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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:\nClinical characteristics and control of the infection of patients with culture-negative (CN) prosthetic joint infection (PJI) have not been well assessed. Prior use of antimicrobial therapy has been speculated but not proven as a risk factor for CNPJI. We therefore determined whether prior use of antimicrobial therapy, prior PJI, and postoperative wound healing complications were associated with CN PJI. We performed a retrospective case-control study of 135 patients with CN PJI treated between January 1, 1985, and December 31, 2000 matched with 135 patients with culture-positive (CP) PJIs (control patients) during the study period. The time to failure of therapy compared between cases and control patients using a Kaplan-Meier analysis. The use of prior antimicrobial therapy and postoperative wound drainage after index arthroplasty were associated with increased odds of PJI being culture-negative (odds ratio, 4.7; 95% CI, 2.8-8.1 and odds ratio, 3.5; 95% CI, 1.5-8.1, respectively). The percent (+/- SE) cumulative incidence free of treatment failure at 2 years followup was similar for CN and CP PJI: 75% (+/- 4%) and 79% (+/- 4%), respectively.\n\nQuestion:\nIs prior use of antimicrobial therapy a risk factor for culture-negative prosthetic joint infection?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTaspine, isolated from Radix et Rhizoma Leonticis has demosntrated potential proctiective effects against cancer. Tas13D, a novel taspine derivative synthetized by structure-based drug design, have been shown to possess interesting biological and pharmacological activities. The current study was designed to evaluate its antiproliferative activity and underlying mechanisms. Antiproliferative activity of tas13D was evaluated by xenograft in athymic mice in vivo, and by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) and cell migration assays with human liver cancer (SMMC-7721) cell lines in vitro. Docking between tas13D and VEGFR and EGFR was studied by with a Sybyl/Surflex module. VEGF and EGF and their receptor expression was determined by ELISA and real-time PCR methods, respectively. Our present study showed that tas13D inhibited SMMC-7721 xenograft tumor growth, bound tightly with the active site of kinase domains of EGFR and VEGFR, and reduced SMMC-7721 cell proliferation (IC=34.7 μmol/L) and migration compared to negative controls. VEGF and EGF mRNAs were significantly reduced by tas13D treatment in a dose-dependent manner, along with VEGF and EGF production.\n\nQuestion:\nDoes tas13D inhibit growth of SMMC-7721 cell via suppression VEGF and EGF expression?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe COLIA1 gene is a strong candidate for susceptibility to osteoporosis. The causal genetic variants are currently unclear, but the most likely are functional polymorphisms in the promoter and intron 1 of COLIA1. The objective of the study was to determine whether promoter and intron 1 polymorphisms of COLIA1 or haplotypes defined by these polymorphisms regulate bone mineral density (BMD) in women. This was a population-based association study involving 3270 women from the United Kingdom who took part in a regional osteoporosis screening program. BMD at the lumbar spine (LS-BMD) and femoral neck (FN-BMD) was measured on two occasions approximately 6 yr apart, in relation to polymorphisms and haplotypes defined by polymorphisms within the COLIA1 intron 1 (+1245G/T; rs1800012) and promoter (-1997G/T; rs1107946; -1663IndelT; rs2412298). The polymorphisms were in strong linkage disequilibrium, and three haplotypes accounted for more than 95% of alleles at the COLIA1 locus. The individual polymorphisms were associated with BMD, but the most consistent associations were with haplotypes defined by all three polymorphisms. Homozygote carriers of haplotype 2 (-1997G/-1663delT/+1245T) had reduced BMD at baseline (P = 0.007 for LS-BMD; P = 0.008 for FN-BMD), whereas homozygotes for haplotype 3 (-1997T/-1663insT/+1245G) had increased BMD (P = 0.007 for LS-BMD). Similar associations were observed at follow-up for haplotype 3, but the association with haplotype 2 was weaker due to increased uptake of hormone replacement therapy in homozygotes for this haplotype.\n\nQuestion:\nDo haplotypes defined by promoter and intron 1 polymorphisms of the COLIA1 gene regulate bone mineral density in women?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe DNA repair enzyme O(6)-methylguanine DNA methyltransferase (MGMT) inhibits the killing of tumor cells by alkylating agents, and its loss in cancer cells is associated with hypermethylation of the MGMT CpG island. Thus, methylation of MGMT has been correlated with the clinical response to 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) in primary gliomas. Here, we investigate whether the presence of MGMT methylation in gliomas is also a good predictor of response to another emergent alkylating agent, temozolomide. Using a methylation-specific PCR approach, we assessed the methylation status of the CpG island of MGMT in 92 glioma patients who received temozolomide as first-line chemotherapy or as treatment for relapses. Methylation of the MGMT promoter positively correlated with the clinical response in the glioma patients receiving temozolomide as first-line chemotherapy (n = 40). Eight of 12 patients with MGMT-methylated tumors (66.7%) had a partial or complete response, compared with 7 of 28 patients with unmethylated tumors (25.0%; P = 0.030). We also found a positive association between MGMT methylation and clinical response in those patients receiving BCNU (n = 35, P = 0.041) or procarbazine/1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (n = 17, P = 0.043) as first-line chemotherapy. Overall, if we analyze the clinical response of all of the first-line chemotherapy treatments with temozolomide, BCNU, and procarbazine/1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea as a group in relation to the MGMT methylation status, MGMT hypermethylation was strongly associated with the presence of partial or complete clinical response (P < 0.001). Finally, the MGMT methylation status determined in the initial glioma tumor did not correlate with the clinical response to temozolomide when this drug was administered as treatment for relapses (P = 0.729).\n\nQuestion:\nDoes cpG island hypermethylation of the DNA repair enzyme methyltransferase predict response to temozolomide in primary gliomas?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nObesity is an increasing burden affecting developed and emerging societies since it is associated with an increased risk of diabetes and consequent cardiovascular complications. Increasing evidence points towards a pivotal role of inflammation in the etiology of vascular dysfunction. Our study aimed to investigate signs of inflammation and their relation to vascular dysfunction in rats receiving a high fat diet. Diet-induced obese (DIO) rats were used as a model since these rats exhibit a human pre-diabetic pathology. Oral glucose and insulin tolerance tests were conducted on DIO rats and their controls prior to the development of insulin resistance. Furthermore, the plasma contents of selected cytokines [macrophage chemoattractant protein (MCP-1), interleukin-6 (IL-6), and interleukin-1 (IL-1)] and the concentration of adiponectin were measured. Using wire myography, we tested the vascular function of isolated small mesenteric arteries. DIO animals had significantly (p < 0.05) increased body weight (721.2 ± 6.3 g) compared to age- and sex-matched controls (643.4 ± 14.6 g), as well as a significant increase (p < 0.01) in body fat percentage (29.7 ± 1.7% and 22.7 ± 0.97%, respectively). No significant difference in fasting plasma insulin levels could be detected between the two groups (chow-fed group 141.5 ± 15.1 pmol/l; high fat-fed group 125.9 ± 18.8 pmol/l). However, the levels of MCP-1 (89.7 ± 4.2 pg/ml vs. 60.8 ± 7.7 pg/ml) and IL-6 (61.6 ± 3.1 pg/ml vs. 41.6 ± 7.4 pg/ml) were significantly elevated in DIO animals (p < 0.05) as compared to controls. Adiponectin levels were also significantly increased (p < 0.01) in DIO rats (10.8 ± 0.7 ng/ml) versus controls (6.9 ± 0.5 ng/ml). No difference in vascular or endothelial function was evident as determined by responses to acetylcholine, sodium nitroprusside, endothelin-1, and calcitonin gene-related peptide.\n\nQuestion:\nDoes early onset inflammation in pre-insulin-resistant diet-induced obese rats affect the vasoreactivity of isolated small mesenteric arteries?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nDendritic cell activation through ligation of pattern recognition receptors leading to full functional maturation causes induction of CD8(+) T-cell immunity through increased delivery of costimulatory signals instead of tolerance. Here we investigate whether organ-resident antigen-presenting cells, such as liver sinusoidal endothelial cells (LSECs), also switch from tolerogenic to immunogenic CD8(+) T-cell activation upon such stimulation. Murine LSECs were isolated by immunomagnetic separation and analyzed for functional maturation upon triggering pattern recognition receptors or viral infection employing gene expression analysis and T cell coculture assays. In vivo relevance of the findings was confirmed with bone-marrow chimeric animals. LSECs expressed numerous pattern recognition receptors that allowed for sentinel function, but ligand-induced activation of these receptors was not sufficient to overcome tolerance induction of CD8(+) T cells. Importantly, viral infection with murine cytomegalovirus caused functional maturation of antigen-presenting LSECs and was sufficient to promote antigen-specific differentiation into effector CD8(+) T cells in the absence of dendritic cells and independent of CD80/86.\n\nQuestion:\nDo virally infected mouse liver endothelial cells trigger CD8+ T-cell immunity?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPatients with gastro-oesophageal reflux disease (GERD) frequently report excessive belching but it is not known what determines the severity of these complaints. To determine what causes troublesome belching symptoms in GERD patients. We included 90 consecutive patients who were referred for ambulatory 24-h pH-impedance measurement as part of the analysis of reflux symptoms. Overall severity of belching was reported by the patients using a 3-point scale. Furthermore, each belch perceived during the ambulatory measurement was reported by the patients using a symptom diary. No significant differences in frequency of gastric belches or combined liquid reflux and gastric belches were observed. However, the number of supragastric belches was significantly higher in patients with severe belching complaints compared to patients with moderate and none to mild complaints. Moreover, the number of supragastric belches which coincided with a liquid reflux episode was significantly higher in patients with severe complaints than in those with moderate and none to mild complaints. Per-patient analysis showed that belches coinciding with a liquid reflux event were more often symptomatic than isolated belches.\n\nQuestion:\nAre supragastric belches the main determinants of troublesome belching symptoms in patients with gastro-oesophageal reflux disease?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nDiabetes is considered a risk factor in the osseointegration of dental implants, which suggests that these patients might benefit from anabolic therapies. Preclinical studies, including investigations by this research group, revealed that intermittent administration of parathyroid hormone (PTH) stimulates bone formation on the surface of titanium implants under physiological conditions. However, the anabolic effect of PTH on osseointegration under the hyperglycemic condition of diabetes is unknown. The ability of PTH to stimulate osseointegration was investigated in 40 female Wistar rats that were randomly divided into the following treatment groups: diabetes, diabetes plus PTH, control, and control plus PTH. Diabetes was induced by intraperitoneal injection of streptozotocin (45 mg/kg) at 1 week before implantation. Rats received PTH at a dose of 60 μg/kg or a vehicle by subcutaneous injection starting at the day of implant insertion into the tibia. Histomorphometric analysis was performed after 4 weeks. The medullary peri-implant bone area significantly increased in rats receiving PTH in comparison with the control group (41±12% to 20±12%; P<0.01). Moreover, there was an increased bone-to-implant contact (BIC) area in animals treated with PTH (47±18% to 27±16%; P<0.05). In contrast, diabetic rats failed to benefit from the anabolic treatment. A similar peri-implant bone area occurred in the diabetes group, independent of treatment with PTH (13±9% to 15±6%; P>0.05). Moreover, PTH did not affect the BIC area under hyperglycemic conditions (16±12% to 16±8%; P>0.05). No significant changes were observed in the cortical compartment of all groups.\n\nQuestion:\nDoes intermittent parathyroid hormone fail to stimulate osseointegration in diabetic rats?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAs hypertension (HT) is one of the risk factors for lower urinary tract symptoms, we investigated the effect of an angiotensin II type I receptor blocker, olmesartan, on bladder dysfunction in the spontaneously hypertensive rat (SHR). Twelve-week-old male SHRs were administered perorally with olmesartan (0, 1, or 3 mg/kg/day) or nifedipine (30 mg/kg/day) for 6 weeks. Wistar rats were used as normotensive controls. The effects of olmesartan or nifedipine on blood pressure (BP), bladder blood flow (BBF), urodynamic parameters, tissue levels of malondialdehyde (MDA), nuclear factor erythroid 2-related factor 2 (Nrf2), and nerve growth factor (NGF) were measured in the bladder. Localization of 4-hydroxy-2-nonenal (4-HNE), Nrf2, and NGF in the bladder was shown by immunohistochemistry. The SHRs showed significant increase in BP, micturition frequency, and expression of MDA, 4-HNE, Nrf2, and NGF when compared to the control Wistar rats. Conversely, there was a decrease in BBF and single voided volume in SHRs when compared to Wistar rats. Treatment with olmesartan and nifedipine significantly improved BP. However, only olmesartan significantly ameliorated urodynamic parameters and oxidative damage compared to the non-treated SHR. The immunoreactivities of 4-HNE, Nrf2, and NGF in SHR urothelium and blood vessels were increased compared to the control. Treatment with a high dose of olmesartan decreased the expressions of 4-HNE, Nrf2, and NGF in the bladder.\n\nQuestion:\nDoes olmesartan ameliorate urinary dysfunction in the spontaneously hypertensive rat via recovering bladder blood flow and decreasing oxidative stress?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nVisfatin is an insulin-mimetic adipokine. In non-rheumatoid arthritis (RA) patients circulating levels of visfatin are correlated with the amount of visceral fat. Recent studies have disclosed an implication of visfatin in inflammation. Chronic systemic inflammation is of major importance in the development of atherosclerosis in RA. In the present study we investigated whether inflammation, obesity or metabolic syndrome are potential determinants of circulating visfatin concentrations in a group of RA patients on periodical treatment with the TNF-alpha blocker infliximab due to severe disease. We also assessed whether the infusion of infliximab may alter circulating visfatin concentrations in patients with severe RA. We investigated 33 non-diabetic patients with RA on periodical treatment with infliximab. Serum visfatin levels were determined immediately prior to and after infliximab infusion. There was no correlation between body mass index of RA patients and baseline serum level of visfatin. Also, no significant correlations between baseline visfatin levels and the age at the time of the study or at the onset of the disease, disease duration, ESR and CRP levels, DAS28, lipids, insulin sensitivity, resistin or the cumulative prednisone dose at the time of the study were found. Visfatin levels did not change upon infliximab infusion.\n\nQuestion:\nIs visfatin associated with inflammation or metabolic syndrome in patients with severe rheumatoid arthritis undergoing anti-TNF-alpha therapy?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nNewborns display distinct immune responses that contribute to susceptibility to infection and reduced vaccine responses. Toll-like receptor (TLR) agonists may serve as vaccine adjuvants, when given individually or in combination, but responses of neonatal leukocytes to many TLR agonists are diminished. TLR8 agonists are more effective than other TLR agonists in activating human neonatal leukocytes in vitro, but little is known about whether different TLR8 agonists may distinctly activate neonatal leukocytes. We characterized the in vitro immuno-stimulatory activities of a novel benzazepine TLR8 agonist, VTX-294, in comparison to imidazoquinolines that activate TLR8 (R-848; (TLR7/8) CL075; (TLR8/7)), with respect to activation of human newborn and adult leukocytes. Effects of VTX-294 and R-848 in combination with monophosphoryl lipid A (MPLA; TLR4) were also assessed. TLR agonist specificity was assessed using TLR-transfected HEK293 cells expressing a NF-κB reporter gene. TLR agonist-induced cytokine production was measured in human newborn cord and adult peripheral blood using ELISA and multiplex assays. Newborn and adult monocytes were differentiated into monocyte-derived dendritic cells (MoDCs) and TLR agonist-induced activation assessed by cytokine production (ELISA) and co-stimulatory molecule expression (flow cytometry). VTX-294 was ≈ 100x more active on TLR8- than TLR7-transfected HEK cells (EC50, ≈ 50 nM vs. ≈ 5700 nM). VTX-294-induced TNF and IL-1β production were comparable in newborn cord and adult peripheral blood, while VTX-294 was 1 log more potent in inducing TNF and IL-1β production than MPLA, R848 or CL075. Combination of VTX-294 and MPLA induced greater blood TNF and IL-1β responses than combination of R-848 and MPLA. VTX-294 also potently induced expression of cytokines and co-stimulatory molecules HLA-DR and CD86 in human newborn MoDCs.\n\nQuestion:\nDoes the ultra-potent and selective TLR8 agonist VTX-294 activate human newborn and adult leukocytes?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis study compared insulin lispro (IL) pharmacokinetics (PK) and pharmacodynamics (PD) delivered via microneedle intradermal (ID) injection with subcutaneous (SC) injection under euglycemic glucose clamp conditions. Ten healthy male volunteers were administered 10 international units (IU) of IL at 3 microneedle lengths (1.25, 1.50, or 1.75 mm) in a randomized, crossover fashion on Days 1-3 followed by a repetitive ID 1.5-mm microneedle dose (Day 4) and an SC dose (Day 5). Microneedle ID delivery resulted in more rapid absorption of IL, with decreased time to maximum insulin concentration (ID vs. SC: 36.0-46.4 vs. 64.3 min, P < 0.05) and higher fractional availability at early postinjection times. ID produced more rapid effects on glucose uptake with shorter times to maximal and early half-maximal glucose infusion rates (GIRs) (ID vs. SC: time to maximum GIR, 106-112 vs. 130 min, P < 0.05; early half-maximal GIR, 29-35 vs. 42 min), increased early GIR area under the curve (AUC), and faster offset of insulin action (shorter time to late half-maximal GIR: 271-287 vs. 309 min). Relative total insulin bioavailability (AUC to 360 min and AUC to infinite measurement) did not significantly differ between administration routes. ID PK/PD parameters showed some variation as a function of needle length. Delivery of ID IL was generally well tolerated, although transient, localized wheal formation and redness were observed at injection sites.\n\nQuestion:\nDoes intradermal microneedle delivery of insulin lispro achieve faster insulin absorption and insulin action than subcutaneous injection?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe aim of the study was to clinically and histologically evaluate the healing of human intrabony defects treated with open flap surgery (OFD) and application of a new, resorbable, fully synthetic, unsintered, nanocrystalline, phase-pure hydroxyapatite (nano-HA). Six patients, each of them displaying very advanced intrabony defects around teeth scheduled for extraction due to advanced chronic periodontitis and further prosthodontic considerations, were included in the study. Following local anaesthesia, mucoperiosteal flaps were reflected; the granulation tissue was removed, and the roots were meticulously debrided by hand and ultrasonic instruments. A notch was placed at the most apical extent of the calculus present on the root surface or at the most apical part of the defect (if no calculus was present) in order to serve as a reference for the histological evaluation. Following defect fill with nano-HA, the flaps were sutured by means of mattress sutures to allow primary intention healing. At 7 months after regenerative surgery, the teeth were extracted together with some of their surrounding soft and hard tissues and processed for histological analysis. The postoperative healing was uneventful in all cases. At 7 months following surgery, mean PPD reduction and mean CAL gain measured 4.0 ± 0.8 and 2.5 ± 0.8 mm, respectively. The histological analysis revealed a healing predominantly characterized by epithelial downgrowth. Limited formation of new cementum with inserting connective tissue fibers and bone regeneration occurred in three out of the six biopsies (i.e. 0-0.86 and 0-1.33 mm, respectively). Complete resorption of the nano-HA was found in four out of the six biopsies. A few remnants of the graft particles (either surrounded by newly formed mineralized tissue or encapsulated in connective tissue) were found in two out of the six biopsies.\n\nQuestion:\nDo histological evaluation of human intrabony periodontal defects treated with an unsintered nanocrystalline hydroxyapatite paste?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo evaluate the impact of surgery on gastrointestinal lymphoma. The Surveillance, Epidemiology, and End Results (SEER) database was queried from 1973 to 2005. A total of 17,222 cases of PGIL were identified. The overall incidence of PGIL was approximately 1.505 cases per 100,000. A significantly increasing incidence for PGIL was observed (APC = +4.67, P < 0.05). In the cases for which treatment data was available, resection occurred in roughly half of the patients. In univariate analysis, surgical extirpation did not improve survival (47 months vs. 76 months, P < 0.001), while radiation treatment improved median survival (77 months vs. 59 months, P < 0.001). Multivariate analysis revealed increasing age and male gender as independent predictors of decreased overall survival. Tumor location also was a significant predictor of outcome. Large B-cell lymphoma type PGIL had a poorer prognosis than marginal zone B-cell lymphoma. By multivariate analysis, surgery was not found to increase the risk of death (HR = 0.99).\n\nQuestion:\nDoes surgery adversely affect survival in primary gastrointestinal lymphoma?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCerebral white matter hyperintensities on magnetic resonance imaging (MRI) scans have been associated with vascular disease and late-life depression, both in the general population and in psychiatric patients. Therefore, a cerebrovascular etiology for late-onset depression has been hypothesized. However, longitudinal studies on the causal role of white matter hyperintensities in the development of depressive symptoms in elderly adults are lacking. To investigate the relation between white matter hyperintensities and depressive symptoms in elderly subjects at risk of cardiovascular disease. In the Dutch sample of the PROSPER (PROspective Study of Pravastatine in the Elderly at Risk of cardiovascular disease) cohort, 527 non-demented elderly, all aged 70 years or older, received a cranial MRI scan and the 15-item Geriatric Depression Scale, at baseline and 33 months (SD 1.6) later. Presence of white matter hyperintensities at baseline was not related to baseline depressive symptoms nor to the development of depressive symptoms during follow-up. Moreover, no association was found between progression of white matter lesion volume and progression of depressive symptoms.\n\nQuestion:\nIs progression of cerebral white matter lesions associated with development of depressive symptoms in elderly subjects at risk of cardiovascular disease : The PROSPER Study?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIntermediate early graft function is associated with increased incidence of graft loss and worse long-term graft function in kidney transplantation. Delayed graft function (DGF) is associated with premature graft loss, increased rate of allograft function decline, and greater incidence of acute rejection episodes (ARE). Regarding early intermediate graft function (IGF), these prognostic observations have not been clearly made. Our objective was to investigate the impact of IGF as compared with excellent graft function (EGF) on these outcomes. Retrospective analysis included all patients who underwent transplantation in a tertiary care center between 1989 and 2009. Definitions are as follows: DGF, need for dialysis in the first 7 days posttransplantation; EGF, serum creatinine (sCr) <3 mg/dL at 5 days posttransplantation; IGF, absence of dialysis need but with a sCr >3 mg/dL at 5 days posttransplantation. For univariate analysis we performed Student t test, Mann- Whitney test, or Chi-square test, as appropriate. For survival analysis we performed Kaplan-Meier method to determine survival curves and we used the log-rank test for comparison. Multivariate logistic regression analysis was used to determine independent predictors of IGF and of graft survival. Five hundred seventy patients were included: 69.0% had EGF, 22.6% had IGF, and 8.4% had DGF. Patients with IGF had worse graft survival at 5 and 10 years posttransplantation (75% vs 92% and 69% vs 85%, respectively; P < .001 for both comparisons) and higher incidence of ARE (41% vs 27%; P = .001), compared with EGF. In multivariate analysis, IGF was independently associated with an increased risk of graft loss compared with EGF (odds ratio [OR], 2.40; 95% confidence interval [CI], 1.32-4.35; P = .004]. Donor age (OR, 1.03 per year; 95% CI, 1.02-1.05; P < .001) was the strongest predictor of the occurrence of IGF. IGF was also associated with worse long-term graft function until 7 years posttransplantation (mean glomerular filtration rate [GFR] 48.3 ± 18.9 vs 57.4 ± 20.4 mL/min/1.73 m(2); P = .008).\n\nQuestion:\nIs intermediate early graft function associated with increased incidence of graft loss and worse long-term graft function in kidney transplantation?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe previously reported that 48 weeks of combination therapy with pegylated interferon-alpha2b (PEG-IFN-alpha2b) and adefovir dipivoxil (ADV) in patients with chronic hepatitis B led to marked decreases of hepatitis B virus (HBV) covalently closed circular DNA (cccDNA) (-2.4 log10 copies/ml). Combination therapy was followed by 96 weeks of ADV monotherapy. Here, we report on the final outcome after 144 weeks of sequential antiviral treatment. Twenty-four patients were analysed, triplet liver biopsies (taken at baseline, week 48 and week 144) were available from 16 patients. At week 144, 12/15 patients positive for hepatitis B virus e antigen (HBeAg) had lost HBeAg, alanine transaminase (ALT) levels were normal in 23 patients (96%), median serum HBV DNA had decreased by -4.9 log10 copies/ml and was undetectable (<100 copies/ml) in 11/24 individuals (46%). Median total intrahepatic HBV DNA had decreased by -2.2 log. Although no further significant cccDNA changes occurred between week 48 and week 144, two years of ADV monotherapy proved capable of controlling cccDNA levels in most patients. Analysis of intrahepatic HBV DNA species demonstrated that combination therapy with PEG-IFN-alpha2b and ADV inhibited viral productivity by 99% and subsequent ADV monotherapy by 76%, respectively. Virus suppression to undetectability within the first 12 weeks of treatment was strongly associated with long-term virological response and HBeAg and hepatitis B virus surface antigen HBsAg seroconversion. Histological improvement was determined in 11/16 patients at week 144. Two patients developed ADV resistance during the third year of treatment.\n\nQuestion:\nDoes sequential combination therapy lead to biochemical and histological improvement despite low ongoing intrahepatic hepatitis B virus replication?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSeveral case reports and clinical studies in the literature demonstrate needle track seeding after core needle biopsy in patients with breast cancer in up to 50% of cases. The impact of this observation on local recurrence and overall survival rate is, however, not fully investigated. We retrospectively analysed 719 patients after breast conserving surgery and postoperative radiotherapy for stage I and II breast cancer. We divided this group into patients with (189) and without (530) preoperative core needle biopsy. Demographic data, local recurrence and overall survival rate were compared between these two groups. Preoperative core needle biopsy did not significantly influence the local free recurrence rate (median follow-up time of 78 and 71 months, respectively). The prognostic factors and the postoperative therapy did not differ significantly between the two groups.\n\nQuestion:\nDoes preoperative core needle biopsy increase local recurrence rate in breast cancer patients?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe explain why traits of interest to behavioral scientists may have a genetic architecture featuring hundreds or thousands of loci with tiny individual effects rather than a few with large effects and why such an architecture makes it difficult to find robust associations between traits and genes. We conducted a genome-wide association study at 2 sites, Harvard University and Union College, measuring more than 100 physical and behavioral traits with a sample size typical of candidate gene studies. We evaluated predictions that alleles with large effect sizes would be rare and most traits of interest to social science are likely characterized by a lack of strong directional selection. We also carried out a theoretical analysis of the genetic architecture of traits based on R.A. Fisher's geometric model of natural selection and empirical analyses of the effects of selection bias and phenotype measurement stability on the results of genetic association studies. Although we replicated several known genetic associations with physical traits, we found only 2 associations with behavioral traits that met the nominal genome-wide significance threshold, indicating that physical and behavioral traits are mainly affected by numerous genes with small effects.\n\nQuestion:\nIs why it hard to find genes associated with social science traits : theoretical and empirical considerations?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nClassical effects of oestrogen involve activation of target genes after binding nuclear receptors. Oestrogenic effects too rapid for DNA transcription (non-genomic) are known to occur. The effect of oestrogen on colonic motility is unknown despite the prevalence of gastrointestinal symptoms in pregnant and premenopausal women. Histologically normal colon was obtained from proximal resection margins of colorectal carcinoma specimens. Circular smooth muscle strips were microdissected and suspended in organ baths under 1 g of tension. After equilibration, they were exposed to 17beta-oestradiol (n = 8) or bovine serum albumin (BSA)-conjugated 17beta-oestradiol (n = 8). Fulvestrant, an oestrogen receptor antagonist, was added to some baths (n = 8). Other strips were exposed to calphostin C or cycloheximide. Carbachol was added in increasing concentrations and contractile activity was recorded isometrically. Oestrogen inhibited colonic contractility (mean difference 19.7 per cent; n = 8, P < 0.001). In keeping with non-genomic, rapid-onset steroid action, the effect was apparent within minutes and reversible. It was observed with both 17beta-oestradiol and BSA-conjugated oestrogen, and was not altered by cycloheximide. Effects were inhibited by fulvestrant, suggesting receptor mediation.\n\nQuestion:\nDoes oestrogen inhibit human colonic motility by a non-genomic cell membrane receptor-dependent mechanism?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThrombotic thrombocytopenic purpura (TTP) and the hemolytic uremic syndrome (HUS) share many clinical features and have been difficult to separate into distinct entities. Histologic examination of organs from autopsied patients suggested that TTP and HUS have dissimilar lesions of different severity and distribution. To perform a retrospective observational review of autopsied patients with TTP or HUS to compare the nature and severity of the lesions found. To examine the pathologic features of these conditions, we reviewed all cases among 51 350 indexed autopsies at The Johns Hopkins Hospital (Baltimore, Md) diagnosed with TTP or HUS, and included those showing multiple arteriolar thrombi or their sequela. The 56 cases that met the inclusion criteria fell into 2 distinct groups, based on distribution and severity of arteriolar lesions. In 25 patients classified as having TTP, platelet-rich thrombi were present-in decreasing severity-in heart, pancreas, kidney, adrenal gland, and brain. In 31 patients with HUS, fibrin/red cell-rich thrombi were present, largely confined to the kidney and often severe, and only 6 cases showed pancreas involvement, 4 adrenal gland involvement, 2 brain involvement, and 1 heart involvement.\n\nQuestion:\nAre thrombotic thrombocytopenic purpura and hemolytic uremic syndrome distinct pathologic entities . A review of 56 autopsy cases?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe molecular mechanisms underlying stress urinary incontinence (SUI) are not clear. This study was conducted to evaluate molecular alterations in the urethras of mice with experimentally induced SUI. Eighteen virgin female mice were equally distributed into three groups as follows: two groups undergoing vaginal distension (VD) for 1 h with 3 mm and 8 mm dilators each, and a non-instrumented control group. Changes in leak point pressure (LPP), morphology, lysyl oxidase (LOX) expression and the metabolism of urethral connective tissue were assessed. The LPP was significantly decreased in the 3 mm and 8 mm VD groups compared with that in the control group. Collagen and elastin expression in the urethra was significantly decreased in the 8 mm VD group compared with that in the control group, while LOX expression was significantly enhanced.\n\nQuestion:\nDoes stress urinary incontinence following vaginal trauma involve remodeling of urethral connective tissue in female mice?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCortactin activates the actin-related 2/3 (Arp2/3) complex promoting actin polymerization to remodel cell architecture in multiple processes (e.g. cell migration, membrane trafficking, invadopodia formation etc.). Moreover, it was called the Achilles' heel of the actin cytoskeleton because many pathogens hijack signals that converge on this oncogenic scaffolding protein. Cortactin is able to modulate N-WASP activation in vitro in a phosphorylation-dependent fashion. Thus Erk-phosphorylated cortactin is efficient in activating N-WASP through its SH3 domain, while Src-phosphorylated cortactin is not. This could represent a switch on/off mechanism controlling the coordinated action of both nucleator promoting factors (NPFs). Pedestal formation by enteropathogenic Escherichia coli (EPEC) requires N-WASP activation. N-WASP is recruited by the cell adapter Nck which binds a major tyrosine-phosphorylated site of a bacterial injected effector, Tir (translocated intimin receptor). Tir-Nck-N-WASP axis defines the current major pathway to actin polymerization on pedestals. In addition, it was recently reported that EPEC induces tyrosine phosphorylation of cortactin. Here we demonstrate that cortactin phosphorylation is absent on N-WASP deficient cells, but is recovered by re-expression of N-WASP. We used purified recombinant cortactin and Tir proteins to demonstrate a direct interaction of both that promoted Arp2/3 complex-mediated actin polymerization in vitro, independently of cortactin phosphorylation.\n\nQuestion:\nDo distinct phosphorylation requirements regulate cortactin activation by TirEPEC and its binding to N-WASP?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis study was designed to assess whether a new method of cardiopulmonary resuscitation (CPR), termed active compression-decompression CPR, or ACD-CPR, improves organ perfusion when compared with standard (S) CPR in a dog model of ventricular fibrillation. ACD-CPR has recently been shown to improve hemodynamic and respiratory parameters during cardiac arrest when compared with standard CPR. However, to our knowledge, the effects of ACD-CPR on tissue perfusion have not been investigated. Ventricular fibrillation was induced in eight anesthetized, intubated animals. ACD-CPR and standard CPR were each performed twice in alternating order. All interventions were preceded by 1 min of ventricular fibrillation, in which no CPR was performed, and consisted of 6 min of CPR with either technique during which tissue perfusion was measured. Compressions were performed at 80/min with a 50 percent duty cycle and 175 to 200 N downward force applied to the chest wall for both techniques. Epinephrine was administered at the beginning of each 6-min CPR interval. Hemodynamic monitoring of aortic and right atrial pressure was performed continuously and myocardial, cerebral, and renal blood flows were measured using the radiolabeled microsphere technique at baseline and during all interventions. Baseline organ perfusion and hemodynamics were similar for all dogs. Baseline left ventricular, brain, and renal blood flows were 62.0 +/- 5.5, 14.1 +/- 2.1, and 476.3 +/- 55.5 ml/min/100 g, respectively (mean +/- SEM). Compared with standard CPR, ACD-CPR resulted in higher global left ventricular (22.5 +/- 6.2 vs 14.1 +/- 4.0 ml/min/100 g, p < 0.01), cerebral (12.0 +/- 2.4 vs 8.5 +/- 2.3 ml/min/100 g, p < 0.01), and renal cortical (27.8 +/- 5.0 vs 17.5 +/- 5.0 ml/min/100 g, p < 0.05) blood flows. Regional flows to the epicardium, endocardium, and midmyocardium as well as to the frontal, parietal, and occipital lobes of the brain were all significantly improved by ACD-CPR. Aortic systolic (61.7 +/- 4.1 vs 49.5 +/- 3.1 mm Hg, p < 0.01), aortic mean (31.6 +/- 2.8 vs 27.2 +/- 2.2 mm Hg, p = 0.001), and myocardial perfusion pressure (12.9 +/- 3.4 vs 10.4 +/- 3.4 mm Hg, ACD-CPR vs standard CPR, p < 0.01) were all higher during ACD-CPR than during standard CPR.\n\nQuestion:\nDoes active compression-decompression CPR improve vital organ perfusion in a dog model of ventricular fibrillation?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe tested the hypothesis that ventilation in the prone position might improve homogenization of tidal ventilation by reducing time-constant inequalities, and thus improving alveolar ventilation. We have recently reported in ARDS patients that these inequalities are responsible for the presence of a \"slow compartment,\" excluded from tidal ventilation at supportive respiratory rate. In 11 ARDS patients treated by ventilation in the prone position because of a major oxygenation impairment (PaO(2)/FIO(2)</=100 mm Hg) we studied mechanical and blood gas changes produced by a low PEEP (6+/-1 cm H(2)O), ventilation in the prone position, and the two combined. Ventilation in the prone position significantly reduced the expiratory time constant from 1.98+/-0.53 s at baseline with ZEEP to 1.53+/-0.34 s, and significantly decreased PaCO(2) from 55+/-11 mm Hg at baseline with ZEEP to 50+/-7 mm Hg. This improvement in alveolar ventilation was accompanied by a significant improvement in respiratory system mechanics, and in arterial oxygenation, the latter being markedly increased by application of a low PEEP (PaO(2)/FIO(2) increasing from 64+/-19 mm Hg in supine position with ZEEP to 137+/-88 mm Hg in prone with a low PEEP).\n\nQuestion:\nDoes prone position improve mechanics and alveolar ventilation in acute respiratory distress syndrome?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe spatial relationship of glioblastoma (GBM) to the subventricular zone (SVZ) is associated with inferior patient survival. However, the underlying molecular phenotype is largely unknown. We interrogated an SVZ-dependent transcriptome and potential location-specific prognostic markers. mRNA microarray data of a discovery set (n = 36 GBMs) were analyzed for SVZ-dependent gene expression and process networks using the MetaCore™ workflow. Differential gene expression was confirmed by qPCR in a validation set of 142 IDH1 wild-type GBMs that was also used for survival analysis. Microarray analysis revealed a transcriptome distinctive of SVZ+ GBM that was enriched for genes associated with Notch signaling. No overlap was found to The Cancer Genome Atlas's molecular subtypes. Independent validation of SVZ-dependent expression confirmed four genes with simultaneous prognostic impact: overexpression of HES4 (p = 0.034; HR 1.55) and DLL3 (p = 0.017; HR 1.61) predicted inferior, and overexpression of NTRK2 (p = 0.049; HR 0.66) and PIR (p = 0.025; HR 0.62) superior overall survival (OS). Additionally, overexpression of DLL3 was predictive of shorter progression-free survival (PFS) (p = 0.043; HR 1.64). Multivariate analysis revealed overexpression of HES4 to be independently associated with inferior OS (p = 0.033; HR 2.03), and overexpression of DLL3 with inferior PFS (p = 0.046; HR 1.65).\n\nQuestion:\nDoes spatial transcriptome analysis reveal Notch pathway-associated prognostic markers in IDH1 wild-type glioblastoma involving the subventricular zone?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSome polyphenols possess anti-allergic activities. Naringenin chalcone is one of the polyphenols that is present in the skin of red tomatoes. In this study, we investigated the effect of naringenin chalcone in allergic responses in vivo using an experimental mouse model system of allergic asthma. Allergic airway inflammation was induced in mice by sensitization and challenge with ovalbumin. Naringenin chalcone was orally administrated every day during the course of the experiment. Airway hyperreactivity, the eosinophilic infiltration in the bronchioalveolar lavage fluid and Th2 cytokine production from splenic CD4 T cells were assessed. Eosinophilic airway inflammation, airway hyperreactivity and Th2 cytokine production from CD4 T cells were significantly suppressed in mice that were treated with naringenin chalcone. Hyperproduction of mucus was slightly reduced.\n\nQuestion:\nDoes naringenin chalcone suppress allergic asthma by inhibiting the type-2 function of CD4 T cells?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe compared two rapid MR imaging T2-weighted pulse sequences with high-resolution turbo spin-echo for the diagnosis of adenomyosis, and we evaluated interobserver variability. Fifty-six consecutive patients referred for hysterectomy prospectively underwent MR imaging. Two fast pulse sequences using a breath-hold technique-true fast imaging with steady-state free precession (FISP) and turbo inversion recovery-and turbo spin-echo T2-weighted images of the pelvis were obtained in each patient. The images were analyzed in a blinded manner and independently by three reviewers with different levels of experience for the accuracy of adenomyosis diagnosis, image quality, anatomic visualization, and image artifacts. The accuracy for the diagnosis of adenomyosis on turbo spin-echo T2-weighted imaging combined with one or two fast pulse sequences was evaluated for each reviewer. Twenty-four patients (42.9%) had a histologic diagnosis of adenomyosis. The accuracy for the diagnosis of adenomyosis for reviewers 1, 2, and 3 using turbo spin-echo T2-weighted, true FISP, and turbo inversion recovery sequences was 83.9%, 67.8%, 75%; 83.9%, 67.8, 78.5%; and 87.5%, 73.2%, and 75%, respectively. A difference in the accuracy rate was found among the observers for the three sequences (p < 0.001). Whatever the pulse sequence, the accuracy rate was higher for the reviewer with more experience in gynecologic imaging. The combination of turbo spin-echo T2-weighted imaging with at least one rapid sequence increased the accuracy of observers with little experience in gynecology. With turbo inversion recovery sequences, the image quality score was low for the three reviewers compared with turbo spin-echo T2-weighted and true FISP sequences. The combination of turbo spin-echo T2-weighted and true FISP sequences gave the highest image quality scores.\n\nQuestion:\nDoes fast breath-hold T2-weighted MR imaging reduce interobserver variability in the diagnosis of adenomyosis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo study whether N-terminal probrain natriuretic peptide (NT-proBNP) is a short-term independent predictor of both all-cause and cardiovascular (CV) mortality in type 2 diabetic patients and to establish whether albuminuria and C-reactive protein (CRP) affect this relationship. The prospective study included 1,825 type 2 diabetic patients from the population-based cohort of the Casale Monferrato study. CV risk factors, preexisting CVD, and NT-proBNP levels were evaluated at baseline. All-cause and CV mortality were assessed 5.5 years after baseline examination. Multivariate Cox proportional hazards modeling was used to estimate mortality hazard ratios (HRs). During the follow-up period, 390 people died (175 for CVD) out of 9,101 person-years of observations. A significantly increased mortality risk by quartiles of NT-proBNP was observed (test for trend, P < 0.001). NT-proBN P values >91 pg/mL conferred HRs of 2.05 (95% CI 1.47-2.86) for all-cause and 4.47 (2.38-8.39) for CV mortality, independently of CV risk factors, including CRP and albumin excretion rate (AER). The association was also significant for modest rises in NT-proBNP levels and in patients without microalbuminuria and CVD at baseline (upper quartiles HRs 3.82 [95% CI 1.24-13.75]) and 3.14 [1.00-9.94]). Albuminuria and NT-proBNP had an additive effect on mortality, though the association was stronger for NT-proBNP.\n\nQuestion:\nIs n-terminal probrain natriuretic peptide a stronger predictor of cardiovascular mortality than C-reactive protein and albumin excretion rate in elderly patients with type 2 diabetes : the Casale Monferrato population-based study?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nVascular and valvular calcifications are a common finding in chronic kidney disease (CKD) patients and are associated with increased morbidity and mortality. We investigated the hypothesis that calcification of the cardiac valves is a marker of coronary artery calcification (CAC) and thoracic aorta calcification (AoC) in hemodialysis (CKD-5) patients. This was a cross-sectional study of 145 maintenance CKD stage 5 (CKD-5) patients. All patients underwent electron beam tomography for quantification of CAC and AoC score via the Agatston score. The presence of calcification of the cardiac valves was assessed by standard bi-dimensional echocardiography. Eighty-four of the study patients (58%) had echocardiographic evidence of valvular calcification. A significant and graded association between valvular calcification and CAC as well as AoC was detected. Patients with 1 or 2 calcified valves had a significantly greater likelihood of having a CAC score >1,000 (odds ratio [OR] = 5.94; 95% confidence interval [95% CI], 1.91-18.44; p=0.002; and OR=3.27; 95%CI, 1.36-7.88; p=0.007, respectively). Similarly, the presence of 1 or 2 calcified valves was associated with an eightfold and threefold increased probability of an AoC score greater than the third quartile, respectively.\n\nQuestion:\nIs cardiac valve calcification a marker of vascular disease in prevalent hemodialysis patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAlthough it is known that Müller cells express the glial fibrillary acidic protein (GFAP) in response to acute retinal damage, the regulatory mechanism is not completely understood. α(2)-Macroglobulin (α(2)M) and its receptor, low-density lipoprotein receptor-related protein 1 (LRP1), have also been found in injured retinas. Herein, the authors examined the involvement of the α(2)M/LRP1 system in GFAP expression in Müller cells using in vitro and in vivo experimental models. Using Western blot analysis and immunocytochemistry, the authors evaluated the effect of α(2)M* on GFAP expression in the Müller cell line MIO-M1, which constitutively expresses LRP1. Intracellular signaling pathways activated by α(2)M* were examined by Western blot analysis. The effect of α(2)M* on GFAP expression in the mouse retina was examined by intravitreal microinjection of α(2)M* in mouse eyes. These data demonstrate that α(2)M* induced GFAP expression in the MIO-M1 cell line, which was selectively blocked by RAP, an antagonist of LRP1 binding ligands. In addition, α(2)M* induced JAK/STAT pathway activation, determined by STAT3 phosphorylation (p-STAT3), which was also blocked by RAP. Finally, the authors showed that GFAP was expressed in the retinas of mice, preferentially in Müller cells at 3 and 6 days after a single intravitreal α(2)M* injection, whereas p-STAT3 staining increased at day 1 in both the ganglion cell layer and the inner nuclear layer.\n\nQuestion:\nDoes alpha2-Macroglobulin induce glial fibrillary acidic protein expression mediated by low-density lipoprotein receptor-related protein 1 in Müller cells?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTissue organization during embryonic development and wound healing depends on the ability of cells on the one hand to exchange adhesive bonds during active rearrangement and on the other to become fixed in place as tissue homeostasis is reached. Cells achieve these contradictory tasks by regulating either cell-cell adhesive bonds, mediated by cadherins, or cell-extracellular matrix (ECM) connections, regulated by integrins. Integrin alpha5beta1 and soluble fibronectin (sFN) are key players in cell-ECM force generation and in ECM polymerization. Here, we explore the interplay between integrin alpha5beta1 and sFN and its influence on tissue mechanical properties and cell sorting behavior. We generated a series of cell lines varying in alpha5beta1 receptor density. We then systematically explored the effects of different sFN concentrations on aggregate biomechanical properties using tissue surface tensiometry. We found previously unreported complex behaviors including the observation that interactions between fibronectin and integrin alpha5beta1 generates biphasic tissue cohesion profiles. Specifically, we show that at constant sFn concentration, aggregate cohesion increases linearly as alpha5beta1 receptor density is increased from low to moderate levels, producing a transition from viscoelastic-liquid to pseudo viscoelastic-solid behavior. However, further increase in receptor density causes an abrupt drop in tissue cohesion and a transition back to viscoelastic-liquid properties. We propose that this may be due to depletion of sFn below a critical value in the aggregate microenvironment at high alpha5beta1 levels. We also show that differential expression of alpha5beta1 integrin can promote phase-separation between cells.\n\nQuestion:\nDo alpha5beta1 integrin-fibronectin interactions specify liquid to solid phase transition of 3D cellular aggregates?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe pathogenesis of immune dysfunction in chronic HIV-1 infection is unclear, and a potential role for oxidized lipids has been suggested. We hypothesize that both oxidized HDL and LDL (HDLox and LDLox) contribute to HIV-1-related immune dysfunction. In the AIDS Clinical Trials Group A5260, 234 HIV-infected antiretroviral therapy (ART)-naive participants were randomized to receive tenofovir-emtricitabine and protease inhibitors or raltegravir and had HIV-1 RNA less than 50 copies/ml by week 24 and thereafter. Associations between biomarkers of inflammation (IL-6, high-sensitivity C-reactive protein and D-dimer), immune activation (sCD163, sCD14, soluble IL-2 receptor, CD38 and HLA-DR), inflammatory monocytes (CD14CD16), T-cell senescence (CD28 and CD57) and exhaustion (PD1), and HDLox, LDLox were assessed at entry and after ART (week 96) with Spearman (partial) correlations. HDLox declined and LDLox increased over 96 weeks of ART. Positive associations were observed at baseline and over time between HDLox (but not consistently for LDLox) and most markers of inflammation and immune activation (but not senescence/exhaustion), even after adjustment for multiple comparisons, demographics, entry CD4 cell count and HIV-1 RNA. HDLox was positively associated with IL-6 (r = 0.19 - 0.29, P < 0.01) and sCD163 (r = 0.14 - 0.41, P ≤ 0.04) at all time points.\n\nQuestion:\nAre oxidized lipoproteins associated with markers of inflammation and immune activation in HIV-1 infection?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMalaria and human immunodeficiency virus (HIV) infection during pregnancy affect the transplacental transfer of antibodies against several pathogens from mother to fetus, although the effect of malaria and HIV infection on the transfer of antimalarial antibodies remains unclear. Levels of total immunoglobulin G (IgG), immunoglobulin M (IgM), and IgG subtypes against the following Plasmodium falciparum antigens were measured in 187 pairs of mother-cord plasma specimens from Mozambique: 19-kDa fragment of merozoite surface protein 1 (MSP119), erythrocyte binding antigen 175 (EBA175), apical membrane antigen 1 (AMA1), and parasite lysate. Placental antibody transfer was defined as the cord-to-mother ratio (CMR) of antibody levels. Maternal malaria was associated with reduced CMR of EBA175 IgG (P = .014) and IgG1 (P = .029), AMA1 IgG (P = .002), lysate IgG1 (P = .001), and MSP1 IgG3 (P = .01). Maternal HIV was associated with reduced CMR of MSP1 IgG1 (P = .022) and IgG3 (P = .023), lysate IgG1 (P = .027) and IgG3 (P = .025), AMA1 IgG1 (P = .001), and EBA175 IgG3 (P = .001). Decreased CMR was not associated with increased adverse pregnancy outcomes or augmented risk of malaria in the infant during the first year of life.\n\nQuestion:\nAre malaria and HIV infection in Mozambican pregnant women associated with reduced transfer of antimalarial antibodies to their newborns?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAngiotensin II (Ang II) is a potent stimulus of vascular smooth muscle cell (VSMC) growth. Activation of extracellular signal-regulated kinase (ERK), the archetypal mitogen-activated protein (MAP) kinase, and phosphatidylinositol 3 (PI3) kinase are critical steps in Ang II-induced mitogenic signaling. However, the mechanism involved in the activation of these kinases upon binding of Ang II to its receptor is poorly understood. In the present study, we examined the role of the epidermal growth factor receptor (EGFR) in Ang II signaling in VSMCs employing immunoprecipitation, Western blot analysis, kinase immunocomplex assay, and [3H]-thymidine incorporation. A time-dependent tyrosine phosphorylation of the EGFR in response to Ang II was observed that was mediated by the Ang II type 1 receptor. This transactivation of the EGFR was blocked in the presence of PP1, an inhibitor of the intracellular Src-like tyrosine kinases. The tyrphostin AG 1478, a selective EGFR antagonist, inhibited both Ang II- and EGF-induced tyrosine phosphorylation of the EGFR. Furthermore, Ang II induced the binding of the adaptor protein Shc to the EGFR, leading to phosphorylation of Shc. In addition, the same nanomolar concentrations of AG 1478 that were effective in EGF signaling blocked the Ang II-induced activation of ERK and PI3 kinase in a dose-dependent manner. Proliferation of VSMCs, detected by measurements of DNA synthesis, following stimulation with Ang II was potently inhibited in the presence of AG 1478 or PP1.\n\nQuestion:\nDoes angiotensin II-induced growth of vascular smooth muscle cells require an Src-dependent activation of the epidermal growth factor receptor?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWith the increased use of nanoparticles in biomedical applications there is a growing need to understand the effects that nanoparticles may have on cell function. Identifying these effects and understanding the mechanism through which nanoparticles interfere with the normal functioning of a cell is necessary for any therapeutic or diagnostic application. The aim of this study is to evaluate if gold nanoparticles can affect the normal function of neurons, namely their activity and coding properties. We synthesized star shaped gold nanoparticles of 180 nm average size. We applied the nanoparticles to acute mouse hippocampal slices while recording the action potentials from single neurons in the CA3 region. Our results show that CA3 hippocampal neurons increase their firing rate by 17% after the application of gold nanostars. The increase in excitability lasted for as much as 50 minutes after a transient 5 min application of the nanoparticles. Further analyses of the action potential shape and computational modeling suggest that nanoparticles block potassium channels responsible for the repolarization of the action potentials, thus allowing the cell to increase its firing rate.\n\nQuestion:\nDoes transient extracellular application of gold nanostars increase hippocampal neuronal activity?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo investigate the relationship between blood riboflavin levels and riboflavin transporter 2 (RFT2) gene expression in gastric carcinoma (GC) development. High-performance liquid chromatography was used to detect blood riboflavin levels in patients with GC. Real-time fluorogenic quantitative polymerase chain reaction and immunohistochemistry were used to analyze the expression of RFT2 mRNA and protein in samples from 60 GC patients consisting of both tumor and normal tissue. A significant decrease in the RFT2 mRNA levels was detected in GC samples compared with those in the normal mucous membrane (0.398 ± 0.149 vs 1.479 ± 0.587; P = 0.040). Tumors exhibited low RFT2 protein expression (75%, 16.7%, 8.3% and 0% for no RFT2 staining, weak staining, medium staining and strong staining, respectively), which was significantly lower than that in the normal mucous membrane (10%, 16.7%, 26.7% and 46.7% for no RFT2 staining, weak staining, medium staining and strong staining, respectively; P < 0.05). Tumors with low RFT2 expression were significantly associated with tumor stage and histological grade. Moreover, a significantly decrease in Uyghur patients was observed compared with Han patients. However, other parameters-gender, tumor location and lymph node metastasis-showed no significant relationship with RFT2 expression. Blood riboflavin levels were reverse correlated with development of GC (1.2000 ± 0.97569 ng/mL in high tumor stage patients vs 2.5980 ± 1.31129 ng/mL in low tumor stage patients; P < 0.05). A positive correlation of plasma riboflavin levels with defective expression of RFT2 protein was found in GC patients (χ² = 2.619; P = 0.019).\n\nQuestion:\nAre decreased blood riboflavin levels correlated with defective expression of RFT2 gene in gastric cancer?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe aimed to investigate relationship between gamma glutamyl transferase (GGT) activity with paraoxonase 1 (PON1) activity and aortic stiffness (AS) parameters such as pulse wave velocity (PWV) and augmentation index (AIx). Measurements were obtained from 324 patients with newly diagnosed essential hypertension (mean age: 55.0 ± 8.2 years). The patients were divided into two groups according to their median GGT values. PWV and AIx were calculated using the single-point method via the Mobil-O-Graph® ARCsolver algorithm. PWV, Aix, and high-sensitive C-reactive protein (hs-CRP) values were higher and PON1 activity values were lower in GGThigh group compared with GGTlow group (P < 0.05, for all). Multiple linear regression analysis showed that GGT activity was independently associated with PWV (β = 0.496, P < 0.001) and PON1 activity (β = -0.343, P < 0.001) as well as hs-CRP (β = 0.334, P < 0.001).\n\nQuestion:\nIs gamma Glutamyl Transferase Activity Associated With Both Paraoxonase Activity and Aortic Stiffness in Hypertensive Patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis article reports our preliminary observation regarding the diagnostic ability of dynamic helical biphasic computed tomography (CT) for proximal arterioportal shunting in hepatoma patients as compared with that of conventional angiography. Three hundred and sixty patients with clinically-suspected liver lesions received both dynamic helical biphasic CT scan and conventional angiography of the liver. The criteria for diagnosis of proximal arterioportal (AP) shunting in dynamic helical biphasic CT included early and strong enhancement of main portal vein or its major branches approaching the density of the aorta, or enhancement of the portal vein earlier than opacification of the splenic vein and superior mesenteric vein in the arterial phase. The angiographic diagnosis of proximal AP shunting was made if there was early opacification of the main portal vein or its major branches in the arterial phase. Peripheral subsegmental small AP shunting was excluded from our study. The existence and extent of AP shunting were compared in these two imaging modalities. Dynamic helical biphasic CT scan demonstrated proximal AP shunting in 23 patients. All of these patients harbored hepatoma. Conventional angiography showed proximal AP shunting in 20 patients, which were all positive on dynamic helical CT. Dynamic helical biphasic CT demonstrated the presence of proximal AP shunting in 3 more patients than conventional angiography did. The extent of AP shunting was well correlated between these two imaging modalities in 17 patients.\n\nQuestion:\nDoes dynamic helical biphasic CT emerge as a potential tool for the diagnosis of proximal arterioportal shunting?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nBivalirudin, a direct thrombin inhibitor, is a widely used adjunctive therapy in patients undergoing percutaneous intervention (PCI). Thrombin is a highly potent agonist of platelets and activates the protease-activated receptors, PAR1 and PAR4, but it is not known whether bivalirudin exerts antiplatelet effects in PCI patients. We tested the hypothesis that bivalirudin acts as an antiplatelet agent in PCI patients by preventing activation of PARs on the platelet surface. The effect of bivalirudin on platelet function and systemic thrombin levels was assessed in patients undergoing elective PCI. Mean plasma levels of bivalirudin were 2.7±0.5 μmol/L during PCI, which correlated with marked inhibition of thrombin-induced platelet aggregation and significantly inhibited cleavage of PAR1. Unexpectedly, bivalirudin also significantly inhibited collagen-platelet aggregation during PCI. Collagen induced a conversion of the platelet surface to a procoagulant state in a thrombin-dependent manner that was blocked by bivalirudin. Consistent with this result, bivalirudin reduced systemic thrombin levels by >50% during PCI. Termination of the bivalirudin infusion resulted in rapid clearance of the drug with a half-life of 29.3 minutes.\n\nQuestion:\nIs bivalirudin a dual inhibitor of thrombin and collagen-dependent platelet activation in patients undergoing percutaneous coronary intervention?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nRecent studies have shown that an increased bleeding tendency can be caused by Selective Serotonin Reuptake Inhibitors (SSRI) use. We aimed to investigate the occurrence and risk of blood transfusion in SSRI users compared to non-SSRI users in a cohort of patients admitted for hip-surgery. We conducted a retrospective cohort study of patients who underwent planned or emergency hip surgery from 1996 to 2011 in the Academic Medical Center in Amsterdam. Primary outcome measure was risk of blood transfusion. Secondary outcome measures were pre- and postoperative hemoglobin level. Multivariate logistic regression was used to adjust for potential confounders. One-hundred and fourteen SSRI users were compared to 1773 non-SSRI users. Risk of blood transfusion during admission was increased for SSRI users in multivariate analyses (OR 1.7 [95% CI 1.1-2.5]). Also, pre-operative hemoglobin levels were lower in SSRI users (7.8 ± 1.0 mmol/L) compared to non-SSRI users (8.0 ± 1.0 mmol/L) (p  =  0.042)), as were postoperative hemoglobin levels (6.2 ± 1.0 mmol/L vs. 6.4 ± 1.0 mmol/L respectively) (p  =  0.017)).\n\nQuestion:\nDo sSRIs increase risk of blood transfusion in patients admitted for hip surgery?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIn adults, pencil-point spinal needles are believed to be less traumatic and therefore to be superior compared to cutting-point needles with respect to success rate and postpuncture complications. The aim of this randomised, parallel groups and prospective study was to record the success rate and to evaluate the incidence of complications following spinal anaesthesia with the two types of needles in children. We studied 215 children aged 1 to 18 years. A 25-gauge needle was used in children up to 7 years (n=96) and a 27-gauge needle in older children (n=119). During lumbar puncture with either a cutting-point (n=109) or a pencil-point (n=106) spinal needle, we recorded puncture characteristics and the success of cerebrospinal fluid (CSF) aspiration. Hyperbaric bupivacaine 5 mg ml(-1) at a dose of 0.3-0.4 mg kg(-1) was used for the spinal anaesthesia. The incidence of postdural puncture complications was recorded from diaries completed by the children and parents one week after the lumbar puncture. The success rate of the spinal anaesthesia was 97% without difference between the needles. The success rate was higher when the aspiration of CSF was easy compared to if it was difficult (98% vs. 88%, P=0.02). Two hundred and seven diaries were returned (97%). Twenty-four children developed a headache, 8 of which were classified as a postdural puncture headache (PDPH), 6 with the cutting-point needle and 2 with the pencil-point needle (n.s.). Nine children developed signs of transient radicular irritation with no difference between the needles.\n\nQuestion:\nDoes needle design affect the success rate of spinal anaesthesia or the incidence of postpuncture complications in children?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCerebral white matter lesions (WML) are known to increase with age, as is left ventricular (LV) diastolic dysfunction with normal contraction. Although aging is a common risk factor, the link between these diseases is not fully understood. The aim was to clarify this relationship, using the ratio between early diastolic mitral inflow and early diastolic mitral annular tissue velocity (E/E'). E/E' measured by tissue Doppler echocardiography offers an indicator of the severity of LV diastolic dysfunction, reflecting both diastolic LV stiffness and diastolic LV filling pressure. Participants comprised 75 patients aged between 65 and 75 years with normal LV contraction and no signs or history of symptomatic heart failure, ischemic heart diseases, atrial fibrillation, stroke, or cognitive dysfunction. The volume of WML was quantified on brain magnetic resonance imaging. The participants were classified into three groups: Low E/E', E/E' ≤ 8; Middle E/E', 8 < E/E' < 15; and High E/E', E/E' ≥ 15. WML volume was 3.6 ± 3.0 mL in Low E/E', 5.4 ± 6.5 mL in Middle E/E' and 12.0 ± 11.0 mL in High E/E', increasing significantly with increased diastolic LV stiffness (Low vs High, P = 0.034; Middle vs High, P = 0.016). Linear regression analysis showed the positive association between the volume of WML and E/E' ratio (r = 0.377, P = 0.0009).\n\nQuestion:\nIs left ventricular diastolic dysfunction associated with cerebral white matter lesions ( leukoaraiosis ) in elderly patients without ischemic heart disease and stroke?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe sought to determine the etiologic mechanism of proinflammatory cytokine, interleukin-6 (IL-6), and statin as regulators of synthesis of plasminogen activator inhibitor-1 (PAI-1), the physiological fibrinolysis inhibitor and an acute-phase reactant. Transient transfection and luciferase assay in HepG2 human hepatoma-derived cells demonstrated that IL-6 increased PAI-1 promoter activity and mevastatin decreased IL-6-inducible response. Systematic deletion assay of the promoter demonstrated that the region (-239 to -210 bp) containing a putative CCAAT/enhancer-binding protein (C/EBP) binding site was necessary. Point mutation in this site abolished the IL-6-inducible response. Electrophoretic mobility shift assay and chromatin immunoprecipitation assay demonstrated that C/EBPalpha, C/EBPbeta, and C/EBPdelta were involved in protein-DNA complex formation in intact cells. Deoxyribonuclease (DNase) I footprinting analysis revealed that 5' flanking region (-232 to -210 bp) is acute-phase response protein-binding site. C/EBPdelta binding activity was increased by IL-6 and attenuated by mevastatin. Mevastatin attenuated IL-6-mediated increase of C/EBPdelta protein in the nuclear extracts. IL-6 also increased PAI-1 and C/EBPdelta mRNA in mouse primary hepatocytes.\n\nQuestion:\nDo interleukin-6 and mevastatin regulate plasminogen activator inhibitor-1 through CCAAT/enhancer-binding protein-delta?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nRestenosis is an undesirable consequence following percutaneous vascular interventions. However, the current strategy for preventing restenosis is inadequate. The aim of this study was to investigate the role of low-voltage gated T-type calcium channels in regulating vascular smooth muscle cell (VSMC) proliferation during neointimal formation. Wire injury of mice carotid arteries resulted in neointimal formation in the wild-type and Ca(v)3.2(-/-) but not Ca(v)3.1(-/-) mice, indicating a critical role of Ca(v)3.1 in neointimal formation. In addition, we found a significant increase of Ca(v)3.1 mRNA and protein in injured arteries. Ca(v)3.1 knockout or knockdown (shCa(v)3.1) reduced VSMC proliferation. Since T-channels are expressed predominantly in the G(1) and S phases in VSMCs, we examined whether an abnormal G(1)/S transition was the cause of the reduced cell proliferation in shCa(v)3.1 VSMCs. We found a disrupted expression of cyclin E in shCa(v)3.1 VSMCs, and calmodulin agonist CALP1 partially rescued the defective cell proliferation. Furthermore, we demonstrated that infusion of NNC55-0396, a selective T-channel blocker, inhibited neointimal formation in wild-type mice.\n\nQuestion:\nIs the Ca ( v ) 3.1 T-type calcium channel required for neointimal formation in response to vascular injury in mice?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nStatins (hydroxymethylglutaryl coenzyme A reductase inhibitors) are effective in reducing the risk of cardiovascular morbidity and mortality in patients with hyperlipidemia, hypertension, or type II diabetes. Next to their cholesterol-lowering activity, statins have immunomodulatory properties. Based on these properties, we hypothesized that statin use may eventually lead to dysregulation of immune responses, possibly resulting in autoimmunity. We have recently shown in an observational study that statin use was associated with an increased risk of developing rheumatoid arthritis. Our objective was to investigate whether a causal relationship could be established for this finding. The mouse collagen type II (CII)-induced arthritis (CIA) model was used, with immunization, challenge, and euthanasia at days 0, 21, and 42, respectively. Statins were given orally before (day -28 until day 21) or after (day 21 until day 42) CIA induction. Atorvastatin (0.2 mg/day) or pravastatin (0.8 mg/day) was administered. Arthritis was recorded three times a week. Serum anti-CII autoantibodies and cytokines in supernatants from Concanavalin-A-stimulated lymph node cells and CII-stimulated spleen cells were measured. Statin administration accelerated arthritis onset and resulted in 100% arthritic animals, whereas only seven out of 12 nonstatin control animals developed arthritis. Atorvastatin administration after CIA induction resulted in earlier onset than atorvastatin administration before induction, or than pravastatin administration before or after induction. The arthritic score of animals given pravastatin before CIA induction was similar to that of the nonstatin controls, whereas the other groups that received statins showed higher arthritic scores. Atorvastatin administration, especially before CIA induction, increased anti-CII autoantibody production. IL-2 and IL-17 production by lymph node and spleen cells was higher in CIA animals than in PBS controls, but was not affected by statin administration. While IFNγ production was not affected by CIA induction, atorvastatin administration before CIA induction increased the production of this cytokine.\n\nQuestion:\nDo statins accelerate the onset of collagen type II-induced arthritis in mice?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSquamous cell carcinoma of tongue (SCCT) is expected to harbor unique clinico-pathological and molecular genetic features since a significant proportion of patients are young and exhibit no association with tobacco or alcohol. We determined P53, epidermal growth factor receptor, microsatellite instability, human papilloma virus infection and loss of heterozygosity status at several tumor suppressor loci in one hundred and twenty one oral SCCT (SSCOT) samples and analyzed their association with clinico-pathological features and patient survival. Our results revealed a significantly higher incidence of p53 nuclear stabilization in early (as against late) onset SCCOT. FHIT loss was significantly associated with p53 nuclear stabilization and the association was stronger in patients with no history of tobacco use. Samples harboring mutation in p53 DNA binding domain or exhibiting p53 nuclear stabilization, were significantly associated with poor survival.\n\nQuestion:\nIs p53 nuclear stabilization associated with FHIT loss and younger age of onset in squamous cell carcinoma of oral tongue?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nEuthyroid sick syndrome is a common finding in critically ill patients with nonthyroidal illness, characterized by low serum levels of free triiodothyronine (fT3) with a peculiar increase in reverse T3 (rT3) and normal-to-low free thyroxine (fT4) as well as thyroid-stimulating hormone (TSH) levels. This condition has been proposed as a prognostic factor of worse outcome in critically ill patients, while no conclusive data are available in burns. Since thyroid function testing is contained in our baseline laboratory tests at admission, we retrospectively evaluated fT3, fT4 and TSH in 295 consecutive burn patients admitted to the Burn Center of Turin from January 2002 to December 2006, comparing hormone levels in survivors and non-survivors. fT3 and TSH levels were significantly lower (p<or=0.0002) in non-survivors compared to survivors, while no significant difference between the two populations was found in fT4 concentrations. Excluding from the study 20 patients who received dopamine administration for more than 21h, serum fT3 levels fell further still (p=0.0003). In addition, fT3 concentrations showed a significant correlation with burn severity expressed by the Roi score (Spearman's correlation coefficient -0.37 with p<0.00001).\n\nQuestion:\nDo low triiodothyronine serum levels as a predictor of poor prognosis in burn patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe comprehension of tense/aspect morphology by children with autism spectrum disorder (ASD) was assessed via Intermodal Preferential Looking (IPL) to determine whether this population's difficulties with producing these morphemes extended to their comprehension. Four-year-old participants were assessed twice, 4 months apart. They viewed a video that presented side-by-side ongoing and completed events paired with familiar verbs with past tense and progressive morphology. Their eye movements were recorded and coded offline; the IPL measures included percentage of looking time at, and latency of first look to, the matching scene. Spontaneous speech samples were also obtained and coded for number of words, past tense, and progressive inflections. Relative to their baseline preferences, these 4-year-old children with ASD looked more quickly to and longer at the matching scene for both morphemes. Children who produced more words, including progressive and past morphemes, and those who performed better on standardized language assessments demonstrated better comprehension of -ing.\n\nQuestion:\nIs grammatical aspect a strength in the language comprehension of young children with autism spectrum disorder?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nNew data suggest that glioma stem-like cells (GSCs) and neural stem/progenitor cells (NSCs) may share common origins. GSCs drive tumor proliferation and appear to be resistant to classic chemotherapy, while the effects of chemotherapy on NSCs are not well studied. As the role of NSCs in learning and memory is increasingly recognized, we need to identify drugs that reduce neurotoxicity but are still effective against glial tumors. We treated 3 human NSC cultures and multiple low- and high-grade GSC cultures with the commonly used agents temozolomide (TMZ) and cisplatin (CIS), and with 2 newer, promising drugs: the proteasome inhibitor bortezomib (BTZ) and the epidermal growth factor receptor tyrosine kinase inhibitor erlotinib (ERL). We measured cell survival, proliferation, cell death induction, and drug resistance markers. TMZ decreased NSC viability, while minimally affecting GSCs. TMZ induced NSC death, which was partially compensated for by increased proliferation. CIS had similar effects. The NSC's sensitivity to TMZ and CIS correlated with low expression of the multidrug resistance gene ABCG2, but not of MGMT or MSH1/MLH2. BTZ caused an 80%decrease in GSCs, while minimally affecting NSCs. GSCs had lower proteasome levels and activity after BTZ treatment. ERL treatment also decreased GSC numbers, but not NSC viability, which correlated with low EGFR expression in NSCs compared to GSCs.\n\nQuestion:\nDo neural stem/progenitors and glioma stem-like cells have differential sensitivity to chemotherapy?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nExogenous bone morphogenetic protein 4 (BMP-4) has been reported to inhibit ureteric branching morphogenesis and regulate the anterior-posterior axis of the developing kidney in vitro. We examined the role of BMP-4 on ureteric branching in vitro using three-dimensional image analysis software and statistical models. Additionally, in vivo ureteric branching was analyzed and the effect of reduced levels of BMP-4 in vivo on nephron number was examined. Embryonic day 12.5 (E12.5) Balb/c mouse metanephroi cultured for 48 hours with or without 260 ng/mL recombinant human BMP-4 (rhBMP-4) were immunostained to identify the ureteric epithelium which was quantified in three dimensions. In vivo ureteric branching morphogenesis in Hoxb7/GFP mice was also analyzed. The effect of reduced in vivo levels of BMP-4 on nephron number was examined in BMP-4(+/-) and wild-type mice using an unbiased stereologic method. Qualitative and quantitative studies identified a decrease in total ureteric length and branch number in wild-type mouse metanephroi cultured in the presence of BMP-4. A marked anterior-posterior asymmetry in both ureteric length and branch number was observed in BMP-4-treated metanephroi. A similar asymmetry was revealed in control metanephroi, both in vitro and in vivo. This asymmetry is the result of reduced ureteric branching morphogenesis in the posterior region of the kidney and appears to be due to slower growth rather than the adoption of an alternate branching pattern. Reduction of endogenous BMP-4 in BMP-4(+/-) mice resulted in no change in total nephron number in macroscopically normal kidneys.\n\nQuestion:\nDoes exogenous BMP-4 amplify asymmetric ureteric branching in the developing mouse kidney in vitro?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nRegional anesthesia has been shown to blunt the response to surgical stress and decrease the use of volatile anesthetics and the consumption of opioids, which may reduce immune compromise and potentially delay tumor recurrence. The goal of this study was to find a possible association between intraoperative regional anesthesia and decreased cancer recurrence. Patients who underwent surgery for ovarian cancer between January 1, 2000, and October 1, 2006, were included. Subjects who had optimal surgical debulking (<1.0 cm of remaining tumor) were evaluated for time to tumor recurrence (carcinoantigen 125 >21 U/mL or computed tomography evidence of disease progression) and/or death. One hundred eighty-two patients were evaluated; 127 did not receive epidural anesthesia/analgesia. Among the 55 who had epidural catheters placed, 26 were used intraoperatively and postoperatively; 29 were used only postoperatively. Cancer recurrence was documented in 121 patients. The median (interquartile range) time to recurrence was 40 (25-52) months. The intraoperative use epidural group had a mean (95% confidence interval) time to recurrence of 73 (56-91) months, which was longer than either the epidural postoperative group 33 (21-45) months (P = 0.002) or the no-epidural group 38 (30-47) months (P = 0.001). The postoperative-only and no-epidural groups were not different (P = 0.92). Intraoperative epidural significantly reduced (hazard ratio, 0.37 [95% confidence interval, 0.19-0.73]) tumor recurrence risk.\n\nQuestion:\nIs intraoperative neuraxial anesthesia but not postoperative neuraxial analgesia associated with increased relapse-free survival in ovarian cancer patients after primary cytoreductive surgery?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nDepartures from power law group size frequency distributions have been proposed as a useful tool to link individual behavior with population patterns and dynamics, although examples are scarce for wild animal populations. We studied a population of Lesser kestrels (Falco naumanni) breeding in groups (colonies) from one to ca. 40 breeding pairs in 10,000 km(2) in NE Spain. A 3.5 fold steady population increase occurred during the eight-year study period, accompanied by a geographical expansion from an initial subpopulation which in turn remained stable in numbers. This population instability was mainly driven by first-breeders, which are less competitive at breeding sites, being relegated to breed solitarily or in small colony sizes, and disperse farther than adults. Colony size frequency distributions shifted from an initial power law to a truncated power law mirroring population increase. Thus, we hypothesized that population instability was behind the truncation of the power law. Accordingly, we found a power law distribution through years in the initial subpopulation, and a match between the power law breakpoint (at ca. ten pairs) and those colony sizes from which the despotic behavior of colony owners started to impair the settlement of newcomers. Moreover, the instability hypothesis was further supported by snapshot data from another population of Lesser kestrels in SW Spain suffering a population decline.\n\nQuestion:\nDo truncated power laws reveal a link between low-level behavioral processes and grouping patterns in a colonial bird?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIsoflurane may be protective in preclinical models of lung injury, but its use in patients with lung injury remains controversial and the mechanism of its protective effects remains unclear. The authors hypothesized that this protection is mediated at the level of alveolar tight junctions and investigated the possibility in a two-hit model of lung injury that mirrors human acute respiratory distress syndrome. Wild-type mice were treated with isoflurane 1 h after exposure to nebulized endotoxin (n = 8) or saline control (n = 9) and then allowed to recover for 24 h before mechanical ventilation (MV; tidal volume, 15 ml/kg, 2 h) producing ventilator-induced lung injury. Mouse lung epithelial cells were similarly treated with isoflurane 1 h after exposure to lipopolysaccharide. Cells were cyclically stretched the following day to mirror the MV protocol used in vivo. Mice treated with isoflurane following exposure to inhaled endotoxin and before MV exhibited significantly less physiologic lung dysfunction. These effects appeared to be mediated by decreased vascular leak, but not altered inflammatory indices. Mouse lung epithelial cells treated with lipopolysaccharide and cyclic stretch and lungs harvested from mice after treatment with lipopolysaccharide and MV had decreased levels of a key tight junction protein (i.e., zona occludens 1) that was rescued by isoflurane treatment.\n\nQuestion:\nDoes isoflurane ameliorate Acute Lung Injury by Preserving Epithelial Tight Junction Integrity?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nDiabetes interferes with bone formation and impairs fracture healing, an important complication in humans and animal models. The aim of this study was to examine the impact of diabetes on mesenchymal stem cells (MSCs) during fracture repair. Fracture of the long bones was induced in a streptozotocin-induced type 1 diabetic mouse model with or without insulin or a specific TNFα inhibitor, pegsunercept. MSCs were detected with cluster designation-271 (also known as p75 neurotrophin receptor) or stem cell antigen-1 (Sca-1) antibodies in areas of new endochondral bone formation in the calluses. MSC apoptosis was measured by TUNEL assay and proliferation was measured by Ki67 antibody. In vitro apoptosis and proliferation were examined in C3H10T1/2 and human-bone-marrow-derived MSCs following transfection with FOXO1 small interfering (si)RNA. Diabetes significantly increased TNFα levels and reduced MSC numbers in new bone area. MSC numbers were restored to normal levels with insulin or pegsunercept treatment. Inhibition of TNFα significantly reduced MSC loss by increasing MSC proliferation and decreasing MSC apoptosis in diabetic animals, but had no effect on MSCs in normoglycaemic animals. In vitro experiments established that TNFα alone was sufficient to induce apoptosis and inhibit proliferation of MSCs. Furthermore, silencing forkhead box protein O1 (FOXO1) prevented TNFα-induced MSC apoptosis and reduced proliferation by regulating apoptotic and cell cycle genes.\n\nQuestion:\nDoes diabetes reduce mesenchymal stem cells in fracture healing through a TNFα-mediated mechanism?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo examine the effect of doxycycline on the activity of matrix metalloproteinases (MMPs) and oxidative stress in gastric tissues of rats following gastric injury. Gastric ulcers were generated in rats by administration of 70% ethanol, and activity of doxycycline was tested by administration 30 min prior to ethanol. Similarly, the effect of doxycycline was tested in an indomethacin-induced gastric ulcer model. The activities and expression of MMPs were examined by zymography and Western blot analysis. Gastric injury in rats as judged by elevated ulcer indices following exposure to ulcerogen, either indomethacin or ethanol, was reversed significantly by doxycycline. Indomethacin-induced ulcerated gastric tissues exhibited about 12-fold higher proMMP-9 activity and about 5-fold higher proMMP-3 activity as compared to control tissues. Similarly, ethanol induced about 22-fold and about 6-fold higher proMMP-9 and proMMP-3 activities, respectively, in rat gastric tissues. Both proMMP-9 and MMP-3 activities were markedly decreased by doxycycline in ulcerogen treated rat gastric tissues. In contrast, the reduced MMP-2 activity in ulcerated tissues was increased by doxycycline during ulcer prevention. On the other hand, doxycycline inhibited significantly proMMP-9, -2 and -3 activities in vitro. In addition, doxycycline reduced oxidative load in gastric tissues and scavenged H₂O₂ in vitro. Our results suggest a novel regulatory role of doxycycline on MMP-2 activity in addition to inhibitory action on MMP-9 and MMP-3 during prevention of gastric ulcers.\n\nQuestion:\nDoes doxycycline block gastric ulcer by regulating matrix metalloproteinase-2 activity and oxidative stress?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCornoid lamella is the hallmark of the group of conditions encompassed by the term porokeratosis (PK). One of the characteristics of cornoid lamella is parakeratosis. Although these explanations are not universally accepted, dermatopathology suggests that parakeratosis is formed either by the acceleration of epidermopoiesis or the faulty maturation of keratinocytes. This study tested the proliferation rate of the cell population underneath the cornoid lamella. An immunohistochemical study was performed in four cases of PK (2 plaque type PK, 1 disseminated superficial actinic PK, and 1 linear PK) with the MIB-1 antibody. The lesions evidenced in the patients were all smaller than 2 cm. The epidermal cells beneath the cornoid lamella showed a proliferation rate that was similar to the one observed in the adjacent epidermal cells in all cases.\n\nQuestion:\nDo small lesions of porokeratosis show a normal proliferation rate with MIB-1?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe use of patient-reported outcome measures to assess clinical outcomes after injury and surgery has become common in treating young athletes with orthopaedic injuries; however, normative data for these measures are limited and often include a wide range of ages and activity levels. To provide normative data for the Knee Injury and Osteoarthritis Outcome Score (KOOS) and Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) in a young and athletic population, and to compare scores between participants with a history of knee ligament injury and those with no history. Cross-sectional study; Level of evidence, 3. We administered the KOOS and WOMAC to 1177 college freshmen entering the United States Military Academy in June 2011. All participants were healthy and had been medically screened to meet the physical induction standards for military service. We calculated means, standard deviations, percentiles, ranges, and interquartile ranges for the KOOS and WOMAC by sex and injury history. We also compared median scale scores for those with a history of knee ligament injury with those with no history using the Kruskal-Wallis test. Among the 1177 participants, 971 were male (age, 18.8 ± 0.9 years), and the remaining 206 were female (age, 18.7 ± 0.8 years). Normative median values and interquartile ranges (IQRs) for the KOOS scale scores among men with no history of knee ligament injury were the following: Symptoms (96.4; IQR, 10.7), Pain (100; IQR, 2.8), Functional Activities of Daily Living (ADL) (100; IQR, 0.0), Sports and Recreation Function (100; IQR, 5.0), and Knee-Related Quality of Life (QOL) (100; IQR, 12.5). For women with no history of knee ligament injury, the KOOS scale scores were the following: Symptoms (92.9; IQR, 14.3), Pain (100; IQR, 5.6), Functional ADL (100; IQR, 2.9), Sports and Recreation Function (100; IQR, 10.0), and Knee-Related QOL (93.8; IQR, 18.8). Among the men, 139 (14%) reported a history of knee ligament injury, while 33 (16%) women also reported a history of injury. All KOOS scale scores and the WOMAC Stiffness and Function scale scores were significantly lower (P < .05) for men who reported a history of knee ligament injury. Similarly, Symptoms, Pain, and Knee-Related QOL on the KOOS and Pain on the WOMAC were significantly lower among women with a history of knee ligament injury.\n\nQuestion:\nIs normative values for the KOOS and WOMAC in a young athletic population : history of knee ligament injury associated with lower scores?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSirtuin 3 (Sirt3), one of the seven Sirtuins family members, plays critical roles in the progression of multiple cancer types. However, its role in the prognosis of hepatocellular carcinoma (HCC) has not yet been investigated systematically. The correlation of Sirtuins expression with prognosis of HCC was determined by immunohistochemistry (IHC) in a large HCC patient cohort (n = 342). Expression of Sirt3 in tumoral and peritumoral tissues of HCC patients were further determined by western blotting (WB). IHC and WB studies both showed a decreased expression of Sirt3 in tumoral tissues compared with peritumoral tissues (P = 0.003 for IHC, P = 0.0042 for WB). Decreased expression of Sirt3 in both tumoral and peritumoral tissues was associated with increased recurrence probability and decreased overall survival rate by univariate analyses (intratumoral Sirt3: P = 0.011 for TTR, P = 0.001 for OS; peritumoral Sirt3: P = 0.017 for TTR, P = 0.023 for OS), the prognostic value was strengthened by multivariate analyses (intratumoral Sirt3: P = 0.031 for TTR, P = 0.001 for OS; peritumoral Sirt3: P = 0.047 for TTR, P = 0.031 for OS). Intratumoral Sirt3 also showed a favorable prognostic value in patients with BCLC stage A (TTR, P = 0.011; OS, P < 0.001). In addition, we found that IHC studies of other sirtuin members showed a decreased expression of Sirt2, Sirt4 and Sirt5 and an increased expression of Sirt1, Sirt6 and Sirt7 in intratumoral tissues compared with peritumoral tissues. In contrast to Sirt3, other members did not showed a remarkable correlation with HCC prognosis.\n\nQuestion:\nIs down-regulation of sirtuin 3 associated with poor prognosis in hepatocellular carcinoma after resection?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHeparin-binding epidermal growth factor-like growth factor (HB-EGF) is produced as a type-I, single-pass transmembrane protein that can be cleaved to release a diffusible peptide. HB-EGF, often overexpressed in damaged or diseased epithelium, is normally expressed in pancreatic islets, but its function is not understood. To understand the function of each isoform of HB-EGF, we made transgenes expressing either a constitutively transmembrane or a constitutively secreted protein. The transmembrane isoform was not an inert precursor protein, but a functional molecule, downregulating the glucose-sensing apparatus of pancreatic islets. Conversely, the secreted form of HB-EGF improved islet function, but had severe fibrotic and neoplastic effects on surrounding tissues. Each isoform had a more severe phenotype than that of full-length HB-EGF, even though the full-length protein was efficiently cleaved, thus producing both isoforms, suggesting that a level of regulation was lost by separating the isoforms.\n\nQuestion:\nDo transmembrane and soluble isoforms of heparin-binding epidermal growth factor-like growth factor regulate distinct processes in the pancreas?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHuman genome-wide association studies have identified genetic variants in the chromosome 9p21 region that confer increased risk of coronary artery disease and other age-related diseases. These variants are located in a block of high linkage disequilibrium with the neighboring Ink4/Arf tumor-suppressor locus (also named CDKN2A/CDKN2B). Since previous studies suggest an atheroprotective role of the Ink4/Arf locus, here we assessed whether gain-of-function of the encoded genes can be exploited therapeutically to reduce atherosclerosis. Generation and characterization of apolipoprotein E-null mice carrying an additional transgenic copy of the entire Ink4/Arf locus (apoE-/-Super-Ink4/Arf) that reproduces the normal expression and regulation of the endogenous locus. Although liver and aorta of apoE-/-Super-Ink4/Arf mice only showed a trend towards increased Ink4/Arf transcript levels compared to apoE-/- controls, cultured macrophages with increased Ink4/Arf gene dosage exhibited augmented apoptosis induced by irradiation with ultraviolet light, indicating that low level of transgene overexpression can lead to augmented Ink4/Arf function. However, increased Ink4/Arf gene dosage did not affect atherosclerosis development in different vascular regions of both male and female apoE-/- mice fed either normal or high-fat diet. Increased gene dosage of Ink4/Arf similarly had no effect on atheroma cell composition or collagen content, an index of plaque stability.\n\nQuestion:\nDoes increased gene dosage of the Ink4/Arf locus attenuate atherosclerosis development in hypercholesterolaemic mice?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nFuture changes in environmental conditions may alter evolutionary processes, including hybridization in nature. Frequency of hybrids could be altered via range shifts by the parental species or by changes in prezygotic or postzygotic reproductive isolation. We examined the potential for range shifts and change in postzygotic isolation by determining effects of increasing and decreasing precipitation on leaf physiology and fitness components in the subalpine herbs Ipomopsis aggregata (Polemoniaceae), I. tenuituba¸ and their natural hybrids in a common garden in the habitat of I. aggregata. Summer precipitation was experimentally doubled or halved over 3 yr in comparison with ambient conditions. We measured relative growth rate, specific leaf area, intrinsic water-use efficiency, survival to reproduction, biomass, number of flowers produced, and floral morphology. Ipomopsis tenuituba increased relative growth rate with higher precipitation more so than did I. aggregata during the first summer, but this response did not result in changes across treatments in relative survival or final reproductive success of the two species. When precipitation was reduced, the relative success of hybrids was greater than that of the home species, I. aggregata. In dry conditions, hybrids increased water-use efficiency and fitness as indexed by number of flowers more so than the other plant types did.\n\nQuestion:\nDoes altered precipitation affect plant hybrids differently than their parental species?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe objective of this study was to examine the associations between objective measures of sleep duration and sleep efficiency with the grades obtained by healthy typically developing children in math, language, science, and art while controlling for the potential confounding effects of socioeconomic status (SES), age, and gender. We studied healthy typically developing children between 7 and 11 years of age. Sleep was assessed for five week nights using actigraphy, and parents provided their child's most recent report card. Higher sleep efficiency (but not sleep duration) was associated with better grades in math, English language, and French as a second language, above and beyond the contributions of age, gender, and SES.\n\nQuestion:\nIs sleep efficiency ( but not sleep duration ) of healthy school-age children associated with grades in math and languages?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo assess the impact of eliminating routine drain placement in patients undergoing robot-assisted laparoscopic prostatectomy (RALP) and pelvic lymph node dissection (PLND) on the risk of postoperative complications. An experienced single surgeon performed RALP on 651 consecutive patients at our institution from 2008 to 2012. Before August 2011, RALP with or without PLND included a routine peritoneal drain placed during surgery. Thereafter, routine intraoperative placement of drains was omitted, except for intraoperatively noted anastomotic leakage. We used multivariable logistic regression to compare complication rates between study periods and the actual drain placement status after adjusting for standard prespecified covariates. Most patients (92%) did not have ≥grade 2 complications after surgery and only two patients (0.3%) experienced a grade 4 complication. The absolute adjusted risk of a grade 2-5 complication was 0.9% greater among those treated before August 2011 (95% confidence interval [CI] -3.3%-5.1%; p=0.7), while absolute adjusted risk of a grade 3-5 complication was 2.8% less (-2.8%; 95% CI-5.3%-0.1%; p=0.061). RESULTS based on drain status were similar.\n\nQuestion:\nDoes impact of routine use of surgical drain on incidence of complications with robot-assisted radical prostatectomy?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe Lancet recently sponsored a commission examining the role of surgery in global health. There is a paucity of published information on the cost-effectiveness of surgery in low- and middle-income countries, a key metric in the prioritisation of limited resources. All patients undergoing emergency laparotomy, elective and emergency inguinal hernia repair, elective and emergency caesarean section, amputation, fracture manipulation, or fracture fixation over a 3 months period in a single district African hospital were assessed. World Health Organisation global burden of disease (GBD) methodology was used to calculate the disability-adjusted life years (DALYs) saved for each patient (using global and local life expectancy). Fully loaded costs were calculated for each patient’s care and providing the overall surgical service. Cost-effectiveness was calculated in year 2012 US$ per DALY saved for each procedure and overall. A total of 428 patients were included, with an overall cost-effectiveness of $10.70 per DALY averted. The cost-effectiveness of individual procedures (global life expectancy) was: Amputation—$17.66; Emergency caesarean section—$7.42; Elective caesarean section—$20.50; Emergency laparotomy—$8.62; Elective hernia repair—$15.26; Emergency hernia repair—$4.36; Fracture/dislocation reduction—$69.03; Fracture/dislocation fixation—$225.89.\n\nQuestion:\nAre surgery and Obstetric Care Highly Cost-Effective Interventions in a Sub-Saharan African District Hospital : A Three-Month Single-Institution Study of Surgical Costs and Outcomes?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe have previously shown that toll-like receptor 3 (TLR3)-mediated signaling plays an important role in the induction of innate cytokine responses to Theiler's murine encephalomyelitis virus (TMEV) infection. In addition, cytokine levels produced after TMEV infection are significantly higher in the glial cells of susceptible SJL mice compared to those of resistant C57BL/6 mice. However, it is not known whether TLR3-mediated signaling plays a protective or pathogenic role in the development of demyelinating disease. SJL/J and B6;129S-Tlr3tm1Flv/J (TLR3KO-B6) mice, and TLR3KO-SJL mice that TLR3KO-B6 mice were backcrossed to SJL/J mice for 6 generations were infected with Theiler's murine encephalomyelitis virus (2 × 105 PFU) with or without treatment with 50 μg of poly IC. Cytokine production and immune responses in the CNS and periphery of infected mice were analyzed. We investigated the role of TLR3-mediated signaling in the protection and pathogenesis of TMEV-induced demyelinating disease. TLR3KO-B6 mice did not develop demyelinating disease although they displayed elevated viral loads in the CNS. However, TLR3KO-SJL mice displayed increased viral loads and cellular infiltration in the CNS, accompanied by exacerbated development of demyelinating disease, compared to the normal littermate mice. Late, but not early, anti-viral CD4+ and CD8+ T cell responses in the CNS were compromised in TLR3KO-SJL mice. However, activation of TLR3 with poly IC prior to viral infection also exacerbated disease development, whereas such activation after viral infection restrained disease development. Activation of TLR3 signaling prior to viral infection hindered the induction of protective IFN-γ-producing CD4+ and CD8+ T cell populations. In contrast, activation of these signals after viral infection improved the induction of IFN-γ-producing CD4+ and CD8+ T cells. In addition, poly IC-pretreated mice displayed elevated PDL-1 and regulatory FoxP3+ CD4+ T cells in the CNS, while poly IC-post-treated mice expressed reduced levels of PDL-1 and FoxP3+ CD4+ T cells.\n\nQuestion:\nIs tLR3 signaling either protective or pathogenic for the development of Theiler 's virus-induced demyelinating disease depending on the time of viral infection?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe aim of our study was to analyze whether there is a gender difference in the effects of maternal chocolate ingestion (80% cocoa) on the fetus, as expressed by the fetal heart rate (FHR). One hundred pregnant women with uncomplicated term gestation, matched for age and parity, underwent computerized FHR recording before and after eating 30 g of 80% cocoa chocolate; 46 carried a male fetus, and 54 carried a female. Computerized cardiotocography parameters (baseline FHR in beats per minute, number of contractions/hour, fetal movements/hour, accelerations of at least 15 bpm for 15 s, episodes of high variation/min and short-term variation in ms) were expressed as the mean and SD. We calculated the difference before and after maternal chocolate eating both in male and female fetuses and then compared the gender differences in the FHR variation. Statistical significance was set at p < 0.05. While baseline FHR and number of contractions did not change, the number of: fetal movements/hour, accelerations, episodes of high variation/min, and the short-term variation significantly increased after chocolate ingestion. The percent variation of the movements (101.7 ± 89.23 males versus 252.0 ± 297.6 females; p = 0.002), accelerations (70.90 ± 46.98 males versus 153.3 ± 178.5 females; p = 0.004) and short-term FHR variation (21.47 ± 18.73 males versus 37.35 ± 27.46 females; p = 0.002) increased to a greater degree in the female fetuses than in the males.\n\nQuestion:\nAre female fetuses more reactive when mother eats chocolate?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMitral valve repair (MVRr) has become the mainstay of surgical treatment for mitral valvular regurgitation. Evaluation of MVRr by intraoperative transesophageal echocardiography (IOE) has been routinely employed to guide the operation. While the main objective of IOE is to assess for residual mitral regurgitation, it is also important to exclude significant mitral stenosis. Utilisation of pressure half-time (PHT) to estimate mitral valve area (MVA) has been shown to be reliable in normal clinical situations. However, in MVRr, the accuracy of MVA calculation by PHT needs to be ascertained. Data from IOE and post-MVRr transthoracic echocardiography (TTE) from the year 1998 to 2002 were analysed and when required, offline PHT measurements were made. The mean time interval between the two echocardiographic examinations was 10.6 (1 to 56) weeks. In our 36 cases, the IOE MVA was found to be 2.1+/-0.5 cm2, with the corresponding TTE MVA to be 2.7+/-1.0 cm2. MVA by PHT with IOE underestimated TTE findings by 0.6+/-0.9 cm2 (95% CI: -0.85 to -0.24, P=0.001). In 6 patients, the IOE MVA was moderately reduced. Subsequent TTE in these patients showed that the MVA was adequate and was significantly underestimated by IOE in 5 of these patients. In all these cases, IOE underestimated MVA by a margin, which may result in a need to revise the repair.\n\nQuestion:\nDoes transesophageal echocardiography during mitral valve repair underestimate mitral valve area by pressure half-time calculation?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nDegree of satisfaction with a knee arthroplasty is said to be correlated to reduced pain and better function. During a validation of the Swedish Knee Arthroplasty Register in 1997, previously operated patients were asked how satisfied they were with their knee. A subgroup of \"satisfied\" patients was identified who underwent revision within 2 years of having expressed satisfaction. Our aim was to study the revision diagnosis, to determine whether the problem leading to revision had been discovered as a result of routine follow-up, and also to find out when the symptoms leading to revision had started. We retrospectively studied the medical records of 181 patients (181 knees), with a median age of 74 (31-88) years. 68% were women and the median time between primary operation and revision was 8 (3-21) years. Aseptic loosening (74/181) was the most common diagnosis. 2 cases were revised as a result of routine follow-up. 44% of the medical records included reports of pain in the replaced knee prior to answering the satisfaction questionnaire.\n\nQuestion:\nIs revision in previously satisfied knee arthroplasty patients the result of their call on the physician , not on pre-planned follow-up : a retrospective study of 181 patients who underwent revision within 2 years?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo determine which respiratory function tests best predicted diaphragmatic strength in patients with amyotrophic lateral sclerosis. Patients referred for pulmonary evaluation were included (n = 25) if they underwent measurement of transdiaphragmatic pressure (Pdi) and one or more of the following on the same day: upright FVC, supine FVC, upright FEV(1), supine FEV(1), maximal inspiratory pressure (MIP), maximal expiratory pressure (MEP), and PaCO(2). Abdominal paradox and use of accessory muscles were also assessed. Bivariate analyses were performed using simple linear regression. Sensitivity and specificity of the potential predictors to detect an abnormal Pdi (< 70 cm H(2)O) were calculated. Pulmonary function laboratory of an academic medical center. Upright FVC, FEV(1), and MEP were all significantly correlated with Pdi, while MIP and PaCO(2) were not. Supine FVC was the most highly correlated predictor of Pdi (R(2) = 0.76). A cutoff of supine FVC that was < 75% predicted was 100% sensitive and specific for predicting an abnormally low Pdi. Accessory muscle use and abdominal paradox were both significantly associated with Pdi, and the presence of accessory muscle use had a sensitivity of 84% and a specificity of 100% for detecting a low Pdi.\n\nQuestion:\nDoes spirometry in the supine position improve the detection of diaphragmatic weakness in patients with amyotrophic lateral sclerosis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPrevious studies showed that serum tartrate-resistant acid phosphatase 5b (TRACP5b) activity was increased in 70% to 94% of breast cancer (BC) patients with bone metastasis (BM). This study aims to determine whether serum TRACP5b is useful for identifying limited or extensive BM in BC patients. Serum TRACP5b activity was measured in 168 BC patients, including 81 who were newly diagnosed with early BC, 20 with extraosseous metastasis, 24 with limited BM, and 43 with extensive BM. Serum TRACP5b activity was also measured monthly in 151 patients with early BC until they developed BM. Four hundred and twenty-seven (427) healthy women ages 18 to 90 served as control. One-way ANOVA was used to compare serum TRACP5b among groups. The sensitivity and specificity of serum TRACP5b as a marker for BM were estimated by receiver operator characteristic (ROC) curves. Serum TRACP5b increased with age in healthy women ( P < 0.0001). It was significantly elevated in patients with extensive BM compared with all other groups ( P < 0.0001). ROC analysis established a cutoff value of 4.026 units/L to identify patients with extensive BM with a specificity of 98% and a sensitivity of 93% (area under the curve = 0.9807; 95% CI = 0.9698-0.9915). Among the 151 patients with early BC, 6 developed limited BM and 2 developed extensive BM during the follow-up period. Serum TRACP5b remained below the cutoff value in patients with limited BM, but became significantly increased in those whose BM became extensive.\n\nQuestion:\nIs tartrate-resistant acid phosphatase 5b a useful serum marker for extensive bone metastasis in breast cancer patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nChanging dietary and physical activity habits has the potential to postpone or prevent the development of type 2 diabetes. However, it needs to be assessed whether moderate interventions, in agreement with current guidelines for the general population, are effective. We evaluated the impact of a 2-year combined diet and physical activity intervention program on glucose tolerance in Dutch subjects at increased risk for developing diabetes. Subjects with glucose intolerance were randomly assigned to either the lifestyle intervention group (INT) or control group (CON). The INT received regular dietary advice and was stimulated to increase their physical activity. The CON received a brief leaflet about healthy diet and increased physical activity. Primary outcome measure was the change in glucose tolerance. In total, 88 subjects completed 2 years of intervention (40 subjects in the INT, 48 subjects in the CON, mean BMI 29.4 kg/m2). Subjects in the INT reduced their body weight, waist circumference, and (saturated) fat intake and improved their aerobic capacity. Two-hour plasma glucose concentration declined from 8.7 to 8.0 mM in the INT and rose from 8.6 to 9.4 mM in the CON (p < 0.01). Subjects adherent to both the diet and exercise intervention showed the largest reduction in 2-hour glucose levels.\n\nQuestion:\nDoes lifestyle intervention according to general recommendations improve glucose tolerance?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe pressure in air-filled endotracheal cuffs increases steadily throughout general anesthesia with nitrous oxide (N2O). High cuff pressures can be responsible for local ischemia, which may induce tracheal mucosal injury. In this study, cuff pressure was monitored in anesthetized patients, and postanesthesia endotracheal lesions were assessed by endoscopy. Sixty-five patients undergoing general anesthesia with tracheal intubation >1 h in duration were randomized into two groups. The endotracheal tube cuff was inflated to 30-40 cm H2O with air in Group 1 (n = 33) and with a gas mixture (N2O 50% in oxygen) in Group 2 (n = 32). At the time of tracheal extubation, a fiberoptic examination via the endotracheal tube was performed by an independent observer. Aspects of trachea at the level of cuff contact area were scored as 0 = normal, 1 = mucosal erythema or edema, 2 = mucosal erosion or hemorrhage, 3 = mucosal erosion or hemorrhage on both anterior and posterior tracheal walls. Cuff pressure increased throughout the procedure (P<0.01) in Group 1 and remained stable in Group 2. In Group 1, tracheal lesions in the area of the cuff were more frequent than they were in Group 2 (79% vs. 37%; P<0.001). Tracheal injury was correlated to cuff pressure (r = 0.62, P<0.001). No postoperative respiratory complication was observed in any patient. In patients anesthetized with N2O, the inflation of the tracheal tube cuff with a gas mixture of the same composition as the inhaled mixture can prevent excessive cuff pressure and reduce the incidence of tracheal injury.\n\nQuestion:\nDoes nitrous oxide increase endotracheal cuff pressure and the incidence of tracheal lesions in anesthetized patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nObese and overweight patients are at increased risk of arterial stiffness, and visceral, epicardial and hepatic fat accumulation is associated with cardiovascular disease risk. In general, muscular lipids are stored either in interstitial adipose tissue (extramyocellular lipid (EMCL)) or in lipid droplets within muscle cells (intramyocellular lipid (IMCL)). However, the association between IMCL or EMCL content and arterial stiffness remains unclear. This cross-sectional study aimed to clarify this association. A total of 237 subjects (18-81 years) were enrolled in this study. The IMCL and EMCL contents of the right vastus lateralis muscle were evaluated by proton magnetic resonance spectroscopy. Arterial stiffness was estimated using brachial-ankle pulse wave velocity (baPWV). There were significant correlations between baPWV and the contents of both IMCL (R = -0.23, P < 0.001) and EMCL (R = 0.53, P < 0.001) in all subjects. The baPWV negatively correlated with IMCL content (R = -0.45, P < 0.001) in females only. In contrast, significant positive correlations were observed between baPWV and EMCL content in both males (R = 0.59, P < 0.001) and females (R = 0.55, P < 0.001). IMCL and EMCL contents contributed independently to baPWV variation after adjustment for age, sex, body mass index, visceral and subcutaneous abdominal fat, upper and lower limb fat, blood pressure, heart rate, and lipid profiles.\n\nQuestion:\nDo intramyocellular and Extramyocellular Lipids Are Associated With Arterial Stiffness?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe function of synaptotagmins (syt) in Ca2+-dependent transmitter release has been attributed primarily to Ca2+-dependent isoforms such as syt I. Recently, syt IV, an inducible Ca2+-independent isoform has been implicated in transmitter release. We postulated that the effects of syt IV on transmitter release are dependent on the expression of syt I. To test this, we increased syt IV expression in PC12 cells by either upregulation with forskolin treatment or overexpression with transfection. Two separately generated stable PC12 cell lines with syt I expression abolished by RNAi targeting were used and compared to control cells. We measured catecholamine release from single vesicles by amperometry and neuropeptide Y release from populations of cells by an immunoassay. In syt I targeted cells with forskolin-induced syt IV upregulation, amperometry measurements showed a reduction in the number of release events and the total amount of transmitter molecules released per cell. In cells with syt IV overexpressed, similar amperometry results were obtained, except that the rate of expansion for full fusion was slowed. Neuropeptide Y (NPY) release from syt I knockdown cells was decreased, and overexpression of syt IV did not rescue this effect.\n\nQuestion:\nDoes upregulation of synaptotagmin IV inhibit transmitter release in PC12 cells with targeted synaptotagmin I knockdown?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nApproximately 20% of laparoscopic colonic tumor resections result in conversion to open surgery. This result may be related to an increased risk in terms of the oncologic outcome. This study aimed to investigate the oncologic consequences of early and late conversion in laparoscopic colonic surgery. For this study, 45 male WAG-Rij rats were randomized into three operation groups of 15 animals each: laparotomy (LT group), laparoscopy followed by early conversion after 20 min (EC group), and laparoscopy followed by late conversion after 40 min (LC group). The total procedure time for the LT and EC groups was 60 min, compared with 80 min for the LC group. Hematogenous metastatic spread was induced in each operation group by tumor cell inoculation of a rat colon adenocarcinoma (CC 531) into the portal vein after 15 min of surgical intervention. A cecal resection was performed after 30 min in the LT and EC groups and after 50 min in the LC group. On day 28 after surgery, hepatic tumor growth was evaluated by measuring the diameter of tumor nodules, the tumor volume, the weight of the liver, and the cancer index. Hepatic tumor volume was significantly increased after LC than after EC (p = 0.01) and LT (p = 0.04). The liver weights in the LC group were significantly higher than in the EC (p = 0.01) and LT (p = 0.01) groups. No significant difference between EC and LT was observed in any parameters surveyed.\n\nQuestion:\nDoes the point of conversion in laparoscopic colonic surgery affect the oncologic outcome in an experimental rat model?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIn this report we show that the adipocytokine leptin directly modulates autophagy in human CD4(+)CD25(-) conventional (Tconv) T cells. In vitro treatment with recombinant human leptin determined an inhibition of autophagy during T cell receptor (TCR) stimulation, and this phenomenon was dose- and time-dependent. The events were secondary to the activation of the mammalian-target of rapamycin (mTOR)-pathway induced by leptin, as testified by its reversion induced by mTOR inhibition with rapamycin. At molecular level these phenomena associated with Bcl-2 up-regulation and its interaction with Beclin-1, whose complex exerts a negative effect on autophagy. The impact of leptin on autophagy of Tconv cells was determined at biochemical level by western blotting and by flow cytometry; the interaction between BCL-2 and Beclin-1 by co-immunoprecipitation assays.\n\nQuestion:\nDoes leptin modulate autophagy in human CD4+CD25- conventional T cells?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe purpose of this study was to evaluate the outcome of the ratio between metastatic and examined lymph nodes (N ratio) in gastric cancer patients with <15 examined lymph nodes after curative resection. A retrospective study of 710 patients who underwent radical gastrectomy (R0) for gastric cancer from January 1980 to December 2000 was analyzed statistically to identify the N ratio. Patients with <15 examined lymph nodes (group 1, n=327) and those with ≥15 examined lymph nodes (group 2, n=383) were analyzed separately. N ratio categories were identified as follows: N ratio 0, 0%; N ratio 1, 1% to 9%; N ratio 2, 10% to 25%; and N ratio 3, >25%. All the enrolled categories were evaluated by the best cutoff approach. The univariate analysis showed that age, tumor site, tumor size, surgery, T categories, number of metastatic nodes, and N ratio significantly affected prognosis in groups 1 and 2. By multivariate analysis, the N ratio (but not the TNM N category) classification was retained as an independent prognostic factor in groups 1 and 2 compared with the N category system. However, patients with N1 disease in group 1 obtained a better postoperative prognosis than those with N1 disease in group 2 according to the N stage classification (P=0.003). When the N ratio classification was applied, no significant differences were found for N ratios 0, 1, 2, or 3 between the 2 groups (P>0.05).\n\nQuestion:\nIs lymph node ratio an independent prognostic factor in gastric cancer after curative resection ( R0 ) regardless of the examined number of lymph nodes?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo evaluate the therapeutic effect of amniotic membrane transplantation(AMT) for ocular burn. Twenty patients with ocular burn(28 eyes) were treated with amniotic membrane transplantation. Of them, there were 6 cases of severe alkali burn(10 eyes), 8 cases of severe acid burn(10 eyes), and 6 cases of thermal burn(8 eyes). In 28 eyes, ocular inflammation was controlled after 3-7 days of surgery; no continued dissolution, perforation and iris atrophy were found. There were corneal transparency in 16 eyes, keratoleukoma in 4 eyes, and total corneal opacity in 8 eyes. All eyeballs were saved and had stable ocular surface. There was no allograft immune rejection and secondary infection.\n\nQuestion:\nDo [ Therapeutic effect of amniotic membrane transplantation for ocular burn ]?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nToll-like receptors (TLRs) are key factors in the innate immune system and initiate the inflammatory response to foreign pathogens such as bacteria, fungi and viruses. In the microenvironment of tumorigenesis, TLRs can promote inflammation and cell survival. Toll-like receptor 2/6 (TLR2/6) signaling in tumor cells is regarded as one of the mechanisms of chronic inflammation but it can also mediate tumor cell immune escape and tumor progression. However, the expression of TLR2 and its biological function in the development and progression of hepatocarcinoma have not been investigated. This study aimed to determine the expression of TLRs 1-10 in the established human hepatocellular carcinoma cell line BLE-7402, to investigate the biological effect of TLR2 on cell growth and survival. TLR expression in BLE-7402 cells was assayed by RT-PCR, real-time PCR and flow cytometry (FCM). To further investigate the function of TLR2 in hepatocarcinoma growth, BLE-7402 cells were transfected with recombinant plasmids expressing one of three forms of TLR2 siRNA (sh-TLR2 RNAi(A, B and C)). TLR2 knockdown was confirmed using RT-PCR, real-time PCR and fluorescence microscopy. Tumor cell proliferation was monitored by MTT assay and secreted cytokines in the supernatant of transfected cells were measured by bead-based FCM, the function of TLR2 siRNA was also investigated in vivo. The BLE-7402 cell line expressed TLRs 2 to 10 at both mRNA and protein levels. TLR2 was the most highly expressed TLR. While all the three siRNAs inhibited TLR2 mRNA and protein expression, sh-TLR2 RNAi(B) had the strongest knockdown effect. TLR2 knockdown with sh-TLR2 RNAi(B) reduced cell proliferation. Furthermore, secretion of IL-6 and IL-8 was also reduced. The result showed a drastic reduction in tumor volume in mice treated with sh-TLR2 RNAi(B).\n\nQuestion:\nDoes gene silencing of Toll-like receptor 2 inhibit proliferation of human liver cancer cells and secretion of inflammatory cytokines?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCurrent cardiovascular magnetic resonance (CMR) methods, such as late gadolinium enhancement (LGE) and oedema imaging (T2W) used to depict myocardial ischemia, have limitations. Novel quantitative T1-mapping techniques have the potential to further characterize the components of ischemic injury. In patients with myocardial infarction (MI) we sought to investigate whether state-of the art pre-contrast T1-mapping (1) detects acute myocardial injury, (2) allows for quantification of the severity of damage when compared to standard techniques such as LGE and T2W, and (3) has the ability to predict long term functional recovery. 3T CMR including T2W, T1-mapping and LGE was performed in 41 patients [of these, 78% were ST elevation MI (STEMI)] with acute MI at 12-48 hour after chest pain onset and at 6 months (6M). Patients with STEMI underwent primary PCI prior to CMR. Assessment of acute regional wall motion abnormalities, acute segmental damaged fraction by T2W and LGE and mean segmental T1 values was performed on matching short axis slices. LGE and improvement in regional wall motion at 6M were also obtained. We found that the variability of T1 measurements was significantly lower compared to T2W and that, while the diagnostic performance of acute T1-mapping for detecting myocardial injury was at least as good as that of T2W-CMR in STEMI patients, it was superior to T2W imaging in NSTEMI. There was a significant relationship between the segmental damaged fraction assessed by either by LGE or T2W, and mean segmental T1 values (P < 0.01). The index of salvaged myocardium derived by acute T1-mapping and 6M LGE was not different to the one derived from T2W (P = 0.88). Furthermore, the likelihood of improvement of segmental function at 6M decreased progressively as acute T1 values increased (P < 0.0004).\n\nQuestion:\nDoes cardiovascular magnetic resonance by non contrast T1-mapping allow assessment of severity of injury in acute myocardial infarction?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo explore the effects of limb ischemic preconditioning (LIP) on cerebral ischemia/reperfusion injuries. Thirty six wistar rats, of which bilateral vertebral arteries were occluded permanently, were randomly divided into the following 6 groups: control group, cerebral ischemic group, limb ischemic group, LIP 0 d group (cerebral ischemia was given immediately after LIP), LIP 1 d group (cerebral ischemia was given 1 d after LIP) and LIP 2 d group (cerebral ischemia was given 2 d after LIP). Global cerebral ischemia was performed by four vessels occlusion in rats. LIP was performed by occluding the bilateral femoral arteries for 10 min 3 times in a interval of 10 min. The histological grade and pyramidal neuronal density in the CA1 hippocampus were measured to quantitate the degree of hippocampal injury under thionin staining. The histological grade was increased and the pyramidal neuronal density was decreased in the CA1 hippocampus of the cerebral ischemic group (P < 0.01). The damage of the CA1 hippocampus in LIP 0 d group was significantly diminished, which represented by decreased histological grade and increased neuronal density compared with the cerebral ischemic group (P < 0.01). But the CA1 hippocampus still showed obvious injuries in the LIP 1 d and LIP 2 d group.\n\nQuestion:\nDoes [ Limb ischemic preconditioning decrease hippocampal ischemia/reperfusion injuries in rats ]?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPrevious studies demonstrated that pre-treatment with malonate, a reversible inhibitor of succinate dehydrogenase, given before ischaemia, reduces infarct size. However, it is unknown whether administration of malonate may reduce reperfusion injury. Isolated mice hearts were treated, under normoxic conditions, with increasing concentrations of disodium malonate (0.03-30 mmol/L, n = 4). Malonate induced a concentration-dependent decrease in left ventricular developed pressure (LVdevP) (EC50 = 8.05 ± 2.11 mmol/L). In isolated hearts submitted to global ischaemia (35 min) followed by reperfusion (60 min), malonate 3 mmol/L given only during the first 15 min of reperfusion reduced lactate dehydrogenase release (125.41 ± 16.82 vs. 189.20 ± 13.74 U/g dry tissue/15 min in controls, P = 0.015) and infarct size (24.57 ± 2.32 vs. 39.84 ± 2.78%, P = 0.001, n = 7-8 per group) and improved recovery of LVdevP (20.06 ± 3.82 vs 7.76 ± 2.53% of baseline LVdevP, P = 0.017). (1)H NMR spectroscopy demonstrated marked changes in the metabolic profile of malonate-treated hearts, including increased accumulation of succinate. Furthermore, malonate reduced reactive oxygen species (ROS) production, as measured by MitoSOX staining in myocardial samples obtained after 5 min of reperfusion and in mitochondrial preparations from these samples, preserved mitochondrial respiration, and reduced mitochondrial permeabilization, assessed by calcein retention. Treatment with malonate did not result in activation of RISK or SAFE signalling pathways in tissue extracts obtained 5 min after reperfusion.\n\nQuestion:\nDoes succinate dehydrogenase inhibition with malonate during reperfusion reduce infarct size by preventing mitochondrial permeability transition?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAstrocytes are an integral component of the blood-brain barrier (BBB) which may be compromised by ischemic or traumatic brain injury. In response to trauma, astrocytes increase expression of the endopeptidase matrix metalloproteinase (MMP)-9. Compromise of the BBB leads to the infiltration of fluid and blood-derived proteins including albumin into the brain parenchyma. Albumin has been previously shown to activate astrocytes and induce the production of inflammatory mediators. The effect of albumin on MMP-9 activation in astrocytes is not known. We investigated the molecular mechanisms underlying the production of MMP-9 by albumin in astrocytes. Primary enriched astrocyte cultures were used to investigate the effects of exposure to albumin on the release of MMP-9. MMP-9 expression was analyzed by zymography. The involvement of mitogen-activated protein kinase (MAPK), reactive oxygen species (ROS) and the TGF-β receptor-dependent pathways were investigated using pharmacological inhibitors. The production of ROS was observed by dichlorodihydrofluorescein diacetate fluorescence. The level of the MMP-9 inhibitor tissue inhibitor of metalloproteinase (TIMP)-1 produced by astrocytes was measured by ELISA. We found that albumin induces a time-dependent release of MMP-9 via the activation of p38 MAPK and extracellular signal regulated kinase, but not Jun kinase. Albumin-induced MMP-9 production also involves ROS production upstream of the MAPK pathways. However, albumin-induced increase in MMP-9 is independent of the TGF-β receptor, previously described as a receptor for albumin. Albumin also induces an increase in TIMP-1 via an undetermined mechanism.\n\nQuestion:\nDoes albumin induce upregulation of matrix metalloproteinase-9 in astrocytes via MAPK and reactive oxygen species-dependent pathways?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAlthough molecular mechanism of growth differentiation factor 15 (GDF15) in tumorigenesis of oral squamous cell carcinoma (OSCC) is not clear, the diagnostic and prognostic value of serum GDF15 detection has been noticed. However, serum GDF15 levels in patients with oral leukoplakia and GDF15 as a potential predictive biomarker for response to induction chemotherapy in patients with OSCC have not been reported. Pretreatment serum GDF15 concentration was detected using an enzyme-linked immunosorbent assay in 30 healthy persons, 24 patients with oral leukoplakia, and 60 patients with OSCC. Serum GDF15 concentration was significantly higher in patients with oral leukoplakia and OSCC, compared with healthy controls (F = 13.701, df = 2, P < 0.001). From a diagnostic standpoint, a cutoff value of 346.9 ng/l of serum GDF15 concentration was calculated using receiver operating characteristic curve, with a sensitivity of 0.750, specificity of 0.867, Youden's Index of 0.617, and area under curve of 0.863. From a prognostic standpoint, patients with serum GDF15 concentration <346.9 ng/l had an improved 3-year disease-free survival rate (64.3% vs 56.5%) compared with those above 346.9 ng/l, but the difference was not statistically significant. A decreased concentration of GDF15 (<346.9 ng/l) showed a predictive trend toward an improved response to induction chemotherapy compared with elevated concentration with clinical response rates of 100% and 71.4%, respectively, but the difference was not significant.\n\nQuestion:\nIs elevated level of serum growth differentiation factor 15 associated with oral leukoplakia and oral squamous cell carcinoma?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIn recent years, the inflammasome has been determined to play an important role in inflammatory diseases. However, the role of the inflammasome in pulpitis remains unclear. Absent in melanoma 2 (AIM2) is a type of inflammasome that recognizes cytosolic double stranded DNA and forms a caspase-1-activating inflammasome with apoptosis-associated speck-like protein containing a caspase activating recruiting domain. In this study, we determined whether AIM2 was expressed in pulp cells and defined the role of AIM2 in the initiation of inflammation within the dental pulp. In the in vivo study, the right maxillary molars from male adult Sprague-Dawley rats (250-350 g) were exposed to the pulp. In the in vitro study, the pulp cells isolated from the mandibular incisors of the Sprague-Dawley rats (2 weeks) were conventionally cultured. Immunofluorescence staining was used to determine the expression and distribution of AIM2 in the rat dental pulp tissues and cells in the presence or absence of inflammatory stimulation. Western blotting and real-time polymerase chain reaction were performed to determine whether there was a correlation between AIM2 expression levels and inflammation both in vivo and in vitro. In healthy dental pulp tissues and cells, AIM2 was only detected in the odontoblast layer. Stimulation significantly increased AIM2 expression in both the dental pulp tissues and cultured cells. The mRNA and protein levels of AIM2 were significantly up-regulated in response to inflammatory stimulation in a dose-dependent manner. Moreover, we also found that AIM2 expression correlated with interleukin-1 levels. These results reveal a direct relationship between the AIM2 inflammasome and pulpitis.\n\nQuestion:\nDoes absent in melanoma 2 ( AIM2 ) in rat dental pulp mediate the inflammatory response during pulpitis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo examine the role of Cd-induced reactive oxygen species (ROS) generation in the apoptosis of neuronal cells. Neuronal cells (primary rat cerebral cortical neurons and PC12 cells) were incubated with or without Cd post-pretreatment with rapamycin (Rap) or N-acetyl-L-cysteine (NAC). Cell viability was determined by MTT assay, apoptosis was examined using flow cytometry and fluorescence microscopy, and the activation of phosphoinositide 3'-kinase/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) and mitochondrial apoptotic pathways were measured by western blotting or immunofluorescence assays. Cd-induced activation of Akt/mTOR signaling, including Akt, mTOR, p70 S6 kinase (p70 S6K), and eukaryotic initiation factor 4E binding protein 1 (4E-BP1). Rap, an mTOR inhibitor and NAC, a ROS scavenger, blocked Cd-induced activation of Akt/mTOR signaling and apoptosis of neuronal cells. Furthermore, NAC blocked the decrease of B-cell lymphoma 2/Bcl-2 associated X protein (Bcl-2/Bax) ratio, release of cytochrome c, cleavage of caspase-3 and poly(ADP-ribose) polymerase (PARP), and nuclear translocation of apoptosis-inducing factor (AIF) and endonuclease G (Endo G).\n\nQuestion:\nDoes cadmium activate Reactive Oxygen Species-dependent AKT/mTOR and Mitochondrial Apoptotic Pathways in Neuronal Cells?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo determine whether the variant of adducin alpha subunit (alpha-adducin) is in association with essential hypertension in the Hans of Chinese population. One hundred and eighty-three patients with essential hypertension and 129 normotensive subjects were included in this study. Genomic DNA was isolated from 3 ml of whole blood. Polymerase chain reaction, single-strand conformational polymorphism and DNA sequencing analysis techniques were used to detect the variant in the exon 10 of alpha-adducin gene. The clinical data of height, weight and blood pressure were also measured in all subjects. A G-->T substitution at nucleotide 614 in exon 10 of alpha-adducin gene which resulted in the Gly460Trp variant was found in the Hans. The distribution of Gly/Gly, Gly/Trp and Trp/Trp genotypes was coincident with Hardy-Weinberg equilibrium and there were no statistical differences in the three genotypes and Trp allele frequencies between hypertensive and normotensive subjects (P>0.05). The variant of alpha-adducin genotypes was not associated with any significant differences in age, body mass index and blood pressure.\n\nQuestion:\nDoes [ be Gly460Trp variant of alpha-adducin associated with essential hypertension in the Hans of Chinese population ]?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe goal of the current study was to investigate the prognostic impact of proliferative activity, together with the other classic clinicopathologic prognostic factors (tumor size, tumor grade, receptor status, ploidy, and lymph node status), in breast carcinoma by counting mitoses and evaluating S phase fraction (SPF) in fresh and frozen tumor samples. From March 1, 1990, to July 1, 1999, a total of 1984 previously untreated invasive breast carcinoma samples were snap-frozen for flow cytometry. After multivariate analysis incorporating all classic prognostic factors, SPF combined with mitotic activity (i.e., proliferative activity) remained the sole prognostic factor in the lymph node-negative group; proliferative activity was accompanied by tumor size as a prognostic factor in patients with lymph node-positive disease and by lymph node status, lymphatic invasion, and receptor status in the overall population. The predictive value of proliferative activity was superior to that of the reference standards (classic prognostic predictors according to the guidelines of our institution [common oncology practice] and the St. Gallen classification). A review of the literature, focusing on series in which fresh material was used, allowed us to demonstrate that there is widespread agreement regarding the correlation between SPF and prognosis, even after multivariate analysis.\n\nQuestion:\nIs proliferative activity in primary breast carcinomas a salient prognostic factor?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo study the interaction of streptococcal collagen-like protein 1 (Scl1) of M41-type group A streptococcus (GAS) ATCC12373 with low-density lipoprotein (LDL). We cloned, expressed and purified the recombinant proteins rScl1 and its V region rScl1-V, designated as C176 and C176V, derived from Scl1. 41 of M41-type GAS. The binding of rScl1 to LDL was detected with affinity chromatography-binding assay, Western blot analysis and enzyme-linked immunosorbent assay (ELISA), and whole cell binding assays were used to detect the interactions of whole GAS cells with LDL. The results demonstrated that C176 and C176V could specifically bind purified LDL, and M41-type GAS cells expressing native Sell could bind LDL whereas M6-type GAS could not.\n\nQuestion:\nDoes [ Scl1 of M41-type group A streptococcus bound low-density lipoprotein ]?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe chronic obstructive pulmonary disease (COPD) assessment test (CAT) is a validated simple instrument to assess health status, and it correlates well with the severity of airway obstruction in COPD patients. However, little is known about the relationships between CAT scores and quantitative computed tomography (CT) measurements of emphysema and airway wall thickness in COPD patients in the People's Republic of China. One hundred and twelve participants including 63 COPD patients and 49 normal control subjects were recruited. All participants were examined with high-resolution CT to get the measurements of emphysema (percentage of pixels below -950 HU [%LAA-950]) and airway wall thickness (wall area percentage and the ratio of airway wall thickness to total diameter). Meanwhile, they completed the CAT and modified Medical Research Council questionnaire independently. Significantly higher CAT scores and CT measurements were found in COPD patients compared with normal control subjects (P<0.05), and there was a tendency of higher CAT scores and CT measurements with increasing disease severity measured by GOLD staging system. Positive correlations were found between CAT scores and CT measurements (P<0.01). Using multiple linear stepwise regression, CAT score =-46.38+0.778× (wall area percentage) +0.203× (%LAA-950) (P<0.001). Meanwhile, CAT scores and CT measurements in COPD patients all positively correlated with the modified Medical Research Council grades and negatively correlated with FEV1% (P<0.01).\n\nQuestion:\nDoes the COPD assessment test correlate well with the computed tomography measurements in COPD patients in China?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nLeber's hereditary optic neuropathy (LHON) is a condition characterised by a rapid bilateral central vision loss due to death of the retinal ganglion cells, leading to visual impairment commonly occurring during young adulthood. The disease manifests itself more in male patients than female patients. The mtDNA mutations m.11778G>A, m.3460G>A and m.14484T>C are by far more frequent in LHON than any other mutation. In this report, a multi-generational Arab family from Kuwait with 14 male members with LHON was investigated. Complete mtDNA mutational analysis by direct Sanger's sequencing was carried out to detect pathogenic mutations, polymorphisms and haplogrouping. All maternally related subjects from this study who were examined expressed the L3 haplotype background, with two concurrent mtDNA mutations, 10609T>C and 10663T>C, that led to non-conservative amino acid changes of Ile47Thr and Val65Ala, respectively. The two variations were absent in 144 normal and ethnicity-matched controls.\n\nQuestion:\nAre nD4L gene concurrent 10609T > C and 10663T > C mutations associated with Leber 's hereditary optic neuropathy in a large pedigree from Kuwait?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis study was performed to investigate the effect of temperature of blood cardioplegia on the recovery of postischemic cardiac function. Pigs on cardiopulmonary bypass were subjected to global ischemia (30 minutes), followed by cold (n = 10) or warm (n = 11) continuous antegrade blood cardioplegia (45 minutes) delivered at 55-60 mm Hg. Global left ventricular function, evaluated by preload recruitable stroke work, decreased with cold cardioplegia from 91 (85-103) [mean (quartile interval)], at baseline, to 73 (55-87) erg x 10(3)/mL postbypass (p = 0.03), but was unchanged after warm cardioplegia; 110 (80-132) to 109 (71-175) erg x 10(3)/mL (p > 0.5). However, the difference between treatment effects was not significant (p = 0.25). Diastolic function, evaluated by end-diastolic pressure-volume relation, deteriorated without any difference between groups. Mean cardioplegic flow was similar between groups. Coronary vascular resistance increased at constant rate during warm cardioplegic delivery, but remained unchanged with cold cardioplegia (p = 0.001 between regression coefficients).\n\nQuestion:\nDoes warm or cold continuous blood cardioplegia provide similar myocardial protection?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCurrent diagnostic methods of renal allograft rejection are neither sensitive nor specific. Needle biopsies are invasive and associated with patient morbidity. Thus, it is desirable to develop noninvasive tests to predict and diagnose rejection. Using a case-control approach, surface-enhanced laser desorption/ionization time-of-flight mass spectrometry was used to identify plasma proteins associated with renal allograft rejection. From each rejection patient (n=16), two plasma samples (one near the biopsy date and the other at a time postbiopsy) were compared. Biopsy-confirmed nonrejection patients (n=48) were further analyzed as controls. Antibody-based quantitative enzyme-linked immunosorbent assay was performed to validate candidate biomarker apolipoprotein A1 (Apo A1) in a subset of the original and a second cohort of biopsy-confirmed rejection (n=40) and nonrejection (n=70) patients. Twenty-two proteins/peptides showed significant differences between rejection and postrejection samples. Peptides 5191 Da and 4467 Da detected rejection with 100% sensitivity and 94% specificity. The 4467 Da peptide was identified as the C-terminal fragment of α-1 antichymotrypsin and a 28 kDa protein was determined as Apo A1. Both protein levels were significantly lower at rejection compared with postrejection. Protein levels of nonrejection patients were similar to the postrejection samples. Apo A1 enzyme-linked immunosorbent assay results showed significantly lower Apo A1 levels (P=0.001 for the original and P=4.14E-11 for the second cohort) at the time of rejection compared with nonrejection which coincides with the SELDI findings.\n\nQuestion:\nAre apolipoprotein A1 and C-terminal fragment of α-1 antichymotrypsin candidate plasma biomarkers associated with acute renal allograft rejection?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nDesflurane and sevoflurane have markedly different pungencies. The tested hypothesis was that patients breathing equivalent concentrations of desflurane or sevoflurane through a laryngeal mask airway (LMA) would have similar responses. After institutional review board approval and informed consent were obtained, 60 patients were enrolled and given intravenous midazolam (14 microg/kg) and fentanyl (1 microg/kg) 5 min before induction of anesthesia. The LMA was inserted at loss of consciousness after 2 mg/kg propofol. When spontaneous breathing returned, a randomly assigned volatile anesthetic was started at an inspired concentration of either 1.8% sevoflurane or 6% desflurane at a fresh gas flow of 6 l/min in air:oxygen (50:50). After 5 min, a controlled movement of the LMA took place. Three minutes later, the inspiratory anesthetic concentration was changed to either 3.6% sevoflurane or 12% desflurane for 3 min. A blinded observer recorded movements and airway events during the start of anesthetic, LMA movement, deepening of the anesthetic, and emergence before LMA removal. There were no differences at anesthetic start and LMA movement. Desflurane titration to 12% increased heart rate, increased mean arterial blood pressure, and initiated frequent coughing (53% vs. 0% sevoflurane) and body movements (47% vs. 0% sevoflurane). During emergence, there was a twofold greater incidence of coughing and a fivefold increase in breath holding in the desflurane group.\n\nQuestion:\nDoes desflurane enhance reactivity during the use of the laryngeal mask airway?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo investigate the impact of maternal diet during breastfeeding on atopic sensitization of infants at risk. Prospective cohort study. Turku University Central Hospital, Finland. Altogether 114 infants with a family history of atopic disease were followed during their first year of life. The mothers completed a 4 day food record during breastfeeding just before the infants were 3 months old. Atopic sensitization of the infants was determined by a positive skin prick test result at 12 months. Positive skin prick test reactivity to at least one antigen was detected in 27/114 (24%) infants at 12 months. The energy intake of the mothers was low, mean 8.0 MJ/day (95% CI 7.7-8. 3), and the proportion of energy derived from fat was high, mean 36. 6 E% (95% CI 35.6-37.6). Atopic mothers had a higher intake of total fat and saturated fat and a lower intake of carbohydrate as a percentage of total energy intake than non-atopic mothers; P=0.017, P=0.050, P=0.004 respectively. Maternal intake of saturated fat during breastfeeding was associated with atopic sensitization of the infant, OR=1.16 (95% CI 1.001-1.36); P=0.048 irrespective of the maternal atopic status.\n\nQuestion:\nIs maternal diet rich in saturated fat during breastfeeding associated with atopic sensitization of the infant?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis study's aim was to assess the use of intravesical injection of botulinum neurotoxin type A (BoNT-A) as a treatment of overactive bladder (OAB) in children. A 6-year retrospective study of children who received BoNT-A for OAB was performed. Treatment outcome was classified as complete success (CS), partial success (PS) or treatment failure (TF). Of the 57 patients who received BoNT-A treatment for OAB, 35 were males. CS occurred in 74.2% of males and 54.5% of females. PS was achieved in 20% of males and 18.2% of females. TF occurred in 2.9% of males and 22.7% of females. Anticholinergics had previously been used and had been effective in 58.6% and 83.3% of males and females. Significant side effects to medications were experienced in 12 (41.4%) males and 4 (22.2%) females. Of these, BoNT-A achieved CS in seven (53.3%) males and two (50%) females and PS in three (25%) males and one (25%) female. BoNT-A was successful in seven (58.3%) males and two (66.7%) females where anticholinergics were ineffective.\n\nQuestion:\nIs urinary incontinence in children : botulinum toxin a safe and effective treatment option?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIncreased body iron stores and hepcidin have been hypothesized to promote atherosclerosis by inducing macrophage iron accumulation and release of cytokines, but direct demonstration in human cells is lacking. The aim of this study was to evaluate the effect of iron on cytokine release in monocytes ex vivo and the correlation with vascular damage and to evaluate the relationship among serum levels of hepcidin, cytokines, and vascular damage in patients with metabolic syndrome alterations. Manipulation of iron status with ferric ammonium citrate and hepcidin-25 induced monocyte chemoattractant protein (MCP)-1 and interleukin-6 in human differentiating monocytes of patients with hyperferritinemia associated with the metabolic syndrome (n=11), but not in subjects with hemochromatosis or HFE mutations impairing iron accumulation (n=15), and the degree of induction correlated with the presence of carotid plaques, detected by echocolor-Doppler. In monocytes of healthy subjects (n=7), iron and hepcidin increased the mRNA levels and release of MCP-1, but not of interleukin-6. In 130 patients with metabolic alterations, MCP-1 levels, as detected by ELISA, were correlated with hepcidin-25 measured by time-of-flight mass spectrometry (P=0.005) and were an independent predictor of the presence of carotid plaques (P=0.05).\n\nQuestion:\nDo serum hepcidin and macrophage iron correlate with MCP-1 release and vascular damage in patients with metabolic syndrome alterations?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nRecent technological advances have stimulated the development of endoscopic optical biopsy technologies. This study compared the accuracy of endoscopic diagnosis using magnifying narrow-band imaging (NBI) and histologic diagnosis of esophageal squamous lesions. Patients at high risk for esophageal squamous cell carcinoma were examined with endoscopy and subsequent biopsy. The lesions diagnosed as cancer on NBI and the lesions diagnosed as cancer on biopsy were resected endoscopically or surgically. Histological diagnoses of resected specimens, the reference standards in this study, were made by a pathologist who was blind to both the endoscopic and biopsy diagnoses. The primary outcome was the accuracy of endoscopic and biopsy diagnosis. A noninferiority trial design with a noninferiority margin of -10% was chosen to investigate the accuracy of endoscopic diagnosis using magnifying NBI. Between November 2010 and October 2012, a total of 111 lesions in 85 patients were included in the analysis. The accuracy of endoscopic diagnosis and biopsy diagnosis for all lesions was 91.0% (101/111) and 85.6% (95/111), respectively. The difference in diagnostic accuracy was 5.4% (95% confidence interval: -2.9%-13.7%). The accuracy of endoscopic diagnosis and biopsy diagnosis of invasive cancers was 94.9% (74/78) and 84.6% (66/78), respectively. The difference was 10.3% (95% confidence interval: 1.6%-19.0%) for invasive cancers. The lower bound of the 95% confidence interval was above the prestated -10% in both cases.\n\nQuestion:\nDoes endoscopic optical diagnosis provide high diagnostic accuracy of esophageal squamous cell carcinoma?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMonoamine reuptake inhibitors can stimulate expression of brain-derived neurotrophic factor (BDNF) and alter long-term potentiation (LTP), a widely used model for the synaptic mechanisms that underlie memory formation. BDNF expression is upregulated during LTP, and BDNF in turn positively modulates LTP. Previously, we found that treatment with venlafaxine, a serotonin and norepinephrine reuptake inhibitor (SNRI), but not citalopram, a selective serotonin reuptake inhibitor (SSRI), reduced LTP in hippocampal area CA1 without changing hippocampal BDNF protein expression. We tested the hypothesis that combined serotonin and norepinephrine reuptake inhibition is necessary for LTP impairment, and we reexamined the potential role of BDNF by testing for region-specific changes in areas CA1, CA3, and dentate gyrus. We also tested whether early events in the LTP signaling pathway were altered to impair LTP. Animals were treated for 21 days with venlafaxine, imipramine, fluoxetine, or maprotiline. In vitro hippocampal slices were used for electrophysiological measurements. Protein expression was measured by enzyme-linked immunosorbent assay (ELISA) and Western blotting. LTP was impaired only following treatment with combined serotonin and norepinephrine reuptake inhibitors (venlafaxine, imipramine) but not with selective serotonin (fluoxetine) or norepinephrine (maprotiline) reuptake inhibitors. BDNF protein expression was not altered by venlafaxine or imipramine treatment, nor were postsynaptic depolarization during LTP inducing stimulation or synaptic membrane NMDA receptor subunit expression affected.\n\nQuestion:\nDo antidepressants that inhibit both serotonin and norepinephrine reuptake impair long-term potentiation in hippocampus?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]