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PubmedQA18732
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: T-bet is crucially implicated in Th1 differentiation due to its strong promoting activity for IFN-gamma gene transcription. However, the regulatory role of T-bet in Th2 cytokines is not fully delineated. The effect of T-bet on mRNA expression as well as the promoter activity of IL-4 in human T cells was investigated by employing quantitative RT-PCR and fluorescence-based promoter reporter assay procedures. IL-4 mRNA expression as well as the transcriptional activity of 5'-flanking region in the IL-4 gene encompassing -1105 to +4 in Jurkat cells was clearly upregulated upon stimulation. The inducible mRNA expression and the promoter activity of IL-4 were significantly diminished by ectopic expression of T-bet.\n Question: Is iL-4 gene transcription in human T cells suppressed by T-bet?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: T-bet is crucially implicated in Th1 differentiation due to its strong promoting activity for IFN-gamma gene transcription. However, the regulatory role of T-bet in Th2 cytokines is not fully delineated. The effect of T-bet on mRNA expression as well as the promoter activity of IL-4 in human T cells was investigated by employing quantitative RT-PCR and fluorescence-based promoter reporter assay procedures. IL-4 mRNA expression as well as the transcriptional activity of 5'-flanking region in the IL-4 gene encompassing -1105 to +4 in Jurkat cells was clearly upregulated upon stimulation. The inducible mRNA expression and the promoter activity of IL-4 were significantly diminished by ectopic expression of T-bet.
Question: Is iL-4 gene transcription in human T cells suppressed by T-bet?
Output:
|
PubmedQA103414
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To investigate the influence of clear surgical resection margin width on disease recurrence rate after intentionally curative resection of colorectal liver metastases. There is consensus that a histological positive resection margin is a predictor of disease recurrence after resection of colorectal liver metastases. The dispute, however, over the width of cancer-free resection margin required is ongoing. Analysis of observational prospectively collected data for 2715 patients who underwent primary resection of colorectal liver metastases from 2 major hepatobiliary units in the United Kingdom. Histological cancer-free resection margin was classified as positive (if cancer cells present at less than 1 mm from the resection margin) or negative (if the distance between the cancer and the margin is 1 mm or more). The negative margin was further classified according to the distance from the tumor in millimeters. Predictors of disease-free survival were analyzed in univariate and multivariate analyses. A case-match analysis by a propensity score method was undertaken to reduce bias. A 1-mm cancer-free resection margin was sufficient to achieve 33% 5-year overall disease-free survival. Extra margin width did not add disease-free survival advantage (P > 0.05). After the propensity case-match analysis, there is no statistical difference in disease-free survival between patients with negative narrow and wider margin clearance [hazard ratio (HR) 1.0; 95% (confidence interval) CI: 0.9-1.2; P = 0.579 at 5-mm cutoff and HR 1.1; 95% CI: 0.96-1.3; P = 0.149 at 10-mm cutoff]. Patients with extrahepatic disease and positive lymph node primary tumor did not have disease-free survival advantage despite surgical margin clearance (9 months for <1-mm vs 12 months for ≥1-mm margin clearance; P = 0.062).\n Question: Is one-millimeter cancer-free margin curative for colorectal liver metastases : a propensity score case-match approach?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To investigate the influence of clear surgical resection margin width on disease recurrence rate after intentionally curative resection of colorectal liver metastases. There is consensus that a histological positive resection margin is a predictor of disease recurrence after resection of colorectal liver metastases. The dispute, however, over the width of cancer-free resection margin required is ongoing. Analysis of observational prospectively collected data for 2715 patients who underwent primary resection of colorectal liver metastases from 2 major hepatobiliary units in the United Kingdom. Histological cancer-free resection margin was classified as positive (if cancer cells present at less than 1 mm from the resection margin) or negative (if the distance between the cancer and the margin is 1 mm or more). The negative margin was further classified according to the distance from the tumor in millimeters. Predictors of disease-free survival were analyzed in univariate and multivariate analyses. A case-match analysis by a propensity score method was undertaken to reduce bias. A 1-mm cancer-free resection margin was sufficient to achieve 33% 5-year overall disease-free survival. Extra margin width did not add disease-free survival advantage (P > 0.05). After the propensity case-match analysis, there is no statistical difference in disease-free survival between patients with negative narrow and wider margin clearance [hazard ratio (HR) 1.0; 95% (confidence interval) CI: 0.9-1.2; P = 0.579 at 5-mm cutoff and HR 1.1; 95% CI: 0.96-1.3; P = 0.149 at 10-mm cutoff]. Patients with extrahepatic disease and positive lymph node primary tumor did not have disease-free survival advantage despite surgical margin clearance (9 months for <1-mm vs 12 months for ≥1-mm margin clearance; P = 0.062).
Question: Is one-millimeter cancer-free margin curative for colorectal liver metastases : a propensity score case-match approach?
Output:
|
PubmedQA97638
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To compare the extent of sensory and motor block with two different nerve stimulation techniques in axillary blocks. Prospective, randomized, investigator-blinded study. Ambulatory surgery unit of a university hospital. 60 ASA physical status I, II, and III patients undergoing surgery at or below the elbow. Patients receiving axillary block were randomized into two nerve stimulation groups with either radial plus musculocutaneous or triple nerve stimulation (radial, median, and musculocutaneous nerves). Thirty milliliters of plain 2% mepivacaine was given to all patients either in a single or fractionated dosing for radial or for radial and median nerves, according to group assignment. Five milliliters of plain 1% mepivacaine for the musculocutaneous nerve was given to all patients. Blocks were assessed at 10, 20, and 30 minutes. Rates of supplementation given as a result of insufficient surgical anesthesia were also noted. Statistically significantly higher rates of anesthesia at the cutaneous distributions of median and medial cutaneous of the arm nerves with multiple nerve stimulation at 30 minutes were found as compared with radial plus musculocutaneous nerve stimulation. The rate of supplementation was lower with multiple nerve stimulation.\n Question: Is radial plus musculocutaneous nerve stimulation for axillary block inferior to triple nerve stimulation with 2 % mepivacaine?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To compare the extent of sensory and motor block with two different nerve stimulation techniques in axillary blocks. Prospective, randomized, investigator-blinded study. Ambulatory surgery unit of a university hospital. 60 ASA physical status I, II, and III patients undergoing surgery at or below the elbow. Patients receiving axillary block were randomized into two nerve stimulation groups with either radial plus musculocutaneous or triple nerve stimulation (radial, median, and musculocutaneous nerves). Thirty milliliters of plain 2% mepivacaine was given to all patients either in a single or fractionated dosing for radial or for radial and median nerves, according to group assignment. Five milliliters of plain 1% mepivacaine for the musculocutaneous nerve was given to all patients. Blocks were assessed at 10, 20, and 30 minutes. Rates of supplementation given as a result of insufficient surgical anesthesia were also noted. Statistically significantly higher rates of anesthesia at the cutaneous distributions of median and medial cutaneous of the arm nerves with multiple nerve stimulation at 30 minutes were found as compared with radial plus musculocutaneous nerve stimulation. The rate of supplementation was lower with multiple nerve stimulation.
Question: Is radial plus musculocutaneous nerve stimulation for axillary block inferior to triple nerve stimulation with 2 % mepivacaine?
Output:
|
PubmedQA77271
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Papillary thyroid carcinoma (PTC) is the most frequent thyroid tumor and is responsible for the overall increase in thyroid cancer incidence. S100A11 (calgizzarin), a member of the S100 Ca(2+)-binding protein family, is involved in several different biological processes. S100A11 has been found up-regulated in PTC, both at the mRNA and protein levels. Through a combination of expression analysis and functional in vitro and in vivo studies, we have attempted to gain insight into the relevance of S100A11 overexpression in PTC biology. The expression of the S100A11 gene in PTC was investigated in several gene expression data sets. The effect of S100A11 silencing on the hallmarks of the malignant phenotype of several PTC-derived cell lines was investigated. In NIH3T3 cells, the cooperation of S100A11 with the different PTC-specific oncogenes was assessed. We found that the S100A11 gene expression is frequently up-regulated in PTC, anaplastic thyroid carcinoma, but not in follicular thyroid carcinoma. S100A11 overexpression was also detected in PTC-derived cell lines, which were then used for functional studies. S100A11 silencing in PTC-derived cell lines did not affect cell proliferation, whereas it reduced the loss of contact inhibition, anchorage-independent growth, and resistance to anoikis. Cotransfection experiments in NIH3T3 cells showed that overexpression of the S100A11 gene was able to enhance the transforming capabilities of the different PTC-associated oncogenes by affecting the loss of contact inhibition, anchorage-independent growth, and in vivo tumor formation.\n Question: Does s100A11 overexpression contribute to the malignant phenotype of papillary thyroid carcinoma?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Papillary thyroid carcinoma (PTC) is the most frequent thyroid tumor and is responsible for the overall increase in thyroid cancer incidence. S100A11 (calgizzarin), a member of the S100 Ca(2+)-binding protein family, is involved in several different biological processes. S100A11 has been found up-regulated in PTC, both at the mRNA and protein levels. Through a combination of expression analysis and functional in vitro and in vivo studies, we have attempted to gain insight into the relevance of S100A11 overexpression in PTC biology. The expression of the S100A11 gene in PTC was investigated in several gene expression data sets. The effect of S100A11 silencing on the hallmarks of the malignant phenotype of several PTC-derived cell lines was investigated. In NIH3T3 cells, the cooperation of S100A11 with the different PTC-specific oncogenes was assessed. We found that the S100A11 gene expression is frequently up-regulated in PTC, anaplastic thyroid carcinoma, but not in follicular thyroid carcinoma. S100A11 overexpression was also detected in PTC-derived cell lines, which were then used for functional studies. S100A11 silencing in PTC-derived cell lines did not affect cell proliferation, whereas it reduced the loss of contact inhibition, anchorage-independent growth, and resistance to anoikis. Cotransfection experiments in NIH3T3 cells showed that overexpression of the S100A11 gene was able to enhance the transforming capabilities of the different PTC-associated oncogenes by affecting the loss of contact inhibition, anchorage-independent growth, and in vivo tumor formation.
Question: Does s100A11 overexpression contribute to the malignant phenotype of papillary thyroid carcinoma?
Output:
|
PubmedQA191931
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The purpose of this study was to investigate tibial changes in volumetric bone mineral density and geometry that take place in athletes from pre- to post-season. Female college athletes (n = 36) and ten controls recruited from the student population were included in the study. Participants had their left tibia scanned by pQCT at 4, 20, and 66 % of the overall length from the distal end before and after their competitive seasons. Subjects were divided into four groups: non-athlete (controls, n = 10), moderate-impact (cross-country runners, n = 13), high-impact (volleyball and basketball, n = 11), and odd-impact (soccer, n = 12). Anterior-posterior and medial-lateral diameter increased at the 4 % site in control subjects. In the moderate-impact group, medial-lateral moment of inertia (MOI) increased by 1.2 ± 1.8 (mean ± SD) percent at the 20 % site. In high-impact group, anterior-posterior MOI increased by 1.6 ± 2.0 percent at the 66 % site. In odd-impact group, cortical area (1.4 ± 2.3 %) and cortical thickness (1.8 ± 2.8 %) increased at the 20 % site increased, as did the polar MOI (1.8 ± 2.2 %) at the 66 % site.\n Question: Does odd-impact loading result in increased cortical area and moments of inertia in collegiate athletes?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: The purpose of this study was to investigate tibial changes in volumetric bone mineral density and geometry that take place in athletes from pre- to post-season. Female college athletes (n = 36) and ten controls recruited from the student population were included in the study. Participants had their left tibia scanned by pQCT at 4, 20, and 66 % of the overall length from the distal end before and after their competitive seasons. Subjects were divided into four groups: non-athlete (controls, n = 10), moderate-impact (cross-country runners, n = 13), high-impact (volleyball and basketball, n = 11), and odd-impact (soccer, n = 12). Anterior-posterior and medial-lateral diameter increased at the 4 % site in control subjects. In the moderate-impact group, medial-lateral moment of inertia (MOI) increased by 1.2 ± 1.8 (mean ± SD) percent at the 20 % site. In high-impact group, anterior-posterior MOI increased by 1.6 ± 2.0 percent at the 66 % site. In odd-impact group, cortical area (1.4 ± 2.3 %) and cortical thickness (1.8 ± 2.8 %) increased at the 20 % site increased, as did the polar MOI (1.8 ± 2.2 %) at the 66 % site.
Question: Does odd-impact loading result in increased cortical area and moments of inertia in collegiate athletes?
Output:
|
PubmedQA38556
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The leucine-75-proline variant of apolipoprotein A-I leads to a new hereditary systemic amyloidosis involving mostly the liver and kidney. The objective of the study was to examine the effects of this amyloidosis on testicular structure and function. This was an observational study in which patients with testicular amyloidosis were characterized. The study was carried out at the Endocrinology Department of Brescia University. Over a 13-yr period, 25 patients were found to be affected by leucine-75-proline apolipoprotein A-I testicular amyloidosis. Thirteen had the testicle as the first or only organ involved (group 1); in 12 testicular damage followed that of other organs (group 2). There were no interventions. Hormone and lipidic profiles, semen analysis, echographic volume of testicles, testicular histology, and genetic analysis were carried out. Group 1 patients were younger than those of group 2. In group 1, eight had hypergonadotropic hypogonadism and five were normogonadic with high gonadotropins; in group 2 all subjects were hypogonadic. All men had low high-density lipoprotein values. Group 1 patients were macroorchid, whereas the testicular volume was at the highest limit in group 2 (group 1 vs. group 2, P < 0.05). All men in the first group and six in the second group were azoospermic; the remaining had oligoposia. Biopsies showed the germinal epithelium replaced by amyloid. Leydig cells were essentially preserved in normogonadic but not hypogonadic patients.\n Question: Does spermatogenic and steroidogenic impairment of the testicle characterize the hereditary leucine-75-proline apolipoprotein a-I amyloidosis?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: The leucine-75-proline variant of apolipoprotein A-I leads to a new hereditary systemic amyloidosis involving mostly the liver and kidney. The objective of the study was to examine the effects of this amyloidosis on testicular structure and function. This was an observational study in which patients with testicular amyloidosis were characterized. The study was carried out at the Endocrinology Department of Brescia University. Over a 13-yr period, 25 patients were found to be affected by leucine-75-proline apolipoprotein A-I testicular amyloidosis. Thirteen had the testicle as the first or only organ involved (group 1); in 12 testicular damage followed that of other organs (group 2). There were no interventions. Hormone and lipidic profiles, semen analysis, echographic volume of testicles, testicular histology, and genetic analysis were carried out. Group 1 patients were younger than those of group 2. In group 1, eight had hypergonadotropic hypogonadism and five were normogonadic with high gonadotropins; in group 2 all subjects were hypogonadic. All men had low high-density lipoprotein values. Group 1 patients were macroorchid, whereas the testicular volume was at the highest limit in group 2 (group 1 vs. group 2, P < 0.05). All men in the first group and six in the second group were azoospermic; the remaining had oligoposia. Biopsies showed the germinal epithelium replaced by amyloid. Leydig cells were essentially preserved in normogonadic but not hypogonadic patients.
Question: Does spermatogenic and steroidogenic impairment of the testicle characterize the hereditary leucine-75-proline apolipoprotein a-I amyloidosis?
Output:
|
PubmedQA29345
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Solid lipid nanoparticles containing cholesteryl butyrate (cholbut SLN) can be a delivery system for the anti-cancer drug butyrate. These nanoparticles inhibit adhesion of polymorphonuclear and tumour cells to endothelial cells and migration of tumour cells, suggesting that they may act as anti-inflammatory and anti-tumour agents. Here we have evaluated the effects of cholbut SLN on tumour cell growth using in vitro and in vivo models. Cholbut SLNs were incubated with cultures of four tumour cell lines, and cell growth was analysed by assessing viability, clonogenic capacity and cell cycle. Effects on intracellular signalling was assessed by Western blot analysis of Akt expression. The in vivo anti-tumour activity was measured in two models of PC-3 cell xenografts in SCID/Beige mice. Cholbut SLN inhibited tumour cell line viability, clonogenic activity, Akt phosphorylation and cell cycle progression. In mice injected i.v. with PC3-Luc cells and treated with cholbut SLN, . in vivo optical imaging and histological analysis showed no metastases in the lungs of the treated mice. In another set of mice injected s.c. with PC-3 cells and treated with cholbut SLN when the tumour diameter reached 2 mm, analysis of the tumour dimensions showed that treatment with cholbut SLN substantially delayed tumour growth.\n Question: Do solid lipid nanoparticles of cholesteryl butyrate inhibit the proliferation of cancer cells in vitro and in vivo models?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Solid lipid nanoparticles containing cholesteryl butyrate (cholbut SLN) can be a delivery system for the anti-cancer drug butyrate. These nanoparticles inhibit adhesion of polymorphonuclear and tumour cells to endothelial cells and migration of tumour cells, suggesting that they may act as anti-inflammatory and anti-tumour agents. Here we have evaluated the effects of cholbut SLN on tumour cell growth using in vitro and in vivo models. Cholbut SLNs were incubated with cultures of four tumour cell lines, and cell growth was analysed by assessing viability, clonogenic capacity and cell cycle. Effects on intracellular signalling was assessed by Western blot analysis of Akt expression. The in vivo anti-tumour activity was measured in two models of PC-3 cell xenografts in SCID/Beige mice. Cholbut SLN inhibited tumour cell line viability, clonogenic activity, Akt phosphorylation and cell cycle progression. In mice injected i.v. with PC3-Luc cells and treated with cholbut SLN, . in vivo optical imaging and histological analysis showed no metastases in the lungs of the treated mice. In another set of mice injected s.c. with PC-3 cells and treated with cholbut SLN when the tumour diameter reached 2 mm, analysis of the tumour dimensions showed that treatment with cholbut SLN substantially delayed tumour growth.
Question: Do solid lipid nanoparticles of cholesteryl butyrate inhibit the proliferation of cancer cells in vitro and in vivo models?
Output:
|
PubmedQA31619
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: There has been increased interest in the possible role of human cytomegalovirus (HCMV) in carcinogenesis during the last decade. HCMV seroprevalence was enhanced in patients with hepatocellular carcinoma (HCC) but a possible relationship between HCC and HCMV infection remained to be assessed. The aim of this work was to investigate the pro-tumor influence of HCMV on primary human hepatocytes (PHH) and HepG2 cells. Following infection of PHH and HepG2 cells by two different strains of HCMV, we measured the production of IL-6 in culture supernatants by ELISA and the protein levels of STAT3, pSTAT3, JAK, cyclin D1, survivin, p53, p21, and Mdm2 by western Blotting in infected and uninfected cells. Cell proliferation and transformation were investigated using Ki67Ag expression measurement and soft-agar colony formation assay respectively. Infection of HepG2 cells and PHH by HCMV resulted in the production of IL-6 and the subsequent activation of the IL-6R-JAK-STAT3 pathway. HCMV increased the expression of cyclin D1 and survivin. Cell proliferation was enhanced in HepG2 and PHH infected with HCMV, despite a paradoxical overexpression of p53 and p21. More importantly, we observed the formation of colonies in soft agar seeded with PHH infected with HCMV and when we challenged the HepG2 cultures to form tumorspheres, we found that the HCMV-infected cultures formed 2.5-fold more tumorspheres than uninfected cultures.\n Question: Does hCMV activate the IL-6-JAK-STAT3 axis in HepG2 cells and primary human hepatocytes?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: There has been increased interest in the possible role of human cytomegalovirus (HCMV) in carcinogenesis during the last decade. HCMV seroprevalence was enhanced in patients with hepatocellular carcinoma (HCC) but a possible relationship between HCC and HCMV infection remained to be assessed. The aim of this work was to investigate the pro-tumor influence of HCMV on primary human hepatocytes (PHH) and HepG2 cells. Following infection of PHH and HepG2 cells by two different strains of HCMV, we measured the production of IL-6 in culture supernatants by ELISA and the protein levels of STAT3, pSTAT3, JAK, cyclin D1, survivin, p53, p21, and Mdm2 by western Blotting in infected and uninfected cells. Cell proliferation and transformation were investigated using Ki67Ag expression measurement and soft-agar colony formation assay respectively. Infection of HepG2 cells and PHH by HCMV resulted in the production of IL-6 and the subsequent activation of the IL-6R-JAK-STAT3 pathway. HCMV increased the expression of cyclin D1 and survivin. Cell proliferation was enhanced in HepG2 and PHH infected with HCMV, despite a paradoxical overexpression of p53 and p21. More importantly, we observed the formation of colonies in soft agar seeded with PHH infected with HCMV and when we challenged the HepG2 cultures to form tumorspheres, we found that the HCMV-infected cultures formed 2.5-fold more tumorspheres than uninfected cultures.
Question: Does hCMV activate the IL-6-JAK-STAT3 axis in HepG2 cells and primary human hepatocytes?
Output:
|
PubmedQA160667
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Anthocyanins are plant-derived dietary components that are highly abundant, for example, in bilberries. We have previously demonstrated that anthocyanins exert anti-inflammatory properties in mouse colitis models and ameliorate disease activity in ulcerative colitis patients. Here, we studied the molecular mechanisms through which anthocyanin-containing bilberry extract (BE) exerts anti-inflammatory effects in human monocytic THP-1 cells. THP-1 cells were pre-incubated with BE 20 min prior to TNF-α or IFN-γ (100 ng/ml each) stimulation. Signalling protein activation was studied by Western blotting, mRNA expression by quantitative PCR and cytokine secretion by ELISA. IFN-γ-induced phosphorylation of STAT1 and STAT3 was significantly reduced by BE co-treatment. Consequently, levels of mRNA expression and/or cytokine secretion of MCP-1, IL-6, TNF-α, ICAM-1, and T-bet were lower with BE co-treatment. In contrast, BE enhanced TNF-α-mediated p65-NF-κB phosphorylation but reduced ERK1/2 phosphorylation. BE co-treatment further increased TNF-α-induced mRNA expression and secretion of NF-κB target genes, such as IL-6, IL-8, and MCP-1, while mRNA levels of ICAM-1 were reduced.\n Question: Do bilberry-derived anthocyanins prevent IFN-γ-induced pro-inflammatory signalling and cytokine secretion in human THP-1 monocytic cells?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Anthocyanins are plant-derived dietary components that are highly abundant, for example, in bilberries. We have previously demonstrated that anthocyanins exert anti-inflammatory properties in mouse colitis models and ameliorate disease activity in ulcerative colitis patients. Here, we studied the molecular mechanisms through which anthocyanin-containing bilberry extract (BE) exerts anti-inflammatory effects in human monocytic THP-1 cells. THP-1 cells were pre-incubated with BE 20 min prior to TNF-α or IFN-γ (100 ng/ml each) stimulation. Signalling protein activation was studied by Western blotting, mRNA expression by quantitative PCR and cytokine secretion by ELISA. IFN-γ-induced phosphorylation of STAT1 and STAT3 was significantly reduced by BE co-treatment. Consequently, levels of mRNA expression and/or cytokine secretion of MCP-1, IL-6, TNF-α, ICAM-1, and T-bet were lower with BE co-treatment. In contrast, BE enhanced TNF-α-mediated p65-NF-κB phosphorylation but reduced ERK1/2 phosphorylation. BE co-treatment further increased TNF-α-induced mRNA expression and secretion of NF-κB target genes, such as IL-6, IL-8, and MCP-1, while mRNA levels of ICAM-1 were reduced.
Question: Do bilberry-derived anthocyanins prevent IFN-γ-induced pro-inflammatory signalling and cytokine secretion in human THP-1 monocytic cells?
Output:
|
PubmedQA34449
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: This study assessed the efficacy of the combination of sotalol and either quinidine or procainamide in preventing sustained ventricular tachycardia inducibility and recurrence and prospectively evaluated the ability of the drug combination to prevent ventricular tachycardia recurrence when the arrhythmia remained inducible but was modified. Individual antiarrhythmic drugs are often ineffective in preventing the induction and recurrence of sustained ventricular tachycardia. Beta-adrenergic blockade and prolongation of refractoriness may be important components of successful antiarrhythmic therapy in patients with ventricular tachycardia. We reasoned that the combination of sotalol, which has beta-adrenergic blocking properties and prolonged ventricular refractoriness, and quinidine or procainamide, two agents that slow conduction and prolong refractory periods, would be effective therapy in such patients. We administered low dose sotalol (205 +/- 84 mg/day) plus quinidine sulfate (1,278 +/- 479 mg/day) or procainamide (2,393 +/- 1,423 mg/day) to 50 patients with spontaneous sustained ventricular tachycardia or fibrillation and inducible ventricular tachycardia. In 21 (46%) of 46 patients, ventricular tachycardia was rendered noninducible at electrophysiologic study (group I), and in 17 patients (37%), inducible tachycardia was modified according to prospectively identified criteria (group II), for a combined 83% response rate. Ventricular refractory periods increased from 252 +/- 24 to 316 +/- 28 ms and from 265 +/- 33 to 316 +/- 24 ms in groups I and II, respectively (p < 0.001), but from 234 +/- 19 to only 286 +/- 13 ms in the group of patients with unmodified ventricular tachycardia inducibility (n = 8, group III, p < 0.001). Cycle length of induced ventricular tachycardia slowed from 324 +/- 62 to 432 +/- 70 ms in group II patients (p < 0.001), whereas it slowed less in group III patients (279 +/- 73 to 314 +/- 63 ms, p = NS). Forty-two of the 50 patients (including all patients in groups I and II) were discharged on treatment with the drug combination. After 25 +/- 19 months of follow-up, the actuarial recurrence rate of ventricular tachycardia was 6%, 6% and 11% at 1, 2 and 3 years, respectively. Among patients in whom this drug combination was unsuccessful at electrophysiologic study (group III) and in those who received alternative therapy after combination therapy was discontinued because of side effects, actuarial recurrence rates were 9%, 14% and 32% at 1, 2 and 3 years, respectively.\n Question: Do sotalol and type IA drugs in combination prevent recurrence of sustained ventricular tachycardia?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: This study assessed the efficacy of the combination of sotalol and either quinidine or procainamide in preventing sustained ventricular tachycardia inducibility and recurrence and prospectively evaluated the ability of the drug combination to prevent ventricular tachycardia recurrence when the arrhythmia remained inducible but was modified. Individual antiarrhythmic drugs are often ineffective in preventing the induction and recurrence of sustained ventricular tachycardia. Beta-adrenergic blockade and prolongation of refractoriness may be important components of successful antiarrhythmic therapy in patients with ventricular tachycardia. We reasoned that the combination of sotalol, which has beta-adrenergic blocking properties and prolonged ventricular refractoriness, and quinidine or procainamide, two agents that slow conduction and prolong refractory periods, would be effective therapy in such patients. We administered low dose sotalol (205 +/- 84 mg/day) plus quinidine sulfate (1,278 +/- 479 mg/day) or procainamide (2,393 +/- 1,423 mg/day) to 50 patients with spontaneous sustained ventricular tachycardia or fibrillation and inducible ventricular tachycardia. In 21 (46%) of 46 patients, ventricular tachycardia was rendered noninducible at electrophysiologic study (group I), and in 17 patients (37%), inducible tachycardia was modified according to prospectively identified criteria (group II), for a combined 83% response rate. Ventricular refractory periods increased from 252 +/- 24 to 316 +/- 28 ms and from 265 +/- 33 to 316 +/- 24 ms in groups I and II, respectively (p < 0.001), but from 234 +/- 19 to only 286 +/- 13 ms in the group of patients with unmodified ventricular tachycardia inducibility (n = 8, group III, p < 0.001). Cycle length of induced ventricular tachycardia slowed from 324 +/- 62 to 432 +/- 70 ms in group II patients (p < 0.001), whereas it slowed less in group III patients (279 +/- 73 to 314 +/- 63 ms, p = NS). Forty-two of the 50 patients (including all patients in groups I and II) were discharged on treatment with the drug combination. After 25 +/- 19 months of follow-up, the actuarial recurrence rate of ventricular tachycardia was 6%, 6% and 11% at 1, 2 and 3 years, respectively. Among patients in whom this drug combination was unsuccessful at electrophysiologic study (group III) and in those who received alternative therapy after combination therapy was discontinued because of side effects, actuarial recurrence rates were 9%, 14% and 32% at 1, 2 and 3 years, respectively.
Question: Do sotalol and type IA drugs in combination prevent recurrence of sustained ventricular tachycardia?
Output:
|
PubmedQA29019
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Insulin-dependent glucose influx in skeletal muscle and adipocytes is believed to rely largely on GLUT4, but this has not been confirmed directly. We assessed the relative functional contribution of GLUT4 in experimental models of skeletal muscle and adipocytes using the HIV-1 protease inhibitor indinavir. Indinavir (up to 100 micro mol/l) was added to the glucose transport solution after insulin stimulation of wild-type L6 muscle cells, L6 cells over-expressing either GLUT4myc or GLUT1myc, 3T3-L1 adipocytes, isolated mouse brown or white adipocytes, and isolated mouse muscle preparations. 100 micro mol/l indinavir inhibited 80% of both basal and insulin-stimulated 2-deoxyglucose uptake in L6GLUT4myc myotubes and myoblasts, but only 25% in L6GLUT1myc cells. Cell-surface density of glucose transporters was not affected. In isolated soleus and extensor digitorum longus muscles, primary white and brown adipocytes, insulin-stimulated glucose uptake was inhibited 70 to 80% by indinavir. The effect of indinavir on glucose uptake was variable in 3T3-L1 adipocytes, averaging 45% and 67% inhibition of basal and maximally insulin-stimulated glucose uptake, respectively. In this cell, fractional inhibition of glucose uptake by indinavir correlated positively with the fold-stimulation of glucose uptake by insulin, and was higher with sub-maximal insulin concentrations. The latter finding coincided with an increase only in GLUT4, but not GLUT1, in plasma membrane lawns.\n Question: Does indinavir uncover different contributions of GLUT4 and GLUT1 towards glucose uptake in muscle and fat cells and tissues?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Insulin-dependent glucose influx in skeletal muscle and adipocytes is believed to rely largely on GLUT4, but this has not been confirmed directly. We assessed the relative functional contribution of GLUT4 in experimental models of skeletal muscle and adipocytes using the HIV-1 protease inhibitor indinavir. Indinavir (up to 100 micro mol/l) was added to the glucose transport solution after insulin stimulation of wild-type L6 muscle cells, L6 cells over-expressing either GLUT4myc or GLUT1myc, 3T3-L1 adipocytes, isolated mouse brown or white adipocytes, and isolated mouse muscle preparations. 100 micro mol/l indinavir inhibited 80% of both basal and insulin-stimulated 2-deoxyglucose uptake in L6GLUT4myc myotubes and myoblasts, but only 25% in L6GLUT1myc cells. Cell-surface density of glucose transporters was not affected. In isolated soleus and extensor digitorum longus muscles, primary white and brown adipocytes, insulin-stimulated glucose uptake was inhibited 70 to 80% by indinavir. The effect of indinavir on glucose uptake was variable in 3T3-L1 adipocytes, averaging 45% and 67% inhibition of basal and maximally insulin-stimulated glucose uptake, respectively. In this cell, fractional inhibition of glucose uptake by indinavir correlated positively with the fold-stimulation of glucose uptake by insulin, and was higher with sub-maximal insulin concentrations. The latter finding coincided with an increase only in GLUT4, but not GLUT1, in plasma membrane lawns.
Question: Does indinavir uncover different contributions of GLUT4 and GLUT1 towards glucose uptake in muscle and fat cells and tissues?
Output:
|
PubmedQA740
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: PTH stimulates bone formation in Fgfr3 knockout mice through promotion of proliferation and differentiation in osteoblasts. Previous studies showed that endogenous fibroblast growth factor 2 (FGF-2) is required for parathyroid hormone (PTH)-stimulated bone anabolic effects, however, the exact mechanisms by which PTH stimulate bone formation and the function of FGF receptors in mediating these actions are not fully defined. FGF receptor 3 (FGFR3) has been characterized as an important regulator of bone metabolism and is confirmed to cross-talk with PTH/PTHrP signal in cartilage and bone development. Fgfr3 knockout and wild-type mice at 2-month-old and 4-month-old were intraperitoneally injected with PTH intermittently for 4 weeks and then the skeletal responses to PTH were assessed by dual energy X-ray absorptiometry (DEXA), micro-computed tomography (μCT) and bone histomorphometry. Intermittent PTH treatment improved bone mineral density (BMD) and femoral mechanical properties in both Fgfr3 (-/-) and wild-type mice. Histomorphometric analysis showed that bone formation and bone resorption were increased in both genotypes following PTH treatment. PTH treatment increased trabecular bone volume (BV/TV) in WT and Fgfr3-deficient mice. The anabolic response in Fgfr3-deficient and wild-type bone is characterized by an increase of both bone formation and resorption-related genes following PTH treatment. In addition, we found that Fgfr3 null osteoblasts (compared to wild-type controls) maintained normal abilities to response to PTH-stimulated increase of proliferation, differentiation, expression of osteoblastic marker genes (Cbfa1, Osteopontin and Osteocalcin), and phosphorylation of Erk1/2.\n Question: Does fibroblast Growth Factor Receptor 3 Deficiency Impair the Osteoanabolic Action of Parathyroid Hormone on Mice?\n Output: "
},
{
"role": "assistant",
"content": "no"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: PTH stimulates bone formation in Fgfr3 knockout mice through promotion of proliferation and differentiation in osteoblasts. Previous studies showed that endogenous fibroblast growth factor 2 (FGF-2) is required for parathyroid hormone (PTH)-stimulated bone anabolic effects, however, the exact mechanisms by which PTH stimulate bone formation and the function of FGF receptors in mediating these actions are not fully defined. FGF receptor 3 (FGFR3) has been characterized as an important regulator of bone metabolism and is confirmed to cross-talk with PTH/PTHrP signal in cartilage and bone development. Fgfr3 knockout and wild-type mice at 2-month-old and 4-month-old were intraperitoneally injected with PTH intermittently for 4 weeks and then the skeletal responses to PTH were assessed by dual energy X-ray absorptiometry (DEXA), micro-computed tomography (μCT) and bone histomorphometry. Intermittent PTH treatment improved bone mineral density (BMD) and femoral mechanical properties in both Fgfr3 (-/-) and wild-type mice. Histomorphometric analysis showed that bone formation and bone resorption were increased in both genotypes following PTH treatment. PTH treatment increased trabecular bone volume (BV/TV) in WT and Fgfr3-deficient mice. The anabolic response in Fgfr3-deficient and wild-type bone is characterized by an increase of both bone formation and resorption-related genes following PTH treatment. In addition, we found that Fgfr3 null osteoblasts (compared to wild-type controls) maintained normal abilities to response to PTH-stimulated increase of proliferation, differentiation, expression of osteoblastic marker genes (Cbfa1, Osteopontin and Osteocalcin), and phosphorylation of Erk1/2.
Question: Does fibroblast Growth Factor Receptor 3 Deficiency Impair the Osteoanabolic Action of Parathyroid Hormone on Mice?
Output:
|
PubmedQA8785
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Thromboembolic disease (TED) after knee arthroplasty occurs infrequently in Iran. The aim of this study was to examine the incidence of TED in patients with osteoarthritis undergoing knee replacement in Southern Iran while on prophylaxis. In a case series study from January to December 2012, 100 consecutive total knee arthroplasty (TKA) candidates were evaluated for TED by clinical evaluation and Doppler sonography preoperatively and 2 months postoperatively and by clinical evaluation one year after surgery. The patients in this study randomly received either warfarin or enoxaparin prophylactically. A total of 77 women and 23 men with mean age of 67 years (52-82 years) entered the study. The average hemoglobin drop of 2.7 g with warfarin and 3.3 with enoxaparin was observed. No case of TED, pulmonary embolus (PE), major bleeding, post-thrombotic syndrome, or hemarthrosis was observed.\n Question: Is thromboembolic disease after knee arthroplasty rare in Southern Iran?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Thromboembolic disease (TED) after knee arthroplasty occurs infrequently in Iran. The aim of this study was to examine the incidence of TED in patients with osteoarthritis undergoing knee replacement in Southern Iran while on prophylaxis. In a case series study from January to December 2012, 100 consecutive total knee arthroplasty (TKA) candidates were evaluated for TED by clinical evaluation and Doppler sonography preoperatively and 2 months postoperatively and by clinical evaluation one year after surgery. The patients in this study randomly received either warfarin or enoxaparin prophylactically. A total of 77 women and 23 men with mean age of 67 years (52-82 years) entered the study. The average hemoglobin drop of 2.7 g with warfarin and 3.3 with enoxaparin was observed. No case of TED, pulmonary embolus (PE), major bleeding, post-thrombotic syndrome, or hemarthrosis was observed.
Question: Is thromboembolic disease after knee arthroplasty rare in Southern Iran?
Output:
|
PubmedQA189718
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Anti-thyroid peroxidase (TPO) autoantibodies (TPOAb) seem to be protective for patients with breast cancer (BC). Thyroid and breast tissues both express the sodium iodide symporter (NIS), similarly both have a peroxidase activity, TPO and lactoperoxidase (LPO) respectively. We hypothesize a common immune response to a thyroid/breast shared antigen suggesting three putative mechanisms: (1) TPOAb react to both TPO and LPO, (2) TPO could be expressed in BC and (3) patients with TPOAb could have autoantibodies to NIS (NISAb). Previous studies excluded NISAb that block NIS activity in sera of patients with thyroid autoimmunity (TA) and/or BC. This study investigates neutral NISAb (binding without affecting function). Clones of CHO cells stably expressing human NIS (hNIS; CHO-NIS) were isolated following transfection of hNIS in pcDNA3 vector. Expression of hNIS mRNA and surface protein was confirmed by PCR and flow cytometry respectively using a hNIS-mouse-monoclonal-antibody. CHO-NIS and controls transfected with the empty pcDNA3 vector (CHO-Empty) were incubated with 42 heat-inactivated human sera followed by an anti-human-IgG-AlexaFluor488-conjugate: 12 with BC, 11 with TA, 10 with both BC and TA and 9 with non-autoimmune thyroid diseases. The Kolmogorov-Smirnov Test was used to compare the fluorescence intensity obtained with CHO-NIS and CHO-Empty, using sera from six young males as a negative control population. None of the 42 sera were positive for NISAb.\n Question: Is the sodium iodide symporter unlikely to be a thyroid/breast shared antigen?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Anti-thyroid peroxidase (TPO) autoantibodies (TPOAb) seem to be protective for patients with breast cancer (BC). Thyroid and breast tissues both express the sodium iodide symporter (NIS), similarly both have a peroxidase activity, TPO and lactoperoxidase (LPO) respectively. We hypothesize a common immune response to a thyroid/breast shared antigen suggesting three putative mechanisms: (1) TPOAb react to both TPO and LPO, (2) TPO could be expressed in BC and (3) patients with TPOAb could have autoantibodies to NIS (NISAb). Previous studies excluded NISAb that block NIS activity in sera of patients with thyroid autoimmunity (TA) and/or BC. This study investigates neutral NISAb (binding without affecting function). Clones of CHO cells stably expressing human NIS (hNIS; CHO-NIS) were isolated following transfection of hNIS in pcDNA3 vector. Expression of hNIS mRNA and surface protein was confirmed by PCR and flow cytometry respectively using a hNIS-mouse-monoclonal-antibody. CHO-NIS and controls transfected with the empty pcDNA3 vector (CHO-Empty) were incubated with 42 heat-inactivated human sera followed by an anti-human-IgG-AlexaFluor488-conjugate: 12 with BC, 11 with TA, 10 with both BC and TA and 9 with non-autoimmune thyroid diseases. The Kolmogorov-Smirnov Test was used to compare the fluorescence intensity obtained with CHO-NIS and CHO-Empty, using sera from six young males as a negative control population. None of the 42 sera were positive for NISAb.
Question: Is the sodium iodide symporter unlikely to be a thyroid/breast shared antigen?
Output:
|
PubmedQA204552
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The polycomb-group (PcG) proteins function as general regulators of stem cells. We previously reported that retrovirus-mediated overexpression of Bmi1, a gene encoding a core component of polycomb repressive complex (PRC) 1, maintained self-renewing hematopoietic stem cells (HSCs) during long-term culture. However, the effects of overexpression of Bmi1 on HSCs in vivo remained to be precisely addressed. In this study, we generated a mouse line where Bmi1 can be conditionally overexpressed under the control of the endogenous Rosa26 promoter in a hematopoietic cell-specific fashion (Tie2-Cre;R26Stop(FL)Bmi1). Although overexpression of Bmi1 did not significantly affect steady state hematopoiesis, it promoted expansion of functional HSCs during ex vivo culture and efficiently protected HSCs against loss of self-renewal capacity during serial transplantation. Overexpression of Bmi1 had no effect on DNA damage response triggered by ionizing radiation. In contrast, Tie2-Cre;R26Stop(FL)Bmi1 HSCs under oxidative stress maintained a multipotent state and generally tolerated oxidative stress better than the control. Unexpectedly, overexpression of Bmi1 had no impact on the level of intracellular reactive oxygen species (ROS).\n Question: Does bmi1 confer resistance to oxidative stress on hematopoietic stem cells?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: The polycomb-group (PcG) proteins function as general regulators of stem cells. We previously reported that retrovirus-mediated overexpression of Bmi1, a gene encoding a core component of polycomb repressive complex (PRC) 1, maintained self-renewing hematopoietic stem cells (HSCs) during long-term culture. However, the effects of overexpression of Bmi1 on HSCs in vivo remained to be precisely addressed. In this study, we generated a mouse line where Bmi1 can be conditionally overexpressed under the control of the endogenous Rosa26 promoter in a hematopoietic cell-specific fashion (Tie2-Cre;R26Stop(FL)Bmi1). Although overexpression of Bmi1 did not significantly affect steady state hematopoiesis, it promoted expansion of functional HSCs during ex vivo culture and efficiently protected HSCs against loss of self-renewal capacity during serial transplantation. Overexpression of Bmi1 had no effect on DNA damage response triggered by ionizing radiation. In contrast, Tie2-Cre;R26Stop(FL)Bmi1 HSCs under oxidative stress maintained a multipotent state and generally tolerated oxidative stress better than the control. Unexpectedly, overexpression of Bmi1 had no impact on the level of intracellular reactive oxygen species (ROS).
Question: Does bmi1 confer resistance to oxidative stress on hematopoietic stem cells?
Output:
|
PubmedQA70938
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: We previously demonstrated that the HLA class II transactivator CIITA inhibits HIV-1 replication in T cells by competing with the viral transactivator Tat for the binding to Cyclin T1 subunit of the P-TEFb complex. Here, we analyzed the anti-viral function of CIITA in myeloid cells, another relevant HIV-1 target cell type. We sinvestigated clones of the U937 promonocytic cell line, either permissive (Plus) or non-permissive (Minus) to HIV-1 replication. This different phenotype has been associated with the expression of TRIM22 in U937 Minus but not in Plus cells. U937 Plus cells stably expressing CIITA were generated and HLA-II positive clones were selected by cell sorting and cloning. HLA and CIITA proteins were analyzed by cytofluorometry and western blotting, respectively. HLA-II DR and CIITA mRNAs were quantified by qRT-PCR. Tat-dependent transactivation was assessed by performing the HIV-1 LTR luciferase gene reporter assay. Cells were infected with HIV-1 and viral replication was evaluated by measuring the RT activity in culture supernatants. CIITA was expressed only in HLA-II-positive U937 Minus cells, and this was strictly correlated with inhibition of Tat-dependent HIV-1 LTR transactivation in Minus but not in Plus cells. Overexpression of CIITA in Plus cells restored the suppression of Tat transactivation, confirming the inhibitory role of CIITA. Importantly, HIV-1 replication was significantly reduced in Plus-CIITA cells with respect to Plus parental cells. This effect was independent of TRIM22 as CIITA did not induce TRIM22 expression in Plus-CIITA cells.\n Question: Does the MHC-II transactivator CIITA inhibit Tat function and HIV-1 replication in human myeloid cells?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: We previously demonstrated that the HLA class II transactivator CIITA inhibits HIV-1 replication in T cells by competing with the viral transactivator Tat for the binding to Cyclin T1 subunit of the P-TEFb complex. Here, we analyzed the anti-viral function of CIITA in myeloid cells, another relevant HIV-1 target cell type. We sinvestigated clones of the U937 promonocytic cell line, either permissive (Plus) or non-permissive (Minus) to HIV-1 replication. This different phenotype has been associated with the expression of TRIM22 in U937 Minus but not in Plus cells. U937 Plus cells stably expressing CIITA were generated and HLA-II positive clones were selected by cell sorting and cloning. HLA and CIITA proteins were analyzed by cytofluorometry and western blotting, respectively. HLA-II DR and CIITA mRNAs were quantified by qRT-PCR. Tat-dependent transactivation was assessed by performing the HIV-1 LTR luciferase gene reporter assay. Cells were infected with HIV-1 and viral replication was evaluated by measuring the RT activity in culture supernatants. CIITA was expressed only in HLA-II-positive U937 Minus cells, and this was strictly correlated with inhibition of Tat-dependent HIV-1 LTR transactivation in Minus but not in Plus cells. Overexpression of CIITA in Plus cells restored the suppression of Tat transactivation, confirming the inhibitory role of CIITA. Importantly, HIV-1 replication was significantly reduced in Plus-CIITA cells with respect to Plus parental cells. This effect was independent of TRIM22 as CIITA did not induce TRIM22 expression in Plus-CIITA cells.
Question: Does the MHC-II transactivator CIITA inhibit Tat function and HIV-1 replication in human myeloid cells?
Output:
|
PubmedQA165778
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To investigate the changes of fibroblast growth factor (FGF) in burn wounds. The FGF expression in the center of wound granulation, the edge of wound, the healed part of wound, the normal skin of patients, and the heal course of second degree burn wounds were detected by immunohistochemical methods. The expression intensity of FGF was different in the different sites of third degree burn wounds. The highest contents of FGF was in the center granulation of burn wounds, the less was in the borderline of wound and healed skin, and the least was in the healed skin. FGF expression mainly concentrated in the middle layer of wound, and almost no FGF expression in normal skin. The most FGF expression was occurred at 14 days after injury in second degree of burn wound.\n Question: Do [ Clinical observation on changes of fibroblast growth factor in burn wounds ]?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To investigate the changes of fibroblast growth factor (FGF) in burn wounds. The FGF expression in the center of wound granulation, the edge of wound, the healed part of wound, the normal skin of patients, and the heal course of second degree burn wounds were detected by immunohistochemical methods. The expression intensity of FGF was different in the different sites of third degree burn wounds. The highest contents of FGF was in the center granulation of burn wounds, the less was in the borderline of wound and healed skin, and the least was in the healed skin. FGF expression mainly concentrated in the middle layer of wound, and almost no FGF expression in normal skin. The most FGF expression was occurred at 14 days after injury in second degree of burn wound.
Question: Do [ Clinical observation on changes of fibroblast growth factor in burn wounds ]?
Output:
|
PubmedQA104765
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Because the number of long-term survivors of colorectal cancer has increased, second primary cancer has become an important issue. However, previous studies were heterogeneous in design, and few data for Asia-Pacific area were available. This was a retrospective population-based study conducted using the national database of the Taiwan Cancer Registry. Patients who have histology-proven primary colon cancer and rectal cancer from 1995 to 2005 were enrolled in this study. All second primary cancer events had to be histology proven. The standardized incidence ratio of second primary cancer was used as an indicator. Standardized incidence ratio was counted as the number of observed second primary cancer divided by the expected number of cancer cases in the general population. A total of 65 648 eligible index patients were enrolled, and 3810 second primary cancer events were identified. The standardized incidence ratio for all of the patients was 1.03 (95% confidence interval: 0.99-1.06), which implied that the risk of second primary cancer was not significantly elevated in the index patients compared with that of the general population. The standardized incidence ratio for the patients aged <50, 50-70 and >70 years was 2.52 (95% confidence interval: 2.28-2.78), 1.18 (95% confidence interval: 1.12-1.23) and 0.80 (95% confidence interval: 0.76-0.84), respectively. In young patients (aged <50 years), the standardized incidence ratio increase was statistically significant and persisted for over 10 years and this significantly increased across all subgroups. The small intestine, the large intestine, the female genital organs and the lungs were the most common sites of second primary cancer in young patients.\n Question: Do young patients with colorectal cancer have increased risk of second primary cancers?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Because the number of long-term survivors of colorectal cancer has increased, second primary cancer has become an important issue. However, previous studies were heterogeneous in design, and few data for Asia-Pacific area were available. This was a retrospective population-based study conducted using the national database of the Taiwan Cancer Registry. Patients who have histology-proven primary colon cancer and rectal cancer from 1995 to 2005 were enrolled in this study. All second primary cancer events had to be histology proven. The standardized incidence ratio of second primary cancer was used as an indicator. Standardized incidence ratio was counted as the number of observed second primary cancer divided by the expected number of cancer cases in the general population. A total of 65 648 eligible index patients were enrolled, and 3810 second primary cancer events were identified. The standardized incidence ratio for all of the patients was 1.03 (95% confidence interval: 0.99-1.06), which implied that the risk of second primary cancer was not significantly elevated in the index patients compared with that of the general population. The standardized incidence ratio for the patients aged <50, 50-70 and >70 years was 2.52 (95% confidence interval: 2.28-2.78), 1.18 (95% confidence interval: 1.12-1.23) and 0.80 (95% confidence interval: 0.76-0.84), respectively. In young patients (aged <50 years), the standardized incidence ratio increase was statistically significant and persisted for over 10 years and this significantly increased across all subgroups. The small intestine, the large intestine, the female genital organs and the lungs were the most common sites of second primary cancer in young patients.
Question: Do young patients with colorectal cancer have increased risk of second primary cancers?
Output:
|
PubmedQA54966
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Pancreatic adenocarcinoma is an aggressive malignancy. Oncolytic adenoviruses (Ads) are modified genetically to target tumor cells while sparing normal cells. We modified the knob domain of the Ad serotype 5 with a serotype 3 knob domain and incorporated the CXCR4 promoter to regulate Ad E1A gene expression (Ad5/3-CXCR4-E1A). These modifications were made to efficiently infect and lyse pancreatic tumors. Human pancreatic cancer lines CFPAC-1, PANC-1, AsPC-1, and BxPC-3 were obtained from the American Type Culture Collection. Efficiency of Ad infection in the cells was determined by the use of an Ad construct expressing the green fluorescence protein (GFP) marker in place of the E1A gene (Ad5/3-CXCR4-GFP) and quantified by flow cytometry. Oncolytic activity in the pancreatic cancer cells was determined with the Ad5/3-CXCR4-E1A oncolytic Ad by a crystal violet staining method. To determine the oncolytic effect in vivo, pancreatic cancer cells were implanted on the flanks of 40 SCID mice (4 groups). Tumors were injected intratumorally for 3 days with Ad5/3-CXCR4-E1A, Ad5 wild-type (a positive control), or phosphate-buffered saline (a no virus control). Tumor size, overall survival, and body condition scale score were recorded. Statistical analyses included the Kaplan-Meier survival curve, the log-rank test, and one-way analysis of variance. The serotype 3 fiber-modified Ad with the CXCR4 promoter (Ad5/3-CXCR4-E1A) was most efficient in infecting and lysing pancreatic cancer cells compared with an Ad containing an unmodified fiber knob (Ad5-CXCR4-E1A). Treatment of pancreatic tumor xenografts in vivo with Ad5/3-CXCR4-E1A group resulted in smaller tumors (P = .001), greater body condition scale score (P = .01), and greater survival time (P = .04) than the other treatment groups.\n Question: Does virotherapy using a novel chimeric oncolytic adenovirus prolong survival in a human pancreatic cancer xenograft model?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Pancreatic adenocarcinoma is an aggressive malignancy. Oncolytic adenoviruses (Ads) are modified genetically to target tumor cells while sparing normal cells. We modified the knob domain of the Ad serotype 5 with a serotype 3 knob domain and incorporated the CXCR4 promoter to regulate Ad E1A gene expression (Ad5/3-CXCR4-E1A). These modifications were made to efficiently infect and lyse pancreatic tumors. Human pancreatic cancer lines CFPAC-1, PANC-1, AsPC-1, and BxPC-3 were obtained from the American Type Culture Collection. Efficiency of Ad infection in the cells was determined by the use of an Ad construct expressing the green fluorescence protein (GFP) marker in place of the E1A gene (Ad5/3-CXCR4-GFP) and quantified by flow cytometry. Oncolytic activity in the pancreatic cancer cells was determined with the Ad5/3-CXCR4-E1A oncolytic Ad by a crystal violet staining method. To determine the oncolytic effect in vivo, pancreatic cancer cells were implanted on the flanks of 40 SCID mice (4 groups). Tumors were injected intratumorally for 3 days with Ad5/3-CXCR4-E1A, Ad5 wild-type (a positive control), or phosphate-buffered saline (a no virus control). Tumor size, overall survival, and body condition scale score were recorded. Statistical analyses included the Kaplan-Meier survival curve, the log-rank test, and one-way analysis of variance. The serotype 3 fiber-modified Ad with the CXCR4 promoter (Ad5/3-CXCR4-E1A) was most efficient in infecting and lysing pancreatic cancer cells compared with an Ad containing an unmodified fiber knob (Ad5-CXCR4-E1A). Treatment of pancreatic tumor xenografts in vivo with Ad5/3-CXCR4-E1A group resulted in smaller tumors (P = .001), greater body condition scale score (P = .01), and greater survival time (P = .04) than the other treatment groups.
Question: Does virotherapy using a novel chimeric oncolytic adenovirus prolong survival in a human pancreatic cancer xenograft model?
Output:
|
PubmedQA92417
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Osteoarthritis (OA) can occur in the ankle joint. It also occurs in an appreciable proportion of subjects with hereditary hemochromatosis (HH). Might these conditions have common genetic characteristics? The aim of this study was to test the hypothesis that HFE gene mutations are associated with primary osteoarthritis in the ankle joint. Consecutive referred patients who had primary or secondary (posttraumatic) OA of the ankle joint were assessed by a single rheumatologist and had a full physical and joint examination. Plain x-rays of the ankle joint, other clinically involved osteoarthritic joints, iron studies, HFE genotyping, and Hb electrophoresis were performed. The significance of differences was evaluated by 2-tailed Fisher exact test. Fourteen patients met the inclusion criteria for primary ankle OA and 6 met the criteria for secondary ankle OA. One of the 14 had had a previous subtalar joint fusion and was excluded. Among the remaining 13, 7 had OA in the index and/or middle finger metacarpophalangeal joints (MCP2,3 OA) with radiologic features similar to those found in hemochromatotic arthropathy (HA). Furthermore, 11 of the 13 had at least one HFE mutation, one subject in this group was homozygous for H63D, one was compound heterozygous for C282Y and S65C, and one was compound heterozygous for H63D and S65C. Eight were heterozygous for H63D. The 13 subjects were compared with the 6 secondary ankle OA subjects and with a previously studied population cohort (n = 3011) from the town of Busselton in whom HFE genotyping had been performed. A statistically significant increase in the frequency of HFE gene mutations was observed in the group with primary OA of the ankle joint compared with that with secondary ankle joint OA (P = 0.0095) and compared with the Busselton cohort (P = 0.0008). Furthermore, a statistically significant association between finger MCP joint OA and primary ankle joint OA was observed (P = 0.0436). Iron studies were normal in the 13 primary and 6 secondary ankle OA subjects. None of the subjects with ankle OA had clinical signs of hemochromatosis or abnormal liver function tests.\n Question: Is primary osteoarthritis in the ankle joint associated with finger metacarpophalangeal osteoarthritis and the H63D mutation in the HFE gene : evidence for a hemochromatosis-like polyarticular osteoarthritis phenotype?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Osteoarthritis (OA) can occur in the ankle joint. It also occurs in an appreciable proportion of subjects with hereditary hemochromatosis (HH). Might these conditions have common genetic characteristics? The aim of this study was to test the hypothesis that HFE gene mutations are associated with primary osteoarthritis in the ankle joint. Consecutive referred patients who had primary or secondary (posttraumatic) OA of the ankle joint were assessed by a single rheumatologist and had a full physical and joint examination. Plain x-rays of the ankle joint, other clinically involved osteoarthritic joints, iron studies, HFE genotyping, and Hb electrophoresis were performed. The significance of differences was evaluated by 2-tailed Fisher exact test. Fourteen patients met the inclusion criteria for primary ankle OA and 6 met the criteria for secondary ankle OA. One of the 14 had had a previous subtalar joint fusion and was excluded. Among the remaining 13, 7 had OA in the index and/or middle finger metacarpophalangeal joints (MCP2,3 OA) with radiologic features similar to those found in hemochromatotic arthropathy (HA). Furthermore, 11 of the 13 had at least one HFE mutation, one subject in this group was homozygous for H63D, one was compound heterozygous for C282Y and S65C, and one was compound heterozygous for H63D and S65C. Eight were heterozygous for H63D. The 13 subjects were compared with the 6 secondary ankle OA subjects and with a previously studied population cohort (n = 3011) from the town of Busselton in whom HFE genotyping had been performed. A statistically significant increase in the frequency of HFE gene mutations was observed in the group with primary OA of the ankle joint compared with that with secondary ankle joint OA (P = 0.0095) and compared with the Busselton cohort (P = 0.0008). Furthermore, a statistically significant association between finger MCP joint OA and primary ankle joint OA was observed (P = 0.0436). Iron studies were normal in the 13 primary and 6 secondary ankle OA subjects. None of the subjects with ankle OA had clinical signs of hemochromatosis or abnormal liver function tests.
Question: Is primary osteoarthritis in the ankle joint associated with finger metacarpophalangeal osteoarthritis and the H63D mutation in the HFE gene : evidence for a hemochromatosis-like polyarticular osteoarthritis phenotype?
Output:
|
PubmedQA140421
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To evaluate whether TiF4 solution and APF gel had any adverse effects on the surface morphology of newly developed glass ionomers. Fifteen disc-shaped specimens of Fuji IX Extra, Fuji II LC and Ketac N100 were prepared and stored in 2 ml of artificial saliva at 37 degrees C for 8 weeks. Specimens of each material were divided randomly into three subgroups as 1 and 4 minutes application of 1.23% APF gel and 1 minute application of 1% TiF4 solution. Specimens were reaged for another 8 weeks. Microhardness, surface roughness values and surface morphology were evaluated by using Vicker's hardness test, surface profilometry and scanning electron microscopy (SEM) for all time interventions, respectively. One-way Anova test was performed and differences were compared by Tukey's HSD and Dunnet T3 test APF and TiF4 applications decreased microhardness significantly in Fuji II LC. In Fuji IX Extra microhardness decreased significantly after 1- and 4-min APF applications. Ketac N100 showed no difference in microhardness after APF and TiF4 applications. Surface roughness was not affected at any time interval for three restorative materials.\n Question: Does microhardness and surface roughness of glass ionomer cement after APF and TiF4 applications?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To evaluate whether TiF4 solution and APF gel had any adverse effects on the surface morphology of newly developed glass ionomers. Fifteen disc-shaped specimens of Fuji IX Extra, Fuji II LC and Ketac N100 were prepared and stored in 2 ml of artificial saliva at 37 degrees C for 8 weeks. Specimens of each material were divided randomly into three subgroups as 1 and 4 minutes application of 1.23% APF gel and 1 minute application of 1% TiF4 solution. Specimens were reaged for another 8 weeks. Microhardness, surface roughness values and surface morphology were evaluated by using Vicker's hardness test, surface profilometry and scanning electron microscopy (SEM) for all time interventions, respectively. One-way Anova test was performed and differences were compared by Tukey's HSD and Dunnet T3 test APF and TiF4 applications decreased microhardness significantly in Fuji II LC. In Fuji IX Extra microhardness decreased significantly after 1- and 4-min APF applications. Ketac N100 showed no difference in microhardness after APF and TiF4 applications. Surface roughness was not affected at any time interval for three restorative materials.
Question: Does microhardness and surface roughness of glass ionomer cement after APF and TiF4 applications?
Output:
|
PubmedQA81775
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Overexpression of epidermal growth factor (EGF) and EGF receptor has been associated with progression and invasive phenotype in pancreatic cancer. However, the underlying molecular mechanism by which EGF worked in pancreatic cancer cells has been poorly understood. In this study, we determined the effect of EGF on the invasiveness and the related regulatory mechanism in two pancreatic cancer cell lines NOR-P1 and KP4. Invasion assay was performed to examine the invasiveness of tumor cells induced by EGF, and the expression of matrix metalloproteinase (MMP)-9, MMP-2, and plasminogen activator (uPA) was determined by reverse transcription-polymerase chain reaction and Western blot. Gelatin zymography was used to detect the activities of MMP-9 and MMP-2, and the nuclear factor-kappaB (NF-kappaB) binding activity was determined by electrophoretic mobility shift assay (EMSA). EGF significantly increased the invasiveness of both cell lines but did not affect cell proliferation or adhesion. Increased invasiveness was associated with the induction of MMP-9 and uPA at both mRNA and protein levels. Furthermore, EGF stimulated NF-kappaB binding activity. Moreover, pretreatment of cells with NF-kappaB inhibitors, pyrrolidine dithiocarbamate or ibuprofen, markedly attenuated EGF-induced NF-kappaB activation. Subsequently, the EGF-induced MMP-9 and uPA expression and MMP-9 activity, as well as cell invasiveness, were also inhibited by these NF-kappaB inhibitors.\n Question: Does epidermal growth factor promote invasiveness of pancreatic cancer cells through NF-kappaB-mediated proteinase productions?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Overexpression of epidermal growth factor (EGF) and EGF receptor has been associated with progression and invasive phenotype in pancreatic cancer. However, the underlying molecular mechanism by which EGF worked in pancreatic cancer cells has been poorly understood. In this study, we determined the effect of EGF on the invasiveness and the related regulatory mechanism in two pancreatic cancer cell lines NOR-P1 and KP4. Invasion assay was performed to examine the invasiveness of tumor cells induced by EGF, and the expression of matrix metalloproteinase (MMP)-9, MMP-2, and plasminogen activator (uPA) was determined by reverse transcription-polymerase chain reaction and Western blot. Gelatin zymography was used to detect the activities of MMP-9 and MMP-2, and the nuclear factor-kappaB (NF-kappaB) binding activity was determined by electrophoretic mobility shift assay (EMSA). EGF significantly increased the invasiveness of both cell lines but did not affect cell proliferation or adhesion. Increased invasiveness was associated with the induction of MMP-9 and uPA at both mRNA and protein levels. Furthermore, EGF stimulated NF-kappaB binding activity. Moreover, pretreatment of cells with NF-kappaB inhibitors, pyrrolidine dithiocarbamate or ibuprofen, markedly attenuated EGF-induced NF-kappaB activation. Subsequently, the EGF-induced MMP-9 and uPA expression and MMP-9 activity, as well as cell invasiveness, were also inhibited by these NF-kappaB inhibitors.
Question: Does epidermal growth factor promote invasiveness of pancreatic cancer cells through NF-kappaB-mediated proteinase productions?
Output:
|
PubmedQA25915
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The purpose of this study was to develop and evaluate a fully automated method that spatially registers anterior, posterior, and lateral ventilation/perfusion (V/Q) images with posteroanterior and lateral digital chest radiographs to retrospectively combine the physiologic information contained in the V/Q scans with the anatomic detail in the chest radiographs. Gray-level thresholding techniques were used to segment the aerated lung regions in the radiographic images. A variable-thresholding technique combined with an analysis of image noise was used to segment the adequately perfused or ventilated lung regions in the scintigraphic images. The physical dimensions of the segmented lung regions in images from both modalities were used to properly scale the radiographic images relative to the radionuclide images. Computer-determined locations of anatomic landmarks were then used to rotate and translate the images to achieve registration. Pairs of corresponding radionuclide and radiographic images were enhanced with color and then merged to create superimposed images. Five observers used a five-point rating scale to subjectively evaluate four image combinations for each of 50 cases. Of these ratings, 95.5% reflected very good, good, or fair registration.\n Question: Does automated registration of frontal and lateral radionuclide lung scan with digital chest radiographs?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: The purpose of this study was to develop and evaluate a fully automated method that spatially registers anterior, posterior, and lateral ventilation/perfusion (V/Q) images with posteroanterior and lateral digital chest radiographs to retrospectively combine the physiologic information contained in the V/Q scans with the anatomic detail in the chest radiographs. Gray-level thresholding techniques were used to segment the aerated lung regions in the radiographic images. A variable-thresholding technique combined with an analysis of image noise was used to segment the adequately perfused or ventilated lung regions in the scintigraphic images. The physical dimensions of the segmented lung regions in images from both modalities were used to properly scale the radiographic images relative to the radionuclide images. Computer-determined locations of anatomic landmarks were then used to rotate and translate the images to achieve registration. Pairs of corresponding radionuclide and radiographic images were enhanced with color and then merged to create superimposed images. Five observers used a five-point rating scale to subjectively evaluate four image combinations for each of 50 cases. Of these ratings, 95.5% reflected very good, good, or fair registration.
Question: Does automated registration of frontal and lateral radionuclide lung scan with digital chest radiographs?
Output:
|
PubmedQA176151
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Application of direct current (DC) to a burn wound limits extension of the zone-of-stasis and reduces wound tissue edema. To study the effects of DC on extravasation of plasma proteins after burn by using Evans blue (EB) as a marker of plasma albumin. Male Sprague-Dawley rats with 20% total body surface area full-thickness scalds (100 degrees C/10 sec) were used as the experimental model. Burn wounds were treated with plain nylon, silver-nylon, silver-nylon and 40 microA DC, or no dressing. EB (30 mg/kg) was injected immediately or at variably delayed postburn (PB) times and accompanied by DC application at various time intervals PB. Tissue content of Evans blue was assessed at different times after injection of the dye or infliction of burn injury. Evans blue albumin (EBA) concentration in untreated burn wounds (307.7 microg/g tissue) was nine times greater than in unburned skin (36.5 microg/g tissue) at 48 hours PB. When animals received a DC and EB injection immediately PB, DC treatment reduced EBA concentration by 60% at any time point PB. When EB was injected immediately PB, or at variably delayed times PB, accompanied by DC immediately PB, or at variably delayed times PB, DC reduced EBA accumulation at all examined times PB by more the 50% (p < 0.001).\n Question: Does direct current reduce accumulation of Evans Blue albumin in full-thickness burns?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Application of direct current (DC) to a burn wound limits extension of the zone-of-stasis and reduces wound tissue edema. To study the effects of DC on extravasation of plasma proteins after burn by using Evans blue (EB) as a marker of plasma albumin. Male Sprague-Dawley rats with 20% total body surface area full-thickness scalds (100 degrees C/10 sec) were used as the experimental model. Burn wounds were treated with plain nylon, silver-nylon, silver-nylon and 40 microA DC, or no dressing. EB (30 mg/kg) was injected immediately or at variably delayed postburn (PB) times and accompanied by DC application at various time intervals PB. Tissue content of Evans blue was assessed at different times after injection of the dye or infliction of burn injury. Evans blue albumin (EBA) concentration in untreated burn wounds (307.7 microg/g tissue) was nine times greater than in unburned skin (36.5 microg/g tissue) at 48 hours PB. When animals received a DC and EB injection immediately PB, DC treatment reduced EBA concentration by 60% at any time point PB. When EB was injected immediately PB, or at variably delayed times PB, accompanied by DC immediately PB, or at variably delayed times PB, DC reduced EBA accumulation at all examined times PB by more the 50% (p < 0.001).
Question: Does direct current reduce accumulation of Evans Blue albumin in full-thickness burns?
Output:
|
PubmedQA77346
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To explore the role of the P38 signaling pathway in the apoptosis of arsenic trioxide (As2 O3)-induced androgen-independent prostate cancer PC-3 cells. Androgen-independent prostate cancer PC-3 cells were treated with different concentrations of As2 O3 for 24, 48 and 72 hours. The inhibitory effect of As2 O3 on the cell growth was measured by MTT, the expression of p- P38 detected by Western blot, and the rate of cell apoptosis determined by Annexin V and PI double staining before and after interfering the P38 signaling pathway by SB203580, a highly selective P38 inhibitor. As2 O3 inhibited the proliferation of PC-3 cells in a concentration- and time-dependent manner, and quickly activated P38 phosphorylation, thus giving full play to its biological activities. After 24 hours of treatment with As2 O3 at the concentrations of 2, 10 and 20 micromol/L, the apoptosis rates of the PC-3 cells were (18.9 +/- 0.43), (24.7 +/- 0.29) and (49.7 +/- 1.79)%, respectively, which were reduced to (14.8 +/- 0.81), (22.1 +/- 0.51) and (39.6 +/- 1.74)% after interfering the P38 pathway with SB203580. Inhibition of the P38 pathway significantly reduced the apoptosis of the PC-3 cells induced by As2 O3 (P < 0.05).\n Question: Does [ Arsenic trioxide induce the apoptosis of prostate cancer PC-3 cells via the P38 signaling pathway ]?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To explore the role of the P38 signaling pathway in the apoptosis of arsenic trioxide (As2 O3)-induced androgen-independent prostate cancer PC-3 cells. Androgen-independent prostate cancer PC-3 cells were treated with different concentrations of As2 O3 for 24, 48 and 72 hours. The inhibitory effect of As2 O3 on the cell growth was measured by MTT, the expression of p- P38 detected by Western blot, and the rate of cell apoptosis determined by Annexin V and PI double staining before and after interfering the P38 signaling pathway by SB203580, a highly selective P38 inhibitor. As2 O3 inhibited the proliferation of PC-3 cells in a concentration- and time-dependent manner, and quickly activated P38 phosphorylation, thus giving full play to its biological activities. After 24 hours of treatment with As2 O3 at the concentrations of 2, 10 and 20 micromol/L, the apoptosis rates of the PC-3 cells were (18.9 +/- 0.43), (24.7 +/- 0.29) and (49.7 +/- 1.79)%, respectively, which were reduced to (14.8 +/- 0.81), (22.1 +/- 0.51) and (39.6 +/- 1.74)% after interfering the P38 pathway with SB203580. Inhibition of the P38 pathway significantly reduced the apoptosis of the PC-3 cells induced by As2 O3 (P < 0.05).
Question: Does [ Arsenic trioxide induce the apoptosis of prostate cancer PC-3 cells via the P38 signaling pathway ]?
Output:
|
PubmedQA70644
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Bisphenol A (BPA) is a base chemical used extensively in many consumer products. BPA and its analogues are present in environmental and human samples. Many endocrine-disrupting chemicals, including BPA, have been shown to activate the pregnane X receptor (PXR), a nuclear receptor that functions as a master regulator of xenobiotic metabolism. However, the detailed mechanism by which these chemicals activate PXR remains unknown. We investigated the mechanism by which BPA interacts with and activates PXR and examined selected BPA analogues to determine whether they bind to and activate PXR. Cell-based reporter assays, in silico ligand-PXR docking studies, and site-directed mutagenesis were combined to study the interaction between BPA and PXR. We also investigated the influence of BPA and its analogues on the regulation of PXR target genes in human LS180 cells. We found that BPA and several of its analogues are potent agonists for human PXR (hPXR) but do not affect mouse PXR activity. We identified key residues within hPXR's ligand-binding pocket that constitute points of interaction with BPA. We also deduced the structural requirements of BPA analogues that activate hPXR. BPA and its analogues can also induce PXR target gene expression in human LS180 cells.\n Question: Do bisphenol A and its analogues activate human pregnane X receptor?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Bisphenol A (BPA) is a base chemical used extensively in many consumer products. BPA and its analogues are present in environmental and human samples. Many endocrine-disrupting chemicals, including BPA, have been shown to activate the pregnane X receptor (PXR), a nuclear receptor that functions as a master regulator of xenobiotic metabolism. However, the detailed mechanism by which these chemicals activate PXR remains unknown. We investigated the mechanism by which BPA interacts with and activates PXR and examined selected BPA analogues to determine whether they bind to and activate PXR. Cell-based reporter assays, in silico ligand-PXR docking studies, and site-directed mutagenesis were combined to study the interaction between BPA and PXR. We also investigated the influence of BPA and its analogues on the regulation of PXR target genes in human LS180 cells. We found that BPA and several of its analogues are potent agonists for human PXR (hPXR) but do not affect mouse PXR activity. We identified key residues within hPXR's ligand-binding pocket that constitute points of interaction with BPA. We also deduced the structural requirements of BPA analogues that activate hPXR. BPA and its analogues can also induce PXR target gene expression in human LS180 cells.
Question: Do bisphenol A and its analogues activate human pregnane X receptor?
Output:
|
PubmedQA154871
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To investigate the effect of short-term statin treatment on impaired endothelium-dependent vasodilatation and haemodynamic abnormalities typically occurring in chronic heart failure (CHF). In a double-blind, crossover study endothelium-dependent vasodilatation was measured in conduit and resistance vessels of 23 patients with non-ischaemic CHF after 6 weeks of placebo and 40 mg atorvastatin. The haemodynamic impact was assessed by cardioendocrine hormones, echocardiography and clinical indicators of CHF. Cholesterol concentrations were population average (low density lipoprotein 3.56 (SEM 0.16) mmol/l, triglycerides 1.70 (0.20) mmol/l and high density lipoprotein 1.17 (0.07) mmol/l). In resistance vessels, the area under the curve ratio during acetylcholine infusion increased from 9.2 (1.9) with placebo to 12.2 (2.1) with statin (p < 0.01). This improvement was reversed during co-infusion with the nitric oxide antagonist N(G)-monomethyl-L-arginine. In conduit arteries, flow-mediated dilatation increased from 5.64 (SEM 0.88)% with placebo to 6.83 (0.97)% with statin (p < 0.05). Endothelium-independent vasodilatation did not change (p = 0.68 for conduit and p = 0.45 for resistance vessels). Endothelin 1 and atrial natriuretic peptide (ANP) decreased from 1.57 (0.08) and 51.3 (1.0) with placebo to 1.42 (0.09) pg/ml (p < 0.05) and 42.1 (7.5) pmol/l (p < 0.05), respectively, with statin.\n Question: Does short-term statin treatment improve endothelial function and neurohormonal imbalance in normocholesterolaemic patients with non-ischaemic heart failure?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To investigate the effect of short-term statin treatment on impaired endothelium-dependent vasodilatation and haemodynamic abnormalities typically occurring in chronic heart failure (CHF). In a double-blind, crossover study endothelium-dependent vasodilatation was measured in conduit and resistance vessels of 23 patients with non-ischaemic CHF after 6 weeks of placebo and 40 mg atorvastatin. The haemodynamic impact was assessed by cardioendocrine hormones, echocardiography and clinical indicators of CHF. Cholesterol concentrations were population average (low density lipoprotein 3.56 (SEM 0.16) mmol/l, triglycerides 1.70 (0.20) mmol/l and high density lipoprotein 1.17 (0.07) mmol/l). In resistance vessels, the area under the curve ratio during acetylcholine infusion increased from 9.2 (1.9) with placebo to 12.2 (2.1) with statin (p < 0.01). This improvement was reversed during co-infusion with the nitric oxide antagonist N(G)-monomethyl-L-arginine. In conduit arteries, flow-mediated dilatation increased from 5.64 (SEM 0.88)% with placebo to 6.83 (0.97)% with statin (p < 0.05). Endothelium-independent vasodilatation did not change (p = 0.68 for conduit and p = 0.45 for resistance vessels). Endothelin 1 and atrial natriuretic peptide (ANP) decreased from 1.57 (0.08) and 51.3 (1.0) with placebo to 1.42 (0.09) pg/ml (p < 0.05) and 42.1 (7.5) pmol/l (p < 0.05), respectively, with statin.
Question: Does short-term statin treatment improve endothelial function and neurohormonal imbalance in normocholesterolaemic patients with non-ischaemic heart failure?
Output:
|
PubmedQA43083
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: IL-21 is the most recently identified member of the IL-2 cytokine family. Here we studied the therapeutic efficacy of IL-21-gene-modified cells (Neuro2a/IL-21) in a syngeneic metastatic neuroblastoma (NB) model. Neuro2a/IL-21 cells were tested as subcutaneous (sc) vaccine both in prophylactic and therapeutic settings. Depletion studies, cytotoxicity assay and immunohistochemical analyses were carried out to evaluate the mechanisms involved in tumor rejection. When injected sc in syngeneic A/J mice viable Neuro2a/IL-21 cells were rejected and induced resistance to a subsequent iv challenge with Neuro2a parental cells (Neuro2a/pc), suggesting the involvement of an immune response. More importantly, in mice bearing Neuro2a/pc micrometastases, a single sc injection of Neuro2a/IL-21 cells significantly increased the mean tumor-free survival of treated animals (43 vs. 22 days) and cured 14% of them. The administration of two or three doses of Neuro2a/IL-21 cell vaccine further increased the mean survival time to 54 and 75 days, and the cure rate to 27 and 33%, respectively, whereas the use of unmodified Neuro2a or mock-transfected cells had no effect. In vivo cell subset depletion and a Winn-assay indicated the involvement of CD8 + CTLs. Immunohistochemical analysis indicated a reduction of CD31+ and VEGFR2+ microvessels in late metastases from therapeutically vaccinated mice. A role of survivin as antigen was suggested by in vitro assays using survivin-synthetic CTL-epitopes.\n Question: Does immunotherapy of neuroblastoma by an Interleukin-21-secreting cell vaccine involve survivin as antigen?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: IL-21 is the most recently identified member of the IL-2 cytokine family. Here we studied the therapeutic efficacy of IL-21-gene-modified cells (Neuro2a/IL-21) in a syngeneic metastatic neuroblastoma (NB) model. Neuro2a/IL-21 cells were tested as subcutaneous (sc) vaccine both in prophylactic and therapeutic settings. Depletion studies, cytotoxicity assay and immunohistochemical analyses were carried out to evaluate the mechanisms involved in tumor rejection. When injected sc in syngeneic A/J mice viable Neuro2a/IL-21 cells were rejected and induced resistance to a subsequent iv challenge with Neuro2a parental cells (Neuro2a/pc), suggesting the involvement of an immune response. More importantly, in mice bearing Neuro2a/pc micrometastases, a single sc injection of Neuro2a/IL-21 cells significantly increased the mean tumor-free survival of treated animals (43 vs. 22 days) and cured 14% of them. The administration of two or three doses of Neuro2a/IL-21 cell vaccine further increased the mean survival time to 54 and 75 days, and the cure rate to 27 and 33%, respectively, whereas the use of unmodified Neuro2a or mock-transfected cells had no effect. In vivo cell subset depletion and a Winn-assay indicated the involvement of CD8 + CTLs. Immunohistochemical analysis indicated a reduction of CD31+ and VEGFR2+ microvessels in late metastases from therapeutically vaccinated mice. A role of survivin as antigen was suggested by in vitro assays using survivin-synthetic CTL-epitopes.
Question: Does immunotherapy of neuroblastoma by an Interleukin-21-secreting cell vaccine involve survivin as antigen?
Output:
|
PubmedQA167740
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To determine whether resveratrol, a natural plant-derived drug, has protective effects against antibody-induced apoptosis of retinal cells in vitro and to provide insights on the mechanism of resveratrol protection. E1A.NR3 retinal cells pretreated with 40 muM resveratrol were grown in the presence of anti-recoverin (Rec-1), anti-enolase (Enol-1) antibodies, and normal purified immunoglobulins. When the cells were exposed to resveratrol before treatment with Enol-1 or Rec-1 antibodies, 30-55% more cells survived compared to the resveratrol-untreated cells. Western blotting showed a reduction in proapoptotic protein Bax in the cytoplasm and mitochondria of resveratrol-treated cells. Resveratrol-pretreated cells also showed a significant decrease in intracellular calcium and an inhibition of caspase-3 activity as compared to the untreated cells. Sirt1 expression was greatly reduced in the cells grown in the presence of Rec-1 and Enol-1, but it increased about five times in the resveratrol-pretreated cells. Immunocytochemistry revealed that Sirt1 expression in the cytoplasm and nucleus was colocalized with Ku70 expression in resveratrol-treated cells, suggesting possible interaction with each other in the cell. The pattern of the Ku70 cellular localization also overlapped with the Bax cellular localization in treated and untreated cells.\n Question: Does resveratrol prevent antibody-induced apoptotic death of retinal cells through upregulation of Sirt1 and Ku70?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To determine whether resveratrol, a natural plant-derived drug, has protective effects against antibody-induced apoptosis of retinal cells in vitro and to provide insights on the mechanism of resveratrol protection. E1A.NR3 retinal cells pretreated with 40 muM resveratrol were grown in the presence of anti-recoverin (Rec-1), anti-enolase (Enol-1) antibodies, and normal purified immunoglobulins. When the cells were exposed to resveratrol before treatment with Enol-1 or Rec-1 antibodies, 30-55% more cells survived compared to the resveratrol-untreated cells. Western blotting showed a reduction in proapoptotic protein Bax in the cytoplasm and mitochondria of resveratrol-treated cells. Resveratrol-pretreated cells also showed a significant decrease in intracellular calcium and an inhibition of caspase-3 activity as compared to the untreated cells. Sirt1 expression was greatly reduced in the cells grown in the presence of Rec-1 and Enol-1, but it increased about five times in the resveratrol-pretreated cells. Immunocytochemistry revealed that Sirt1 expression in the cytoplasm and nucleus was colocalized with Ku70 expression in resveratrol-treated cells, suggesting possible interaction with each other in the cell. The pattern of the Ku70 cellular localization also overlapped with the Bax cellular localization in treated and untreated cells.
Question: Does resveratrol prevent antibody-induced apoptotic death of retinal cells through upregulation of Sirt1 and Ku70?
Output:
|
PubmedQA23515
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Malignant melanoma has high metastatic potential, is highly resistant to chemotherapy, and has a poor survival rate. Gambogic acid (GA), a polyprenylated xanthone extracted from a traditional Chinese medicinal herb, has been proven to exhibit antitumor activity. The present study aimed to investigate the signaling pathways that mediated GA-induced inhibition of human malignant skin melanoma proliferation. The study was conducted using A375 cells and the corresponding tumor transplanted in nude mice. Incubation of A375 cells with 1-10 μg/ml GA decreased cell viability and increased apoptosis. GA concentration-dependently increased p66shc expression and intracellular ROS levels. GA also decreased the oxygen consumption rate and the mitochondrial membrane potential (MMP) in A375 cells. Experimental inhibition of p66shc by siRNA suppressed GA-induced increase of ROS, decrease of oxygen consumption rate, MMP and cell viability, whilst suppressing GA-induced increase of apoptosis. GA concentration-dependently upregulated p53 and Bax expression in A375 cells. GA also increased p53-TA-luciferase activity and p53-binding to Bax promoter, which was inhibited by Sip53. Experimental inhibition of p53 with Sip53 blocked GA-induced decrease of the oxygen consumption rate and cell viability, and blocked the increase of apoptosis. In tumor-bearing nude mice, GA notably inhibited tumor growth, and this action was suppressed by N-acetylcysteine (NAC), a potent antioxidant, and by PFT-α, a p53 inhibitor. In A375 tumors transplanted in nude mice, GA increased both p66shc and p53 expression. NAC and PFT-α treatment did not significantly affect p66shc expression in tumors grown in mice treated with GA. In contrast, both NAC and PFT-α treatment inhibited GA-induced p53 expression in mouse tumors.\n Question: Does gambogic Acid inhibit Malignant Melanoma Cell Proliferation Through Mitochondrial p66shc/ROS-p53/Bax-Mediated Apoptosis?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Malignant melanoma has high metastatic potential, is highly resistant to chemotherapy, and has a poor survival rate. Gambogic acid (GA), a polyprenylated xanthone extracted from a traditional Chinese medicinal herb, has been proven to exhibit antitumor activity. The present study aimed to investigate the signaling pathways that mediated GA-induced inhibition of human malignant skin melanoma proliferation. The study was conducted using A375 cells and the corresponding tumor transplanted in nude mice. Incubation of A375 cells with 1-10 μg/ml GA decreased cell viability and increased apoptosis. GA concentration-dependently increased p66shc expression and intracellular ROS levels. GA also decreased the oxygen consumption rate and the mitochondrial membrane potential (MMP) in A375 cells. Experimental inhibition of p66shc by siRNA suppressed GA-induced increase of ROS, decrease of oxygen consumption rate, MMP and cell viability, whilst suppressing GA-induced increase of apoptosis. GA concentration-dependently upregulated p53 and Bax expression in A375 cells. GA also increased p53-TA-luciferase activity and p53-binding to Bax promoter, which was inhibited by Sip53. Experimental inhibition of p53 with Sip53 blocked GA-induced decrease of the oxygen consumption rate and cell viability, and blocked the increase of apoptosis. In tumor-bearing nude mice, GA notably inhibited tumor growth, and this action was suppressed by N-acetylcysteine (NAC), a potent antioxidant, and by PFT-α, a p53 inhibitor. In A375 tumors transplanted in nude mice, GA increased both p66shc and p53 expression. NAC and PFT-α treatment did not significantly affect p66shc expression in tumors grown in mice treated with GA. In contrast, both NAC and PFT-α treatment inhibited GA-induced p53 expression in mouse tumors.
Question: Does gambogic Acid inhibit Malignant Melanoma Cell Proliferation Through Mitochondrial p66shc/ROS-p53/Bax-Mediated Apoptosis?
Output:
|
PubmedQA176955
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Clinical practice guidelines summarize evidence from science and attempt to translate those findings into clinical practice. Pervasive and consistent adoption of these guidelines into daily provider practice has proven slow. Using postoperative nausea and vomiting (PONV) prophylaxis guideline compliance as our metric, we compared the effects of continuing medical education (CME) alone (I), CME with a single snapshot of provider compliance (II), and ongoing reporting of provider compliance data without further CME (III). We retrospectively analyzed guideline compliance of 23,279 anesthetics at the University of Texas M.D. Anderson Cancer Center. Compliance was defined as a patient with 1 risk factor for PONV receiving at least 1 antiemetic, 2 risk factors receiving at least 2 antiemetics, and 3 risk factors receiving at least 3 antiemetics. Drugs of the same class were counted as single antiemetic administration. Propofol-based anesthetic techniques were counted as receiving 1 antiemetic. Patients with 0 risk factors for PONV were not included. We estimated the compliance rates for each of the 4 time periods of the study adjusting for multiple observations on the same clinician. Individual performance feedback was given once at 6 months after intervention I coincident with a refresher presentation on PONV (start of intervention II) and on an ongoing quarterly basis during intervention III. Compliance rates were not significantly influenced with CME (intervention I) compared with baseline behavior (54.5% vs 54.4%, P = 0.9140). Significant improvement occurred during the time period when CME was paired with performance data (intervention II) compared with intervention I (59.2% vs 54.4%, P = 0.0002). Further significant improvement occurred when data alone were presented (intervention III) compared with intervention II (65.1% vs 59.2%, P < 0.0001). For patients with 3 risk factors, we saw significant improvement in compliance rates during intervention III (P = 0.0002). In post hoc analysis of overtreatment, the percentage differences between the baseline and time period III decreased as the number of risk factors increased.\n Question: Does ongoing provision of individual clinician performance data improve practice behavior?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Clinical practice guidelines summarize evidence from science and attempt to translate those findings into clinical practice. Pervasive and consistent adoption of these guidelines into daily provider practice has proven slow. Using postoperative nausea and vomiting (PONV) prophylaxis guideline compliance as our metric, we compared the effects of continuing medical education (CME) alone (I), CME with a single snapshot of provider compliance (II), and ongoing reporting of provider compliance data without further CME (III). We retrospectively analyzed guideline compliance of 23,279 anesthetics at the University of Texas M.D. Anderson Cancer Center. Compliance was defined as a patient with 1 risk factor for PONV receiving at least 1 antiemetic, 2 risk factors receiving at least 2 antiemetics, and 3 risk factors receiving at least 3 antiemetics. Drugs of the same class were counted as single antiemetic administration. Propofol-based anesthetic techniques were counted as receiving 1 antiemetic. Patients with 0 risk factors for PONV were not included. We estimated the compliance rates for each of the 4 time periods of the study adjusting for multiple observations on the same clinician. Individual performance feedback was given once at 6 months after intervention I coincident with a refresher presentation on PONV (start of intervention II) and on an ongoing quarterly basis during intervention III. Compliance rates were not significantly influenced with CME (intervention I) compared with baseline behavior (54.5% vs 54.4%, P = 0.9140). Significant improvement occurred during the time period when CME was paired with performance data (intervention II) compared with intervention I (59.2% vs 54.4%, P = 0.0002). Further significant improvement occurred when data alone were presented (intervention III) compared with intervention II (65.1% vs 59.2%, P < 0.0001). For patients with 3 risk factors, we saw significant improvement in compliance rates during intervention III (P = 0.0002). In post hoc analysis of overtreatment, the percentage differences between the baseline and time period III decreased as the number of risk factors increased.
Question: Does ongoing provision of individual clinician performance data improve practice behavior?
Output:
|
PubmedQA209494
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: This study was undertaken to investigate the ability of a high-pressure CO2 environment to aerosolize tumor cells in both in vitro and in vivo models. (An aerosol is defined as a stable gaseous suspension of insoluble particles). Also, this study was designed to determine if rapid desufflation is capable of transporting fluid laden with tumor cells. The four in vitro aerosol experiments were performed in an 18.9-1 plastic vessel fitted with two 7-mm ports and a compliant latex balloon affixed to the top. After CO2 insufflation, the vessel was desufflated through a sterile soluset containing 25 ml of culture media that was subsequently emptied into a culture dish, incubated for two weeks, and periodically assessed for growth. At the bottom of the vessel, one of the following was placed: Study 1 and 2, a suspension of B16 melanoma or colon 26 tumor cells in liquid culture media; Study 3, colon 26 cells in saline solution; Study 4, several pieces of solid colon 26 tumor. In Studies 1 to 3, cell preparations were subjected to the following high-pressure CO2 conditions (pneumo): 1) static pneumo of 15 and 30 mmHg (10 minute dwell); 2) a continuous flow (CF) of CO2 (1O l) while maintaining a pressure of 15 or 30 mmHg in the vessel. In Study 4, only the 30 mmHg static and CF conditions were tested. Between 6 and 12 determinations were performed for each condition and cell preparation. In vivo aerosol experiments consisted of Spraque Dawley rats that received intraperitoneal injections of 10-5 B16 cells in 0.1 ml of liquid media. Two laparoscopic ports were placed in the abdomen, one each for insufflation and desufflation. Study groups were: 1, static CO2 pneumo of 15 mmHg; 2 and 3, continuous CO2 flow (10 l) at a stable pneumo pressure of 5 and 10 mmHg. Desufflation was performed via the same collecting device and handled in an identical manner to the in vitro experiments described above. The in vitro balloon experiment was designed to investigate the ability of desufflation to transport fluid-containing tumor cells; latex balloon model was used. To prevent complete loss of volume on desufflation, a wire coil was placed inside the balloon. Twenty ml of media containing 20 x 10(-6) B16 cells was placed in the bottom of the balloon. The balloon was insufflated with 1 to 2 l of gas. There were three study groups that differed in the degree to which the cell suspension was agitated before desufflation. Study conditions were as follows: 1) no agitation; 2) moderate agitation to coat the lower walls and coil; 3) maximum agitation to coat the entire balloon. To verify the viability of tumor cells, at the end of each in vitro and in vivo study, a sample of tumor cells or peritoneal washing was incubated in sterile media. These samples served as positive controls. In vitro aerosol studies consisted of the following. At the end of two weeks of incubation, no tumor growth was noted in any of the 124 test dishes. The 14 control samples all demonstrated tumor growth. In vivo aerosol studies consisted of the following. Zero of 18 experimental dishes grew tumor. All three peritoneal washing samples demonstrated growth. In vitro balloon studies consisted of the following. Zero of 12 test dishes in Groups 1 and 2 demonstrated growth, whereas five of six dishes did so in Group 3 (maximally agitated before desufflation). Again, positive controls all grew tumor cells.\n Question: Is trocar site recurrence unlikely to result from aerosolization of tumor cells?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: This study was undertaken to investigate the ability of a high-pressure CO2 environment to aerosolize tumor cells in both in vitro and in vivo models. (An aerosol is defined as a stable gaseous suspension of insoluble particles). Also, this study was designed to determine if rapid desufflation is capable of transporting fluid laden with tumor cells. The four in vitro aerosol experiments were performed in an 18.9-1 plastic vessel fitted with two 7-mm ports and a compliant latex balloon affixed to the top. After CO2 insufflation, the vessel was desufflated through a sterile soluset containing 25 ml of culture media that was subsequently emptied into a culture dish, incubated for two weeks, and periodically assessed for growth. At the bottom of the vessel, one of the following was placed: Study 1 and 2, a suspension of B16 melanoma or colon 26 tumor cells in liquid culture media; Study 3, colon 26 cells in saline solution; Study 4, several pieces of solid colon 26 tumor. In Studies 1 to 3, cell preparations were subjected to the following high-pressure CO2 conditions (pneumo): 1) static pneumo of 15 and 30 mmHg (10 minute dwell); 2) a continuous flow (CF) of CO2 (1O l) while maintaining a pressure of 15 or 30 mmHg in the vessel. In Study 4, only the 30 mmHg static and CF conditions were tested. Between 6 and 12 determinations were performed for each condition and cell preparation. In vivo aerosol experiments consisted of Spraque Dawley rats that received intraperitoneal injections of 10-5 B16 cells in 0.1 ml of liquid media. Two laparoscopic ports were placed in the abdomen, one each for insufflation and desufflation. Study groups were: 1, static CO2 pneumo of 15 mmHg; 2 and 3, continuous CO2 flow (10 l) at a stable pneumo pressure of 5 and 10 mmHg. Desufflation was performed via the same collecting device and handled in an identical manner to the in vitro experiments described above. The in vitro balloon experiment was designed to investigate the ability of desufflation to transport fluid-containing tumor cells; latex balloon model was used. To prevent complete loss of volume on desufflation, a wire coil was placed inside the balloon. Twenty ml of media containing 20 x 10(-6) B16 cells was placed in the bottom of the balloon. The balloon was insufflated with 1 to 2 l of gas. There were three study groups that differed in the degree to which the cell suspension was agitated before desufflation. Study conditions were as follows: 1) no agitation; 2) moderate agitation to coat the lower walls and coil; 3) maximum agitation to coat the entire balloon. To verify the viability of tumor cells, at the end of each in vitro and in vivo study, a sample of tumor cells or peritoneal washing was incubated in sterile media. These samples served as positive controls. In vitro aerosol studies consisted of the following. At the end of two weeks of incubation, no tumor growth was noted in any of the 124 test dishes. The 14 control samples all demonstrated tumor growth. In vivo aerosol studies consisted of the following. Zero of 18 experimental dishes grew tumor. All three peritoneal washing samples demonstrated growth. In vitro balloon studies consisted of the following. Zero of 12 test dishes in Groups 1 and 2 demonstrated growth, whereas five of six dishes did so in Group 3 (maximally agitated before desufflation). Again, positive controls all grew tumor cells.
Question: Is trocar site recurrence unlikely to result from aerosolization of tumor cells?
Output:
|
PubmedQA63893
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Prospective memory, or remembering to do things in the future, is crucial for independent living in old age. Although there is evidence of substantial age-related deficits in memory for intentions, older adults have demonstrated the ability to compensate for their deficits in everyday life. The present study investigated feedback as a strategy for facilitating prospective memory in the elderly. Young and older adults played a computer-based task, Virtual Week, in which they had to remember to carry out life-like intentions. After each virtual day, specific feedback on prospective memory performance was automatically provided on the computer screen that participants either proceeded through by themselves (non-social feedback) or were taken through by an experimenter (social feedback). The control group received no feedback. We found that, compared with no-feedback group, only social feedback substantially reduced the age-related deficit in prospective memory. Older adults significantly benefited from feedback provided by the experimenter on the tasks of intermediate difficulty. Unexpectedly, prospective memory with non-social feedback was not only worse than with social feedback, but it was not any better than without any feedback at all.\n Question: Does only social feedback reduce age-related prospective memory deficits in `` Virtual Week ''?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Prospective memory, or remembering to do things in the future, is crucial for independent living in old age. Although there is evidence of substantial age-related deficits in memory for intentions, older adults have demonstrated the ability to compensate for their deficits in everyday life. The present study investigated feedback as a strategy for facilitating prospective memory in the elderly. Young and older adults played a computer-based task, Virtual Week, in which they had to remember to carry out life-like intentions. After each virtual day, specific feedback on prospective memory performance was automatically provided on the computer screen that participants either proceeded through by themselves (non-social feedback) or were taken through by an experimenter (social feedback). The control group received no feedback. We found that, compared with no-feedback group, only social feedback substantially reduced the age-related deficit in prospective memory. Older adults significantly benefited from feedback provided by the experimenter on the tasks of intermediate difficulty. Unexpectedly, prospective memory with non-social feedback was not only worse than with social feedback, but it was not any better than without any feedback at all.
Question: Does only social feedback reduce age-related prospective memory deficits in `` Virtual Week ''?
Output:
|
PubmedQA158927
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The variation in serum uric acid concentrations is under significant genetic influence. Elevated SUA concentrations have been linked to increased risk for gout, kidney stones, chronic kidney disease, and cardiovascular disease whereas reduced serum uric acid concentrations have been linked to multiple sclerosis, Parkinson's disease and Alzheimer's disease. Previously, we identified a novel locus on chromosome 3p26 affecting serum uric acid concentrations in Mexican Americans from San Antonio Family Heart Study. As a follow up, we examined genome-wide single nucleotide polymorphism data in an extended cohort of 1281 Mexican Americans from multigenerational families of the San Antonio Family Heart Study and the San Antonio Family Diabetes/Gallbladder Study. We used a linear regression-based joint linkage/association test under an additive model of allelic effect, while accounting for non-independence among family members via a kinship variance component. Univariate genetic analysis indicated serum uric acid concentrations to be significant heritable (h (2) = 0.50 ± 0.05, p < 4 × 10(-35)), and linkage analysis of serum uric acid concentrations confirmed our previous finding of a novel locus on 3p26 (LOD = 4.9, p < 1 × 10(-5)) in the extended sample. Additionally, we observed strong association of serum uric acid concentrations with variants in following candidate genes in the 3p26 region; inositol 1,4,5-trisphosphate receptor, type 1 (ITPR1), contactin 4 (CNTN4), decapping mRNA 1A (DCP1A); transglutaminase 4 (TGM4) and rho guanine nucleotide exchange factor (GEF) 26 (ARHGEF26) [p < 3 × 10(-7); minor allele frequencies ranged between 0.003 and 0.42] and evidence of cis-regulation for ITPR1 transcripts.\n Question: Do gWAS and transcriptional analysis prioritize ITPR1 and CNTN4 for a serum uric acid 3p26 QTL in Mexican Americans?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: The variation in serum uric acid concentrations is under significant genetic influence. Elevated SUA concentrations have been linked to increased risk for gout, kidney stones, chronic kidney disease, and cardiovascular disease whereas reduced serum uric acid concentrations have been linked to multiple sclerosis, Parkinson's disease and Alzheimer's disease. Previously, we identified a novel locus on chromosome 3p26 affecting serum uric acid concentrations in Mexican Americans from San Antonio Family Heart Study. As a follow up, we examined genome-wide single nucleotide polymorphism data in an extended cohort of 1281 Mexican Americans from multigenerational families of the San Antonio Family Heart Study and the San Antonio Family Diabetes/Gallbladder Study. We used a linear regression-based joint linkage/association test under an additive model of allelic effect, while accounting for non-independence among family members via a kinship variance component. Univariate genetic analysis indicated serum uric acid concentrations to be significant heritable (h (2) = 0.50 ± 0.05, p < 4 × 10(-35)), and linkage analysis of serum uric acid concentrations confirmed our previous finding of a novel locus on 3p26 (LOD = 4.9, p < 1 × 10(-5)) in the extended sample. Additionally, we observed strong association of serum uric acid concentrations with variants in following candidate genes in the 3p26 region; inositol 1,4,5-trisphosphate receptor, type 1 (ITPR1), contactin 4 (CNTN4), decapping mRNA 1A (DCP1A); transglutaminase 4 (TGM4) and rho guanine nucleotide exchange factor (GEF) 26 (ARHGEF26) [p < 3 × 10(-7); minor allele frequencies ranged between 0.003 and 0.42] and evidence of cis-regulation for ITPR1 transcripts.
Question: Do gWAS and transcriptional analysis prioritize ITPR1 and CNTN4 for a serum uric acid 3p26 QTL in Mexican Americans?
Output:
|
PubmedQA141388
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Anti-CD3 immunotoxin (IT), a T-cell-depleting agent, prolongs survival of renal allografts in a rhesus monkey model without the need for long-term immunosuppression. In this study we sought to further prolong allograft survival by giving short-term conventional immunosuppression simultaneous with IT administration. MHC class II mismatched, juvenile rhesus monkeys were paired as donor and recipient for renal transplantation. Recipients received two to three daily doses of IT starting on the day of transplantation. Additional immunosuppression was given for no more than 60 days. Graft function was monitored by serum creatinine and renal biopsies. Flow cytometry was used to monitor T-cell recovery. Graft survival time (GST) in animals receiving IT was prolonged compared with controls with 50% of IT-treated monkeys surviving >100 days. Animals treated with IT plus mycophenolate mofetil (MMF) and steroids had significantly enhanced GST (mean GST, 305 days) compared with those treated with IT alone (mean GST, 94 days). In contrast, addition of cyclosporine or 40-O-[2-Hydroxyethyl]rapamycin did not significantly increase graft survival time. A comparison among animals from all treatment groups with short (<100 days) and long (>100 days) GST demonstrated that those with the shorter GST had a higher blood T-cell count 2 weeks after transplantation. Full recovery of CD4+ T cells required longer than 6 months.\n Question: Is graft survival in a rhesus renal transplant model after immunotoxin-mediated T-cell depletion enhanced by mycophenolate and steroids?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Anti-CD3 immunotoxin (IT), a T-cell-depleting agent, prolongs survival of renal allografts in a rhesus monkey model without the need for long-term immunosuppression. In this study we sought to further prolong allograft survival by giving short-term conventional immunosuppression simultaneous with IT administration. MHC class II mismatched, juvenile rhesus monkeys were paired as donor and recipient for renal transplantation. Recipients received two to three daily doses of IT starting on the day of transplantation. Additional immunosuppression was given for no more than 60 days. Graft function was monitored by serum creatinine and renal biopsies. Flow cytometry was used to monitor T-cell recovery. Graft survival time (GST) in animals receiving IT was prolonged compared with controls with 50% of IT-treated monkeys surviving >100 days. Animals treated with IT plus mycophenolate mofetil (MMF) and steroids had significantly enhanced GST (mean GST, 305 days) compared with those treated with IT alone (mean GST, 94 days). In contrast, addition of cyclosporine or 40-O-[2-Hydroxyethyl]rapamycin did not significantly increase graft survival time. A comparison among animals from all treatment groups with short (<100 days) and long (>100 days) GST demonstrated that those with the shorter GST had a higher blood T-cell count 2 weeks after transplantation. Full recovery of CD4+ T cells required longer than 6 months.
Question: Is graft survival in a rhesus renal transplant model after immunotoxin-mediated T-cell depletion enhanced by mycophenolate and steroids?
Output:
|
PubmedQA43511
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: In our study, we describe the use of spider silk fibres as a new material in nerve tissue engineering, in a 20-mm sciatic nerve defect in rats. We compared isogenic nerve grafts to vein grafts with spider silk fibres, either alone or supplemented with Schwann cells, or Schwann cells and matrigel. Controls, consisting of veins and matrigel, were transplanted. After 6 months, regeneration was evaluated for clinical outcome, as well as for histological and morphometrical performance. Nerve regeneration was achieved with isogenic nerve grafts as well as with all constructs, but not in the control group. Effective regeneration by isogenic nerve grafts and grafts containing spider silk was corroborated by diminished degeneration of the gastrocnemius muscle and by good histological evaluation results. Nerves stained for S-100 and neurofilament indicated existence of Schwann cells and axonal re-growth. Axons were aligned regularly and had a healthy appearance on ultrastructural examination. Interestingly, in contrast to recently published studies, we found that bridging an extensive gap by cell-free constructs based on vein and spider silk was highly effective in nerve regeneration.\n Question: Do spider silk fibres in artificial nerve constructs promote peripheral nerve regeneration?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: In our study, we describe the use of spider silk fibres as a new material in nerve tissue engineering, in a 20-mm sciatic nerve defect in rats. We compared isogenic nerve grafts to vein grafts with spider silk fibres, either alone or supplemented with Schwann cells, or Schwann cells and matrigel. Controls, consisting of veins and matrigel, were transplanted. After 6 months, regeneration was evaluated for clinical outcome, as well as for histological and morphometrical performance. Nerve regeneration was achieved with isogenic nerve grafts as well as with all constructs, but not in the control group. Effective regeneration by isogenic nerve grafts and grafts containing spider silk was corroborated by diminished degeneration of the gastrocnemius muscle and by good histological evaluation results. Nerves stained for S-100 and neurofilament indicated existence of Schwann cells and axonal re-growth. Axons were aligned regularly and had a healthy appearance on ultrastructural examination. Interestingly, in contrast to recently published studies, we found that bridging an extensive gap by cell-free constructs based on vein and spider silk was highly effective in nerve regeneration.
Question: Do spider silk fibres in artificial nerve constructs promote peripheral nerve regeneration?
Output:
|
PubmedQA170307
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To investigate the effect of pre-freezing equilibration on the cryo-survival of human sperm and to optimize the protocol of direct fumigation for the freeze-thawing of human sperm. We collected 50 semen samples from healthy donors, each subjected to cryopreservation with 3 different methods: non-equilibration freezing (Group A), 10-min equilibration at room temperature before freezing (Group B), and 10-min equilibration at 4 degrees C before freezing (Group C). We examined all the post-thaw semen samples by computer-assisted semen analysis for the sperm motility parameters, and detected the sperm vitality and deformity index (SDI). The recovery rate of progressive sperm motility was (61.88 +/- 16.94)% in Group C, remarkably higher than in A ([48.61 +/- 16.44]%) and B ([49.41 +/- 13.77]%) (P < 0.05), but with no significant difference between the latter two. And there were no significant differences in sperm vitality and SDI among the three groups.\n Question: Does [ Pre-freezing equilibration improve post-thaw human semen parameters ]?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To investigate the effect of pre-freezing equilibration on the cryo-survival of human sperm and to optimize the protocol of direct fumigation for the freeze-thawing of human sperm. We collected 50 semen samples from healthy donors, each subjected to cryopreservation with 3 different methods: non-equilibration freezing (Group A), 10-min equilibration at room temperature before freezing (Group B), and 10-min equilibration at 4 degrees C before freezing (Group C). We examined all the post-thaw semen samples by computer-assisted semen analysis for the sperm motility parameters, and detected the sperm vitality and deformity index (SDI). The recovery rate of progressive sperm motility was (61.88 +/- 16.94)% in Group C, remarkably higher than in A ([48.61 +/- 16.44]%) and B ([49.41 +/- 13.77]%) (P < 0.05), but with no significant difference between the latter two. And there were no significant differences in sperm vitality and SDI among the three groups.
Question: Does [ Pre-freezing equilibration improve post-thaw human semen parameters ]?
Output:
|
PubmedQA24104
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To characterize nocturia in men based on frequency volume chart data and symptom profiles assessed using the Core Lower Urinary Tract Symptom Score and Athens Insomnia Scale questionnaires. The Core Lower Urinary Tract Symptom Score and Athens Insomnia Scale questionnaires were administered to 299 consecutive treatment naïve men with nocturia (≥one time per night). Frequency volume chart data were recorded for 2 days. Correlations between nocturia and clinical characteristics including symptom scores, clinical diagnosis, Charlson Comorbidity Index, estimated glomerular filtration rate, uroflowmetry and prostate volume were analyzed. Patients were divided into five groups: one time (n = 36), two times (n = 65), three times (n = 85), four times (n = 78) and five times (n = 34) of nocturia. Age, prevalence or severity of chronic kidney disease, hyperlipidemia, low bladder capacity, nocturnal polyuria, urgency, bladder pain and sleep disorders were significantly correlated with the severity of nocturia. The Spearman correlation analysis identified eight possible independent factors for nocturia: age, estimated glomerular filtration rate, urgency, bladder pain, sleep quality, sleepiness during the day, average voided volume and nocturnal volume divided by body weight. Logistic regression analysis showed that nocturnal volume divided by body weight was the strongest factor of nocturia, and ≥7, 9 and 9.7 mL/kg were practical cut-off values of three, four and five times per night of nocturia, respectively.\n Question: Is nocturia in men a chaotic condition dominated by nocturnal polyuria?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To characterize nocturia in men based on frequency volume chart data and symptom profiles assessed using the Core Lower Urinary Tract Symptom Score and Athens Insomnia Scale questionnaires. The Core Lower Urinary Tract Symptom Score and Athens Insomnia Scale questionnaires were administered to 299 consecutive treatment naïve men with nocturia (≥one time per night). Frequency volume chart data were recorded for 2 days. Correlations between nocturia and clinical characteristics including symptom scores, clinical diagnosis, Charlson Comorbidity Index, estimated glomerular filtration rate, uroflowmetry and prostate volume were analyzed. Patients were divided into five groups: one time (n = 36), two times (n = 65), three times (n = 85), four times (n = 78) and five times (n = 34) of nocturia. Age, prevalence or severity of chronic kidney disease, hyperlipidemia, low bladder capacity, nocturnal polyuria, urgency, bladder pain and sleep disorders were significantly correlated with the severity of nocturia. The Spearman correlation analysis identified eight possible independent factors for nocturia: age, estimated glomerular filtration rate, urgency, bladder pain, sleep quality, sleepiness during the day, average voided volume and nocturnal volume divided by body weight. Logistic regression analysis showed that nocturnal volume divided by body weight was the strongest factor of nocturia, and ≥7, 9 and 9.7 mL/kg were practical cut-off values of three, four and five times per night of nocturia, respectively.
Question: Is nocturia in men a chaotic condition dominated by nocturnal polyuria?
Output:
|
PubmedQA126181
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Cystoisosporiasis is an opportunistic infection seen more commonly in patients with acquired immunodeficiency syndrome. Although uncommon, Cystoisospora infection can occur in immunocompetent individuals but tend to be benign and self-limiting. Chronic infection however, has been described but diagnosis can often be challenging and requires a high clinical index of suspicion. We present a case of delayed diagnosis of Cystoisospora belli (C. belli) in an immunocompetent 28-year-old refugee from Myanmar. She had a history of chronic diarrhea where exhaustive investigations over many years failed to reveal a diagnosis. Cystoisospora belli cysts were finally detected in stool 4 years after investigation commenced, and PCR testing on stored colon biopsies amplified a molecular product with 99 % sequence homology to C. belli. The patient improved promptly with trimethoprim-sulfamethoxazole treatment.\n Question: Is chronic Cystoisospora belli infection in an immunocompetent Myanmar refugee - microscopy sensitive enough?\n Output: "
},
{
"role": "assistant",
"content": "no"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Cystoisosporiasis is an opportunistic infection seen more commonly in patients with acquired immunodeficiency syndrome. Although uncommon, Cystoisospora infection can occur in immunocompetent individuals but tend to be benign and self-limiting. Chronic infection however, has been described but diagnosis can often be challenging and requires a high clinical index of suspicion. We present a case of delayed diagnosis of Cystoisospora belli (C. belli) in an immunocompetent 28-year-old refugee from Myanmar. She had a history of chronic diarrhea where exhaustive investigations over many years failed to reveal a diagnosis. Cystoisospora belli cysts were finally detected in stool 4 years after investigation commenced, and PCR testing on stored colon biopsies amplified a molecular product with 99 % sequence homology to C. belli. The patient improved promptly with trimethoprim-sulfamethoxazole treatment.
Question: Is chronic Cystoisospora belli infection in an immunocompetent Myanmar refugee - microscopy sensitive enough?
Output:
|
PubmedQA195656
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Evidence reveals that histone deacetylase (HDAC) inhibition has potential for the treatment of inflammatory diseases. The protective effect of HDAC inhibition involves multiple mechanisms. Heme oxygenase-1 (HO-1) is protective in lung injury as a key regulator of antioxidant response. The authors examined whether HDAC inhibition provided protection against ischemia-reperfusion (I/R) lung injury in rats by up-regulating HO-1 activity. Acute lung injury was induced by producing 40 min of ischemia followed by 60 min of reperfusion in isolated perfused rat lungs. The rats were randomly allotted to control group, I/R group, or I/R + valproic acid (VPA) group with or without an HO-1 activity inhibitor (zinc protoporphyrin IX) (n = 6 per group). I/R caused significant increases in the lung edema, pulmonary arterial pressure, lung injury scores, tumor necrosis factor-α, and cytokine-induced neutrophil chemoattractant-1 concentrations in bronchoalveolar lavage fluid. Malondialdehyde levels, carbonyl contents, and myeloperoxidase-positive cells in lung tissue were also significantly increased. I/R stimulated the degradation of inhibitor of nuclear factor-κB-α, nuclear translocation of nuclear factor-κB, and up-regulation of HO-1 activity. Furthermore, I/R decreased B-cell lymphoma-2, heat shock protein 70, acetylated histone H3 protein expression, and increased the caspase-3 activity in the rat lungs. In contrast, VPA treatment significantly attenuated all the parameters of lung injury, oxidative stress, apoptosis, and inflammation. In addition, VPA treatment also enhanced HO-1 activity. Treatment with zinc protoporphyrin IX blocked the protective effect of VPA.\n Question: Does valproic acid attenuate acute lung injury induced by ischemia-reperfusion in rats?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Evidence reveals that histone deacetylase (HDAC) inhibition has potential for the treatment of inflammatory diseases. The protective effect of HDAC inhibition involves multiple mechanisms. Heme oxygenase-1 (HO-1) is protective in lung injury as a key regulator of antioxidant response. The authors examined whether HDAC inhibition provided protection against ischemia-reperfusion (I/R) lung injury in rats by up-regulating HO-1 activity. Acute lung injury was induced by producing 40 min of ischemia followed by 60 min of reperfusion in isolated perfused rat lungs. The rats were randomly allotted to control group, I/R group, or I/R + valproic acid (VPA) group with or without an HO-1 activity inhibitor (zinc protoporphyrin IX) (n = 6 per group). I/R caused significant increases in the lung edema, pulmonary arterial pressure, lung injury scores, tumor necrosis factor-α, and cytokine-induced neutrophil chemoattractant-1 concentrations in bronchoalveolar lavage fluid. Malondialdehyde levels, carbonyl contents, and myeloperoxidase-positive cells in lung tissue were also significantly increased. I/R stimulated the degradation of inhibitor of nuclear factor-κB-α, nuclear translocation of nuclear factor-κB, and up-regulation of HO-1 activity. Furthermore, I/R decreased B-cell lymphoma-2, heat shock protein 70, acetylated histone H3 protein expression, and increased the caspase-3 activity in the rat lungs. In contrast, VPA treatment significantly attenuated all the parameters of lung injury, oxidative stress, apoptosis, and inflammation. In addition, VPA treatment also enhanced HO-1 activity. Treatment with zinc protoporphyrin IX blocked the protective effect of VPA.
Question: Does valproic acid attenuate acute lung injury induced by ischemia-reperfusion in rats?
Output:
|
PubmedQA38351
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: DNA microarrays provide a powerful method for global analysis of gene expression. The application of this technology to specific cell types and tissues, however, is typically limited by small amounts of available mRNA, thereby necessitating amplification. Here we compare microarray results obtained with two different methods of RNA amplification to profile gene expression in the C. elegans larval nervous system. We used the mRNA-tagging strategy to isolate transcripts specifically from C. elegans larval neurons. The WT-Ovation Pico System (WT-Pico) was used to amplify 2 ng of pan-neural RNA to produce labeled cDNA for microarray analysis. These WT-Pico-derived data were compared to microarray results obtained with a labeled aRNA target generated by two rounds of In Vitro Transcription (IVT) of 25 ng of pan-neural RNA. WT-Pico results in a higher fraction of present calls than IVT, a finding consistent with the proposal that DNA-DNA hybridization results in lower mismatch signals than the RNA-DNA heteroduplexes produced by IVT amplification. Microarray data sets from these samples were compared to a reference profile of all larval cells to identify transcripts with elevated expression in neurons. These results were validated by the high proportion of known neuron-expressed genes detected in these profiles and by promoter-GFP constructs for previously uncharacterized genes in these data sets. Together, the IVT and WT-Pico methods identified 2,173 unique neuron-enriched transcripts. Only about half of these transcripts (1,044), however, are detected as enriched by both IVT and WT-Pico amplification.\n Question: Do complementary RNA amplification methods enhance microarray identification of transcripts expressed in the C. elegans nervous system?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: DNA microarrays provide a powerful method for global analysis of gene expression. The application of this technology to specific cell types and tissues, however, is typically limited by small amounts of available mRNA, thereby necessitating amplification. Here we compare microarray results obtained with two different methods of RNA amplification to profile gene expression in the C. elegans larval nervous system. We used the mRNA-tagging strategy to isolate transcripts specifically from C. elegans larval neurons. The WT-Ovation Pico System (WT-Pico) was used to amplify 2 ng of pan-neural RNA to produce labeled cDNA for microarray analysis. These WT-Pico-derived data were compared to microarray results obtained with a labeled aRNA target generated by two rounds of In Vitro Transcription (IVT) of 25 ng of pan-neural RNA. WT-Pico results in a higher fraction of present calls than IVT, a finding consistent with the proposal that DNA-DNA hybridization results in lower mismatch signals than the RNA-DNA heteroduplexes produced by IVT amplification. Microarray data sets from these samples were compared to a reference profile of all larval cells to identify transcripts with elevated expression in neurons. These results were validated by the high proportion of known neuron-expressed genes detected in these profiles and by promoter-GFP constructs for previously uncharacterized genes in these data sets. Together, the IVT and WT-Pico methods identified 2,173 unique neuron-enriched transcripts. Only about half of these transcripts (1,044), however, are detected as enriched by both IVT and WT-Pico amplification.
Question: Do complementary RNA amplification methods enhance microarray identification of transcripts expressed in the C. elegans nervous system?
Output:
|
PubmedQA68707
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To examine whether pain sensitivity and pain catastrophizing are associated with persistent pain and disability after lumbar spine surgery. Prospective observational cohort study. Academic medical center. Patients (N=68; mean age, 57.9±13.1y; 40 women [58.8%]) undergoing spine surgery for a degenerative condition from March 1, 2012 to April 30, 2013 were assessed 6 weeks, 3 months, and 6 months after surgery. Not applicable. The main outcome measures were persistent back pain intensity, pain interference, and disability. Patients with persistent back pain intensity, pain interference, or disability were identified as those patients reporting Brief Pain Inventory scores ≥4 and Oswestry Disability Index scores ≥21 at all postoperative time points. From 6 weeks to 6 months after surgery, approximately 12.9%, 24.2%, and 46.8% of patients reported persistent back pain intensity, pain interference, or disability, respectively. Increased pain sensitivity at 6 weeks was associated with having persistent back pain intensity (odds ratio [OR], 2.0; 95% confidence interval [CI], 1.0-4.1) after surgery. Increased pain catastrophizing at 6 weeks was associated with having persistent back pain intensity (OR, 1.1; 95% CI, 1.0-1.2), pain interference (OR, 1.1; 95% CI, 1.0-1.2), and disability (OR, 1.3; 95% CI, 1.1-1.4). An interaction effect was not found between pain sensitivity and pain catastrophizing on persistent outcomes (P>.05).\n Question: Do pain Sensitivity and Pain Catastrophizing Are Associated With Persistent Pain and Disability After Lumbar Spine Surgery?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To examine whether pain sensitivity and pain catastrophizing are associated with persistent pain and disability after lumbar spine surgery. Prospective observational cohort study. Academic medical center. Patients (N=68; mean age, 57.9±13.1y; 40 women [58.8%]) undergoing spine surgery for a degenerative condition from March 1, 2012 to April 30, 2013 were assessed 6 weeks, 3 months, and 6 months after surgery. Not applicable. The main outcome measures were persistent back pain intensity, pain interference, and disability. Patients with persistent back pain intensity, pain interference, or disability were identified as those patients reporting Brief Pain Inventory scores ≥4 and Oswestry Disability Index scores ≥21 at all postoperative time points. From 6 weeks to 6 months after surgery, approximately 12.9%, 24.2%, and 46.8% of patients reported persistent back pain intensity, pain interference, or disability, respectively. Increased pain sensitivity at 6 weeks was associated with having persistent back pain intensity (odds ratio [OR], 2.0; 95% confidence interval [CI], 1.0-4.1) after surgery. Increased pain catastrophizing at 6 weeks was associated with having persistent back pain intensity (OR, 1.1; 95% CI, 1.0-1.2), pain interference (OR, 1.1; 95% CI, 1.0-1.2), and disability (OR, 1.3; 95% CI, 1.1-1.4). An interaction effect was not found between pain sensitivity and pain catastrophizing on persistent outcomes (P>.05).
Question: Do pain Sensitivity and Pain Catastrophizing Are Associated With Persistent Pain and Disability After Lumbar Spine Surgery?
Output:
|
PubmedQA42801
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To create a fast, sensitive and specific method for identifying Fusarium oxysporum f. sp. cucumerinum and F. o. luffae. Specific DNA bands were selected as probes from RAPD profiles of 13 formae speciales of F. oxysporum. The forma specialis-specific probe OPC18300c and OPC18520f could be used to identify F. o. cucumerinum and F. o. luffae by RAPD-PCR followed dot blot hybridization, respectively.\n Question: Do identification of F. o. cucumerinum and F. o. luffae by RAPD-generated DNA probes?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To create a fast, sensitive and specific method for identifying Fusarium oxysporum f. sp. cucumerinum and F. o. luffae. Specific DNA bands were selected as probes from RAPD profiles of 13 formae speciales of F. oxysporum. The forma specialis-specific probe OPC18300c and OPC18520f could be used to identify F. o. cucumerinum and F. o. luffae by RAPD-PCR followed dot blot hybridization, respectively.
Question: Do identification of F. o. cucumerinum and F. o. luffae by RAPD-generated DNA probes?
Output:
|
PubmedQA48175
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Cytokines and chemokines are key mediators of anti-malarial immunity. We evaluated whether Intermittent Preventive Treatment in infants with Sulfadoxine-Pyrimethamine (IPTi-SP) had an effect on the acquisition of these cellular immune responses in Mozambican children. Multiple cytokines and chemokines were quantified in plasma by luminex, and antigen-specific cytokine production in whole blood was determined by intracellular cytokine staining and flow cytometry, at ages 5, 9, 12 and 24 months. IPTi-SP did not significantly affect the proportion of CD3+ cells producing IFN-γ, IL-4 or IL-10. Overall, plasma cytokine or chemokine concentrations did not differ between treatment groups. Th1 and pro-inflammatory responses were higher than Th2 and anti-inflammatory responses, respectively, and IFN-γ:IL-4 ratios were higher for placebo than for SP recipients. Levels of cytokines and chemokines varied according to age, declining from 5 to 9 months. Plasma concentrations of IL-10, IL-12 and IL-13 were associated with current infection or prior malaria episodes. Higher frequencies of IFN-γ and IL-10 producing CD3+ cells and elevated IL-10, IFN-γ, MCP-1 and IL-13 in plasma were individually associated with increased malaria incidence, at different time points. When all markers were analyzed together, only higher IL-17 at 12 months was associated with lower incidence of malaria up to 24 months.\n Question: Does intermittent preventive treatment with sulfadoxine-pyrimethamine modify plasma cytokines and chemokines or intracellular cytokine responses to Plasmodium falciparum in Mozambican children?\n Output: "
},
{
"role": "assistant",
"content": "no"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Cytokines and chemokines are key mediators of anti-malarial immunity. We evaluated whether Intermittent Preventive Treatment in infants with Sulfadoxine-Pyrimethamine (IPTi-SP) had an effect on the acquisition of these cellular immune responses in Mozambican children. Multiple cytokines and chemokines were quantified in plasma by luminex, and antigen-specific cytokine production in whole blood was determined by intracellular cytokine staining and flow cytometry, at ages 5, 9, 12 and 24 months. IPTi-SP did not significantly affect the proportion of CD3+ cells producing IFN-γ, IL-4 or IL-10. Overall, plasma cytokine or chemokine concentrations did not differ between treatment groups. Th1 and pro-inflammatory responses were higher than Th2 and anti-inflammatory responses, respectively, and IFN-γ:IL-4 ratios were higher for placebo than for SP recipients. Levels of cytokines and chemokines varied according to age, declining from 5 to 9 months. Plasma concentrations of IL-10, IL-12 and IL-13 were associated with current infection or prior malaria episodes. Higher frequencies of IFN-γ and IL-10 producing CD3+ cells and elevated IL-10, IFN-γ, MCP-1 and IL-13 in plasma were individually associated with increased malaria incidence, at different time points. When all markers were analyzed together, only higher IL-17 at 12 months was associated with lower incidence of malaria up to 24 months.
Question: Does intermittent preventive treatment with sulfadoxine-pyrimethamine modify plasma cytokines and chemokines or intracellular cytokine responses to Plasmodium falciparum in Mozambican children?
Output:
|
PubmedQA166316
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The aim was to assess the effect of dietary patterns on postpartum body weight change (BWC). A Food Frequency Questionnaire (FFQ) with 81 items was applied in 278 women having the first six months after delivery as the time frame. Body weight (BW) was measured at 15 days (baseline) and at 2.6 and 9 months postpartum. Principal components analysis was used to extract the dietary patterns. Linear mixed models were performed having BWC as the outcome and the dietary patterns as independent variables. Two major dietary patterns were identified: healthy and mixed. Energy intake was 2,838 kcal (DP = 624) and 2,233 kcal (DP = 455), for women classified in the highest quartiles of mixed and healthy dietary patterns, respectively. Mean BWC declined -0.151 kg/ month (SE = 0.02) independently of the dietary pattern. Predicted values of BWC among women that have adhered to mixed dietary pattern indicated a lower BWC of 0.830 kg/month (SE = 0.24; p < 0.001) at 6 months and 0.938 kg/month (SE = 0.24; p < 0.001) at 9 months postpartum.\n Question: Is mixed dietary pattern associated with a slower decline of body weight change during postpartum in a cohort of Brazilian women?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: The aim was to assess the effect of dietary patterns on postpartum body weight change (BWC). A Food Frequency Questionnaire (FFQ) with 81 items was applied in 278 women having the first six months after delivery as the time frame. Body weight (BW) was measured at 15 days (baseline) and at 2.6 and 9 months postpartum. Principal components analysis was used to extract the dietary patterns. Linear mixed models were performed having BWC as the outcome and the dietary patterns as independent variables. Two major dietary patterns were identified: healthy and mixed. Energy intake was 2,838 kcal (DP = 624) and 2,233 kcal (DP = 455), for women classified in the highest quartiles of mixed and healthy dietary patterns, respectively. Mean BWC declined -0.151 kg/ month (SE = 0.02) independently of the dietary pattern. Predicted values of BWC among women that have adhered to mixed dietary pattern indicated a lower BWC of 0.830 kg/month (SE = 0.24; p < 0.001) at 6 months and 0.938 kg/month (SE = 0.24; p < 0.001) at 9 months postpartum.
Question: Is mixed dietary pattern associated with a slower decline of body weight change during postpartum in a cohort of Brazilian women?
Output:
|
PubmedQA166105
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Clustering sequences into families has long been an important step in characterization of genes and proteins. There are many algorithms developed for this purpose, most of which are based on either direct similarity between gene pairs or some sort of network structure, where weights on edges of constructed graphs are based on similarity. However, conserved synteny is an important signal that can help distinguish homology and it has not been utilized to its fullest potential. Here, we present GenFamClust, a pipeline that combines the network properties of sequence similarity and synteny to assess homology relationship and merge known homologs into groups of gene families. GenFamClust identifies homologs in a more informed and accurate manner as compared to similarity based approaches. We tested our method against the Neighborhood Correlation method on two diverse datasets consisting of fully sequenced genomes of eukaryotes and synthetic data.\n Question: Does quantitative synteny scoring improve homology inference and partitioning of gene families?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Clustering sequences into families has long been an important step in characterization of genes and proteins. There are many algorithms developed for this purpose, most of which are based on either direct similarity between gene pairs or some sort of network structure, where weights on edges of constructed graphs are based on similarity. However, conserved synteny is an important signal that can help distinguish homology and it has not been utilized to its fullest potential. Here, we present GenFamClust, a pipeline that combines the network properties of sequence similarity and synteny to assess homology relationship and merge known homologs into groups of gene families. GenFamClust identifies homologs in a more informed and accurate manner as compared to similarity based approaches. We tested our method against the Neighborhood Correlation method on two diverse datasets consisting of fully sequenced genomes of eukaryotes and synthetic data.
Question: Does quantitative synteny scoring improve homology inference and partitioning of gene families?
Output:
|
PubmedQA140263
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To investigate the association between B-mode ultrasound classification of small hepatocellular carcinoma (HCC) and outcome after radiofrequency ablation (RFA). Ninety-seven cases of HCC treated using RFA between April 2001 and March 2006 were reviewed. Ultrasound images were classified as follows: type 1, with halo (n = 29); and type 2, without halo (n = 68). Type 2 was further categorized into three subgroups: type 2a, homogenous hyperechoic (n = 9); type 2b, hypoechoic with smooth margins (n = 43); and type 2c (n = 16), hypoechoic with irregular or unclear margins. Patients with type 2a HCC were excluded from analysis due to the small number of cases. Two year recurrence rates for type 2b, type 1 and type 2c were 26%, 42% and 69%, respectively, with significant differences between type 2b and type 2c (P < 0.01), and between type 1 and type 2c (P < 0.05). Five year survival rates were 89%, 43% and 65%, respectively. Survival was significantly longer for type 2b than for other types (type 1 vs type 2b, P < 0.01; type 2b vs type 2c, P < 0.05). On univariate analysis, factors contributing to recurrence were number of tumors, tumor stage, serum level of lens culinaris agglutinin-reactive alpha-fetoprotein and ultrasound classification (P < 0.05). Factors contributing to survival were tumor stage and ultrasound classification (P < 0.05). Multivariate analysis identified ultrasound classification as the only factor independently associated with both recurrence and survival (P < 0.05).\n Question: Is ultrasonogram of hepatocellular carcinoma associated with outcome after radiofrequency ablation?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To investigate the association between B-mode ultrasound classification of small hepatocellular carcinoma (HCC) and outcome after radiofrequency ablation (RFA). Ninety-seven cases of HCC treated using RFA between April 2001 and March 2006 were reviewed. Ultrasound images were classified as follows: type 1, with halo (n = 29); and type 2, without halo (n = 68). Type 2 was further categorized into three subgroups: type 2a, homogenous hyperechoic (n = 9); type 2b, hypoechoic with smooth margins (n = 43); and type 2c (n = 16), hypoechoic with irregular or unclear margins. Patients with type 2a HCC were excluded from analysis due to the small number of cases. Two year recurrence rates for type 2b, type 1 and type 2c were 26%, 42% and 69%, respectively, with significant differences between type 2b and type 2c (P < 0.01), and between type 1 and type 2c (P < 0.05). Five year survival rates were 89%, 43% and 65%, respectively. Survival was significantly longer for type 2b than for other types (type 1 vs type 2b, P < 0.01; type 2b vs type 2c, P < 0.05). On univariate analysis, factors contributing to recurrence were number of tumors, tumor stage, serum level of lens culinaris agglutinin-reactive alpha-fetoprotein and ultrasound classification (P < 0.05). Factors contributing to survival were tumor stage and ultrasound classification (P < 0.05). Multivariate analysis identified ultrasound classification as the only factor independently associated with both recurrence and survival (P < 0.05).
Question: Is ultrasonogram of hepatocellular carcinoma associated with outcome after radiofrequency ablation?
Output:
|
PubmedQA200115
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Periodontitis, a chronic oral infection caused mainly by gram-negative bacteria, induces endotoxemia and associates with the risk for atherosclerosis. We investigated the effect of periodontal treatment on proatherogenic properties of very low density lipoproteins (VLDL). VLDL were isolated from 30 systemically healthy periodontitis patients before (pre-treatment) and 3 months after treatment (post-treatment). The mass compositions were analyzed, and VLDL-induced changes in cellular cholesterol content and expression of selected genes of human THP-1 macrophages were measured. Periodontal treatment decreased the local inflammation in the periodontium, but did not have a significant effect on C-reactive protein (CRP) levels, VLDL composition, or VLDL potential to induce cholesterol uptake or gene expression by the macrophages. Incubation of macrophages in the presence of VLDL resulted in more than twofold increase in their cellular cholesterol content. Uptake of VLDL with ensuing macrophage cholesterol accumulation correlated positively with VLDL-associated lipopolysaccharide (LPS) activity (r=0.436, P=.016) and apolipoprotein E content (r=0.374, P=.046). Pre-treatment VLDL derived from the patients with high CRP levels displayed higher LPS activity than that of VLDL derived from patients with low CRP (above vs. below median, P=.007). In addition, pre-treatment VLDL isolated from patients with high systemic inflammation induced higher relative mRNA expression of CD14, TNF-α, MCP-1, and IL-6 in the macrophages.\n Question: Do very low density lipoproteins derived from periodontitis patients facilitate macrophage activation via lipopolysaccharide function?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Periodontitis, a chronic oral infection caused mainly by gram-negative bacteria, induces endotoxemia and associates with the risk for atherosclerosis. We investigated the effect of periodontal treatment on proatherogenic properties of very low density lipoproteins (VLDL). VLDL were isolated from 30 systemically healthy periodontitis patients before (pre-treatment) and 3 months after treatment (post-treatment). The mass compositions were analyzed, and VLDL-induced changes in cellular cholesterol content and expression of selected genes of human THP-1 macrophages were measured. Periodontal treatment decreased the local inflammation in the periodontium, but did not have a significant effect on C-reactive protein (CRP) levels, VLDL composition, or VLDL potential to induce cholesterol uptake or gene expression by the macrophages. Incubation of macrophages in the presence of VLDL resulted in more than twofold increase in their cellular cholesterol content. Uptake of VLDL with ensuing macrophage cholesterol accumulation correlated positively with VLDL-associated lipopolysaccharide (LPS) activity (r=0.436, P=.016) and apolipoprotein E content (r=0.374, P=.046). Pre-treatment VLDL derived from the patients with high CRP levels displayed higher LPS activity than that of VLDL derived from patients with low CRP (above vs. below median, P=.007). In addition, pre-treatment VLDL isolated from patients with high systemic inflammation induced higher relative mRNA expression of CD14, TNF-α, MCP-1, and IL-6 in the macrophages.
Question: Do very low density lipoproteins derived from periodontitis patients facilitate macrophage activation via lipopolysaccharide function?
Output:
|
PubmedQA13469
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Recently, many antioxidants have been tested in cardiovascular disease. The effect of antioxidants on alleviation of coronary vasospasm, however, remains unclear. We investigated whether chronic administration of ascorbic acid and glutathione prevents coronary vasospasm in pigs. Balloon-induced endothelial injury in the left anterior descending coronary artery was performed every 2 weeks until 6 weeks (0, 2, 4, 6 weeks). Ten micrograms per kilogram serotonin-induced vasoconstriction was assessed before each endothelial injury and at eighth week by coronary angiography. In endothelial injury without antioxidant group (ED group, n=12), serotonin-induced left anterior descending coronary artery vasoconstriction was augmented from 7+/-4% (0 week) to 88+/-8% (8th week, P<0.01) with electrocardiogram-ST elevation, and an increase of cyclooxygenase-2 expression and a decrease of endothelial nitric oxide synthase expression was observed at the spasm portion removed from the endothelial denuded site. In the endothelial injury group with oral administration of ascorbic acid 3 g/day and glutathione 1 g/day after the first endothelial injury (ASC+GSH group, n=12), serotonin-induced vasoconstriction was suppressed (8th week, 60+/-6%, P<0.01 vs. ED group) and endothelial nitric oxide synthase expression was fairly well maintained. Intimal thickening was observed at the left anterior descending artery spasm portion in the endothelial injury without antioxidant group but not at the corresponding portion in the ASC+GSH group.\n Question: Is antioxidant a useful supportive agent for the treatment of coronary vasospasm with endothelial dysfunction in pig?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Recently, many antioxidants have been tested in cardiovascular disease. The effect of antioxidants on alleviation of coronary vasospasm, however, remains unclear. We investigated whether chronic administration of ascorbic acid and glutathione prevents coronary vasospasm in pigs. Balloon-induced endothelial injury in the left anterior descending coronary artery was performed every 2 weeks until 6 weeks (0, 2, 4, 6 weeks). Ten micrograms per kilogram serotonin-induced vasoconstriction was assessed before each endothelial injury and at eighth week by coronary angiography. In endothelial injury without antioxidant group (ED group, n=12), serotonin-induced left anterior descending coronary artery vasoconstriction was augmented from 7+/-4% (0 week) to 88+/-8% (8th week, P<0.01) with electrocardiogram-ST elevation, and an increase of cyclooxygenase-2 expression and a decrease of endothelial nitric oxide synthase expression was observed at the spasm portion removed from the endothelial denuded site. In the endothelial injury group with oral administration of ascorbic acid 3 g/day and glutathione 1 g/day after the first endothelial injury (ASC+GSH group, n=12), serotonin-induced vasoconstriction was suppressed (8th week, 60+/-6%, P<0.01 vs. ED group) and endothelial nitric oxide synthase expression was fairly well maintained. Intimal thickening was observed at the left anterior descending artery spasm portion in the endothelial injury without antioxidant group but not at the corresponding portion in the ASC+GSH group.
Question: Is antioxidant a useful supportive agent for the treatment of coronary vasospasm with endothelial dysfunction in pig?
Output:
|
PubmedQA164282
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Parathyroid gland localization and lateralization are important before surgery, particularly for minimally invasive parathyroidectomy (MIP) and recurrent hyperparathyroidism. We hypothesized that readings of Tc sestamibi scans with single photon emission computed tomography (SPECT) by a surgeon and nuclear medicine physician together (NMP+S) compared to a nuclear medicine physician alone (NMP alone) might affect scan interpretation accuracy. Between May 1999 and December 2002, 127 hyperparathyroid patients had preoperative localization with sestamibi SPECT. Scans were prospectively interpreted by an endocrine surgeon and nuclear medicine physician attending together (NMP+S) and a nuclear medicine physician attending alone (NMP alone). These readings were compared to intra-operative findings, which served as the 'gold standard'. There were 120 patients with primary hyperparathyroidism (55 underwent MIP) and seven with secondary or tertiary hyperparathyroidism; seven patients had recurrent hyperparathyroidism. Of 127 patients, 83 had single adenomas; 27, double adenomas; 15, hyperplasia; one, MENIIA; and one, parathyroid cancer. Sensitivity and positive predictive values were 58.6% and 67.4% for NMP alone compared to 81.9% and 70.0% for NMP+S. The overall accuracy of correct localization was 45.7% vs. 60.6% (P<0.01) and of correct lateralization was 69.3% vs. 80.3% (P<0.01) for NMP alone versus NMP+S respectively. The most common finding interpreted incorrectly by NMP alone and correctly by NMP+S was an ectopic superior parathyroid adenoma in the inferior position. Ninety-eight per cent of patients were cured of their hyperparathyroidism.\n Question: Is interpretation of 99mTc sestamibi parathyroid SPECT scan improved when read by the surgeon and nuclear medicine physician together?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Parathyroid gland localization and lateralization are important before surgery, particularly for minimally invasive parathyroidectomy (MIP) and recurrent hyperparathyroidism. We hypothesized that readings of Tc sestamibi scans with single photon emission computed tomography (SPECT) by a surgeon and nuclear medicine physician together (NMP+S) compared to a nuclear medicine physician alone (NMP alone) might affect scan interpretation accuracy. Between May 1999 and December 2002, 127 hyperparathyroid patients had preoperative localization with sestamibi SPECT. Scans were prospectively interpreted by an endocrine surgeon and nuclear medicine physician attending together (NMP+S) and a nuclear medicine physician attending alone (NMP alone). These readings were compared to intra-operative findings, which served as the 'gold standard'. There were 120 patients with primary hyperparathyroidism (55 underwent MIP) and seven with secondary or tertiary hyperparathyroidism; seven patients had recurrent hyperparathyroidism. Of 127 patients, 83 had single adenomas; 27, double adenomas; 15, hyperplasia; one, MENIIA; and one, parathyroid cancer. Sensitivity and positive predictive values were 58.6% and 67.4% for NMP alone compared to 81.9% and 70.0% for NMP+S. The overall accuracy of correct localization was 45.7% vs. 60.6% (P<0.01) and of correct lateralization was 69.3% vs. 80.3% (P<0.01) for NMP alone versus NMP+S respectively. The most common finding interpreted incorrectly by NMP alone and correctly by NMP+S was an ectopic superior parathyroid adenoma in the inferior position. Ninety-eight per cent of patients were cured of their hyperparathyroidism.
Question: Is interpretation of 99mTc sestamibi parathyroid SPECT scan improved when read by the surgeon and nuclear medicine physician together?
Output:
|
PubmedQA44499
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: We minimized the influence of image quality variability, as measured by signal strength (SS), on optical coherence tomography (OCT) thickness measurements using the histogram matching (HM) method. We scanned 12 eyes from 12 healthy subjects with the Cirrus HD-OCT device to obtain a series of OCT images with a wide range of SS (maximal range, 1-10) at the same visit. For each eye, the histogram of an image with the highest SS (best image quality) was set as the reference. We applied HM to the images with lower SS by shaping the input histogram into the reference histogram. Retinal nerve fiber layer (RNFL) thickness was automatically measured before and after HM processing (defined as original and HM measurements), and compared to the device output (device measurements). Nonlinear mixed effects models were used to analyze the relationship between RNFL thickness and SS. In addition, the lowest tolerable SSs, which gave the RNFL thickness within the variability margin of manufacturer recommended SS range (6-10), were determined for device, original, and HM measurements. The HM measurements showed less variability across a wide range of image quality than the original and device measurements (slope = 1.17 vs. 4.89 and 1.72 μm/SS, respectively). The lowest tolerable SS was successfully reduced to 4.5 after HM processing.\n Question: Does histogram Matching extend Acceptable Signal Strength Range on Optical Coherence Tomography Images?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: We minimized the influence of image quality variability, as measured by signal strength (SS), on optical coherence tomography (OCT) thickness measurements using the histogram matching (HM) method. We scanned 12 eyes from 12 healthy subjects with the Cirrus HD-OCT device to obtain a series of OCT images with a wide range of SS (maximal range, 1-10) at the same visit. For each eye, the histogram of an image with the highest SS (best image quality) was set as the reference. We applied HM to the images with lower SS by shaping the input histogram into the reference histogram. Retinal nerve fiber layer (RNFL) thickness was automatically measured before and after HM processing (defined as original and HM measurements), and compared to the device output (device measurements). Nonlinear mixed effects models were used to analyze the relationship between RNFL thickness and SS. In addition, the lowest tolerable SSs, which gave the RNFL thickness within the variability margin of manufacturer recommended SS range (6-10), were determined for device, original, and HM measurements. The HM measurements showed less variability across a wide range of image quality than the original and device measurements (slope = 1.17 vs. 4.89 and 1.72 μm/SS, respectively). The lowest tolerable SS was successfully reduced to 4.5 after HM processing.
Question: Does histogram Matching extend Acceptable Signal Strength Range on Optical Coherence Tomography Images?
Output:
|
PubmedQA44088
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To explore the association between quality of life and social support in elderly osteoporosis patients in a Chinese population. A total of 214 elderly patients who underwent bone mineral density screening were divided into two groups: elderly patients with primary osteoporosis (case group, n = 112) and normal elderly patients (control group, n = 102). Quality of life and social support were compared between the two groups. Quality of life and social support were significantly different between the case and control groups. The physical function, role-physical, bodily pain, general health, vitality, social-functioning, role-emotional and mental health scores in case group were significantly lower than those in the control group (P < 0.01). The objective support, subjective support, utilization of support, and total scores in case group were significantly lower than those in the control group (P < 0.01). Quality of life and social support were positively correlated in the case group (r = 0.672, P < 0.01).\n Question: Does quality of Life be Related to Social Support in Elderly Osteoporosis Patients in a Chinese Population?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To explore the association between quality of life and social support in elderly osteoporosis patients in a Chinese population. A total of 214 elderly patients who underwent bone mineral density screening were divided into two groups: elderly patients with primary osteoporosis (case group, n = 112) and normal elderly patients (control group, n = 102). Quality of life and social support were compared between the two groups. Quality of life and social support were significantly different between the case and control groups. The physical function, role-physical, bodily pain, general health, vitality, social-functioning, role-emotional and mental health scores in case group were significantly lower than those in the control group (P < 0.01). The objective support, subjective support, utilization of support, and total scores in case group were significantly lower than those in the control group (P < 0.01). Quality of life and social support were positively correlated in the case group (r = 0.672, P < 0.01).
Question: Does quality of Life be Related to Social Support in Elderly Osteoporosis Patients in a Chinese Population?
Output:
|
PubmedQA162391
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The morbidity associated with transurethral resection of the prostate (TURP) for large-volume prostates has prompted attempts to modify the standard equipment and techniques. Patients with large prostates (>70 g) need longer operative time, and have greater blood loss and higher irrigant fluid requirements; therefore, the traditional surgical recommendation for the management of benign prostatic hyperplasia (BPH) >70 g is open surgery. We assessed the effectiveness and safety of transurethral vapor resection of the prostate (TUVRP) for the management of prostate glands with a volume >70 g. Eighty-nine patients with a diagnosis of BPH who had a prostate volume >70 grams determined by abdominal ultrasonography underwent TUVRP between July 2002 and March 2006. Preoperative evaluation included assessment of International Prostate Symptom Score (IPSS), prostate volume, postvoid residual (PVR), and maximum flow rate (Q(max)). Intraoperative and postoperative parameters, including operative time, total irrigant requirement, blood loss, duration of postoperative catheterization, hospital stay, and complications were also analyzed. The mean prostate volume for the 89 patients was 83.3 g (range 70-169 g). The mean age was 67.25 years (range 55-87 yr). Symptom duration varied from 2 months to 7 years. Twenty-two patients used a catheter preoperatively. The mean IPSS score, Q(max), and PVR were 23, 7.1 mL/sec, and 116 mL, respectively. The mean operative time was 64 minutes, and mean irrigant used was 21.4 L. The mean weight of resected tissue was 31.3 g. The average postoperative catheter duration was 2.25 days. Complications included transient dysuria in 11 patients, hyponatremia in two patients, and urethral stricture in two patients. No patient required a blood transfusion postoperatively. The effectiveness as assessed at 6 months was IPSS 5.1, Q(max) 22.5 mL/sec, and PVR not significant.\n Question: Is transurethral vapor resection of prostate a good alternative for prostates > 70 g?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: The morbidity associated with transurethral resection of the prostate (TURP) for large-volume prostates has prompted attempts to modify the standard equipment and techniques. Patients with large prostates (>70 g) need longer operative time, and have greater blood loss and higher irrigant fluid requirements; therefore, the traditional surgical recommendation for the management of benign prostatic hyperplasia (BPH) >70 g is open surgery. We assessed the effectiveness and safety of transurethral vapor resection of the prostate (TUVRP) for the management of prostate glands with a volume >70 g. Eighty-nine patients with a diagnosis of BPH who had a prostate volume >70 grams determined by abdominal ultrasonography underwent TUVRP between July 2002 and March 2006. Preoperative evaluation included assessment of International Prostate Symptom Score (IPSS), prostate volume, postvoid residual (PVR), and maximum flow rate (Q(max)). Intraoperative and postoperative parameters, including operative time, total irrigant requirement, blood loss, duration of postoperative catheterization, hospital stay, and complications were also analyzed. The mean prostate volume for the 89 patients was 83.3 g (range 70-169 g). The mean age was 67.25 years (range 55-87 yr). Symptom duration varied from 2 months to 7 years. Twenty-two patients used a catheter preoperatively. The mean IPSS score, Q(max), and PVR were 23, 7.1 mL/sec, and 116 mL, respectively. The mean operative time was 64 minutes, and mean irrigant used was 21.4 L. The mean weight of resected tissue was 31.3 g. The average postoperative catheter duration was 2.25 days. Complications included transient dysuria in 11 patients, hyponatremia in two patients, and urethral stricture in two patients. No patient required a blood transfusion postoperatively. The effectiveness as assessed at 6 months was IPSS 5.1, Q(max) 22.5 mL/sec, and PVR not significant.
Question: Is transurethral vapor resection of prostate a good alternative for prostates > 70 g?
Output:
|
PubmedQA174384
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To investigate the effect of necrotic cells on the secretion of inflammatory cytokines. RAW264.7 macrophages and necrotic mouse thymocytes induced by heating were incubated for 18 h at a ratio of 5:1 in the absence or presence of lipopolysaccharide (LPS, 100 ng/ml). The supernatant of the cell culture was collected and the expression and secretion of the pro-inflammatory cytokines were measured using Bio-Plex suspension system. The secretions of tumor necrosis factor-alpha (TNF-alpha) and interlukine-6 (IL-6) by macrophages co-cultured with the necrotic cells were significantly enhanced as compared with the control cells. The necrotic cells also significantly augmented the secretion of the pro-inflammatory cytokines induced by LPS.\n Question: Do [ Necrotic cells induce and promote inflammatory responses in vitro ]?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To investigate the effect of necrotic cells on the secretion of inflammatory cytokines. RAW264.7 macrophages and necrotic mouse thymocytes induced by heating were incubated for 18 h at a ratio of 5:1 in the absence or presence of lipopolysaccharide (LPS, 100 ng/ml). The supernatant of the cell culture was collected and the expression and secretion of the pro-inflammatory cytokines were measured using Bio-Plex suspension system. The secretions of tumor necrosis factor-alpha (TNF-alpha) and interlukine-6 (IL-6) by macrophages co-cultured with the necrotic cells were significantly enhanced as compared with the control cells. The necrotic cells also significantly augmented the secretion of the pro-inflammatory cytokines induced by LPS.
Question: Do [ Necrotic cells induce and promote inflammatory responses in vitro ]?
Output:
|
PubmedQA50570
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To describe the preferences for disclosure of individual biomarker results among mothers participating in a longitudinal birth cohort. We surveyed 343 mothers that participated in the Health Outcomes and Measures of the Environment Study about their biomarker disclosure preferences. Participants were told that the study was measuring pesticide metabolites in their biological specimens, and that the health effects of these low levels of exposure are unknown. Participants were asked whether they wanted to receive their results and their child's results. In addition, they were asked about their preferred method (letter vs in person) and format (more complex vs less complex) for disclosure of results. Almost all of the study participants wanted to receive their individual results (340/343) as well as their child's results (342/343). However, preferences for receiving results differed by education level. Mothers with less than a college degree preferred in-person disclosure of results more often than mothers with some college education or a college degree (34.3% vs 17.4% vs 7.9%, p<0.001). Similarly, mothers with less than a college education preferred a less complex disclosure format than mothers with some college education or a college degree (59.7% vs 79.1% vs 86.3%, p<0.0001).\n Question: Does understanding preferences for disclosure of individual biomarker result among participants in a longitudinal birth cohort?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To describe the preferences for disclosure of individual biomarker results among mothers participating in a longitudinal birth cohort. We surveyed 343 mothers that participated in the Health Outcomes and Measures of the Environment Study about their biomarker disclosure preferences. Participants were told that the study was measuring pesticide metabolites in their biological specimens, and that the health effects of these low levels of exposure are unknown. Participants were asked whether they wanted to receive their results and their child's results. In addition, they were asked about their preferred method (letter vs in person) and format (more complex vs less complex) for disclosure of results. Almost all of the study participants wanted to receive their individual results (340/343) as well as their child's results (342/343). However, preferences for receiving results differed by education level. Mothers with less than a college degree preferred in-person disclosure of results more often than mothers with some college education or a college degree (34.3% vs 17.4% vs 7.9%, p<0.001). Similarly, mothers with less than a college education preferred a less complex disclosure format than mothers with some college education or a college degree (59.7% vs 79.1% vs 86.3%, p<0.0001).
Question: Does understanding preferences for disclosure of individual biomarker result among participants in a longitudinal birth cohort?
Output:
|
PubmedQA60340
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To determine how hypochlorous acid (HOCl), the principal product of myeloperoxidase, modulates vascular function. Rabbit arterial rings exposed to HOCl (0 to 500 micromol/L) exhibited dose- and time-dependent impairment of endothelium-dependent arterial relaxation to acetylcholine and A23187, but not the NO donor, diethylamine NONOate, suggesting that HOCl targets the endothelium. This effect was not because of cytotoxicity, as HOCl treatment produced no significant change in endothelial cell morphology or lactate dehydrogenase release. We observed HOCl-mediated endothelial cell protein oxidation by immunoreactivity to HOP-1, a monoclonal antibody specific for HOCl-oxidized protein. In support of this notion, known HOCl scavengers, such as methionine and N-acetylcysteine, partially preserved endothelium-derived NO bioactivity in response to HOCl. In an unanticipated observation, HOCl-mediated impairment of NO bioactivity was prevented by manganese superoxide dismutase in a manner dependent on its enzymatic activity. Finally, we found that HOCl reduced endothelial nitric oxide synthase dimer stability, an effect that was also inhibited by superoxide dismutase.\n Question: Does hypochlorous acid impair endothelium-derived nitric oxide bioactivity through a superoxide-dependent mechanism?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To determine how hypochlorous acid (HOCl), the principal product of myeloperoxidase, modulates vascular function. Rabbit arterial rings exposed to HOCl (0 to 500 micromol/L) exhibited dose- and time-dependent impairment of endothelium-dependent arterial relaxation to acetylcholine and A23187, but not the NO donor, diethylamine NONOate, suggesting that HOCl targets the endothelium. This effect was not because of cytotoxicity, as HOCl treatment produced no significant change in endothelial cell morphology or lactate dehydrogenase release. We observed HOCl-mediated endothelial cell protein oxidation by immunoreactivity to HOP-1, a monoclonal antibody specific for HOCl-oxidized protein. In support of this notion, known HOCl scavengers, such as methionine and N-acetylcysteine, partially preserved endothelium-derived NO bioactivity in response to HOCl. In an unanticipated observation, HOCl-mediated impairment of NO bioactivity was prevented by manganese superoxide dismutase in a manner dependent on its enzymatic activity. Finally, we found that HOCl reduced endothelial nitric oxide synthase dimer stability, an effect that was also inhibited by superoxide dismutase.
Question: Does hypochlorous acid impair endothelium-derived nitric oxide bioactivity through a superoxide-dependent mechanism?
Output:
|
PubmedQA180127
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Structural changes in the extracranial carotid artery are associated with an increase in left ventricular (LV) mass and relative wall thickness. The present study was performed to determine the relation of LV mass index and relative wall thickness to suspected atherosclerotic steno-occlusive disease of the intracranial arteries on magnetic resonance angiography (MRA) in noncardioembolic ischaemic stroke patients. We retrospectively analysed the records of acute ischaemic stroke patients who underwent echocardiography and intracranial MRA. Patients with potential sources of cardioembolism, or known causes of vascular steno-occlusive disease including dissection, vasculitis, and moyamoya disease, were excluded from the study. LV mass indexes and relative wall thicknesses were estimated using echocardiography. Patients were divided into four groups according to their LV mass index and relative wall thickness: concentric LV hypertrophy, eccentric LV hypertrophy, concentric LV remodelling, and normal geometry. MRA was used to evaluate steno-occlusive disease in the basilar artery (BA) and the horizontal portion of the middle cerebral artery. A total of 212 patients were included, and logistic regression analysis revealed that BA steno-occlusive disease was related to LV relative wall thickness, but not LV mass index. The prevalence of BA disease was significantly higher in the concentric LV hypertrophy group than in the normal geometry group. Steno-occlusive disease of the middle cerebral artery was not closely related to the structural changes in the left ventricle.\n Question: Is basilar artery steno-occlusive disease associated with structural changes in the left ventricle?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Structural changes in the extracranial carotid artery are associated with an increase in left ventricular (LV) mass and relative wall thickness. The present study was performed to determine the relation of LV mass index and relative wall thickness to suspected atherosclerotic steno-occlusive disease of the intracranial arteries on magnetic resonance angiography (MRA) in noncardioembolic ischaemic stroke patients. We retrospectively analysed the records of acute ischaemic stroke patients who underwent echocardiography and intracranial MRA. Patients with potential sources of cardioembolism, or known causes of vascular steno-occlusive disease including dissection, vasculitis, and moyamoya disease, were excluded from the study. LV mass indexes and relative wall thicknesses were estimated using echocardiography. Patients were divided into four groups according to their LV mass index and relative wall thickness: concentric LV hypertrophy, eccentric LV hypertrophy, concentric LV remodelling, and normal geometry. MRA was used to evaluate steno-occlusive disease in the basilar artery (BA) and the horizontal portion of the middle cerebral artery. A total of 212 patients were included, and logistic regression analysis revealed that BA steno-occlusive disease was related to LV relative wall thickness, but not LV mass index. The prevalence of BA disease was significantly higher in the concentric LV hypertrophy group than in the normal geometry group. Steno-occlusive disease of the middle cerebral artery was not closely related to the structural changes in the left ventricle.
Question: Is basilar artery steno-occlusive disease associated with structural changes in the left ventricle?
Output:
|
PubmedQA32141
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: We report an interesting case of monosymptomatic hypochondriacal psychosis (MHP) which, because of its rarity, tends to be neglected in differential diagnosis. The patient presented with delusions including smelling the odour of detergent and thinking detergent was circulating in his blood. He had many medical and paramedical treatments over 2½ years, and was finally diagnosed with MHP. Risperidone was then started, and gradually increased. A significant improvement was observed. However, risperidone was discontinued, because of its hypomanic effects.\n Question: Is `` The detergent circulating in my blood '' : a case report?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: We report an interesting case of monosymptomatic hypochondriacal psychosis (MHP) which, because of its rarity, tends to be neglected in differential diagnosis. The patient presented with delusions including smelling the odour of detergent and thinking detergent was circulating in his blood. He had many medical and paramedical treatments over 2½ years, and was finally diagnosed with MHP. Risperidone was then started, and gradually increased. A significant improvement was observed. However, risperidone was discontinued, because of its hypomanic effects.
Question: Is `` The detergent circulating in my blood '' : a case report?
Output:
|
PubmedQA120158
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: MR is being used increasingly as an intraoperative imaging technique. The purpose of this study was to test the hypothesis that intraoperative MR imaging increases the extent of tumor resection, thus improving surgical results in patients with high-grade gliomas. Thirty-eight patients with intracranial high-grade gliomas underwent 41 operations. Using a neuronavigation system, tumors were resected in all patients to the point at which the neurosurgeon would have terminated the operation because he thought that all enhancing tumor had been removed. Intraoperative MR imaging (0.2 T) was performed, and surgery, if necessary and feasible, was continued. All patients underwent early postoperative MR imaging (1.5 T). By comparing the proportions of patients in whom complete resection of all enhancing tumor was shown by intraoperative and early postoperative MR imaging, respectively, the impact of intraoperative MR imaging on surgery was determined. Intraoperative MR imaging showed residual enhancing tumor in 22 cases (53.7%). In 15 patients (36.6%), no residual tumor was seen, whereas the results of the remaining four intraoperative MR examinations (9.7%) were inconclusive. In 17 of the 22 cases in which residual tumor was seen, surgery was continued. Early postoperative MR imaging showed residual tumor in eight patients (19.5%) and no residual tumor in 31 cases (75.6%); findings were uncertain in two patients (4.9%). The difference in the proportion of \"complete removals\" was statistically highly significant (P = .0004).\n Question: Does intraoperative MR imaging increase the extent of tumor resection in patients with high-grade gliomas?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: MR is being used increasingly as an intraoperative imaging technique. The purpose of this study was to test the hypothesis that intraoperative MR imaging increases the extent of tumor resection, thus improving surgical results in patients with high-grade gliomas. Thirty-eight patients with intracranial high-grade gliomas underwent 41 operations. Using a neuronavigation system, tumors were resected in all patients to the point at which the neurosurgeon would have terminated the operation because he thought that all enhancing tumor had been removed. Intraoperative MR imaging (0.2 T) was performed, and surgery, if necessary and feasible, was continued. All patients underwent early postoperative MR imaging (1.5 T). By comparing the proportions of patients in whom complete resection of all enhancing tumor was shown by intraoperative and early postoperative MR imaging, respectively, the impact of intraoperative MR imaging on surgery was determined. Intraoperative MR imaging showed residual enhancing tumor in 22 cases (53.7%). In 15 patients (36.6%), no residual tumor was seen, whereas the results of the remaining four intraoperative MR examinations (9.7%) were inconclusive. In 17 of the 22 cases in which residual tumor was seen, surgery was continued. Early postoperative MR imaging showed residual tumor in eight patients (19.5%) and no residual tumor in 31 cases (75.6%); findings were uncertain in two patients (4.9%). The difference in the proportion of "complete removals" was statistically highly significant (P = .0004).
Question: Does intraoperative MR imaging increase the extent of tumor resection in patients with high-grade gliomas?
Output:
|
PubmedQA560
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Mass spectrometry-based proteomics experiments generate spectra that are rich in information. Often only a fraction of this information is used for peptide/protein identification, whereas a significant proportion of the peaks in a spectrum remain unexplained. In this paper we explore how a specific class of data mining techniques termed \"frequent itemset mining\" can be employed to discover patterns in the unassigned data, and how such patterns can help us interpret the origin of the unexpected/unexplained peaks. First a model is proposed that describes the origin of the observed peaks in a mass spectrum. For this purpose we use the classical correlative database search algorithm. Peaks that support a positive identification of the spectrum are termed explained peaks. Next, frequent itemset mining techniques are introduced to infer which unexplained peaks are associated in a spectrum. The method is validated on two types of experimental proteomic data. First, peptide mass fingerprint data is analyzed to explain the unassigned peaks in a full scan mass spectrum. Interestingly, a large numbers of experimental spectra reveals several highly frequent unexplained masses, and pattern mining on these frequent masses demonstrates that subsets of these peaks frequently co-occur. Further evaluation shows that several of these co-occurring peaks indeed have a known common origin, and other patterns are promising hypothesis generators for further analysis. Second, the proposed methodology is validated on tandem mass spectrometral data using a public spectral library, where associations within the mass differences of unassigned peaks and peptide modifications are explored. The investigation of the found patterns illustrates that meaningful patterns can be discovered that can be explained by features of the employed technology and found modifications.\n Question: Does unravelling associations between unassigned mass spectrometry peak with frequent itemset mining techniques?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Mass spectrometry-based proteomics experiments generate spectra that are rich in information. Often only a fraction of this information is used for peptide/protein identification, whereas a significant proportion of the peaks in a spectrum remain unexplained. In this paper we explore how a specific class of data mining techniques termed "frequent itemset mining" can be employed to discover patterns in the unassigned data, and how such patterns can help us interpret the origin of the unexpected/unexplained peaks. First a model is proposed that describes the origin of the observed peaks in a mass spectrum. For this purpose we use the classical correlative database search algorithm. Peaks that support a positive identification of the spectrum are termed explained peaks. Next, frequent itemset mining techniques are introduced to infer which unexplained peaks are associated in a spectrum. The method is validated on two types of experimental proteomic data. First, peptide mass fingerprint data is analyzed to explain the unassigned peaks in a full scan mass spectrum. Interestingly, a large numbers of experimental spectra reveals several highly frequent unexplained masses, and pattern mining on these frequent masses demonstrates that subsets of these peaks frequently co-occur. Further evaluation shows that several of these co-occurring peaks indeed have a known common origin, and other patterns are promising hypothesis generators for further analysis. Second, the proposed methodology is validated on tandem mass spectrometral data using a public spectral library, where associations within the mass differences of unassigned peaks and peptide modifications are explored. The investigation of the found patterns illustrates that meaningful patterns can be discovered that can be explained by features of the employed technology and found modifications.
Question: Does unravelling associations between unassigned mass spectrometry peak with frequent itemset mining techniques?
Output:
|
PubmedQA9816
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To analyze the effect of allogeneic blood transfusion on clinical outcome in 119 patients with stage IIB cervical cancer who were treated with radiotherapy +/- chemotherapy. Medical records were examined for hemoglobin levels before and during radiotherapy, history of allogeneic blood transfusions and the time point when transfusions were given. These factors were retrospectively analyzed along with other clinical risk factors for influences on the patients' clinical outcomes. Thirty-two patients (26.9%) received packed red blood cell transfusion (mean, 3.4 units; range, 1-12 units) before or during radiotherapy. Median follow-up period was 39.3 months (range, 7.6-58.4 months). Patients with history of transfusion showed poorer metastasis-free survival and a trend toward poorer overall survival than non-transfused patients. When patients who received transfusions were sub-divided by the time of transfusion, those who received transfusions before radiotherapy had significantly poorer clinical outcome than those who received transfusions during radiotherapy. In a multivariable analysis, patients with pretreatment transfusion showed a higher risk of distant metastasis (HR = 3.75, 95% CI: 1.28-12.15, p = 0.017) and decreased overall survival rates (HR = 4.62, 95% CI: 1.15-18.54, p = 0.031) compared with those of other patients.\n Question: Is allogeneic blood transfusion given before radiotherapy associated with the poor clinical outcome in patients with cervical cancer?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To analyze the effect of allogeneic blood transfusion on clinical outcome in 119 patients with stage IIB cervical cancer who were treated with radiotherapy +/- chemotherapy. Medical records were examined for hemoglobin levels before and during radiotherapy, history of allogeneic blood transfusions and the time point when transfusions were given. These factors were retrospectively analyzed along with other clinical risk factors for influences on the patients' clinical outcomes. Thirty-two patients (26.9%) received packed red blood cell transfusion (mean, 3.4 units; range, 1-12 units) before or during radiotherapy. Median follow-up period was 39.3 months (range, 7.6-58.4 months). Patients with history of transfusion showed poorer metastasis-free survival and a trend toward poorer overall survival than non-transfused patients. When patients who received transfusions were sub-divided by the time of transfusion, those who received transfusions before radiotherapy had significantly poorer clinical outcome than those who received transfusions during radiotherapy. In a multivariable analysis, patients with pretreatment transfusion showed a higher risk of distant metastasis (HR = 3.75, 95% CI: 1.28-12.15, p = 0.017) and decreased overall survival rates (HR = 4.62, 95% CI: 1.15-18.54, p = 0.031) compared with those of other patients.
Question: Is allogeneic blood transfusion given before radiotherapy associated with the poor clinical outcome in patients with cervical cancer?
Output:
|
PubmedQA81924
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The influence of diabetes on carotid revascularization techniques is controversial, with few data regarding angioplasty and stenting (CAS). Our purpose was to analyze whether its presence constitutes a risk factor for poor outcome of patients with carotid stenosis treated with CAS. We compared 30-day and long term morbidity and mortality, as well as restenosis rates, of non diabetic and diabetic patients with symptomatic carotid stenosis treated with endovascular techniques. 318 consecutive patients, 116 (36.5%) of them diabetics, were followed for a median of 56 months. Cumulative 30-day stroke, ischemic cardiopathy and death rate was 4% for non diabetics and 5.2% for diabetics (non significant). Long term stroke and mortality rate was 26.4% for the first group and 34.3% for the second (non significant). The most frequent causes of death were myocardial infarction (17.5% non diabetics, 44% diabetics, p = 0.04), ischemic stroke (12.5% non diabetics, 4% diabetics, non significant) and cancer (30% non diabetics, 16% diabetics, non significant). Twelve patients (6.4%) had restenosis ≥ 50%, 5.9% non diabetic, 7.4% diabetic, also without statistical significance.\n Question: Does diabetes affect outcome of symptomatic carotid stenosis treated with endovascular techniques?\n Output: "
},
{
"role": "assistant",
"content": "no"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: The influence of diabetes on carotid revascularization techniques is controversial, with few data regarding angioplasty and stenting (CAS). Our purpose was to analyze whether its presence constitutes a risk factor for poor outcome of patients with carotid stenosis treated with CAS. We compared 30-day and long term morbidity and mortality, as well as restenosis rates, of non diabetic and diabetic patients with symptomatic carotid stenosis treated with endovascular techniques. 318 consecutive patients, 116 (36.5%) of them diabetics, were followed for a median of 56 months. Cumulative 30-day stroke, ischemic cardiopathy and death rate was 4% for non diabetics and 5.2% for diabetics (non significant). Long term stroke and mortality rate was 26.4% for the first group and 34.3% for the second (non significant). The most frequent causes of death were myocardial infarction (17.5% non diabetics, 44% diabetics, p = 0.04), ischemic stroke (12.5% non diabetics, 4% diabetics, non significant) and cancer (30% non diabetics, 16% diabetics, non significant). Twelve patients (6.4%) had restenosis ≥ 50%, 5.9% non diabetic, 7.4% diabetic, also without statistical significance.
Question: Does diabetes affect outcome of symptomatic carotid stenosis treated with endovascular techniques?
Output:
|
PubmedQA58582
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Endotoxin and its purified derivative LPS are important contaminants of both domestic and occupational environments that have been related to airway diseases. A body of data suggests that there is considerable interindividual variability in LPS sensitivity. The aim of the study was to relate the individual clinical responses to inhaled LPS with the inflammatory process and the atopic status. Fifteen healthy subjects were challenged each week by inhalation with saline solution or LPS (0.5, 5, or 50 microg). The systemic response was defined by the increase in body temperature, blood neutrophilia, acute-phase proteins (C-reactive protein and LPS-binding protein [LBP]), and E-selectin. The LPS-induced airway response was defined as the increase in airway responsiveness and related to the cell count and concentration of TNF-alpha, myeloperoxidase, and eosinophil cationic protein in induced sputum. The atopic status was defined as an increase in IgE or a positive skin prick test result. Subjects (n = 7) with a significant increase in body temperature had a larger increase in the systemic inflammatory response (blood neutrophilia; P <.01) and in blood concentrations of C-reactive protein (P <.02) and LBP (P <.01). Subjects with a significant increase in airway responsiveness (n = 8) had an increase in the sputum concentration of eosinophil cationic protein (P <.01). The amplitude of the systemic response (increase in body temperature [P <.001], blood neutrophilia [P <.02], and rise in LBP [P <.05] and decrease in FEV(1) [P <.01]) were inversely associated with the atopic status, suggesting a link between atopy and LPS responsiveness.\n Question: Do healthy subjects express differences in clinical responses to inhaled lipopolysaccharide that are related with inflammation and with atopy?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Endotoxin and its purified derivative LPS are important contaminants of both domestic and occupational environments that have been related to airway diseases. A body of data suggests that there is considerable interindividual variability in LPS sensitivity. The aim of the study was to relate the individual clinical responses to inhaled LPS with the inflammatory process and the atopic status. Fifteen healthy subjects were challenged each week by inhalation with saline solution or LPS (0.5, 5, or 50 microg). The systemic response was defined by the increase in body temperature, blood neutrophilia, acute-phase proteins (C-reactive protein and LPS-binding protein [LBP]), and E-selectin. The LPS-induced airway response was defined as the increase in airway responsiveness and related to the cell count and concentration of TNF-alpha, myeloperoxidase, and eosinophil cationic protein in induced sputum. The atopic status was defined as an increase in IgE or a positive skin prick test result. Subjects (n = 7) with a significant increase in body temperature had a larger increase in the systemic inflammatory response (blood neutrophilia; P <.01) and in blood concentrations of C-reactive protein (P <.02) and LBP (P <.01). Subjects with a significant increase in airway responsiveness (n = 8) had an increase in the sputum concentration of eosinophil cationic protein (P <.01). The amplitude of the systemic response (increase in body temperature [P <.001], blood neutrophilia [P <.02], and rise in LBP [P <.05] and decrease in FEV(1) [P <.01]) were inversely associated with the atopic status, suggesting a link between atopy and LPS responsiveness.
Question: Do healthy subjects express differences in clinical responses to inhaled lipopolysaccharide that are related with inflammation and with atopy?
Output:
|
PubmedQA111565
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Chromosomal aberrations are frequently associated with birth defects and pregnancy losses. Trisomy 13, Trisomy 18 and Trisomy 21 are the most common, clinically relevant fetal aneusomies. This study used a transcriptomics approach to identify the molecular signatures at the maternal-fetal interface in each aneuploidy. We profiled placental gene expression (13-22 weeks) in T13 (n = 4), T18 (n = 4) and T21 (n = 8), and in euploid pregnancies (n = 4). We found differentially expressed transcripts (≥2-fold) in T21 (n = 160), T18 (n = 80) and T13 (n = 125). The majority were upregulated and most of the misexpressed genes were not located on the relevant trisomic chromosome, suggesting genome-wide dysregulation. A smaller number of the differentially expressed transcripts were encoded on the trisomic chromosome, suggesting gene dosage. In T21, <10% of the genes were transcribed from the Down syndrome critical region (21q21-22), which contributes to the clinical phenotype. In T13, 15% of the upregulated genes were on the affected chromosome (13q11-14), and in T18, the percentage increased to 24% (18q11-22 region).\n Question: Do placental transcriptomes in the common aneuploidies reveal critical regions on the trisomic chromosomes and genome-wide effects?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Chromosomal aberrations are frequently associated with birth defects and pregnancy losses. Trisomy 13, Trisomy 18 and Trisomy 21 are the most common, clinically relevant fetal aneusomies. This study used a transcriptomics approach to identify the molecular signatures at the maternal-fetal interface in each aneuploidy. We profiled placental gene expression (13-22 weeks) in T13 (n = 4), T18 (n = 4) and T21 (n = 8), and in euploid pregnancies (n = 4). We found differentially expressed transcripts (≥2-fold) in T21 (n = 160), T18 (n = 80) and T13 (n = 125). The majority were upregulated and most of the misexpressed genes were not located on the relevant trisomic chromosome, suggesting genome-wide dysregulation. A smaller number of the differentially expressed transcripts were encoded on the trisomic chromosome, suggesting gene dosage. In T21, <10% of the genes were transcribed from the Down syndrome critical region (21q21-22), which contributes to the clinical phenotype. In T13, 15% of the upregulated genes were on the affected chromosome (13q11-14), and in T18, the percentage increased to 24% (18q11-22 region).
Question: Do placental transcriptomes in the common aneuploidies reveal critical regions on the trisomic chromosomes and genome-wide effects?
Output:
|
PubmedQA129111
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: There is evidence for genetic susceptibility to Crohn's disease, and a tentative association with tumour necrosis factor (TNF) and HLA class II alleles. To examine the potential of genetic linkage between Crohn's disease and the MHC region on chromosome 6p. TNF microsatellite markers and, for some families, additional HLA antigens were typed for 323 individuals from 49 Crohn's disease multiplex families to generate informative haplotypes. Non-parametric linkage analysis methods, including sib pair and affected relative pair methods, were used. Increased sharing of haplotypes was observed in affected sib pairs: 92% (48/52) shared one or two haplotypes versus an expected 75% if linkage did not exist (p=0.004). After other affected relative pairs were included, the significance level reached 0.001. The mean proportion of haplotype sharing was increased for both concordant affected (pi=0.60, p=0.002) and unaffected sib pairs (pi=0.58, p=0. 031) compared with the expected value (pi=0.5). In contrast, sharing in discordant sib pairs was significantly decreased (pi=0.42, p=0. 007). Linear regression analysis using all three types of sib pairs yielded a slope of -0.38 at p=0.00003. It seemed that the HLA effect was stronger in non-Jewish families than in Jewish families.\n Question: Is linkage of Crohn 's disease to the major histocompatibility complex region detected by multiple non-parametric analyses?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: There is evidence for genetic susceptibility to Crohn's disease, and a tentative association with tumour necrosis factor (TNF) and HLA class II alleles. To examine the potential of genetic linkage between Crohn's disease and the MHC region on chromosome 6p. TNF microsatellite markers and, for some families, additional HLA antigens were typed for 323 individuals from 49 Crohn's disease multiplex families to generate informative haplotypes. Non-parametric linkage analysis methods, including sib pair and affected relative pair methods, were used. Increased sharing of haplotypes was observed in affected sib pairs: 92% (48/52) shared one or two haplotypes versus an expected 75% if linkage did not exist (p=0.004). After other affected relative pairs were included, the significance level reached 0.001. The mean proportion of haplotype sharing was increased for both concordant affected (pi=0.60, p=0.002) and unaffected sib pairs (pi=0.58, p=0. 031) compared with the expected value (pi=0.5). In contrast, sharing in discordant sib pairs was significantly decreased (pi=0.42, p=0. 007). Linear regression analysis using all three types of sib pairs yielded a slope of -0.38 at p=0.00003. It seemed that the HLA effect was stronger in non-Jewish families than in Jewish families.
Question: Is linkage of Crohn 's disease to the major histocompatibility complex region detected by multiple non-parametric analyses?
Output:
|
PubmedQA3184
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: For slim patients eligible to breast reconstruction, clinical concerns exist on availability of adequate amount of donor tissue to restore breast volume and challenges in donor-site closure, when using the deep inferior epigastric perforator (DIEP) flap. The purpose of the current study is to analyze whether the DIEP flap can provide adequate volume for breast reconstruction in slim patients, without increased complication rates or prolonged hospital stay. All patients receiving a unilateral DIEP breast reconstruction at the center 2007-2010 were included (n = 171). The patients were analyzed in subgroups of delayed and immediate reconstruction and of BMI. Complications were analyzed according to Clavien-Dindo. Flap weight was compared to mastectomy specimen weight among immediate reconstructions (n = 91). There was no difference in specimen to flap weight ratio between the different BMI-groups (BMI <25, 25-29.9 and >30: 0.81, 0.87 and 0.96 respectively, P = 0.360. Overall complication rate was 43.1% (BMI <25); 43.0% (BMI 25-29.9): and 70.0% (BMI >30) (P = 0.018). The results were similar for both the immediate and the delayed reconstructions. Length of hospital stay was similar in the different BMI groups. Delayed donor-site healing was higher in patients with BMI <25; 17.2%, compared to patients with BMI 25-29.9; 11.8%, but lower than for patients with BMI >30; 29.7% (P = 0.033).\n Question: Is breast reconstruction with the deep inferior epigastric perforator flap a reliable alternative in slim patients?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: For slim patients eligible to breast reconstruction, clinical concerns exist on availability of adequate amount of donor tissue to restore breast volume and challenges in donor-site closure, when using the deep inferior epigastric perforator (DIEP) flap. The purpose of the current study is to analyze whether the DIEP flap can provide adequate volume for breast reconstruction in slim patients, without increased complication rates or prolonged hospital stay. All patients receiving a unilateral DIEP breast reconstruction at the center 2007-2010 were included (n = 171). The patients were analyzed in subgroups of delayed and immediate reconstruction and of BMI. Complications were analyzed according to Clavien-Dindo. Flap weight was compared to mastectomy specimen weight among immediate reconstructions (n = 91). There was no difference in specimen to flap weight ratio between the different BMI-groups (BMI <25, 25-29.9 and >30: 0.81, 0.87 and 0.96 respectively, P = 0.360. Overall complication rate was 43.1% (BMI <25); 43.0% (BMI 25-29.9): and 70.0% (BMI >30) (P = 0.018). The results were similar for both the immediate and the delayed reconstructions. Length of hospital stay was similar in the different BMI groups. Delayed donor-site healing was higher in patients with BMI <25; 17.2%, compared to patients with BMI 25-29.9; 11.8%, but lower than for patients with BMI >30; 29.7% (P = 0.033).
Question: Is breast reconstruction with the deep inferior epigastric perforator flap a reliable alternative in slim patients?
Output:
|
PubmedQA11820
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Previously, the authors have reported the acceleration of tooth movement and osteoclastogenesis on the pressure site in an experimental tooth movement model by low-energy laser irradiation (LELI), which stimulated the RANK/RANKL system and c-fms/macrophage colony-stimulating factor system. However, the effect of LELI on osteogenesis on the tension site is not known clearly. Moreover, the temporal changes in alveolar bone during tooth movement have not been investigated as yet. Therefore, the present study was designed to examine the effects of LELI on alveolar bone remodeling during experimental tooth movement, and observe the temporal bone mineral density (BMD) using micro-computed tomography (muCT). To induce experimental tooth movement in rats, 10 g force was applied to the upper right first molar with Nickel titanium closed-coil. Next, a gallium-aluminum-arsenide (Ga-Al-As) diode laser was used to irradiate the area around the moved tooth, and BMD and the amount of tooth movement were measured by muCT scanning for 21 days. Histopathological examination was also performed. The amount of tooth movement in the LELI group was significantly greater than in the non-irradiation group by the end of the experimental period. Further, compared with the non-irradiation group, the fall of BMD was less in the LELI group.\n Question: Does low-energy laser irradiation accelerate the velocity of tooth movement via stimulation of the alveolar bone remodeling?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Previously, the authors have reported the acceleration of tooth movement and osteoclastogenesis on the pressure site in an experimental tooth movement model by low-energy laser irradiation (LELI), which stimulated the RANK/RANKL system and c-fms/macrophage colony-stimulating factor system. However, the effect of LELI on osteogenesis on the tension site is not known clearly. Moreover, the temporal changes in alveolar bone during tooth movement have not been investigated as yet. Therefore, the present study was designed to examine the effects of LELI on alveolar bone remodeling during experimental tooth movement, and observe the temporal bone mineral density (BMD) using micro-computed tomography (muCT). To induce experimental tooth movement in rats, 10 g force was applied to the upper right first molar with Nickel titanium closed-coil. Next, a gallium-aluminum-arsenide (Ga-Al-As) diode laser was used to irradiate the area around the moved tooth, and BMD and the amount of tooth movement were measured by muCT scanning for 21 days. Histopathological examination was also performed. The amount of tooth movement in the LELI group was significantly greater than in the non-irradiation group by the end of the experimental period. Further, compared with the non-irradiation group, the fall of BMD was less in the LELI group.
Question: Does low-energy laser irradiation accelerate the velocity of tooth movement via stimulation of the alveolar bone remodeling?
Output:
|
PubmedQA203419
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Nod like receptor pyrin domain containing 3 (NLRP3) is the best characterized member of nod like receptor family. Recent studies suggest that NLRP3 plays a crucial role in the pathogenesis of type-2 diabetes (T2DM), and variants in NLRP3 affect its mRNA stability and expression. Therefore, we hypothesize that the variants in NLRP3 gene may contribute to T2DM susceptibility. The aim of this study is to evaluate the association of NLRP3 SNPs with T2DM in Chinese Han patients. Two common variants in NLRP3 gene, rs10754558 and rs4612666, were detected using the polymerase chain reaction-restriction fragment length polymorphism procedure in 952 unrelated T2DM patients and 871 healthy controls. All participants were unrelated Chinese Hans. The GG genotype and G allele frequencies of rs10754558 were significantly higher in T2DM patients than those in controls (for GG genotype, 19.6% vs. 14.5%, p=0.019; for G allele, 43.9% vs. 39.8%, p=0.013). The GG genotype of rs10754558 was significantly associated with higher LDL-C levels and more prone to insulin resistance, as evaluated by HOMA-IR or QUICK indexes.\n Question: Are variants of NLRP3 gene associated with insulin resistance in Chinese Han population with type-2 diabetes?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Nod like receptor pyrin domain containing 3 (NLRP3) is the best characterized member of nod like receptor family. Recent studies suggest that NLRP3 plays a crucial role in the pathogenesis of type-2 diabetes (T2DM), and variants in NLRP3 affect its mRNA stability and expression. Therefore, we hypothesize that the variants in NLRP3 gene may contribute to T2DM susceptibility. The aim of this study is to evaluate the association of NLRP3 SNPs with T2DM in Chinese Han patients. Two common variants in NLRP3 gene, rs10754558 and rs4612666, were detected using the polymerase chain reaction-restriction fragment length polymorphism procedure in 952 unrelated T2DM patients and 871 healthy controls. All participants were unrelated Chinese Hans. The GG genotype and G allele frequencies of rs10754558 were significantly higher in T2DM patients than those in controls (for GG genotype, 19.6% vs. 14.5%, p=0.019; for G allele, 43.9% vs. 39.8%, p=0.013). The GG genotype of rs10754558 was significantly associated with higher LDL-C levels and more prone to insulin resistance, as evaluated by HOMA-IR or QUICK indexes.
Question: Are variants of NLRP3 gene associated with insulin resistance in Chinese Han population with type-2 diabetes?
Output:
|
PubmedQA194555
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Studies conducted in 2013 in Świnoujście area aimed at determining mosquito species distribution and analyzing sites, productivity and dynamics of larva and adult breeding as well as developing guidelines for effective mosquito control in this area. Entomological studies were conducted from March to September 2013. Distribution of mosquito larvae and adults was investigated. Mosquito larvae were observed mainly in April in transient snow-melt pools. Ochlerotatus cantans, Oc. communis, Oc. annulipes, Oc. punctor were the most predominant mosquito species. Since July, larvae of the following genera: Culex spp., Culiseta spp., Anopheles spp. were collected in standing water bodies. A total of 17 species adult mosquito were identified. Of them, Oc. communis, Aedes vexans, Culex pipiens/torrentium, Oc. Cantans, Oc. caspius predominated over other species.\n Question: Do methods of mosquito plague control in Świnoujście area based on the analysis of species distribution?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Studies conducted in 2013 in Świnoujście area aimed at determining mosquito species distribution and analyzing sites, productivity and dynamics of larva and adult breeding as well as developing guidelines for effective mosquito control in this area. Entomological studies were conducted from March to September 2013. Distribution of mosquito larvae and adults was investigated. Mosquito larvae were observed mainly in April in transient snow-melt pools. Ochlerotatus cantans, Oc. communis, Oc. annulipes, Oc. punctor were the most predominant mosquito species. Since July, larvae of the following genera: Culex spp., Culiseta spp., Anopheles spp. were collected in standing water bodies. A total of 17 species adult mosquito were identified. Of them, Oc. communis, Aedes vexans, Culex pipiens/torrentium, Oc. Cantans, Oc. caspius predominated over other species.
Question: Do methods of mosquito plague control in Świnoujście area based on the analysis of species distribution?
Output:
|
PubmedQA182777
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Ebbert et al. reported gene-gene interactions between rs11136000-rs670139 (CLU-MS4A4E) and rs3865444-rs670139 (CD33-MS4A4E). We evaluate these interactions in the largest data set for an epistasis study. We tested interactions using 3837 cases and 4145 controls from Alzheimer's Disease Genetics Consortium using meta-analyses and permutation analyses. We repeated meta-analyses stratified by apolipoprotein E (APOE) ε4 status, estimated combined odds ratio (OR) and population attributable fraction (cPAF), and explored causal variants. Results support the CLU-MS4A4E interaction and a dominant effect. An association between CLU-MS4A4E and APOE ε4 negative status exists. The estimated synergy factor, OR, and cPAF for rs11136000-rs670139 are 2.23, 2.45, and 8.0, respectively. We identified potential causal variants.\n Question: Does interaction between variants in CLU and MS4A4E modulate Alzheimer 's disease risk?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Ebbert et al. reported gene-gene interactions between rs11136000-rs670139 (CLU-MS4A4E) and rs3865444-rs670139 (CD33-MS4A4E). We evaluate these interactions in the largest data set for an epistasis study. We tested interactions using 3837 cases and 4145 controls from Alzheimer's Disease Genetics Consortium using meta-analyses and permutation analyses. We repeated meta-analyses stratified by apolipoprotein E (APOE) ε4 status, estimated combined odds ratio (OR) and population attributable fraction (cPAF), and explored causal variants. Results support the CLU-MS4A4E interaction and a dominant effect. An association between CLU-MS4A4E and APOE ε4 negative status exists. The estimated synergy factor, OR, and cPAF for rs11136000-rs670139 are 2.23, 2.45, and 8.0, respectively. We identified potential causal variants.
Question: Does interaction between variants in CLU and MS4A4E modulate Alzheimer 's disease risk?
Output:
|
PubmedQA115314
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Intrathecal administration of morphine has been shown to suppress natural killer (NK) cell activity. We tested the hypothesis that combined administration of morphine and noradrenaline would further modify NK cell activity in patients undergoing hysterectomy. Thirty female patients were randomly divided into three groups of ten patients each. Groups MN and M received intrathecal morphine (0.5 mg) dissolved in 5 ml of physiological saline with and without 5 micro g noradrenaline, respectively. Group C received saline alone. After the intrathecal administration, general anesthesia was induced. Blood samples were withdrawn before and 2 h after surgery and on postoperative days 1, 2, and 7 to determine the NK cell activity, the ratio of T-helper/inducer cells (CD4) to T-suppressor/cytotoxic cells (CD8), the levels of interleukin-6 (IL-6) and interleukin-8 (IL-8), and the plasma concentrations of catecholamines and cortisol. NK cell activity decreased on postoperative day 1 in groups MN (12.0 +/- 2.7%) and M (25.4 +/- 9.6%) compared with their respective baseline levels. In group MN, NK cell activity remained lower (23.7 +/- 8.0%) on postoperative day 2 than the baseline value before surgery.\n Question: Does addition of noradrenaline to intrathecal morphine augment the postoperative suppression of natural killer cell activity?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Intrathecal administration of morphine has been shown to suppress natural killer (NK) cell activity. We tested the hypothesis that combined administration of morphine and noradrenaline would further modify NK cell activity in patients undergoing hysterectomy. Thirty female patients were randomly divided into three groups of ten patients each. Groups MN and M received intrathecal morphine (0.5 mg) dissolved in 5 ml of physiological saline with and without 5 micro g noradrenaline, respectively. Group C received saline alone. After the intrathecal administration, general anesthesia was induced. Blood samples were withdrawn before and 2 h after surgery and on postoperative days 1, 2, and 7 to determine the NK cell activity, the ratio of T-helper/inducer cells (CD4) to T-suppressor/cytotoxic cells (CD8), the levels of interleukin-6 (IL-6) and interleukin-8 (IL-8), and the plasma concentrations of catecholamines and cortisol. NK cell activity decreased on postoperative day 1 in groups MN (12.0 +/- 2.7%) and M (25.4 +/- 9.6%) compared with their respective baseline levels. In group MN, NK cell activity remained lower (23.7 +/- 8.0%) on postoperative day 2 than the baseline value before surgery.
Question: Does addition of noradrenaline to intrathecal morphine augment the postoperative suppression of natural killer cell activity?
Output:
|
PubmedQA127834
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Decreased arterial oxygen pressure obtained at peak exercise is strong evidence of walking-induced hypoxemia, assuming that the lower pressure occurs just before exercise is stopped. Using empirical predefined models and transcutaneous oximetry, we have shown that some patients reporting exercise intolerance show a minimal value at the onset of walking and a post-exercise overshoot. These changes are referred to as transcutaneous \"walking-induced transient hacks\". In 245 patients, walking-induced transcutaneous oxygen pressure changes in the chest were analyzed using observer-independent clustering techniques. Clustering classes were compared to the profile types previously proposed with the cross-correlation technique. The classifications of patients according to both approaches were compared using kappa statistics. In 10 patients showing a hack on transcutaneous oximetry, we analyzed the results of direct iterative arterial sampling recorded during a new walking treadmill test. Clustering analysis resulted in 4 classes that closely fit the 4 most frequently proposed empirical models (cross-correlation coefficients: 0.93 to 0.97). The kappa between the two classifications was 0.865. In 10 patients showing transcutaneous hacks, the minimal direct arterial oxygen pressure value occurred at exercise onset, and these patients exhibited a recovery overshoot reaching a maximum at two minutes of recovery, confirming the walking-induced transient hypoxemia.\n Question: Is the walking-induced transient hack concept valid & relies on a transient early-exercise hypoxemia?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Decreased arterial oxygen pressure obtained at peak exercise is strong evidence of walking-induced hypoxemia, assuming that the lower pressure occurs just before exercise is stopped. Using empirical predefined models and transcutaneous oximetry, we have shown that some patients reporting exercise intolerance show a minimal value at the onset of walking and a post-exercise overshoot. These changes are referred to as transcutaneous "walking-induced transient hacks". In 245 patients, walking-induced transcutaneous oxygen pressure changes in the chest were analyzed using observer-independent clustering techniques. Clustering classes were compared to the profile types previously proposed with the cross-correlation technique. The classifications of patients according to both approaches were compared using kappa statistics. In 10 patients showing a hack on transcutaneous oximetry, we analyzed the results of direct iterative arterial sampling recorded during a new walking treadmill test. Clustering analysis resulted in 4 classes that closely fit the 4 most frequently proposed empirical models (cross-correlation coefficients: 0.93 to 0.97). The kappa between the two classifications was 0.865. In 10 patients showing transcutaneous hacks, the minimal direct arterial oxygen pressure value occurred at exercise onset, and these patients exhibited a recovery overshoot reaching a maximum at two minutes of recovery, confirming the walking-induced transient hypoxemia.
Question: Is the walking-induced transient hack concept valid & relies on a transient early-exercise hypoxemia?
Output:
|
PubmedQA124984
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The purpose of this study is to report the clinical course of fatigue-type subchondral fractures of the femoral head in young healthy adults. We retrospectively reviewed 28 consecutive patients (34 hips) who had a clear history of a sudden increase in physical activity without trauma on the hip and pelvis, and were diagnosed as having a fatigue-type subchondral fracture of the femoral head. The diagnosis was made primarily on the basis of sequential plain radiographs and magnetic resonance images. Of the 34 hips, 19 hips with no bony collapse experienced gradual disappearance of subjective pain a few months after onset, and there were no recurrences. Other 2 hips that showed bony collapse, but preserved the articular margin, also experienced no definite deterioration of collapse or arthritic change and did not need surgical intervention. In the remaining13 hips with bony collapse and destroyed articular margin or arthritic change, hip pain gradually worsened necessitating surgery.\n Question: Does fate of subchondral fatigue fractures of femoral head in young adults differ from general outcome of fracture healing?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: The purpose of this study is to report the clinical course of fatigue-type subchondral fractures of the femoral head in young healthy adults. We retrospectively reviewed 28 consecutive patients (34 hips) who had a clear history of a sudden increase in physical activity without trauma on the hip and pelvis, and were diagnosed as having a fatigue-type subchondral fracture of the femoral head. The diagnosis was made primarily on the basis of sequential plain radiographs and magnetic resonance images. Of the 34 hips, 19 hips with no bony collapse experienced gradual disappearance of subjective pain a few months after onset, and there were no recurrences. Other 2 hips that showed bony collapse, but preserved the articular margin, also experienced no definite deterioration of collapse or arthritic change and did not need surgical intervention. In the remaining13 hips with bony collapse and destroyed articular margin or arthritic change, hip pain gradually worsened necessitating surgery.
Question: Does fate of subchondral fatigue fractures of femoral head in young adults differ from general outcome of fracture healing?
Output:
|
PubmedQA150445
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The study's purpose was to analyze the effects of exercise training on exercise tolerance and left ventricular systolic function and structure in heart failure patients with preserved, mild, and moderate to severe reduction of left ventricular ejection fraction (LVEF). Ninety-eight patients with moderate to severe (n = 34), mild (n = 33), and preserved (n = 31) LVEF were randomly assigned to exercise training plus usual care (n = 65) or usual care alone (n = 33) in a randomization ratio of 2:1. Left ventricular function, left ventricular dimensions, and exercise tolerance were assessed before and after each intervention. Exercise tolerance and LVEF increased with exercise training in all patient groups, whereas they remained unchanged after usual care alone. Exercise training increased the mean ratio of early to late mitral inflow velocities (E/A ratio) and decreased deceleration time (DT) of early filling in patients with mild and preserved LVEF. In patients with moderate to severe systolic dysfunction and advanced diastolic dysfunction (DT < 160 ms), exercise training decreased E/A ratio and increased DT, both of which were unchanged after usual care alone. In the remaining patients (DT > 160 ms), exercise training also improved mitral inflow patterns. Exercise training decreased left ventricular dimensions in patients with mild and moderate to severe reduction of LVEF but not in patients with preserved LVEF.\n Question: Does exercise training improve diastolic function in heart failure patients?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: The study's purpose was to analyze the effects of exercise training on exercise tolerance and left ventricular systolic function and structure in heart failure patients with preserved, mild, and moderate to severe reduction of left ventricular ejection fraction (LVEF). Ninety-eight patients with moderate to severe (n = 34), mild (n = 33), and preserved (n = 31) LVEF were randomly assigned to exercise training plus usual care (n = 65) or usual care alone (n = 33) in a randomization ratio of 2:1. Left ventricular function, left ventricular dimensions, and exercise tolerance were assessed before and after each intervention. Exercise tolerance and LVEF increased with exercise training in all patient groups, whereas they remained unchanged after usual care alone. Exercise training increased the mean ratio of early to late mitral inflow velocities (E/A ratio) and decreased deceleration time (DT) of early filling in patients with mild and preserved LVEF. In patients with moderate to severe systolic dysfunction and advanced diastolic dysfunction (DT < 160 ms), exercise training decreased E/A ratio and increased DT, both of which were unchanged after usual care alone. In the remaining patients (DT > 160 ms), exercise training also improved mitral inflow patterns. Exercise training decreased left ventricular dimensions in patients with mild and moderate to severe reduction of LVEF but not in patients with preserved LVEF.
Question: Does exercise training improve diastolic function in heart failure patients?
Output:
|
PubmedQA76106
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The number of transplanted solid organs and life expectancy after transplantation are steadily rising worldwide. Inflammation is widely recognized as playing a pivotal role in transplant rejection, and several studies have shown that serum interleukin-6 (IL-6) levels can identify individuals who are at greater risk for rejection. Given the known association between IL-6 and chronic periodontitis, the aim of our study was to assess the periodontal status of solid-organ transplant subjects compared to systemically healthy controls, to quantify the IL-6 levels in the serum and periodontal tissues, and to explore their association. Forty-seven heart and kidney transplant and 18 systemically healthy age-matched individuals were recruited. Subjects received a complete periodontal examination, and blood and periodontal tissue samples were collected for quantification of IL-6 protein and mRNA levels, respectively. Transplant subjects had significantly higher serum IL-6 levels and slightly but statistically significantly increased mean probing depths than healthy controls. Multivariable linear regression analysis adjusting for gender, diabetes, smoking, and immunosuppressant dose showed that the mean probing depth, number of missing teeth, and mean percentage of sites with > or =4 mm attachment loss were independent predictors for elevated serum IL-6 levels. Transplant subjects with chronic periodontitis had higher mean serum IL-6 levels than those without chronic periodontitis, and there was a positive correlation between periodontal IL-6 gene expression levels and serum IL-6 protein levels.\n Question: Is elevated serum interleukin-6 ( IL-6 ) in solid-organ transplant recipients positively associated with tissue destruction and IL-6 gene expression in the periodontium?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: The number of transplanted solid organs and life expectancy after transplantation are steadily rising worldwide. Inflammation is widely recognized as playing a pivotal role in transplant rejection, and several studies have shown that serum interleukin-6 (IL-6) levels can identify individuals who are at greater risk for rejection. Given the known association between IL-6 and chronic periodontitis, the aim of our study was to assess the periodontal status of solid-organ transplant subjects compared to systemically healthy controls, to quantify the IL-6 levels in the serum and periodontal tissues, and to explore their association. Forty-seven heart and kidney transplant and 18 systemically healthy age-matched individuals were recruited. Subjects received a complete periodontal examination, and blood and periodontal tissue samples were collected for quantification of IL-6 protein and mRNA levels, respectively. Transplant subjects had significantly higher serum IL-6 levels and slightly but statistically significantly increased mean probing depths than healthy controls. Multivariable linear regression analysis adjusting for gender, diabetes, smoking, and immunosuppressant dose showed that the mean probing depth, number of missing teeth, and mean percentage of sites with > or =4 mm attachment loss were independent predictors for elevated serum IL-6 levels. Transplant subjects with chronic periodontitis had higher mean serum IL-6 levels than those without chronic periodontitis, and there was a positive correlation between periodontal IL-6 gene expression levels and serum IL-6 protein levels.
Question: Is elevated serum interleukin-6 ( IL-6 ) in solid-organ transplant recipients positively associated with tissue destruction and IL-6 gene expression in the periodontium?
Output:
|
PubmedQA198087
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Tumor-initiating cells are resistant to chemotherapy, but how microRNAs play a role in regulating drug resistance of breast tumor-initiating cells (BT-IC) needs to be clarified. Lentivirus-mediated miR-128 transduction was done in BT-ICs, enriched by mammosphere cultures or CD44(+)CD24(-) fluorescence-activated cell sorting. Apoptosis and DNA damage were determined upon treatment with doxorubicin. Expression of miR-128 in breast cancer tissues was examined by in situ hybridization and correlated with breast tumor response to neoadjuvant chemotherapy and patient survival. MiR-128 was significantly reduced in chemoresistant BT-ICs enriched from breast cancer cell lines and primary breast tumors (P < 0.01), accompanied by an overexpression of Bmi-1 and ABCC5, which were identified as targets of miR-128. Ectopic expression of miR-128 reduced the protein levels of Bmi-1 and ABCC5 in BT-ICs, along with decreased cell viability (P < 0.001) and increased apoptosis (P < 0.001) and DNA damage (P < 0.001) in the presence of doxorubicin. Reduced miR-128 expression in breast tumor tissues was associated with chemotherapeutic resistance (P < 0.001) and poor survival of breast cancer patients (P < 0.05; n = 57).\n Question: Does reduced miR-128 in breast tumor-initiating cells induce chemotherapeutic resistance via Bmi-1 and ABCC5?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Tumor-initiating cells are resistant to chemotherapy, but how microRNAs play a role in regulating drug resistance of breast tumor-initiating cells (BT-IC) needs to be clarified. Lentivirus-mediated miR-128 transduction was done in BT-ICs, enriched by mammosphere cultures or CD44(+)CD24(-) fluorescence-activated cell sorting. Apoptosis and DNA damage were determined upon treatment with doxorubicin. Expression of miR-128 in breast cancer tissues was examined by in situ hybridization and correlated with breast tumor response to neoadjuvant chemotherapy and patient survival. MiR-128 was significantly reduced in chemoresistant BT-ICs enriched from breast cancer cell lines and primary breast tumors (P < 0.01), accompanied by an overexpression of Bmi-1 and ABCC5, which were identified as targets of miR-128. Ectopic expression of miR-128 reduced the protein levels of Bmi-1 and ABCC5 in BT-ICs, along with decreased cell viability (P < 0.001) and increased apoptosis (P < 0.001) and DNA damage (P < 0.001) in the presence of doxorubicin. Reduced miR-128 expression in breast tumor tissues was associated with chemotherapeutic resistance (P < 0.001) and poor survival of breast cancer patients (P < 0.05; n = 57).
Question: Does reduced miR-128 in breast tumor-initiating cells induce chemotherapeutic resistance via Bmi-1 and ABCC5?
Output:
|
PubmedQA138512
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Pancreatic autoantibodies (PABs) specifically recognizing GP2 and/or CUZD1 are present in more than 35% of patients with Crohn's disease (CrD). We have recently provided evidence of the presence of GP2-specific PABs in ruminants with paratuberculosis (ptb), a Mycobacterium avium paratuberculosis (MAP)-induced disease resembling CrD. To assess whether anti-CUZD1 antibodies are also present in ruminants with ptb. A total of 110 samples (73 cattle/37 sheep) were studied including 40 with ptb (24 cattle/16 sheep; 20 anti-GP2 antibody pos) and 70 without ptb (49 cattle/21 sheep; 10 anti-GP2 antibody pos). The samples were pre-characterized for anti-MAP and anti-GP2 antibodies by ELISA. Evidence of MAP was confirmed by PCR. Anti-CUZD1 antibody testing was performed by indirect immunofluorescence (IIF) based on transfected HEK293 cells expressing CUZD1. Anti-sheep or anti-cattle specific antisera were used as revealing antibodies. None of the ruminant sera had anti-CUZD1 antibodies by IIF testing at dilutions varying from 1/10 to 1/160. Methodological flaws were prevented by a series of tests. Control sera from anti-CUZD1 positive CrD samples have shown anti-CUZD1 antibody reactivity at various concentrations. Antibody reactivity to GP2-expressing HEK293 cells has confirmed the reactivity to GP2 in ruminant sera found positive for anti-GP2 antibodies by ELISA.\n Question: Are crohn 's disease-specific anti-CUZD1 pancreatic antibodies absent in ruminants with paratuberculosis?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Pancreatic autoantibodies (PABs) specifically recognizing GP2 and/or CUZD1 are present in more than 35% of patients with Crohn's disease (CrD). We have recently provided evidence of the presence of GP2-specific PABs in ruminants with paratuberculosis (ptb), a Mycobacterium avium paratuberculosis (MAP)-induced disease resembling CrD. To assess whether anti-CUZD1 antibodies are also present in ruminants with ptb. A total of 110 samples (73 cattle/37 sheep) were studied including 40 with ptb (24 cattle/16 sheep; 20 anti-GP2 antibody pos) and 70 without ptb (49 cattle/21 sheep; 10 anti-GP2 antibody pos). The samples were pre-characterized for anti-MAP and anti-GP2 antibodies by ELISA. Evidence of MAP was confirmed by PCR. Anti-CUZD1 antibody testing was performed by indirect immunofluorescence (IIF) based on transfected HEK293 cells expressing CUZD1. Anti-sheep or anti-cattle specific antisera were used as revealing antibodies. None of the ruminant sera had anti-CUZD1 antibodies by IIF testing at dilutions varying from 1/10 to 1/160. Methodological flaws were prevented by a series of tests. Control sera from anti-CUZD1 positive CrD samples have shown anti-CUZD1 antibody reactivity at various concentrations. Antibody reactivity to GP2-expressing HEK293 cells has confirmed the reactivity to GP2 in ruminant sera found positive for anti-GP2 antibodies by ELISA.
Question: Are crohn 's disease-specific anti-CUZD1 pancreatic antibodies absent in ruminants with paratuberculosis?
Output:
|
PubmedQA184575
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: In vital pulp therapy such as direct pulp capping, clinical success rates depend on achieving hemostasis in exposed pulp tissue. For hemostasis of exposed pulp tissue, gentle pressure by cotton pellets moistened with sodium hypochlorite is most commonly used. However, more rapid and reliable methods are necessary. Therefore, we focused on high-frequency radio waves (HRW). To evaluate reparative dentin induction by HRW, we used a rat direct pulp capping model and performed hemostasis by using HRW of several strengths, covering the pulp with calcium hydroxide as a direct capping agent. After 14 or 28 days, rats were killed, and reparative dentin and pulp inflammation were investigated histologically. Radio wave-induced hemostasis required less time when compared with the control group. Reparative dentin with regularly arranged dentinal tubules was observed in the HRW group.\n Question: Do application of high-frequency radio waves to direct pulp capping?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: In vital pulp therapy such as direct pulp capping, clinical success rates depend on achieving hemostasis in exposed pulp tissue. For hemostasis of exposed pulp tissue, gentle pressure by cotton pellets moistened with sodium hypochlorite is most commonly used. However, more rapid and reliable methods are necessary. Therefore, we focused on high-frequency radio waves (HRW). To evaluate reparative dentin induction by HRW, we used a rat direct pulp capping model and performed hemostasis by using HRW of several strengths, covering the pulp with calcium hydroxide as a direct capping agent. After 14 or 28 days, rats were killed, and reparative dentin and pulp inflammation were investigated histologically. Radio wave-induced hemostasis required less time when compared with the control group. Reparative dentin with regularly arranged dentinal tubules was observed in the HRW group.
Question: Do application of high-frequency radio waves to direct pulp capping?
Output:
|
PubmedQA169029
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Hemodynamic forces play a crucial role in regulating vascular cell phenotype. However, the underlying molecular mechanisms are largely unknown. The objective of this study was to test our hypothesis that cyclic strain could affect smooth muscle cell (SMC) differentiation. A murine embryonic mesenchymal progenitor cell line (C3H/10T1/2) was cultured with or without cyclic strain for 6 days. Changes in cell morphology were studied with fluorescence dye Calcein-AM staining. Expression of specific SMC markers, smooth muscle specific alpha-actin (alpha-SMA), and smooth muscle myosin heavy chain (SMMHC), was determined by real-time polymerase chain reaction (PCR) and Western blot. Transforming growth factor- beta (TGF-beta) was used as a positive control. With cyclic strain, CH3/10T1/2 cells demonstrated spindle-shaped morphology and parallel alignment. Cells exposed to cyclic strain illustrated significantly increased mRNA levels of alpha-SMA and SMMHC by 3- and 2-fold, respectively, compared with static cells (P<.05). In addition, cells cultured under cyclic strain with TGF-beta (2 ng/ml) supplementation demonstrated increased mRNA levels of alpha-SMA and SMMHC by 10- and 2-fold, respectively, compared with static cells (P<.05). Furthermore, protein levels of alpha-SMA and SMMHC were also significantly increased by more than 3-fold in cyclic strain-treated cells compared with static cultures (P<.05). TGF-beta synergistically enhanced the effect of cyclic strain on alpha-SMA mRNA expression in CH3/10T1/2 cells.\n Question: Does cyclic strain induce vascular smooth muscle cell differentiation from murine embryonic mesenchymal progenitor cells?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Hemodynamic forces play a crucial role in regulating vascular cell phenotype. However, the underlying molecular mechanisms are largely unknown. The objective of this study was to test our hypothesis that cyclic strain could affect smooth muscle cell (SMC) differentiation. A murine embryonic mesenchymal progenitor cell line (C3H/10T1/2) was cultured with or without cyclic strain for 6 days. Changes in cell morphology were studied with fluorescence dye Calcein-AM staining. Expression of specific SMC markers, smooth muscle specific alpha-actin (alpha-SMA), and smooth muscle myosin heavy chain (SMMHC), was determined by real-time polymerase chain reaction (PCR) and Western blot. Transforming growth factor- beta (TGF-beta) was used as a positive control. With cyclic strain, CH3/10T1/2 cells demonstrated spindle-shaped morphology and parallel alignment. Cells exposed to cyclic strain illustrated significantly increased mRNA levels of alpha-SMA and SMMHC by 3- and 2-fold, respectively, compared with static cells (P<.05). In addition, cells cultured under cyclic strain with TGF-beta (2 ng/ml) supplementation demonstrated increased mRNA levels of alpha-SMA and SMMHC by 10- and 2-fold, respectively, compared with static cells (P<.05). Furthermore, protein levels of alpha-SMA and SMMHC were also significantly increased by more than 3-fold in cyclic strain-treated cells compared with static cultures (P<.05). TGF-beta synergistically enhanced the effect of cyclic strain on alpha-SMA mRNA expression in CH3/10T1/2 cells.
Question: Does cyclic strain induce vascular smooth muscle cell differentiation from murine embryonic mesenchymal progenitor cells?
Output:
|
PubmedQA210232
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Venous occlusion is a recognized complication of transvenous pacing, and lead cross-sectional area indexed to body surface area (BSA) has been used to predict venous obstruction in children. The aim of this study was to identify the risk factors and incidence of angiographic venous obstruction after transvenous lead implantation in both children and young adults. Contrast venography was obtained in 85 of 90 consecutive patients undergoing repeat pacemaker or ICD procedures from 2002 to 2004 at a single cardiac center. Venograms were graded as complete venous obstruction, significant partial obstruction (>70% with collaterals), or patent. The cohort had a median age of 15.0 years at implant and was divided into two age groups: 3-12 years (n = 35) and 13 years and over (n = 50). After a median interval of 6.5 years, complete obstruction was seen in 11 of 85 patients (13%) and partial obstruction in another 10 patients (12%). No significant differences were seen in the incidence of obstruction between the two age groups although younger patients had a larger lead indexed to BSA ratio (6.82 vs 5.05, P = 0.005). There were no significant differences between obstructed and nonobstructed patients in relation to age, size, growth, or lead factors.\n Question: Do age , size , and lead factors alone predict venous obstruction in children and young adults with transvenous lead systems?\n Output: "
},
{
"role": "assistant",
"content": "no"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Venous occlusion is a recognized complication of transvenous pacing, and lead cross-sectional area indexed to body surface area (BSA) has been used to predict venous obstruction in children. The aim of this study was to identify the risk factors and incidence of angiographic venous obstruction after transvenous lead implantation in both children and young adults. Contrast venography was obtained in 85 of 90 consecutive patients undergoing repeat pacemaker or ICD procedures from 2002 to 2004 at a single cardiac center. Venograms were graded as complete venous obstruction, significant partial obstruction (>70% with collaterals), or patent. The cohort had a median age of 15.0 years at implant and was divided into two age groups: 3-12 years (n = 35) and 13 years and over (n = 50). After a median interval of 6.5 years, complete obstruction was seen in 11 of 85 patients (13%) and partial obstruction in another 10 patients (12%). No significant differences were seen in the incidence of obstruction between the two age groups although younger patients had a larger lead indexed to BSA ratio (6.82 vs 5.05, P = 0.005). There were no significant differences between obstructed and nonobstructed patients in relation to age, size, growth, or lead factors.
Question: Do age , size , and lead factors alone predict venous obstruction in children and young adults with transvenous lead systems?
Output:
|
PubmedQA24284
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Anti-acetylcholine receptor (AChR) autoantibodies target muscles in spontaneous human myasthenia gravis (MG) and its induced experimental autoimmune model MG (EAMG). The aim of this study was to identify novel functional mechanisms occurring in the muscle pathology of myasthenia. A transcriptome analysis performed on muscle tissue from MG patients (compared with healthy controls) and from EAMG rats (compared with control rats) revealed a deregulation of genes associated with the Interleukin-6 (IL-6) and Insulin-Like Growth Factor 1 (IGF-1) pathways in both humans and rats. The expression of IL-6 and its receptor IL-6R transcripts was found to be altered in muscles of EAMG rats and mice compared with control animals. In muscle biopsies from MG patients, IL-6 protein level was higher than in control muscles. Using cultures of human muscle cells, we evaluated the effects of anti-AChR antibodies on IL-6 production and on the phosphorylation of Protein Kinase B (PKB/Akt). Most MG sera and some monoclonal anti-AChR antibodies induced a significant increase in IL-6 production by human muscle cells. Furthermore, Akt phosphorylation in response to insulin was decreased in the presence of monoclonal anti-AChR antibodies.\n Question: Are iL-6 and Akt involved in muscular pathogenesis in myasthenia gravis?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Anti-acetylcholine receptor (AChR) autoantibodies target muscles in spontaneous human myasthenia gravis (MG) and its induced experimental autoimmune model MG (EAMG). The aim of this study was to identify novel functional mechanisms occurring in the muscle pathology of myasthenia. A transcriptome analysis performed on muscle tissue from MG patients (compared with healthy controls) and from EAMG rats (compared with control rats) revealed a deregulation of genes associated with the Interleukin-6 (IL-6) and Insulin-Like Growth Factor 1 (IGF-1) pathways in both humans and rats. The expression of IL-6 and its receptor IL-6R transcripts was found to be altered in muscles of EAMG rats and mice compared with control animals. In muscle biopsies from MG patients, IL-6 protein level was higher than in control muscles. Using cultures of human muscle cells, we evaluated the effects of anti-AChR antibodies on IL-6 production and on the phosphorylation of Protein Kinase B (PKB/Akt). Most MG sera and some monoclonal anti-AChR antibodies induced a significant increase in IL-6 production by human muscle cells. Furthermore, Akt phosphorylation in response to insulin was decreased in the presence of monoclonal anti-AChR antibodies.
Question: Are iL-6 and Akt involved in muscular pathogenesis in myasthenia gravis?
Output:
|
PubmedQA112023
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Brain atrophy, as assessed by magnetic resonance imaging (MRI), has been correlated with disability in patients with multiple sclerosis (MS). Recent evidence indicates that both white matter (WM) and gray matter (GM) are subject to atrophy in patients with MS. Although neurological deficiencies in MS are primarily due to loss of WM, the clinical significance of GM atrophy has not been fully explored in MS. We have undertaken a three-year, open-label study, comparing 26 patients who elected to receive intramuscular interferon beta-1a (IFN beta-1a) therapy, with 28 patients who elected not to receive therapy. Both groups had quantitative cranial MRI scans at study entry and after three years, and standardized clinical assessments every six months. Brain parenchymal fraction (BPF), GM fraction (GMF), and WM fraction (WMF) percent changes were calculated, and T2- and T1-lesion volumes (LVs) assessed. After three years, mean percent (%) change in BPF favored the IFN beta-1a treatment group (IFN beta-1a -1.3% versus the control group -2.5%, P=0.009), as did the mean percent change in GMF (+0.2 versus -1.4%, P=0.014), and the mean percent change in T1-LV (-9.3 versus +91.6%, P=0.011). At the end of the study, there was a significant within-patient decrease in BPF for both groups (P=0.02 for the IFN beta-1a treatment group, and P<0.001 for the control group), a significant within-patient decrease in WMF for the IFN beta-1a treatment group (P=0.01), and a significant decrease in GMF for the control group (P=0.013) when compared with baseline.\n Question: Does interferon beta-1a slow progression of brain atrophy in relapsing-remitting multiple sclerosis predominantly by reducing gray matter atrophy?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Brain atrophy, as assessed by magnetic resonance imaging (MRI), has been correlated with disability in patients with multiple sclerosis (MS). Recent evidence indicates that both white matter (WM) and gray matter (GM) are subject to atrophy in patients with MS. Although neurological deficiencies in MS are primarily due to loss of WM, the clinical significance of GM atrophy has not been fully explored in MS. We have undertaken a three-year, open-label study, comparing 26 patients who elected to receive intramuscular interferon beta-1a (IFN beta-1a) therapy, with 28 patients who elected not to receive therapy. Both groups had quantitative cranial MRI scans at study entry and after three years, and standardized clinical assessments every six months. Brain parenchymal fraction (BPF), GM fraction (GMF), and WM fraction (WMF) percent changes were calculated, and T2- and T1-lesion volumes (LVs) assessed. After three years, mean percent (%) change in BPF favored the IFN beta-1a treatment group (IFN beta-1a -1.3% versus the control group -2.5%, P=0.009), as did the mean percent change in GMF (+0.2 versus -1.4%, P=0.014), and the mean percent change in T1-LV (-9.3 versus +91.6%, P=0.011). At the end of the study, there was a significant within-patient decrease in BPF for both groups (P=0.02 for the IFN beta-1a treatment group, and P<0.001 for the control group), a significant within-patient decrease in WMF for the IFN beta-1a treatment group (P=0.01), and a significant decrease in GMF for the control group (P=0.013) when compared with baseline.
Question: Does interferon beta-1a slow progression of brain atrophy in relapsing-remitting multiple sclerosis predominantly by reducing gray matter atrophy?
Output:
|
PubmedQA163408
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Irritable bowel syndrome (IBS) is a chronic, episodic gastrointestinal disorder that is prevalent in a significant fraction of western human populations; and changes in the microbiota of the large bowel have been implicated in the pathology of the disease. Using a novel comprehensive, high-density DNA microarray (PhyloChip) we performed a phylogenetic analysis of the microbial community of the large bowel in a rat model in which intracolonic acetic acid in neonates was used to induce long lasting colonic hypersensitivity and decreased stool water content and frequency, representing the equivalent of human constipation-predominant IBS. Our results revealed a significantly increased compositional difference in the microbial communities in rats with neonatal irritation as compared with controls. Even more striking was the dramatic change in the ratio of Firmicutes relative to Bacteroidetes, where neonatally irritated rats were enriched more with Bacteroidetes and also contained a different composition of species within this phylum. Our study also revealed differences at the level of bacterial families and species.\n Question: Does phyloChip microarray analysis reveal altered gastrointestinal microbial communities in a rat model of colonic hypersensitivity?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Irritable bowel syndrome (IBS) is a chronic, episodic gastrointestinal disorder that is prevalent in a significant fraction of western human populations; and changes in the microbiota of the large bowel have been implicated in the pathology of the disease. Using a novel comprehensive, high-density DNA microarray (PhyloChip) we performed a phylogenetic analysis of the microbial community of the large bowel in a rat model in which intracolonic acetic acid in neonates was used to induce long lasting colonic hypersensitivity and decreased stool water content and frequency, representing the equivalent of human constipation-predominant IBS. Our results revealed a significantly increased compositional difference in the microbial communities in rats with neonatal irritation as compared with controls. Even more striking was the dramatic change in the ratio of Firmicutes relative to Bacteroidetes, where neonatally irritated rats were enriched more with Bacteroidetes and also contained a different composition of species within this phylum. Our study also revealed differences at the level of bacterial families and species.
Question: Does phyloChip microarray analysis reveal altered gastrointestinal microbial communities in a rat model of colonic hypersensitivity?
Output:
|
PubmedQA21373
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Research is equivocal regarding endurance performance benefits of external nasal dilators, and currently research focusing on internal nasal dilators is non-existent. Both devices are used within competitive cycling. This study examined the influence of external and internal nasal dilation on cycling economy of motion and 20-km time trial performance. The study utilized a randomized, counterbalanced cross-over design. Fifteen trained cyclists completed three exercise sessions consisting of a 15min standardized warm up and 20-km cycling time trial while wearing either a Breathe Right No differences were observed for mean 20-km power output between the internal (270±45W) or external dilator (271±44W) and control (272±44W). No differences in the economy of motion were observed throughout the 15-min warm up between conditions.\n Question: Does neither internal nor external nasal dilation improve cycling 20-km time trial performance?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Research is equivocal regarding endurance performance benefits of external nasal dilators, and currently research focusing on internal nasal dilators is non-existent. Both devices are used within competitive cycling. This study examined the influence of external and internal nasal dilation on cycling economy of motion and 20-km time trial performance. The study utilized a randomized, counterbalanced cross-over design. Fifteen trained cyclists completed three exercise sessions consisting of a 15min standardized warm up and 20-km cycling time trial while wearing either a Breathe Right No differences were observed for mean 20-km power output between the internal (270±45W) or external dilator (271±44W) and control (272±44W). No differences in the economy of motion were observed throughout the 15-min warm up between conditions.
Question: Does neither internal nor external nasal dilation improve cycling 20-km time trial performance?
Output:
|
PubmedQA79603
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The aim of this study was to investigate whether the inability of chronic renal failure patients to mount an adequate antibody response following hepatitis B vaccination was due to an inherent defect in the antibody producing capacity of their B cells. Peripheral blood mononuclear cells of end stage renal disease (ESRD) patients, who were not on maintenance hemodialysis (CRF) and those undergoing long-term hemodialysis (HD) were stimulated in vitro with pokeweed mitogen, a B cell mitogen or hepatitis B surface antigen. The total immunoglobulin (IgG, IgM and IgA) levels and anti-HBs specific IgM and IgG were quantitiated by sandwich ELISA and levels between patients who had a good antibody response in vivo and those who failed to mount an antibody response were compared. Spontaneous IgG production was significantly higher than normals in CRF and HD group; PWM induced IgM, IgG and IgA production was comparable to normals in both groups of patients. The spontaneous IgG and PWM stimulated IgM and IgG production was significantly higher in HD patients as compared to CRF. The in vitro Ig levels in the vaccine responders and non-responders was comparable except for the spontaneous IgG which was highest in the responders. The in vitro anti-HBs production was comparable in HB vaccine responders and non-responders; the in vivo and in vitro anti-HBs titers showed a significant correlation coefficient thereby indicating that the in vitro assay reflects the in vivo functional status of B cells.\n Question: Is low response to HBsAg vaccine in chronic renal failure patients due to intrinsic defect of B cells?\n Output: "
},
{
"role": "assistant",
"content": "no"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: The aim of this study was to investigate whether the inability of chronic renal failure patients to mount an adequate antibody response following hepatitis B vaccination was due to an inherent defect in the antibody producing capacity of their B cells. Peripheral blood mononuclear cells of end stage renal disease (ESRD) patients, who were not on maintenance hemodialysis (CRF) and those undergoing long-term hemodialysis (HD) were stimulated in vitro with pokeweed mitogen, a B cell mitogen or hepatitis B surface antigen. The total immunoglobulin (IgG, IgM and IgA) levels and anti-HBs specific IgM and IgG were quantitiated by sandwich ELISA and levels between patients who had a good antibody response in vivo and those who failed to mount an antibody response were compared. Spontaneous IgG production was significantly higher than normals in CRF and HD group; PWM induced IgM, IgG and IgA production was comparable to normals in both groups of patients. The spontaneous IgG and PWM stimulated IgM and IgG production was significantly higher in HD patients as compared to CRF. The in vitro Ig levels in the vaccine responders and non-responders was comparable except for the spontaneous IgG which was highest in the responders. The in vitro anti-HBs production was comparable in HB vaccine responders and non-responders; the in vivo and in vitro anti-HBs titers showed a significant correlation coefficient thereby indicating that the in vitro assay reflects the in vivo functional status of B cells.
Question: Is low response to HBsAg vaccine in chronic renal failure patients due to intrinsic defect of B cells?
Output:
|
PubmedQA93375
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To determine the effect of human recombinant TIGR/myocilin (MYOC) protein on outflow resistance in the human anterior segment. A cDNA for MYOC was inserted into a bacterial expression system and purified with nickel ion affinity chromatography. The anterior segments of 12 pairs of human eyes were placed in perfusion organ culture. One eye received an anterior chamber exchange with partially purified recombinant MYOC (25 microgram), whereas the other eye received either heat-denatured recombinant MYOC (25 microgram), partially purified ss-galactosidase (25 or 250 microgram), or partially purified control proteins isolated from a null expression lysate (25 microgram). Eyes were fixed up to 72 hours after infusion, and immunohistochemistry was performed using anti-MYOC polyclonal antibody. Recombinant MYOC caused an increase in IOP over 12 hours, increasing outflow resistance 94%, whereas the fellow eye infused with null expression sample increased 12% (n = 7; P = 0.0005). When compared with recombinant MYOC, neither heat-denatured MYOC, recombinant ss-galactosidase, bovine serum albumin, nor fetal calf serum caused an increase in outflow resistance. MYOC IOP remained above baseline levels for 48 to 72 hours. Immunohistochemistry results confirmed the presence of recombinant MYOC in the trabecular meshwork.\n Question: Does recombinant TIGR/MYOC increase outflow resistance in the human anterior segment?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To determine the effect of human recombinant TIGR/myocilin (MYOC) protein on outflow resistance in the human anterior segment. A cDNA for MYOC was inserted into a bacterial expression system and purified with nickel ion affinity chromatography. The anterior segments of 12 pairs of human eyes were placed in perfusion organ culture. One eye received an anterior chamber exchange with partially purified recombinant MYOC (25 microgram), whereas the other eye received either heat-denatured recombinant MYOC (25 microgram), partially purified ss-galactosidase (25 or 250 microgram), or partially purified control proteins isolated from a null expression lysate (25 microgram). Eyes were fixed up to 72 hours after infusion, and immunohistochemistry was performed using anti-MYOC polyclonal antibody. Recombinant MYOC caused an increase in IOP over 12 hours, increasing outflow resistance 94%, whereas the fellow eye infused with null expression sample increased 12% (n = 7; P = 0.0005). When compared with recombinant MYOC, neither heat-denatured MYOC, recombinant ss-galactosidase, bovine serum albumin, nor fetal calf serum caused an increase in outflow resistance. MYOC IOP remained above baseline levels for 48 to 72 hours. Immunohistochemistry results confirmed the presence of recombinant MYOC in the trabecular meshwork.
Question: Does recombinant TIGR/MYOC increase outflow resistance in the human anterior segment?
Output:
|
PubmedQA2824
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Adenoid cystic carcinomas are rare tumors with an indolent clinical course, but frequent local relapses. The identification of tumors with a higher relapse risk seems to be interesting. Hence we investigated parameters of glucose metabolism, which were found associated with poor prognosis in other malignancies. Specimen of 29 patients were investigated immunohistochemically with antibodies against p-AKT, TKTL-1 (transketolase-like 1), M2PK (M2 pyruvate kinase), and GLUT-1. Proliferation was investigated by staining with Ki67. The tumors were located at the major or minor salivary glands. Only the typical cribriform subtype was investigated. The initial tumor stage was pT1 or pT2. Expression of p-AKT was significantly (P = 0.036) associated with a higher relapse risk in multivariate analysis. Low expression of M2PK was non-significantly (P = 0.065) predictive for a higher risk. TKTL-1 and GLUT-1 were expressed in the majority of cases, albeit not associated with relapse risk.\n Question: Does expression of p-AKT characterize adenoid cystic carcinomas of head and neck with a higher risk for tumor relapses?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Adenoid cystic carcinomas are rare tumors with an indolent clinical course, but frequent local relapses. The identification of tumors with a higher relapse risk seems to be interesting. Hence we investigated parameters of glucose metabolism, which were found associated with poor prognosis in other malignancies. Specimen of 29 patients were investigated immunohistochemically with antibodies against p-AKT, TKTL-1 (transketolase-like 1), M2PK (M2 pyruvate kinase), and GLUT-1. Proliferation was investigated by staining with Ki67. The tumors were located at the major or minor salivary glands. Only the typical cribriform subtype was investigated. The initial tumor stage was pT1 or pT2. Expression of p-AKT was significantly (P = 0.036) associated with a higher relapse risk in multivariate analysis. Low expression of M2PK was non-significantly (P = 0.065) predictive for a higher risk. TKTL-1 and GLUT-1 were expressed in the majority of cases, albeit not associated with relapse risk.
Question: Does expression of p-AKT characterize adenoid cystic carcinomas of head and neck with a higher risk for tumor relapses?
Output:
|
PubmedQA129266
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: In vertebrate development, the segmental pattern of the body axis is established as somites, masses of mesoderm distributed along the two sides of the neural tube, are formed sequentially in the anterior-posterior axis. This mechanism depends on waves of gene expression associated with the Notch, Fgf and Wnt pathways. The underlying transcriptional regulation has been studied by whole-transcriptome mRNA profiling; however, interpretation of the results is limited by poor resolution, noisy data, small sample size and by the absence of a wall clock to assign exact time for recorded points. We present a method of Maximum Entropy deconvolution in both space and time and apply it to extract, from microarray timecourse data, the full spatiotemporal expression profiles of genes involved in mouse somitogenesis. For regulated genes, we have reconstructed the temporal profiles and determined the timing of expression peaks along the somite cycle to a single-minute resolution. Our results also indicate the presence of a new class of genes (including Raf1 and Hes7) with two peaks of activity in two distinct phases of the somite cycle. We demonstrate that the timeline of gene expression precisely reflects their functions in the biochemical pathways and the direction of causation in the regulatory networks.\n Question: Does the precise timeline of transcriptional regulation reveal causation in mouse somitogenesis network?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: In vertebrate development, the segmental pattern of the body axis is established as somites, masses of mesoderm distributed along the two sides of the neural tube, are formed sequentially in the anterior-posterior axis. This mechanism depends on waves of gene expression associated with the Notch, Fgf and Wnt pathways. The underlying transcriptional regulation has been studied by whole-transcriptome mRNA profiling; however, interpretation of the results is limited by poor resolution, noisy data, small sample size and by the absence of a wall clock to assign exact time for recorded points. We present a method of Maximum Entropy deconvolution in both space and time and apply it to extract, from microarray timecourse data, the full spatiotemporal expression profiles of genes involved in mouse somitogenesis. For regulated genes, we have reconstructed the temporal profiles and determined the timing of expression peaks along the somite cycle to a single-minute resolution. Our results also indicate the presence of a new class of genes (including Raf1 and Hes7) with two peaks of activity in two distinct phases of the somite cycle. We demonstrate that the timeline of gene expression precisely reflects their functions in the biochemical pathways and the direction of causation in the regulatory networks.
Question: Does the precise timeline of transcriptional regulation reveal causation in mouse somitogenesis network?
Output:
|
PubmedQA69922
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Patients who undergo endovascular treatment of superficial femoral artery (SFA) disease vary greatly in lesion complexity and treatment options. This study examined the association of lesion severity and cost of SFA stenting and to determine if procedure cost affects primary patency at 1 year. A retrospective record review identified patients undergoing initial SFA stenting between January 1, 2010, and February 1, 2012. Medical records were reviewed to collect data on demographics, comorbidities, indication for the procedure, TransAtlantic Inter-Society Consensus (TASC) II severity, and primary patency. The interventional radiology database and hospital accounting database were queried to determine cost drivers of SFA stenting. Procedure supply cost included any item with a bar code used for the procedure. Associations between cost drivers and lesion characteristics were explored. Primary patency was determined using Kaplan-Meier survival curves and a log-rank test. During the study period, 95 patients underwent stenting in 98 extremities; of these, 61% of SFA stents were performed for claudication, with 80% of lesions classified as TASC II A or B. Primary patency at 1 year was 79% for the entire cohort. The mean total cost per case was $10,333. Increased procedure supply cost was associated with adjunct device use, the number of stents, and TASC II severity. Despite higher costs of treating more complex lesions, primary patency at 1 year was similar at 80% for high-cost (supply cost >$4000) vs 78% for low-cost (supply cost <$4000) interventions.\n Question: Does lesion complexity drive the cost of superficial femoral artery endovascular interventions?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Patients who undergo endovascular treatment of superficial femoral artery (SFA) disease vary greatly in lesion complexity and treatment options. This study examined the association of lesion severity and cost of SFA stenting and to determine if procedure cost affects primary patency at 1 year. A retrospective record review identified patients undergoing initial SFA stenting between January 1, 2010, and February 1, 2012. Medical records were reviewed to collect data on demographics, comorbidities, indication for the procedure, TransAtlantic Inter-Society Consensus (TASC) II severity, and primary patency. The interventional radiology database and hospital accounting database were queried to determine cost drivers of SFA stenting. Procedure supply cost included any item with a bar code used for the procedure. Associations between cost drivers and lesion characteristics were explored. Primary patency was determined using Kaplan-Meier survival curves and a log-rank test. During the study period, 95 patients underwent stenting in 98 extremities; of these, 61% of SFA stents were performed for claudication, with 80% of lesions classified as TASC II A or B. Primary patency at 1 year was 79% for the entire cohort. The mean total cost per case was $10,333. Increased procedure supply cost was associated with adjunct device use, the number of stents, and TASC II severity. Despite higher costs of treating more complex lesions, primary patency at 1 year was similar at 80% for high-cost (supply cost >$4000) vs 78% for low-cost (supply cost <$4000) interventions.
Question: Does lesion complexity drive the cost of superficial femoral artery endovascular interventions?
Output:
|
PubmedQA157827
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To define a minimal set of descriptive parameters for cochlear morphology and study its influence on the cochlear implant electrode position in relation to surgical insertion distance. Cochlear morphology and electrode position were analyzed using multiplanar reconstructions of the pre- and postoperative CT scans in a population of 336 patients (including 26 bilaterally implanted ones) with a CII HiFocus1 or HiRes90K HiFocus1J implant. Variations in cochlear diameter and cochlear canal size were analyzed. The relationship between the outer and inner walls was investigated. Size differences based on sex, age, and ear side were investigated using linear mixed models. Two new methods, spiral fitting and principal component analysis, were proposed to describe cochlear shape, and the goodness of fit was investigated. The relationship between cochlear shape and electrode position, in terms of modiolus proximity and insertion depth, was analyzed using clustering, one-way analysis of variance (ANOVA) and simple linear regression analysis. Large variations in cochlear morphology were found, with cochlear canal sizes ranging from 0.98 to 2.96 mm and average cochlear diameters between 8.85 and 5.92 mm (with standard deviations of around 0.4 mm). The outer and inner walls were significantly correlated (p < 0.01), and a size difference of 4% in favor of males was found. Spiral fitting shows good alignment of the true measurements, with residuals having a mean of 0.01 mm and a standard deviation of 0.29 mm. Principal component analysis (PCA) showed that the use of one component, which describes size, is sufficient to explain 93.6% of the cochlear shape variance. A significant sex difference was also found with spiral fitting and PCA. Cochlear size was found to have a significant influence on modiolus proximity and insertion depth of the electrode (p < 0.01). Cochlear size explained around 13% of the variance in electrode position. When cochlear size was combined with surgical insertion, more than 81% of the variance in insertion depth can be explained.\n Question: Do diversity in cochlear morphology and its influence on cochlear implant electrode position?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To define a minimal set of descriptive parameters for cochlear morphology and study its influence on the cochlear implant electrode position in relation to surgical insertion distance. Cochlear morphology and electrode position were analyzed using multiplanar reconstructions of the pre- and postoperative CT scans in a population of 336 patients (including 26 bilaterally implanted ones) with a CII HiFocus1 or HiRes90K HiFocus1J implant. Variations in cochlear diameter and cochlear canal size were analyzed. The relationship between the outer and inner walls was investigated. Size differences based on sex, age, and ear side were investigated using linear mixed models. Two new methods, spiral fitting and principal component analysis, were proposed to describe cochlear shape, and the goodness of fit was investigated. The relationship between cochlear shape and electrode position, in terms of modiolus proximity and insertion depth, was analyzed using clustering, one-way analysis of variance (ANOVA) and simple linear regression analysis. Large variations in cochlear morphology were found, with cochlear canal sizes ranging from 0.98 to 2.96 mm and average cochlear diameters between 8.85 and 5.92 mm (with standard deviations of around 0.4 mm). The outer and inner walls were significantly correlated (p < 0.01), and a size difference of 4% in favor of males was found. Spiral fitting shows good alignment of the true measurements, with residuals having a mean of 0.01 mm and a standard deviation of 0.29 mm. Principal component analysis (PCA) showed that the use of one component, which describes size, is sufficient to explain 93.6% of the cochlear shape variance. A significant sex difference was also found with spiral fitting and PCA. Cochlear size was found to have a significant influence on modiolus proximity and insertion depth of the electrode (p < 0.01). Cochlear size explained around 13% of the variance in electrode position. When cochlear size was combined with surgical insertion, more than 81% of the variance in insertion depth can be explained.
Question: Do diversity in cochlear morphology and its influence on cochlear implant electrode position?
Output:
|
PubmedQA143538
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: It is useful to decide whether lymphatic involvement or lymph node metastasis exists before polypectomy or operation in submucosal colorectal cancer. Whether vascular endothelial growth factor-C (VEGF-C) or VEGF-D could predict lymph node metastasis and lymphatic involvement is uncertain. Expression of the VEGF-C and VEGF-D in human submucosal colorectal cancers was investigated in paraffin-embedded stepwise sections by means of immunohistochemistry, and the correlation between immunohistochemical expression pattern and clinicopathological features was also evaluated. The results showed that VEGF-C overexpression correlated with lymphatic involvement (P = 0.01) and lymph node metastasis (P = 0.02), but VEGF-D overexpression did not correlate significantly. In multivariate analysis lymphatic invasion was the predictive factor (P = 0.0129), but VEGF-C positivity was not predictive (P = 0.3437).\n Question: Is vascular endothelial growth factor-C ( VEGF-C ) a more specific risk factor for lymph node metastasis than VEGF-D in submucosal colorectal cancer?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: It is useful to decide whether lymphatic involvement or lymph node metastasis exists before polypectomy or operation in submucosal colorectal cancer. Whether vascular endothelial growth factor-C (VEGF-C) or VEGF-D could predict lymph node metastasis and lymphatic involvement is uncertain. Expression of the VEGF-C and VEGF-D in human submucosal colorectal cancers was investigated in paraffin-embedded stepwise sections by means of immunohistochemistry, and the correlation between immunohistochemical expression pattern and clinicopathological features was also evaluated. The results showed that VEGF-C overexpression correlated with lymphatic involvement (P = 0.01) and lymph node metastasis (P = 0.02), but VEGF-D overexpression did not correlate significantly. In multivariate analysis lymphatic invasion was the predictive factor (P = 0.0129), but VEGF-C positivity was not predictive (P = 0.3437).
Question: Is vascular endothelial growth factor-C ( VEGF-C ) a more specific risk factor for lymph node metastasis than VEGF-D in submucosal colorectal cancer?
Output:
|
PubmedQA135052
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Beyond their lipid-lowering abilities, statins have anti-inflammatory and immunomodulatory properties. In view of these effects, a growing interest has emerged in the possible role of statins, in preventing or decreasing morbidity and mortality from infection. The aim of this study was to determine whether previous statin use is associated with reduced risk of acute bacterial infections and better outcome of these infections. In this historical cohort study, consecutive adult patients admitted with acute bacterial infection were enrolled. Control group were selected from adult outpatient and without history of acute bacterial infections. Acute bacterial infections included in this study were; pneumonia, acute pyelonephritis, cellulitis and sepsis with unknown origin. Data about baseline characteristics, co-morbidities and statins use of two groups was obtained. Finally 144 patients met inclusion criteria and were enrolled. Same numbers of controls were selected. Two groups were matched based on most baseline characteristics and co-morbidities. The patients' categories were as follows: pneumonia 42.3%, acute pyelonephritis 23.6%, cellulitis 16% and sepsis 18%. From all participants 29.9% of patients and 45.8% controls were statin users. There was significant association between previous statin use and reduced risk of acute bacterial infections (Mantel Haenszel Weighted Odds Ratio=0.51, 95% CI: 0.30-0.85, p=0.009). Duration of hospitalization was significantly shorter in statin users (p=0.002). Hospital mortality rate was lower (14.6%) in statins users when compared with non-users (18.8%) with significant difference (p=0.028).\n Question: Do the Effect of Statins Use on the Risk and Outcome of Acute Bacterial Infections in Adult Patients?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Beyond their lipid-lowering abilities, statins have anti-inflammatory and immunomodulatory properties. In view of these effects, a growing interest has emerged in the possible role of statins, in preventing or decreasing morbidity and mortality from infection. The aim of this study was to determine whether previous statin use is associated with reduced risk of acute bacterial infections and better outcome of these infections. In this historical cohort study, consecutive adult patients admitted with acute bacterial infection were enrolled. Control group were selected from adult outpatient and without history of acute bacterial infections. Acute bacterial infections included in this study were; pneumonia, acute pyelonephritis, cellulitis and sepsis with unknown origin. Data about baseline characteristics, co-morbidities and statins use of two groups was obtained. Finally 144 patients met inclusion criteria and were enrolled. Same numbers of controls were selected. Two groups were matched based on most baseline characteristics and co-morbidities. The patients' categories were as follows: pneumonia 42.3%, acute pyelonephritis 23.6%, cellulitis 16% and sepsis 18%. From all participants 29.9% of patients and 45.8% controls were statin users. There was significant association between previous statin use and reduced risk of acute bacterial infections (Mantel Haenszel Weighted Odds Ratio=0.51, 95% CI: 0.30-0.85, p=0.009). Duration of hospitalization was significantly shorter in statin users (p=0.002). Hospital mortality rate was lower (14.6%) in statins users when compared with non-users (18.8%) with significant difference (p=0.028).
Question: Do the Effect of Statins Use on the Risk and Outcome of Acute Bacterial Infections in Adult Patients?
Output:
|
PubmedQA86428
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Pooled analysis of major placebo-controlled trials suggests that the earlier thrombolysis is given after ischemic stroke, the better the outcome. We report a single-center assessment of the effect of ultraearly thrombolysis on the outcome of our patients. Between January 2003, and December 2008, a total of 878 patients with ischemic stroke received thrombolysis within 4.5 hours from the symptom onset at the Helsinki University Central Hospital. Using univariate methods and multivariable logistic regression, we assessed the association between onset-to-treatment time (OTT) and favorable 3-month outcome (modified Rankin Scale 0 to 2). Median age was 70.5 years, median OTT 115 minutes, and median National Institutes of Health Stroke Scale (NIHSS) on admission 9. After adjustment for baseline stroke severity, more patients with OTT <70 minutes had a favorable outcome than those with OTT > or = 70 minutes. Specifically, OR of 5.15 (1.50 to 27.5) was for the patients with NIHSS 7 to 12, and 2.74 (1.26 to 5.90) for those with NIHSS > or = 13. Of the patients with OTT < or = 90 minutes, those with NIHSS 7 to 12 had an OR of 1.72 (1.00 to 2.96) for a favorable outcome, and those with NIHSS > or = 13 had lower mortality than the ones with OTT >90 minutes (16.4% versus 29.5%; P=0.01). Multivariable model showed an association of better outcome with lower baseline glucose level, younger age, lower baseline NIHSS, and OTT <70 minutes.\n Question: Is ultraearly thrombolysis in acute ischemic stroke associated with better outcome and lower mortality?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Pooled analysis of major placebo-controlled trials suggests that the earlier thrombolysis is given after ischemic stroke, the better the outcome. We report a single-center assessment of the effect of ultraearly thrombolysis on the outcome of our patients. Between January 2003, and December 2008, a total of 878 patients with ischemic stroke received thrombolysis within 4.5 hours from the symptom onset at the Helsinki University Central Hospital. Using univariate methods and multivariable logistic regression, we assessed the association between onset-to-treatment time (OTT) and favorable 3-month outcome (modified Rankin Scale 0 to 2). Median age was 70.5 years, median OTT 115 minutes, and median National Institutes of Health Stroke Scale (NIHSS) on admission 9. After adjustment for baseline stroke severity, more patients with OTT <70 minutes had a favorable outcome than those with OTT > or = 70 minutes. Specifically, OR of 5.15 (1.50 to 27.5) was for the patients with NIHSS 7 to 12, and 2.74 (1.26 to 5.90) for those with NIHSS > or = 13. Of the patients with OTT < or = 90 minutes, those with NIHSS 7 to 12 had an OR of 1.72 (1.00 to 2.96) for a favorable outcome, and those with NIHSS > or = 13 had lower mortality than the ones with OTT >90 minutes (16.4% versus 29.5%; P=0.01). Multivariable model showed an association of better outcome with lower baseline glucose level, younger age, lower baseline NIHSS, and OTT <70 minutes.
Question: Is ultraearly thrombolysis in acute ischemic stroke associated with better outcome and lower mortality?
Output:
|
PubmedQA125507
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Recently, some growth factors have been shown to play roles not only as growth factors but also as cell-surviving factors. Transforming growth factor (TGF)-alpha is expressed in normal gastric mucosa. In this study, we investigated the cell-surviving effect of TGF-alpha on gastric mucosal cells and its signaling mechanism. We used a gastric mucosal cell line, GSM06, and gastric cancer cell line, AGS. Apoptosis was induced by serum depletion or exposure to sodium butyrate. Analysis of apoptosis was performed by DNA ladder assay, measuring the DNA fragmentation ratio (Burton method), and 4',6-diamidino-2-phenylindole staining. TGF-alpha protected gastric mucosal cells against apoptosis induced by serum depletion or sodium butyrate in a dose-dependent manner. This antiapoptotic effect of TGF-alpha was blocked by the pretreatment with reagents that can potentially inhibit NF-kappaB activation, whereas neither MEK inhibitor PD098059 nor PI-3-kinase inhibitor wortmannin abolished this effect. Electrophoretic mobility shift assay showed nuclear factor kappaB (NF-kappaB) activation by TGF-alpha stimulation. TGF-alpha also enhanced the expression of Bcl-2 family proteins in an NF-kappaB-dependent manner.\n Question: Does tGF-alpha inhibit apoptosis of murine gastric pit cells through an NF-kappaB-dependent pathway?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Recently, some growth factors have been shown to play roles not only as growth factors but also as cell-surviving factors. Transforming growth factor (TGF)-alpha is expressed in normal gastric mucosa. In this study, we investigated the cell-surviving effect of TGF-alpha on gastric mucosal cells and its signaling mechanism. We used a gastric mucosal cell line, GSM06, and gastric cancer cell line, AGS. Apoptosis was induced by serum depletion or exposure to sodium butyrate. Analysis of apoptosis was performed by DNA ladder assay, measuring the DNA fragmentation ratio (Burton method), and 4',6-diamidino-2-phenylindole staining. TGF-alpha protected gastric mucosal cells against apoptosis induced by serum depletion or sodium butyrate in a dose-dependent manner. This antiapoptotic effect of TGF-alpha was blocked by the pretreatment with reagents that can potentially inhibit NF-kappaB activation, whereas neither MEK inhibitor PD098059 nor PI-3-kinase inhibitor wortmannin abolished this effect. Electrophoretic mobility shift assay showed nuclear factor kappaB (NF-kappaB) activation by TGF-alpha stimulation. TGF-alpha also enhanced the expression of Bcl-2 family proteins in an NF-kappaB-dependent manner.
Question: Does tGF-alpha inhibit apoptosis of murine gastric pit cells through an NF-kappaB-dependent pathway?
Output:
|
PubmedQA90353
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Sialic acid-binding immunoglobulin-like lectins (Siglecs) are a family of receptors that bind sialic acid and mostly contain immunoreceptor tyrosine-based inhibitory motifs, suggesting that these molecules possess inhibitory functions. We have recently identified Siglec-8 as an eosinophil-prominent Siglec, and cross-linking of Siglec-8 on human eosinophils induces apoptosis. In this article, we address the in vivo consequences of Siglec engagement. We and others have identified mouse Siglec-F as the closest functional paralog of human Siglec-8, based on shared ligand-binding and expression pattern. We therefore hypothesized that Siglec-F engagement would affect levels and viability of eosinophils in vivo. Wild type and hypereosinophilic mice were administered Siglec-F antibody and levels of eosinophils in peripheral blood and tissue were measured. Eosinophil apoptosis (in vivo and in vitro) was determined by binding of Annexin-V. Studies in IL-5 transgenic mice, displaying hypereosinophilia, show that administration of a single dose of Siglec-F antibody results in rapid reductions in quantum of eosinophils in the blood. This decrease was accompanied by reductions in tissue eosinophils. Quantum of eosinophils in blood was decreased using two separate antibodies, as well as in other mouse models (wild type mice and in a mouse model of chronic eosinophilic leukemia). Mechanistic studies demonstrated that Siglec-F antibody administration induced apoptosis of eosinophils in vivo and in vitro.\n Question: Does siglec-F antibody administration to mice selectively reduce blood and tissue eosinophils?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Sialic acid-binding immunoglobulin-like lectins (Siglecs) are a family of receptors that bind sialic acid and mostly contain immunoreceptor tyrosine-based inhibitory motifs, suggesting that these molecules possess inhibitory functions. We have recently identified Siglec-8 as an eosinophil-prominent Siglec, and cross-linking of Siglec-8 on human eosinophils induces apoptosis. In this article, we address the in vivo consequences of Siglec engagement. We and others have identified mouse Siglec-F as the closest functional paralog of human Siglec-8, based on shared ligand-binding and expression pattern. We therefore hypothesized that Siglec-F engagement would affect levels and viability of eosinophils in vivo. Wild type and hypereosinophilic mice were administered Siglec-F antibody and levels of eosinophils in peripheral blood and tissue were measured. Eosinophil apoptosis (in vivo and in vitro) was determined by binding of Annexin-V. Studies in IL-5 transgenic mice, displaying hypereosinophilia, show that administration of a single dose of Siglec-F antibody results in rapid reductions in quantum of eosinophils in the blood. This decrease was accompanied by reductions in tissue eosinophils. Quantum of eosinophils in blood was decreased using two separate antibodies, as well as in other mouse models (wild type mice and in a mouse model of chronic eosinophilic leukemia). Mechanistic studies demonstrated that Siglec-F antibody administration induced apoptosis of eosinophils in vivo and in vitro.
Question: Does siglec-F antibody administration to mice selectively reduce blood and tissue eosinophils?
Output:
|
PubmedQA50442
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Expression of exogenous sequences in plants is often suppressed through one of the earliest described RNA silencing pathways, sense post-transcriptional gene silencing (S-PTGS). This type of suppression has made significant contributions to our knowledge of the biology of RNA silencing pathways and has important consequences in plant transgenesis applications. Although significant progress has been made in recent years, factors affecting the stability of transgene expression are still not well understood. It has been shown before that the efficiency of RNA silencing in plants is influenced by various environmental factors. Here we report that a major environmental factor, light intensity, significantly affects the induction and systemic spread of S-PTGS. Moreover, we show that photoadaptation to high or low light intensity conditions differentially affects mRNA levels of major components of the RNA silencing machinery.\n Question: Does light intensity affect RNA silencing of a transgene in Nicotiana benthamiana plants?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Expression of exogenous sequences in plants is often suppressed through one of the earliest described RNA silencing pathways, sense post-transcriptional gene silencing (S-PTGS). This type of suppression has made significant contributions to our knowledge of the biology of RNA silencing pathways and has important consequences in plant transgenesis applications. Although significant progress has been made in recent years, factors affecting the stability of transgene expression are still not well understood. It has been shown before that the efficiency of RNA silencing in plants is influenced by various environmental factors. Here we report that a major environmental factor, light intensity, significantly affects the induction and systemic spread of S-PTGS. Moreover, we show that photoadaptation to high or low light intensity conditions differentially affects mRNA levels of major components of the RNA silencing machinery.
Question: Does light intensity affect RNA silencing of a transgene in Nicotiana benthamiana plants?
Output:
|
PubmedQA36339
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Uncertainties remain over whether prophylactic surgery or surveillance is the better management option for intraductal papillary mucinous neoplasm of the pancreas. The aim of this preliminary study was to determine if differences in anxiety and quality of life exist between patients who have surgery or undergo surveillance. Recruited patients were given the Hospital Anxiety and Depression Scale, a general survey that evaluates anxiety, and the Functional Assessment of Cancer Therapy-Pancreas, a disease-specific survey that assesses quality of life. Questionnaires were scored by standardized algorithms and compared using Student's t test or Wilcoxon rank-sum test. Sixteen patients had surgery and 16 patients were undergoing surveillance. Mean age was 66.8 ± 19.9 years. Responses from both groups were remarkably similar. Surgery patients scored higher on the anxiety questionnaire than surveillance patients, although not statistically significant (p = 0.09). Surgery patients scored lower on the functional well-being domain of the quality-of-life instrument (p = 0.03), though there were no differences in overall quality of life.\n Question: Does prophylactic pancreatectomy for intraductal papillary mucinous neoplasm negatively impact quality of life : a preliminary study?\n Output: "
},
{
"role": "assistant",
"content": "no"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Uncertainties remain over whether prophylactic surgery or surveillance is the better management option for intraductal papillary mucinous neoplasm of the pancreas. The aim of this preliminary study was to determine if differences in anxiety and quality of life exist between patients who have surgery or undergo surveillance. Recruited patients were given the Hospital Anxiety and Depression Scale, a general survey that evaluates anxiety, and the Functional Assessment of Cancer Therapy-Pancreas, a disease-specific survey that assesses quality of life. Questionnaires were scored by standardized algorithms and compared using Student's t test or Wilcoxon rank-sum test. Sixteen patients had surgery and 16 patients were undergoing surveillance. Mean age was 66.8 ± 19.9 years. Responses from both groups were remarkably similar. Surgery patients scored higher on the anxiety questionnaire than surveillance patients, although not statistically significant (p = 0.09). Surgery patients scored lower on the functional well-being domain of the quality-of-life instrument (p = 0.03), though there were no differences in overall quality of life.
Question: Does prophylactic pancreatectomy for intraductal papillary mucinous neoplasm negatively impact quality of life : a preliminary study?
Output:
|
PubmedQA174404
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The aim of this study was to evaluate coronary vasomotor function in cardiac transplant recipients maintained on sirolimus (SRL)- or cyclosporin (CyA)-based immunosuppression. Endothelium-independent response to intracoronary nitroglycerin and adenosine and endothelium-dependent response to intracoronary acetylcholine (Ach) were assessed in 15 SRL- and 21 CyA- treated subjects with angiographically normal coronary arteries. Baseline mean blood pressure was lower in the SRL group (85.6 +/- 10.3 vs. 105.2 +/- 8.7 mmHg, P = 0.002). There was no difference between the groups in coronary flow reserve after adenosine administration in multivariable analysis (P = 0.34). Nitroglycerin administration resulted in increase in coronary artery diameter in the SRL compared with the CyA groups (2.79 +/- 0.54 vs. 2.57 +/- 0.61, P = 0.0036). In 13 SRL-treated subjects without evidence of cardiac allograft vasculopathy (CAV), Ach administration resulted in less epicardial vasoconstriction compared with CyA-treated subjects (2.7 +/- 17.7 vs. -15.6 +/- 17.2%, P = 0.005). Two SRL-treated subjects with three-dimensional intravascular ultrasound evidence of CAV developed coronary spasm in response to Ach 10(-4). Microvascular endothelial function did not differ between the groups.\n Question: Is sirolimus as primary immunosuppression associated with improved coronary vasomotor function compared with calcineurin inhibitors in stable cardiac transplant recipients?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: The aim of this study was to evaluate coronary vasomotor function in cardiac transplant recipients maintained on sirolimus (SRL)- or cyclosporin (CyA)-based immunosuppression. Endothelium-independent response to intracoronary nitroglycerin and adenosine and endothelium-dependent response to intracoronary acetylcholine (Ach) were assessed in 15 SRL- and 21 CyA- treated subjects with angiographically normal coronary arteries. Baseline mean blood pressure was lower in the SRL group (85.6 +/- 10.3 vs. 105.2 +/- 8.7 mmHg, P = 0.002). There was no difference between the groups in coronary flow reserve after adenosine administration in multivariable analysis (P = 0.34). Nitroglycerin administration resulted in increase in coronary artery diameter in the SRL compared with the CyA groups (2.79 +/- 0.54 vs. 2.57 +/- 0.61, P = 0.0036). In 13 SRL-treated subjects without evidence of cardiac allograft vasculopathy (CAV), Ach administration resulted in less epicardial vasoconstriction compared with CyA-treated subjects (2.7 +/- 17.7 vs. -15.6 +/- 17.2%, P = 0.005). Two SRL-treated subjects with three-dimensional intravascular ultrasound evidence of CAV developed coronary spasm in response to Ach 10(-4). Microvascular endothelial function did not differ between the groups.
Question: Is sirolimus as primary immunosuppression associated with improved coronary vasomotor function compared with calcineurin inhibitors in stable cardiac transplant recipients?
Output:
|
PubmedQA156504
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Shock index (SI) (ratio between heart rate and systolic blood pressure) has been shown to be associated with poor mortality outcomes in trauma and pneumonia; however it has yet to be examined in stroke. We aimed to examine the relationship between SI and acute outcomes of inpatient, 3-day and 7-day mortality in stroke. Secondly, we aimed to compare SI and systolic blood pressure (SBP) alone in predicting above outcomes. Data from a multicentre prospective cohort study conducted between October 2009 and September 2012 in eight NHS trusts in East of England were analysed. The relationships between SI, SBP and study outcomes were assessed using multivariable logistic regression models using mid-quintile groups as the reference category. Receiver operating characteristic (ROC) curves assessed the discriminating ability between the SI and SBP models. A total of 2121 stroke patients were included (47.4% men; mean age 77.10 (sd) 12.40) years. The lowest quintile of the SI, had an increased odds of 3-day and 7-day mortality, adjusted odds ratio (AOR) 2.45 (95% CI:1.16-5.17) and 1.88 (1.01-3.49), respectively. Patients with the highest quintile of SI also had increased odds of in-patient, 3-day and 7-day mortality, AORs 1.85 (1.17-2.92), 2.18 (1.03-4.63) and 2.45 (1.34-4.49), respectively. Similarly, SBP had a U-shape relationship with mortality. All measures had an ROC area under the curve >0.8 but there was no difference in the discriminating ability between SI and SBP.\n Question: Does the shock index predict acute mortality outcomes in stroke?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Shock index (SI) (ratio between heart rate and systolic blood pressure) has been shown to be associated with poor mortality outcomes in trauma and pneumonia; however it has yet to be examined in stroke. We aimed to examine the relationship between SI and acute outcomes of inpatient, 3-day and 7-day mortality in stroke. Secondly, we aimed to compare SI and systolic blood pressure (SBP) alone in predicting above outcomes. Data from a multicentre prospective cohort study conducted between October 2009 and September 2012 in eight NHS trusts in East of England were analysed. The relationships between SI, SBP and study outcomes were assessed using multivariable logistic regression models using mid-quintile groups as the reference category. Receiver operating characteristic (ROC) curves assessed the discriminating ability between the SI and SBP models. A total of 2121 stroke patients were included (47.4% men; mean age 77.10 (sd) 12.40) years. The lowest quintile of the SI, had an increased odds of 3-day and 7-day mortality, adjusted odds ratio (AOR) 2.45 (95% CI:1.16-5.17) and 1.88 (1.01-3.49), respectively. Patients with the highest quintile of SI also had increased odds of in-patient, 3-day and 7-day mortality, AORs 1.85 (1.17-2.92), 2.18 (1.03-4.63) and 2.45 (1.34-4.49), respectively. Similarly, SBP had a U-shape relationship with mortality. All measures had an ROC area under the curve >0.8 but there was no difference in the discriminating ability between SI and SBP.
Question: Does the shock index predict acute mortality outcomes in stroke?
Output:
|
PubmedQA191250
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To evaluate the feasibility of using iron oxide nanoparticles as gene vector and the effect of magnetic field on efficiency of transfection. Iron oxide nanoparticles were prepared by alkaline precipitation of divalent and trivalent iron chloride. The surface of iron oxide nanoparticles was modified by self-assembled poly-L-lysine to form particle complexes (IONP-PLL). Transfection was determined by delivering reporter gene, PGL2-control encoding luciferase, to different cell lines using IONP-PLL as vector. The effect of magnetic field on efficiency of transfection was determined using Nd-Fe-B permanent magnet. Foreign gene could be delivered to various cell lines by IONP-PLL and expressed with high efficiency, but the transfection efficiency and time course varied in the different cell lines studied. Magnetic field could enhance the efficiency of transfection by 5 - 10 fold.\n Question: Does [ In vitro gene transfection by magnetic iron oxide nanoparticles and magnetic field increase transfection efficiency ]?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To evaluate the feasibility of using iron oxide nanoparticles as gene vector and the effect of magnetic field on efficiency of transfection. Iron oxide nanoparticles were prepared by alkaline precipitation of divalent and trivalent iron chloride. The surface of iron oxide nanoparticles was modified by self-assembled poly-L-lysine to form particle complexes (IONP-PLL). Transfection was determined by delivering reporter gene, PGL2-control encoding luciferase, to different cell lines using IONP-PLL as vector. The effect of magnetic field on efficiency of transfection was determined using Nd-Fe-B permanent magnet. Foreign gene could be delivered to various cell lines by IONP-PLL and expressed with high efficiency, but the transfection efficiency and time course varied in the different cell lines studied. Magnetic field could enhance the efficiency of transfection by 5 - 10 fold.
Question: Does [ In vitro gene transfection by magnetic iron oxide nanoparticles and magnetic field increase transfection efficiency ]?
Output:
|
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