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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:\nAdjuvant interferon based chemoradiation has rendered promising results against pancreatic cancer. This study evaluated the in vivo effect of interferon α on two human pancreatic carcinoma cell lines implanted in nude. MiaPaCa-2 expressed the interferon α/β receptor and Panc-1 cells did not. Regimen I consisted of intraperitoneal single-agent gemcitabine and Regimen II consisted of IFN-α and gemcitabine biweekly for 30 d. Regimen I and II significantly decreased median tumor volume compared with control mice (P < 0.001). However, MiaPaCa-2 showed a more dramatic response to Regimen II compared with Panc-1 implanted mice. MiaPaCa-2 and treated with Regimen II showed less metastasis and less local invasion compared with Panc-1 treated with same regimen. Regimen II was more effective on MiaPaCa-2 compared with Regimen I (P < 0.001). There were no differences between Regimens I and II in the Panc-1 group.\n\nQuestion:\nIs the expression of interferon receptor α/β in human pancreatic cancer in nude mice essential for tumor response to interferon α treatment?\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:\nZebrafish mutants generated by ethylnitrosourea-mutagenesis provide a powerful tool for dissecting the genetic regulation of developmental processes, including organogenesis. One zebrafish mutant, \"flotte lotte\" (flo), displays striking defects in intestinal, liver, pancreas, and eye formation at 78 hours postfertilization (hpf). In this study, we sought to identify the underlying mutated gene in flo and link the genetic lesion to its phenotype. Positional cloning was employed to map the flo mutation. Subcellular characterization of flo embryos was achieved using histology, immunocytochemistry, bromodeoxyuridine incorporation analysis, and confocal and electron microscopy. The molecular lesion in flo is a nonsense mutation in the elys (embryonic large molecule derived from yolk sac) gene, which encodes a severely truncated protein lacking the Elys C-terminal AT-hook DNA binding domain. Recently, the human ELYS protein has been shown to play a critical, and hitherto unsuspected, role in nuclear pore assembly. Although elys messenger RNA (mRNA) is expressed broadly during early zebrafish development, widespread early defects in flo are circumvented by the persistence of maternally expressed elys mRNA until 24 hpf. From 72 hpf, elys mRNA expression is restricted to proliferating tissues, including the intestinal epithelium, pancreas, liver, and eye. Cells in these tissues display disrupted nuclear pore formation; ultimately, intestinal epithelial cells undergo apoptosis.\n\nQuestion:\nDoes abnormal nuclear pore formation trigger apoptosis in the intestinal epithelium of elys-deficient zebrafish?\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:\nSerum concentrations of conventional nutrition-related proteins, such as albumin, prealbumin, transferrin, and retinol-binding protein, are usually inconsistent with changes in anthropometric measurements in the postnatal period. The aim of this study was to evaluate how reliable growth hormone (GH), insulin-like growth factors (IGFs), IGF-binding proteins (IGFBPs), and leptin, the proteins known to be involved in the regulation of growth, are in reflecting postnatal growth and nutritional status in preterm neonates. Blood samples and anthropometric measurements were collected from 55 preterm neonates (chronological age 30.4 +/- 2.8 weeks) for 4 continuous weeks (weeks 0 to 3). After adjusting for chronological age, body weights and serum IGF-II concentrations were significantly greater and serum transferrin concentrations were significantly lower in weeks 2 and 3 than in week 0 (repeated-measures analysis of variance (ANOVA) and Bonferroni test, p < .05). Forward stepwise multivariate regression analysis showed that change in total IGF-I (week 0 to week 3) was a positive predictor, and changes in insulin and prealbumin were negative predictors of postnatal weight gain. In addition, daily fat intake was a positive predictor of postnatal length increases, and changes in prealbumin, insulin, and GH were negative predictors of postnatal changes in the ponderal index (weight x length(-3)). Changes in GH and IGFBP-2 were negative predictors of changes in head circumference and triceps skinfold thickness, respectively.\n\nQuestion:\nAre changes in serum insulin-like growth factors , not leptin , associated with postnatal weight gain in preterm neonates?\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:\nObstructive sleep apnea (OSA) is often observed in patients with metabolic syndrome (MetS). In addition, the association of MetS and OSA substantially increases sympathetic nerve activity. However, the mechanisms involved in sympathetic hyperactivation in patients with MetS + OSA remain to be clarified. We tested the hypothesis that chemoreflex sensitivity is heightened in patients with MetS and OSA. Prospective clinical study. Forty-six patients in whom MetS was newly diagnosed (ATP-III) were allocated into: (1) MetS + OSA (n = 24, 48 ± 1.8 yr); and (2) MetS - OSA (n = 22, 44 ± 1.7 yr). Eleven normal control subjects were also studied (C, 47 ± 2.3 yr). OSA was defined as an apnea-hypopnea index ≥ 15 events/hr (polysomnography). Muscle sympathetic nerve activity (MSNA) was measured by microneurography technique. Peripheral chemoreflex sensitivity was assessed by inhalation of 10% oxygen and 90% nitrogen (carbon dioxide titrated), and central chemoreflex sensitivity by 7% carbon dioxide and 93% oxygen. Physical characteristics and MetS measures were similar between MetS + OSA and MetS - OSA. MSNA was higher in MetS + OSA patients compared with MetS - OSA and C (33 ± 1.3 versus 28 ± 1.2 and 18 ± 2.2 bursts/min, P < 0.05). Isocapnic hypoxia caused a greater increase in MSNA in MetS + OSA than MetS - OSA and C (P = 0.03). MSNA in response to hyperoxic hypercapnia was greater in MetS + OSA compared with C (P = 0.005). Further analysis showed a significant association between baseline MSNA and peripheral (P < 0.01) and central (P < 0.01) chemoreflex sensitivity. Min ventilation in response to hyperoxic hypercapnia was greater in MetS + OSA compared with C (P = 0.001).\n\nQuestion:\nIs obstructive sleep apnea associated with increased chemoreflex sensitivity in patients with metabolic 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:\nThis study sought to determine if there is a relationship between the consumption of alcohol and tobacco and oral colonization by mutans streptococci and Candida species. Subjects were recruited from the University Dental Clinic of CEU Cardenal Herrera University (Moncada, Valencia). Information on alcohol and tobacco consumption was obtained by questionnaire. Individual stimulated saliva samples from 105 patients were obtained and selective media was used to isolate and quantify mutans streptococci and Candida spp. colony forming units per millilitre of saliva (CFU ml(-1) ). Samples were stratified by duration and quantity of alcohol and tobacco consumption. Alcohol consumption statistically significantly decreased oral carriage of mutans streptococci, whereas there was no effect on Candida albicans colonization levels. Tobacco users were found to harbour elevated levels of C. albicans; however, there was no observed effect on bacterial colonization by mutans streptococci. The carriage of other species investigated, such as Candida krusei, Candida tropicalis and lactobacilli, do not show a response to the consumption of the stimulants analysed. Microbial colonization of the oral cavity changes in a species-specific manner in response to dietary and social habits such as drinking alcohol and smoking.\n\nQuestion:\nDo alcohol and tobacco consumption affect the oral carriage of Candida albicans and mutans streptococci?\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:\nRiboflavin is the precursor of flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD), essential cofactors for many metabolic enzymes that catalyze a variety of biochemical reactions. Previously we showed that free flavin (riboflavin, FMN, and FAD) concentrations were decreased in leaves of transgenic Arabidopsis plants expressing a turtle riboflavin-binding protein (RfBP). Here, we report that flavin downregulation by RfBP induces the early flowering phenotype and enhances expression of floral promoting photoperiod genes. Early flowering was a serendipitous phenomenon and was prudently characterized as a constant phenotype of RfBP-expressing transgenic Arabidopsis plants in both long days and short days. The phenotype was eliminated when leaf free flavins were brought back to the steady-state levels either by the RfBP gene silencing and consequently nullified production of the RfBP protein, or by external riboflavin feeding treatment. RfBP-induced early flowering was correlated with enhanced expression of floral promoting photoperiod genes and the florigen gene FT in leaves but not related to genes assigned to vernalization, autonomous, and gibberellin pathways, which provide flowering regulation mechanisms alternative to the photoperiod. RfBP-induced early flowering was further correlated with increased expression of the FD gene encoding bZIP transcription factor FD essential for flowering time control and the floral meristem identity gene AP1 in the shoot apex. By contrast, the expression of FT and photoperiod genes in leaves and the expression of FD and AP1 in the shoot apex were no longer enhanced when the RfBP gene was silenced, RfBP protein production canceled, and flavin concentrations were elevated to the steady-state levels inside plant leaves.\n\nQuestion:\nDoes downregulation of leaf flavin content induce early flowering and photoperiod gene expression in Arabidopsis?\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:\nLin28 has been known to control the proliferation and pluripotency of embryonic stem cells. The purpose of this study was to determine the downstream effectors of Lin28 in mouse embryonic stem cells (mESCs) by RNA interference and microarray analysis. The control siRNA and Lin28 siRNA (Dharmacon) were transfected into mESCs. Total RNA was prepared from each type of transfected mESC and subjected to reverse transcription-polymerase chain reaction (RT-PCR) analysis to confirm the downregulation of Lin28. The RNAs were labeled and hybridized with an Affymetrix Gene-Chip Mouse Genome 430 2.0 array. The data analysis was accomplished by GenPlex 3.0 software. The expression levels of selected genes were confirmed by quantitative real-time RT-PCR. According to the statistical analysis of the cDNA microarray, a total of 500 genes were altered in Lin28-downregulated mESCs (up-regulated, 384; down-regulated, 116). After differentially expressed gene filtering, 31 genes were selected as candidate genes regulated by Lin28 downregulation. Among them, neuropeptide Y5 receptor and oocyte-specific homeobox 5 genes were significantly upregulated in Lin28-downregulated mESCs. We also showed that the families of neuropeptide Y receptor (Npyr) and oocyte-specific homeobox (Obox) genes were upregulated by downregulation of Lin28.\n\nQuestion:\nDoes lin28 regulate the expression of neuropeptide Y receptors and oocyte-specific homeobox genes in mouse embryonic stem 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 INT6 gene was first discovered as a site of integration in mouse mammary tumors by the mouse mammary tumor virus; however, INT6's role in the development of human breast cancer remains largely unknown. By gene silencing, we have previously shown that repressing INT6 promotes transforming activity in untransformed human mammary epithelial cells. In the present study, guided by microarray data of human tumors, we have discovered a role of Int6 in stromal fibroblasts. We searched microarray databases of human tumors to assess Int6's role in breast cancer. While INT6 expression levels, as expected, were lower in breast tumors than in adjacent normal breast tissue samples, INT6 expression levels were also substantially lower in tumor stroma. By immunohistochemistry, we determined that the low levels of INT6 mRNA observed in the microarray databases most likely occurs in stromal fibroblasts, because far fewer fibroblasts in the tumor tissue showed detectable levels of the Int6 protein. To directly investigate the effects of Int6 repression on fibroblasts, we silenced INT6 expression in immortalized human mammary fibroblasts (HMFs). When these INT6-repressed HMFs were co-cultured with breast cancer cells, the abilities of the latter to form colonies in soft agar and to invade were enhanced. We analyzed INT6-repressed HMFs and found an increase in the levels of a key carcinoma-associated fibroblast (CAF) marker, smooth muscle actin. Furthermore, like CAFs, these INT6-repressed HMFs secreted more stromal cell-derived factor 1 (SDF-1), and the addition of an SDF-1 antagonist attenuated the INT6-repressed HMFs' ability to enhance soft agar colony formation when co-cultured with cancer cells. These INT6-repressed HMFs also expressed high levels of mesenchymal markers such as vimentin and N-cadherin. Intriguingly, when mesenchymal stem cells (MSCs) were induced to form CAFs, Int6 levels were reduced.\n\nQuestion:\nDoes int6 reduction activate stromal fibroblasts to enhance transforming activity in breast epithelial 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 hypothesized that the Infant/Child Monitoring Questionnaire (ICMQ) could be used to identify at-risk infants eligible for developmental interventional services. Of this cross-sectional observational study, group A (n = 108) included a retrospective review of moderate risk infants scheduled for developmental assessment clinic (DAC) visits. Group B (n = 108) included moderate-risk infants whose parents completed the ICMQ. Group C (n = 67) included high-risk infants who were seen in the DAC and whose parents completed the ICMQ. For group A infants, 43.5% were seen in the DAC; 10.6% of these visits resulted in an intervention. For group B infants, 56.5% of parents completed the ICMQ; 66.7% of subsequent visits resulted in an intervention. For group C infants, comparison of ICMQ and DAC visits showed moderate agreement (kappa = 0.50).\n\nQuestion:\nDoes the value of the Infant/Child Monitoring Questionnaire for identification of developmental disability among neonatal intensive care unit graduate?\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 cyclophilin (Cyp) inhibitors - cyclosporine A (CsA), NIM811, Debio 025, and SCY 635 - block HCV replication both in vitro and in vivo, and represent a novel class of potent anti-HCV agents. We and others showed that HCV relies on cyclophilin A (CypA) to replicate. We demonstrated that the hydrophobic pocket of CypA, where Cyp inhibitors bind, and which controls the isomerase activity of CypA, is critical for HCV replication. Recent studies showed that under Cyp inhibitor selection, mutations arose in the HCV nonstructural 5A (NS5A) protein. This led us to postulate that CypA assists HCV by acting on NS5A. We tested this hypothesis by developing several interaction assays including GST pull-down assays, ELISA, and mammalian two-hybrid binding assays. We demonstrated that full-length NS5A and CypA form a stable complex. Remarkably, CsA prevents the CypA-NS5A interaction in a dose-dependent manner. Importantly, the CypA-NS5A interaction is conserved among genotypes and is interrupted by CsA. Surprisingly, the NS5A mutant protein, which arose in CsA-resistant HCV variants, behaves similarly to wild-type NS5A in terms of both CypA binding and CsA-mediated release from CypA. This latter finding suggests that HCV resistance to CsA does not correlate with a resistance of the CypA-NS5A interaction to Cyp inhibitors. Moreover, we found that CypA, devoid of its isomerase activity, fails to bind NS5A.\n\nQuestion:\nDoes hCV resistance to cyclosporin A correlate with a resistance of the NS5A-cyclophilin A interaction to cyclophilin inhibitors?\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:\nThe heat shock protein H11 is silenced in melanoma cell lines, where its forced expression by demethylation with Aza-C triggers apoptosis. To examine whether H11 is silenced by aberrant DNA methylation in melanoma as compared to nevi and normal skin tissues. Cell suspensions from benign intradermal nevi, atypical nevi and malignant melanoma tissues were used in reverse-transcriptase PCR and methylation-specific PCR. Paraffin-embedded tissues were stained with H11 antibody. H11 is methylated in 60-75% of melanoma and atypical nevi, but not in normal skin or most benign nevi. Methylation is inversely correlated with H11 expression.\n\nQuestion:\nDoes aberrant DNA methylation silence the novel heat shock protein H11 in melanoma but not benign melanocytic lesions?\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:\nAccumulated evidence indicates that the incidence of early-onset breast cancer has rapidly increased in Taiwan and other Asian compared to Western countries. The mismatch repair (MMR) pathway might be one of the crucial mechanisms of predisposition to early breast cancer. In this study, we explored whether MMR gene polymorphisms contribute to the risk of breast cancer in young women. This was a 2-stage case-control study including 737 cases and 719 controls. After eight single nucleotide polymorphisms (SNPs) were genotyped in MMR pathway genes in the stage I study, a promising SNP, MSH2 rs2303425, was selected for validation in the stage II study. A luciferase reporter assay was used to evaluate the transcriptional activity of MSH2. Logistic regression analysis showed that individuals with the MSH2 rs2303425 C/C genotype had a significantly increased risk of breast cancer compared to those with the T/T genotype (adjusted odds ratio 2.0; 95 % confidence interval 1.1-3.8), particularly in early-onset breast cancer patients with the luminal A subtype. The luciferase assay in three cell lines indicated that the MSH2 rs2303425 T/C substitution decreased MSH2 expression, which is consistent with the finding of an association study.\n\nQuestion:\nIs mSH2 rs2303425 Polymorphism Associated with Early-Onset Breast Cancer in Taiwan?\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:\nTest the hypothesis that the link between respiratory viruses and pulmonary exacerbation in cystic fibrosis (CF) reflects increased frequency or severity of lower airways infection. Molecular respiratory viral panels (RVPs), cell counts, and quantitative bacterial cultures were assessed in 235 bronchoalveolar lavage fluid (BALF) samples from 138 children with CF. Relationships among the data were analyzed using multivariate methods. RVPs were positive in 67 (28.5%) BALF samples from 52 (37.7%) patients, with rhinovirus/enterovirus most common (82.4% of RVP+). RVP+ patients were younger (5.4 years, IQR 3.0-9.7 vs. 8.0 years, IQR 3.5-12.9; P < 0.01), more likely to have respiratory symptoms (74.6% vs. 55.2%, P < 0.01), and had higher BALF percent neutrophils (70.5%, IQR 46-85% vs. 59.3%, IQR 34-77%; P < 0.05). Percent predicted FEV1 at bronchoscopy was diminished from baseline in both groups, but recovered in the RVP- (90.2 ± 22.2% vs. 89.6 ± 19.7%, P = 0.62) but not the RVP+ subjects (95.7 ± 21.1% vs. 89.1 ± 18.0%, P < 0.05). RVP status did not alter recovery rates of typical CF respiratory pathogens including Staphylococcus aureus (44.8% vs. 42.9%) and Pseudomonas aeruginosa (25.4% vs. 25.6%). However, common respiratory pathogens (Haemophilus species, Moraxella species, and Streptococcus pneumoniae) were recovered more frequently from RVP+ samples independent of age (OR 3.6, 95% CI 1.8-7.5, P < 0.001).\n\nQuestion:\nAre respiratory viruses associated with common respiratory pathogens in cystic fibrosis?\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 quantified absolute myocardial blood flow (MBF) using a spin-labeling MRI (SL-MRI) method after transplantation of endothelial cells (ECs) into the infarcted heart. Our aims were to study the temporal changes in MBF in response to EC transplantation and to compare regional MBF with contractile function (wall motion) and microvascular density. We first validated the SL-MRI method with the standard microsphere technique in normal rats. We then induced myocardial infarction in athymic rats and injected 5 million ECs (human umbilical vein endothelial cells) suspended in Matrigel or Matrigel alone (vehicle) along the border of the blanched infarcted area. At 2 weeks after myocardial infarction, MBF averaged over the entire slice (P=0.038) and in the infarcted region (P=0.0086) was significantly higher in EC versus vehicle group; the greater MBF was accompanied by an increase of microvasculature density in the infarcted region (P=0.0105 versus vehicle). At 4 weeks after myocardial infarction, MBF in the remote region was significantly elevated in EC-treated hearts (P=0.0277); this was accompanied by increased wall motion in this region assessed by circumferential strains (P=0.0075). Intraclass correlation coefficients and Bland-Altman plot revealed a good reproducibility of the SL-MRI method.\n\nQuestion:\nDoes spin-labeling magnetic resonance imaging detect increased myocardial blood flow after endothelial cell transplantation in the infarcted heart?\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:\nIodine is an essential micronutrient for normal human growth and development. It is estimated that more than 1.6 billion people live in iodine-deficient environments, yet there are still some countries and areas where the prevalence of iodine-deficiency disorders is unknown. To establish the prevalence of iodine-deficiency disorders in the Zanzibar Islands, a community assumed to have ready access to iodine-rich seafoods. In a cross-sectional study, 11,967 schoolchildren were palpated for goiter prevalence, a subsample was evaluated for urinary iodine concentration, and the availability of iodated salt was assessed at the household and retail levels. The mean total goiter prevalence was 21.3% for Unguja and 32.0% for Pemba. The overall median urinary iodine concentration was 127.5 microg/L. For Unguja the median was 185.7 microg/L, a higher value than the median of 53.4 microg/L for Pemba (p < .01). The household availability of iodated salt was 63.5% in Unguja and 1.0% in Pemba. The community was not aware of the iodine-deficiency problem and had never heard of iodated salt.\n\nQuestion:\nDoes iodine deficiency persist in the Zanzibar Islands of Tanzania?\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:\nMatrix metalloprotease-2 (MMP-2) and matrix metalloprotease-9 (MMP-9) play a key role in tissue remodelling after processes such as joint destruction in rheumatoid arthritis. Their expression may reflect the disease activity and they could therefore represent a useful marker to assess the efficacy of therapy. In this study MMP-2 and MMP-9 serum were evaluated in patients with chronic arthritis during therapy with the anti-TNFalpha mAb, infliximab. Fifty patients with chronic arthritis, 26 with rheumatoid arthritis and 24 with undifferentiated chronic arthritis, were recruited and treated with infliximab (3 mg/kg). Serum concentrations of MMP-2 and MMP-9 were serially measured by gelatine zymography at baseline and after two and fourteen weeks of infliximab therapy. DAS-28 and ACR response criteria were applied to assess disease activity and clinical improvement. Twenty-four healthy donors were included in the study as controls. Although therapy with infliximab induced a statistically significant reduction of the DAS-28 score and improvement of the ACR clinical response, MMP-2 and MMP-9 serum concentrations were not modulated during therapy with infliximab.\n\nQuestion:\nDoes infliximab therapy modify MMP-2 and MMP-9 serum concentrations in chronic arthritis?\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:\nThe purpose was to investigate the efficacy and complications of nonvalved glaucoma drainage implant (GDI) surgery and GDI combined with trabeculectomy. Serial Japanese patients who received GDI were retrospectively investigated. The survival rate of eyes was analyzed using the Kaplan-Meier method, defining death as: (1) Intraocular pressure (IOP) <6 mmHg, or ≥22 mmHg, and <20% reduction of preoperative IOP, (2) additional glaucoma surgery, (3) loss of light perception. Prognostic factors of age, sex, previous surgery, type of glaucoma, synechial closure, preoperative IOP, type of GDI (single-, double-plate Molteno, Baerveldt 350) and GDI combined with trabeculectomy were investigated employing proportional hazards analysis. One hundred and twenty-four eyes of 109 patients aged 53.3 ± 7.8 years old were analyzed. Types of GDI were single-plate (15.3%), double-plate Molteno (71.8%), and Baerveldt 350 (12.9%). The results of survival rate analysis were 86.1, 71.1, 71.1, and 64.6% for 1, 3, 5, and 10 years respectively. Thirty-four eyes (27.4%) died because of uncontrolled IOP (19.4%), loss of light perception (5.6%), and additional glaucoma surgery (2.4%). Single-plate Molteno was the only risk factor for failure. Persistent unphysiological hypotony (0.8%) and bullous keratopathy (5.6%) were observed.\n\nQuestion:\nDo long-term results of non-valved glaucoma drainage implant surgery and glaucoma drainage implant combined with trabeculectomy?\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:\nAlterations in the serotonin (5-HT) system have been suggested as a mechanism of sleep apnea in humans and rodents. The objective is to evaluate the contribution of 5-HT to this disorder. We studied sleep and breathing (whole-body plethysmography) in mutant mice that lack monoamine oxidase A (MAOA) and have increased concentrations of monoamines, including 5-HT. Compared to wild-type mice, the mutants showed similar amounts of slow wave sleep (SWS) and rapid eye movement sleep (REMS), but exhibited a 3-fold increase in SWS and REMS apnea indices. Acute administration of the MAOA inhibitor clorgyline decreased REMS amounts and increased the apnea index in wild-type but not mutant mice. Parachlorophenylalanine, a 5-HT synthesis inhibitor, reduced whole brain concentrations of 5-HT in both strains, and induced a decrease in apnea index in mutant but not wild-type mice.\n\nQuestion:\nAre sleep apneas increased in mice lacking monoamine oxidase A?\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:\nMeasures of health-related quality of life (HRQoL), like the Short Form (SF)-36, have been suggested to correlate with inflammatory biomarkers. It is, however, unclear whether a joint measure of two inflammatory biomarkers would bring additional information in comparison with evaluation of one inflammatory biomarker. To evaluate associations between SF-36 and low-grade inflammation in a Swedish population, with emphasis on a combined measure of C-reactive protein (CRP) and interleukin-6 (IL-6) as a proxy for low-grade inflammation. In a randomly selected sample of a middle-aged Swedish general population (n = 905; aged 45-69 years, 50% women), relations between SF-36 parameters and the biomarkers were tested. Regression and correlation analyses were adjusted for sex, age, presence of disease, lifestyle, and psychological factors. After adjustment for sex and age, HRQoL was significantly lower in the group with a joint elevation of CRP and IL-6 in comparison with either the group with no elevation or the groups showing elevation of one of the two biomarkers. Also after full adjustments, the combined measure of elevated CRP and IL-6, with few exceptions, was associated with significantly lower HRQoL in comparison with elevations in one of them, difference ranging from 4 (Mental Health scale) to 18 scale steps (Role-Physical scale).\n\nQuestion:\nIs the joint subclinical elevation of CRP and IL-6 associated with lower health-related quality of life in comparison with no elevation or elevation of only one of the biomarkers?\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:\nInvasive plants represent a significant threat to ecosystem biodiversity. To decrease the impacts of invasive species, a major scientific undertaking of the last few decades has been aimed at understanding the mechanisms that drive invasive plant success. Most studies and theories have focused on a single mechanism for predicting the success of invasive plants and therefore cannot provide insight as to the relative importance of multiple interactions in predicting invasive species' success. We examine four mechanisms that potentially contribute to the success of invasive velvetgrass Holcus lanatus: direct competition, indirect competition mediated by mammalian herbivores, interference competition via allelopathy, and indirect competition mediated by changes in the soil community. Using a combination of field and greenhouse approaches, we focus on the effects of H. lanatus on a common species in California coastal prairies, Erigeron glaucus, where the invasion is most intense. We found that H. lanatus had the strongest effects on E. glaucus via direct competition, but it also influenced the soil community in ways that feed back to negatively influence E. glaucus and other native species after H. lanatus removal.\n\nQuestion:\nDo multiple mechanisms enable invasive species to suppress native 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:\nControl measures which reduce individual exposure to malaria are expected to reduce disease, but also to eventually reduce immunity. Reassuringly, long term data following community wide ITN distribution show sustained benefits at a population level. However, the more common practice in Sub-Saharan Africa is to target ITN distribution on young children. There are few data on the long term outcomes of this practice. Episodes of febrile malaria were identified by active surveillance in 383 children over 18 months of follow up. In order to compare the short and long term outcomes of ITN use, we examined interactions between ITN use and age (12-42 months of age versus 42-80 months) in determining the risk of febrile malaria. ITN use and older age protected against the first or only episode of malaria (Hazard Ratio [HR] = 0.33, 95%CI 0.17-0.65 and HR = 0.30, 95%CI 0.17-0.51, respectively). The interaction term between ITN use and older age was HR = 2.91, 95%CI 1.02-8.3, p = 0.045, indicating that ITNs did not protect older children. When multiple episodes were included in analysis, ITN use and older age were again protective against malaria episodes (Incident Rate Ratio [IRR] = 0.43 95%CI 0.27-0.7) and IRR = 0.23, 95%CI 0.13-0.42, respectively) and the interaction term indicated that ITNs did not protect older children (IRR = 2.71, 95%CI 1.3-5.7, p = 0.008).\n\nQuestion:\nDo interactions between age and ITN use determine the risk of febrile malaria in children?\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:\nStudies have postulated that cyclooxygenase-2 (COX-2) selective inhibitors affect cardiovascular risk through various mechanisms. Some of these mechanisms could increase risk (for example, inhibition of prostacyclin production), and some could decrease risk (for example, inhibition of inflammation). To determine the effect of COX-2 inhibitors on risk for nonfatal myocardial infarction (MI). Case-control study. 36 hospitals in a 5-county area. 1718 case-patients with a first, nonfatal MI admitted to these hospitals and 6800 controls randomly selected from the same counties. Self-reported medication use assessed through telephone interviews. The adjusted odds ratio for MI among celecoxib users, relative to persons who did not use nonaspirin nonsteroidal anti-inflammatory drugs (NSAIDs), was 0.43 (95% CI, 0.23 to 0.79) compared with 1.16 (CI, 0.70 to 1.93) among rofecoxib users. The use of rofecoxib was associated with a statistically significant higher odds of MI compared with the use of celecoxib (adjusted odds ratio for rofecoxib vs. celecoxib, 2.72 [CI, 1.24 to 5.95]; P = 0.01). Nonselective NSAIDs were associated with a reduced odds of nonfatal MI relative to nonusers. Comparisons of COX-2 inhibitors with nonselective NSAIDs were the following: rofecoxib versus naproxen (odds ratio, 3.39 [CI, 1.37 to 8.40]) and celecoxib versus ibuprofen or diclofenac (odds ratio, 0.77 [CI, 0.40 to 1.48]).\n\nQuestion:\nDo patients exposed to rofecoxib and celecoxib have different odds of nonfatal 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:\nSeveral viruses have been recently isolated from Mediterranean phlebotomine sand flies; some are known to cause human disease while some are new to science. To monitor the Phlebotomus-borne viruses spreading, field studies are in progress using different sand fly collection and storage methods. Two main sampling techniques consist of CDC light traps, an attraction method allowing collection of live insects in which the virus is presumed to be fairly preserved, and sticky traps, an interception method suitable to collect dead specimens in high numbers, with a risk for virus viability or integrity. Sand flies storage requires a \"deep cold chain\" or specimen preservation in ethanol. In the present study the influence of sand fly collection and storage methods on viral isolation and RNA detection performances was evaluated experimentally. Specimens of laboratory-reared Phlebotomus perniciosus were artificially fed with blood containing Toscana virus (family Bunyaviridae, genus Phlebovirus). Various collection and storage conditions of blood-fed females were evaluated to mimic field procedures using single and pool samples. Isolation on VERO cell cultures, quantitative Real time-Retro-transcriptase (RT)-PCR and Nested-RT-PCR were performed according to techniques commonly used in surveillance studies. Live engorged sand flies stored immediately at -80 °C were the most suitable sample for phlebovirus identification by both virus isolation and RNA detection. The viral isolation rate remained very high (26/28) for single dead engorged females frozen after 1 day, while it was moderate (10/30) for specimens collected by sticky traps maintained up to 3 days at room temperature and then stored frozen without ethanol. Opposed to viral isolation, molecular RNA detection kept very high on dead sand flies collected by sticky traps when left at room temperature up to 6 days post blood meal and then stored frozen in presence (88/95) or absence (87/88) of ethanol. Data were confirmed using sand fly pools.\n\nQuestion:\nDo experimental evaluation of sand fly collection and storage methods for the isolation and molecular detection of Phlebotomus-borne viruses?\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 analyze retinal nerve fiber layer (RNFL) thickness in eyes with band atrophy by use of optical coherence tomography (OCT) and to evaluate the ability of OCT to detect this characteristic pattern of RNFL loss. Cross-sectional, retrospective study. Thirty-four eyes of 18 patients with bitemporal hemianopia caused by optic chiasm compression by chiasmal tumors were studied. All eyes were divided into 3 groups according to visual field loss grading after Goldmann perimetry. Retinal nerve fiber layer thickness measurements with OCT. Retinal nerve fiber layer thickness around the optic disc was measured by OCT (3.4-mm diameter circle). Calculation of the changes in OCT parameters, including the horizontal (nasal + temporal quadrant RNFL thickness) and vertical values (superior + inferior quadrant RNFL thickness) was based on data from 160 normal eyes. Comparison between the 3 visual field grading groups was done with the analysis of variance test. The receiver operating characteristic (ROC) curve for the horizontal and vertical value were calculated, and the areas under the curve (AUC) were compared. Retinal nerve fiber layer thickness in eyes with band atrophy decreased in all OCT parameters. The reduction rate in average and temporal RNFL thickness and horizontal value was correlated with visual field grading. The AUC of horizontal value was 0.970+/-0.011, which was significantly different from AUC of vertical value (0.903+/-0.022).\n\nQuestion:\nDoes optical coherence tomography detect characteristic retinal nerve fiber layer thickness corresponding to band atrophy of the optic discs?\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:\nPrenatal infection is a major risk factor for the occurrence of neuropsychiatric disorders. These have been associated with hippocampal neuroanatomical and functional abnormalities. In the present study, we evaluated the occurrence of pyramidal cell disarray and reelin neuronal deficit in the hippocampus, and the protective role of N-acetyl-cysteine (NAC) in a rodent experimental model of prenatal immune challenge. Sprague-Dawley rats received either 500 μg/kg of endotoxin (lipopolysaccharide, LPS) or 2 ml/kg of isotonic saline by i.p. injection on day 19 of gestation. After LPS injection, rats were or were not maintained on a preventive treatment of NAC (5 g/l in tap water), up to delivery. The pyramidal cell orientation and the number and type of reelin-expressing neurons were determined in male offspring. Prenatal LPS challenge led to permanent pyramidal cell disarray and to an early and transient decreased density of reelin-immunoreactive neurons. These disorders, more pronounced in the CA3 area, were prevented by NAC.\n\nQuestion:\nDoes n-acetyl-cysteine prevent pyramidal cell disarray and reelin-immunoreactive neuron deficiency in CA3 after prenatal immune challenge 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:\nThe heat shock protein gp96 is an endoplasmic reticulum chaperone involved in endoplasmic reticulum stress reactions. gp96 binds antigens and is secreted into extracellular space on cell stress. After reinternalization by antigen presenting cells, antigens can be transferred to major histocompatibility complex molecules. In recent studies, we found induction of gp96 during differentiation of intestinal macrophages, whereas it was absent in intestinal macrophages of patients with Crohn's disease. To study immuno-modulating effects of gp96 in T-cell transfer colitis BALB/c donor mice were injected with 2 × 100 μg gp96. After 1 week, 2.5 × 10(5) CD4+CD62L+ cells were isolated from spleens and injected into severe combined immunodeficiency recipients. Another group received cells from untreated donors and was treated with 100 μg gp96 after transfer. Control groups received cells from untreated donors, or buffer alone. After transfer of CD4+CD62L+ T cells from gp96-pretreated donors, mice (TBT gp96) showed an initial weight loss, but after 3 weeks, they recovered and reached the starting weight after 5 weeks. Mice treated with gp96 after transfer (TAT gp96) showed a delayed weight loss in comparison with the CD4+CD62L+ group. The histological scores in CD4CD62L mice were 2.6 ± 0.1, in TBT gp96 mice 1.3 ± 0.3 (CD4+CD62L+ versus TBT gp96: P < 0.05) and in mice treated after transfer 1.9 ± 0.1 (CD4+CD62L+ versus TAT gp96: P < 0.05).\n\nQuestion:\nDoes exogenous heat shock protein gp96 ameliorate CD4+CD62L+ T-cell-mediated transfer colitis?\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:\nConversion of factor XI (FXI) to FXIa is enhanced by polymers of inorganic phosphate (polyP). This process requires FXI to bind to polyP. Each FXIa subunit contains anion-binding sites (ABSs) on the apple 3 (A3) and catalytic domains that are required for normal heparin-mediated enhancement of FXIa inhibition by antithrombin. To determine the importance of FXI ABSs to polyP enhancement of FXI activation. Recombinant FXI variants lacking one or both ABSs were tested in polyP-dependent purified protein systems, plasma clotting assays, and a murine thrombosis model. In the presence of polyP, activation rates for FXI lacking either ABS were reduced compared with wild-type FXI, and FXI lacking both sites had an even greater defect. In contrast to heparin, polyP binding to FXIa did not enhance inhibition by antithrombin and did not interfere with FXIa activation of FIX. FXI lacking one or both ABSs does not reconstitute FXI-deficient plasma as well as wild-type FXI when polyP was used to initiate coagulation. In FXI-deficient mice, FXI lacking one or more ABSs was inferior to wild-type FXI in supporting arterial thrombus formation.\n\nQuestion:\nAre factor XI anion-binding sites required for productive interactions with polyphosphate?\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:\nSuberoylanilide hydroxamic acid (SAHA) has been studied in adult solid and hematologic malignancies. However, little information has been reported on the effects of SAHA on central nervous system (CNS) tumors including medulloblastoma, the most common malignant brain tumor in children. We investigated SAHA in preclinical medulloblastoma models to determine its anti-cancer efficacy as well as its ability to affect intracranial lesions when administered systemically. Tissue culture studies were performed treating primary human fibroblasts, established medulloblastoma cell lines, and primary human medulloblastoma tumors with SAHA. At 10 microM concentration, SAHA had little effect on normal fibroblasts but caused >90% apoptosis in cultured medulloblastoma cells. Primary medulloblastomas from patients were sensitive to SAHA compared to vehicle alone in ex vivo studies. In athymic mice with medulloblastoma xenograft tumors, oral SAHA resulted in apoptosis of tumor tissue and significantly slowed tumor growth. In the ND2:Smo transgenic mouse medulloblastoma model, SAHA treatment caused significant apoptosis in these cerebellar tumors.\n\nQuestion:\nIs suberoylanilide hydroxamic acid effective in preclinical studies of medulloblastoma?\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 the practice of parathyroid and thyroid surgery shifts toward short stay and outpatient treatment, the occurrence and management of postoperative nausea and vomiting (PONV) increases in importance due to its potential to delay discharge. PONV also may contribute negatively to the patient's experience and thus their level of satisfaction. The purpose of this study was to determine whether anesthetic technique based on propofol decreases the incidence of PONV and, consequently, improves patient satisfaction with their care. A prospective, randomized trial included patients undergoing thyroidectomy and parathyroidectomy under general anesthetic with (75 patients) or without (73 patients) propofol. Occurrences of nausea, vomiting, and the resultant treatment were tracked during the perioperative period. Repeated questionnaires at multiple time points determined patient expectations and experiences related to PONV after their operation. Statistical analyses compared differences between the propofol and non-propofol groups. PONV was significantly less likely in the propofol group at the early time points (in the operating room and postanesthesia care unit) but not at later time points (postoperative day 1 or 2). Patients were largely satisfied with different aspects of their management despite the specifics of their anesthetic regimen.\n\nQuestion:\nDoes propofol decrease early postoperative nausea and vomiting in patients undergoing thyroid and parathyroid operations?\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 randomized clinical equivalence trial was designed to evaluate health-related quality of life (HRQoL) after fast-track treatment for low-risk coronary artery bypass (CABG) patients. Four hundred and ten CABG patients were randomly assigned to undergo either short-stay intensive care treatment (SSIC, 8 h of intensive care stay) or control treatment (care as usual, overnight intensive care stay). HRQoL was measured at baseline and 1 month, and one year after surgery using the multidimensional index of life quality (MILQ), the EQ-5D, the Beck Depression Inventory and the State-Trait Anxiety Inventory. At one month after surgery, no statistically significant difference in overall HRQoL was found (MILQ-score P-value=.508, overall MILQ-index P-value=.543, EQ-5D VAS P-value=.593). The scores on the MILQ-domains, physical, and social functioning were significantly higher at one month postoperatively in the SSIC group compared to the control group (P-value=.049; 95%CI: 0.01-2.50 and P-value=.014, 95% CI: 0.24-2.06, respectively). However, these differences were no longer observed at long-term follow-up.\n\nQuestion:\nDoes health-related quality of life after fast-track treatment result from a randomized controlled clinical equivalence trial?\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:\nCholecystokinin regulates gut motility and visceral sensation. The aim of the study was to determine the diagnostic value of plasma cholecystokinin octapeptide (CCK-8) concentration in children with functional abdominal pain (FAP). Fifty-two children (33 girls and 19 boys) aged 6-17 years with chronic abdominal pain were included in this study. On the basis of clinical data, results of endoscopy and Criteria for Functional Disorders the patients were divided into three groups: group 1--functional dyspepsia (FD), group 2--irritable bowel syndrome (IBS), group 3--non-specific FAP. The control group consisted of children without abdominal pain in anamnesis. CCK-8 concentrations in plasma were measured with radio immunoassay technique, after plasma extraction. In study protocol we analysed CCK-8 levels in fasting state and 15, 30, 60 minutes after a standard test meal. In the fasting state plasma levels of CCK-8 were similar in each group and in controls. In the IBS patients CCK-8 levels were not increased after meal. In groups 1, 3 and controls postprandial levels were higher when compared to fasting state (p<0.05). Area under curve of CCK-8 plasma concentration was the lowest in group 2, but not significant compared to controls and other groups. No correlation was found between main symptoms of FD and IBS and CCK-8 concentration in plasma.\n\nQuestion:\nIs cholecystokinin octapeptide ( CCK-8 ) concentration in plasma affected in functional abdominal pain 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:\nPre-emptive therapy with valganciclovir (VGCV) has become the standard therapy for preventing cytomegalovirus (CMV) infection after allogeneic hematopoietic stem cell transplantation (HSCT). The effectiveness of low-dose VGCV (900 mg per day) has been shown to be equal to that of standard-dose VGCV (900 mg twice daily); however, individualized optimal dosing and toxicity of VGCV have not been reported. We conducted a retrospective study to evaluate the optimal dose of VGCV as pre-emptive therapy for preventing CMV infection by comparing the frequency of adverse events (AEs) and clinical efficacy in a low-dose VGCV group with those in a standard-dose VGCV group. Thirty-eight patients who were administered VGCV because of CMV antigenemia after HSCT were analyzed. Neutropenia (standard-dose group: 33%, low-dose group: 15%, P = 0.26) and thrombocytopenia (standard-dose group: 39%, low-dose group: 15%, P = 0.14) were frequent AEs of VGCV, and a significantly higher frequency of overall AEs was detected in the standard-dose group than in the low-dose group (P < 0.01). In comparison of dosage based on weight, dosage of VGCV >27 mg/kg was closely related to onset of AEs (P = 0.04).\n\nQuestion:\nIs occurrence of adverse events caused by valganciclovir as pre-emptive therapy for cytomegalovirus infection after allogeneic stem cell transplantation reduced by low-dose administration?\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 whether hyaluronan (HA)-CD44 promotes head and neck squamous cell carcinoma (HNSCC) cisplatin resistance and whether HA-CD44 promotes phospholipase C (PLC)-mediated Ca2+ signaling to alter cisplatin sensitivity in HNSCC. Cell line study. Tumor cell growth with the chemotherapeutic drug cisplatin was measured in the presence or absence of HA, anti-CD44 antibody plus HA, and other inhibitors of the PLC-mediated Ca2+ signaling pathway. Ca2+ mobilization was measured with fluorescence spectrophotometry using the Ca2+ binding dye Fura/2AM. In the absence of HA, cisplatin inhibited tumor cell growth. The addition of HA, but not HA plus anti-CD44 antibody, resulted in a 5-fold reduced ability of cisplatin to cause HNSCC cell death, suggesting that HA can promote CD44-dependent cisplatin resistance. Fluorescence spectrophotometry demonstrated that HA can promote CD44-dependent Ca2+ mobilization in HNSCC. On the other hand, the presence of U73122, a PLC inhibitor, and 2-aminoethoxydiphenyl borate, an inositol-1,4,5-triphosphate receptor inhibitor, eliminated HA-mediated Ca2+ mobilization and HA-mediated cisplatin resistance in these cell lines.\n\nQuestion:\nDoes hyaluronan-CD44 promote phospholipase C-mediated Ca2+ signaling and cisplatin resistance in head and neck 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:\nTo determine if the platelet glass bead retention assay can predict bleeding after cardiac surgery. Prospective, observational study. Large, tertiary care, academic medical center. Forty-three adult patients scheduled to undergo elective cardiac surgery employing cardiopulmonary bypass (CPB). Whole blood samples were observed for platelet count, prothrombin time, and platelet (glass bead) retention assay. The platelet retention and prothrombin times were independent univariant and multivariant predictors of bleeding after CPB (r = 0.554, p = 0.0002 and r = 0.655, p = 0.00001).\n\nQuestion:\nDoes platelet glass bead retention predict bleeding after cardiac 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:\nCarbohydrate antigen 19-9 (CA19-9) is used as a biomarker to differentiate benign from malignant gastrointestinal disorders. We examined the value of CA19-9 measurement in polycystic livers after observing high CA19-9 cyst fluid levels in a benign polycystic liver case. We determined CA19-9 levels in serum (n=120) and hepatic cyst fluid (n=81), from patients with polycystic livers (n=109) and simple hepatic cysts (n=24). Further, we analysed CA19-9 expression in normal and polycystic liver tissue (n=17). Cyst fluid CA19-9 levels from both polycystic livers and simple hepatic cysts were extremely high (median 91 000 U/ml, range 14-15 870 000 U/ml; median 85 000 U/ml, range 332-1 744 000 U/ml respectively). Serum CA19-9 levels were significantly higher in polycystic liver patients (median 30 U/ml, range 0-1200 U/ml) compared with patients with simple hepatic cysts (median 10 U/ml, range 3-200 U/ml, P=0.0011). Serum CA19-9 levels correlated with those in cyst fluid (r=0.3979, P=0.0399), polycystic liver volume (r=0.3870, P=0.0025) and the size of the largest cyst (simple cysts group; r=0.5319, P=0.0280). Cyst epithelia showed strong CA19-9 expression. Evacuation of cyst fluid in four patients resulted in a dramatic decrease in the serum CA19-9 levels (60-95%).\n\nQuestion:\nIs carbohydrate antigen 19-9 extremely elevated in polycystic liver 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:\nLong-term labelling of mice with halogenated thymidine analogues is an established method for quantifying the contribution of beta cell proliferation to in vivo beta cell mass expansion in (re)generation models. The method is believed to give accurate information on the accrued number of cycling beta cells over a period of time. Multiple thymidine analogue labelling is applied for evaluating the duration of postmitotic quiescence in beta cells. We hypothesise, however, that long-term labelling by thymidine analogues hampers beta cell proliferation. Thymidine analogues were administered for 7-14 days via the i.p. route to neonatal mice, or via drinking water to young mice with normal pancreases or adult mice with injured pancreases. The proliferation of insulin-positive cells was assessed by their expression of the proliferation markers Ki67 or phosphorylated histone H3 and by their incorporation of nucleotide analogues. In the mouse models of beta cell proliferation investigated herein, long-term administration of thymidine analogues decreased the percentage of Ki67(+) and phosphorylated histone H3(+) beta cells as compared with administration of normal drinking water. Proliferation was restored by washout of the analogue. Labelling with one analogue decreased the subsequent incorporation of another analogue by beta cells.\n\nQuestion:\nIs mouse beta cell proliferation inhibited by thymidine analogue labelling?\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:\nIt is believed that the stretch of cardiomyocytes is the most important stimulus of brain natriuretic peptide (BNP) release; however, its correlation with volume status represented by global end diastolic volume index (GEDVI) is less well established. The study aimed to investigate the correlation between the changes in BNP and the changes in GEDVI measured with transpulmonary thermodilution technique. Critically ill patients requiring hemodynamic monitoring (PiCCO system) in a tertiary 18-bed intensive care unit were prospectively enrolled. Hemodynamic variables were measured simultaneously with blood sampling for BNP concentration. Correlations between changes in BNP and changes in GEDVI were tested using pairwise correlation analysis. A total of 46 patients were included in the study. BNP level (median 4,602 pg/mL; IQR 1,988 to 12,439 pg/mL) was markedly elevated in the study population, but was not correlated with GEDVI (rho=-0.09, P=0.56). The changes in BNP (ΔBNP) showed significant correlation with changes in GEDVI (ΔGEDVI) (Figure 2; rho=0.52, P<0.01). Variables including Age (r=0.43, P=0.002), serum creatinine (r=0.36, P=0.012) and cardiac index (CI) (r=-0.35, P=0.016) were also significantly correlated with logBNP. Other variables such as APACHE II score, central venous pressure (CVP), heart rate (HR), intrathoracic blood volume (ITBVI), extravascular lung water (EVLWI) and systemic vascular resistance index (SVRI) were not significantly correlated with logBNP.\n\nQuestion:\nAre changes in brain natriuretic peptide correlated with changes in global end-diastolic volume index?\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:\nEnvironmental alternations leading to fetal programming of cardiovascular diseases in later life have been attributed to maternal factors. However, animal studies showed that paternal obesity may program cardio-metabolic diseases in the offspring. In the current study we tested the hypothesis that paternal BMI may be associated with fetal growth. We analyzed the relationship between paternal body mass index (BMI) and birth weight, ultrasound parameters describing the newborn's body shape as well as parameters describing the newborns endocrine system such as cortisol, aldosterone, renin activity and fetal glycated serum protein in a birth cohort of 899 father/mother/child triplets. Since fetal programming is an offspring sex specific process, male and female offspring were analyzed separately. Multivariable regression analyses considering maternal BMI, paternal and maternal age, hypertension during pregnancy, maternal total glycated serum protein, parity and either gestational age (for birth weight) or time of ultrasound investigation (for ultrasound parameters) as confounding showed that paternal BMI is associated with growth of the male but not female offspring. Paternal BMI correlated with birth parameters of male offspring only: birth weight; biparietal diameter, head circumference; abdominal diameter, abdominal circumference; and pectoral diameter. Cortisol was likewise significantly correlated with paternal BMI in male newborns only.\n\nQuestion:\nIs paternal body mass index ( BMI ) associated with offspring intrauterine growth in a gender dependent manner?\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 effects of local applied NO-active compounds on glutamate (GLU)-evoked responses were investigated in globus pallidus (GP) neurons. Extracellularly recorded single units from anesthetized rats were treated with GLU before and during the microiontophoretic application of S-nitrosoglutathione (SNOG), a NO donor, and Nω-nitro-l-arginine methyl ester (L-NAME), a NOS inhibitor. Most GP cells were excited by SNOG whereas administration of L-NAME induced decrease of GP neurons activity. Nearly all neurons responding to SNOG and/or L-NAME showed significant modulation of their excitatory responses to the administration of iontophoretic GLU. In these cells, the changes induced by NO-active drugs in the magnitude of GLU-evoked responses were used as indicators of NO modulation. In fact, when a NO-active drug was co-iontophoresed with GLU, significant changes in GLU-induced responses were observed: generally, increased magnitudes of GLU-evoked responses were observed during SNOG ejection, whereas the administration of L-NAME decreased responses to GLU.\n\nQuestion:\nDo nitric oxide-active compounds modulate the intensity of glutamate-evoked responses in the globus pallidus of the rat?\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:\nMutations of PCDH15, the gene encoding protocadherin 15, cause either nonsyndromic deafness DFNB23 or Usher syndrome type 1F (USH1F) in humans and deafness with balance problems in Ames waltzer (av) mice. Persons with USH1 usually begin to exhibit signs of retinitis pigmentosa (RP) in early adolescence, but av mice are reported to have functional retinas. In this study, the auditory, visual and molecular biological phenotype of Pcdh15av-5J and Pcdh15av-Jfb mice is characterized, and their usefulness as animal models of USH1 is evaluated. Hearing thresholds of mice between 6 and 10 weeks of age were measured by auditory brain stem response (ABR). Immunohistochemistry and histology were used to examine the effect of homozygosity of Pcdh15av-5J on stereocilia bundles of inner ear hair cells and on the photoreceptor cells of the retina. Scotopic and photopic Ganzfeld ERGs were recorded from homozygous Pcdh15av-5J and Pcdh15av-Jfb mice at different ages. Heterozygous littermates served as control subjects. Measurements of the width of the outer nuclear layer (ONL) and the length of rod photoreceptor outer segment (ROS) were made. Homozygous Pcdh15av-5J mice have profound hearing loss and disorganized stereocilia bundles of inner ear hair cells. Compared with heterozygous littermates, homozygous Pcdh15av-5J and Pcdh15av-Jfb mutant mice had scotopic ERG amplitudes consistently reduced by approximately 40% at all light intensities. The b-to-a-wave ratio confirmed that the a- and b-waves were reduced proportionally in homozygous mutant mice. Histologic measurements of retinal sections revealed no significant differences in either the ONL width or the ROS length as a function of genotype. The protocadherin 15 labeling pattern with antisera PB303 in the retina of both heterozygous and homozygous Pcdh15av-5J mice was indistinguishable from the wild type. Wild-type Pcdh15 have many alternatively spliced isoforms. A novel isoform was found in the retina of homozygous Pcdh15av-5J mice, which appears to circumvent the effect of the mutant allele (IVS14-2A-->G), which causes skipping of exon 14, a shift in the translation reading frame and a premature stop codon in exon 15.\n\nQuestion:\nDo ames Waltzer deaf mice have reduced electroretinogram amplitudes and complex alternative splicing of Pcdh15 transcripts?\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:\nCurrently available clinicopathologic prognostic factors are imperfect predictors of clinical course in advanced-stage epithelial ovarian cancer patients. New molecular predictors are needed to identify patients with higher risk of relapse or death from disease. In a retrospective study, we investigated the prognostic impact of activated leukocyte cell adhesion molecule (ALCAM) expression in epithelial ovarian cancer. We analyzed the effect of cell-anchorage loss on ALCAM cellular localization in vitro and assessed ALCAM expression by immunohistochemistry in a series of 109 well-characterized epithelial ovarian cancer patient samples. Chi-square test, Kaplan-Meier method, and Cox proportional hazard analyses were used to relate ALCAM cellular localization to clinical-pathologic parameters and to overall survival (OS) rate. Loss of epithelial ovarian cancer cell anchorage was associated both in vitro and in vivo with decreased ALCAM membrane expression. In vivo, ALCAM was localized to cell membrane in normal surface ovarian epithelium, whereas in 67% of the epithelial ovarian cancer samples, membrane localization was decreased or even lost, and the molecule was mainly expressed in cytoplasm. Median OS in this group of patients was 58 months, whereas a median OS was not yet reached in patients with ALCAM membrane localization (P = 0.036, hazard ratio [HR] = 2.0, 95% confidence interval [CI] 1.1 to 3.5). In a multivariate Cox regression model including all the available clinicopathologic variables, loss of ALCAM membrane expression was an independent factor of unfavorable prognosis (P = 0.042, HR = 2.15, 95% CI: 1.0 to 4.5).\n\nQuestion:\nIs subcellular localization of activated leukocyte cell adhesion molecule a molecular predictor of survival in ovarian carcinoma 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 dihydropyrimidinase-related protein (DRP) family, also called the collapsin response mediator protein, is implicated in the developmental process of the nervous system. Dysfunction of DRPs may result in neurodevelopmental abnormalities, which may be a factor in the pathogenesis of schizophrenia. The expression of one member of DRP-2 in humans has been reported to be decreased in the brains of people with schizophrenia. In addition, the DRP-2 gene (Dihydropyrimidinase-like 2; DPYSL2) is located on chromosome 8p21, a region that has been implicated in schizophrenia in genetic linkage studies. We investigated a genetic association between five polymorphisms of the DRP-2 gene and schizophrenia in the Japanese population. The *2236T>C polymorphism in the 3' untranslated region (3'UTR) exhibited significant differences with respect to the distribution of the genotype and allele in patients compared with control subjects. The frequency of the *2236C allele was significantly higher in control subjects than patients with schizophrenia (p =.0097) and paranoid-type schizophrenia (p =.0083).\n\nQuestion:\nIs the human dihydropyrimidinase-related protein 2 gene on chromosome 8p21 associated with paranoid-type schizophrenia?\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 diabetes mellitus in Lithuania have access to almost all the latest blood glucose-lowering drugs available in the rest of the world. This study evaluated the effects of prescribing of treatment (oral medications, insulin, or both) in Lithuanian patients with type 1 or 2 diabetes and poor blood glucose control. The relevant information was obtained from specialized questionnaires completed by 26 consulting endocrinologists in Lithuania between October 1, 2008 and December 31, 2008. The study cohort comprised 865 randomly selected patients with diabetes mellitus and a glycosylated (HbA1c) level ≥7%. In total, there were 95 patients with type 1 diabetes and 770 with type 2 diabetes. Linear regression for patients with type 1 diabetes revealed a weak trend towards higher doses of insulin reflecting lower HbA1c values. The mean dose of insulin in patients with type 1 diabetes before an endocrinology consultation was 57.1 ± 15.7 U/day (0.8 ± 0.2 U/kg), which increased significantly to 63.3 ± 16.5 U/day (0.9 ± 0.2 U/kg) after an endocrinology consultation (P < 0.05). Treatment prescribed for patients with type 2 diabetes depended on the duration of disease. Earlier treatment recommended for 68% of patients with type 2 diabetes was subsequently changed by the endocrinologist. Linear regression showed that the insulin dose prescribed before a specialist consultation as well as that recommended by an endocrinologist was significantly correlated with body mass index.\n\nQuestion:\nDoes adequate prescribing of medication necessarily translate into good control of diabetes mellitus?\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:\nCalifornian Granny Smith apples are very susceptible to bitter pit (BP) and superficial scald symptoms that develop during cold storage. The main preventive means are diphenylamine dipping and/or gaseous application of the ethylene inhibitor 1-methylcylclopropene (1-MCP), which is effective against superficial scald but not against BP. This study investigated the efficacy of a non-chemical alternative, low-O(2) (LO2) stress, in preventing these two physiological disorders. Application of LO2 stress at 20 degrees C for 10 days prior to cold storage of Granny Smith apples reduced superficial scald and BP incidence and severity during 8 months at 0 degrees C. LO2 treatments induced volatile alcohols and reduced ethylene and 6-methyl-5-hepten-2-one (MHO-on) production, thereby reducing superficial scald development after 4 months at 0 degrees C. In addition, LO2-treated fruits had higher pectin methyl esterase (MdPME) gene expression, similar to that of 1-MCP-treated fruits, associated with their higher firmness. Conversion of MHO-on to 6-methyl-5-hepten-2-ol (MHO-ol) in LO2-treated fruits may explain the lower scald development.\n\nQuestion:\nDoes short anaerobiosis period prior to cold storage alleviate bitter pit and superficial scald in Granny Smith apples?\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 this study was to determine if the haptoglobin phenotype was predictive of cardiovascular disease (CVD) in diabetic mellitus (DM). Cardiovascular disease is the most frequent, severe, and costly complication of type 2 DM. There are clear geographic and ethnic differences in the risk of CVD among diabetic patients that cannot be fully explained by differences in conventional CVD risk factors. We have demonstrated that a functional allelic polymorphism in the haptoglobin gene acts as a major determinant of susceptibility for the development of diabetic microvascular complications. We sought to determine if this paradigm concerning the haptoglobin gene could be extended to CVD in DM. We tested this hypothesis in a case-control sample from the Strong Heart study, a population-based longitudinal study of CVD in American Indians. Haptoglobin phenotype was determined by polyacrylamide gel electrophoresis in 206 CVD cases and 206 matched controls age 45 to 74 years. Median follow-up was six years. In multivariate analyses controlling for conventional CVD risk factors, haptoglobin phenotype was a highly statistically significant, independent predictor of CVD in DM. The odds ratio of having CVD in DM with the haptoglobin 2-2 phenotype was 5.0 times greater than in DM with the haptoglobin 1-1 phenotype (p = 0.002). An intermediate risk of CVD was associated with the haptoglobin 2-1 phenotype.\n\nQuestion:\nIs haptoglobin phenotype an independent risk factor for cardiovascular disease in individuals with diabetes : The Strong Heart 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:\nThere is some evidence suggesting that factors other than autoantibodies to FceRI or IgE and histamine released from mast cells may play a role in skin autoreactivity that characterizes many patients with chronic urticaria (CU) and, possibly, in the pathogenesis of this disease. The effect of antihistamine treatment on autologous plasma skin test (APST) in patients with CU was assessed. 24 patients with CU underwent autologous plasma skin test (APST) as well as SPT with histamine 10 mg/ml while taking antihistamines. In 6 cases the same tests had been carried out also before the start of antihistamine treatment. Plasma levels of D-dimer, prothrombin F 1+2 fragment, and vascular endothelial growth factor (VEGF) were measured in 21 patients. 21/24 (87%) patients showed a large flare on APST while taking antihistamines while the skin reaction to histamine 10 mg/ml was abolished or negligible. Little difference in the autologous plasma-induced flare was seen before and after the start of cetirizine therapy in 6 cases, whereas the drug exerted a marked effect on the histamine SPT as well as on the autologous plasma-induced wheal. The APST-induced flare was not associated with patients' response to antihistamine. Plasma levels of VEGF, prothrombin F 1+2 fragment, and D-dimer were increased in plasmas from 8, 9, and 2 patients, respectively.\n\nQuestion:\nDo antihistamines inhibit the flare induced by the intradermal injection of autologous plasma in chronic urticaria 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:\nThe involvement of B cells in allergen tolerance induction remains largely unexplored. This study investigates the role of B cells in this process, by comparing B-cell responses in allergic patients before and during allergen immunotherapy (AIT) and naturally exposed healthy beekeepers before and during the beekeeping season. Circulating B cells were characterized by flow cytometry. Phospholipase A2 (PLA)-specific B cells were identified using dual-color staining with fluorescently labeled PLA. Expression of regulatory B-cell-associated surface markers, interleukin-10, chemokine receptors, and immunoglobulin heavy-chain isotypes, was measured. Specific and total IgG1, IgG4, IgA, and IgE from plasma as well as culture supernatants of PLA-specific cells were measured by ELISA. Strikingly, similar responses were observed in allergic patients and beekeepers after venom exposure. Both groups showed increased frequencies of plasmablasts, PLA-specific memory B cells, and IL-10-secreting CD73\n\nQuestion:\nDoes high-dose bee venom exposure induce similar tolerogenic B-cell responses in allergic patients and healthy beekeepers?\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:\nBody mass index (BMI) may alter serum prostate specific antigen (PSA) and percent free PSA (%fPSA) and may mask the risk of prostate cancer. We investigated the relationship between BMI and PSA or %fPSA. Height, weight, PSA and %fPSA were assessed in 616 consecutive screened men without prostate cancer. Continuously coded and categorised BMI was studied. Statistical analyses consisted of ANOVA, linear regression, bivariate and partial correlations. Median age was 57 years. Median PSA was 1.0 and median %fPSA was 26. Median BMI was 25.8 kg/m(2). Neither continuously coded nor categorised BMI correlated with either PSA or %fPSA in unadjusted or age-adjusted analyses (all p values > or = 0.3).\n\nQuestion:\nDoes body mass index predict prostate-specific antigen or percent free prostate-specific antigen in men undergoing prostate cancer screening?\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:\nRight ventricular failure does not explain all cases of death in patients with chronic pulmonary hypertension. Searching for alternative explanations, we evaluated the prognostic significance of main pulmonary artery (PA) dilatation in patients with pulmonary arterial hypertension (PAH) or chronic thromboembolic pulmonary hypertension (CTEPH). A retrospective outcome analysis was made of 264 patients (aged 46 ± 17 years; women, 69%; PAH, 82%) who underwent both CT scan measurement of the PA and right-sided heart catheterization (mean PA pressure, 57.6 ± 16.5 mm Hg) at initial evaluation. The diameter of the PA ranged from 28 to 120 mm (mean, 39 ± 8.6 mm; median, 38 mm) and was largest in patients with unrepaired congenital defects (42.6 ± 7.6 mm). Pulmonary pulse pressure (P = .04), lower age (P = .03), and duration of symptoms (P &lt; .001) were independently but weakly related to PA diameter. During follow-up (median, 38 months), 99 patients (37%) died. Of these 99 deaths, 73 (74%) were due to heart failure or comorbidities, and 26 (26%) were unexpected deaths (UE-Ds). PA diameter (hazard ratio [HR], 1.06 per 1 mm; 95% CI, 1.03-1.08), heart rate (HR, 1.30 per 10 beats/min; 95% CI, 1.01-1.66), and systolic pulmonary arterial pressure (HR, 1.02 per 1 mm Hg; 95% CI, 1.01-1.04) were the only independent predictors of UE-D and differed from the usual predictors found in the study group for all-cause mortality. PA diameter ≥ 48 mm had 95% specificity and 39% sensitivity and carried 7.5 times higher risk of UE-D (95% CI, 3.4-16.5; P &lt; .0001) during follow-up.\n\nQuestion:\nDoes pulmonary artery dilatation correlate with the risk of unexpected death in chronic arterial or thromboembolic pulmonary hypertension?\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 predict adherent perinephric fat (APF) at minimally invasive partial nephrectomy (MIPN) using the Mayo adhesive probability (MAP) score and to determine the impact of MAP score and APF on MIPN outcomes. A total of 245 patients undergoing MIPN were included in the study. The presence of APF was determined through keywords in operating notes, and radiographic data were obtained from preoperative cross-sectional imaging. Posterior fat thickness was measured between the renal capsule and the posterior abdominal wall at the level of the renal vein. Perinephric stranding was graded on a 0-3 severity scale. The study included 123 men and 122 women, with a median age of 55 years, body mass index of 31.7, tumour size of 2.7 cm and nephrometry score of 6. The median posterior fat thickness was 1.79 cm and MAP score 2.63. In all, 26 patients (10.6%) had evidence of APF at the time of renal surgery. Factors predictive of APF included increasing age (P = 0.001), male gender (P = 0.045), perinephric stranding (P = 0.002), posterior fat thickness (P < 0.001) and MAP score (P < 0.001). APF was associated with adverse pathological and peri-operative outcomes including malignant renal histology (P = 0.04), longer operating time (P = 0.005) and greater estimated blood loss (EBL; P = 0.025).\n\nQuestion:\nIs adherent perinephric fat at minimally invasive partial nephrectomy associated with adverse peri-operative outcomes and malignant renal histology?\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 angiotensin-converting enzyme (ACE) inhibitors has increased markedly during the last decade. It has been claimed that doses of ACE inhibitors prescribed in clinical practice are considerably lower than the target doses used in randomized clinical trials. The aim of the study was to investigate dosing of ACE inhibitors in patients discharged from the hospital after an acute myocardial infarction (AMI) and, furthermore, to compare these doses with the doses actually reached in clinical trials. From 16 hospitals, we drew a sample of patients who were discharged alive with the diagnosis of AMI during a 3-month period in 1999/2000. From medical records, physicians in each hospital obtained the observed rate of cardiovascular drugs at discharge, including type and doses of ACE inhibitors. The clinicians' main indication for ACE inhibitor use was also reported. Outcome variables, including deaths and drug utilization with dosing after 6 months, were collected. Of a total of 767 patients discharged alive, 274 patients received an ACE inhibitor. The daily mean doses of the four ACE inhibitors used in the study were as follows: captopril 69.8+/-36.9 mg (n=44), enalapril 13.6+/-8.1 mg (n=75), lisinopril 11.0+/-7.2 mg (n=114), and ramipril 8.4+/-4.5 mg (n=38). The doses were unchanged after 6 months except for captopril, which showed a rise in mean daily dose to 84.4+/-36.7 mg. Ramipril compared most favorably with clinical trial medications, while captopril deviated most. The indication of hypertension was associated with slightly higher doses than the indication of secondary prevention.\n\nQuestion:\nIs the problem of underdosing of angiotensin-converting enzyme inhibitors markedly overrated : results from a study of patients discharged from hospital after an 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:\nDimethylarginine dimethylaminohydrolase 1 (DDAH1) modulates NO production by degrading the endogenous nitric oxide (NO) synthase (NOS) inhibitors asymmetrical dimethylarginine (ADMA) and L-NG-monomethyl arginine (L-NMMA). This study examined whether, in addition to degrading ADMA, DDAH1 exerts ADMA-independent effects that influence endothelial function. Using selective gene silencing of DDAH1 with small interfering RNA and overexpression of DDAH1 in human umbilical vein endothelial cells, we found that DDAH1 acts to promote endothelial cell proliferation, migration, and tube formation by Akt phosphorylation, as well as through the traditional role of degrading ADMA. Incubation of human umbilical vein endothelial cells with the NOS inhibitors l-NG-nitro-arginine methyl ester (L-NAME) or ADMA, the soluble guanylyl cyclase inhibitor 1H-(1,2,4)oxadiazolo-(4,3-2)quinoxalin-1-one, or the cGMP analog 8-(4-Chlorophenylthio)-cGMP had no effect on phosphorylated (p)-Akt(Ser473), indicating that the increase in p-Akt(Ser473) produced by DDAH1 was independent of the NO-cGMP signaling pathway. DDAH1 formed a protein complex with Ras, and DDAH1 overexpression increased Ras activity. The Ras inhibitor manumycin-A or dominant-negative Ras significantly attenuated the DDAH1-induced increase in p-Akt(Ser473). Furthermore, DDAH1 knockout impaired endothelial sprouting from cultured aortic rings, and overexpression of constitutively active Akt or DDAH1 rescued endothelial sprouting in the aortic rings from these mice.\n\nQuestion:\nDoes dimethylarginine dimethylaminohydrolase 1 modulate endothelial cell growth through nitric oxide and Akt?\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:\nMultiple types of substance use are associated with HIV risk behaviors, but relatively little research has examined the association between marijuana use and risky sexual activities in treatment-seeking polysubstance abusing patients. This study evaluated the relationship between marijuana use and sexual behaviors in 239 patients with cocaine, opioid or alcohol use disorders who were initiating outpatient substance use treatment. Participants completed the HIV Risk Behavior Scale and were classified into one of three groups based on their marijuana use histories: never (n = 66), past but not current use (n = 124) or current use (n = 49). Compared to never marijuana users, current and former marijuana users had a greater likelihood of having more than 50 lifetime sexual partners (odds ratio [OR] and 95% confidence interval [CI] = 3.9 [1.0-15.7] and 5.2 [1.6-17.3], respectively). Former marijuana users had increased risk of low frequency condom use with casual partners relative to never users (OR [95% CI] = 2.9 [1.1-7.6]). Moreover, current marijuana users were more likely than never users to have had more than two recent sexual partners (OR [95% CI] = 8.1 [1.94-33.44]).\n\nQuestion:\nIs marijuana use associated with risky sexual behaviors in treatment-seeking polysubstance abusers?\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:\nChronic obstructive pulmonary disease (COPD) is a serious disease that is increasing in prevalence, yet is under-diagnosed and under-recognised in Australia. The goal is to bring this to the attention of public health and offer recommendations in order to reduce the present and future burden from COPD. The increase in prevalence, particularly in women, and the impact upon personal and public health demonstrate that COPD is a major public health issue. A proactive approach for public health is suggested, including strategies to increase smoking cessation among at-risk groups, reduce delayed diagnosis, extend disease management strategies, and establish an Australian research base.\n\nQuestion:\nIs chronic obstructive pulmonary disease ( COPD ) a major personal and public health burden in Australia?\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:\nTremor is frequently associated with dystonia, but its pathophysiology is still unclear. Dysfunctions of cerebellar circuits are known to play a role in the pathophysiology of action-induced tremors, and cerebellar impairment has frequently been associated to dystonia. However, a link between dystonic tremor and cerebellar abnormalities has not been demonstrated so far. Twenty-five patients with idiopathic isolated cervical dystonia, with and without tremor, were enrolled. We studied the excitability of inhibitory circuits in the brainstem by measuring the R2 blink reflex recovery cycle (BRC) and implicit learning mediated by the cerebellum by means of eyeblink classical conditioning (EBCC). Results were compared with those obtained in a group of age-matched healthy subjects (HS). Statistical analysis did not disclose any significant clinical differences among dystonic patients with and without tremor. Patients with dystonia (regardless of the presence of tremor) showed decreased inhibition of R2 blink reflex by conditioning pulses compared with HS. Patients with dystonic tremor showed a decreased number of conditioned responses in the EBCC paradigm compared to HS and dystonic patients without tremor.\n\nQuestion:\nDoes impaired eye blink classical conditioning distinguish dystonic patients with and without tremor?\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:\nMechanical ventilation of preterm babies increases survival but can also cause ventilator-induced lung injury (VILI), leading to the development of bronchopulmonary dysplasia (BPD). It is not known whether shear stress injury from gases flowing into the preterm lung during ventilation contributes to VILI. Preterm lambs of 131 days' gestation (term = 147 d) were ventilated for 2 hours with a bias gas flow of 8 L/min (n = 13), 18 L/min (n = 12) or 28 L/min (n = 14). Physiological parameters were measured continuously and lung injury was assessed by measuring mRNA expression of early injury response genes and by histological analysis. Control lung tissue was collected from unventilated age-matched fetuses. Data were analysed by ANOVA with a Tukey post-hoc test when appropriate. High bias gas flows resulted in higher ventilator pressures, shorter inflation times and decreased ventilator efficiency. The rate of rise of inspiratory gas flow was greatest, and pulmonary mRNA levels of the injury markers, EGR1 and CTGF, were highest in lambs ventilated with bias gas flows of 18 L/min. High bias gas flows resulted in increased cellular proliferation and abnormal deposition of elastin, collagen and myofibroblasts in the lung.\n\nQuestion:\nDoes high bias gas flow increase lung injury in the ventilated preterm lamb?\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:\nRheumatoid arthritis (RA) is associated with an increased mortality rate from cardiovascular disease. This may relate to insulin resistance and dyslipidemia, which were both reported to correlate with the acute phase response in RA. We investigated whether insulin resistance and dyslipidemia could be explained by the acute phase response as well as excess weight in inflammatory arthritis. We investigated 87 patients, 38 with RA, 29 with spondyloarthropathy, 20 with undifferentiated inflammatory arthritis. Thirty age, sex, and race matched healthy volunteers served as controls. Fasting blood samples were taken for determination of erythrocyte sedimentation rate (ESR), plasma glucose, serum insulin, and total cholesterol (chol), low density lipoprotein cholesterol (LDL-chol), high density lipoprotein cholesterol (HDL-chol), and triglycerides. Insulin resistance was estimated by the homeostasis model assessment for insulin resistance (HOMA) and the quantitative insulin sensitivity check index (QUICKI). In controls the mean (SD) HOMA (microU x mmol/ml x l), QUICKI, body mass index (BMI, kg/m2), and ESR (mm/h) were 1.1 (0.5), 0.393 (0.048), 22.9 (2.8), and 13 (8) in patients; they were 1.9 (1.3), 0.357 (0.037), 26.5 (4.2), and 26 (18) in controls, respectively. Each of these differences was highly significant (p < 0.001). HDL-chol concentrations were lower (p = 0.002) and chol/HDL-chol ratios and triglyceride levels were higher (p < 0.001 and p = 0.004, respectively) in patients compared to controls. A high ESR predicted insulin resistance and dyslipidemia, while a high BMI similarly predicted insulin resistance but not dyslipidemia. After controlling for ESR and BMI, insulin sensitivity was no longer different between patients and controls, while HDL-chol concentrations remained lower (p = 0.015) and chol/HDL-chol ratios remained higher (p = 0.003) in patients compared to controls.\n\nQuestion:\nDoes the acute phase response fully predict the presence of insulin resistance and dyslipidemia in inflammatory arthritis?\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 have previously reported that brief pressure overload of the left ventricle reduced myocardial infarct (MI) size. However, the role of protein kinase C (PKC) remains uncertain. In this study, we investigated whether pressure overload reduces MI size by activating PKC. MI was induced by a 40-minute occlusion of the left anterior descending coronary artery and a 3-hour reperfusion in anesthetized Sprague-Dawley rats. MI size was determined using triphenyl tetrazolium chloride staining. Brief pressure overload was achieved by two 10-minute partial snarings of the ascending aorta, raising the systolic left ventricular pressure 50% above the baseline value. Ischemic preconditioning was elicited by two 10-minute coronary artery occlusions and 10-minute reperfusions. Dimethyl sulfoxide (vehicle) or calphostin C (0.1 mg/kg, a specific inhibitor of PKC) was administered intravenously as pretreatment. The MI size, expressed as the percentage of the area at risk, was significantly reduced in the pressure overload group and the ischemic preconditioning group (19.0 ± 2.9% and 18.7 ± 3.0% vs. 26.1 ± 2.6% in the control group, where p < 0.001). Pretreatment with calphostin C significantly limited the protection by pressure overload and ischemic preconditioning (25.2 ± 2.4% and 25.0 ± 2.3%, where p < 0.001). Calphostin C itself did not significantly affect MI size (25.5 ± 2.4%). Additionally, the hemodynamics, area at risk, and mortality were not significantly different.\n\nQuestion:\nDoes brief pressure overload of the left ventricle reduce myocardial infarct size via activation of protein kinase C?\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 ornithine decarboxylase (ODC) gene expression in colorectal carcinoma, ODC mRNA was assayed by RT-PCR and ODC protein was detected by a monoclonal antibody against fusion of human colon ODC prepared by hybridoma technology. Total RNA was extracted from human colorectal cancer tissues and their normal counterpart tissues. ODC mRNA levels were examined by RT-PCR. ODC genes amplified from RT-PCR were cloned into a prokaryotic vector pQE-30. The expressed proteins were purified by chromatography. Anti-ODC mAb was prepared with classical hybridoma techniques and used to determine the ODC expression in colon cancer tissues by immunohistochemical and Western blotting assay. A cell line, which could steadily secrete anti-ODC mAb, was selected through subcloning four times. Western blotting reconfirmed the mAb and ELISA showed that its subtype was IgG2a. RT-PCR showed that the ODC mRNA level increased greatly in colon cancer tissues (P<0.01). Immunohistochemical staining showed that colorectal carcinoma cells expressed a significantly higher level of ODC than normal colorectal mucosa (98.6+/-1.03% vs 5.26+/-5%, P<0.01).\n\nQuestion:\nIs ornithine decarboxylase gene overexpressed in colorectal 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:\nGenome-wide RNA interference screening study revealed that loss of expression of insulin-like growth factor binding protein 7 (IGFBP7) is a critical step in development of a malignant melanoma (MM), and this secreted protein plays a central role in apoptosis of MM. In this study we constructed pcDNA3.1-IGFBP7 to obtain high expression of IGBPF7 and to inhibit the growth of MM in C57BL/6J mice. pcDNA3.1-IGFBP7 was transfected into B16-F10 cell, the expression of IGFBP7 was detected by RT-PCR and western blot. The proliferations and apoptosis rates of transfected and control cells were measured by CCK8 and FCM, respectively. The tumorigenicity and tumor growth in both pcDNA3.1-IGFBP7 group and control groups were studied in C57BL/6J mice model. IGFBP7, caspase-3, and VEGF expressions in tumor tissue were measured by immunohistochemistry. Apoptosis of tumors were detected by TUNEL. We demonstrated this plasmid inhibited proliferation of B16-F10 melanoma cells efficiently in vivo, exploiting the high expression of IGFBP7. More importantly, in-vivo transfection of pcDNA3.1-IGFBP7 inhibited MM growth in C57BL/6J mice. The inhibition of MM growth was proved owing to apoptosis and reduced expression of VEGF induced by pcDNA3.1-IGFBP7.\n\nQuestion:\nDoes in-vivo transfection of pcDNA3.1-IGFBP7 inhibit melanoma growth in mice through apoptosis induction and VEGF downexpression?\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:\nEndothelin-1 (ET-1) is elevated and participates in the regulation of several brain inflammatory disorders. The deleterious effects of ET-1 on endothelial cells may aggravate brain inflammation mediated through the upregulation of cyclooxygenase-2 (COX-2) gene expression. However, the signaling mechanisms underlying ET-1-induced COX-2 expression in brain microvascular endothelial cells remain unclear. The goal of this study was to examine whether ET-1-induced COX-2 expression and prostaglandin E2 (PGE2) release were mediated through a c-Src-dependent transactivation of epidermal growth factor receptor (EGFR) pathway in brain microvascular endothelial cells (bEnd.3 cells). The expression of COX-2 induced by ET-1 was evaluated by Western blotting and RT-PCR analysis. The COX-2 regulatory signaling pathways were investigated by pretreatment with pharmacological inhibitors, short hairpin RNA (shRNA) or small interfering RNA (siRNA) transfection, chromatin immunoprecipitation (ChIP), and promoter activity reporter assays. Finally, we determined the PGE2 level as a marker of functional activity of COX-2 expression. First, the data showed that ET-1-induced COX-2 expression was mediated through a c-Src-dependent transactivation of EGFR/PI3K/Akt cascade. Next, we demonstrated that ET-1 stimulated activation (phosphorylation) of c-Src/EGFR/Akt/MAPKs (ERK1/2, p38 MAPK, and JNK1/2) and then activated the c-Jun/activator protein 1 (AP-1) via Gq/i protein-coupled ETB receptors. The activated c-Jun/AP-1 bound to its corresponding binding sites within COX-2 promoter, thereby turning on COX-2 gene transcription. Ultimately, upregulation of COX-2 by ET-1 promoted PGE2 biosynthesis and release in bEnd.3 cells.\n\nQuestion:\nDoes c-Src-dependent EGF receptor transactivation contribute to ET-1-induced COX-2 expression in brain microvascular endothelial 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:\nβ-Adrenoceptors modulate acute wound healing; however, few studies have shown the effects of β-adrenoceptor blockade on chronic wounds. Therefore, this study investigated the effect of β1-/β2-adrenoceptor blockade in wound healing of pressure ulcers. Male mice were daily treated with propranolol (β1-/β2-adrenoceptor antagonist) until euthanasia. One day after the beginning of treatment, two cycles of ischemia-reperfusion by external application of two magnetic plates were performed in skin to induce pressure ulcer formation. Propranolol administration reduced keratinocyte migration, transforming growth factor-β protein expression, re-epithelialization, and necrotic tissue loss. Neutrophil number and neutrophil elastase protein expression were increased in propranolol-treated group when compared with control group. Propranolol administration delayed macrophage mobilization and metalloproteinase-12 protein expression and reduced monocyte chemoattractant protein-1 protein expression. Myofibroblastic differentiation, angiogenesis, and wound closure were delayed in the propranolol-treated animals. Propranolol administration increased neo-epidermis thickness, reduced collagen deposition, and enhanced tenascin-C expression resulting in the formation of an immature and disorganized collagenous scar.\n\nQuestion:\nDoes propranolol impair the closure of pressure ulcers 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:\nSerum levels of hepcidin-25, a peptide hormone that reduces blood iron content, are elevated when patients with cystic fibrosis (CF) develop pulmonary exacerbation (PEx). Because hepcidin-25 is unavailable as a clinical laboratory test, we questioned whether a one-time serum iron level was associated with the subsequent number of days until PEx, as defined by the need to receive systemic antibiotics (ABX) for health deterioration. Clinical, biochemical, and microbiological parameters were simultaneously checked in 54 adults with CF. Charts were reviewed to determine when they first experienced a PEx after these parameters were assessed. Time to ABX was compared in subgroups with and without specific attributes. Multivariate linear regression was used to identify parameters that significantly explained variation in time to ABX. In univariate analyses, time to ABX was significantly shorter in subjects with Aspergillus-positive sputum cultures and CF-related diabetes. Multivariate linear regression models demonstrated that shorter time to ABX was associated with younger age, lower serum iron level, and Aspergillus sputum culture positivity.\n\nQuestion:\nDoes serum Iron Level be Associated with Time to Antibiotics in Cystic Fibrosis?\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 whether modes of commuting to school at baseline and changes in commuting were related to 6-year changes in cardiorespiratory fitness in youth. A total of 262 (142 girls) Swedish children (9 years at entry) were measured at baseline (1998/9) and follow-up (2004/5). Mode of commuting to school was assessed by questionnaire and fitness by a maximal bicycle test. At baseline, 34% of children used passive modes of commuting (e.g., car, motorcycle, bus, train), 54% walked, and 12% bicycled to school. Six years later the percentage of bicyclists increased 19% and the percentage of walkers decreased 19%. On average, children who bicycled to school increased their fitness 13% (p=0.03) more than those who used passive modes and 20% (p=0.002) more than those who walked. Children who used passive modes or walked at baseline and bicycled to school at 6 years later increased their fitness 14% (p=0.001) more than those who remained using passive modes or walking at follow-up.\n\nQuestion:\nIs bicycling to school associated with improvements in physical fitness over a 6-year follow-up period in Swedish children?\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:\nOrthostatic hypotension and cerebral autoregulation have been extensively studied in the rabbit. However, these physiologic responses have not been previously studied utilizing a rabbit in the sitting position under anesthesia. This unusual position was obtained as the preferred orientation based on geometry requirements of associated equipment for a study of osteoarthritis of the knee. Rabbits for this experiment did not survive and an additional experimental condition was developed to elucidate the mechanism and cause of death. The carotid artery pressure was measured under general anesthesia with incremental tilt testing to achieve the sitting position. Under this condition, rabbits developed orthostatic hypotension and did not survive.\n\nQuestion:\nDoes orthostatic hypotension in the anesthetized rabbit in the sitting position exceed cerebral autoregulation?\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 on high grade sarcomas using mass spectrometry imaging showed proteasome activator complex subunit 1 (PSME1) to be associated with poor survival in soft tissue sarcoma patients. PSME1 is involved in immunoproteasome assembly for generating tumor antigens presented by MHC class I molecules. In this study, we aimed to validate PSME1 as a prognostic biomarker in an independent and larger series of soft tissue sarcomas by immunohistochemistry. Tissue microarrays containing leiomyosarcomas (n = 34), myxofibrosarcomas (n = 14), undifferentiated pleomorphic sarcomas (n = 15), undifferentiated spindle cell sarcomas (n = 4), pleomorphic liposarcomas (n = 4), pleomorphic rhabdomyosarcomas (n = 2), and uterine leiomyomas (n = 7) were analyzed for protein expression of PSME1 using immunohistochemistry. Survival times were compared between high and low expression groups using Kaplan-Meier analysis. Cox regression models as multivariate analysis were performed to evaluate whether the associations were independent of other important clinical covariates. PSME1 expression was variable among soft tissue sarcomas. In leiomyosarcomas, high expression was associated with overall poor survival (p = 0.034), decreased metastasis-free survival (p = 0.002) and lower event-free survival (p = 0.007). Using multivariate analysis, the association between PSME1 expression and metastasis-free survival was still significant (p = 0.025) and independent of the histological grade.\n\nQuestion:\nDoes high nuclear expression of proteasome activator complex subunit 1 predict poor survival in soft tissue leiomyosarcomas?\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:\nDebate continues as to whether allopatric speciation or peripatric speciation through a founder effect is the predominant force driving evolution in vertebrates. The mouse lemurs of Madagascar are a system in which evolution has generated a large number of species over a relatively recent time frame. Here, we examine speciation patterns in a pair of sister species of mouse lemur, Microcebus murinus and M. griseorufus. These two species have ranges that are disparately proportioned in size, with M. murinus showing a much more extensive range that marginally overlaps that of M. griseorufus. Given that these two species are sister taxa, the asymmetric but overlapping geographic ranges are consistent with a model of peripatric speciation. To test this hypothesis, we analyze DNA sequence data from four molecular markers using coalescent methods. If the peripatric speciation model is supported, we predict substantially greater genetic diversity in M. murinus, relative to M. griseorufus. Further, we expect a larger effective population size in M. murinus and in the common ancestor of the two species than in M. griseorufus, with a concomitant decrease in gene tree/species tree incongruence in the latter and weak signs of demographic expansion in M. murinus. Our results reject a model of peripatric divergence. Coalescent effective population size estimates were similar for both extant species and larger than that estimated for their most recent common ancestor. Gene tree results show similar levels of incomplete lineage sorting within species with respect to the species tree, and locus-specific estimates of genetic diversity are concordant for both species. Multilocus demographic analyses suggest range expansions for M. murinus, with this species also experiencing more recent population declines over the past 160 thousand years.\n\nQuestion:\nDo multilocus coalescent analyses reveal the demographic history and speciation patterns of mouse lemur sister 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 inhaled anesthetic sevoflurane has been demonstrated to protect against myocardial ischemia/reperfusion (MI/R) injury via mechanisms involving AMP-activated protein kinase (AMPK) and caveolin-3 (Cav-3). However, the relative contributions of AMPK and Cav-3 to sevoflurane preconditioning (SF-PreCon)-mediated cardioprotection and their precise underlying mechanisms of action remain incompletely understood. SF-PreCon (consisting of 3 cycles of 15-minute exposure to 2% sevoflurane before 30 minutes of MI) decreased MI/R injury in wild-type mice (caspase-3 activity, -29.1%; infarct size, -20.2%; and left ventricular end diastolic pressure, -33.8%). In cardiac-specific AMPKα2 dominant-negative overexpressing mice, the cardioprotective effect of SF-PreCon was largely retained (caspase-3 activity, -26.7%; infarct size, -16.7%; and left ventricular end-diastolic pressure, -25.9%; P<0.01). In contrast, SF-PreCon failed to significantly protect Cav-3 knockout mice against MI/R injury (P>0.05). SF-PreCon significantly decreased MI/R-induced superoxide generation in wild-type (-43.6%) and AMPK dominant-negative overexpressing mice (-35.5%; P<0.01) but not in Cav-3 knockout mice. SF-PreCon did not affect nicotinamide adenine dinucleotide phosphate oxidase expression but significantly inhibited cyclooxygenase-2 expression in wild-type (-38.7%) and AMPK dominant-negative overexpressing mice (-35.8%) but not in Cav-3 knockout mice.\n\nQuestion:\nDoes sevoflurane preconditioning attenuate myocardial ischemia/reperfusion injury via caveolin-3-dependent cyclooxygenase-2 inhibition?\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:\nNumerous studies have investigated the effects of isolated CLA supplementation on glucose homeostasis in humans and rodents. However, both the amount and relative abundance of CLA isomers in supplemental form are not representative of what is consumed from natural sources. No study to date has examined the effects of altered CLA isomer content within a natural food source. Our goal was to increase the content of the insulin desensitizing CLAt10,c12 isomer relative to the CLAc9,t11 isomer in cow's milk by inducing subacute rumenal acidosis (SARA), and subsequently investigate the effects of this milk fat on parameters related to glucose and insulin tolerance in rats. We fed female rats (~2.5 to 3 months of age) CLA t10,c12 -enriched (SARA) butter or non-SARA butter based diets for 4 weeks in either low (10% of kcal from fat; 0.18% total CLA by weight) or high (60% of kcal from fat; 0.55% total CLA by weight) amounts. In an effort to extend these findings, we then fed rats high (60% kcal) amounts of SARA or non-SARA butter for a longer duration (8 weeks) and assessed changes in whole body glucose, insulin and pyruvate tolerance in comparison to low fat and 60% lard conditions. There was a main effect for increased fasting blood glucose and insulin in SARA vs. non-SARA butter groups after 4 weeks of feeding (p < 0.05). However, blood glucose and insulin concentration, and maximal insulin-stimulated glucose uptake in skeletal muscle were similar in all groups. Following 8 weeks of feeding, insulin tolerance was impaired by the SARA butter, but not glucose or pyruvate tolerance. The non-SARA butter did not impair tolerance to glucose, insulin or pyruvate.\n\nQuestion:\nDoes feeding butter with elevated content of trans-10 , cis-12 conjugated linoleic acid to lean rats impair glucose tolerance or muscle insulin response?\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:\nTo determine whether the D1 agonistic action of (-)-stepholidine (SPD) on the medial prefrontal cortex (mPFC) neuron is involved in the modulation of evoked subcortical dopamine (DA) release from nucleus accumbens (NAc) of rats. With the microinjection of SPD into the mPFC, the ventral tegmental area (VTA)-stimulated or amphetamine (AMP)-evoked DA efflux in the NAc was detected by microdialysis + HPLC-ECD in the 6-hydroxydopamine (6-OHDA)-lesioned and intact rats. The depletion of DA in the mPFC did not modify both the basal level and the VTA-stimulated DA efflux in the NAc, but significantly facilitated the AMP (20 mumol.L-1)-evoked DA efflux within the NAc. It indicates that the mPFC DA system is involved in the regulation of evoked DA release in the NAc. Besides, the AMP-evoked increase of the extracellular DA release in the NAc was significantly attenuated by SPD (10, 30 mmol.L-1) microinjection into the mPFC, though this injection of SPD could not alter the response of DA release by the stimulation of the VTA. Furthermore, the inhibitory effect of SPD on the AMP-evoked DA efflux could be partially reversed by intravenous administration of D1 antagonist Sch-23390 (1 mg.kg-1), but not by D2 antagonist spiperone.\n\nQuestion:\nDoes i-stepholidine facilitate inhibition of mPFC DA receptors on subcortical NAc DA release?\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 paired box gene 8 (PAX8) plays crucial roles in organ patterning and cellular differentiation during development and tumorigenesis. Although its function is partly understood in vertebrate development, there is poor data concerning human central nervous system (CNS) development and brain tumours. We investigated developing human (n = 19) and mouse (n = 3) brains as well as medulloblastomas (MBs) (n = 113) for PAX8 expression by immunohistochemistry. Human MB cell lines were assessed for PAX8 expression using polymerase chain reaction and immunoblotting and analysed for growth and migration following PAX8 knock-down by small interfering ribonucleic acid (siRNA). PAX8 protein expression was associated with germinal layers in human and murine forebrain and hindbrain development. PAX8 expression significantly decreased over time in the external granule cell layer but increased in the internal granule cell layer. In MB subtypes, we observed an association of PAX8 expression with sonic hedgehog (SHH) and wingless int subtypes but not with group 3 and 4 MBs. Beyond that, we detected high PAX8 levels in desmoplastic MB subtypes. Univariate analyses revealed high PAX8 levels as a prognostic factor associated with a significantly better patient prognosis in human MB (overall survival: Log-Rank P = 0.0404, Wilcoxon P = 0.0280; progression-free survival: Log-Rank P = 0.0225; Wilcoxon P = 0.0136). In vitro assays revealed increased proliferation and migration of MB cell lines after PAX8 siRNA knock-down.\n\nQuestion:\nIs paired box gene 8 ( PAX8 ) expression associated with sonic hedgehog ( SHH ) /wingless int ( WNT ) subtypes , desmoplastic histology and patient survival in human medulloblastomas?\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:\nIgA nephropathy is one of the most common forms of primary glomerulonephritis in adults. Its pathogenesis is complex. The nature of infiltrating and proliferating cells and of cellular mediators could contribute to the progression of IgA nephropathy towards end-stage renal failure. To evaluate this hypothesis, we attempted to quantify the magnitude of intrarenal gene expression of various cytokines (IL-1 beta, TNF-alpha, IL-6, IL-15, IL-2, IFN-gamma, IL-10) and chemokines (IL-8, RANTES, MCP-1) in 48 renal core biopsy specimens, diagnosed as IgA nephropathy by immunofluorescence microscopy. Semi-quantitative reverse-transcriptase polymerase chain reaction using internal competitors was used for the quantification of gene transcripts. The expression of intrarenal gene transcripts of various cytokines and chemokines was closely interrelated, but not associated with the pathological grading system. The IFN-gamma/IL-10 ratio was higher in patients with renal dysfunction than in those with normal renal function (P=0.0483). Gene transcript levels of proinflammatory cytokines were related to the amount of proteinuria. In patients with severe glomerular sclerosis, the ratio of IFN-gamma/IL-10 gene transcripts was high (P=0.04). IL-10 gene transcript level was related to the severity of tubulointerstitial damage. The levels of gene expression of IL-10 (P=0.009), IFN-gamma (P=0.03), and TNF-alpha (P=0.005) were related to the degree of mesangial matrix expansion and the extent of intrarenal arteriolar changes correlated with the expression of the IL-8 gene transcript (r=0.43, P=0.004).\n\nQuestion:\nDo th1/Th2 predominance and proinflammatory cytokines determine the clinicopathological severity of IgA nephropathy?\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 current study aimed to examine links between appearance evaluation and skin cancer risk behaviors in men and women. Data (N = 1,535; men, n = 873; women, n = 662) were extracted from Wave 4 of the National Longitudinal Study of Adolescent Health, a nationally representative, longitudinal dataset of U.S. adolescents and young adults. Skin cancer risk (i.e., number of hours spent outside for those with a history of severe sunburn and who were unlikely to use sunscreen) was significantly associated with participant gender, appearance evaluation, and their interaction. Both men and women who negatively evaluated their appearance were at significantly increased skin cancer risk, and this was particularly true for men.\n\nQuestion:\nIs negative appearance evaluation associated with skin cancer risk behaviors among American men and 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:\nHemolysis, occurring during cardiopulmonary bypass, is associated with lipid peroxidation and postoperative acute kidney injury. Acetaminophen inhibits lipid peroxidation catalyzed by hemeproteins and in an animal model attenuated rhabdomyolysis-induced acute kidney injury. This pilot study tests the hypothesis that acetaminophen attenuates lipid peroxidation in children undergoing cardiopulmonary bypass. Single-center prospective randomized double-blinded study. University-affiliated pediatric hospital. Thirty children undergoing elective surgical correction of a congenital heart defect. Patients were randomized to acetaminophen (OFIRMEV [acetaminophen] injection; Cadence Pharmaceuticals, San Diego, CA) or placebo every 6 hours for four doses starting before the onset of cardiopulmonary bypass. Markers of hemolysis, lipid peroxidation (isofurans and F2-isoprostanes), and acute kidney injury were measured throughout the perioperative period. Cardiopulmonary bypass was associated with a significant increase in free hemoglobin (from a prebypass level of 9.8 ± 6.2 mg/dL to a peak of 201.5 ± 42.6 mg/dL postbypass). Plasma and urine isofuran and F2-isoprostane concentrations increased significantly during surgery. The magnitude of increase in plasma isofurans was greater than the magnitude in increase in plasma F2-isoprostanes. Acetaminophen attenuated the increase in plasma isofurans compared with placebo (p = 0.02 for effect of study drug). There was no significant effect of acetaminophen on plasma F2-isoprostanes or urinary makers of lipid peroxidation. Acetaminophen did not affect postoperative creatinine, urinary neutrophil gelatinase-associated lipocalin, or prevalence of acute kidney injury.\n\nQuestion:\nDoes acetaminophen attenuate lipid peroxidation in children undergoing cardiopulmonary bypass?\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:\nApelin-13 (A13) regulates cardiac homeostasis. However, the effects and mechanism of A13 infusion after an acute myocardial injury (AMI) have not been elucidated. This study assesses the restorative effects and mechanism of A13 on the peri-infarct region in murine AMI model. 51 FVB/N mice (12weeks, 30g) underwent AMI. A week following injury, continuous micro-pump infusion of A13 (0.5μg/g/day) and saline was initiated for 4-week duration. Dual contrast MRI was conducted on weeks 1, 2, 3, and 5, consisting of delayed-enhanced and manganese-enhanced MRI. Four mice in each group were followed for an extended period of 4weeks without further infusion and underwent MRI scans on weeks 7 and 9. A13 infusion demonstrated preserved LVEF compared to saline from weeks 1 to 4 (21.9±3.2% to 23.1±1.7%* vs. 23.5±1.7% to 16.9±2.8%, *p=0.02), which persisted up to 9weeks post-MI (+1.4%* vs. -9.4%, *p=0.03). Mechanistically, dual contrast MRI demonstrated significant decrease in the peri-infarct and scar % volume in A13 group from weeks 1 to 4 (15.1 to 7.4% and 34.3 to 25.1%, p=0.02, respectively). This was corroborated by significant increase in 5-ethynyl-2'-deoxyuridine (EdU(+)) cells by A13 vs. saline groups in the peri-infarct region (16.5±3.1% vs. 8.1±1.6%; p=0.04), suggesting active cell mitosis. Finally, significantly enhanced mobilization of CD34(+) cells in the peripheral blood and up-regulation of APJ, fibrotic, and apoptotic genes in the peri-infarct region were found.\n\nQuestion:\nDoes apelin-13 infusion salvage the peri-infarct region to preserve cardiac function after severe myocardial injury?\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:\nMutations in the KRAS gene occur at an early stage in the development of colorectal carcinoma. Importantly, KRAS mutation predicts resistance to anti-epidermal growth factor receptor therapy in stage IV disease. The aim of the current study is to correlate histologic features of colon cancer with the presence of KRAS mutations. Tumor tissue from 145 colon cancer resections was tested for KRAS mutations. KRAS mutation status was correlated with demographic and histologic characteristics. Statistical analysis was performed using the Pearson χ2 test and multivariate analysis. KRAS mutations were present in 55/145 cases (37.9%), consistent with reported rates. KRAS mutations were significantly associated with usual adenocarcinoma morphology (multivariate P=0.014), peritumoral lymphocytic response (χ2, P=0.028; multivariate P=0.017), T3-T4 status (χ2, P=0.012; multivariate P=0.015), right-sided location (multivariate P=0.027), absence of lymphovascular invasion (multivariate P=0.008), and metastases at the time of resection (multivariate P=0.034). No association was found between KRAS mutation status and other factors.\n\nQuestion:\nAre kRAS mutations associated with specific morphologic features in colon 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 previously demonstrated that the anticholinesterase eserine provokes interictal-like discharges in the CA3 area of hippocampal slices from rats in which generalized seizures had been induced by pentylenetetrazol (PTZ) when immature. In this study, we investigated several factors as the possible mechanism for this effect, including age at convulsions. Rats were injected with PTZ on postnatal day (P) 18-20 or >P60, and neuronal activity was recorded intra- and extracellularly from CA3 5-10 or >40 days later. In additional experiments, convulsions were triggered by kainate or were blocked by pentobarbital. Hippocampal (a) acetylcholine (ACh) innervation density was measured by immunocytochemistry, and ACh and gamma-aminobutyric acid (GABA) contents were determined by high-performance liquid chromatography (HPLC)-electrospray ionization. The excitatory effect of eserine was the most consistent in slices from rats PTZ-treated when immature and after the long interval, whereas the reverse was true in rats treated as adults. This effect was dependent on the occurrence of a seizure and was less prevalent when the seizure had been provoked by kainate. Adult animals PTZ-treated at P20 did not differ from control in (a) poly- or monosynaptic GABAA and GABAB CA3 inhibitory postsynaptic potentials (IPSPs); (b) density of ACh innervation; or (c) tissue content of ACh and GABA.\n\nQuestion:\nDo pentylenetetrazol-induced seizures in immature rats provoke long-term changes in adult hippocampal cholinergic excitability?\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:\nRetinal pigment epithelial (RPE) cells are believed to play a pivotal role in the formation and contraction of epiretinal membranes in proliferative vitreoretinopathy (PVR). In the present study, an organ culture method was used that mimics the contractile stage of PVR, to investigate the contribution of a variety of growth factors in human RPE cell-mediated contraction of the retina. Cultured human RPE cells were seeded onto bovine retinal explants. After attachment, cultures received one of the following exogenous growth factors: platelet-derived growth factor (PDGF)-AB, PDGF-BB, basic fibroblast growth factor (bFGF), transforming growth factor (TGF)-beta1, TGF-beta2, or interleukin (IL)-10; or a neutralizing antibody to PDGF and/or TGF-beta2. Control explants were either untreated or received a null antibody. Contraction was assessed by image analysis and expressed as percentage reduction in retinal area. RPE cells produced a more than 50% contraction of the retina after 7 days in untreated samples. PDGF and TGF-beta2 stimulated RPE-mediated contraction by a further 20% at 100 ng/ml. IL-10 decreased contraction by 63%, whereas the other growth factors gave rise to similar contraction to untreated controls. Neutralizing antibodies against PDGF and TGF-beta2 reduced RPE-mediated contraction by up to 70% in comparison with untreated controls. The neutralizing antibodies also inhibited the effects of exogenous PDGF and TGF-beta2 on RPE-mediated contraction of the retina (P < 0.01).\n\nQuestion:\nDo iL-10 and antibodies to TGF-beta2 and PDGF inhibit RPE-mediated retinal contraction?\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:\nAtopic dermatitis (AD) is a common chronic inflammatory skin disease. Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine that has been implicated in the pathogenesis of AD. Recently, we developed a novel DNA vaccine that generates neutralizing endogenous anti-MIF antibodies. This study explores the preventive and therapeutic effects of this MIF-DNA vaccine in mouse models of AD. Two different AD model mice (DS-Nh and NC/Nga) received MIF-DNA vaccination to analyze preventive and therapeutic effects, as assessed by clinical skin scores, histologic findings, and serum IgE levels. In murine models of AD, MIF-DNA vaccination prevented the occurrence of the AD skin phenotype. Furthermore, administration of MIF-DNA vaccine to mice that had already developed AD produced a rapid improvement in AD skin manifestation. There were reduced histologic signs of inflammation and lower serum IgE levels in treated mice compared with those seen in control animals. Finally, passive transfer of IgG from MIF-DNA vaccinated mice to AD mice also produced a significant therapeutic effect. These results demonstrate that MIF-DNA vaccination not only prevents the development of AD but also improves the symptoms of pre-existing AD.\n\nQuestion:\nDoes dNA vaccination against macrophage migration inhibitory factor improve atopic dermatitis in murine models?\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:\nSocial communication difficulties represent an autistic trait that is highly heritable and persistent during the course of development. However, little is known about the underlying genetic architecture of this phenotype. We performed a genome-wide association study on parent-reported social communication problems using items of the children's communication checklist (age 10 to 11 years) studying single and/or joint marker effects. Analyses were conducted in a large UK population-based birth cohort (Avon Longitudinal Study of Parents and their Children, ALSPAC, N = 5,584) and followed-up within a sample of children with comparable measures from Western Australia (RAINE, N = 1364). Two of our seven independent top signals (P-discovery <1.0E-05) were replicated (0.009 <P-replication ≤0.02) within RAINE and suggested evidence for association at 6p22.1 (rs9257616, meta-P = 2.5E-07) and 14q22.1 (rs2352908, meta-P = 1.1E-06). The signal at 6p22.1 was identified within the olfactory receptor gene cluster within the broader major histocompatibility complex (MHC) region. The strongest candidate locus within this genomic area was TRIM27. This gene encodes an ubiquitin E3 ligase, which is an interaction partner of methyl-CpG-binding domain (MBD) proteins, such as MBD3 and MBD4, and rare protein-coding mutations within MBD3 and MBD4 have been linked to autism. The signal at 14q22.1 was found within a gene-poor region.Single-variant findings were complemented by estimations of the narrow-sense heritability in ALSPAC suggesting that approximately a fifth of the phenotypic variance in social communication traits is accounted for by joint additive effects of genotyped single nucleotide polymorphisms throughout the genome (h2(SE) = 0.18(0.066), P = 0.0027).\n\nQuestion:\nDoes common variation contribute to the genetic architecture of social communication traits?\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 Kangaroo mother care (KMC) facilitates mother baby attachment in low birth weight infants. Over 16 month period 110 neonates were randomized into kangaroo mother care group and control group using a random number table. The kangaroo group was subjected to Kangaroo mother care for at least 6 hours per day. The babies also received kangaroo care after shifting out from NICU and at home. The control group received standard care (incubator or open care system). After 3 months followup, structured maternal interview was conducted to assess attachment between mothers and their babies. Mean birth weight was 1.69 +/- 0.11 Kg in KMC group compared to 1.690 +/- 0.12 Kg in control group (p>0.05). Mean gestational age was 35.48 +/- 1.20 week in KMC group and 35.04+/-1.09 week in the control group (p>0.05). KMC was initiated at a mean age of 1.72+/-0.45 days. The duration of KMC in first month was 10.21+/-1.50 hour, in the 2nd month was 10.03+/-1.57 hour and in the 3rd month was 8.97+/-1.37 hours. The duration of hospital stay was significantly shorter in the KMC group (3.56+/-0.57 days) compared to control group (6.80+/-1.30 days). The total attachment score (24.46+/-1.64) in the KMC group was significantly higher than that obtained in control group (18.22+/-1.79, p< 0.001). In KMC group, mother was more often the main caretaker of the baby. Mothers were significantly more involved in care taking activities like bathing, diapering, sleeping with their babies and spent more time beyond usual care taking. They went out without their babies less often and only for unavoidable reasons. They derived greater pleasure from their babies.\n\nQuestion:\nDoes kMC facilitate mother baby attachment in low birth weight infants?\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:\nSuppressor of cytokine signaling 3 (SOCS3) is an inducible endogenous negative regulator of signal transduction and activator of transcription 3 (STAT3). Epigenetic silencing of SOCS3 has been shown in head and neck squamous cell carcinoma (HNSCC), which is associated with increased activation of STAT3. There is scarce information on the functional role of the reduction of SOCS3 expression and no information on altered subcellular localization of SOCS3 in HNSCC. We assessed endogenous SOCS3 expression in different HNSCC cell lines by RT-qPCR and western blot. Immunofluorescence and western blot were used to study the subcellular localization of endogenous SOCS3 induced by IL-6. Overexpression of SOCS3 by CMV-driven plasmids and siRNA-mediated inhibition of endogenous SOCS3 were used to verify the role of SOCS3 on tumor cell proliferation, viability, invasion and migration in vitro. In vivo relevance of SOCS3 expression in HNSCC was studied by quantitative immunohistochemistry of commercially-available tissue microarrays. Endogenous expression of SOCS3 was heterogeneous in four HNSCC cell lines and surprisingly preserved in most of these cell lines. Subcellular localization of endogenous SOCS3 in the HNSCC cell lines was predominantly nuclear as opposed to cytoplasmic in non-neoplasic epithelial cells. Overexpression of SOCS3 produced a relative increase of the protein in the cytoplasmic compartment and significantly inhibited proliferation, migration and invasion, whereas inhibition of endogenous nuclear SOCS3 did not affect these events. Analysis of tissue microarrays indicated that loss of SOCS3 is an early event in HNSCC and was correlated with tumor size and histological grade of dysplasia, but a considerable proportion of cases presented detectable expression of SOCS3.\n\nQuestion:\nIs loss of expression and function of SOCS3 an early event in HNSCC : altered subcellular localization as a possible mechanism involved in proliferation , migration and invasion?\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:\nAutoimmune polyendocrine syndrome type 1 (APS-1) is caused by mutations of the autoimmune regulator (AIRE) gene. Mouse studies have shown that this results in defective negative selection of T cells and defective early seeding of peripheral organs with regulatory T cells (Tregs). Aire deficiency in humans and mice manifests as spontaneous autoimmunity against multiple organs, and 20% of patients develop an autoimmune hepatitis (AIH). To study AIH in APS-1, we generated a murine model of human AIH on a BALB/c mouse background, in which Aire is truncated at exon 2. A subgroup of 24% of mice is affected by AIH, characterized by lymphoplasmacytic and periportal hepatic infiltrates, autoantibodies, elevated aminotransferases, and a chronic and progressive course of disease. Disease manifestation was dependent on specific Aire mutations and the genetic background of the mice. Though intrahepatic Treg numbers were increased and hyperproliferative, the intrahepatic CD4/CD8 ratio was decreased. The targets of the adaptive autoimmune response were polyspecific and not focussed on essential autoantigens, as described for other APS-1-related autoimmune diseases. The AIH could be treated with prednisolone or adoptive transfer of polyspecific Tregs.\n\nQuestion:\nIs autoimmune hepatitis in a murine autoimmune polyendocrine syndrome type 1 model directed against multiple autoantigens?\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 long-term effects of the development of chronic metabolic diseases such as type 2 diabetes and obesity have been associated with nutritional insults in critical life stages. In this study, we evaluated the effect of a low-protein diet on metabolism in mid-adulthood male rats. At 90 days of age, Wistar male rats were fed a low-protein diet (4.0 %, LP group) for 30 days, whereas control rats were fed a normal-protein diet (20.5 %, NP group) throughout their lifetimes. To allow for dietary rehabilitation, from 120 to 180 days of age, the LP rats were fed a normal-protein diet. Then, we measured body composition, fat stores, glucose-insulin homeostasis and pancreatic islet function. At 120 days of age, just after low-protein diet treatment, the LP rats displayed a strong lean phenotype, hypoinsulinemia, as assessed under fasting and glucose tolerance test conditions, as well as weak pancreatic islet insulinotropic response to glucose and acetylcholine (p < 0.01). At 180 days of age, after poor-protein diet rehabilitation, the LP rats displayed a slight lean phenotype (p < 0.05), which was associated with a high body weight gain (p < 0.001). Additionally, fat pad accumulation, glycemia and insulinemia, as well as the pancreatic islet insulinotropic response, were not significantly different between the LP and NP rats (p > 0.05).\n\nQuestion:\nDoes protein-energy malnutrition at mid-adulthood imprint long-term metabolic consequences in male rats?\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:\nMotor learning is essential to gain skills with neurorehabilitation. To investigate whether capacity for motor learning affects rehabilitation outcome and its relevant brain activation in ataxic patients with stroke. Twelve patients presenting with ataxia admitted for inpatient rehabilitation 2 to 3 months after infratentorial stroke and 6 control subjects performed 8 repetitions of 30-second pursuit rotor (PR) task. Cortical oxygenated hemoglobin (oxyHb) signals were measured using functional near-infrared spectroscopy. Both patients and controls learned the PR skill, although the gains in PR performance were significantly lower in patients. In patients, the less learning significantly correlated with smaller rehabilitation gains assessed by the Functional Independence Measure. The Fugl-Meyer score for coordination and balance did not change. Center of task-related increase of cortical oxyHb signals shifted from the presupplementary motor area (preSMA) to the supplementary motor area (SMA) with task repetitions in controls but not in patients. Accordingly, serial changes of ratio of oxyHb increase in the preSMA to SMA (preSMA/SMA ratio) were significantly different between the groups. In patients and controls, gains in PR performance and changes of the preSMA/SMA ratio correlated.\n\nQuestion:\nDoes impaired motor learning by a pursuit rotor test reduce functional outcomes during rehabilitation of poststroke ataxia?\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:\nPredominantly theoretical courses are employed to teach German dental students in implant dentistry at pre-clinical stage. As implant dentistry is an important part of the clinical treatment spectra, practical implementation of this field at an early stage of education seems to be appropriate. By a newly developed interdisciplinary implant dentistry course, students should assess an improved competence level as well as first practical experiences in the field of implant dentistry at the pre-clinical stage of their education. Interdisciplinary implant dentistry education was integrated in the final pre-clinical course Phantom II at the Department of Prosthodontics, LMU, Munich. In total 120 pre-clinical students participated at the implant dentistry education course. After theoretical introduction into implant surgery and implant prosthetics, 30 simulation units were employed for the practical training of the participants. All important treatment steps were carried out by the students under instruction by the supervisors, including interdisciplinary planning, the use of the drilling template, the template guided insertion of two implants, as well as the integration of two ball attachments into a pre-existing full denture. After the course participants were asked by questionnaire about the quality of the course and their personal opinion. The course received an extraordinary positive feedback. In total 108 students evaluated the course with the overall grade of 1.68 according to the German school-mark system (1 = excellent, 6 = unsatisfactory). Also the single parts of the course were voted constantly positively.\n\nQuestion:\nDo description and evaluation of a new approach on pre-clinical implant dentistry education based on an innovative simulation 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:\nThe aim of this study was to test the hypothesis that preoperative prostate health index (PHI) levels could help to predict early biochemical recurrence (BCR) in a contemporary population of patients with prostate cancer treated with robot-assisted radical prostatectomy (RARP). The study population consisted of 313 patients treated with RARP for clinically localized prostate cancer at a single institution between 2010 and 2011. Patients subjected to neoadjuvant or adjuvant therapies and patients with a follow-up of<2 years were excluded. BCR was defined as a postoperative level of total prostate-specific antigen ≥0.2 ng/ml and elevating after RARP. The minimum P-value method was used to determine the most significant PHI cutoff value to discriminate between patients with and without BCR. The Kaplan-Meier method was used to determine BCR-free survival rates. Finally, Cox regression models were fitted to determine the predictors of BCR, and the predictive accuracy (area under the curve) of each predictor was determined with the Harrell concordance index. Mean total prostate-specific antigen and mean PHI levels were 5.76 ng/ml (interquartile range: 4.2-8.7) and 46.0 (35-62), respectively. Biopsy Gleason score was 6 in 173 (55.3%), 7 in 121 (38.7%), and ≥8 in 19 (6.1%) patients. At final pathology, extracapsular extension was observed in 59 (18.8%), seminal vesicle invasion in 24 (7.7%), and lymph node invasion in 11 (3.5%) patients, whereas 228 (72.8%) patients had organ-confined disease. The 2-year BCR-free survival rate was 92.5% in the overall population and was 96.7% in patients with organ-confined disease. The most significant PHI cutoff value to discriminate between patients with and without BCR was 82. Specifically, the 2-year BCR-free survival rate was 97.7% in patients with a preoperative PHI level<82 relative to 69.7% in patients with a PHI level ≥82 (log-rank test: P<0.001). Finally, in multivariable Cox regression analyses, PHI level emerged as an independent predictor of BCR in both the preoperative and the postoperative settings and was more accurate than several established BCR predictors were.\n\nQuestion:\nIs preoperative prostate health index an independent predictor of early biochemical recurrence after radical prostatectomy : Results from a prospective single-center 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:\nStreptococcus pneumoniae (pneumococcus) causes respiratory and systemic infections that are a major public health problem worldwide. It has been postulated that pneumococci persist in vivo in biofilm communities. In this study, we analyzed whether pneumococci form biofilms in vivo, and if so, whether biofilms correlated with bacterial persistence. Chinchillas were infected with S. pneumoniae TIGR4 and euthanized at varying times after infection, after which the superior ear bullae were excised and examined by culture and microscopy. Dense material, resembling the biofilms of other otitis media pathogens, was visible in the middle ear as late as 12 days after infection. Scanning electron microscopy revealed bacteria within an electron-dense matrix, similar to pneumococcal biofilms formed in vitro. Viability staining revealed groups of viable diplococci, as well as viable and nonviable host cells, attached to a fibrous matrix that was positive when stained with propidium iodide. Cryosections of biofilms were treated with polyclonal antibodies against the pneumococcal surface components pneumococcal surface protein A family 2, pneumococcal surface protein C, choline-binding protein, and neuraminidase, coupled with appropriate secondary antibody conjugates. Immunofluorescent staining showed the presence of pneumococcal communities within the material recovered from the middle ear chamber.\n\nQuestion:\nDoes streptococcus pneumoniae form surface-attached communities in the middle ear of experimentally infected chinchillas?\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:\nSuccessful lung transplantation has been limited by the scarcity of donors. Brain death (BD) donors are major source of lung transplantation. Whereas BD process induces acute lung injury and aggravates lung ischemia reperfusion injury. Carbon monoxide (CO) inhalation at 50-500 parts per million (ppm) can ameliorate lung injury in several models. We examined in rats whether CO inhalation in BD donor would show favorable effects on lung grafts. Rats were randomly divided into 4 groups. In sham group, donor rats received insertion of a balloon catheter into the cranial cavity, but the balloon was not inflated. In BD-only group, donor rats were ventilated with 40% oxygen after BD confirmation. In BD+CO250 and BD+CO500 groups, donor rats inhaled, after BD confirmation, 250 ppm or 500 ppm CO for 120 minutes prior to lung procurement, and orthotopic lung transplantation was performed. The rats were sacrificed 120 minutes after the lung transplantation by exsanguination, and their blood and lung graft samples were obtained. A total of 8 rats fulfilling the criteria were included in each group. The inhalation decreased the severity of lung injury in grafts from BD donors checked by histological examination. CO pretreatment reversed the aggravation of PaO2/FiO2 in recipients from BD donors. The CO inhalation down-regulated pro-inflammatory cytokines (TNF-alpha, IL-6) along with the increase of anti-inflammatory cytokine (IL-10) in recipient serum, and inhibited the activity of myeloperoxidase in grafts tissue. The inhalation significantly decreased cell apoptosis in lung grafts, inhibiting mRNA and protein expression of intercellular adhesion molecule-1 (ICAM-1) and caspase-3 in lung grafts. Further, the inhalation activated phosphorylation of p38 expression and inhibited phosphorylation of anti-extracellular signal-regulated kinase (ERK) expression in lung grafts. The effects of CO at 500 ppm were greater than those at 250 ppm.\n\nQuestion:\nDoes carbon monoxide inhalation ameliorate conditions of lung grafts from rat brain death donors?\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:\nInterleukin-8 (IL8) is a chemokine produced by malignant cells of multiple cancer types. It exerts various functions in shaping protumoral vascularization and inflammation/immunity. We evaluated sequential levels of serum IL8 in preclinical tumor models and in patients to assess its ability to estimate tumor burden. IL8 levels were monitored by sandwich ELISAs in cultured tumor cells supernatants, tumor-xenografted mice serum, and in samples from 126 patients with cancer. We correlated IL8 serum levels with baseline tumor burden and with treatment-induced changes in tumor burden, as well as with prognosis. IL8 concentrations correlated with the number of IL8-producing tumor cells in culture. In xenografted neoplasms, IL8 serum levels rapidly dropped after surgical excision, indicating an accurate correlation with tumor burden. In patients with melanoma (n = 16), renal cell carcinoma (RCC; n = 23), non-small cell lung cancer (NSCLC; n = 21), or hepatocellular carcinoma (HCC; n = 30), serum IL8 concentrations correlated with tumor burden and stage, survival (melanoma, n = 16; RCC, n = 23; HCC, n = 33), and objective responses to therapy, including those to BRAF inhibitors (melanoma, n = 16) and immunomodulatory monoclonal antibodies (melanoma, n = 8). IL8 concentrations in urine (n = 18) were mainly elevated in tumors with direct contact with the urinary tract.\n\nQuestion:\nDoes serum interleukin-8 reflect tumor burden and treatment response across malignancies of multiple tissue origins?\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:\nIt is unclear whether plasma homocysteine (Hcy) level affects long-term outcomes in patients with previous percutaneous coronary intervention (PCI). Accordingly, we investigated the association of plasma Hcy level with long-term major adverse cardiovascular events (MACEs), especially with recurrence of angina pectoris (AP) or new myocardial infarction (MI) in patients with previous PCI. A total of 231 patients with previous (>12 months) PCI were followed up for a median period of 49 months. The primary end point was recurrence of AP or new MI. The secondary end points were MACEs (cardiovascular death, recurrence of AP, new MI, revascularization therapy, hospitalization for heart failure, or stroke). During the follow-up period, 35 patients (15.2%) had a primary end point, and 58 (25.1%) had a secondary end point. A univariate analysis by a Cox proportional hazards regression model showed that plasma Hcy level was not associated with the primary (hazard ratio [HR] 1.13, 95% confidence interval [CI] 0.41-3.08, p=0.82) and secondary (HR 1.60, 95% CI 0.75-3.42, p=0.23) end points. The adjustment for other clinical variables did not alter the results.\n\nQuestion:\nIs plasma homocysteine level unrelated to long-term cardiovascular events in patients with previous 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:\nTo investigate the pharmacokinetics of talipexole hydrochloride tablets and the potential influence of Madopar (benserazide and levodopa combination; co-beneldopa) tablets on talipexole's pharmacokinetics when the two tablets are co-administered orally to healthy Chinese volunteers. A sensitive liquid chromatography-tandem mass spectrometry (LC-MS/MS) method was developed to measure talipexole concentration in human plasma in an open-label, randomized, two-way crossover, single-dose study, with 1-week washout period. Healthy Chinese volunteers were randomized to receive talipexole tablets either alone or together with Madopar tablets by oral administration after an overnight fast. Serial blood samples were collected for a period of 36 h after the administration. Pharmacokinetic parameters C(max), t(max), t(1/2z), mean residence time (MRT), AUC(0-tau), AUC(0-infinity), CL(z)/F and V(z)/F were determined under the non-compartmental model. Pharmacokinetic values of talipexole administered alone to the subjects were compared with those administered simultaneously with Madopar to determine whether or not the differences were statistically significant. The subjects experienced mild gastrointestinal irritation when talipexole was administered alone as well as together with Madopar. For talipexole hydrochloride, there were no significant differences in the pharmacokinetic values between the two administrations. No pharmacokinetic differences based on gender were observed either.\n\nQuestion:\nIs pharmacokinetic profile of talipexole in healthy volunteers altered when it is co-administered with Madopar ( co-beneldopa )?\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:\nPaclitaxel and docetaxel are two taxanes approved for the treatment of non-small-cell lung cancer (NSCLC). However, there is limited evidence regarding the efficacy of docetaxel in NSCLC previously treated with a paclitaxel-platinum doublet (PP). The aim of our study was to evaluate the response to docetaxel in NSCLC patients with prior PP treatment. Patients with stage IV NSCLC treated with PP that presented disease progression and received docetaxel as second-line treatment were included. Demographics, clinical characteristics, EGFR mutation status, objective response (OR), overall survival (OS), progression-free survival (PFS), and PFS without chemotherapy after first line with PP were analyzed. Sixty-three patients were evaluated. Median age was 58 years, 54% of patients were women, 53% were never-smokers, and 39% had EGFR mutations. OR and median PFS for PP were 36.5% and 6.7 months, respectively. OR and median PFS for docetaxel were 19% and 3.8 months, respectively. Patients with EGFR mutations had better response to docetaxel compared with wild-type patients (26 vs. 17%, p = 0.028). However, only long PFS (>6 months) to first-line PP was independently associated with a higher OR [RR 6.3, 95% CI (1.03-38.4), p = 0.046], and longer PFS [0.49 (0.25-0.9)] and OS [0.2 (0.06-0.7), p = 0.008] to second-line docetaxel compared with patients with short PFS (≤6 months) to PP.\n\nQuestion:\nIs long progression-free survival with first-line paclitaxel plus platinum associated with improved response and progression-free survival with second-line docetaxel in advanced non-small-cell lung 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:\nThe objective of this study was to assess whether the angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism influences the adequacy of the neurohormonal response to ACE inhibitors in patients with chronic heart failure (CHF). The renin-angiotensin-aldosterone system (RAAS) plays an important role in the pathophysiology of CHF, and aldosterone levels closely relate to outcome in patients with CHF. Angiotensin-converting enzyme inhibitors suppress the RAAS, but a significant proportion of patients exhibit elevated serum levels of aldosterone despite long-term administration of apparently adequate doses of these agents. We prospectively studied 132 patients with CHF (ejection fraction <45%) receiving long-term therapy with ACE inhibitors for over six months. Patients taking aldosterone antagonists were excluded from the study. \"Aldosterone escape\" was defined as being present when plasma aldosterone levels were above the normal range in our laboratory (>42 nmol/L). Patients were then divided into two subgroups according to the presence (group 1) or absence (group 2) of aldosterone escape. Genotype analysis for the ACE I/D polymorphism was performed by polymerase chain reaction. The prevalence of aldosterone escape in our patients was 10% (13/132). The two groups of patients did not differ regarding the dose of ACE inhibitor, diuretics and their renal function. There was a statistically significant different distribution of genotypes between the two groups, with a higher proportion of DD genotype in group 1 compared with group 2 (62% vs. 24%, p = 0.005).\n\nQuestion:\nIs failure of aldosterone suppression despite angiotensin-converting enzyme ( ACE ) inhibitor administration in chronic heart failure associated with ACE DD genotype?\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:\nInduction of HIV-1-specific T-cell responses relevant to diverse subtypes is a major goal of HIV vaccine development. Prime-boost regimens using heterologous gene-based vaccine vectors have induced potent, polyfunctional T cell responses in preclinical studies. The first opportunity to evaluate the immunogenicity of DNA priming followed by recombinant adenovirus serotype 5 (rAd5) boosting was as open-label rollover trials in subjects who had been enrolled in prior studies of HIV-1 specific DNA vaccines. All subjects underwent apheresis before and after rAd5 boosting to characterize in depth the T cell and antibody response induced by the heterologous DNA/rAd5 prime-boost combination. rAd5 boosting was well-tolerated with no serious adverse events. Compared to DNA or rAd5 vaccine alone, sequential DNA/rAd5 administration induced 7-fold higher magnitude Env-biased HIV-1-specific CD8(+) T-cell responses and 100-fold greater antibody titers measured by ELISA. There was no significant neutralizing antibody activity against primary isolates. Vaccine-elicited CD4(+) and CD8(+) T-cells expressed multiple functions and were predominantly long-term (CD127(+)) central or effector memory T cells and that persisted in blood for >6 months. Epitopes mapped in Gag and Env demonstrated partial cross-clade recognition.\n\nQuestion:\nDoes priming immunization with DNA augment immunogenicity of recombinant adenoviral vectors for both HIV-1 specific antibody and T-cell responses?\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:\nElectrical stimulation (ES) of the lower esophageal sphincter (LES) increases resting LES pressure (LESP) in animal models. Our aims were to evaluate the safety of such stimulation in humans, and test the hypothesis that ES increases resting LESP in patients with gastroesophageal reflux disease (GERD). A total of 10 subjects (nine female patients, mean age 52.6 years), with symptoms of GERD responsive to PPIs, low resting LES pressure, and abnormal 24-h intraesophageal pH test were enrolled. Those with hiatal hernia >2 cm and/or esophagitis >Los Angeles Grade B were excluded. Bipolar stitch electrodes were placed longitudinally in the LES during an elective laparoscopic cholecystectomy, secured by a clip and exteriorized through the abdominal wall. Following recovery, an external pulse generator delivered two types of stimulation for periods of 30 min: (i) low energy stimulation; pulse width of 200 μs, frequency of 20 Hz and current of 5-15 mA (current was increased up to 15 mA if LESP was less than 15 mmHg), and (ii) high energy stimulation; pulse width of 375 ms, frequency of 6 cpm, and current 5 mA. Resting LESP, amplitude of esophageal contractions and residual LESP in response to swallows were assessed before and after stimulation. Symptoms of chest pain, abdominal pain, and dysphagia were recorded before, during, and after stimulation and 7-days after stimulation. Continuous cardiac monitoring was performed during and after stimulation. All patients were successfully implanted nine subjects received high frequency, low energy, and four subjects received low frequency, high energy stimulation. Both types of stimulation significantly increased resting LESP: from 8.6 mmHg (95% CI 4.1-13.1) to 16.6 mmHg (95% CI 10.8-19.2), P < 0.001 with low energy stimulation and from 9.2 mmHg (95% CI 2.0-16.3) to 16.5 mmHg (95% CI 2.7-30.1), P = 0.03 with high energy stimulation. Neither type of stimulation affected the amplitude of esophageal peristalsis or residual LESP. No subject complained of dysphagia. One subject had retrosternal discomfort with stimulation at 15 mA that was not experienced with stimulation at 13 mA. There were no adverse events or any cardiac rhythm abnormalities with either type of stimulation.\n\nQuestion:\nDoes short-term electrical stimulation of the lower esophageal sphincter increase sphincter pressure in patients with gastroesophageal 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:\nThe purpose of this study was to examine the effects of caffeine (CAF) on physical, vigilance, and marksmanship tasks in soldiers during a sustained 55-h field exercise. There were 30 soldiers (23.6 +/- 4.5 yr, 81.8 +/- 10.3 kg) who were divided into a placebo (PLAC) and a CAF group. After a period of restricted sleep of 3 h during the first night, a period of sustained wakefulness began that ended at 11:00 of the third day. PLAC or CAF doses of 100 mg, 200 mg, 100 mg, and 200 mg were administered at 21:45, 23:45, 01:45, and 03:45, respectively. At 22:00 of day 2, subjects began two cycles of marksmanship, urban operations vigilance, and psychomotor vigilance (PVT) testing which ended at 06:00 of day 3. CAF maintained marksmanship vigilance at 85% throughout the second night as compared with PLAC, who significantly declined to 61.4 +/- 28.2% overnight. Marksmanship accuracy also decreased significantly in PLAC from 95.1 +/- 8.3% to 83.3 +/- 19.2%, but no change was observed in CAF. Urban operations vigilance decreased for both groups over the night, but the decrease was less for CAF (81.2 +/- 14.4% to 63.4 +/- 24.1%) compared with PLAC (77.6 +/- 19.2% to 44.0 +/- 30.2%). Reaction time and the number of major and minor lapses with the PVT significantly increased in PLAC but were unaffected in CAF.\n\nQuestion:\nDoes caffeine maintain vigilance and marksmanship in simulated urban operations with sleep deprivation?\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 examined the relationships between parent-child mealtime interactions and dietary adherence and glycemic control in young children with type 1 diabetes. It was hypothesized that young children who exhibited disruptive mealtime behaviors would have more dietary deviations (poorer dietary adherence) and poor glycemic control. It was also hypothesized that parents of young children who used ineffective/coercive parenting strategies at mealtimes would have children with more dietary deviations and poor glycemic control. A total of 35 families of children (aged 2.2-7.9 years) with type 1 diabetes were recruited from a pediatric hospital. Families had at least three meals videotaped in their home, which were coded for parent, child, and eating behaviors, using the Dyadic Interaction Nomenclature for Eating. Children's dietary adherence was assessed according to deviations from the prescribed number of carbohydrate units per meal. Children's average glycemic excursion was assessed prospectively for 2 weeks, using a standardized home blood glucose meter. Findings demonstrated significant positive relationships between children's mealtime behavior, dietary deviations, and glycemic control. An examination of parent behaviors revealed significant positive correlations between parents' use of ineffective/coercive parenting strategies and children's dietary deviations and glycemic control.\n\nQuestion:\nDo mealtime interactions relate to dietary adherence and glycemic control in young children with type 1 diabetes?\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 radiofrequency treatment applied to an intact anterior cruciate ligament, and to quantify the mechanical effects of controlled cyclic loading (simulating activities of daily living) post-treatment. An in vitro radiofrequency energy application to the rabbit anterior cruciate ligament and cyclic loading of the treated ligament. Effect of cyclic loading on the radiofrequency treated ligament in a controlled environment is not known. In the treatment group radiofrequency treatment was applied to an intact ligament and then the ligament was cyclically loaded for 3000 cycles, and stretched-to-failure. Control group was similar to treatment, except that the radiofrequency treatment was not applied. The cyclic loading (approximately 6% tensile strain) was kept below the injury threshold of the rabbit anterior cruciate ligament and was designed to simulate loading post-treatment. A relaxation test (5% constant strain for 180 s) was used to compare the results at different steps in the experiment; within each group and between the two groups. Relaxation force increased in the treatment group (average 108% of intact, P<0.05), but decreased after the cyclic loading (average 71% of intact, P<0.05). There were significant differences in the force-deformation-failure curves between the treatment and control groups: average treated ligament failed at 59% and 57% of the control values respectively for the deformation and force (P<0.05).\n\nQuestion:\nDoes radiofrequency treatment weaken the fatigue characteristics of rabbit anterior cruciate ligament?\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:\nEarly-life immune deviation is suspected in the inception of atopic disease. To investigate the association between cord blood chemokines and the subsequent development of atopic biomarkers and clinical end-points during the first 6 years of life. The Th1-associated chemokines CXCL10 and CXCL11 and the Th2-associated chemokines CCL17 and CCL22 were assessed in cord blood of asymptomatic at-risk newborn children from the Copenhagen Prospective Study on Asthma in Childhood (COPSAC(2000) ) birth cohort and associated with the longitudinal development of biomarkers and clinical end-points of asthma, eczema, and allergic rhinitis during the first 6 years of life. Cord blood CCL22 levels were significantly associated to total-IgE levels measured at four time-points during the first 6 years of life; overall odds ratio, 1.54 [CI, 1.25-1.89; P < 0.0001]. CXCL10 and CXCL11 were not associated with development of any atopic disorders or biomarkers.\n\nQuestion:\nDo cord blood Th2-related chemokine CCL22 levels associate with elevated total-IgE during preschool age?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]