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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:\nNonviral vectors based on polyethylenimine (PEI) usually contain an excess of PEI that is not complexed to DNA. Since unbound PEI contributes to cellular and systemic toxicity, purification of polyplexes from unbound PEI is desirable. Size exclusion chromatography (SEC) was used to purify PEI polyplexes of free PEI. Transfection properties of purified polyplexes and the effect of free PEI on gene delivery were studied in vitro and in vivo after systemic application into mice. SEC did not change the size and zeta-potential of polyplexes. Independent of the amount of PEI used for complex formation, purified PEI polyplexes had the same final PEI nitrogen/DNA phosphate ratio of 2.5. Notably, purified PEI polyplexes demonstrated low cellular and systemic toxicity. High transfection efficiency was achieved with purified polyplexes at high DNA concentrations (8-15 microg/ml). At low DNA concentrations (2-4 microg/ml) gene transfer with purified particles was less efficient than with polyplexes containing free PEI both in vitro and in vivo. Mechanistic studies showed that free PEI partly blocked cellular association of DNA complexes but was essential for the following intracellular gene delivery. Adding free PEI to cells treated with purified particles with a delay of up to 4 h resulted in significantly enhanced transfection efficiency compared with non-purified particles or purified particles without free PEI.\n\nQuestion:\nDoes purification of polyethylenimine polyplexes highlight the role of free polycations in gene transfer?\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:\nTouch preparation cytology (TPC) has proven to be a quick and accurate intraoperative diagnostic tool for excisional breast biopsy, margins and sentinel nodes. We hypothesized that TPC of core needle biopsy (CNB) specimens can provide a same-day diagnosis in the outpatient setting. Outpatients presenting with breast lesions underwent TPC of biopsy cores performed by biopsy gun or vacuum-assisted CNB. The TPC results were compared with the final diagnosis of CNB specimens. In all, 199 CNB and TP were performed between August 1997 and October 2002. Twenty-nine percent of lesions were malignant. Touch preparation was deferred in 21% of cases. In the remaining 157 evaluable cases, TPC had an accuracy of 89% and a false negative rate of 26%. The sensitivity, specificity, positive predictive value and negative predictive value of TPC were 74%, 97%, 93%, and 86% respectively.\n\nQuestion:\nIs touch preparation of breast core needle specimens a new method for same-day diagnosis?\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:\nGreen tea extract (GTE) has been shown to have antioxidative properties due to its high content of polyphenols and catechin gallates. Previous studies indicated that catechin gallates scavenge free radicals and attenuate the effects of reactive oxygen species. Cyclophosphamide (CP) produces reactive oxidative species, which can have adverse effects on development, causing limb, digit, and cranial abnormalities. The current study was performed to determine if exposure to GTE can decrease teratogenic effects induced by CP in CD-1 mice. From gestation days (GD) 6-13, mated CD-1 mice were dosed with 400 or 800 mg/kg/d GTE; 100, 200, 400, or 800 mg/kg/d GTE + CP; CP alone, or the vehicle. GTE was given by gavage. CP (20 mg/kg) was given by intraperitoneal injection on GD 10. Dams were sacrificed on GD 17, and their litters were examined for adverse effects. The highest GTE dose did not effectively attenuate, and in some cases exacerbated the negative effect of CP. GTE alone was also associated with an increased incidence of microblepharia. Conversely, moderate GTE doses (200 and/or 400 mg/kg/d) attenuated the effect of CP on fetal weight and (GTE 200 mg/kg/d) decreased the incidences of certain defects resulting from CP exposure.\n\nQuestion:\nDoes exposure to green tea extract alter the incidence of specific cyclophosphamide-induced malformations?\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:\nA previous study has demonstrated that endogenous male sex hormones do not alter neuronal nitric oxide (NO) release in rat mesenteric artery. However, the regulatory role of endogenous male sex hormones on noradrenaline (NA) release in rat mesenteric artery is not known. The present study was designed to analyze whether endogenous male sex hormones influence the NA release induced by electrical field stimulation (EFS), as well as the possible modification in NA and neuronal NO release by presynaptic beta-adrenoceptor activation. For this purpose, mesenteric arteries from control and orchidectomized male Sprague-Dawley rats were used. Basal and EFS-induced neuronal NO and NA release, as well as the contractile effect induced by EFS, was measured. Basal and EFS-induced neuronal NO and NA release were similar in arteries from control and orchidectomized rats. The beta-adrenoceptor agonist clenbuterol did not modify EFS-induced neuronal NO and NA release in arteries from control rats. In contrast, in arteries from orchidectomized animals, clenbuterol increased both neuronal NO and NA release; this increase was prevented by incubation with the beta-adrenoceptor antagonist propranolol. However, the contractile response elicited by EFS was not modified by clenbuterol in either group of rats.\n\nQuestion:\nDoes orchidectomy increase beta-adrenoceptor activation-mediated neuronal nitric oxide and noradrenaline release in rat mesenteric artery?\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:\nOncogenic mutations of PIK3CA, RAS (KRAS, NRAS), and BRAF have been identified in various malignancies, and activate the PI3K/AKT/mTOR and RAS/RAF/MEK pathways, respectively. Both pathways are critical drivers of tumorigenesis. Tumor tissues from 504 patients with diverse cancers referred to the Clinical Center for Targeted Therapy at MD Anderson Cancer Center starting in October 2008 were analyzed for PIK3CA, RAS (KRAS, NRAS), and BRAF mutations using polymerase chain reaction-based DNA sequencing. PIK3CA mutations were found in 54 (11%) of 504 patients tested; KRAS in 69 (19%) of 367; NRAS in 19 (8%) of 225; and BRAF in 31 (9%) of 361 patients. PIK3CA mutations were most frequent in squamous cervical (5/14, 36%), uterine (7/28, 25%), breast (6/29, 21%), and colorectal cancers (18/105, 17%); KRAS in pancreatic (5/9, 56%), colorectal (49/97, 51%), and uterine cancers (3/20, 15%); NRAS in melanoma (12/40, 30%), and uterine cancer (2/11, 18%); BRAF in melanoma (23/52, 44%), and colorectal cancer (5/88, 6%). Regardless of histology, KRAS mutations were found in 38% of patients with PIK3CA mutations compared to 16% of patients with wild-type (wt)PIK3CA (p = 0.001). In total, RAS (KRAS, NRAS) or BRAF mutations were found in 47% of patients with PIK3CA mutations vs. 24% of patients wtPIK3CA (p = 0.001). PIK3CA mutations were found in 28% of patients with KRAS mutations compared to 10% with wtKRAS (p = 0.001) and in 20% of patients with RAS (KRAS, NRAS) or BRAF mutations compared to 8% with wtRAS (KRAS, NRAS) or wtBRAF (p = 0.001).\n\nQuestion:\nDo pIK3CA mutations frequently coexist with RAS and BRAF mutations in patients with advanced cancers?\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 bacterial loads in meningococcal disease (MCD), their relation with disease severity, and the factors which determine bacterial load. Meningococcal DNA quantification was performed by the Taqman PCR method on admission and sequential blood samples from patients with MCD. Disease severity was assessed using the Glasgow Septicaemia Prognostic Score (GMSPS, range 0-15, severe disease > or =8). Median admission bacterial load was 1.6 x 10(6) DNA copies/ml of blood (range 2.2 x 10(4) to 1.6 x 10(8)). Bacterial load was significantly higher in patients with severe (8.4 x 10(6)) compared to milder disease (1.1 x 10(6), p = 0.018). This difference was greater in septicaemic patients (median 1.6 x 10(7) versus 9.2 x 10(5), p < 0.001). Bacterial loads were significantly higher in patients that died (p = 0.017). Admission bacterial load was independent of the duration of clinical symptoms prior to admission, with no difference between the duration of symptoms in mild or severe cases (median, 10.5 and 11 hours respectively). Bacterial loads were independent of DNA elimination rates following treatment.\n\nQuestion:\nDoes meningococcal bacterial DNA load at presentation correlate with disease severity?\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 role of exogenous normal lymph (ENL) on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats. ALI was induced by the jugular vein injection of LPS (iv, 15 mg/kg) in rats of the LPS and LPS+ENL groups within 15 min, then, ENL without cell components (5 ml/kg) was infused at the speed of 0.5 ml per minute in the LPS+ENL group, the same amount of saline was administered in the LPS group. The rats in the sham group received the same surgical procedure and saline. The histomorphology and the levels of P-selectin, intercellular adhesion molecule-1 (ICAM-1), myeloperoxidase (MPO) in pulmonary tissue were assessed. LPS induced pulmonary injury as well as increased the wet/dry weight ratio (W/D) and the levels of P-selectin, ICAM-1, and MPO in pulmonary tissues. These deleterious effects of LPS were significantly ameliorated by ENL treatment.\n\nQuestion:\nDoes exogenous normal lymph alleviate lipopolysaccharide-induced acute lung injury through lessening the adhesion molecules?\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:\nSingle nucleotide polymorphisms in the 5,10-methylenetetrahydrofolate reductase (MTHFR), vascular endothelial growth factor (VEGF), endothelial nitric oxide synthase (eNOS), monocyte chemoattractant protein-1 (MCP-1) and apolipoprotein E (ApoE) genes appear to be a genetic risk factor for atherosclerosis. Common carotid intima-media thickness (cIMT) provides information on the severity of atherosclerosis. To investigate the relationship between cIMT and gene polymorphisms associated with atherosclerosis in Turkish patients with coronary artery disease (CAD). Sixty-two patients with angiographically diagnosed stable CAD were divided into two groups according to their cIMT values (group 1: n=35, cIMT of 1 mm or greater; group 2: n=27, cIMT of less than 1 mm). MTHFR 677 C/T, VEGF --460 C/T, eNOS 894 G/T, MCP-1 --2518 A/G and ApoE (E2, E3 and E4) gene polymorphisms (where A is adenine, C is cytosine, G is guanine and T is thymine) were analyzed by polymerase chain reaction and restriction fragment length polymorphism. Evaluations of cardiovascular risk factors and coronary atherosclerotic lesions were performed in all patients. Serum homocysteine and high-sensitivity C-reactive protein were measured and compared between the two groups. Serum high-sensitivity C-reactive protein (P=0.04) and homocysteine (P=0.006) levels were higher in group 1 than in group 2. The ratio of multivessel CAD and previous myocardial infarction was significantly higher in group 1 than in group 2 (P=0.014). In the study population, no significant difference in cIMT was observed according to the polymorphisms studied. Only hyperhomocysteinemia (OR 1.17 [95% CI 1.01 to 1.35], P=0.033) and previous myocardial infarction (OR 3.76 [95% CI 1.10 to 12.81], P=0.034) maintained a significant correlation with cIMT on multiple logistic regression analysis.\n\nQuestion:\nAre polymorphisms of the methylenetetrahydrofolate reductase , vascular endothelial growth factor , endothelial nitric oxide synthase , monocyte chemoattractant protein-1 and apolipoprotein E genes associated with carotid intima-media thickness?\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:\nMicrobubbles and contrast-enhanced ultrasound (CEUS) is a new technique for locating sentinel lymph node (SLN). The aim of this study is to explore the feasibility of SLNs tracing by CEUS using microbubbles in breast cancer patients and the value of enhancing patterns in diagnosing lymph nodes metastases. A clinical trial was registered (trial registration: ChiCTR-DDT-13003778). One hundred and one consecutive consenting patients with breast cancer undergoing SLN biopsy were enrolled. Before the surgery, microbubble was injected periareolarly. Lymphatic drainage pathway was detected by CEUS, and guidewire was deployed to locate the SLN before the operation. Blue dye was also used to help in tracing sentinel lymph node during the operation. The identification rate and the accuracy rate were recorded. Enhancing patterns of lymph nodes were recorded and compared with the pathological diagnosis. Of the 101 cases, SLNs in 99 cases were successfully identified by at least one tracer, including 98 cases identified by CEUS and 97 cases by blue dye. There was no significant difference between the two methods (P = 0.705). Guidewires were deployed successfully in all 98 cases, and the localized SLNs were all isolated successfully in the following operations. The status of SLNs isolated by CEUS was completely identical to that of the whole axillary lymph node while 7.1 % cases were misdiagnosed as negative by blue dye method. The sensitivity of predicting SLNs metastases by CEUS enhancing pattern was 81.8 %, the specificity was 86.2 %, and the positive and negative predictive values were 75.0 and 90.3 %, respectively.\n\nQuestion:\nIs intradermal microbubbles and contrast-enhanced ultrasound ( CEUS ) a feasible approach for sentinel lymph node identification in early-stage breast 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:\nObesity is associated with a number of diseases with metabolic abnormalities such as type 2 diabetes (T2D). We investigate the effects of tectorigenin on 3T3-L1 preadipocyte differentiation and adipocytokines secretion. The effects of tectorigenin on adipocyte differentiation were studied using Oil Red O staining. Effects of tectorigenin on adipogenesis-related genes expression and adipocytokines secretion were measured by the real-time quantitative RT-PCR and ELISA method, respectively. Reporter gene assays were performed to determine the PPARγ and NF-κB transactivation. We also used [(3)H]-2-deoxy-d-glucose to study the glucose uptake, and the IKK/NF-κB signaling pathway was assessed by western blot analysis. HFD/STZ rats were used to evaluate the therapeutic efficacies of tectorigenin. Tectorigenin 10, 25, 50, and 75 μM inhibited 3T3-L1 adipogenesis and related genes transcription. TNF-α-induced changes of IL-6, MCP-1, as well as adiponectin in 3T3-L1 were markedly reversed by tectorigenin at 75 μM. Further investigation using reporter gene revealed that tectorigenin was a partial PPARγ agonist with an IC50 value of 13.3 μM. Tectorigenin improved basal and insulin-stimulated glucose uptake in mature 3T3-L1 adipocytes. Moreover, tectorigenin antagonized TNF-α-induced NF-κB transactivation and p65 nuclear translocation. Although tectorigenin (50 and 100 mg/kg) displayed the ability to promote insulin sensitivity and improve glucose metabolism in HFD/STZ rats, it did not cause significant side effects such as body weight gain, fluid retention, or cardiac hypertrophy.\n\nQuestion:\nDoes tectorigenin regulate adipogenic differentiation and adipocytokines secretion via PPARγ and IKK/NF-κB signaling?\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 lines of evidence indicate that mutational activation of KRAS is an early event in the carcinogenesis of non-small cell lung cancer (NSCLC). Nonetheless, previous studies report high frequencies of divergent KRAS mutational status between primary NSCLC and corresponding metastases. This suggests heterogeneity of the primary tumor in respect to its KRAS status. We therefore aimed to examine the frequency and the extent of such intratumoral heterogeneity. 40 NSCLC were examined for intratumoral heterogeneity of KRAS mutation (20 adenocarcinomas, 10 squamous cell carcinomas and 10 large cell carcinomas). Three to eight different tumor areas were analyzed for KRAS mutation and up to four corresponding lymph node metastases were included for analysis in nineteen cases. A combination of different methods for screening of heterogeneity and its validation were used including direct sequencing, laser-capture microdissection for tumor cell enrichment and the very sensitive ARMS/S method. Mutations of KRAS were found in 13/30 adenocarcinomas and large cell carcinomas. No mutations were detected in 10 squamous cell carcinomas. Four cases showed heterogeneous KRAS results by direct sequencing. More sensitive methods for KRAS mutation analysis revealed false negative results due to admixture of non-neoplastic cells in all of these samples. Intratumoral heterogeneity of KRAS mutational status was therefore confirmed in none of the analyzed cases. In addition, identical KRAS mutations were present in the primary tumor and the corresponding lymph node metastases in 19 cases examined.\n\nQuestion:\nIs intratumoral heterogeneity of KRAS mutation rare in 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:\nHepcidin is a key regulator of iron homeostasis and levels are elevated in patients with chronic kidney disease (CKD). Hepcidin may explain the often observed imbalance in iron metabolism in patients with CKD. We evaluated the influence of estimated glomerular filtration rate (eGFR) on serum levels of hepcidin-25 and its isoforms in patients with renal dysfunction. Serum levels of the biologically active hepcidin-25 and its isoforms were determined in CKD and dialysis patients by a mass spectrometry-based assay. In 83 patients with CKD not requiring dialysis, serum hepcidin-25 levels were not significantly increased (5.1 nM versus 4.2 nM, P = 0.30) and positively correlated with ferritin (r = 0.74, P < 0.01). Multiple regression analysis showed ferritin to be the only significant predictor of hepcidin-25 levels. Serum hepcidin-25 levels were not dependent on eGFR. In contrast, hepcidin-20 and total hepcidin levels showed an independent significant inverse correlation with eGFR. In 48 haemodialysis patients, median hepcidin-25 levels were significantly higher than in CKD patients (9.4 nM versus 5.1 nM, P < 0.001) and again strongly correlated with ferritin (r = 0.79, P < 0.001).\n\nQuestion:\nAre serum hepcidin-25 levels in patients with chronic kidney disease independent of glomerular filtration rate?\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:\nGranulocyte-colony stimulating factor (G-CSF) is used routinely in clinical practice for the treatment of neutropenia and to increase generation of hematopoietic stem cells in bone marrow donors. A growing body of literature on the neurotrophic effects of G-CSF has led to clinical trials in stroke, Alzheimer's disease (AD) and Parkinson's disease (PD). The primary objective of this study was to determine if G-CSF administration would rescue the nigro-striatal system and restore locomotor function after completion of a sub-acute course of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration (30mg/kg i.p. for 5 days) in 12 month-old mice. A secondary aim was to determine if G-CSF affects the neuro-inflammatory response by modulating microglial activation in striatum and midbrain. MPTP-treated mice were impaired on the rotometer test after the last dose of the toxicant and remained impaired until euthanasia. MPTP-treated mice that were given an 8-day regimen of G-CSF starting 2 days after the last dose of toxicant enhanced motor performance compared to the MPTP alone group. MPTP treatment depleted striatal DA (DA) levels; G-CSF given after MPTP resulted in a partial, significant repletion of DA levels. Total microglial burden in the striatum was increased significantly in MPTP-treated mice and was reduced after G-CSF rescue.\n\nQuestion:\nDoes granulocyte-colony stimulating factor ( G-CSF ) enhance recovery in mouse model of Parkinson 's 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:\nWe tested whether cortical activation anticipating painful stimuli is reduced more by integrative processes on somatosensory painful and motor information relative to the same hand than when that information refers to different hands. In 3 conditions, visual warning stimuli were followed by visual target stimuli associated with an electrical painful stimulation at left index finger. In the Pain (control) condition, no task was required after the target stimuli. In the \"Pain + ipsilateral movement\" condition, the subjects had to perform a movement of the left index finger. In the \"Pain + contralateral movement\" condition, they had to perform a movement of the right index finger. Meanwhile, electroencephalographic data were recorded (n = 18) from 128 scalp electrodes. Off line, these data were spatially enhanced by surface Laplacian transformation. Sensorimotor cortical activation before the painful stimulation was probed by the percentage power reduction of alpha rhythms at approximately 8 to 12 Hz (event-related desynchronization, ERD). Results showed that the subjects perceived a lower stimulus intensity in both \"Pain + ipsilateral\" and \"Pain + contralateral\" conditions compared with the control \"Pain\" condition. Furthermore, wide anticipatory alpha ERD (approximately 10-12 Hz) was lower in amplitude in the \"Pain + ipsilateral\" than in the \"Pain + contralateral\" condition. These results suggest that modulation of alpha rhythms is a putative physiological mechanism underlying anticipatory processes preceding the integration of painful and motor information at cortical level. Furthermore, these processes show a marked interference (\"gating\") when the sensorimotor integration refer to the same hand as opposed to both hands.\n\nQuestion:\nAre cortical alpha rhythms related to the anticipation of sensorimotor interaction between painful stimuli and movements : a high-resolution EEG 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:\nOral Squamous Cell Carcinoma (OSCC) is a major cause of cancer death worldwide, which is mainly due to recurrence leading to treatment failure and patient death. Histological status of surgical margins is a currently available assessment for recurrence risk in OSCC; however histological status does not predict recurrence, even in patients with histologically negative margins. Therefore, molecular analysis of histologically normal resection margins and the corresponding OSCC may aid in identifying a gene signature predictive of recurrence. We used a meta-analysis of 199 samples (OSCCs and normal oral tissues) from five public microarray datasets, in addition to our microarray analysis of 96 OSCCs and histologically normal margins from 24 patients, to train a gene signature for recurrence. Validation was performed by quantitative real-time PCR using 136 samples from an independent cohort of 30 patients. We identified 138 significantly over-expressed genes (> 2-fold, false discovery rate of 0.01) in OSCC. By penalized likelihood Cox regression, we identified a 4-gene signature with prognostic value for recurrence in our training set. This signature comprised the invasion-related genes MMP1, COL4A1, P4HA2, and THBS2. Over-expression of this 4-gene signature in histologically normal margins was associated with recurrence in our training cohort (p = 0.0003, logrank test) and in our independent validation cohort (p = 0.04, HR = 6.8, logrank test).\n\nQuestion:\nIs a gene signature in histologically normal surgical margins predictive of oral carcinoma recurrence?\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 inducible production of antimicrobial peptides is a major immune response in Drosophila. The genes encoding these peptides are activated by NF-kappaB transcription factors that are controlled by two independent signaling cascades: the Toll pathway that regulates the NF-kappaB homologs, Dorsal and DIF; and the IMD pathway that regulates the compound NF-kappaB-like protein, Relish. Although numerous components of each pathway that are required to induce antimicrobial gene expression have been identified, less is known about the mechanisms that either repress antimicrobial genes in the absence of infection or that downregulate these genes after infection. In a screen for factors that negatively regulate the IMD pathway, we isolated two partial loss-of-function mutations in the SkpA gene that constitutively induce the antibacterial peptide gene, Diptericin, a target of the IMD pathway. These mutations do not affect the systemic expression of the antifungal peptide gene, Drosomycin, a target of the Toll pathway. SkpA encodes a homolog of the yeast and human Skp1 proteins. Skp1 proteins function as subunits of SCF-E3 ubiquitin ligases that target substrates to the 26S proteasome, and mutations affecting either the Drosophila SCF components, Slimb and dCullin1, or the proteasome also induce Diptericin expression. In cultured cells, inhibition of SkpA and Slimb via RNAi increases levels of both the full-length Relish protein and the processed Rel-homology domain.\n\nQuestion:\nDoes a ubiquitin-proteasome pathway repress the Drosophila immune deficiency signaling cascade?\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:\nMicroRNAs play important roles in the development and progression of various cancers. Recent studies have shown that miR-638 was downregulated in several tumors; however, its role in gastric cancer (GC) has not been investigated in detail. The purpose of this study was to determine the role of miR-638 and to elucidate its regulatory mechanism in GC. The expression levels of miR-638 and specificity protein 2 (Sp2) were detected by real-time PCR and Western blotting in GC. After pcDNA6.2-GW/EmGFP-miR-638 vector, miR-638 inhibitor and Sp2-siRNA transfection, the AGS cell proliferation was investigated by MTT assay and cell cycle, and apoptosis was detected using the Annexin V/PI. In addition, the regulation of Sp2 by miR-638 was evaluated by real-time RT-PCR, Western blot and luciferase reporter assays; cyclin D1 expression was measured by Western blotting. The expression of miR-638 is dramatically down-regulated and Sp2 expression is remarkably up-regulated in GC tissues. Luciferase assays revealed that miR-638 inhibited Sp2 expression by targeting the 3'-UTR of Sp2 mRNA. Overexpression of miR-638 and Sp2-siRNA reduced Sp2 expression at both the mRNA and protein levels in vitro, and inhibition of miR-638 increased Sp2 expression. Moreover, we found that miR-638 overexpression and Sp2-siRNA markedly suppressed cell proliferation with decreasing expression of cyclin D1 and inducing G1-phase cell-cycle arrest in vitro; inhibition of miR-638 significantly promoted cell proliferation by increasing expression of cyclin D1 and leading more cells into the S and G2/M phase.\n\nQuestion:\nDoes miR-638 suppress cell proliferation in gastric cancer by targeting Sp2?\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 the muscle strength decrease that follows anterior cruciate ligament (ACL) reconstruction would lead to different cardiorespiratory adjustments during dynamic exercise. Eighteen active male subjects were submitted to isokinetic evaluation of knee flexor and extensor muscles four months after ACL surgery. Thigh circumference was also measured and an incremental unilateral cardiopulmonary exercise test was performed separately for both involved and uninvolved lower limbs in order to compare heart rate, oxygen consumption, minute ventilation, and ventilatory pattern (breath rate, tidal volume, inspiratory time, expiratory time, tidal volume/inspiratory time) at three different workloads (moderate, anaerobic threshold, and maximal). There was a significant difference between isokinetic extensor peak torque measured in the involved (116.5 ± 29.1 Nm) and uninvolved (220.8 ± 40.4 Nm) limbs, p=0.000. Isokinetic flexor peak torque was also lower in the involved limb than in the uninvolved limb (107.8 ± 15.4 and 132.5 ± 26.3 Nm, p=0.004, respectively). Lower values were also found in involved thigh circumference as compared with uninvolved limb (46.9 ± 4.3 and 48.5 ± 3.9 cm, p=0.005, respectively). No differences were found between the lower limbs in any of the variables of the incremental cardiopulmonary tests at all exercise intensities.\n\nQuestion:\nDo differences in muscle strength after ACL reconstruction influence cardiorespiratory responses to isometabolic exercise?\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:\nCancer risk and Lhermitte-Duclos disease (LDD) risk estimates for Cowden syndrome (CS) are broad and based on a small number of patients. Risk estimates are vital to the development of diagnostic criteria, genetic counseling, and cancer surveillance. To further elaborate and estimate the risks associated with CS, a large cohort of patients was evaluated. CS patients were identified from the medical literature and the Mayo Clinic's records. All patients met accepted diagnostic criteria for CS. A total of 211 CS patients (age 44 +/- 16 years, 64% female, 46% PTEN mutation) were included (published literature 90% and Mayo Clinic series 10%). The cumulative lifetime (age 70 years) risks were 89% for any cancer diagnosis (95% confidence interval (CI) = 80%,95%), breast cancer [female] 81% (CI = 66%,90%), LDD 32% (CI = 19%,49%), thyroid cancer 21% (CI = 14%,29%), endometrial cancer 19% (CI = 10%,32%), and renal cancer 15% (CI = 6%,32%). A previously unreported increased lifetime risk for colorectal cancer was identified (16%, CI = 8%,24%). Male CS patients had fewer cancers diagnosed than female patients and often had cancers not classically associated with CS. Seven percent of breast and thyroid cancers occurred in patients who were younger than the recommended age to commence radiographic cancer screening. There was a trend for patients with a family history of CS and PTEN mutations to have a lower cancer risk than those without.\n\nQuestion:\nAre cancer and Lhermitte-Duclos disease common in Cowden syndrome 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:\nBased on the development of minimal-invasive techniques and introduction of new implants enabling secure reconstruction an increasing number of patients are treated by isolated anterior column surgery. Most biomechanical studies dealing with thoracolumbar fracture models use worst-case scenarios of complete corpectomies to simulate vertebral body defects neglecting the influence of remaining cortical bone in partial corpus instability. Using a standardized partial and total corpectomy model we investigated the effect of the extent of corpectomy on stiffness in an anterior reconstruction model. Twelve human thoracolumbar specimens (Th11-L3) were loaded in a spine simulator with pure moments in the three motion planes. Following intact testing partial corp- and discectomy and later complete corpectomy of L1 were performed. Defects were instrumented by vertebral body replacements and additional anterior plating systems bridging the defect from Th12 to L2. Intersegmental rotations were measured between Th12 and L2. Significantly (P<0.05) increased range of motion was found in reconstructions of total compared to partial corpectomy. Total corpectomy reconstructions showed solely in lateral bending a significant reduction of range of motion compared to the intact state, while in axial rotation and flexion/extension it was significantly increased. Partial corpectomy reconstructions resulted in significantly reduced range of motion for lateral bending and flexion/extension compared to the intact specimen.\n\nQuestion:\nDoes extent of corpectomy determine primary stability following isolated anterior reconstruction in a thoracolumbar fracture 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:\nTo evaluate the clinical significance of mathematical coupling on the correlation between cardiac output and right ventricular end-diastolic volume (RVEDV) through measurement of cardiac output by two independent techniques. Prospective, observational study. Surgical intensive care unit in a level 1 trauma center. Twenty-eight critically ill surgical patients who received mechanical ventilation and hemodynamic monitoring with a pulmonary artery catheter. A pulmonary artery catheter designed to measure right ventricular ejection fraction (RVEF) and cardiac output by the intermittent bolus thermodilution (TDCO) method and continuous cardiac output by the pulsed thermal energy technique was placed. A computerized data logger was used to collect data simultaneously from the RVEF/TDCO system and the continuous cardiac output system. Two hundred forty-nine data sets from 28 patients were compared. There is statistical correlation between TDCO and continuous cardiac output measurements (r = 0.95, p < 0.0001) with an acceptable bias (-0.11 L/min) and precision (+/-0.74 L/min). The correlation was maintained over a wide range of cardiac outputs (2.3-17.8 L/min). There is a high degree of correlation between RVEDV and both TDCO (r = 0.72, p < 0.0001) and independently measured continuous cardiac output (r = 0.68, p < 0.0001). These correlation coefficients are not statistically different (p = 0.15).\n\nQuestion:\nDoes mathematical coupling explain the relationship between right ventricular end-diastolic volume and cardiac output?\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:\nWith the exception of the head, the vertebrate embryonic body is formed progressively in an anterior-posterior direction, originating from a posteriorly located bipotential neural-mesodermal progenitor population. The T-box transcription factor Brachyury is expressed within the progenitors and is essential for the formation of the posterior mesoderm. A novel cold-sensitive mutant of Zebrafish Brachyury (ntla(cs) ) is described that allows exploration of the temporal role of this key factor. The ntla(cs) mutant is used to show that Ntla has an essential role during early gastrulation, but as gastrulation proceeds the importance of Ntla declines as Ntlb acquires a capacity to form the posterior mesoderm. Remarkably, ntla(cs) embryos held at the nonpermissive temperature just during the gastrula stages show recovery of normal levels of mesodermal gene expression, demonstrating the plasticity of the posterior progenitors.\n\nQuestion:\nDoes a novel cold-sensitive mutant of ntla reveal temporal roles of brachyury in 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:\nTo investigate the effect of Cpd 861 on nuclear factor-kappa B (NF-kappa B) binding activity of hepatic stellate cells (HSC) in vitro. The study was carried out on the culture of hepatic stellate cell line, 5mg/ml of Cpd 861 was added and incubated for 48 hours. NF-kappa B binding activity was evaluated by electrophoretic mobility shift assays. IL-6 and sICAM-1 levels in the cultured supernatant were detected by ELISA. Cell apoptosis was detected by flow cytometry and TUNEL. Cpd 861 suppressed the binding activity of NF-kappa B in HSCs compared with the control group. Moreover, IL-6 and sICAM-1 levels in the cultured supernatant were decreased (P<0.05) and apoptosis rate of HSCs was increased after Cpd 861 incubation (P<0.01).\n\nQuestion:\nDoes [ Herbal compound 861 inhibit NF-kappa B binding activity of hepatic stellate cells in vitro ]?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTelomerase activation, a critical step in cell immortalization and oncogenesis, is partly regulated by alternative splicing. In this study, we aimed to use the Marek's disease virus (MDV) T-cell lymphoma model to evaluate TERT regulation by splicing during lymphomagenesis in vivo, from the start point to tumor establishment. We first screened cDNA libraries from the chicken MDV lymphoma-derived MSB-1 T- cell line, which we compared with B (DT40) and hepatocyte (LMH) cell lines. The chTERT splicing pattern was cell line-specific, despite similar high levels of telomerase activity. We identified 27 alternative transcripts of chicken TERT (chTERT). Five were in-frame alternative transcripts without in vitro telomerase activity in the presence of viral or chicken telomerase RNA (vTR or chTR), unlike the full-length transcript. Nineteen of the 22 transcripts with a premature termination codon (PTC) harbored a PTC more than 50 nucleotides upstream from the 3' splice junction, and were therefore predicted targets for nonsense-mediated decay (NMD). The major PTC-containing alternatively spliced form identified in MSB1 (ie10) was targeted to the NMD pathway, as demonstrated by UPF1 silencing. We then studied three splicing events separately, and the balance between in-frame alternative splice variants (d5f and d10f) plus the NMD target i10ec and constitutively spliced chTERT transcripts during lymphomagenesis induced by MDV indicated that basal telomerase activity in normal T cells was associated with a high proportion of in-frame non functional isoforms and a low proportion of constitutively spliced chTERT. Telomerase upregulation depended on an increase in active constitutively spliced chTERT levels and coincided with a switch in alternative splicing from an in-frame variant to NMD-targeted variants.\n\nQuestion:\nDo alternative splicing and nonsense-mediated decay regulate telomerase reverse transcriptase ( TERT ) expression during virus-induced lymphomagenesis in vivo?\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:\nBecause the mechanisms leading to bile duct damage in sclerosing cholangitis are unknown, we aimed to determine the pathogenesis of bile duct injury in multidrug resistance gene (Mdr2) (Abcb4) knockout mice (Mdr2(-/-)) as a novel model of the disease. Mdr2(-/-) and wild-type controls (Mdr2(+/+)) were studied at 2, 4, and 8 weeks of age. Liver histology, ultrastructure, immunofluorescence microscopy (to study inflammatory cells, tight junction protein ZO-1, basement membrane protein laminin, fluorescence-labeled ursodeoxycholic acid), immunohistochemistry (for alpha-smooth muscle actin, nitrotyrosine), sirius red staining, bacterial cultures of intra-abdominal organs, and polymerase chain reaction (PCR) for Helicobacter bilis DNA were compared between both genotypes. Hepatic cytokine expression was determined by reverse-transcription PCR. Bile ducts of Mdr2(-/-) showed disrupted tight junctions and basement membranes, bile acid leakage into portal tracts, induction of a portal inflammatory (CD11b, CD4-positive) infiltrate, and activation of proinflammatory (tumor necrosis factor [TNF]-alpha, interleukin [IL]-1beta) and profibrogenic cytokines (transforming growth factor [TGF]-beta1). This resulted in activation of periductal myofibroblasts, leading to periductal fibrosis, separating the peribiliary plexus from bile duct epithelial cells and, finally, causing atrophy and death of the bile duct epithelium. Bacterial translocation was not increased and H. bilis was not detectable in Mdr2(-/-).\n\nQuestion:\nDoes regurgitation of bile acids from leaky bile ducts cause sclerosing cholangitis in Mdr2 ( Abcb4 ) knockout 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:\nThe occurrence of esophageal dilation after laparoscopic adjustable silicone gastric banding (LASGB) had not been yet investigated systematically. In this study, standardized barium swallow studies were used to assess 45 LASGB patients for the development of esophageal dilation after the operation and after a mean follow-up period of 39.3 months. The diameter of the esophagus postoperatively and during the follow-up period was calculated in millimeters using the known diameter of the gastric band. An increase in diameter exceeding 130% compared with the postoperative diameter was considered as dilation. Symptoms were assessed by a questionnaire. For 11 patients with dilation, the band was emptied and a barium swallow performed to assess whether the dilation was reversible. A significant increase in the esophageal diameter (median and interquartile range [IQR]) was found by comparing the early postoperative and follow-up data: median, 16.3 mm (IQR, 14-18.7 mm) versus median, 20.7 mm (IQR, 18.1-26.8 mm; p < 0.01). For 25 (55.6%) of the 45 patients, the dilation percentage exceeded 130%. For 7 of the 11 patients, the dilation after emptying of the band still exceeded 130%. The increase in esophageal diameter was significantly correlated with the duration of follow-up evaluation, regurgitation, heartburn at night, and slow esophageal clearance.\n\nQuestion:\nIs esophageal dilation after laparoscopic adjustable gastric banding : a more systematic approach needed?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nRecent evidence suggests that obese animals exhibit increased endoplasmic reticulum (ER) stress in the liver and adipose tissue. Although ER stress is closely associated with lipid homeostasis, it is largely unknown how ER stress contributes to hepatic steatosis. In this study, we demonstrate that the induction of ER stress stimulates hepatic steatosis through increased expression of the hepatic very low-density lipoprotein receptor (VLDLR). Among the unfolded protein response sensors, the protein kinase RNA-like ER kinase-activating transcription factor 4 signaling pathway was required for hepatic VLDLR up-regulation. In primary hepatocytes, ER stress-dependent VLDLR expression induced intracellular triglyceride accumulation in the presence of very low-density lipoprotein. Moreover, ER stress-dependent hepatic steatosis was diminished in the livers of VLDLR-deficient and apolipoprotein E-deficient mice compared with wild-type mice. In addition, the VLDLR-deficient mice exhibited decreased hepatic steatosis upon high-fat diet feeding.\n\nQuestion:\nDoes endoplasmic reticulum stress induce hepatic steatosis via increased expression of the hepatic very low-density lipoprotein receptor?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe mechanism by which hemodynamic forces influence the function of the endothelium lining a blood vessel are unknown. The aim of this study was to determine the effect of in vitro cyclic strain on endothelial cell (EC) activation of protein kinase C (PKC). Confluent bovine aortic ECs grown on flexible-bottomed culture plates were subjected to 24% maximum strain at a frequency of 60 cycles/min for 24 hours. Changes in PKC activity and evidence of translocation from cytosol to membrane fractions were assessed by immunocytochemical staining of ECs with antibodies specific to PKC and direct measurement of PKC activity in cytosol and membrane. To determine whether activation of PKC was responsible for some effects of cyclic stretch on ECs, a specific PKC inhibitor, calphostin C, was added to ECs subjected to cyclic stretch for 5 days and control ECs grown under static conditions. Immunocytochemical staining of ECs demonstrated translocation of PKC alpha- and beta-antibody fluorescence from the cytosol to the perinuclear and nuclear regions in ECs subjected to cyclic strain. This was confirmed by direct measurements of PKC activity, which demonstrated an early transient translocation of PKC activity from cytosol to membrane fraction at 10 seconds followed by a sustained elevation in PKC activity in the membrane at 100 seconds. Calphostin C abrogated the increase in EC proliferation that occurs in response to stretch.\n\nQuestion:\nIs protein kinase C a mediator of the adaptation of vascular endothelial cells to cyclic strain in vitro?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nClinical studies suggest a survival advantage in cancer patients receiving low molecular weight heparin (LMWH). A suggested mechanism for this beneficial effect may reside in the antiangiogenic activity of heparins. In this study we investigated whether two different LMWHs, i.e. enoxaparin and dalteparin, and unfractionated heparin (UFH), affect the angiogenic potential of human microvascular endothelial cells (HMEC-1) promoted by tumor cells. HMEC-1 cells were incubated with tumor cell conditioned media (TCM) derived from human breast cancer and leukemic cells (i.e. MCF-7, MDA.MB.231, and NB4 cell lines) or recombinant cytokines (i.e. VEGF, FGF-2, TNF-alpha) +/-heparins. Capillary-like tube formation in Matrigel and cell proliferation were evaluated. All three TCM induced a significant (p<0.05) increase in total length of tubes formed by HMEC-1 in Matrigel. These increases were significantly counteracted (62 to 100% mean inhibition) by enoxaparin and dalteparin, but were significantly less affected by UFH. Similarly, the tube formation induced by standard VEGF, FGF-2, or TNF-alpha was 100% inhibited by enoxaparin, and 70-90% by dalteparin, whereas minor or no inhibition was observed with UFH. VEGF was the most active cytokine in TCM of both breast cancer and leukemic cells. EC proliferation was significantly increased by standard angiogenic factors, and slightly affected by breast cancer TCM (p=ns). The addition of heparins significantly counteracted the proliferative stimuli.\n\nQuestion:\nAre endothelial capillary tube formation and cell proliferation induced by tumor cells affected by low molecular weight heparins and unfractionated heparin?\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 our developed volume supplement protocol in preventing hypernatremia after head injury. Iso-sodium solution was infused to keep the 8-hour water balance positive in 20 head-injured patients with hypotonic urine. Serum sodium concentrations moved to within a normal range in 6 patients and were temporarily increased in 12 patients. Seven of the 12 showed a negative cumulative water balance and slightly low creatinine clearance. Mean arterial pressure in the other five patients was lower after supplementation and was positively related to sodium excretion. Hypernatremia could not be prevented in the other two patients and they did not survive. Creatinine clearance was below 40 mL/min/m2 in these two patients before supplementation.\n\nQuestion:\nDoes volume supplementation with iso-sodium solution prevent hypernatremia after head 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:\nIn vitro studies discovered intestinal proton-coupled folate transporter (PCFT) as a vitamin D hormone-responsive gene. In vivo effects of vitamin D on PCFT and folate status are currently not available. Three experiments were conducted. At first, vitamin D receptor knockout (VDR(-/-)) mice and corresponding wild-type (WT) mice were compared for their plasma and hepatic folate concentration and PCFT mRNA expression in intestinal mucosa. In a second experiment with rats, we analyzed the folate status of offspring in response to a maternal vitamin D-adequate (1,000 IU/kg) or vitamin D-deficient (0 IU/kg) diet that was fed for 11 weeks. Finally, the plasma folate concentration of healthy individuals was studied at baseline (in winter) and in response to an oral treatment for 8 weeks with 2,000 IU vitamin D3 per day or a placebo, respectively. Here, we show that folate status and intestinal PCFT mRNA abundance did not differ between the VDR(-/-) and the WT mice. No effect of vitamin D on folate status was also found in rat dams and their offspring, and plasma folate levels of individuals did not change in response to vitamin D.\n\nQuestion:\nIs vitamin D linked to folate status and mRNA expression of intestinal proton-coupled folate transporter?\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:\nExtracorporeal membrane oxygenation (ECMO) is an effective technique to provide emergency mechanical circulatory or respiratory assistance in critically ill patients. A Mobile Remote Cardiac Assist unit was created to implant ECMO in patients from outside our institution and bring them back in our intensive care unit for follow-up when stabilized. This study was undertaken to evaluate the feasibility and the preliminary results of this procedure. Between March 2006 and June 2008, 38 consecutive patients with acute cardiac or respiratory failure were implanted with percutaneous ECMO. The logistic concerns, indications, complications, and outcomes of these patients were analyzed. There were no logistic or technical problems during the round trip or ECMO implantation. Mean distance from our intensive care unit was 68 km (1 to 230). Maximal time limit between the phone call and implantation was 90 minutes. The indications were fulminant myocarditis, pharmacologic suicide attempt, acute myocardial infarction, postpartum cardiopathy, end-stage cardiomyopathy, with left ventricular ejection fraction of 0.19 ± 0.05 (n = 32), or acute respiratory distress syndrome without cardiac failure (n = 6). Patients received a percutaneous venoarterial femoral ECMO with immediate reperfusion of the limb or venovenous ECMO for isolated lung failure. Seventeen patients (45%) were successfully weaned from ECMO after 9.4 ± 8.7 days. Four patients (11%) were transplanted. One patient was switched to a left ventricular assist device and was then successfully transplanted. Twenty-one patients (55%) survived to hospital discharge.\n\nQuestion:\nDoes mobile extracorporeal membrane oxygenation unit expand cardiac assist surgical programs?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe have shown that autophagy and mitophagy are required for preconditioning. While statin's cardioprotective effects are well known, the role of autophagy/mitophagy in statin-mediated cardioprotection is not. In this study, we used HL-1 cardiomyocytes and mice subjected to ischemia/reperfusion to elucidate the mechanism of statin-mediated cardioprotection. HL-1 cardiomyocytes exposed to simvastatin for 24 h exhibited diminished protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling, increased activation of unc-51-like kinase 1, and upregulation of autophagy and mitophagy. Similar findings were obtained in hearts of mice given simvastatin. Mevalonate abolished simvastatin's effects on Akt/mTOR signaling and autophagy induction in HL-1 cells, indicating that the effects are mediated through inhibition of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase. Simvastatin-treated HL-1 cells exhibited mitochondrial translocation of Parkin and p62/SQSTM1, fission, and mitophagy. Because Parkin is required for mitophagy and is expressed in heart, we investigated the effect of simvastatin on infarct size in Parkin knockout mice. Simvastatin reduced infarct size in wild-type mice but showed no benefit in Parkin knockout mice. Inhibition of HMG-CoA reductase limits mevalonate availability for both cholesterol and coenzyme Q10 (CoQ) biosynthesis. CoQ supplementation had no effect on statin-induced Akt/mTOR dephosphorylation or macroautophagy in HL-1 cells, but it potently blocked mitophagy. Importantly, CoQ supplementation abolished statin-mediated cardioprotection in vivo.\n\nQuestion:\nIs mitophagy required for acute cardioprotection by simvastatin?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe have previously described a second window of protection against infarction in rabbits 24 to 72 hours after adenosine A(1) receptor (A(1)R) activation. In this study, we examined the potential role of the mitochondrial antioxidant manganese superoxide dismutase (Mn-SOD) as a potential end effector in mediating this protection. Rats were treated with an intravenous bolus of the A(1)R agonist 2-chloro-N(6)-cyclopentyladenosine (CCPA, 75 microg/kg) or saline vehicle. They were also given a 5 mg/kg IV infusion of a 22-mer phosphorothioate oligodeoxynucleotide (ODN) with sequence antisense to the initiation site of rat Mn-SOD mRNA. Sense ODN and scrambled ODN were used as controls. Twenty-four hours later, hearts were isolated and perfused with buffer at constant pressure and subjected to 35 minutes of regional ischemia and 2 hours of reperfusion. Treatment with CCPA compared with saline vehicle (control) significantly reduced infarct size, expressed as percentage of myocardium at risk (22.3+/-3.3% versus 42.1+/-3.8%, respectively; P=0.001). This protection was completely abolished by prior treatment with antisense ODN, which had no effect on its own. Neither sense ODN nor scrambled ODN had an effect on the CCPA-induced delayed cardioprotection. In separate animals, 24 hours after the same treatment, hearts were assayed for Mn-SOD content and activity. CCPA treatment induced a significant increase in myocardial Mn-SOD content and activity compared with the control condition; this increase was abolished by pretreatment with antisense ODN.\n\nQuestion:\nDoes adenosine A ( 1 ) receptor activation induce delayed preconditioning in rats mediated by manganese superoxide dismutase?\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:\nAccumulating evidence has revealed the significant role of glucagon-like peptide-1 (GLP-1) in weight loss. Sirtuin 1 (SIRT1) plays a vital role in the regulation of lipid metabolism. Here, we investigated the contribution of lipolytic and oxidative changes in white adipose tissue (WAT) to the weight-lowering effect induced by the GLP-1 receptor (GLP-1R) agonist exenatide (exendin-4) in mice. We also looked at the role of SIRT1 in this process. C57BL/6J mice and Sirt1 (+/-) mice were treated with exenatide (24 nmol/kg) or an NaCl solution (154 mmol/l) control i.p. for 8 weeks while receiving a high-fat diet (HFD) after a 12 week HFD challenge. Systemic phenotypic evaluations were carried out during and after the intervention. A lentivirus-mediated short hairpin (sh)RNA vector of the Sirt1 gene was transfected into differentiated 3T3-L1 adipocytes. An in vitro model system used adipocytes induced from Sirt1-null mouse embryonic fibroblasts (MEFs). Exenatide reduced fat mass and enhanced the lipolytic and oxidative capacity of WAT in diet-induced obese C57BL/6J mice. However, these effects were significantly impaired in Sirt1 (+/-) mice compared with wild-type controls. In vitro, exendin-4 increased lipolysis and fatty acid oxidation by upregulating SIRT1 expression and activity in differentiated 3T3-L1 adipocytes. Conversely, RNA interference (i)-induced knockdown of SIRT1 attenuated the lipolytic and oxidative responses to exendin-4 in differentiated 3T3-L1 adipocytes. Again, these responses were entirely abolished in Sirt1-null MEFs after induction into adipocytes.\n\nQuestion:\nDoes gLP-1 receptor agonist promote brown remodelling in mouse white adipose tissue through SIRT1?\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 increasingly clear that hepatocellular carcinoma (HCC) has a distinct microRNA (miRNA) expression profile that is involved in malignancy; however, little is known about how functional miRNA modulates the metastasis of hepatitis B virus (HBV)-related HCC (HBV-HCC). In the present study, we demonstrate that the levels of miRNA-143 (miR-143) are dramatically increased in metastatic HBV-HCC of both p21-HBx transgenic mice and HCC patients. Moreover, we show that overexpression of this miRNA is transcribed by nuclear factor kappa B (NF-kappaB) and favors liver tumor cell invasive and metastatic behavior. Intratumoral administration of miR-143 shows that high levels of miR-143 can significantly promote HCC metastasis in an athymic nude mouse model. An in vivo study that used p21-HBx transgenic mice also showed that local liver metastasis and distant lung metastasis are significantly inhibited by blocking miR-143. Additionally, fibronectin type III domain containing 3B (FNDC3B), which regulates cell motility, was identified as the direct and functional target of miR-143 both in vivo and in vitro.\n\nQuestion:\nDoes up-regulated microRNA-143 transcribed by nuclear factor kappa B enhance hepatocarcinoma metastasis by repressing fibronectin expression?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe immune response to influenza vaccine may be influenced by many factors, e.g. age, comorbidities or inflammation, and iron status. We studied the vaccine-induced production of hemagglutination-inhibition antibodies (HI) in 133 hemodialysis patients (HD) and 40 controls. To identify variables associated with the immune response, uni- and multivariate regression analyses were performed with seroconversion in HI titers as a dependent variable, with demographics, comorbidities, previous vaccination, inflammation, and iron status as independent variables. Seroconversion rates were lower in HD than in controls [43% versus 73% (H1N1 strain; p < 0.05); 43% versus 53% (H3N2; P=NS); 36% versus 62% (B; p < 0.05)]. In both HD and control groups, the predictors of the inferior HI production were pre-vaccination seroprotection, vaccination in the previous season, and old age. We did not find associations between seroconversion rates and inflammation and iron status in the studied populations. This was also true for a subanalysis of patients without pre-vaccination seroprotection.\n\nQuestion:\nAre previous Vaccination and Age More Important Predictors of Immune Response to Influenza Vaccine than Inflammation and Iron Status in Dialysis 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:\nIn the nonobese diabetic (NOD) mouse model of Sjögren's syndrome, lymphocytic infiltration is preceded by an accumulation of dendritic cells in the submandibular glands (SMGs). NOD mice also exhibit an increased frequency of mature, fractalkine receptor (CX3C chemokine receptor [CX3CR]1) expressing monocytes, which are considered to be precursors for tissue dendritic cells. To unravel further the role played by fractalkine-CX3CR1 interactions in the salivary gland inflammation, we studied the expression of fractalkine in NOD SMGs. We studied protein expression using Western blot analysis of whole tissue lysates. Protease activity was measured in salivary gland tissue lysates using fluorimetric substrates. Digestive capacity of enzymes was determined by in vitro incubation of recombinant enzyme and fractalkine, followed by protein staining and Western blot. Fractalkine was detected in salivary glands of both NOD and control mice at all ages. Western blot analysis showed fractalkine cleavage with increasing age, which was more pronounced in NOD mice. This cleavage resulted in a decrease in the 31 kDa form of the protein, and the generation of an approximately 19 kDa band. Furthermore, in NOD animals older than 15 weeks, we noted the presence of a unique approximately 17 kDa fragment. This cleavage was organ specific, because it did not occur in brain or pancreas. Increased gelatinase and alpha-secretase activity were detected in NOD SMG and contributed to cleavage of the 31 kDa protein. Because aberrant cleavage products may induce autoimmunity, we studied the presence of autoantibodies against fractalkine. Indeed, NOD mice exhibited significantly more antibodies against fractalkine than did control animals.\n\nQuestion:\nDoes altered fractalkine cleavage potentially promote local inflammation in NOD salivary gland?\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:\nFractional technology overcomes the problems of ablative lasers, such as inaccurate depth control and damage to the epidermis. Minimally invasive fractional radiofrequency microneedle devices allow for more-selective heating of the dermis. To evaluate the clinical efficacy of fractional radiofrequency microneedle (ERM) treatment in acne scars and large facial pores. Thirty patients with acne scars and large facial pores were enrolled. Bipolar radiofrequency energy was delivered to the skin through the electrodes of the FRM device. Skin lesions were evaluated according to grade of acne scars, Investigator Global Assessment of large pores, skin surface roughness, transepidermal water loss (TEWL), dermal density, microscopic and composite image, sebum measurement, and questionnaires regarding patient satisfaction. The grade of acne scars and Investigator Global Assessment of large pores improved in more than 70% of all patients. Skin surface roughness, dermal density, and microscopic and composite images also improved, whereas TEWL and sebum measurement did not change.\n\nQuestion:\nDoes evaluation of the clinical efficacy of fractional radiofrequency microneedle treatment in acne scars and large facial pore?\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 outcomes of carotid angioplasty and stenting (CAS) in patients with critical carotid stenosis who are deemed high risk for carotid endarterectomy. Medical records were retrospectively analyzed for patients undergoing CAS between September 2002 and March 2011 at a single institution. Patients were classified as having either critical (≥ 90%) or high-grade (70%-89%) carotid stenosis based on angiography. The primary composite end point was stroke, myocardial infarction, or death from any cause during the periprocedural period or any ipsilateral stroke during the follow-up period. A total of 245 patients underwent 257 CAS procedures during the study period. Fifty-one percentage (n = 130) of cases involved critical stenosis (66.2% male; mean age, 71 ± 10 y), with the remaining group (n = 127) involving high-grade stenosis (67.7% male; mean age, 71 ± 9 y). Symptomatic carotid disease was present in 25% of the critical stenosis and 31% of the high-grade stenosis groups (P = 0.33). Chronic obstructive pulmonary disease was more commonly found in the high-grade stenosis group (20% versus 8%, P = 0.01). No difference was observed between the groups relative to other baseline demographic characteristics, presence of contralateral carotid occlusion, stent diameter or length, maximum balloon diameter or length, use of embolic protection device, or procedural duration. Technical success was achieved in all cases. There was no difference in the need to predilate before the introduction of the filter or stent based on the degree of stenosis. We found no difference in the primary composite end point between the high-grade or critical stenosis groups (7.1% versus 7.7%, P = 0.74), or there were no differences between the individual components of the composite end point. Mid-term survival was similar between the two groups at a mean follow-up period of 2.4 y.\n\nQuestion:\nAre results of carotid angioplasty and stenting equivalent for critical versus high-grade lesions in patients deemed high risk for carotid endarterectomy?\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:\nPrimary pyogenic liver abscess (PLA) with septic complication by Klebsiella pneumoniae is an emerging infectious disease. Using DNA microarray hybridization, we identified a 20-kb chromosomal region that contained 15 open-reading frames (ORFs), including an iron-uptake system (kfu), a phosphoenolpyruvate sugar phosphotransferase system (PTS), and 6 unknown ORFs. The region was more prevalent among tissue-invasive strains (35/46) than among noninvasive strains (19/98) (P<.0001, chi2 test). To test the role played by this region in pathogenesis, 3 different deletion mutants (NTUH-K2044 [Delta kfu], K2044 [Delta ORF7-9], and K2044 [Delta PTS]) were constructed. Only the Delta kfuABC mutants showed decreased virulence in mice, compared with the wild-type strain. An in vitro assay confirmed the involvement of kfu in iron acquisition. There was a high correlation rate (85%) between the kfu/PTS region and 2 tissue invasion-associated chromosomal regions (allS and magA). Moreover, all 3 regions were present in strains that caused PLA plus endophthalmitis or meningitis.\n\nQuestion:\nIs genomic heterogeneity in Klebsiella pneumoniae strains associated with primary pyogenic liver abscess and metastatic infection?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nInfections of Reoviridae consisting of a double-stranded RNA (dsRNA) genome are a possible cause of biliary atresia (BA). The aim of the present study is to clarify the pathophysiological function of dsRNA viruses in the pathogenesis of BA. The expression of dsRNA pattern-recognizing receptors, Toll-like receptor 3 (TLR3), retinoic acid inducible gene I (RIG-I), melanoma differentiation-associated gene-5 (MDA-5), and dsRNA-activated protein kinase R (PKR) was constitutively detected in cultured human biliary epithelial cells (BECs). Stimulation with polyinosinic-polycytidylic acid [poly(I:C), a synthetic analog of viral dsRNA] induced the activation of transcription factors [nuclear factor (NF)-kappaB and interferon regulatory factor 3 (IRF3)] and the production of interferon-beta1 (IFN-beta1) and MxA as potent antiviral responses. Moreover, poly(I:C) up-regulated the expression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), and both poly(I:C) and TRAIL reduced the viability of cultured human BECs by enhancing apoptosis. Experiments in vivo using tissue sections of extrahepatic bile ducts from patients with BA and controls (choledochal cysts and nonbiliary diseases) showed that the activation of NF-kappaB, interferon regulatory factor-3 (IRF-3), and PKR, and the enhancement of TRAIL and single-stranded DNA (ssDNA)-positive apoptosis were significant in BA, although extrahepatic bile ducts diffusely and constantly expressed TLR3 in all diseases.\n\nQuestion:\nIs innate immune response to double-stranded RNA in biliary epithelial cells associated with the pathogenesis of biliary atresia?\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:\nActivation of bone morphogenetic protein (BMP)4 signalling in human ovarian cancer cells induces a number of phenotypic changes in vitro, including altered cell morphology, adhesion, motility and invasion, relative to normal human ovarian surface epithelial cells. From these in vitro analyses, we had hypothesized that active BMP signalling promotes the metastatic potential of ovarian cancer. To test this directly, we engineered OVCA429 human ovarian cancer cells possessing doxycycline-inducible expression of a constitutively-active mutant BMP receptor, ALK3QD, and administered these cells to immunocompromised mice. Further characterization was performed in vitro to address the role of activated BMP signalling on the EOC phenotype, with particular emphasis on epithelial-mesenchymal transition (EMT) and cell adhesion. Unexpectedly, doxycycline-induced ALK3QD expression in OVCA429 cells reduced tumour implantation on peritoneal surfaces and ascites formation when xenografted into immunocompromised mice by intraperitoneal injection. To determine the potential mechanisms controlling this in vivo observation, we followed with several cell culture experiments. Doxycycline-induced ALK3QD expression enhanced the refractile, spindle-shaped morphology of cultured OVCA429 cells eliciting an EMT-like response. Using in vitro wound healing assays, we observed that ALK3QD-expressing cells migrated with long, cytoplasmic projections extending into the wound space. The phenotypic alterations of ALK3QD-expressing cells correlated with changes in specific gene expression patterns of EMT, including increased Snail and Slug and reduced E-cadherin mRNA expression. In addition, ALK3QD signalling reduced beta1- and beta3-integrin expression, critical molecules involved in ovarian cancer cell adhesion. The combination of reduced E-cadherin and beta-integrin expression correlates directly with the reduced EOC cell cohesion in spheroids and reduced cell adhesion to the extracellular matrix substrates fibronectin and vitronectin that was observed.\n\nQuestion:\nDoes constitutive activation of BMP signalling abrogate experimental metastasis of OVCA429 cells via reduced cell adhesion?\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:\nImmunochemical fecal occult blood test (iFOBT) is widely used for colorectal cancer screening; however, its sensitivity is insufficient. We recently reported a fecal microRNA (miRNA) test (FmiRT) to detect colorectal cancer. In this study, we investigated a new colorectal cancer screening method combining iFOBT and FmiRT to improve the sensitivity compared with iFOBT alone. In total, 117 colorectal cancer patients and 107 healthy volunteers were enrolled. Ten-milligram fecal samples were collected and iFOBT was conducted. Fecal RNA was extracted from residuum of iFOBT and then the expression of 14 kinds of miRNA was analyzed for the FmiRT using real-time reverse transcription PCR. Levels of fecal miR-106a expression in iFOBT+ patients and iFOBT- patients were significantly higher than in healthy volunteers (P = 0.001). The sensitivity and specificity of FmiRT using miR-106a were 34.2% and 97.2%, and those of iFOBT were 60.7% and 98.1%, respectively. The overall sensitivity and specificity of the new screening method combining iFOBT and FmiRT were 70.9% and 96.3%, respectively. One quarter of colorectal cancer patients with false-negative iFOBT seemed to be true positive upon adding FmiRT using fecal miR-106a.\n\nQuestion:\nIs fecal miR-106a a useful marker for colorectal cancer patients with false-negative results in immunochemical fecal occult blood test?\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 expression of a specific set of genes controls the different structures of heparan sulfate proteoglycans (HSPGs), which are involved in the growth, invasion and metastatic properties of cancerous cells. The purpose of this study is to increase knowledge of HSPG alterations in breast cancer. Twenty-three infiltrating ductal adenocarcinomas (IDCs), both metastatic and non-metastatic were studied. A transcriptomic approach to the structure of heparan sulfate (HS) chains was used, employing qPCR to analyze both the expression of the enzymes involved in their biosynthesis and editing, as well as the proteoglycan core proteins. Since some of these proteoglycans can also carry chondroitin sulfate chains, we extended the study to include the genes involved in the biosynthesis of these glycosaminoglycans. Histochemical techniques were also used to analyze tissular expression of particular genes showing significant expression differences, of potential interest. No significant change in transcription was detected in approximately 70% of analyzed genes. However, 13 demonstrated changes in both tumor types (40% showing more intense deregulation in the metastatic), while 5 genes showed changes only in non-metastatic tumors. Changes were related to 3 core proteins: overexpression of syndecan-1 and underexpression of glypican-3 and perlecan. HS synthesis was affected by lower levels of some 3-O-sulfotransferase transcripts, the expression of NDST4 and, only in non metastatic tumors, higher levels of extracellular sulfatases. Furthermore, the expression of chondroitin sulfate also was considerably affected, involving both the synthesis of the saccharidic chains and sulfations at all locations. However, the pro-metastatic enzyme heparanase did not exhibit significant changes in mRNA expression, although in metastatic tumors it appeared related to increased levels of the most stable form of mRNA. Finally, the expression of heparanase 2, which displays anti-metastatic features, experienced a strong deregulation in all patients analyzed.\n\nQuestion:\nDo specific genes involved in synthesis and editing of heparan sulfate proteoglycans show altered expression patterns in breast 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:\nTherapies to target prostate cancer bone metastases have only limited effects. New treatments are focused on the interaction between cancer cells, bone marrow cells and the bone matrix. Osteoclasts play an important role in the development of bone tumors caused by prostate cancer. Since Src kinase has been shown to be necessary for osteoclast function, we hypothesized that dasatinib, a Src family kinase inhibitor, would reduce osteoclast activity and prostate cancer (PC-3) cell-induced osteoclast formation. Dasatinib inhibited RANKL-induced osteoclast differentiation of bone marrow-derived monocytes with an EC(50) of 7.5 nM. PC-3 cells, a human prostate cancer cell line, were able to differentiate RAW 264.7 cells, a murine monocytic cell line, into osteoclasts, and dasatinib inhibited this differentiation. In addition, conditioned medium from PC-3 cell cultures was able to differentiate RAW 264.7 cells into osteoclasts and this too, was inhibited by dasatinib. Even the lowest concentration of dasatinib, 1.25 nmol, inhibited osteoclast differentiation by 29%. Moreover, dasatinib inhibited osteoclast activity by 58% as measured by collagen 1 release. We performed in vitro experiments utilizing the Src family kinase inhibitor dasatinib to target osteoclast activation as a means of inhibiting prostate cancer bone metastases.\n\nQuestion:\nDoes dasatinib inhibit both osteoclast activation and prostate cancer PC-3-cell-induced osteoclast formation?\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:\nCompliance with long-term inhaled therapy in asthma is often poor, but it is likely to be improved with a simplified administration, once daily. The present study was designed to assess whether, in childhood asthma, a single dose of nebulized beclomethasone dipropionate once daily was as effective and safe as the same total daily dose administered twice daily. Asthmatic children, not treated with inhaled steroids for at least a month preceding the study and using short-acting bronchodilators more than once a week were enrolled in a double-blind, double dummy, randomised, multicentric study. After a two week run-in period on nebulised twice daily 400 mcg beclomethasone dipropionate, patients were randomly assigned to twelve weeks of treatment with 800 mcg nebulised beclomethasone dipropionate daily, either in single dose (o.d. group) or divided into two 400 mcg doses (b.i.d. group). 65 children (mean age 8.6 years, mean FEV1 81% of predicted), were valuable for intention to treat. During the run-in period, a significant improvement in FEV1, FVC, morning and evening PEF values and clinical scores was observed. Children then entered the randomised trial: 32 were included in the o.d. group and 33 in the b.i.d. group. During the twelve week treatment period, the observed improvement in pulmonary function parameters was maintained in both treatment groups. Morning and evening PEF showed a progressive slight increase as well as PEF diurnal variability showed a progressive reduction in the two treatment groups during the whole study period without reaching statistical significance. Moreover, in both treatment groups a similar progressive increase in symptom free nights and days and in the percentage of children achieving total asthma symptoms control was detected. Finally, no significant changes in urinary cortisol/creatinine ratio were observed throughout the study period and between groups.\n\nQuestion:\nIs once daily nebulized beclomethasone effective in maintaining pulmonary function and improving symptoms in asthmatic 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:\nLess than 20% of Pakistani women with early-onset or familial breast/ovarian cancer harbor germ line mutations in the high-penetrance genes BRCA1, BRCA2 and TP53. Thus, mutations in other genes confer genetic susceptibility to breast cancer, of which CHEK2 is a plausible candidate. CHEK2 encodes a checkpoint kinase, involved in response to DNA damage. In the present study we assessed the prevalence of CHEK2 germ line mutations in 145 BRCA1/2-negative early-onset and familial breast/ovarian cancer patients from Pakistan (Group 1). Mutation analysis of the complete CHEK2 coding region was performed using denaturing high-performance liquid chromatography analysis, followed by DNA sequencing of variant fragments. Two potentially deleterious missense mutations, c.275C>G (p.P92R) and c.1216C>T, (p.R406C), were identified (1.4%). The c.275C>G mutation is novel and has not been described in other populations. It was detected in a 30-year-old breast cancer patient with a family history of breast and multiple other cancers. The c.1216C>T mutation was found in a 34-year-old ovarian cancer patient from a family with two breast cancer cases. Both mutations were not detected in 229 recently recruited BRCA1/2-negative high risk patients (Group 2).\n\nQuestion:\nAre constitutional CHEK2 mutations infrequent in early-onset and familial breast/ovarian cancer patients from Pakistan?\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:\nType 2 diabetes is characterized by progressive beta-cell failure and apoptosis is probably the main form of beta-cell death in this disease. It was reported that circulating levels of interleukin-6 are elevated in type 2 diabetic patients, but whether this is involved in the pathogenesis of type 2 diabetes is still debated. In this study, we examined whether interleukin-6 can induce beta-cell damage in vitro and elucidated its mechanisms. To examine the effect of interleukin-6 on beta cells, glucose-stimulated insulin secretion (GSIS) by enzyme immunoassay (EIA) method and cell apoptosis by propidium iodide and annexin-V staining were measured in a rat beta-cell line (INS-1 or INS-832/13) after treatment with interleukin-6. The expression of apoptosis-related molecules was measured using western blotting and nitric oxide (NO) production was measured using Griess assay. AG490 and N-monomethyl-L-arginine were used to inhibit Janus kinase-mediated signal transducers and activators of transcription signalling and NO production, respectively. Exposure (48 h) of INS-1 cells to 20 ng/mL interleukin-6 significantly decreased GSIS as well as cell viability. We found that sub-G1/G0 population was increased as compared with untreated cells and expression of cleaved caspase-3, cleaved poly(ADP-ribose) polymerase, phosphorylated p38 mitogen-activated protein kinase and phosphorylated nuclear factor-κB was increased in interleukin-6-treated INS-1 cells. Interleukin-6 increased the amount of early apoptotic cells; this increase was blocked by AG490 or N-monomethyl-L-arginine treatment. Moreover, NO production, which is known to induce apoptosis, was increased by interleukin-6 treatment but abrogated in AG490-treated cells.\n\nQuestion:\nDoes interleukin-6 treatment induce beta-cell apoptosis via STAT-3-mediated nitric oxide production?\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:\nOxytocin is believed to be involved in ejaculation by increasing sperm number and contracting ejaculatory tissues. However, oxytocin may mediate these effects via oxytocin or vasopressin (AVP) receptors. The aim of this study was to determine the effect of oxytocin and AVP on peripheral tissues involved in ejaculation and to identify the receptor subtype(s) involved. Standard tissue bath techniques were used to measure isometric tension from tissues involved in ejaculation and erection. Oxytocin and AVP failed to elicit a tonic contractile response in rat and rabbit testes, vas deferens, epididymis, seminal vesicles and prostate. In contrast, oxytocin and AVP elicited large tonic contractions in erectile (corpus spongiosum and corpus cavernosum) and ejaculatory (prostatic urethra, bladder neck and ejaculatory duct) tissues in a concentration-dependent manner. The selective oxytocin agonist, [Thr4,Gly7]-oxytocin and the V2 agonist, [deamino-Cys1,Val4,D-Arg8]-vasopressin (dDAVP), failed to contract tissues. Oxytocin and AVP-induced contractions were weakly antagonized by the selective oxytocin antagonist, L-368899 but potently antagonized by the V1A antagonist, SR49059. The V1B antagonist SSR149415 failed to antagonize AVP contractions except in rabbit bladder neck. Neither L-368899 nor SR49059 antagonized endothelin-1-induced contractions.\n\nQuestion:\nAre oxytocin-induced contractions within rat and rabbit ejaculatory tissues mediated by vasopressin V1A receptors and not oxytocin receptors?\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:\nMorphology alone is not enough for the selection of the embryo (s) with the highest implantation potential and time-lapse imaging has added embryo development kinetics as another selection criterion. Therefore, a combination of morphology with kinetics has inspired a new field termed \"morphokinetics\", providing a new way of evaluating and selecting embryos. The aim of the study was to identify a criterion solely based on morphokinetic data and available up to the 8-cell stage (t8) to predict blastocyst formation and quality. The study included 3,354 embryos, with annotations up to t8, and cultured until day 5 from 626 infertile patients. A total of 17 kinetic expressions, either absolute cleavage timings and time intervals or time ratios were tested retrospectively for the prediction of blastocyst formation and quality. Relative timings (t8-t5, the cleavage synchronicity from 4 to 8 cells and from 2 to 8 cells) were found to be better indicators of blastocyst formation and quality when compared to absolute time-points. Especially, the cleavage synchronicity from 2 to 8 cells (CS2-8) = ((t3-t2) + (t5-t4))/(t8-t2)) was found to be the best predictor available on day 3 for blastocyst formation and quality (AUC:0.786; sensitivity: 83.43; specificity: 62.46).\n\nQuestion:\nAre relative kinetic expressions defining cleavage synchronicity better predictors of blastocyst formation and quality than absolute time points?\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 esophageal cancer related gene 4 (ECRG4) was initially identified and cloned in our laboratory from human normal esophageal epithelium (GenBank accession no.AF325503). ECRG4 was a new tumor suppressor gene in esophageal squamous cell carcinoma (ESCC) associated with prognosis. In this study, we investigated the novel tumor-suppressing function of ECRG4 in cancer cell migration, invasion, adhesion and cell cycle regulation in ESCC. Transwell and Boyden chamber experiments were utilized to examined the effects of ECRG4 expression on ESCC cells migration, invasion and adhesion. And flow cytometric analysis was used to observe the impact of ECRG4 expression on cell cycle regulation. Finally, the expression levels of cell cycle regulating proteins p53 and p21 in human ESCC cells transfected with ECRG4 gene were evaluated by Western blotting. The restoration of ECRG4 expression in ESCC cells inhibited cancer cells migration and invasion (P < 0.05), which did not affect cell adhesion capacity (P > 0.05). Furthermore, ECRG4 could cause cell cycle G1 phase arrest in ESCC (P < 0.05), through inducing the increased expression of p53 and p21 proteins.\n\nQuestion:\nDoes the candidate tumor suppressor gene ECRG4 inhibit cancer cells migration and invasion in esophageal 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:\n5-HT3 receptor antagonists are being evaluated as possible agents to prevent nausea and vomiting associated with radiation exposure in a non-clinical military setting. Because of concern about potential cardiovascular toxicity and the observation that certain developmental 5-HT3 antagonists produced undesirable effects, all drugs in this class are being carefully scrutinized for possible adverse cardiac effects. In this study, nine subjects underwent ambulatory ECG monitoring for an average of 21.6 h after a 2-mg oral dose of granisetron or placebo in a double-blind crossover protocol. Monitoring included a 3-h period of submaximal exercise in a 40 degrees C environment. Although isolated ventricular and supraventricular ectopic activity, sinus bradycardia, and pauses were found, there were no sustained arrhythmias observed in either the placebo or granisetron conditions.\n\nQuestion:\nDoes granisetron show no pro-arrhythmic effect in normal subjects during or after exercise in a hot environment?\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:\nCilostazol is known to be a selective inhibitor of phosphodiesterase 3 and is generally used to treat intermittent claudication caused by peripheral arterial disease. However, there is little information concerning the effect of cilostazol on angiogenesis. Here, we investigated whether cilostazol modulates the angiogenic process in vivo employing a hindlimb model of ischaemia-induced angiogenesis. This was an experimental study. Wild-type (WT) mice were randomly divided into two groups and were treated with or without cilostazol. One week later, the mice were subjected to unilateral hindlimb ischaemia. Angiogenesis was determined by laser Doppler analysis and capillary density stained with CD31. The expression of endothelial nitric oxide synthase (eNOS) was assessed by immunoblotting. WT mice treated with cilostazol showed accelerated neo-vascularisation following hindlimb ischaemic surgery on post-operative day 14 based upon laser Doppler measurements of blood flow (cilostazol-treated group, 0.54 ± 0.13 vs. control group, 0.38 ± 0.11; P-<-0.05). The capillary density in the ischaemic hindlimb was also significantly greater in WT mice treated with cilostazol than in non-treated WT mice (cilostazol-treated group, 1.63 ± 0.10 vs. control group, 1.15 ± 0.12; P-<-0.01). Cilostazol stimulated an ischaemia-induced increase in the phosphorylation of eNOS in the ischaemic limbs. Administration of NOS inhibitor N-nitro-l-arginine methyl ester (l-NAME) abolished cilostazol-induced increase in limb perfusion.\n\nQuestion:\nDoes cilostazol stimulate revascularisation in response to ischaemia via an eNOS-dependent mechanism?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCyclospora cayetanensis is an apicomplexan that causes diarrhea in humans. The investigation of foodborne outbreaks of cyclosporiasis has been hampered by a lack of genetic data and poor understanding of pathogen biology. In this study we sequenced the genome of C. cayetanensis and inferred its metabolism and invasion components based on comparative genomic analysis. The genome organization, metabolic capabilities and potential invasion mechanism of C. cayetanensis are very similar to those of Eimeria tenella. Propanoyl-CoA degradation, GPI anchor biosynthesis, and N-glycosylation are some apparent metabolic differences between C. cayetanensis and E. tenella. Unlike Eimeria spp., there are no active LTR-retrotransposons identified in C. cayetanensis. The similar repertoire of host cell invasion-related proteins possessed by all coccidia suggests that C. cayetanensis has an invasion process similar to the one in T. gondii and E. tenella. However, the significant reduction in the number of identifiable rhoptry protein kinases, phosphatases and serine protease inhibitors indicates that monoxenous coccidia, especially C. cayetanensis, have limited capabilities or use a different system to regulate host cell nuclear activities. C. cayetanensis does not possess any cluster of genes encoding the TA4-type SAG surface antigens seen in E. tenella, and may use a different family of surface antigens in initial host cell interactions.\n\nQuestion:\nDoes comparative genomics reveal Cyclospora cayetanensis possesses coccidia-like metabolism and invasion components but unique surface antigens?\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 role of DAXX in ovarian cancer development and metastasis has not been investigated before now. Overexpression of DAXX enhanced ovarian cancer cell proliferation, colony formation, and migration, whereas Daxx depletion had the opposite effects.\n\nQuestion:\nDoes death domain-associated protein DAXX promote ovarian cancer development and chemoresistance?\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 have suggested that endogenous glutamate and its N-methyl-D-aspartate receptors (NMDARs) play important roles in hyperoxia-induced acute lung injury in newborn rats. We hypothesized that NMDAR activation also participates in the development of chronic lung injury after withdrawal of hyperoxic conditions. In order to rule out the anti-inflammatory effects of NMDAR inhibitor on acute lung injury, the efficacy of MK-801 was evaluated in vivo using newborn Sprague-Dawley rats treated starting 4 days after cessation of hyperoxia exposure (on postnatal day 8). The role of NMDAR activation in hyperoxia-induced lung fibroblast proliferation and differentiation was examined in vitro using primary cells derived from the lungs of 8-day-old Sprague-Dawley rats exposed to hyperoxic conditions. Hyperoxia for 3 days induced acute lung injury in newborn rats. The acute injury almost completely disappeared 4 days after cessation of hyperoxia exposure. However, pulmonary fibrosis, impaired alveolarization, and decreased pulmonary compliance were observed on postnatal days 15 and 22. MK-801 treatment during the recovery period was found to alleviate the chronic damage induced by hyperoxia. Four NMDAR 2 s were found to be upregulated in the lung fibroblasts of newborn rats exposed to hyperoxia. In addition, the proliferation and upregulation of alpha-smooth muscle actin and (pro) collagen I in lung fibroblasts were detected in hyperoxia-exposed rats. MK-801 inhibited these changes.\n\nQuestion:\nDoes n-methyl-D-aspartate receptor activation mediate lung fibroblast proliferation and differentiation in hyperoxia-induced chronic lung disease in newborn 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:\nAdenovirus (Ad)-mediated E2F-1 gene transfer induces apoptosis in cancer cells in vitro and in vivo, but clinical application of E2F-1 in cancer gene therapy remains controversial because of the oncogenic potential of E2F-1. This barrier can be circumvented by using the truncated form of the E2F-1 gene (E2Ftr) (amino acids 1 through 375), which lacks the E2F-1 transactivation domain and cell cycle-promoting effects. The authors constructed 3 adenoviral vectors that expressed E2Ftr under regulation of the tetracycline (Tet)-off system (AdTet-E2Ftr1, AdTet-E2Ftr2, and AdTet-E2Ftr3). These vectors were compared for E2Ftr expression and apoptosis induction in cancer cells and normal cells. E2Ftr antitumor activity in vivo also was assessed in a melanoma xenograft model. One of the 3 vectors, AdTet-E2Ftr3, had the highest E2Ftr protein expression levels, which were correlated with the greatest induction of apoptosis and inhibition of cancer cell growth. E2Ftr induced apoptosis in a variety of cancer cell lines independent of p53 status with little cytotoxicity in normal cell lines. In a mouse melanoma xenograft model, AdTet-E2Ftr3 exhibited an approximately 80% decrease in tumor size compared with controls in vivo.\n\nQuestion:\nDoes adenovirus-mediated expression of truncated E2F-1 suppress tumor growth in vitro and in vivo?\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:\nSevere toxicity to 5-fluorouracil (5-FU) based chemotherapy in gastrointestinal cancer has been associated with constitutional genetic alterations of the dihydropyrimidine dehydrogenase gene (DPYD). In this study, we evaluated DPYD promoter methylation through quantitative methylation-specific PCR and screened DPYD for large intragenic rearrangements in peripheral blood from 45 patients with gastrointestinal cancers who developed severe 5-FU toxicity. DPYD promoter methylation was also assessed in tumor tissue from 29 patients Two cases with the IVS14+1G > A exon 14 skipping mutation (c.1905+1G > A), and one case carrying the 1845 G > T missense mutation (c.1845G > T) in the DPYD gene were identified. However, DPYD promoter methylation and large DPYD intragenic rearrangements were absent in all cases analyzed.\n\nQuestion:\nAre promoter methylation and large intragenic rearrangements of DPYD implicated in severe toxicity to 5-fluorouracil-based chemotherapy in gastrointestinal cancer patients?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nOxidative stress is involved in cholestasis-induced hepatic damage. Therefore, antioxidant therapy is a recommended therapeutic strategy. Studies have illustrated that chromium can enhance antioxidative capacity leading to a resolution of oxidative stress. The aim of this study was to assess whether chromium has protective effects against cholestasis-related liver damage. Cholestasis was produced by bile duct ligation (BDL) in male Sprague-Dawley rats for 3 weeks. Rats were randomly divided into four groups. Control and BDL groups were subjected to sham and BDL operation, respectively, and were supplemented with placebo for 3 weeks. The BDL-post Cr group was supplemented with chromium chloride for 3 weeks after BDL operation. The BDL-pre Cr group was supplemented with chromium chloride for 6 weeks starting from 3 weeks before BDL operation. In comparison with the control group, the BDL group showed hepatic damage as evidenced by elevation in serum biochemicals, ductular reaction, and fibrosis. These pathophysiological changes were attenuated in the BDL-Pre Cr and BDL-Post Cr groups. However, there was no significant difference between these two groups. The anti-fibrotic effect of chromium was accompanied by reductions in alpha-smooth muscle actin-positive matrix-producing cells and Smad 2/3 activity critical to the fibrogenic potential of transforming growth factor beta 1 (TGF-beta1). In addition, chromium effectively attenuated BDL-induced hepatic oxidative stress.\n\nQuestion:\nDoes chromium attenuate hepatic damage in a rat model of chronic cholestasis?\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:\nAn acquired deficiency of blood coagulation factor XIII has been proposed to cause an impairment of intestinal wound healing and hemostasis in patients with inflammatory bowel diseases. Substitution of factor XIII seems to result in a rapid improvement of intestinal wound healing. Our aim was therefore to characterize the role of factor XIII in the modulation of intestinal wound healing in vitro. Factor XIII was added to subconfluent cultures of two non-transformed small-intestinal epithelial cell lines (IEC-6, IEC-18) and three human colon cancer-derived epithelial cell lines (T84, CaCo-2, HT-29) with subsequent assessment of cell proliferation with a colorimetric 3-(4,5-dimethylthiazole-2-yl)-2,5-diphenylformazan (MTT) assay. The effects on epithelial cell migration in vitro were assessed with an in vitro wounding model of confluent IEC-6 cell monolayers. Factor XIII caused a modest inhibition of proliferation of IEC-6 and IEC-18 cells. However, factor XIII significantly stimulated proliferation of T84, CaCo-2. and HT-29 cell lines. In addition, thrombin-activated factor Xill promoted intestinal epithelial cell restitution in vitro on average 2.5-fold. The modulatory effects of factor XIII could not be significantly blocked by anti-transforming growth factor beta (TGFbeta).\n\nQuestion:\nDoes factor XIII modulate intestinal epithelial wound healing in vitro?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe neurotrophin nerve growth factor (NGF) has been implicated as a mediator in allergic asthma. Direct evidence that inhibition of NGF-induced activation of neurotrophin receptors leads to improvement of airway symptoms is lacking. We therefore studied the effects of inhibitors of NGF signal transduction on the development of airway hyper-responsiveness (AHR) and pulmonary inflammation in a guinea-pig model for allergic asthma. Airway responsiveness to the contractile agonist histamine was measured in vivo in guinea-pigs that were sensitized and challenged with ovalbumin (OVA). Inflammatory cell influx and NGF levels were determined in bronchoalveolar lavage fluid (BALF). Substance P, a key mediator of inflammation, was measured in lung tissue by radioimmunoassay, while substance P immunoreactive neurons in nodose ganglia were measured by immunohistochemistry. OVA challenge induced an AHR after 24 h in OVA-sensitized guinea-pigs. This coincided with an increase in the amount of NGF in BALF. Simultaneously, an increase in the percentage of substance P immunoreactive neurons in the nodose ganglia and an increase in the amount of substance P in lung tissue were found. We used tyrosine kinase inhibitors to block the signal transduction of the high-affinity NGF receptor, tyrosine kinase A (trkA). Treatment with the tyrosine kinase inhibitors (K252a or tyrphostin AG879) both inhibited the development of AHR, and prevented the increase in substance P in the nodose ganglia and lung tissue completely whereas both inhibitors had no effect on baseline airway resistance. Neither treatment with K252a or tyrphostin AG879 changed the influx of inflammatory cells in the BALF due to allergen challenge.\n\nQuestion:\nIs airway hyper-responsiveness in allergic asthma in guinea-pigs mediated by nerve growth factor via the induction of substance P : a potential role for trkA?\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:\nSkeletal muscle trauma leads to severe functional deficits, which cannot be addressed by current treatment options. Our group could show the efficacy of local transplantation of mesenchymal stroma cells (MSCs) for the treatment of injured muscles. While local application of MSCs has proven to be effective, we hypothesized that a selective intra-arterial transplantation would lead to a better distribution of the cells and so improved physiological recovery of muscle function. 18 female Sprague Dawley rats received an open crush trauma of the left soleus muscle. Autologous MSC were transduced using dsCOP-GFP and 2.5 x 10(6)cells were transplanted into the femoral artery of 9 animals one week after trauma. Control animals (n=9) received a saline injection. Cell tracking, analysis of tissue fibrosis and muscle force measurements were performed after 3 weeks. Systemic MSC-therapy improved the muscle force significantly compared to control (fast twitch: 82.4%, tetany: 61.6%, p = 0.02). The histological analysis showed no differences in the quantity of fibrotic tissue. Histological examination revealed no cells in the traumatized muscle tissue 21 days after transplantation.\n\nQuestion:\nDoes intra-Arterial MSC Transplantation restore Functional Capacity After Skeletal Muscle Trauma?\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 plant immune system employs intracellular NLRs (nucleotide binding [NB], leucine-rich repeat [LRR]/nucleotide-binding oligomerization domain [NOD]-like receptors) to detect effector proteins secreted into the plant cell by potential pathogens. Activated plant NLRs trigger a range of immune responses, collectively known as the hypersensitive response (HR), which culminates in death of the infected cell. Plant NLRs show structural and functional resemblance to animal NLRs involved in inflammatory and innate immune responses. Therefore, knowledge of the activation and regulation of animal NLRs can help us understand the mechanism of action of plant NLRs, and vice versa. This review provides an overview of the innate immune pathways in plants and animals, focusing on the available structural and biochemical information available for both plant and animal NLRs. We highlight the gap in knowledge between the animal and plant systems, in particular the lack of structural information for plant NLRs, with crystal structures only available for the N-terminal domains of plant NLRs and an integrated decoy domain, in contrast to the more complete structures available for animal NLRs. We assess the similarities and differences between plant and animal NLRs, and use the structural information on the animal NLR pair NAIP/NLRC4 to derive a plausible model for plant NLR activation.\n\nQuestion:\nDo animal NLRs provide structural insights into plant NLR function?\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:\nCancers of the bile duct and the pancreas are virtually indistinguishable using conventional histopathological and clinical characteristics. We sought to use microRNA (miR) profiling to differentiate these two cancers. RNA was harvested from the tumors of patients undergoing curative resection for cholangiocarcinoma or pancreatic adenocarcinoma and compared with adjacent normal bile duct or pancreas, respectively. There were 31 pairs of cholangiocarcinoma with matched tumor and adjacent bile duct and nine pairs of pancreatic cancer with matched tumor and adjacent uninvolved pancreas that had sufficient quantity of RNA that were included in the final analysis. Differential microRNA expression profiles were determined using the nCounter System from nanoString Technologies (Seattle, WA,USA). A total of 41 differentially expressed miRs were identified in cholangiocarcinoma (25 overexpressed, 16 underexpressed) and 52 differentially expressed miRs were found in pancreatic adenocarcinoma (30 overexpressed, 22 underexpressed) relative to adjacent normal tissue. Of these two profiles, 15 miRs were commonly dysregulated between tumor types. Also, eight miRs were similarly overexpressed or underexpressed in cholangiocarcinoma and pancreatic adenocarcinoma, whereas the other seven miRs had inverse expression levels.\n\nQuestion:\nDoes a differential microRNA profile distinguish cholangiocarcinoma from pancreatic adenocarcinoma?\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:\nLittle is known about the association between self-weighing frequency and weight gain prevention, particularly in worksite populations. The degree to which self-weighing frequency predicted 2-year body weight change in working adults was examined. The association between self-weighing frequency (monthly or less, weekly, daily, or more) and 24-month weight change was analyzed in a prospective cohort analysis (n = 1,222) as part of the larger HealthWorks trial. There was a significant interaction between follow-up self-weighing frequency and baseline body mass index. The difference in weight change ranged from -4.4 ± 0.8 kg weight loss among obese daily self-weighers to 2.1 ± 0.4 kg weight gain for participants at a healthy weight who reported monthly self-weighing.\n\nQuestion:\nIs self-weighing frequency associated with weight gain prevention over 2 years among working adults?\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 increasing cartilage cross-links through in vitro glycation of cartilage explants can alter the biomechanical response of chondrocytes to compressive deformation. Bovine osteochondral explants were either incubated with cell culture solution supplemented with (n = 7) or without (n = 7) ribose for 42 h in order to induce glycation. Deformation-induced changes in cell volume, dimensions and local tissue strains were determined through confocal laser scanning microscopy (CLSM) and the use of a custom built micro-compression device. Osteochondral explants were also utilized to demonstrate changes in depth-wise tissue properties, biomechanical tissue properties and cross-links such as pentosidine (Pent), hydroxylysyl pyridinoline (HP) and lysyl pyridinoline (LP). The ribose treated osteochondral samples experienced reduced cell volume deformation in the upper tissue zone by ∼ 8% (P = 0.005), as compared the control samples, through restricting cell expansion. In the deeper tissue zone, cell volume deformation was increased by ∼ 12% (P < 0.001) via the transmission of mechanical signals further into the tissue depth. Biomechanical testing of the ribose treated osteochondral samples demonstrated an increase in the equilibrium and dynamic strain dependent moduli (P < 0.001 and P = 0.008, respectively). The biochemical analysis revealed an increase in Pent cross-links (P < 0.001). Depth-wise tissue property analyses revealed increased levels of carbohydrate content, greater levels of fixed charge density and an increased carbohydrate to protein ratio from 6 to 16%, 55-100% and 72-79% of the normalized tissue thickness (from the surface), respectively, in the ribose-treated group (P < 0.05).\n\nQuestion:\nDoes in vitro glycation of articular cartilage alter the biomechanical response of chondrocytes in a depth-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:\nDespite intense research efforts, the aetiology and pathogenesis of idiopathic pulmonary fibrosis remain poorly understood. Gelsolin, an actin-binding protein that modulates cytoskeletal dynamics, was recently highlighted as a likely disease modifier through comparative expression profiling and target prioritisation. To decipher the possible role of gelsolin in pulmonary inflammation and fibrosis, immunocytochemistry on tissue microarrays of human patient samples was performed followed by computerised image analysis. The results were validated in the bleomycin-induced animal model of pulmonary inflammation and fibrosis using genetically-modified mice lacking gelsolin expression. Moreover, to gain mechanistic insights into the mode of gelsolin activity, a series of biochemical analyses was performed ex vivo in mouse embryonic fibroblasts. Increased gelsolin expression was detected in lung samples of patients with idiopathic interstitial pneumonia as well as in modelled pulmonary inflammation and fibrosis. Genetic ablation of gelsolin protected mice from the development of modelled pulmonary inflammation and fibrosis attributed to attenuated epithelial apoptosis.\n\nQuestion:\nIs gelsolin expression necessary for the development of modelled pulmonary inflammation and 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:\nThe purpose of this study was to investigate the effect of recombinant pigment epithelium-derived factor (rPEDF), secreted by ARPE-19 cells transfected with the human PEDF gene and transplanted subconjunctivally in normal and in rabbits in which corneal neovascularization was elicited by a chemical burn. Twenty grey Chinchilla Bastard rabbits were randomly assigned to four groups; neovascularization was induced in groups A, B, and C by alkali cauterization. Seven days later, group A received no cell implantation, non-transfected ARPE-19 cells were implanted subconjunctivally in group B, and PEDF-transfected ARPE-19 cells were implanted subconjunctivally in groups C and D (non-cauterized). In-vivo rPEDF secretion was analyzed by immunoblotting, and ELISA of extracts of conjunctival tissue samples taken at different time points. Digital photographs acquired on days 7, 14, and 21 after cauterization were evaluated for lead vessel length, vascular invasion area, and overall neovascularization rate. At days 14 and 21 after cauterization, significant differences were observed between groups A, B, and C in lead vessel length (day 21: 5.91 ± 0.45, 5.11 ± 1.22, 3.79 ± 0.59 mm, repectively), vascular invasion area (day 21: 35.5 ± 8.65, 34.86 ± 4.92, 19.2 ± 5.03 mm(2) respectively), and rate of corneal neovascularization. Compared to controls, neovascularization was reduced by 37.5 % on day 14 and 47 % on day 21. Analysis of conjunctival tissue extracts showed that rPEDF was secreted by the transplanted PEDF-transfected cells.\n\nQuestion:\nDoes transplantation of PEDF-transfected pigment epithelial cells inhibit corneal neovascularization in a rabbit 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:\nMaternal prenatal depression predicts post-partum depression and increases risk of prematurity and low birth weight. These effects may be mediated by altered placental function. We hypothesized that placental function would be influenced by the gestational week of experiencing depressive symptoms and aimed to examine associations between maternal depressive symptoms during pregnancy and placental expression of genes involved in glucocorticoid and serotonin transfer between mother and fetus. We studied women participating in a prospective pregnancy cohort: the Prediction and Prevention of Preeclampsia (PREDO) Study, Helsinki, Finland. Maternal depressive symptoms were assessed at 2-week intervals throughout pregnancy in 56 healthy women with singleton, term pregnancies. Messenger ribonucleic acid (mRNA) levels of glucocorticoid (GR) and mineralocorticoid (MR) receptors and serotonin transporter (SLC6A4), 11β-hydroxysteroid dehydrogenase type 1 (HSD1) and 2 (HSD2) were quantified in placental biopsies. In adjusted analyses women who reported higher depressive symptoms across the whole pregnancy had higher mRNA levels of GR [effect size 0.31 s.d. units, 95% confidence interval (CI) 0.01-0.60, p = 0.042] and MR (effect size 0.34 s.d. units, 95% CI 0.01-0.68, p = 0.047). These effects were significant for symptoms experienced in the third trimester of pregnancy for GR; findings for MR were also significant for symptoms experienced in the second trimester. GR and MR mRNA levels increased linearly by having the trimester-specific depressive symptoms scores 0, 1 or 2-3 times above the clinical cut-off for depression (p = 0.003, p = 0.049, respectively, and p = 0.004, p = 0.15 in adjusted analyses).\n\nQuestion:\nAre maternal depressive symptoms throughout pregnancy associated with increased placental glucocorticoid sensitivity?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo examine the independent association of discordant virologic and immunologic responses to highly active antiretroviral therapy (HAART) with mortality. A population-based study of 1527 treatment-naive individuals initiating HAART used Cox proportional hazards modeling to determine the independent association of treatment response at 3 to 9 months with nonaccidental mortality. Logistic regression was used to examine associations with discordant responses. Viral load (VL)/CD4 discordant responses were seen in 235 (15.4%) of subjects, and VL/CD4 responses were seen in 179 (11.7%) of subjects. In adjusted Cox regression models, discordant responses were found to be independently associated with an increased risk of mortality (VL/CD4: relative hazard [RH] = 1.87, 95% confidence interval [CI]: 1.15 to 3.04; VL/CD4: RH = 2.47, 95% CI: 1.54 to 3.95). VL/CD4 discordance was found to be associated with increasing age, baseline HIV RNA load <100,000 copies/mL, baseline CD4 counts <50 cells/muL, the use of lamivudine (3TC)/zidovudine (ZDV), and poor adherence to therapy. VL/CD4 discordance was associated with younger age; injection drug use; baseline HIV RNA load >100,000 copies/mL; the use of 3TC/ZDV, didanosine (ddI)/3TC, or ddI/stavudine; and poor adherence to therapy.\n\nQuestion:\nAre discordant immunologic and virologic responses to highly active antiretroviral therapy associated with increased mortality and poor adherence to therapy?\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 the present study was to investigate the relation between the dose of tumor cell inoculation (especially the doses less than minimum required to evoke tumor growth) and the anti-tumor immune system, particularly lymphoblast formation and cytotoxic activity of lymphcytes. We inoculated rats with various doses of SST-2 tumor cells and examined natural killer (NK) cell activity and lymphoblast formationin vitro. The results showed that the cytotoxicities against SST-2 cells and lymphoblast formation of lymphocytes were enhanced by small dose inoculation of tumor cells that could not induce tumor growth.\n\nQuestion:\nIs sST-2 tumor inoculation a useful model for studying the anti-tumor immune response in SHR 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:\nTo observe the effect and mechanism of wild-type Smad3 gene on the proliferation and osteoblastic differentiation of rat bone marrow-derived mesenchymal stem cell (MSC). Rat bone-derived MSC were cultured and transfected with the complexes of pcDNA3.0-Myc-Smad3 or pcDNA3.0-Myc-Smad3DeltaC and LipofectAMINE reagent. Immunofluorescence technique was performed to evaluate the c-Myc expression. The cell proliferation was detected by MTT method. In order to observe the osteoblastic characteristics in stable expression MSC, alkaline phosphatase (ALP) mRNA and core binding factor alpha1 (cbfa1) mRNA were investigated by RT-PCR technique, and ALP activity and mineralization were examined by PNP method and alizarin red staining respectively. PD98059 was used to interdict selectively ERK pathway in order to investigate the effect of ERK pathway on Smad3 regulating MSC. c-Myc protein was expressed in Smad3-MSC and Smad3DeltaC-MSC. The proliferation of Smad3-MSC was slower than that of Smad3DeltaC-MSC or V-MSC. The relative levels of ALP mRNA and cbfa1 mRNA in Smad3-MSC were higher markedly than those in Smad3DeltaC-MSC or V-MSC, as well as ALP activity and mineralization. However, without a significant difference ALP activity and mineralization was after PD98059 treatment (both slightly decreased P > 0.05).\n\nQuestion:\nDoes [ Wild-type Smad3 gene promote osteoblastic differentiation of rat bone marrow-derived mesenchymal stem cells in vitro ]?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPostoperative pain control is essential for optimal patient outcomes. Ketorolac is an attractive alternative for achieving pain control postoperatively, but concerns over postoperative bleeding have limited its use. Computer searches of the MEDLINE, EMBASE, and Cochrane Library databases were performed. Twenty-seven double-blind, randomized, controlled studies were reviewed by two independent investigators for the incidence of adverse events, including postoperative bleeding. Comprehensive meta-analysis software was used to evaluate the differences between ketorolac and control groups. Twenty-seven studies with 2314 patients were analyzed. Postoperative bleeding occurred in 33 of 1304 patients (2.5 percent) in the ketorolac group compared with 21 of 1010 (2.1 percent) in the control group (OR, 1.1; 95 percent CI, 0.61 to 2.06; p = 0.72). Adverse events were similar in the groups, 31.7 percent in the control group and 27.9 percent in the ketorolac group (OR, 0.64; 95 percent CI, 0.41 to 1.01; p = 0.06). There was a lower incidence of adverse effects with low-dose ketorolac (OR, 0.49; 95 percent CI, 0.27 to 0.91; p = 0.02). Pain control with ketorolac was superior to controls and equivalent to opioids.\n\nQuestion:\nDoes ketorolac increase perioperative bleeding : a meta-analysis of randomized controlled trials?\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 measure serum concentrations of progesterone, estradiol and 5α- and 5β-reduced progesterone metabolites in the follicular and luteal phases of the menstrual cycle in women with latent acute intermittent porphyria and manifest acute intermittent porphyria in comparison with healthy control women. A descriptive study with repeated measurements during a complete, ovulatory menstrual cycle. University hospital out-patient clinic. Thirty-two women with DNA-diagnosed acute intermittent porphyria and 20 healthy control women. Blood samples for serum progesterone, estradiol, allopregnanolone and pregnanolone were drawn on predefined menstrual cycle days, twice in the follicular phase and three times in the luteal phase. Serum levels of estradiol and progesterone were analysed with commercial kits. Allopregnanolone and pregnanolone levels were analysed with radioimmunoassay following diethylether extraction and celite column chromatography. Changes in serum levels of progesterone, estradiol, allopregnanolone and pregnanolone throughout the menstrual cycle. Women with acute intermittent porphyria displayed lower serum concentrations of allopregnanolone in comparison with healthy control women, the difference being most prominent in the luteal phase (p < 0.001). Levels of pregnanolone did not differ significantly between groups. No significant difference was found between women with latent acute intermittent porphyria and manifest acute intermittent porphyria.\n\nQuestion:\nDo women with acute intermittent porphyria have a defect in 5α-steroid production during the menstrual cycle?\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:\nHigh levels of thymidine kinase 1 (TK1) and thymidine phosphorylase (TYMP) are key molecular targets by thymidine therapeutics in cancer treatment. The dual roles of TYMP as a tumor growth factor and a key activation enzyme of anticancer metabolites resulted in a mixed outcome in cancer patients. In this study, we investigated the roles of TK1 and TYMP on a thymidine quinoxaline conjugate to evaluate an alternative to circumvent the contradictive role of TYMP. TK1 and TYMP levels in multiple liver cell lines were assessed along with the cytotoxicity of the thymidine conjugate. Cellular accumulation of the thymidine conjugate was determined with organelle-specific dyes. The impacts of TK1 and TYMP were evaluated with siRNA/shRNA suppression and pseudoviral overexpression. Immunohistochemical analysis was performed on both normal and tumor tissues. In vivo study was carried out with a subcutaneous liver tumor model. We found that the thymidine conjugate had varied activities in liver cancer cells with different levels of TK1 and TYMP. The conjugate mainly accumulated at endothelial reticulum and was consistent with cytosolic pathways. TK1 was responsible for the cytotoxicity yet high levels of TYMP counteracted such activities. Levels of TYMP and TK1 in the liver tumor tissues were significantly higher than those of normal liver tissues. Induced TK1 overexpression decreased the selectivity of dT-QX due to the concurring cytotoxicity in normal cells. In contrast, shRNA suppression of TYMP significantly enhanced the selective of the conjugate in vitro and reduced the tumor growth in vivo.\n\nQuestion:\nIs anticancer activity of a thymidine quinoxaline conjugate modulated by cytosolic thymidine pathways?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe Ca2+ -paradox is an important phenomenon to study cell injury induced by Ca2+ -overload in myocardium. Although intracellular Ca2+ -overload acts as a trigger and modulator of cell death due to apoptosis under various pathophysiological conditions, the presence of apoptosis in hearts subjected to Ca2+ -paradox has not been demonstrated. Since taurine attenuates the changes in cardiac function due to Ca2+ -paradox, this study investigated the occurrence and mechanisms of apoptosis in Ca2+ -paradoxic hearts treated in the absence and presence of taurine. Ca2+ -paradox was induced by perfusing the isolated rat heart with Ca2+ -free medium for 5 min followed by reperfusion with Ca2+ -containing medium for 30 min. Apoptosis related signal transduction mechanisms were determined in Ca2+ -paradoxic hearts perfused with or without 10 mM taurine. Marked alterations in cardiac function and the presence of apoptosis were seen in Ca2+ -paradoxic hearts reperfused for 30 min. Unlike the total protein contents in hearts subjected to Ca2+ -paradox, the contents of phosphorylated p38 mitogen-activated protein kinase (MAPK), extracellular signal regulated kinase (ERK)1, ERK2 and c-jun amino-terminal kinase were increased by 125 +/- 8.6%, 296 +/- 14.3%, 213 +/- 8.5% and 133 +/- 4.2%, respectively vs. control. Caspase-3 and phosphorylated Bcl-2 contents were also increased by 193 +/- 10.2% and 134 +/- 5.0% vs. control whereas phosphorylated Bad and the ratio of Bcl-2/Bad were depressed by 32 +/- 10.8% and 0.23 +/- 0.5% vs. control in Ca2+ -paradoxic hearts. The apoptosis as seen in Ca2+ -paradoxic hearts reperfused for 30 min was not evident in hearts at 10 min Ca2+ -repletion but was similar to hearts subjected to 60 min Ca2+ -repletion. These changes in the apoptotic pathway in cardiomyocytes subjected to Ca2+ -paradox were prevented by taurine. Furthermore, taurine attenuated the KCl- or ATP-induced increase in intracellular concentration of Ca2+ in cardiomyocytes.\n\nQuestion:\nAre mAPK activation and apoptotic alterations in hearts subjected to calcium paradox attenuated by taurine?\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:\nAgave, which is well known for tequila and other liquor production in Mexico, has recently gained attention because of its attractive potential to launch sustainable bioenergy feedstock solutions for semi-arid and arid lands. It was previously found that agave cell walls contain low lignin and relatively diverse non-cellulosic polysaccharides, suggesting unique recalcitrant features when compared to conventional C4 and C3 plants. Here, we report sugar release data from fungal enzymatic hydrolysis of non-pretreated and hydrothermally pretreated biomass that shows agave to be much less recalcitrant to deconstruction than poplar or switchgrass. In fact, non-pretreated agave has a sugar release five to eight times greater than that of poplar wood and switchgrass . Meanwhile, state of the art techniques including glycome profiling, nuclear magnetic resonance (NMR), Simon's Stain, confocal laser scanning microscopy and so forth, were applied to measure interactions of non-cellulosic wall components, cell wall hydrophilicity, and enzyme accessibility to identify key structural features that make agave cell walls less resistant to biological deconstruction when compared to poplar and switchgrass.\n\nQuestion:\nDoes agave prove to be a low recalcitrant lignocellulosic feedstock for biofuels production on semi-arid lands?\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:\nMost of our knowledge about how antiretrovirals and host immune responses influence the HIV-1 protease gene is derived from studies of subtype B virus. We investigated the effect of protease resistance-associated mutations (PRAMs) and population-based HLA haplotype frequencies on polymorphisms found in CRF01_AE pro. We used all CRF01_AE protease sequences retrieved from the LANL database and obtained regional HLA frequencies from the dbMHC database. Polymorphisms and major PRAMs in the sequences were identified using the Stanford Resistance Database, and we performed phylogenetic and selection analyses using HyPhy. HLA binding affinities were estimated using the Immune Epitope Database and Analysis. Overall, 99% of CRF01_AE sequences had at least 1 polymorphism and 10% had at least 1 major PRAM. Three polymorphisms (L10 V, K20RMI and I62 V) were associated with the presence of a major PRAM (P < 0.05). Compared to the subtype B consensus, six additional polymorphisms (I13 V, E35D, M36I, R41K, H69K, L89M) were identified in the CRF01_AE consensus; all but L89M were located within epitopes recognized by HLA class I alleles. Of the predominant HLA haplotypes in the Asian regions of CRF01_AE origin, 80% were positively associated with the observed polymorphisms, and estimated HLA binding affinity was estimated to decrease 19-40 fold with the observed polymorphisms at positions 35, 36 and 41.\n\nQuestion:\nDo protease polymorphisms in HIV-1 subtype CRF01_AE represent selection by antiretroviral therapy and host immune pressure?\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 determine influence of prognostic factors in addition to UICC staging systems, on cancer-specific and overall survival rates for patients with colorectal cancer (CRC) undergoing surgical treatment. Between January 1996 and December 2006, a total of 1367 CRC patients who underwent surgical treatment in Kaohsiung Medical University Hospital were analyzed. We retrospectively investigated clinicopathologic features of these patients. All patients were followed up intensively, and their outcomes were investigated completely. Of 1367 CRC patients, there were seven hundred and fifty-seven males (55.4%) and 610 (44.6%) females. The median follow-up period was 60 months (range, 3-132 months). A multivariate analysis identified that low serum albumin level (P = 0.011), advanced UICC stage (P < 0.001), and high carcinoembryonic antigen (CEA) level (P < 0.001) were independent prognostic factors of cancer-specific survival. Meanwhile, a multivariate analysis showed age over 65 years (P < 0.001), advanced UICC stage (P < 0.001), and high CEA level (P < 0.001) were independent prognostic factors of overall survival. Furthermore, combination of UICC stage, serum CEA and albumin levels as predictors of cancer-specific survival showed that the poorer the prognostic factors involved, the poorer the cancer-specific survival rate. Likewise, combination of UICC stage, age and serum CEA level as predictors of overall survival showed that the poorer the prognostic factors involved, the poorer the overall survival rate. Of these prognostic factors, preoperative serum CEA level was the only significant prognostic factor for patients with stage II and III CRCs in both cancer-specific and overall survival categories.\n\nQuestion:\nAre preoperative serum carcinoembryonic antigen , albumin and age supplementary to UICC staging systems in predicting survival for colorectal cancer patients undergoing surgical 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:\nVariation in the human fecal microbiota has previously been associated with body mass index (BMI). Although obesity is a global health burden, the accumulation of abdominal visceral fat is the specific cardio-metabolic disease risk factor. Here, we explore links between the fecal microbiota and abdominal adiposity using body composition as measured by dual-energy X-ray absorptiometry in a large sample of twins from the TwinsUK cohort, comparing fecal 16S rRNA diversity profiles with six adiposity measures. We profile six adiposity measures in 3666 twins and estimate their heritability, finding novel evidence for strong genetic effects underlying visceral fat and android/gynoid ratio. We confirm the association of lower diversity of the fecal microbiome with obesity and adiposity measures, and then compare the association between fecal microbial composition and the adiposity phenotypes in a discovery subsample of twins. We identify associations between the relative abundances of fecal microbial operational taxonomic units (OTUs) and abdominal adiposity measures. Most of these results involve visceral fat associations, with the strongest associations between visceral fat and Oscillospira members. Using BMI as a surrogate phenotype, we pursue replication in independent samples from three population-based cohorts including American Gut, Flemish Gut Flora Project and the extended TwinsUK cohort. Meta-analyses across the replication samples indicate that 8 OTUs replicate at a stringent threshold across all cohorts, while 49 OTUs achieve nominal significance in at least one replication sample. Heritability analysis of the adiposity-associated microbial OTUs prompted us to assess host genetic-microbe interactions at obesity-associated human candidate loci. We observe significant associations of adiposity-OTU abundances with host genetic variants in the FHIT, TDRG1 and ELAVL4 genes, suggesting a potential role for host genes to mediate the link between the fecal microbiome and obesity.\n\nQuestion:\nAre heritable components of the human fecal microbiome associated with visceral fat?\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 action of prostaglandin E1 on hepatic encephalopathy. Prospective, randomised, controlled animal study. University animal laboratory. Male Wistar rats. After passive avoidance learning, acute liver failure was induced by occlusion of the left portal vein and the hepatic artery for 90 min. Then memory retention was evaluated 48 h later. The effects of prostaglandin E1 on memory retention were examined in animals treated with the agent systemically (intravenous injections with prostaglandin E1 twice before and after surgery, 20 microg/kg each time) and animals treated with the agent topically (intracerebroventricular injection with prostaglandin E1, 0.1 microg/h for 48 h beginning at liver ischaemia). Marked damage was found on plasma analysis in animals subjected to liver ischaemia, and the memory retention was also impaired. Intravenous administration of prostaglandin E1 improved both the liver injury and memory retention. However, intracerebroventricular administration of prostaglandin E1 alleviated neither.\n\nQuestion:\nDoes prostaglandin E1 improve hepatic encephalopathy produced by ischaemia-reperfusion liver injury 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:\nWe outlined the putative significance of GST in renal cell carcinoma biology by investigating the influence of its deletion polymorphisms on renal cell carcinoma progression. Genomic DNA was purified from peripheral blood leukocytes. GSTM1 and GSTT1 genes were polymerase chain reaction amplified and gene fragments were separated by agarose gel electrophoresis. Intact GSTM1 and GSTT1 alleles were identified by the presence of 230 and 480 bp fragments, respectively. Genotypes were associated with clinicopathological variables and survival. Of 147 patients with renal cell carcinoma 80 (54%) had the GSTM1 null and 27 (18%) had the GSTT1 null genotype. The GST genotype distribution did not differ significantly from that in 112 controls without renal cell carcinoma. However, the GSTM1 null genotype was associated with 60% lower odds of the papillary subtype (OR 0.40, 95% CI 0.18 to 0.92, p = 0.032), lower Fuhrman grade (chi-square 9.77, p = 0.008) and a lower risk of metastatic disease in patients with the clear cell subtype (chi-square 4.48, p = 0.034). Of patients with the clear cell subtype those with the GSTM1 null genotype had improved cancer specific survival (p = 0.0412). GSTT1 did not correlate with any pathological variable except age at renal cell carcinoma onset since patients with renal cell carcinoma and the GSTT1 null genotype were significantly younger than their counterparts (mean +/- SD age 58.5 +/- 14.2 vs 65.4 +/- 12.8 years, p = 0.016).\n\nQuestion:\nDo renal cell carcinoma Fuhrman grade and histological subtype correlate with complete polymorphic deletion of glutathione S-transferase M1 gene?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIncreased intestinal permeability has been reported in one study of adult asthmatics. To determine whether children with asthma have altered intestinal permeability. Thirty two asthmatic children, and 32 sex and age matched controls were recruited. The dual sugar (lactulose and mannitol) test was used to evaluate intestinal permeability, and the percentage of ingested lactulose (L) and mannitol (M) in the urine, and the L:M ratio were determined. All patients were skin prick tested for common aeroallergens, and specific IgE to some food items was determined. The median value of L in asthmatic children (2.29, IQR 0.91-4.07) was significantly higher than that in controls (0.69, IQR 0.45-1.08), and that of M was almost similar. The ratio L:M was significantly higher in asthmatic children (0.20, IQR 0.11-0.40) than in controls (0.06, IQR 0.04-0.09). Intestinal permeability did not correlate with eczema, inhaled steroids, positive skin prick test to aeroallergens, or severity of asthma.\n\nQuestion:\nIs intestinal permeability increased in bronchial asthma?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHuman neonates are highly susceptible to a wide range of infections, which has been attributed to deficiencies in their innate and adaptive immunity. In contrast to the well-documented immaturity in neonatal adaptive immunity, deficiencies in their innate immunity are less defined. This study examined the inflammatory response of neonatal monocytes to bacterial lipopolysaccharide (LPS) and peptidoglycan (PGN) stimulation and discriminated the underlying Toll-like receptor (TLR)-mediated signal transduction pathways. Cord blood from 30 healthy newborns of full-term elective cesarean sections and peripheral blood from 25 healthy adult volunteers were collected. Ex vivo production of inflammatory cytokines was assessed by cytometric bead array, and expression of CD14, TLR4, TLR2, phosphorylated NF-κB p65 and p38 on monocytes were detected by FACScan analysis. Neonatal whole blood showed significantly decreased ex vivo TNF-α and IL-1β production in response to stimulation with the TLR4 agonist LPS, but not the TLR2 agonist PGN, when compared with adult whole blood. Consistent with the diminished inflammatory cytokine response to LPS stimulation, neonatal monocytes exhibited substantially impaired TLR-mediated signal transduction pathways characterized by down-regulated expression of CD14 and TLR4, and suppressed phosphorylation of NF-κB p65 at Ser536 and p38 following LPS stimulation. In addition, neonates had a significantly lower percentage of TLR4(+)/CD14(+) monocytes than adults.\n\nQuestion:\nIs an impaired inflammatory cytokine response to gram-negative LPS in human neonates associated with the defective TLR-mediated signaling pathway?\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), a condition with a strong genetic etiology, is associated with excess cardiovascular disease (CVD). Dyslipidemia in RA may be driven by inflammation and genetic factors. Apolipoprotein E (ApoE) is important for the regulation of lipid levels and CVD risk and immune function in the general population. We compared the frequency of 2 ApoE single-nucleotide polymorphisms (SNP) in patients with RA and controls, and studied the relationship of ApoE genotypes with lipids and inflammation in RA. A total of 387 patients with well-characterized RA and 420 non-RA controls were studied. Two ApoE SNP, rs7412 (ApoE2) and rs429358 (ApoE4), were identified. Genotypic (p = 0.908) and allelic (p = 0.894) frequencies did not differ between RA and controls. Within RA, the E2 allele was associated with the lowest and E4 allele with the highest levels of total cholesterol (p = 0.007), low-density lipoproteins (p = 0.004), and apolipoprotein B (p = 0.009). The E4 allele was also associated with lower C-reactive protein (p = 0.007), erythrocyte sedimentation rate (p = 0.001), and Disease Activity Score (p = 0.015) compared to the E3 allele. E2 or E4 alleles were not associated with CVD in RA, although a trend was observed (p = 0.074).\n\nQuestion:\nAre apolipoprotein E gene polymorphisms strong predictors of inflammation and dyslipidemia in rheumatoid arthritis?\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:\nEthanol (EtOH) decreases muscle protein synthesis, and this is associated with reduced mammalian target of rapamycin complex (mTORC)1 and increased mTORC2 activities. In contrast, phospholipase D (PLD) and its metabolite phosphatidic acid (PA) positively regulate mTORC1 signaling, whereas their role in mTORC2 function is less well defined. Herein, we examine the role that PLD and PA play in EtOH-mediated mTOR signaling. C2C12 myoblasts were incubated with EtOH for 18 to 24 hours. For PA experiments, cells were pretreated with the drug for 25 minutes followed by 50-minute incubation with PA in the presence or absence of EtOH. The phosphorylation state of various proteins was assessed by immunoblotting. Protein-protein interactions were determined by immunoprecipitation and immunoblotting. PLD activity was measured using the Amplex Red PLD assay kit. PA concentrations were determined with a total PA assay kit. PA levels and PLD activity increased in C2C12 myocytes exposed to EtOH (100 mM). Increased PLD activity was blocked by inhibitors of AMP-activated protein kinase (AMPK) (compound C) and phosphoinositide 3-kinase (PI3K) (wortmannin). Likewise, suppression of PLD activity with CAY10594 prevented EtOH-induced Akt (S473) phosphorylation. PLD inhibition also enhanced the binding of Rictor to mSin1 and the negative regulatory proteins Deptor and 14-3-3. Addition of PA to myocytes decreased Akt phosphorylation, but changes in mTORC2 activity were not associated with altered binding of complex members and 14-3-3. PA increased S6K1 phosphorylation, with the associated increase in mTORC1 activity being regulated by reduced phosphorylation of AMPKα (T172) and its target tuberous sclerosis protein complex (TSC)2 (S1387). This resulted in increased Rheb and RagA/RagC GTPase interactions with mTOR, as well as suppression of mTORC2.\n\nQuestion:\nDoes activation of AMPK/TSC2/PLD by alcohol regulate mTORC1 and mTORC2 assembly in C2C12 myocytes?\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:\nHepatitis C virus (HCV) infection is a significant global public health problem. In clinical studies, zinc has been closely related to the pathogenesis of chronic hepatitis C. However, the role of zinc in both viral replication and the expression of viral proteins remains unclear. We aimed to clarify the effect of zinc on the replication of HCV in vitro. We incubated subgenomic HCV replicon cells (sO) and genome-length HCV RNA-replicating cells (O) treated with several chemicals including trace elements. Total RNAs were collected and subjected to real-time reverse-transcriptase polymerase chain reaction in order to examine the level of HCV RNA replication, and Western blotting was performed to confirm the expression of viral proteins. Iron salts and interferon-alpha suppressed HCV RNA replication and protein expression in both sO and O cells. Zinc salts effectively reduced the viral replication in the genome-length HCV RNA replication system but not in the subgenomic HCV replicon system.\n\nQuestion:\nIs zinc a negative regulator of hepatitis C virus RNA replication?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAlthough the predictive and prognostic value of thymidylate synthase (TS) expression and gene polymorphism in colon cancer has been widely studied, the results are inconclusive probably because of methodological differences. With this study, we aimed to elucidate the role of TS gene polymorphisms genotyping in therapy response in stage III colon carcinoma patients treated with 5-FU adjuvant chemotherapy. 251 patients diagnosed with stage III colon carcinoma treated with surgery followed by 5-FU based adjuvant therapy were selected. The variable number of tandem repeats (VNTR) and the single nucleotide polymorphism (SNP) in the 5'untranslated region of the TS gene were genotyped. There was a positive association between tumor T stage and the VNTR genotypes (p = 0.05). In both univariate and multivariate survival analysis no effects of the studied polymorphisms on survival were found. However, there was an association between both polymorphisms and age. Among patients younger than 60 years, the patients homozygous for 2R seemed to have a better overall survival, whereas among the patients older than 67 this longer survival was seen by the carriers of other genotypes.\n\nQuestion:\nAre tS gene polymorphisms good markers of response to 5-FU therapy in stage III colon cancer patients?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe retention of plasma low-density lipoprotein (LDL) particles in subendothelial space following transcytosis across the endothelium is the initial step of atherosclerosis. Whether or not C-reactive protein (CRP) can directly affect the transcytosis of LDL is not clear. Here we have examined the effect of CRP on transcytosis of LDL across endothelial cells and have explored the underlying mechanisms. Effects of CRP on transcytosis of FITC-labelled LDL were examined with human umbilical vein endothelial cells and venous rings in vitro and, in vivo, ApoE(-/-) mice. Laser scanning confocal microscopy, immunohistochemistry and Oil Red O staining were used to assay LDL. CRP increased transcytosis of LDL. An NADPH oxidase inhibitor, diphenylene iodonium, and the reducing agent, dithiothreitol partly or completely blocked CRP-stimulated increase of LDL transcytosis. The PKC inhibitor, bisindolylmaleimide I and the Src kinase inhibitor, PP2, blocked the trafficking of the molecules responsible for transcytosis. Confocal imaging analysis revealed that CRP stimulated LDL uptake by endothelial cells and vessel walls. In ApoE(-/-) mice, CRP significantly promoted early changes of atherosclerosis, which were blocked by inhibitors of transcytosis.\n\nQuestion:\nDoes c-reactive protein promote atherosclerosis by increasing LDL transcytosis across 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:\nExpression of disaccharidase sucrase-isomaltase (SI) is significantly enhanced during neoplastic transformation of colonic epithelium. Our study was designed to determine whether expression of SI within primary tumors was significantly associated with survival in patients with colorectal carcinoma (CRC). SI expression was analyzed by immunohistochemistry in paraffin sections from 182 Stage I to III CRC that had been resected for cure at the New England Deaconess Hospital between 1965 and 1977. Expression was scored as absent or present in 1 to 50 percent or more than 50 percent of tumor cells. Associations were explored among SI expression, other clinical or pathologic variables, and overall survival. The data set is mature, with 91 (56 percent) patients who had died of CRC at a median follow-up of 96 months. Fifty-five percent of primary CRC expressed SI. When the multivariate Cox analysis was performed, nodal status, T stage, primary site, grade, and SI expression were independent covariates. SI expression was not associated with the expression of other clinicopathologic variables but increased the risk of death from colorectal carcinoma by 1.83-fold.\n\nQuestion:\nIs sucrase-isomaltase an independent prognostic marker for 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:\nRegulation of apoptosis is an important mechanism during the development of tumors including non-small cell lung cancer (NSCLC). The aim of this study was to assess the relationship between p53 and bcl-2 expression and various clinicopathological features and survival in patients with NSCLC. Histological specimens obtained from 120 patients with stage I-III NSCLC were examined immunohistochemically for p53 and bcl-2. Positive immunostaining for p53 was observed in 50 and for bcl-2 in 35 patients. Tumors with lymph node metastasis were significantly more likely to be bcl-2-positive. However, there was no correlation between p53 immunostaining and clinicopathological parameters. Cox proportional hazard multiple regression analyses identified gender, N status and bcl-2 expression as independent prognostic factors. When advanced stage tumors or tumors with lymph node metastasis were analyzed, a more favorable survival was noted in patients with bcl-2-positive tumors than those with bcl-2-negative tumors.\n\nQuestion:\nDoes bcl-2 protein expression correlate with better prognosis in patients with 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:\nIn sepsis, the reduced systemic vascular resistance (SVR) can lead to a compensatory increase in cardiac output (CO). This may mimic a normal cardiac function although there is already a sepsis-induced myocardial depression. On a cohort of patients with septic multi-organ dysfunction syndrome, we have recently developed a method to correlate the actual CO to the afterload (estimated by SVR) and introduced the parameter \"afterload-related cardiac performance\" (ACP), which indicates if the rise of CO is adequate for the particular SVR. In this present study it was to be investigated, if ACP can reveal septic cardiomyopathy in patients with community-acquired sepsis in the early state soon after admission to the emergency department (ED), and if there is a prognostic relevance of septic cardiomyopathy defined by ACP. Results were compared to cardiac index (CI) and cardiac power index (CPI). Adults presenting at the ED with sepsis were included. ACP, CI and CPI were calculated at the time of admission, after 24, and 72 h. They were correlated to severity of disease and the prognostic values were analyzed. A total of 141 patients were included. Only ACP was significantly influenced by severity of sepsis, whereas CI and CPI were not. ACP was the only hemodynamic parameter predicting mortality: nonsurvivors had lower ACP values at the time of admission to the ED (66.9 vs. 88.9 %, p < 0.05) and ACP predicted non-survival with an AUC value of 0.72, p = 0.003. Cardiac impairment defined by an ACP value of 80 % or below determined worse prognosis.\n\nQuestion:\nDoes severity of cardiac impairment in the early stage of community-acquired sepsis determine worse prognosis?\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:\nOver 70% of smokers visit a physician annually, and physicians are well-positioned to assist patients in smoking cessation. Residency offers the ideal setting to train physicians in best practices for treatment of nicotine dependence. We hypothesized that experiential learning during a smoking cessation medical clinic (SCMC) rotation would be associated with an improvement in smoking cessation practice of internal medicine (IM) interns in outpatient primary care and inpatient settings. This was a prospective study performed at a large university-affiliated hospital. Forty IM interns rotated through SCMC. After a lecture on nicotine addiction and treatment, interns treated SCMC patients under direct supervision of an attending pulmonologist. Interns' smoking cessation practices before and after SCMC rotation were evaluated through chart review over 1 year. Upon study completion, a survey to assess confidence was administered. Paired t tests measured changes in rates of identifying smokers, offering pharmacological treatment and counseling. A total of 5,622 outpatient and 683 inpatient charts of interns' encounters with patients were reviewed. Following SCMC rotation, there was an increase in identifying active smokers (7.1% versus 18.7%), prescribing therapy for smoking cessation (6.5% versus 18.0%), and providing counseling (30.9% versus 42.3%) to outpatients. For inpatients, there was an increase in nicotine replacement during admission (12.9% versus 37.4%) and prescription of therapy upon discharge (5.7% versus 16.1%). Interns reported confidence in providing appropriate counseling and treatment.\n\nQuestion:\nDoes rotation in a Smoking Cessation Clinic improve Nicotine Dependence Treatment Provided by First-Year Internal Medicine Trainees?\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:\nCenicriviroc is a potent antagonist of the chemokine coreceptors 5 and 2 (CCR5/CCR2) and blocks HIV-1 entry. The CCR5 inhibitor maraviroc has been shown in tissue culture to be able to repel cell-free virions from the cell surface into extracellular space. We hypothesized that cenicriviroc might exhibit a similar effect, and tested this using clinical samples from the Phase IIb study 652-2-202, by measuring rates of intracellular DNA decline. We also monitored viral RNA levels in culture fluids. We infected PM-1 cells with CCR5-tropic HIV-1 BaL in the presence or absence of inhibitory concentrations of cenicriviroc (20 nM) or maraviroc (50 nM) or controls. Viral load levels and p24 were measured by ELISA, quantitative PCR and quantitative real-time reverse transcription PCR at 4 h post-infection. Frozen PBMC DNA samples from 30 patients with virological success in the Phase IIb study were studied, as were early and late reverse transcript levels. Docking studies compared binding between cenicriviroc/CCR5 and maraviroc/CCR5. Unlike maraviroc, cenicriviroc did not cause an increase in the amount of virus present in culture fluids at 4 h compared with baseline. The use of cenicriviroc did, however, result in lower levels of intracellular viral DNA after 4 h. Structural modelling indicates that cenicriviroc binds more deeply than maraviroc to the hydrophobic pocket of CCR5, providing an explanation for the absence of viral rebound with cenicriviroc.\n\nQuestion:\nDoes the dual CCR5 and CCR2 inhibitor cenicriviroc redistribute HIV into extracellular space : implications for plasma viral load and intracellular DNA decline?\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:\nLaparoscopic adrenalectomy (LA) has become the established procedure for adrenal masses less than 6 cm. The role of LA for large adrenal masses is well defined to a lesser extent. Thirty-six LAs were performed in 32 patients (including four patients with single stage bilateral adrenalectomies) over a period of 3 years, from May 2002 to 2005. Patients were divided into two groups based on the tumour size, i.e. masses less than 6 cm (group I) and masses 6 cm or more (group II).The results with respect to mean (95% confidence interval) operative time, blood loss, postoperative course and complications were compared. Group II included 11 LAs performed in 10 patients including one bilateral LA for bilateral phaeochromocytomas in multiple endocrine neoplasia 2A. The mean size (+/-standard deviation) of masses was 8 cm (+/-1.47). In comparison, 22 patients in group I underwent 25 adrenalectomies (including three bilateral single stage procedures for Cushing's syndrome). The mean size of masses was 4.1 cm (+/-1.27). There were eight and six phaeochromocytomas in groups I and II, respectively. By comparing groups I and II, only minimal increase in blood loss and operating time was noted with no significant difference in hospital stay and morbidity. Two cases required conversion to hand assistance towards the end of the procedure in view of their large size.\n\nQuestion:\nIs laparoscopic adrenalectomy feasible for large adrenal masses > 6 cm?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIn patients suffering from major depressive disorders (MDD), improvements in MDD are related to increased activation of brain-derived neurotrophic factor (BDNF), an endogenous protein that facilitates neural functioning. To treat patients suffering from severe MDD, electroconvulsive therapy (ECT) is considered an efficacious and safe intervention, though the impact of ECT on plasma BDNF levels has thus far barely been investigated. The aim of the present study was therefore to assess plasma BDNF levels and depression of patients suffering from severe MDD treated with additional ECT compared to patients treated with citalopram only. A total of 40 patients (mean age: M = 31.45 years; females 30%) suffering from MDD and all receiving 40 mg/d citalopram were assigned either to a control group (N = 20), or to a target group (N = 20) undergoing additional 12 sessions of ECT. Plasma BDNF and symptom severity were assessed at baseline and four weeks later. Plasma BDNF increased in both groups over time, though the significant Time by Group-interaction revealed an increase of 101% in the target group as compared to the control group. Symptom severity significantly decreased in both groups over time, though without being related to plasma BDNF levels.\n\nQuestion:\nDoes additional ECT increase BDNF-levels in patients suffering from major depressive disorders compared to patients treated with citalopram only?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe purpose of this study was to evaluate whether the ipsilateral knee alignment secondary to knee osteoarthritis affect positioning of the femoral component anteversion during total hip arthroplasty. Preoperative and postoperative computed tomography-based 3-D femoral models were reconstructed for 20 total hip arthroplasty patients. Prosthetic femoral stem and native femoral anteversion was measured and compared. An average increase by 4.5° ± 8.1° in femoral anteversion was found following total hip arthroplasty (p = 0.02). Strong positive correlation was found between the knee varus angle and the changes in femoral anteversion (R = 0.87, p&lt;0.0001). The knee alignment was an independent factor for predicting the intraoperative positioning of femoral stem anteversion.\n\nQuestion:\nDoes ipsilateral varus knee alignment correlate with increased femoral stem anteversion in primary total hip arthroplasty?\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:\nSpecific demographic and illness characteristics have been identified as predictors of overall morbidity and treatment course among individuals with bipolar disorder. However, the role of specific cognitive limitations on disease severity and treatment response is unclear. The present study evaluated whether impulsiveness during acute mania was a significant predictor of achieving euthymia within one year following psychiatric hospitalization. Participants were 94 adult inpatients (60 manic) with bipolar I disorder. Baseline symptom severity was assessed using the Young Mania Rating Scale and the Montgomery-Åsberg Depression Rating Scale. Impulsivity was measured with the Stop Signal Task, Degraded Stimulus Continuous Performance Task, Delayed Response Task, and Barratt Impulsiveness Scale-11. Individual predictors of time to reach euthymia included fewer depressive symptoms and better impulse control at baseline, later age at illness onset, shorter illness duration, and the absence of comorbid attention-deficit hyperactivity disorder. Self-reported impulsivity was a significant independent predictor of time to euthymia, even after accounting for relevant clinical variables.\n\nQuestion:\nDoes impulsivity predict time to reach euthymia in adults with bipolar disorder?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo test the utility of zinc protoporphyrin to heme ratio (ZnPP/H) as an indicator of iron status in premature infants and to evaluate the effect of oral iron supplements on oxidative injury. We hypothesized that iron sulfate supplementation would decrease the ZnPP/H in preterm infants. Infants eligible for this prospective study were: hospitalized, 24 to 32 weeks of gestation, 7 to 60 days old, feeding > or = 70 mL/kg/d, with a ZnPP/H > or = the mean for age. Iron dose was determined by the ZnPP/H. Iron status and oxidative injury were evaluated at study entry and completion. Concurrent control subjects met entry criteria but were not enrolled and were not treated with iron during the study interval. Statistical evaluation included repeated measures analysis of variance and Z-score conversions. Entry ZnPP/H of iron-treated subjects (n = 16) and control subjects (n = 16) were not different. The ZnPP/H of iron-treated infants was lower at study end (P < .05) but did not change in control infants. Iron treatment (3 to 12 mg/kg/day) was not associated with changes in conventional measures of iron status nor in measures of oxidative injury.\n\nQuestion:\nDoes iron sulfate supplementation decrease zinc protoporphyrin to heme ratio in premature infants?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]