ingredient improved antioxidant status in HCO group, as it was evidenced by ABTS(•+) and FRAP values and SOD and GPx enzyme activities compared to the HC-fed group, reduced the increment in NOX activity and reversed endothelial dysfunction promoted by the HC diet. Scavenging of superoxide with TEMPOL or inhibition of NOX with apocynin improved endothelium-dependent vasodilation only in HC-fed rats.\n\nQuestion:\nDoes high-cholesterol diet enriched with onion affect endothelium-dependent relaxation and NADPH oxidase activity in mesenteric microvessels from Wistar 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:\nAnatomic sublobar resection is being assessed as a substitute to lobectomy for primary lung cancers. However, persistent air leak after anatomic sublobar resection is prevalent and increasing surgical morbidity and costs. The use of electrocautery is being popularized recently in anatomic sublobar resection. We have retrospectively evaluated the safety and efficacy of intersegmental plane dissection using electrocautery. Between April 2009 to September 2010, 47 patients were treated with segmentectomy for clinical T1N0M0 non-small cell lung cancers. The intersegmental plane was dissected using electrocautery alone or in combination with staplers. We evaluated the methods of dividing intersegmental plane (electrocautery alone or combination with electrocautery and staplers), intraoperative blood loss, duration of chest tube placement, duration of surgery, preoperative FEV1.0%, incidence of prolonged air leak, length of postoperative hospital stay, postoperative pulmonary function at 6 months after surgery and the cost for sealing intersegmental plane. Among the 47 patients, 22 patients underwent intersegmental plane dissection with electrocautery alone and 25 patients did in combination with electrocautery and staplers. The mean number of stapler cartridges used was only 1.3 in electrocautery and staplers group. Mean age, gender, number of patients whose FEV1% < 70% were similar between two groups. There was no statistical difference between electrocautery alone and combination with electrocautery and staplers group in duration of surgery (282 vs. 290 minutes), intraoperative blood loss (203 vs.151 ml), duration of chest tube placement (3.2 vs. 3.1 days), postoperative hospital stay (11.0 vs.10.0 days), postoperative loss of FEV1.0 (13 vs.8 %), loss of FVC (11 vs. 6 %) or incidence of minor postoperative complications [9 % (2/22) vs. 16 % (4/25), p = 0.30)]. However, incidence of prolonged air leak was higher in electrocautery alone group than in combination with electrocautery and staplers group [14 % (3/22) vs. 4 % (1/25), p = 0.025)]. The cost of materials for sealing air leaks amounted to €964 per patient in the electrocautery alone group and €1594 per patient in combination with electrocautery and staplers group.\n\nQuestion:\nIs dissection of lung parenchyma using electrocautery a safe and acceptable method for anatomical sublobar resection?\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:\nAllergy is commoner in developed than in developing countries. Chronic worm infections show inverse associations with allergy, and prenatal exposures may be critical to allergy risk. To determine whether anthelminthic treatment during pregnancy increases the risk of allergy in infancy. A randomised, double-blind, placebo-controlled trial on treatment in pregnancy with albendazole versus placebo and praziquantel versus placebo was conducted in Uganda, with a 2 × 2 factorial design; 2507 women were enrolled; infants' allergy events were recorded prospectively. The main outcome was doctor-diagnosed infantile eczema. Worms were detected in 68% of women before treatment. Doctor-diagnosed infantile eczema incidence was 10.4/100 infant years. Maternal albendazole treatment was associated with a significantly increased risk of eczema [Cox HR (95% CI), p: 1.82 (1.26-2.64), 0.002]; this effect was slightly stronger among infants whose mothers had no albendazole-susceptible worms than among infants whose mothers had such worms, although this difference was not statistically significant. Praziquantel showed no effect overall but was associated with increased risk among infants of mothers with Schistosoma mansoni [2.65 (1.16-6.08), interaction p = 0.02]. In a sample of infants, skin prick test reactivity and allergen-specific IgE were both associated with doctor-diagnosed eczema, indicating atopic aetiology. Albendazole was also strongly associated with reported recurrent wheeze [1.58 (1.13-2.22), 0.008]; praziquantel showed no effect.\n\nQuestion:\nIs anthelminthic treatment during pregnancy associated with increased risk of infantile eczema : randomised-controlled trial results?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe nuclear receptor peroxisome proliferator-activated receptor-gamma (PPARgamma) has become a potential target for the prevention and treatment of breast cancer. However, recent in vitro and in vivo studies have raised the question of whether activation of PPARgamma leads to the promotion or reduction of tumor formation. Studies using several cancer cell lines, animal models, and a variety of PPARgamma agonists have shown discordant results, including changes in cellular proliferation, differentiation, and apoptosis of cancer cells and tumors. We studied the effects of low-, moderate-, and high-dose treatment of the PPARgamma ligands 15-deoxy-delta1214 prostaglandin J2 (15dPGJ2) and troglitazone (TGZ) on parameters of cell growth, differentiation, and apoptosis in the epithelial breast cancer cell line MDA-MB-231. The biologic effects of these compounds depend largely on ligand concentration and the degree of PPARgamma activation. For example, low concentrations of 15dPGJ2 (<2.5 microM) and TGZ (<5 microM) increased cellular proliferation, but concentrations of 15dPGJ2 > or = 10 microM and of TGZ at 100 microM blocked cell growth. TGZ (100 microM) slowed cell cycle progression, and 15dPGJ2 (10 microM) caused an S-phase arrest in the cell cycle and induced morphological characteristics consistent with apoptosis. Expression of CD36, a marker of differentiation in these cells, was induced by 2.5 microM 15dPGJ2 or 5 to 100 microM TGZ. However, higher concentrations of 15dPGJ2 did not alter CD36 expression. Transcriptional activation studies demonstrated that 15dPGJ2 is a more potent PPARgamma ligand than TGZ. Regardless of the ligand used, though, low transcriptional activation correlated with an increased cellular proliferation, whereas higher levels of activation correlated with cell cycle arrest and apoptosis.\n\nQuestion:\nIs magnitude of peroxisome proliferator-activated receptor-gamma activation associated with important and seemingly opposite biological responses in breast cancer cells?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMaternal immune responses may interfere with offspring allergy development as maternal immunization may suppress IgE development, while maternal allergy may promote allergy. Therefore, we investigated the effect of two different maternal treatments on airway allergy in female and male offspring. Pregnant mice were immunized (IMM) with ovalbumin (OVA) or immunized and airway-challenged (IMM+AI). At different ages, airway allergy to OVA was induced in offspring by intranasal sensitization. Maternal IgG1 was found at higher levels in IMM+AI than in IMM offspring. After sensitization, the suppression of OVA-specific IgE and IgG1 was complete in juvenile offspring but waned with age concurrently with maternal IgG1 levels. Cytokine secretion, lung inflammation, and B cell priming were not suppressed although IgE responses were.\n\nQuestion:\nAre offspring IgE responses influenced by levels of maternal IgG transferred in early life?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMultiple intracellular transport pathways drive the formation, maintenance, and function of cilia, a compartmentalized organelle associated with motility, chemo-/mechano-/photosensation, and developmental signaling. These pathways include cilium-based intraflagellar transport (IFT) and poorly understood membrane trafficking events. Defects in ciliary transport contribute to the etiology of human ciliary disease such as Bardet-Biedl syndrome (BBS). In this study, we employ the genetically tractable nematode Caenorhabditis elegans to investigate whether endocytosis genes function in cilium formation and/or the transport of ciliary membrane or ciliary proteins. Here we show that localization of the clathrin light chain, AP-2 clathrin adaptor, dynamin, and RAB-5 endocytic proteins overlaps with a morphologically discrete periciliary membrane compartment associated with sensory cilia. In addition, ciliary transmembrane proteins such as G protein-coupled receptors concentrate at periciliary membranes. Disruption of endocytic gene function causes expansion of ciliary and/or periciliary membranes as well as defects in the ciliary targeting and/or transport dynamics of ciliary transmembrane and IFT proteins. Finally, genetic analyses reveal that the ciliary membrane expansions in dynamin and AP-2 mutants require bbs-8 and rab-8 function and that sensory signaling and endocytic genes may function in a common pathway to regulate ciliary membrane volume.\n\nQuestion:\nDo endocytosis genes facilitate protein and membrane transport in C. elegans sensory cilia?\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:\nWhen medical students move from the classroom into clinical practice environments, their roles and learning challenges shift dramatically from a formal curricular approach to a workplace learning model. Continuity among peers during clinical clerkships may play an important role in this different mode of learning. We explored students' perceptions about how they achieved workplace learning in the context of intentionally formed or ad hoc peer groups. We invited students in clerkship program models with continuity (CMCs) and in traditional block clerkships (BCs) to complete a survey about peer relationships with open-ended questions based on a workplace learning framework, including themes of workplace-based relationships, the nature of work practices, and selection of tasks and activities. We conducted qualitative content analysis to characterize students' experiences. In both BCs and CMCs, peer groups provided rich resources, including anticipatory guidance about clinical expectations of students, best practices in interacting with patients and supervisors, helpful advice in transitioning between rotations, and information about implicit rules of clerkships. Students also used each other as benchmarks for gauging strengths and deficits in their own knowledge and skills.\n\nQuestion:\nDo workplace learning through peer groups in medical school clerkships?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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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:\nThere are many patients that exhibit connective tissue related cardiac malformations but do not have mutations in collagen genes. The Small Leucine Rich Proteoglycans (SLRP) fibromodulin (FMOD) and lumican (LUM) bind collagen and regulate fibril assembly in other biological contexts. FMOD deficient mice and double deficient FMOD; LUM mice exhibited anomalies in regions where cardiac valve tissue interdigitates with adjacent muscle for support. Ectopic connective and/or myocardial tissue(s) was associated with the more severe cardiac valve anomalies in FMOD; LUM deficient mice. At postnatal day 0 (P0) there was an increase in the mesenchymal cell number in the regions where valve cusps anchor in FMOD; LUM deficient mice compared to WT. The cardiac valve anomalies correlated with the highest levels of FMOD expression in the heart and also where myotendinous junctions (MTJ) components biglycan, collagen type I alpha 1, and collagen type VI, are also localized.\n\nQuestion:\nDo development of myotendinous-like junctions that anchor cardiac valves requires fibromodulin and lumican?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nFew previous studies have evaluated primary adherence (whether a new prescription is filled within 30 d) to controller medications in individuals with persistent asthma. To compare adherence to the major controller medication regimens for asthma. This was a retrospective cohort study of enrollees from five large health plans. We used electronic medical data on patients of all ages with asthma who had experienced an asthma-related exacerbation in the prior 12 months. We studied adherence measures including proportion of days covered and primary adherence (first prescription filled within 30 d). Our population included 69,652 subjects who had probable persistent asthma and were prescribed inhaled corticosteroids (ICSs), leukotriene antagonists (LTRAs), or ICS/long-acting β-agonists (ICS/LABAs). The mean age was 37 years and 58% were female. We found that 14-20% of subjects who were prescribed controller medicines for the first time did not fill their prescriptions. The mean proportion of days covered was 19% for ICS, 30% for LTRA, and 25% for ICS/LABA over 12 months. Using multivariate logistic regression, subjects prescribed LTRA were less likely to be primary adherent than subjects prescribed ICS (odds ratio, 0.82; 95% confidence interval, 0.74-0.92) or ICS/LABA (odds ratio, 0.88; 95% confidence interval, 0.80-0.97). Black and Latino patients were less likely to fill the prescription compared with white patients.\n\nQuestion:\nIs primary adherence to controller medications for asthma poor?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe function of peroxisome proliferator-activated receptor-gamma (PPARgamma) in hepatic inflammation and injury is unclear. In this study, we sought to determine the role of PPARgamma in hepatic ischemia/reperfusion injury in mice. Male mice were subjected to 90 minutes of partial hepatic ischemia followed by up to 8 hours of reperfusion. PPARgamma was found to be constitutively activated in hepatocytes but not in nonparenchymal cells. Upon induction of ischemia, hepatic PPARgamma activation rapidly decreased and remained suppressed throughout the 8-hour reperfusion period. This reduced activation was not a result of decreased protein availability as hepatic nuclear PPARgamma, retinoid X receptor-alpha (RXRalpha), and PPARgamma/RXRalpha heterodimer expression was maintained. Accompanying the decrease in PPARgamma activation was a decrease in the expression of the natural ligand 15-deoxy-Delta(12,14)-prostaglandin J(2). This was associated with reduced interaction of PPARgamma and the coactivator, p300. To determine whether PPARgamma activation is hepatoprotective during hepatic ischemia/reperfusion injury, mice were treated with the PPARgamma agonists, rosiglitazone and connecting peptide. These treatments increased PPARgamma activation and reduced liver injury compared to untreated mice. Furthermore, PPARgamma-deficient mice had more liver injury after ischemia/reperfusion than their wild-type counterparts.\n\nQuestion:\nDoes peroxisome proliferator-activated receptor-gamma protect against hepatic ischemia/reperfusion injury in mice?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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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 stromal microenvironment has a profound influence on tumour cell behaviour. In tumours, the extracellular matrix (ECM) composition differs from normal tissue and allows novel interactions to influence tumour cell function. The ECM protein tenascin-C (TNC) is frequently up-regulated in breast cancer and we have previously identified two novel isoforms - one containing exon 16 (TNC-16) and one containing exons 14 plus 16 (TNC-14/16). The present study has analysed the functional significance of this altered TNC isoform profile in breast cancer. TNC-16 and TNC-14/16 splice variants were generated using PCR-ligation and over-expressed in breast cancer cells (MCF-7, T47D, MDA-MD-231, MDA-MB-468, GI101) and human fibroblasts. The effects of these variants on tumour cell invasion and proliferation were measured and compared with the effects of the large (TNC-L) and fully spliced small (TNC-S) isoforms. TNC-16 and TNC-14/16 significantly enhanced tumour cell proliferation (P < 0.05) and invasion, both directly (P < 0.01) and as a response to transfected fibroblast expression (P < 0.05) with this effect being dependent on tumour cell interaction with TNC, because TNC-blocking antibodies abrogated these responses. An analysis of 19 matrix metalloproteinases (MMPs) and tissue inhibitor of matrix metalloproteinases 1 to 4 (TIMP 1 to 4) revealed that TNC up-regulated expression of MMP-13 and TIMP-3 two to four fold relative to vector, and invasion was reduced in the presence of MMP inhibitor GM6001. However, this effect was not isoform-specific but was elicited equally by all TNC isoforms.\n\nQuestion:\nDo tumour-associated tenascin-C isoforms promote breast cancer cell invasion and growth by matrix metalloproteinase-dependent and independent mechanisms?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nNearly one-half of Guatemalan children experience growth faltering, more so in indigenous than in nonindigenous children. On the basis of ethnographic interviews in Totonicapán, Guatemala, which revealed differences in maternal perceptions about food needs in infant girls and boys, we predicted a cumulative sex difference in favor of girls that occurred at ∼6 mo of age and diminished markedly thereafter. We examined whether the predicted differences in age-sex patterns were observed in the village, replicated the examination nationally for indigenous children, and examined whether the pattern in nonindigenous children was different. Ethnographic interviews (n = 24) in an indigenous village were conducted. Anthropometric measurements of the village children aged 0-35 mo (n = 119) were obtained. National-level growth patterns were analyzed for indigenous (n = 969) and nonindigenous (n = 1374) children aged 0-35 mo with the use of Demographic and Health Survey (DHS) data. Mothers reported that, compared with female infants, male infants were hungrier, were not as satisfied with breastfeeding alone, and required earlier complementary feeding. An anthropometric analysis confirmed the prediction of healthier growth in indigenous girls than in indigenous boys throughout the first year of life, which resulted in a 2.98-cm height-for-age difference (HAD) between sexes in the village and a 1.61-cm HAD (P < 0.001) in the DHS data between 6 and 17 mo of age in favor of girls. In both data sets, the growth sex differences diminished in the second year of life (P < 0.05). No such pattern was seen in nonindigenous children.\n\nQuestion:\nDo gender perceptions predict sex differences in growth patterns of indigenous Guatemalan infants and young children?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nDysfunction in the ventromedial prefrontal cortex (vmPFC) is believed to play a pivotal role in the pathogenesis of mood and anxiety disorders. Leading neurocircuitry models of these disorders propose that hypoactivity in the vmPFC engenders disinhibited activity of the amygdala and, consequently, pathologically elevated levels of negative affect. This model predicts that a selective loss or diminution of function of the vmPFC would result in heightened activity of the amygdala. Although this prediction has been borne out in rodent lesion and electrophysiologic studies using fear conditioning and extinction paradigms, there has not yet been a definitive test of this prediction in humans. We tested this prediction through a novel use of functional magnetic resonance imaging in four neurosurgical patients with focal, bilateral vmPFC damage. Relative to neurologically healthy comparison subjects, the patients with vmPFC lesions exhibited potentiated amygdala responses to aversive images and elevated resting-state amygdala functional connectivity. No comparable group differences were observed for activity in other brain regions.\n\nQuestion:\nIs ventromedial prefrontal cortex critical for the regulation of amygdala activity in humans?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nBmi-1 had been found to involve in self renewal of stem cells and tumorigenesis in various malignancies. In this study, we investigated the role of Bmi-1 in the development of salivary adenoid cystic carcinoma (SACC). At first, we confirmed that the deregulation of Bmi-1 was a frequent event in SACC; up-regulation of Bmi-1 was correlated with clinical stages, vital status and distant metastasis and associated with reduced overall survival and disease free survival. SACC-LM cells, higher migration and invasion abilities, elevated the expression of Bmi-1 protein, epithelial-mesenchymal transition (EMT) related proteins (Snail, Slug and Vimentin) and cancer stem cells (CSCs) related proteins (ABCG2, Notch, ALDH-1, Oct-4, Nanog and Epcam) compared to the SACC-83 cells (lower migration and invasion abilities). The migration and invasion abilities were inhibited in SACC-LM cells upon Bmi-1 knockdown. Meanwhile, Bmi-1 knockdown resulted in simultaneous loss of stem cell markers and EMT markers in SACC-LM cells.\n\nQuestion:\nIs deregulation of Bmi-1 associated with enhanced migration , invasion and poor prognosis in salivary adenoid cystic carcinoma?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nEndotracheal intubation (ET) in intensive care unit (ICU) patients is regarded as more challenging than elective intubations in the operating room. Despite challenging conditions in ICU, trainees are often the initial operators performing ET. Because nonanesthesiologist intensivists with limited experience in ET run most of the nonsurgical ICUs, it is of exceptional importance to identify patients with predictable difficult ET in advance to prepare for a difficult airway scenario and thus avoid severe complications. In this prospective, observational, single-center study, we used a truncated MACOCHA score to evaluate intubation performance of nonanesthesiologist ICU trainees in an interdisciplinary medical ICU. We show that (a) ET could be performed safely and without fatal complications in all cases; (b) the MACOCHA score is feasible on a nonanesthesiologist ICU; (c) a truncated MACOCHA score of at least 8 predicts failure of ICU trainees; and (d) availability of an ear, nose, and throat physician and an anesthesiologist is required to warrant successful management of difficult airways.\n\nQuestion:\nIs the MACOCHA score feasible to predict intubation failure of nonanesthesiologist intensive care unit trainees?\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:\nAbrus agglutinin (AGG) from the seeds of Indian medicinal plant Abrus precatorius belongs to the class II ribosome inactivating protein family. In this study we investigated the anticancer effects of AGG against human hepatocellular carcinoma in vitro and in vivo. Cell proliferation, DNA fragmentation, Annexin V binding, immunocytofluorescence, Western blotting, caspase activity assays and luciferase assays were performed to evaluate AGG in human liver cancer cells HepG2. Immunohistochemical staining and TUNEL expression were studied in tumor samples of HepG2-xenografted nude mice. AGG induced apoptosis in HepG2 cells in a dose- and time-dependent manner. AGG-treated HepG2 cells demonstrated an increase in caspase 3/7, 8 and 9 activities and a sharp decrease in the Bcl-2/Bax ratio, indicating activation of a caspase cascade. Co-treatment of HepG2 cells with AGG and a caspase inhibitor or treatment of AGG in Bax knockout HepG2 cells decreased the caspase 3/7 activity in comparison to HepG2 cells exposed only to AGG. Moreover, AGG decreased the expression of Hsp90 and suppressed Akt phosphorylation and NF-κB expression in HepG2 cells. Finally, AGG treatment significantly reduced tumor growth in nude mice bearing HepG2 xenografts, increased TUNEL expression and decreased CD-31 and Ki-67 expression compared to levels observed in the untreated control mice bearing HepG2 cells.\n\nQuestion:\nDoes abrus agglutinin suppress human hepatocellular carcinoma in vitro and in vivo by inducing caspase-mediated cell death?\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 ubiquitin-proteasome pathway (UPP) is an important protein quality control mechanism for selective degradation of abnormal proteins. The objective of this study was to test the hypothesis that enhancement of the UPP capacity could attenuate the accumulation and aggregation of misfolded proteins using V76D-γD-crystallin as a model substrate. Wild type (wt) and V76D mutant γD-crystallin were fused to red fluorescence protein (RFP) and expressed in human lens epithelial cells. The cellular distribution of the expressed proteins was compared by fluorescence microscopy. The solubility of wt- and V76D-γD-crystallin was determined by cellular fractionation and Western blotting. Wt-γD-RFP and V76D-γD-RFP were also cotransfected along with a ubiquitin ligase (CHIP) or a ubiquitin-conjugating enzyme (Ubc5) into cells. Levels of wt- and V76D-γD-crystallin, the percentage of transfected cells with aggregates, and aggregate size were quantified and compared among different groups. Wt-γD-crystallin was evenly distributed in cells, whereas V76D-γD-crystallin formed intracellular aggregates. Eighty percent of wt-γD-crystallin was detected in the soluble fraction, whereas only 7% of V76D-γD-crystallin was soluble. CHIP or Ubc5 coexpression reduced the protein level of V76D-γD and concomitantly its aggregation in transfected cells; these effects could be attenuated by proteasome inhibitor. Mutant CHIP with defect TPR (tetratricopeptide repeat) or U-box domain failed to reduce levels of V76D-γD-crystallin.\n\nQuestion:\nDoes enhancement of ubiquitin conjugation activity reduce intracellular aggregation of V76D mutant γD-crystallin?\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 the present study was to examine the effect of massage on nausea, anxiety, and depression in patients with breast cancer undergoing chemotherapy. This work was a single-center, prospective, randomized, controlled trial. This study was conducted in an oncology clinic, in a hospital in southwestern Sweden. Thirty-nine (39) women (mean age = 51.8) with breast cancer undergoing chemotherapy were enrolled. The patients were randomly assigned to a massage therapy group (20 minutes of massage on five occasions) or a control group (five 20-minute visits). All patients recorded nausea and anxiety on the Visual Analogue Scale before and after each intervention. They also completed the Hospital Anxiety and Depression Scale. Massage treatment significantly reduced nausea compared with control treatment (p = 0.025) when improvement was measured as a percentage of the five treatment periods. Differences in anxiety and depression between the two treatment regimes could not be statistically demonstrated.\n\nQuestion:\nDoes massage relieve nausea in women with breast cancer who are undergoing chemotherapy?\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:\nRecent evidence suggests that patients with a normal cranial CT scan after head injury can be safely discharged home from the emergency department. However, supporting data from previous studies has relied on incomplete patient follow-up. We utilized a statewide comprehensive hospital abstract reporting system (CHARS) to assess whether children with normal CT scans after head injury subsequently developed intracranial sequelae in the month following their initial injury. Retrospective case-series study, with comprehensive statewide follow-up for 1 month. The emergency department of a Level 1 Trauma Center in Seattle, Washington. All children (n = 400) with head injury, Glasgow Coma Score of 13 to 15, and initial normal CT scan seen over a 4.5-year time period. All were matched against CHARS to evaluate admissions within 30 days after emergency department disposition. For readmissions, International Classification of Diseases (9th revision) discharge and procedure information was collected. All children were also matched against the state death files. Four children were readmitted for neurologic reasons within 1 month following injury. One child on coumadin for heart disease developed a symptomatic subdural hematoma 5 days after head injury, requiring neurosurgical drainage. One child developed a symptomatic hemorrhagic contusion 3 days after injury, requiring observation only. Two children were readmitted 1 day after injury for concussive symptoms; both were discharged home after observation only. There were no deaths among the study population.\n\nQuestion:\nDoes the use of cranial CT scan in the triage of pediatric patients with mild head injury?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe studied the effect of Lactobacillus reuteri strain SD2112 Tablets Reuterina (ERINA Co., Inc.), in suppressing H. pylori urease activity and to use the urea breath test (UBT) as a marker for the burden of infection. Method 1: Assessment of UBT and H. pylori density. Subjects were 33 H. pylori-positive patients from whom were obtained gastric biopsy specimens by upper gastrointestinal endoscopy. The correlation between UBT and H. pylori density was investigated. Individual UBT was established for each patient. Patients were divided by H. pylori density was 3 groups: Group I (low-density), Group II (moderate-density), and Group III (high-density). The individual UBTs were then correlated to the established H. pylori quantity. Method 2: Assessment of suppressive effect of L. reuteri on H. pylori urease activity. Subjects were 40 asymptomatic volunteers with an UBT exceeding 15 per thousand, randomly allocated to four groups: Subjects in Group A underwent active treatment for 4 weeks (period 1) and placebo treatment for the following 4 weeks (period 2). These in Group B underwent treatment in reverse order. Those in Group C underwent placebo. Group D consisted of volunteers with negative UBT undergoing active treatment for the full 8 weeks. Result 1: UBT was 11.6+/-2.0 per thousand, 22.1+/-2.6 per thousand, and 35.4+/-7.6 per thousand in Groups I, II, and III, showing UBT that increased significantly (I vs. II: p< 0.01 and I vs. III: p<0.05) based on H. pylori density. Result 2:Significant differences were seen in the decrease in UBT before versus after medication in Groups A and B. In Group A, lower UBT was maintained until the end of the full 8-week period. The overall decrease in UBT due to medication with L. reuteri Tablets was 69.7+/-4.0% (p<0.05).\n\nQuestion:\nDo lactobacillus reuteri tablets suppress Helicobacter pylori infection -- a double-blind randomised placebo-controlled cross-over clinical 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:\nBaked egg is tolerated by a majority of egg-allergic children. To characterize immunologic changes associated with ingestion of baked egg and evaluate the role that baked egg diets play in the development of tolerance to regular egg. Egg-allergic subjects who tolerated baked egg challenge incorporated baked egg into their diet. Immunologic parameters were measured at follow-up visits. A comparison group strictly avoiding egg was used to evaluate the natural history of the development of tolerance. Of the 79 subjects in the intent-to-treat group followed for a median of 37.8 months, 89% now tolerate baked egg and 53% now tolerate regular egg. Of 23 initially baked egg-reactive subjects, 14 (61%) subsequently tolerated baked egg and 6 (26%) now tolerate regular egg. Within the initially baked egg-reactive group, subjects with persistent reactivity to baked egg had higher median baseline egg white (EW)-specific IgE levels (13.5 kU(A)/L) than those who subsequently tolerated baked egg (4.4 kU(A)/L; P= .04) and regular egg (3.1 kU(A)/L; P= .05). In subjects ingesting baked egg, EW-induced skin prick test wheal diameter and EW-, ovalbumin-, and ovomucoid-specific IgE levels decreased significantly, while ovalbumin- and ovomucoid-specific IgG(4) levels increased significantly. Subjects in the per-protocol group were 14.6 times more likely than subjects in the comparison group (P< .0001) to develop regular egg tolerance, and they developed tolerance earlier (median 50.0 vs 78.7 months; P< .0001).\n\nQuestion:\nDoes dietary baked egg accelerate resolution of egg allergy in children?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo determine how magnesium affects human coronary arteries and whether endothelium derived nitric oxide (EDNO) is involved in the coronary arterial response to magnesium. Quantitative coronary angiography and Doppler flow velocity measurements were used to determine the effects of the nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA) on magnesium induced dilation of the epicardial and resistance coronary arteries. Hiroshima University Hospital a tertiary cardiology centre. 17 patients with angiographically normal coronary arteries. Magnesium sulfate (MgSO(4)) (0.02 mmol/min and 0.2 mmol/min) was infused for two minutes into the left coronary ostium before and after intracoronary infusion of L-NMMA. Diameter of the proximal and distal segments of the epicardial coronary arteries and coronary blood flow. At a dose of 0.02 mmol/min, MgSO(4) did not affect the coronary arteries. At a dose of 0.2 mmol/min, MgSO(4) caused coronary artery dilation (mean (SEM) proximal diameter 3.00 (0.09) to 3.11 (0.09) mm; distal 1.64 (0.06) to 1.77 (0.07) mm) and increased coronary blood flow (79.3 (7.5) to 101.4 (9.9) ml/min, p < 0.001 v baseline for all). MgSO(4) increased the changes in these parameters after the infusion of L-NMMA (p < 0.001 v baseline).\n\nQuestion:\nDoes magnesium cause nitric oxide independent coronary artery vasodilation in humans?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe enrolled 65 to 75 year-old community-dwelling women and measured muscle power, strength, physical activity using accelerometry and tibial bone strength using peripheral quantitative computed tomography (pQCT). Muscle power contributed 6.6% of the variance in the bone strength-strain index and 8.9% in the section modulus after accounting for age, height, weight, and physical activity; moderate to vigorous physical activity was related to muscle power in the lower extremity. Muscle power is associated with DXA measurements of bone mass, but it is not known whether muscle power is associated with bone strength. There are no reports of investigations that have tested the effect of muscle power on bone compartments using advanced imaging. We enrolled 74 community-dwelling women aged 65-75 years. We measured muscle power and strength of leg extension using Keiser air-pressure resistance equipment. All participants wore a waist-mounted Actigraph accelerometer to record physical activity. We used peripheral quantitative computed tomography (pQCT) to measure tibial mid-shaft (50% of the site) bone strength (strength-strain index, section modulus). We used Pearson correlations and multi-level linear regression to investigate the associations between muscle and bone. Muscle power contributed 6.6% (p = 0.007) of the variance in the bone strength-strain index and 8.9% (p = 0.001) the variance in the section modulus in older women after accounting for age, height, weight, and physical activity. Moderate to vigorous physical activity was significantly related to muscle power in the lower extremity (r = 0.260; p = 0.041).\n\nQuestion:\nIs muscle power related to tibial bone strength in older women?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe aim of this study was to examine the significance of EBP50 (ezrin-radixin-moesin binding phosphoprotein 50) expression in esophageal squamous cell carcinoma (ESCC). Real-time PCR (qRT-PCR), western blotting, and immunohistochemical staining were performed to detect EBP50 expression in pairs of ESCCs and matched non-tumor tissues, and the relationships between EBP50 expression and other clinical factors in ESCC were analyzed. An iRNA targeting EBP50 was transfected into EC9706 cells. MTT and plate colony assays were performed to assess the effects of EBP50 down-regulation on cell growth, and flow cytometry was used to evaluate the influence of inhibiting EBP50 on cell cycle progression. The real-time PCR (qRT-PCR), western blotting, and immunohistochemical staining results showed that EBP50 expression was significantly lower in ESCCs compared to matched non-tumor tissues. In addition, decreased EBP50 expression correlated with differentiation, T stage, lymph node (LN) metastasis, and poor prognosis in patients with ESCC. The down-regulation of EBP50 may significantly promote the growth and proliferation of EC9706 cells while accelerating cell cycle progression from the G1to S phase.\n\nQuestion:\nIs reduced EBP50 expression or mis-localization of the EBP50 protein associated with the malignant progression of esophageal squamous cell carcinoma?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHelicobacter pylori infection has been described as a risk factor for hepatic encephalopathy in patients with chronic liver disease although the topic remains controversial. To determine whether Helicobacter pylori infection is an independent predictive factor for encephalopathy in patients with liver cirrhosis. Clinical, epidemiological, analytical and nutritional parameters of 205 patients were collected. Helicobacter pylori infection was determined by serology. Encephalopathy (grade II or higher) was clinically assessed during follow-up. The relationship between each parameter and encephalopathy was analysed by Kaplan-Meier curves and the Log rank test. The most significant parameters underwent multivariate analysis by Cox regression. Twenty-five variables were related to encephalopathy in the bivariate analysis. Multivariate analysis selected five independent factors: previous bouts of encephalopathy (Odds ratio 3.79; 95% confidence interval 1.94-7.38), albumin (Odds ratio 0.86; 95% confidence interval 0.80-0.92), tricipital skin fold (Odds ratio 0.79; 95% confidence interval 0.66-0.95) chronic pulmonary disease (Odds ratio 2.78, 95% confidence interval; 1.31-5.92), and on-going alcoholism (Odds ratio 2.62; 95% confidence interval 1.16-5. BB).\n\nQuestion:\nIs helicobacter pylori a risk factor for hepatic encephalopathy?\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:\nVascular endothelial growth factor-a (VEGF)-targeted therapies have become an important treatment for a number of human malignancies. The VEGF inhibitors are actually effective in several types of cancers, however, the benefits are transiently, and the vast majority of patients who initially respond to the therapies will develop resistance. One of possible mechanisms for the acquired resistance may be the direct effect(s) of VEGF inhibitors on tumor cells expressing VEGF receptors (VEGFR). Thus, we investigated here the direct effect of chronic VEGF inhibition on phenotype changes in human colorectal cancer (CRC) cells. To chronically inhibit cancer cell-derived VEGF, human CRC cell lines (HCT116 and RKO) were chronically exposed (2 months) to an anti-VEGF monoclonal antibody (mAb) or were disrupted the Vegf gene (VEGF-KO). Effects of VEGF family members were blocked by treatment with a VEGF receptor tyrosine kinase inhibitor (VEGFR-TKI). Hypoxia-induced apoptosis under VEGF inhibited conditions was measured by TUNEL assay. Spheroid formation ability was assessed using a 3-D spheroid cell culture system. Chronic inhibition of secreted/extracellular VEGF by an anti-VEGF mAb redundantly increased VEGF family member (PlGF, VEGFR1 and VEGFR2), induced a resistance to hypoxia-induced apoptosis, and increased spheroid formation ability. This apoptotic resistance was partially abrogated by a VEGFR-TKI, which blocked the compensate pathway consisted of VEGF family members, or by knockdown of Vegf mRNA, which inhibited intracellular function(s) of all Vegf gene products. Interestingly, chronic and complete depletion of all Vegf gene products by Vegf gene knockout further augmented these phenotypes in the compensate pathway-independent manner. These accelerated phenotypes were significantly suppressed by knockdown of hypoxia-inducible factor-1α that was up-regulated in the VEGF-KO cell lines.\n\nQuestion:\nDoes chronic inhibition of tumor cell-derived VEGF enhance the malignant phenotype of colorectal cancer cells?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe gastrointestinal tract is the most common site of primary extranodal non-Hodgkin lymphoma, and the prognostic factors of primary gastric diffuse large B-cell lymphoma (PG-DLBCL) differ in various studies. We retrospectively searched for PG-DLBCL in a single institution, performed immunohistochemical analysis, classified tumor phenotype (Hans and Muris algorithms), reviewed medical records, and analyzed the clinical and immunophenotypic variables using Cox proportional hazard regression model. A total of 46 cases were identified including 25 males and 21 females with a median age of 63.5; 18 (39%) were at stage I and 28 (61%) at stage II. Seven (15%) patients underwent surgery as initial treatment including total (n = 3, 7%) and subtotal (n = 4, 9%) gastrectomy. Thirty-three patients (72%) received frontline chemotherapy treatment including ten with additional rituximab (MabThera) injection, and two (6%) of these patients developed perforation after chemotherapy. Four patients passed away shortly after diagnosis and the remaining three were lost to follow-up. The overall 2- and 5- year survival rates were 55% and 50%, respectively. The expression of various differentiation markers was CD10 (25%), bcl-2 (50%), bcl-6 (84%), and MUM1 (64%). Half of the cases studied (22/44) were classified as germinal center B-cell (GCB) phenotype and the remaining half as non-GCB according to Hans algorithm; 66% and 34% cases belonged to groups 1 and 2, respectively, according to Muris algorithm. Univariate analysis showed the expression of bcl-6 by the tumor cells as a favorable factor, while elevated serum lactate dehydrogenase (LDH) level, bcl-2 expression, and Muris group 2 were associated with poorer outcome. Multivariate analysis revealed that the two prognostic factors were bcl-6 expression and elevated LDH level, with hazard ratios of 0.09 (p = 0.002) and 3.72 (p = 0.024), respectively.\n\nQuestion:\nDo bcl-6 expression and lactate dehydrogenase level predict prognosis of primary gastric diffuse large B-cell lymphoma?\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:\nalpha 1-Antitrypsin (AAT) and alpha 2-macroglobulin (AMG) are elastase inhibitors that bind the enzyme and reduce measured levels of free elastase. It was recently demonstrated that some patients with intracranial aneurysms have significantly elevated plasma elastase (PE) levels. Although this elevation is unrelated to plasma AAT, it is unknown whether abnormal AAT phenotypes or reduced AMG levels play a role. Moreover, the pathological significance of this elevation is not understood. Plasma from 24 patients with aneurysms (ruptured, n = 15; unruptured, n = 9) and 10 age-matched patients who comprised a control group was analyzed for PE and AMG levels by enzyme-linked immunosorbent assay and for AAT phenotype by isoelectric focusing. Sections of superficial temporal temporal artery obtained from these patients at the time of surgery were examined for evidence of elastin degradation by using a van Gieson stain, with scoring on a nine-point quantitative scale. Patients with aneurysms showed significantly elevated PE levels (119 +/- 28 versus 17 +/- 7 micrograms/ml, P < 0.05), but AMG levels were not decreased. AAT phenotypic abnormalities were observed in 10% (2 of 20) of the patients with aneurysms, but this was not different from the expected population incidence (7%). Elastin degradation scores were significantly higher in patients with aneurysms than in patients control group (4.26 +/- 0.54 versus 1.21 +/- 0.43, P < 0.05). In addition, patients with higher elastase levels (> 80 micrograms/ml) demonstrated 55% higher degradation scores than did those with lower elastase levels (< 80 micrograms/ml).\n\nQuestion:\nDoes elastin degradation in the superficial temporal arteries of patients with intracranial aneurysms reflect changes in plasma elastase?\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:\nRespiratory alterations have been associated with subsequent coronary heart diseases in numerous population-based studies. The underlying mechanisms remain largely unknown. The objective of this study was to examine the association between bronchial hyperresponsiveness (BHR) to methacholine (which reflects local inflammation in the bronchus) and common carotid intima-media thickness (CCA-IMT). As part of the European Community Respiratory Health Survey follow-up, in Paris Center, we assessed BHR to methacholine (> or =20% decrease in FEV1 for a maximum methacholine dose of 4 mg) and measured CCA-IMT by ultrasonography in 255 adults free of cardiovascular diseases aged 29 to 56 years (123 men, 132 women; mean age 44.5 years, 43.5% never smokers). In men, CCA-IMT mean value was higher in subjects with BHR than in those without (0.68+/-0.11 versus 0.62+/-0.09 mm, P=0.002). No association was found in women. Multivariate analysis confirmed the independent association between BHR and CCA-IMT in men (adjusted odds ratio for a 0.10-mm increase in CCA-IMT=2.1, 95% confidence interval: 1.1 to 4.3; P=0.02). These results remained similar after exclusion of asthmatic subjects (n=11). In each strata of smoking status (nonsmoker, ex-smoker, and current smokers), CCA-IMT mean values tended to be higher in subjects with BHR than in those without, although the difference between the 2 groups was more pronounced in current smokers.\n\nQuestion:\nIs bronchial hyperresponsiveness to methacholine associated with increased common carotid intima-media thickness in men?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo investigate aerobic capacity with and without an ankle-foot orthosis (AFO) in subacute hemiparetic stroke patients. Prospective crossover intervention study. Rehabilitation clinic in secondary care. Patients diagnosed with first-ever cerebral stroke involving the cortical or subcortical area resulting in hemiparesis (n = 15, 8 men and 7 women; average age, 62.1 years). All subjects participated in 2 continuous, symptom-limited, low-velocity graded treadmill exercise stress tests under 2 different conditions, namely, with and without an AFO. The rest interval between tests was at least 48 hours. The order of exercise stress tests was randomized. To assess cardiorespiratory responses, oxygen consumption, heart rate, systolic blood pressure, diastolic blood pressure, rate-pressure product, and respiratory exchange ratio were measured continuously throughout the test, and peak values were obtained. The rating of perceived exertion was recorded immediately after each test. The percentage of the age-predicted maximal heart rate and total exercise duration were also measured. Gait function was assessed by the Six-Minute Walk Test. Using an AFO significantly increased peak oxygen consumption and Six-Minute Walk Test results. Peak values of each of heart rate, systolic blood pressure, diastolic blood pressure, rate-pressure product, and respiratory exchange ratio, rating of perceived exertion, percentage of age-predicted maximal heart rate, and total exercise duration were similar regardless of AFO use.\n\nQuestion:\nDoes use of an ankle-foot orthosis improve aerobic capacity in subacute hemiparetic stroke 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:\nThe objective of the present study was to elucidate the separate effects of energy restriction and weight loss on blood pressure (BP) and to assess the relationship between sodium intake, weight loss, and BP. Two hundred and eight overweight and obese subjects (age: 52.4 +/- 0.8 yrs; BMI 33.6 +/- 0.3 kg/m(2)) completed a weight loss diet program consisting of 8-12 weeks of moderate energy restriction (ER; approximately 30% energy deficit, unrestricted salt intake) and four weeks of energy balance (EB). Body weight and BP were measured at baseline, the midpoint, and the end of ER and after EB. 24-hr Na+ excretion was measured at baseline and at the end of EB. Overall, body weight reduced progressively by 7.0 +/- 0.2 kg (7.5%; p < 0.001) with the hypocaloric diet. BP fell substantially during the first phase of ER (-5.7 +/- 0.7/-2.6 +/- 0.4 mmHg, p = 0.001), corresponding to a 4.5 +/- 0.2 kg weight reduction, with no further BP changes during the second phase of ER, despite further weight loss (2.4 +/- 0.1 kg). During EB, BP remained stable. The hypotensive effects of caloric restriction and weight loss were similar across clinical subgroups defined by age, sex, diabetes, insulin sensitivity, and hypertensive status. BP responses to weight loss were independent of 24-hr urinary Na+ excretion. 24-hr urinary Na+ excretion was similar at baseline and at the end of EB (146.5 +/- 5.3 vs. 146.9 +/- 5.3 mmol/24-hr).\n\nQuestion:\nDo reductions in blood pressure following energy restriction for weight loss rebound after re-establishment of energy balance in overweight and obese subjects?\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:\nHypermethylation of DNA silences gene expression and is an important event in colorectal cancer (CRC). This study aimed to identify aberrantly methylated genes that contribute to a poor prognosis for patients with CRC. The study comprehensively explored DNA methylation microarray profiles from 396 CRC samples and 45 normal control samples in a database and selected aberrantly methylated transcription factors associated with prognosis and metastasis. Using quantitative reverse transcription polymerase chain reaction, the identified genes in 140 patients with CRC were validated to assess the relationship between expression of methylated genes and prognosis. In the study, FOXE1 was newly identified as a gene associated with prognosis and metastasis in CRC. Expression of FOXE1 in CRC tissues was significantly lower than in normal colorectal tissues (p = 0.01). The survival rate for the patients with low expression of FOXE1 was significantly lower than that for patients with high expression of FOXE1 in uni- and multivariate analyses. Inhibition of DNA methylation recovered FOXE1 expression in CRC cells.\n\nQuestion:\nDoes aberrant Methylation of FOXE1 contribute to a Poor Prognosis for Patients with Colorectal Cancer?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nX chromosome inactivation is the transcriptional silencing of one X chromosome in the somatic cells of female mammals. In eutherian mammals (e.g. humans) one of the two X chromosomes is randomly chosen for silencing, with about 15% (usually in younger evolutionary strata of the X chromosome) of genes escaping this silencing. In contrast, in the distantly related marsupial mammals the paternally derived X is silenced, although not as completely as the eutherian X. A chromosome wide examination of X inactivation, using RNA-seq, was recently undertaken in grey short-tailed opossum (Monodelphis domestica) brain and extraembryonic tissues. However, no such study has been conduced in Australian marsupials, which diverged from their American cousins ~80 million years ago, leaving a large gap in our understanding of marsupial X inactivation. We used RNA-seq data from blood or liver of a family (mother, father and daughter) of tammar wallabies (Macropus eugenii), which in conjunction with available genome sequence from the mother and father, permitted genotyping of 42 expressed heterozygous SNPs on the daughter's X. These 42 SNPs represented 34 X loci, of which 68% (23 of the 34) were confirmed as inactivated on the paternally derived X in the daughter's liver; the remaining 11 X loci escaped inactivation. Seven of the wallaby loci sampled were part of the old X evolutionary stratum, of which three escaped inactivation. Three loci were classified as part of the newer X stratum, of which two escaped inactivation. A meta-analysis of previously published opossum X inactivation data revealed that 5 of 52 genes in the old X stratum escaped inactivation.\n\nQuestion:\nDoes paternal X inactivation correlate with X chromosome evolutionary strata in marsupials?\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 clinical complications of Extracorporeal Circulation (ECC) have been linked to disturbances in the microcirculation. In order to prevent these deleterious effects, a biodegradeable agent to coat the extracorporeal circuit was tested. Intravital fluorescence microscopy was used on the hamster skinfold chamber model in permanently instrumented, awake animals. ECC was introduced via a micro-roller-pump and a silicon tube shunted between the carotid artery and the jugular vein. The ECC-tube system was coated with PEG-Hirudin-Iloprost, two additional groups received either Iloprost i.v. (0.8 mg/kg/h) or Hirudin i.v. (1 mg/kg b.w.). ECC for 20 minutes resulted in an increase in rolling and adherent leukocytes in postcapillary venules (Roller 9 to 36 [%]; Sticker 24 to 330 [n/mm2]). Use of the coated tube system reduced L/E cell interaction (Roller 9 to 24* [%], Sticker 28 to 194* [n/mm2]; *p<0.05), whereas Hirudin i.v. nearly abolished it.\n\nQuestion:\nDoes hirudin protect from leukocyte/endothelial cell interaction induced by extracorporeal circulation?\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 explore the efficacy of inductible nitric oxide synthase (iNOS) inhibitor 1400W in vivo in blocking the death pathway of lipopolysaccharide (LPS)-induced activated-microglia to preoligodendrocytes (preOLs) in neonatal rats with infective-type periventricular leukomalacia (PVL) induced by LPS. Two-day-old neonatal rats were randomly divided into: a sham-operated group, an untreated PVL group, and four 1400W-treated PVL groups that were subcutaneously administrated with 20 mg/kg of 1400W at 0 h, 8 hrs, 16 hrs, and 24 hrs after LPS induction, respectively. The brain specimens were obtained 5 days after LPS induction. The pathological assessment of cerebral white matter was performed under a light microscope. Concentrations of nitric oxide (NO) were measured by nitric acid-deoxidize colorimetry. Synthesis of iNOS was determined by Western blot analysis. Peroxynitrite (ONOO(-)) level and the amount of preOLs were determined by immunocytochemistry. RETHODS: The obvious injuries of periventricular white matter, massive loss of positive O4-labelled preOLs, and increased levels of NO, ONOO(-) and iNOS were observed in neonatal rats with PVL. Compared to the untreated PVL group, the use of 1400W at 0 h, 8 hrs and 16 hrs after LPS induction significantly improved white matter injuries, reduced the levels of NO, ONOO(-) and iNOS, and increased the amount of O4-labelled preOLs. However, the use of 1400W at 24 hrs after LPS induction did not result in the improvements.\n\nQuestion:\nDoes [ 1400W block death pathway of LPS-induced activated-microglia to preOLs ]?\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 precise pathophysiological mechanisms of radiation-induced lung injury are poorly understood, but have been shown to correlate with dysregulation of different cytokines. The purpose of this study was to evaluate the time course of the pro-inflammatory cytokines tumor necrosis factor-(TNF-)alpha, interleukin-(IL-)1alpha and IL-6 after whole-lung irradiation. The thoraces of C57BL/6J mice were irradiated with 12 Gy. Treated and control mice were sacrificed at 0.5, 1, 3, 6, 12, 24, 48, 72 h, 1, 2, 4, 8, 16, and 24 weeks post irradiation (p. i.). Real-time multiplex RT-PCR (reverse transcriptase polmyerase chain reaction) was established to evaluate the expression of TNF-alpha, IL-1alpha and IL-6 in the lung tissue of the mice. For histological analysis, lung tissue sections were stained by hematoxylin and eosin. Multiplex RT-PCR analysis revealed a biphasic expression of these pro-inflammatory cytokines in the lung tissue after irradiation. After an initial increase at 1 h p. i. for TNF-alpha and at 6 h p. i. for IL-1alpha and IL-6, the mRNA expression of these pro-inflammatory cytokines returned to basal levels (48 h, 72 h, 1 week, 2 weeks p. i.). During the pneumonic phase, TNF-alpha, IL-1alpha and IL-6 were significantly elevated and revealed their maximum at 8 weeks p. i. Histopathologic evaluation of the lung sections obtained within 4 weeks p. i. revealed only minor lung damage in 5-30% of the lung tissue. By contrast, at 8, 16, and 24 weeks p. i., 70-90% of the lung tissue revealed histopathologically detectable organizing alveolitis.\n\nQuestion:\nDoes irradiation induce a biphasic expression of pro-inflammatory cytokines in the lung?\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 gene for the renal phosphate wasting disorder autosomal-dominant hypophosphatemic rickets (ADHR) is FGF23, which encodes a secreted protein related to the fibroblast growth factors (FGFs). We previously detected missense mutations R176Q, R179W, and R179Q in FGF23 from ADHR kindreds. The mutations replace R residues within a subtilisin-like proprotein convertase (SPC) cleavage site 176RHTR-179 (RXXR motif). The goal of these studies was to determine if the ADHR mutations lead to protease resistance of FGF-23. The ADHR mutations were introduced into human FGF-23 cDNA clones with or without an N-terminal FLAG tag by site-directed mutagenesis and were transiently transfected into HEK293 cells. Protein expression was determined by Western analyses. Antibodies directed toward the C-terminal portion of FGF-23 revealed that the native FGF-23 protein resolved as 32 kD and 12 kD species in HEK293 conditioned media; however, the three mutated proteins were detected only as the 32 kD band. An N-terminal FLAG-tagged native FGF-23 resolved as two bands of 36 kD and 26 kD when detected with a FLAG antibody, whereas the R176Q mutant resolved primarily as the 36 kD protein species. Cleavage of FGF-23 was not enhanced by extracellular incubation of FGF-23 with HEK293 cells. Native and mutant FGF-23s bound heparin.\n\nQuestion:\nDo autosomal-dominant hypophosphatemic rickets ( ADHR ) mutations stabilize FGF-23?\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 serum creatine kinase (CK) activity after resistance exercise bouts with different rest intervals between sets and exercises in high responding (HR) and normal responding (NR) subjects. During each resistance exercise bout, three sets with 10-repetition maximum (10RM) loads were completed for the chest press, cable pulldown, biceps curl, triceps extension, leg extension, and prone leg curl. Each bout differed in the length of the rest interval between sets and exercises, specifically either 1 or 3 min. After blood analysis, subjects were separated into NR or HR on the basis of the peak serum CK activity being in the 90th percentile. The volume completed (load x sets x repetitions) was significantly greater for the 3-min bout versus the 1-min bout, with no significant differences between the HR and the NR groups. For the NR group, serum CK was significantly elevated from 24 to 72 h after each bout, with no significant differences between bouts. Conversely, for the HR group, the 1-min bout resulted in serum CK activity levels that were approximately 70% greater than the 3-min bout at the 48- and 72-h time points.\n\nQuestion:\nDoes short recovery augment magnitude of muscle damage in high responders?\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:\nPrevalence data of herpes simplex virus (HSV) in oral mucositis in children on treatment for cancer is limited. Quantitative polymerase chain reaction (PCR) has been seldom utilized for detection of HSV-1/2 in oral mucosa. Children on treatment for cancer with oral mucositis were enrolled as cases and healthy children as controls. An oral swab from the lesion in cases and mucosal scraping in controls were obtained. Both qualitative and real-time quantitative PCR for HSV-1/2 were performed. Serum ELISA-IgG/IgM for HSV-1/2 antibodies (NovaLisa™-Dietzenbach-Germany) were measured. Thirty-two cases (Age, 6.3±3.4 years) and 30 controls were enrolled. Majority (69%) of cases had ALL. All patients had febrile neutropenia, except two. ELISA-IgM-HSV-1/2 was not positive in any case or control. ELISA-IgG-HSV-1/2 was positive in 11 (34%) cases and nine (30%) controls (p=1.0). Qualitative PCR for HSV-1 detected the virus in eight (25%) cases and nil controls (p=0.009). HSV-2 was not detected in any case/control by qualitative PCR. Quantitative PCR detected HSV-1 in 21 (66%) and HSV-2 in 22 (69%) cases. In controls, quantitative PCR detected HSV-1 in three (10%) and HSV-2 in none. In patients, the mean viral load of HSV-1 (5,500±15,987×10(4) copies/nanogram DNA) was more than HSV-2 (4.03±8.5×10(4)) (p=0.11). There was no correlation of HSV-1/2 with grading of mucositis.\n\nQuestion:\nIs hSV-1 as well as HSV-2 frequent in oral mucosal lesions of children on chemotherapy?\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:\nLong intervening non-coding RNAs (lincRNAs) are a recently discovered subclass of non-coding RNAs. LincRNAs are expressed across the mammalian genome and contribute to the pervasive transcription phenomenon. They display a tissue-specific and species-specific mode of expression and are present abundantly in the brain. Here, we report the expression patterns of oligodendrocyte maturation-associated long intervening non-coding RNA (OLMALINC), which is highly expressed in the white matter (WM) of the human frontal cortex compared to the grey matter (GM) and peripheral tissues. Moreover, we identified a novel isoform of OLMALINC that was also up-regulated in the WM. RNA-interference (RNAi) knockdown of OLMALINC in oligodendrocytes, which are the major cell type in the WM, caused significant changes in the expression of genes regulating cytostructure, cell activation and membrane signaling. Gene ontology enrichment analysis revealed that over 10% of the top 25 up- and down-regulated genes were involved in oligodendrocyte maturation. RNAi experiments in neuronal cells resulted in the perturbation of genes controlling cell proliferation. Furthermore, we identified a novel cis-natural antisense non-coding RNA, which we named OLMALINC-AS, which maps to the first exon of the dominant isoform of OLMALINC.\n\nQuestion:\nIs high expression of long intervening non-coding RNA OLMALINC in the human cortical white matter associated with regulation of oligodendrocyte maturation?\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 role of T cell induction of matrix metalloproteinase 13 (MMP-13) production by human osteoblasts in order to better understand the process of bone loss in rheumatoid arthritis (RA). Activated T cell-conditioned medium (ACTTCM) was used to mimic the physiologic conditions of inflammation. MMP-13 production by human osteoblasts was assessed using a specific enzyme-linked immunosorbent assay. Specific inhibitors of the p38 mitogen-activated protein (MAP) kinase and the extracellular signal-regulated kinase 1/2 (ERK-1/2) MAP kinase signaling pathways were used to assess their roles in T cell-mediated MMP-13 production. Finally, recombinant cytokines representative of the major components in ACTTCM were assessed for their ability to induce MMP-13. ACTTCM powerfully induced MMP-13 in human osteoblasts. Inhibition of p38 activity abolished, while inhibition of ERK-1/2 activity enhanced, MMP-13 production. We next investigated physiologic levels of the T cell cytokines tumor necrosis factor alpha (TNFalpha), transforming growth factor beta (TGFbeta), interferon-gamma (IFNgamma), and interleukin-17 (IL-17) for their roles in MMP-13 induction. Although individual cytokines had no significant effect, the combination of TNFalpha, TGFbeta, IFNgamma, and IL-17 resulted in a dramatic p38-dependent induction of MMP-13 identical to that produced by ACTTCM.\n\nQuestion:\nDo t cells regulate the expression of matrix metalloproteinase in human osteoblasts via a dual mitogen-activated protein kinase mechanism?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe balance between apoptosis susceptibility and efferocytosis of macrophages is central to plaque remodeling and inflammation. LRP-1 and its ligand, apolipoprotein E, have been implicated in efferocytosis and apoptosis in some cell types. We investigated the involvement of the macrophage LRP-1/apolipoprotein E axis in controlling plaque apoptosis and efferocytosis. Method and Results- LRP-1(-/-) macrophages displayed nearly 2-fold more TUNEL positivity compared to wild-type cells in the presence of DMEM alone or with either lipopolysaccharide or oxidized low-density lipoprotein. The survival kinase, phosphorylated Akt, was barely detectable in LRP-1(-/-) cells, causing decreased phosphorylated Bad and increased cleaved caspase-3. Regardless of the apoptotic stimulation and degree of cell death, LRP-1(-/-) macrophages displayed enhanced inflammation with increased IL-1 beta, IL-6, and tumor necrosis factor-alpha expression. Efferocytosis of apoptotic macrophages was reduced by 60% in LRP-1(-/-) vs wild-type macrophages despite increased apolipoprotein E expression by both LRP-1(-/-) phagocytes and wild-type apoptotic cells. Compared to wild-type macrophage lesions, LRP-1(-/-) lesions had 5.7-fold more necrotic core with more dead cells not associated with macrophages.\n\nQuestion:\nDoes macrophage LRP-1 control plaque cellularity by regulating efferocytosis and Akt activation?\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:\nEpileptogenesis is a hallmark of severe cortical trauma, with up to approximately 80% of patients experiencing seizures in the first 24 hours after penetrating head injury. An in vitro model of traumatic brain injury was developed to investigate hyperexcitability and epileptogenesis and their prevention. We determined whether sodium valproate would prevent epileptiform activity in this experimental model. Rat cortical slices were prepared and maintained in vitro using standard methods. Trauma was effected by removing the superficial 450-500 microm of slices. Traumatized slices were exposed to valproate at various time points. Intracellular and extracellular recordings were used to assess evoked activities. In untreated traumatized deep segments, hyperexcitability was manifested by depressed inhibition and often (54%) by epileptiform activity. Preparations exposed to valproate at 30 minutes or later after trauma showed abnormal activity similar to control traumatized slices. Epileptogenicity in deep segments was significantly reduced when slices were exposed to valproate (a) continuously immediately after trauma, (b) after a 20-minute delay, or (c) immediately after trauma for 1 hour and then returned to physiological solution. Finally, slices that were exposed to valproate or pentobarbital beginning 20 minutes after trauma for only 1 hour and then returned to physiological medium showed a significant reduction in abnormal activity. Valproate was found to enhance fast gamma-aminobutyric acid(A)-ergic inhibitory strength.\n\nQuestion:\nDoes valproate prevent epileptiform activity after trauma in an in vitro model in neocortical slices?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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