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YBXL
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PubmedQA_train

id stringlengths 9 14	conversations listlengths 2 2	text stringlengths 231 5.9k
PubmedQA181746	[ { "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 second generation of cholinesterase inhibitors (ChEIs) is approved in the United Kingdom for the treatment of mild to moderate Alzheimer's disease (AD). The UK National Institute of Clinical Excellence has raised questions, however, about whether ChEIs are cost-effective for the treatment of dementia. To address these concerns, it is important to identify factors that predict which patients may have the best response to ChEl treatment. We reviewed animal studies and human clinical studies to address whether sex can predict and influence the response to ChEI treatment based on differences in neuroanatomy, pharmacokinetics, and prevalence of dementia. Relevant articles examining the use of ChEIs in humans with dementia (especially in AD) and in animals were identified through searches of several databases, including MEDLINE, PubMed, and EMBASE for general medical topics, the Cochrane Controlled Clinical Trials Register and CINAHL DIRECT for nursing and allied health issues, and PsycLIT for reviews of psychology and psychiatry topics (1980 June 2006). Articles reviewed were limited to those that discussed the use of ChEIs in relation to sex. Animal studies have produced a substantial amount of evidence to support the hypothesis that sex may influence the response to ChEIs and, in particular, that testosterone may play a significant role in producing this difference by its influence on the entry of ChEIs into the brain. The results of clinical studies in humans, on the other hand, have been mixed. Two double-label and open-label clinical studies suggested that there may be a 3-way interaction between apolipoprotein E genotype, sex, and tacrine (range, P = 0.03 to P = 0.05). Seven double-blind, open-label clinical trials and 13 case studies of donepezil, rivastigmine, and galantamine produced little evidence of an association between treatment outcomes (as measured with clinical rating scales) and sex, although in an open-label 2-year study in women with AD treated with donepezil, women had lower mortality rates than men (10% and 20%, respectively; P = 0.003). One study produced weak evidence that women treated with ChEIs may experience more adverse effects than men, but this may have been attributable to low body weight rather than to sex differences.\n Question: Does sex influence on cholinesterase inhibitor treatment in elderly individuals with Alzheimer 's disease?\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 second generation of cholinesterase inhibitors (ChEIs) is approved in the United Kingdom for the treatment of mild to moderate Alzheimer's disease (AD). The UK National Institute of Clinical Excellence has raised questions, however, about whether ChEIs are cost-effective for the treatment of dementia. To address these concerns, it is important to identify factors that predict which patients may have the best response to ChEl treatment. We reviewed animal studies and human clinical studies to address whether sex can predict and influence the response to ChEI treatment based on differences in neuroanatomy, pharmacokinetics, and prevalence of dementia. Relevant articles examining the use of ChEIs in humans with dementia (especially in AD) and in animals were identified through searches of several databases, including MEDLINE, PubMed, and EMBASE for general medical topics, the Cochrane Controlled Clinical Trials Register and CINAHL DIRECT for nursing and allied health issues, and PsycLIT for reviews of psychology and psychiatry topics (1980 June 2006). Articles reviewed were limited to those that discussed the use of ChEIs in relation to sex. Animal studies have produced a substantial amount of evidence to support the hypothesis that sex may influence the response to ChEIs and, in particular, that testosterone may play a significant role in producing this difference by its influence on the entry of ChEIs into the brain. The results of clinical studies in humans, on the other hand, have been mixed. Two double-label and open-label clinical studies suggested that there may be a 3-way interaction between apolipoprotein E genotype, sex, and tacrine (range, P = 0.03 to P = 0.05). Seven double-blind, open-label clinical trials and 13 case studies of donepezil, rivastigmine, and galantamine produced little evidence of an association between treatment outcomes (as measured with clinical rating scales) and sex, although in an open-label 2-year study in women with AD treated with donepezil, women had lower mortality rates than men (10% and 20%, respectively; P = 0.003). One study produced weak evidence that women treated with ChEIs may experience more adverse effects than men, but this may have been attributable to low body weight rather than to sex differences. Question: Does sex influence on cholinesterase inhibitor treatment in elderly individuals with Alzheimer 's disease? Output:
PubmedQA182746	[ { "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 morning hours are associated with increased cardiovascular (CV) risk, and vascular endothelial function (VEF) is a strong predictor of CV disease. A diurnal rhythm in VEF has been established but the morning variation in VEF is not well-documented. Thus, we tested if VEF is impaired across the vulnerable morning period. After overnight fasts, eight healthy men (age 26.3 ± 3 yr) underwent assessments of VEF under standardized testing conditions every 2 h from 0700 to 1300 h on two separate days. VEF was estimated following 5 min brachial artery occlusions by hyperemic flow-mediated dilation (FMD). There was no significant change in FMD or hyperemic shear stimulus across the 6 h vulnerable period on either day, despite changes in physical activity and meals across these periods.\n Question: Is brachial artery endothelial function stable across the morning in young men?\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 morning hours are associated with increased cardiovascular (CV) risk, and vascular endothelial function (VEF) is a strong predictor of CV disease. A diurnal rhythm in VEF has been established but the morning variation in VEF is not well-documented. Thus, we tested if VEF is impaired across the vulnerable morning period. After overnight fasts, eight healthy men (age 26.3 ± 3 yr) underwent assessments of VEF under standardized testing conditions every 2 h from 0700 to 1300 h on two separate days. VEF was estimated following 5 min brachial artery occlusions by hyperemic flow-mediated dilation (FMD). There was no significant change in FMD or hyperemic shear stimulus across the 6 h vulnerable period on either day, despite changes in physical activity and meals across these periods. Question: Is brachial artery endothelial function stable across the morning in young men? Output:
PubmedQA2360	[ { "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 identify genes whose depletion is detrimental to Pim1-overexpressing prostate cancer cells and to validate this finding in vitro and in vivo. RNAi screening was used to identify genes whose depletion is detrimental to Pim1-overexpressing cells. Our finding was validated using shRNA or PLK1-specific inhibitor BI 2536. Xenograft studies were performed using both PLK1-knockdown cells and BI 2536 to investigate the effects of PLK1 inhibition on tumorigenesis in Pim1-overexpressing cells. Finally, PLK1 and PIM1 expression patterns in human prostate tumors were examined by immunohistochemistry using tissue microarrays. We identified the mitotic regulator polo-like kinase (PLK1) as a gene whose depletion is particularly detrimental to the viability of Pim1-overexpressing prostate cancer. Inhibition of PLK1 by shRNA or BI 2536 in Pim1-overexpressing prostate cancer xenograft models resulted in a dramatic inhibition of tumor progression. Notably, Pim1-overexpressing cells were more prone to mitotic arrest followed by apoptosis due to PLK1 inhibition than control cells. Furthermore, inhibition of PLK1 led to the reduction of MYC protein levels both in vitro and in vivo. Our data also suggest that PIM1 and PLK1 physically interact and PIM1 might phosphorylate PLK1. Finally, PLK1 and PIM1 are frequently co-expressed in human prostate tumors, and co-expression of PLK1 and PIM1 was significantly correlated to higher Gleason grades.\n Question: Does rNAi screen identify a synthetic lethal interaction between PIM1 overexpression and PLK1 inhibition?\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 identify genes whose depletion is detrimental to Pim1-overexpressing prostate cancer cells and to validate this finding in vitro and in vivo. RNAi screening was used to identify genes whose depletion is detrimental to Pim1-overexpressing cells. Our finding was validated using shRNA or PLK1-specific inhibitor BI 2536. Xenograft studies were performed using both PLK1-knockdown cells and BI 2536 to investigate the effects of PLK1 inhibition on tumorigenesis in Pim1-overexpressing cells. Finally, PLK1 and PIM1 expression patterns in human prostate tumors were examined by immunohistochemistry using tissue microarrays. We identified the mitotic regulator polo-like kinase (PLK1) as a gene whose depletion is particularly detrimental to the viability of Pim1-overexpressing prostate cancer. Inhibition of PLK1 by shRNA or BI 2536 in Pim1-overexpressing prostate cancer xenograft models resulted in a dramatic inhibition of tumor progression. Notably, Pim1-overexpressing cells were more prone to mitotic arrest followed by apoptosis due to PLK1 inhibition than control cells. Furthermore, inhibition of PLK1 led to the reduction of MYC protein levels both in vitro and in vivo. Our data also suggest that PIM1 and PLK1 physically interact and PIM1 might phosphorylate PLK1. Finally, PLK1 and PIM1 are frequently co-expressed in human prostate tumors, and co-expression of PLK1 and PIM1 was significantly correlated to higher Gleason grades. Question: Does rNAi screen identify a synthetic lethal interaction between PIM1 overexpression and PLK1 inhibition? Output:
PubmedQA206814	[ { "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 limited information on the clinimetric properties of questionnaires of activity limitation in people after ankle fracture. The purpose of this study was to investigate the clinimetric properties of the Lower Extremity Functional Scale, an activity limitation questionnaire, in people with ankle fracture. This was a measurement study using data collected from 2 previous randomized controlled trials and 1 inception cohort study. Participants with ankle fracture (N=306) were recruited within 7 days of cast removal. Data were collected at baseline and at short- and medium-term follow-ups. Internal consistency and construct validity were assessed using Rasch analysis. Concurrent validity, responsiveness, and floor and ceiling effects were evaluated. The Lower Extremity Functional Scale demonstrated high internal consistency (alpha > .90). The variance in activity limitation explained by the items was high (98.3%). Each item had a positive correlation with the overall scale, and most items supported the unidimensionality of the scale. These findings suggest that the scale has high internal consistency and construct validity. The scale also demonstrated high concurrent validity and responsiveness in the short term and no floor or ceiling effects. However, the scale would benefit from more-challenging items, as evident at the medium-term follow-up.\n Question: Does the lower extremity functional scale have good clinimetric properties in people with ankle fracture?\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 limited information on the clinimetric properties of questionnaires of activity limitation in people after ankle fracture. The purpose of this study was to investigate the clinimetric properties of the Lower Extremity Functional Scale, an activity limitation questionnaire, in people with ankle fracture. This was a measurement study using data collected from 2 previous randomized controlled trials and 1 inception cohort study. Participants with ankle fracture (N=306) were recruited within 7 days of cast removal. Data were collected at baseline and at short- and medium-term follow-ups. Internal consistency and construct validity were assessed using Rasch analysis. Concurrent validity, responsiveness, and floor and ceiling effects were evaluated. The Lower Extremity Functional Scale demonstrated high internal consistency (alpha > .90). The variance in activity limitation explained by the items was high (98.3%). Each item had a positive correlation with the overall scale, and most items supported the unidimensionality of the scale. These findings suggest that the scale has high internal consistency and construct validity. The scale also demonstrated high concurrent validity and responsiveness in the short term and no floor or ceiling effects. However, the scale would benefit from more-challenging items, as evident at the medium-term follow-up. Question: Does the lower extremity functional scale have good clinimetric properties in people with ankle fracture? Output:
PubmedQA166467	[ { "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 are few comparative studies regarding morphologic changes after kyphoplasty and vertebroplasty. The purpose of this study was to compare restoration of vertebral body height and wedge angle and cement leakage with kyphoplasty and vertebroplasty in osteoporotic compression fractures. Forty patients (57 vertebrae) were treated with kyphoplasty, and 66 patients (124 vertebrae) were treated with vertebroplasty. Cement leakage into the disk space and paravertebral soft tissues or veins was analyzed on immediate postoperative CT scans. The height and wedge angle were measured before and after treatment and analyzed with the Mann-Whitney U test and chi(2) test. Kyphoplasty and vertebroplasty both improved vertebral body height and the wedge angles (P < .05). However, these differences were not statistically significant when the 2 techniques were compared (P > .05). There were 18% of the kyphoplasty group and 49% of the vertebroplasty group that showed cement leakage into the paravertebral soft tissues or veins (P < .01). Cement leakage into the disk space occurred in 12% of the kyphoplasty group and in 25% of the vertebroplasty group (P < .01). However, no complications related to cement leakage were noted.\n Question: Do kyphoplasty and vertebroplasty produce the same degree of height restoration?\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 are few comparative studies regarding morphologic changes after kyphoplasty and vertebroplasty. The purpose of this study was to compare restoration of vertebral body height and wedge angle and cement leakage with kyphoplasty and vertebroplasty in osteoporotic compression fractures. Forty patients (57 vertebrae) were treated with kyphoplasty, and 66 patients (124 vertebrae) were treated with vertebroplasty. Cement leakage into the disk space and paravertebral soft tissues or veins was analyzed on immediate postoperative CT scans. The height and wedge angle were measured before and after treatment and analyzed with the Mann-Whitney U test and chi(2) test. Kyphoplasty and vertebroplasty both improved vertebral body height and the wedge angles (P < .05). However, these differences were not statistically significant when the 2 techniques were compared (P > .05). There were 18% of the kyphoplasty group and 49% of the vertebroplasty group that showed cement leakage into the paravertebral soft tissues or veins (P < .01). Cement leakage into the disk space occurred in 12% of the kyphoplasty group and in 25% of the vertebroplasty group (P < .01). However, no complications related to cement leakage were noted. Question: Do kyphoplasty and vertebroplasty produce the same degree of height restoration? Output:
PubmedQA28979	[ { "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: Chlamydia pneumoniae is known to cause acute respiratory infection and more recently it has been studied as a pathogen causing inflammatory changes in chronic diseases such as atherosclerosis. This study addresses the antichlamydial effect of levofloxacin and its role in modulation of a proinflammatory cytokine IL-6 production by uninfected and infected HEp-2 cells. HEp-2 cell monolayers were infected with previously prepared and frozen aliquots of C.pneumoniae [1 x 10(3) inclusion-forming units (IFU)/ml] by centrifugation for 30 min and incubation at 37 degrees C for 1 h. Infected monolayers were treated with levofloxacin (3 or 8 microg/ml) immediately after infection (0 h) or 24 h after infection. Monolayers were examined daily for 96 h after infection by counting inclusions with fluorescently labeled antichlamydial monoclonal antibody. Aliquots of disrupted monolayers were titrated to determine the numbers of viable C. pneumoniae IFU/ml. IL-6 concentrations in cell supernatants were determined by ELISA assays. Infected HEp-2 cells produced IL-6. Noninfected HEp-2 cells demonstrated modulation of IL-6 production by levofloxacin. No viable C. Pneumoniae were detected in infected HEp-2 cells when the monolayer was treated with levofloxacin immediately after infection (0 h). In contrast, when cells were treated 24 h after infection, a gradual decline in the number of viable C. pneumoniae occurred; by 96 h into the assay >or=98% of C. pneumoniae were killed. IL-6 concentrations were similar in the supernatants of levofloxacin-treated and nontreated HEp-2 cells.\n Question: Does levofloxacin kill Chlamydia pneumoniae and modulates interleukin 6 production by HEp-2 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: Chlamydia pneumoniae is known to cause acute respiratory infection and more recently it has been studied as a pathogen causing inflammatory changes in chronic diseases such as atherosclerosis. This study addresses the antichlamydial effect of levofloxacin and its role in modulation of a proinflammatory cytokine IL-6 production by uninfected and infected HEp-2 cells. HEp-2 cell monolayers were infected with previously prepared and frozen aliquots of C.pneumoniae [1 x 10(3) inclusion-forming units (IFU)/ml] by centrifugation for 30 min and incubation at 37 degrees C for 1 h. Infected monolayers were treated with levofloxacin (3 or 8 microg/ml) immediately after infection (0 h) or 24 h after infection. Monolayers were examined daily for 96 h after infection by counting inclusions with fluorescently labeled antichlamydial monoclonal antibody. Aliquots of disrupted monolayers were titrated to determine the numbers of viable C. pneumoniae IFU/ml. IL-6 concentrations in cell supernatants were determined by ELISA assays. Infected HEp-2 cells produced IL-6. Noninfected HEp-2 cells demonstrated modulation of IL-6 production by levofloxacin. No viable C. Pneumoniae were detected in infected HEp-2 cells when the monolayer was treated with levofloxacin immediately after infection (0 h). In contrast, when cells were treated 24 h after infection, a gradual decline in the number of viable C. pneumoniae occurred; by 96 h into the assay >or=98% of C. pneumoniae were killed. IL-6 concentrations were similar in the supernatants of levofloxacin-treated and nontreated HEp-2 cells. Question: Does levofloxacin kill Chlamydia pneumoniae and modulates interleukin 6 production by HEp-2 cells? Output:
PubmedQA108701	[ { "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: Several lines of in vitro and in vivo studies have demonstrated that interleukin-18 (IL-18) shows both antiallergic and allergy-promoting activities. But its expression in allergic diseases remains unknown. Serum IL-18 levels from atopic dermatitis (AD) model mice, NC/Nga and control mice and from patients with AD and healthy volunteers were measured by ELISA. The relationship between IL-18 levels and serum IgE levels or clinical severity was also examined. Serum IL-18 levels from NC/Nga mice were significantly increased compared to those from control mice. The elevation of IL-18 in the sera was observed prior to the onset and during the development of dermatitis in NC/Nga mice. In addition, IL-18 levels in the sera from patients with AD were significantly (p < 0.05) elevated compared to those from healthy volunteers. However, serum IL-18 levels tended to correlate negatively with serum IgE levels in patients with AD and NC/Nga mice.\n Question: Is interleukin-18 elevated in the sera from patients with atopic dermatitis and from atopic dermatitis model mice , NC/Nga?\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: Several lines of in vitro and in vivo studies have demonstrated that interleukin-18 (IL-18) shows both antiallergic and allergy-promoting activities. But its expression in allergic diseases remains unknown. Serum IL-18 levels from atopic dermatitis (AD) model mice, NC/Nga and control mice and from patients with AD and healthy volunteers were measured by ELISA. The relationship between IL-18 levels and serum IgE levels or clinical severity was also examined. Serum IL-18 levels from NC/Nga mice were significantly increased compared to those from control mice. The elevation of IL-18 in the sera was observed prior to the onset and during the development of dermatitis in NC/Nga mice. In addition, IL-18 levels in the sera from patients with AD were significantly (p < 0.05) elevated compared to those from healthy volunteers. However, serum IL-18 levels tended to correlate negatively with serum IgE levels in patients with AD and NC/Nga mice. Question: Is interleukin-18 elevated in the sera from patients with atopic dermatitis and from atopic dermatitis model mice , NC/Nga? Output:
PubmedQA204435	[ { "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 performed to elucidate the mechanism of high bone turnover during androgen deprivation therapy (ADT) in terms of osteogenic endocrine activity by testosterone, adrenal androgens, and insulin-like growth factor-1 (IGF-I), and to identify markers reflecting the bone mineral density (BMD) during ADT. BMD and samples of blood and urine were studied before and after 6months of ADT in 70 patients with localized prostate cancer. Before ADT, serum free-testosterone, dehydroepiandrosterone sulfate (DHEA-S), androstenedione, and IGF-I levels were correlated with BMD (rs=0.344, p=0.004; rs=0.264, p=0.027; rs=0.329, p=0.005; rs=0.300, p=0.012, respectively). The serum IGF-I level was independently correlated with the pretreatment BMD (Multivariate p=0.001). These relationships disappeared after ADT (p=0.519, 0.316, 0.116, and 0.597, respectively). After ADT, serum levels of free-testosterone decreased (7.9 to 0.2pg/mL), and DHEA-S and androstenedione were also reduced (3.6 to 2.3μmol/L and 5.6 to 2.9nmol/L, respectively) (p<0.001 in all). In contrast, IGF-I levels were elevated after ADT by 11.6% (19.9 to 22.3nmol/L, p<0.001). Delta-values of IGF-I (post- minus pretreatment levels, mean: +2.2, ranged between -7.1 and +15.3) were inversely correlated with the pretreatment (rs=-0.333 p=0.005) and post-treatment (rs=-0.408, p=0.001) BMD. After ADT, the serum IGF-I level was closely correlated with the serum level of the bone formation marker bone-specific alkaline phosphatase (BAP) (rs=0.328, p=0.006), and delta-IGF-I and delta-BAP showed a close positive correlation (rs=0.388, p=0.001). The post-treatment BMD was correlated only with the urine deoxypyridinoline (DPD) concentration (rs=-0.302, p=0.024) among the bone formation/resorption markers including serum/urine N-telopeptide.\n Question: Are deficiency in androgens and upregulation of insulin-like growth factor-1 involved in high bone turnover in men receiving androgen deprivation therapy for prostate 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: This study was performed to elucidate the mechanism of high bone turnover during androgen deprivation therapy (ADT) in terms of osteogenic endocrine activity by testosterone, adrenal androgens, and insulin-like growth factor-1 (IGF-I), and to identify markers reflecting the bone mineral density (BMD) during ADT. BMD and samples of blood and urine were studied before and after 6months of ADT in 70 patients with localized prostate cancer. Before ADT, serum free-testosterone, dehydroepiandrosterone sulfate (DHEA-S), androstenedione, and IGF-I levels were correlated with BMD (rs=0.344, p=0.004; rs=0.264, p=0.027; rs=0.329, p=0.005; rs=0.300, p=0.012, respectively). The serum IGF-I level was independently correlated with the pretreatment BMD (Multivariate p=0.001). These relationships disappeared after ADT (p=0.519, 0.316, 0.116, and 0.597, respectively). After ADT, serum levels of free-testosterone decreased (7.9 to 0.2pg/mL), and DHEA-S and androstenedione were also reduced (3.6 to 2.3μmol/L and 5.6 to 2.9nmol/L, respectively) (p<0.001 in all). In contrast, IGF-I levels were elevated after ADT by 11.6% (19.9 to 22.3nmol/L, p<0.001). Delta-values of IGF-I (post- minus pretreatment levels, mean: +2.2, ranged between -7.1 and +15.3) were inversely correlated with the pretreatment (rs=-0.333 p=0.005) and post-treatment (rs=-0.408, p=0.001) BMD. After ADT, the serum IGF-I level was closely correlated with the serum level of the bone formation marker bone-specific alkaline phosphatase (BAP) (rs=0.328, p=0.006), and delta-IGF-I and delta-BAP showed a close positive correlation (rs=0.388, p=0.001). The post-treatment BMD was correlated only with the urine deoxypyridinoline (DPD) concentration (rs=-0.302, p=0.024) among the bone formation/resorption markers including serum/urine N-telopeptide. Question: Are deficiency in androgens and upregulation of insulin-like growth factor-1 involved in high bone turnover in men receiving androgen deprivation therapy for prostate cancer? Output:
PubmedQA84357	[ { "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 a practical need for the identification of robust cell-surface markers that can be used to enrich for living keratinocyte progenitor cells. Breast cancer resistance protein (ABCG2), a member of the ATP binding cassette (ABC) transporter family, is known to be a marker for stem/progenitor cells in many tissues and organs. We investigated the expression of ABCG2 protein in normal human epidermis to evaluate its potential as a cell surface marker for identifying and enriching for clonogenic epidermal keratinocytes outside the pilosebaceous tract. Immunofluorescence and immunoblotting studies of human skin showed that ABCG2 is expressed in a subset of basal layer cells in the epidermis. Flow cytometry analysis showed approximately 2-3% of keratinocytes in non-hair-bearing epidermis expressing ABCG2; this population also expresses p63, β1 and α6 integrins and keratin 14, but not CD34, CD71, C-kit or involucrin. The ABCG2-positive keratinocytes showed significantly higher colony forming efficiency when co-cultured with mouse 3T3 feeder cells, and more extensive long-term proliferation capacity in vitro, than did ABCG2-negative keratinocytes. Upon clonal analysis, most of the freshly isolated ABCG2-positive keratinocytes formed holoclones and were capable of generating a stratified differentiating epidermis in organotypic culture models.\n Question: Does breast cancer resistance protein identify clonogenic keratinocytes in human interfollicular epidermis?\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 a practical need for the identification of robust cell-surface markers that can be used to enrich for living keratinocyte progenitor cells. Breast cancer resistance protein (ABCG2), a member of the ATP binding cassette (ABC) transporter family, is known to be a marker for stem/progenitor cells in many tissues and organs. We investigated the expression of ABCG2 protein in normal human epidermis to evaluate its potential as a cell surface marker for identifying and enriching for clonogenic epidermal keratinocytes outside the pilosebaceous tract. Immunofluorescence and immunoblotting studies of human skin showed that ABCG2 is expressed in a subset of basal layer cells in the epidermis. Flow cytometry analysis showed approximately 2-3% of keratinocytes in non-hair-bearing epidermis expressing ABCG2; this population also expresses p63, β1 and α6 integrins and keratin 14, but not CD34, CD71, C-kit or involucrin. The ABCG2-positive keratinocytes showed significantly higher colony forming efficiency when co-cultured with mouse 3T3 feeder cells, and more extensive long-term proliferation capacity in vitro, than did ABCG2-negative keratinocytes. Upon clonal analysis, most of the freshly isolated ABCG2-positive keratinocytes formed holoclones and were capable of generating a stratified differentiating epidermis in organotypic culture models. Question: Does breast cancer resistance protein identify clonogenic keratinocytes in human interfollicular epidermis? Output:
PubmedQA183509	[ { "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 lower childhood socioeconomic status (SES) was associated with fewer psychosocial resources independent of adult SES, and whether these associations differed by race/ethnicity. Cross-sectional study of 342 middle-aged (M = 60.5 ± 4.7) African American (n = 49) and Caucasian (n = 293) adults. Childhood SES and adult SES were assessed via highest parental education and participant education, respectively. Participants completed: (a) 6 days of ecological momentary assessment via electronic diaries to assess social support and the number of social interactions and (b) self-report measures of social support, social network diversity, and coping-specifically, active, planning, and emotion focused coping. The interaction term for childhood SES and race/ethnicity significantly predicted several psychosocial resources. Lower childhood SES was associated with less perceived social support in daily life, a less diverse social network, and more limited use of proactive coping strategies in adulthood among African Americans, regardless of adult SES. Comparable associations were not observed among Caucasians.\n Question: Is childhood socioeconomic status associated with psychosocial resources in African Americans : the Pittsburgh Healthy Heart Project?\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 lower childhood socioeconomic status (SES) was associated with fewer psychosocial resources independent of adult SES, and whether these associations differed by race/ethnicity. Cross-sectional study of 342 middle-aged (M = 60.5 ± 4.7) African American (n = 49) and Caucasian (n = 293) adults. Childhood SES and adult SES were assessed via highest parental education and participant education, respectively. Participants completed: (a) 6 days of ecological momentary assessment via electronic diaries to assess social support and the number of social interactions and (b) self-report measures of social support, social network diversity, and coping-specifically, active, planning, and emotion focused coping. The interaction term for childhood SES and race/ethnicity significantly predicted several psychosocial resources. Lower childhood SES was associated with less perceived social support in daily life, a less diverse social network, and more limited use of proactive coping strategies in adulthood among African Americans, regardless of adult SES. Comparable associations were not observed among Caucasians. Question: Is childhood socioeconomic status associated with psychosocial resources in African Americans : the Pittsburgh Healthy Heart Project? Output:
PubmedQA75540	[ { "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 introduce how nursing students discursively construct their dyslexic identities. Identity mediates many important facets of a student's scholarly journey and the availability and use of discourses play a critical part in their ongoing construction. A discourse-based design was used to examine the language employed by students in constructing their dyslexic identities. Using narrative methods, 12 student nurses with dyslexia from two higher education institutions in the Republic of Ireland were interviewed during the period February-July 2012. Discourse analysis of interviews entailed a two-stage approach: leading identity analysis followed by thematic analysis. Discourses used by students to construct their dyslexic identity correspond with positions on an 'Embracer, Passive Engager and Resister' continuum heuristic. The majority of students rejected any reference to using medical or disabled discourses and instead drew on contemporary language in constructing their dyslexic identity. Nine of the 12 students did not disclose their dyslexic identity in practice settings and drew on not being understood to support this position. In addition, a discourse linking 'being stupid' with dyslexia was pervasive in most student narratives and evolved from historical as well as more recent interactions in nurse education.\n Question: Am ' I a dyslexic person I 'm a person with dyslexia ' : identity constructions of dyslexia among students in nurse education?\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: To introduce how nursing students discursively construct their dyslexic identities. Identity mediates many important facets of a student's scholarly journey and the availability and use of discourses play a critical part in their ongoing construction. A discourse-based design was used to examine the language employed by students in constructing their dyslexic identities. Using narrative methods, 12 student nurses with dyslexia from two higher education institutions in the Republic of Ireland were interviewed during the period February-July 2012. Discourse analysis of interviews entailed a two-stage approach: leading identity analysis followed by thematic analysis. Discourses used by students to construct their dyslexic identity correspond with positions on an 'Embracer, Passive Engager and Resister' continuum heuristic. The majority of students rejected any reference to using medical or disabled discourses and instead drew on contemporary language in constructing their dyslexic identity. Nine of the 12 students did not disclose their dyslexic identity in practice settings and drew on not being understood to support this position. In addition, a discourse linking 'being stupid' with dyslexia was pervasive in most student narratives and evolved from historical as well as more recent interactions in nurse education. Question: Am ' I a dyslexic person I 'm a person with dyslexia ' : identity constructions of dyslexia among students in nurse education? Output:
PubmedQA189166	[ { "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 the proportion of acid and weakly acidic refluxes preceding cough bursts could be different in infants, preschool- and school-aged children with chronic, unexplained cough. One hundred six children with unexplained chronic cough, not receiving acid suppressive therapy, underwent impedance-pH monitoring. They were divided into Group A: <2 years (21 pts), Group B: ≥2 to ≤6 years (41 pts), and Group C: >6 years (44 pts). Reflux was defined as acid (pH <4), weakly acidic (WA; pH 4-7), and weakly alkaline (pH >7).Cough episodes were considered temporally associated with gastroesophageal reflux (GER) when occurring within 2 min after a GER episode. Impedance-pH detected 55.50 (39.00-76.00) reflux episodes/patient with an acid-to-WA reflux event ratio of 3.31 (1.55-8.33). This parameter was significantly lower in Group A (1.33 [0.41-3.40]) than in Group B (3.06 [2.00-6.50]; P < 0.05] and Group C (5.09 [2.34-12.43; P < 0.001]). No cough episode was preceded by weakly alkaline refluxes in any patient. During impedance-pH recording, 93 patients (87.7%) had at least one cough episode that had been preceded by impedance refluxes in 83 patients. In this latter group (83 pts), the median number of cough episodes was 12.0 (5.0-25.5), of which 48.15% (30.15-71.43%) were preceded by refluxes; GER-preceded cough episodes were similar in the three groups. The majority of children had cough episodes preceded by acid refluxes in the total population (78.3%), in Group B (80.5%) and in Group C (93.7%), but not in Group A (40.0%; P < 0.001).\n Question: Are weakly acidic gastroesophageal refluxes frequently triggers in young children with chronic cough?\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 the proportion of acid and weakly acidic refluxes preceding cough bursts could be different in infants, preschool- and school-aged children with chronic, unexplained cough. One hundred six children with unexplained chronic cough, not receiving acid suppressive therapy, underwent impedance-pH monitoring. They were divided into Group A: <2 years (21 pts), Group B: ≥2 to ≤6 years (41 pts), and Group C: >6 years (44 pts). Reflux was defined as acid (pH <4), weakly acidic (WA; pH 4-7), and weakly alkaline (pH >7).Cough episodes were considered temporally associated with gastroesophageal reflux (GER) when occurring within 2 min after a GER episode. Impedance-pH detected 55.50 (39.00-76.00) reflux episodes/patient with an acid-to-WA reflux event ratio of 3.31 (1.55-8.33). This parameter was significantly lower in Group A (1.33 [0.41-3.40]) than in Group B (3.06 [2.00-6.50]; P < 0.05] and Group C (5.09 [2.34-12.43; P < 0.001]). No cough episode was preceded by weakly alkaline refluxes in any patient. During impedance-pH recording, 93 patients (87.7%) had at least one cough episode that had been preceded by impedance refluxes in 83 patients. In this latter group (83 pts), the median number of cough episodes was 12.0 (5.0-25.5), of which 48.15% (30.15-71.43%) were preceded by refluxes; GER-preceded cough episodes were similar in the three groups. The majority of children had cough episodes preceded by acid refluxes in the total population (78.3%), in Group B (80.5%) and in Group C (93.7%), but not in Group A (40.0%; P < 0.001). Question: Are weakly acidic gastroesophageal refluxes frequently triggers in young children with chronic cough? Output:
PubmedQA100241	[ { "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: Endovascular aneurysm repair offers improved perioperative morbidity and mortality compared to open repair, counterbalanced by a higher incidence of graft-related complications and re-interventions. Randomized studies comparing EVAR to open repair are yet to report greater than ten-year outcomes. This study reports the outcomes of patients who underwent EVAR greater than ten years ago. Retrospective review of prospectively collected data of all patients who underwent EVAR between 1997 and 2001, supplemented with case-note review, interrogation of imaging and correspondence with general practitioners and coroners' offices. Fifty-eight patients underwent EVAR. Technical success was 100% and 30-day mortality was 0%. The re-intervention rate was 27.3%, including 5 elective open conversions, 2 emergency open repairs, 5 embolizations of endoleaks and 3 extensions. Median time to primary re-intervention was 30 months (1-98). Four graft related complications occurred beyond 5 years however only one reintervention was performed beyond this time point. Four patients died from ruptured AAA.\n Question: Is reintervention following endovascular abdominal aneurysm repair uncommon after five-years : results of greater than a decade follow-up?\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: Endovascular aneurysm repair offers improved perioperative morbidity and mortality compared to open repair, counterbalanced by a higher incidence of graft-related complications and re-interventions. Randomized studies comparing EVAR to open repair are yet to report greater than ten-year outcomes. This study reports the outcomes of patients who underwent EVAR greater than ten years ago. Retrospective review of prospectively collected data of all patients who underwent EVAR between 1997 and 2001, supplemented with case-note review, interrogation of imaging and correspondence with general practitioners and coroners' offices. Fifty-eight patients underwent EVAR. Technical success was 100% and 30-day mortality was 0%. The re-intervention rate was 27.3%, including 5 elective open conversions, 2 emergency open repairs, 5 embolizations of endoleaks and 3 extensions. Median time to primary re-intervention was 30 months (1-98). Four graft related complications occurred beyond 5 years however only one reintervention was performed beyond this time point. Four patients died from ruptured AAA. Question: Is reintervention following endovascular abdominal aneurysm repair uncommon after five-years : results of greater than a decade follow-up? Output:
PubmedQA203679	[ { "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 sufficient evidence that blood group related Lewis antigens are tumour-associated molecules. The Lewisy and Lewisb antigens are complex carbohydrates that are over-expressed by breast, lung, colon and ovarian cancers. The SC101 mAb is a unique Lewisy/b binding antibody that binds to native and extended Lewisy and Lewisb haptens, displaying no cross reactivity with H type 1, H type 2, Lewisx or normal blood group antigens. Immunohistochemical detection of Lewisy/b was performed on 660 formalin-fixed, paraffin embedded breast tumour specimens using a streptavidin-biotin peroxidase technique. Tissue from these patients had previously been included in tissue microarrays. This cohort comprises a well characterized series of patients with primary operable breast cancer diagnosed between 1987 and 1992, obtained from the Nottingham Tenovus Primary Breast Carcinoma Series. This includes patients 70 years of age or less, with a mean follow up of 7 years. Of the breast carcinomas, 370 of 660 (56%) were negative for Lewisy/b expression, 110 (17%) cases showed a low level of expression (<25% of positive cells) and only 54 cases (8%) showed extensive expression of Lewisy/b (>75% of positive cells). We found significant positive associations between histological grade (p < 0.001), Nottingham Prognostic Index (p = 0.016), tumour type (p = 0.007) and the level of Lewis y/b expression. There was a significant correlation between the proportion of Lewisy/b positive tumour cells and survival in lymph-node negative patients (p = 0.006).\n Question: Is high expression of Lewis y/b antigens associated with decreased survival in lymph node negative breast carcinomas?\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 sufficient evidence that blood group related Lewis antigens are tumour-associated molecules. The Lewisy and Lewisb antigens are complex carbohydrates that are over-expressed by breast, lung, colon and ovarian cancers. The SC101 mAb is a unique Lewisy/b binding antibody that binds to native and extended Lewisy and Lewisb haptens, displaying no cross reactivity with H type 1, H type 2, Lewisx or normal blood group antigens. Immunohistochemical detection of Lewisy/b was performed on 660 formalin-fixed, paraffin embedded breast tumour specimens using a streptavidin-biotin peroxidase technique. Tissue from these patients had previously been included in tissue microarrays. This cohort comprises a well characterized series of patients with primary operable breast cancer diagnosed between 1987 and 1992, obtained from the Nottingham Tenovus Primary Breast Carcinoma Series. This includes patients 70 years of age or less, with a mean follow up of 7 years. Of the breast carcinomas, 370 of 660 (56%) were negative for Lewisy/b expression, 110 (17%) cases showed a low level of expression (<25% of positive cells) and only 54 cases (8%) showed extensive expression of Lewisy/b (>75% of positive cells). We found significant positive associations between histological grade (p < 0.001), Nottingham Prognostic Index (p = 0.016), tumour type (p = 0.007) and the level of Lewis y/b expression. There was a significant correlation between the proportion of Lewisy/b positive tumour cells and survival in lymph-node negative patients (p = 0.006). Question: Is high expression of Lewis y/b antigens associated with decreased survival in lymph node negative breast carcinomas? Output:
PubmedQA140392	[ { "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 examine the heart rate reserve (HRR) at first and second ventilatory thresholds (VT's) in postmenopausal women and compare it with optimal intensity range recommended by the ACSM (40-84%HRR). An additional aim was to evaluate whether a higher aerobic power level corresponded to a higher HRR at VT's. Fifty-eight postmenopausal women participated in this study (aged 48-69). A graded 25 Wmin(-2) cycle ergometer (Monark E839) exercise protocol was performed in order to assess aerobic power. The heart rate and gas-exchange variables were measured continuously using a portable gas analyzer system (Cosmed K4b). The first (VT1) and the second (VT2) VT's were determined by the time course curves of ventilation and O2 and CO2 ventilatory equivalents. A K-means clustering analysis was used in order to identify VO2max groups (cut-off of 30.5 mlkg(-1)min(-1)) and differences were evaluated by an independent sample t-test. Bland-Altman plots were performed to illustrate the agreement between methods. The women's HRR values at VT1 were similar to 40% HRR in both VO2max groups. At VT2 both VO2max groups exhibited negative differences (P<0.01) for the predicted 84%HRR intensity (-14.46% in the lower VO2max group and -16.32% in the higher VO2max group).\n Question: Is the upper limit of the cardiorespiratory training zone ( 40-84 % HRR ) overestimated for postmenopausal 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 purpose of this study was to examine the heart rate reserve (HRR) at first and second ventilatory thresholds (VT's) in postmenopausal women and compare it with optimal intensity range recommended by the ACSM (40-84%HRR). An additional aim was to evaluate whether a higher aerobic power level corresponded to a higher HRR at VT's. Fifty-eight postmenopausal women participated in this study (aged 48-69). A graded 25 Wmin(-2) cycle ergometer (Monark E839) exercise protocol was performed in order to assess aerobic power. The heart rate and gas-exchange variables were measured continuously using a portable gas analyzer system (Cosmed K4b). The first (VT1) and the second (VT2) VT's were determined by the time course curves of ventilation and O2 and CO2 ventilatory equivalents. A K-means clustering analysis was used in order to identify VO2max groups (cut-off of 30.5 mlkg(-1)min(-1)) and differences were evaluated by an independent sample t-test. Bland-Altman plots were performed to illustrate the agreement between methods. The women's HRR values at VT1 were similar to 40% HRR in both VO2max groups. At VT2 both VO2max groups exhibited negative differences (P<0.01) for the predicted 84%HRR intensity (-14.46% in the lower VO2max group and -16.32% in the higher VO2max group). Question: Is the upper limit of the cardiorespiratory training zone ( 40-84 % HRR ) overestimated for postmenopausal women? Output:
PubmedQA83917	[ { "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: Ionic remodeling has a close correlation with the occurrence of atrial fibrillation (AF). Atrial tachypacing remodeling is associated with characteristic ionic remodeling. The purpose of this study was to assess the efficacy of cilostazol, an oral phosphodiesterase 3 inhibitor, for preventing atrial ionic remodeling in long-term rapid atrial pacing (RAP) dogs. We use the methods of patch-clamp and molecular biology to investigate the effect of cilostazol on ion channel and channel gene expression in long-term RAP dogs. Twenty-one dogs were randomly assigned to sham, control paced, and paced+cilostazol (5 mg/kg/d, cilo) groups, with 7 dogs in each group. The sham group was instrumented with a pacemaker but without pacing. RAP at 500 beats/min was maintained for 2 weeks in the paced and cilo groups. During the pacing, cilostazol was given orally in the cilo group. Whole-cell patch-clamp technique was used to record atrial L-type Ca2+ (ICaL) and fast sodium channel (INa) ionic currents. Western blot and RT-PCR were applied to estimate the gene expression of the ICaLα) 1C (Cav1.2) and INav1.5α) Nav1.5α) subunits. Statistical analysis was performed using SPSS 13.0. The density of ICaL and INa currents (pA/pF) was significantly reduced in the paced group (ICaL: -6.55±1.42 vs. -4.46±0.59 pA/pF; INa: -48.24±10.54 vs. -30.48±5.20 pA/pF, p<0.01). The paced+cilo group could not increase the density of ICaL currents (ICaL: -4.37±1.25 pA/pF, p>0.05), while the INa currents were recovered (-44.54±12.65 pA/pF, p<0.01) compared with the paced group. The mRNA and protein expression levels of Cav1.2 and Nav1.5α were apparently down-regulated in the paced group (p<0.01), but after cilostazol treatment, both of these subunits were up-regulated significantly (p<0.01).\n Question: Does cilostazol ameliorate atrial ionic remodeling in long-term rapid atrial pacing dogs?\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: Ionic remodeling has a close correlation with the occurrence of atrial fibrillation (AF). Atrial tachypacing remodeling is associated with characteristic ionic remodeling. The purpose of this study was to assess the efficacy of cilostazol, an oral phosphodiesterase 3 inhibitor, for preventing atrial ionic remodeling in long-term rapid atrial pacing (RAP) dogs. We use the methods of patch-clamp and molecular biology to investigate the effect of cilostazol on ion channel and channel gene expression in long-term RAP dogs. Twenty-one dogs were randomly assigned to sham, control paced, and paced+cilostazol (5 mg/kg/d, cilo) groups, with 7 dogs in each group. The sham group was instrumented with a pacemaker but without pacing. RAP at 500 beats/min was maintained for 2 weeks in the paced and cilo groups. During the pacing, cilostazol was given orally in the cilo group. Whole-cell patch-clamp technique was used to record atrial L-type Ca2+ (ICaL) and fast sodium channel (INa) ionic currents. Western blot and RT-PCR were applied to estimate the gene expression of the ICaLα) 1C (Cav1.2) and INav1.5α) Nav1.5α) subunits. Statistical analysis was performed using SPSS 13.0. The density of ICaL and INa currents (pA/pF) was significantly reduced in the paced group (ICaL: -6.55±1.42 vs. -4.46±0.59 pA/pF; INa: -48.24±10.54 vs. -30.48±5.20 pA/pF, p<0.01). The paced+cilo group could not increase the density of ICaL currents (ICaL: -4.37±1.25 pA/pF, p>0.05), while the INa currents were recovered (-44.54±12.65 pA/pF, p<0.01) compared with the paced group. The mRNA and protein expression levels of Cav1.2 and Nav1.5α were apparently down-regulated in the paced group (p<0.01), but after cilostazol treatment, both of these subunits were up-regulated significantly (p<0.01). Question: Does cilostazol ameliorate atrial ionic remodeling in long-term rapid atrial pacing dogs? Output:
PubmedQA27125	[ { "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: Colorectal cancer is (CRC) one of the commonest cancers and its therapy is still based on few drugs. Currently, no biological criteria are used to choose the most effective of the established drugs for treatment. A panel of 77 CRC cell lines was tested for sensitivity to 5-fluorouracil (5FU) using the SRB assay. The responses were grouped into three categories and correlated with genetic changes in the cell lines. The strongest and most clearcut correlation was between 5-fluorouracil response and replication error status (mismatch repair deficiency). All the other significant correlations (loss of heterozygosity for DCC and mutations in TGFbIIR) are secondary to the association with replication error status.\n Question: Is 5-Fluorouracil response in a large panel of colorectal cancer cell lines associated with mismatch repair deficiency?\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: Colorectal cancer is (CRC) one of the commonest cancers and its therapy is still based on few drugs. Currently, no biological criteria are used to choose the most effective of the established drugs for treatment. A panel of 77 CRC cell lines was tested for sensitivity to 5-fluorouracil (5FU) using the SRB assay. The responses were grouped into three categories and correlated with genetic changes in the cell lines. The strongest and most clearcut correlation was between 5-fluorouracil response and replication error status (mismatch repair deficiency). All the other significant correlations (loss of heterozygosity for DCC and mutations in TGFbIIR) are secondary to the association with replication error status. Question: Is 5-Fluorouracil response in a large panel of colorectal cancer cell lines associated with mismatch repair deficiency? Output:
PubmedQA1625	[ { "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 are still many questions related to aseptic femoral stem loosening. Systemic and local immune responses to the implanted \"foreign body\" is one of the reasons for loosening. The purpose of the study was to measure metal ion concentration (Ti, Co, Cr, Mo, Ni, Al) around loosened femoral stems and compare their levels around uncemented and cemented implants. This paper reports 50 hips operated for isolated stem loosening, in 50 patients at the mean age of 57 years (from 21 to 87). There were 25 cemented (Co,Cr29,Mo,Ni) and 25 uncemented (Ti, Al) stems. The mean follow-up from primary hip replacement to revision was 10.1 years (from 0.5 to 17). During the procedure, scar tissue around the stem was taken for analysis of metal ions. The concentrations of titanium and aluminium in soft tissues around uncemented loosened stems were higher than cemented ones (p < 0.001, p < 0.001 respectively). However, no statistically significant differences were observed between both types of stems in terms of ions of the metal of which cemented implants had been made of (Co, Cr, Mo, Ni).\n Question: Does metal debris concentrations in soft tissues adjacent to loosened femoral stem is higher in uncemented than cemented implants?\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 are still many questions related to aseptic femoral stem loosening. Systemic and local immune responses to the implanted "foreign body" is one of the reasons for loosening. The purpose of the study was to measure metal ion concentration (Ti, Co, Cr, Mo, Ni, Al) around loosened femoral stems and compare their levels around uncemented and cemented implants. This paper reports 50 hips operated for isolated stem loosening, in 50 patients at the mean age of 57 years (from 21 to 87). There were 25 cemented (Co,Cr29,Mo,Ni) and 25 uncemented (Ti, Al) stems. The mean follow-up from primary hip replacement to revision was 10.1 years (from 0.5 to 17). During the procedure, scar tissue around the stem was taken for analysis of metal ions. The concentrations of titanium and aluminium in soft tissues around uncemented loosened stems were higher than cemented ones (p < 0.001, p < 0.001 respectively). However, no statistically significant differences were observed between both types of stems in terms of ions of the metal of which cemented implants had been made of (Co, Cr, Mo, Ni). Question: Does metal debris concentrations in soft tissues adjacent to loosened femoral stem is higher in uncemented than cemented implants? Output:
PubmedQA54281	[ { "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 if highly active antiretroviral therapy (HAART) with combination anti-hepatitis B virus (HBV) therapy compared to HAART with HBV monotherapy leads to greater HBV DNA suppression in an HIV/HBV coinfected cohort. A cross-sectional analysis of 122 HIV/HBV coinfected patients from Australia and the United States. Univariate analysis and ordinal logistic regression were used to determine factors associated with an HBV DNA less than 100 IU/ml. The majority of patients were on HAART (85%), had an HIV RNA less than 50 copies/ml, a median CD4 cell count of 438 cells/microl, and had prior or current lamivudine therapy (98%). The majority (89%) of those on HAART were on HBV-active drugs including 54% on tenofovir (TDF) with either lamivudine (LAM) or emtrictabine (FTC), 34% receiving LAM or FTC monotherapy, and 12% on TDF monotherapy. Only 4% of patients in the combination (TDF + LAM/FTC) group had HBV DNA greater than 20 000 IU/ml compared to 54% in the group on no HBV-active therapy, 31% in the LAM or FTC monotherapy group, and 30% in the TDF monotherapy group (P < 0.0001). In an ordinal logistic regression model, monotherapy with either TDF or LAM remained independently associated with higher HBV DNA.\n Question: Is combination HBV therapy linked to greater HBV DNA suppression in a cohort of lamivudine-experienced HIV/HBV coinfected individuals?\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 if highly active antiretroviral therapy (HAART) with combination anti-hepatitis B virus (HBV) therapy compared to HAART with HBV monotherapy leads to greater HBV DNA suppression in an HIV/HBV coinfected cohort. A cross-sectional analysis of 122 HIV/HBV coinfected patients from Australia and the United States. Univariate analysis and ordinal logistic regression were used to determine factors associated with an HBV DNA less than 100 IU/ml. The majority of patients were on HAART (85%), had an HIV RNA less than 50 copies/ml, a median CD4 cell count of 438 cells/microl, and had prior or current lamivudine therapy (98%). The majority (89%) of those on HAART were on HBV-active drugs including 54% on tenofovir (TDF) with either lamivudine (LAM) or emtrictabine (FTC), 34% receiving LAM or FTC monotherapy, and 12% on TDF monotherapy. Only 4% of patients in the combination (TDF + LAM/FTC) group had HBV DNA greater than 20 000 IU/ml compared to 54% in the group on no HBV-active therapy, 31% in the LAM or FTC monotherapy group, and 30% in the TDF monotherapy group (P < 0.0001). In an ordinal logistic regression model, monotherapy with either TDF or LAM remained independently associated with higher HBV DNA. Question: Is combination HBV therapy linked to greater HBV DNA suppression in a cohort of lamivudine-experienced HIV/HBV coinfected individuals? Output:
PubmedQA5438	[ { "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: Systemic hypertension is one of the main risk factors for atherothrombosis. Tissue factor (TF) is found in the adventitia of blood vessels and in the lipid core of atherosclerotic plaques, and is specifically expressed on monocyte or macrophage cell membrane surfaces. TF plays a pivotal role in blood clotting physiology and is involved in pro-inflammatory action and atherosclerotic plaque destabilization. In this study we investigated whether there is any relationship between TF messenger RNA expression and activity in blood monocytes isolated from hypertensive patients with clinical signs of atherosclerosis, uncomplicated hypertensive individuals and normotensive control subjects. Eighty subjects (41 men and 39 women, mean age 41 +/- 12 years) with untreated essential hypertension and 41 control subjects matched for sex and age were enrolled in the study. Patients were classified according to whether they had a normal (</= 1 mm, 41 patients) or abnormal (> 1 mm, 39 patients) intima-media thickness (IMT). TF mRNA expression and activity in hypertensive individuals with no carotid atherosclerosis were no different from control subjects in unstimulated and stimulated monocytes. Abnormal IMT patients showed a higher TF mRNA expression compared with normal IMT hypertensive subjects (P < 0.001).\n Question: Are tissue factor expression and activity increased in peripheral monocytes isolated from uncomplicated hypertensive patients?\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: Systemic hypertension is one of the main risk factors for atherothrombosis. Tissue factor (TF) is found in the adventitia of blood vessels and in the lipid core of atherosclerotic plaques, and is specifically expressed on monocyte or macrophage cell membrane surfaces. TF plays a pivotal role in blood clotting physiology and is involved in pro-inflammatory action and atherosclerotic plaque destabilization. In this study we investigated whether there is any relationship between TF messenger RNA expression and activity in blood monocytes isolated from hypertensive patients with clinical signs of atherosclerosis, uncomplicated hypertensive individuals and normotensive control subjects. Eighty subjects (41 men and 39 women, mean age 41 +/- 12 years) with untreated essential hypertension and 41 control subjects matched for sex and age were enrolled in the study. Patients were classified according to whether they had a normal (</= 1 mm, 41 patients) or abnormal (> 1 mm, 39 patients) intima-media thickness (IMT). TF mRNA expression and activity in hypertensive individuals with no carotid atherosclerosis were no different from control subjects in unstimulated and stimulated monocytes. Abnormal IMT patients showed a higher TF mRNA expression compared with normal IMT hypertensive subjects (P < 0.001). Question: Are tissue factor expression and activity increased in peripheral monocytes isolated from uncomplicated hypertensive patients? Output:
PubmedQA69414	[ { "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: Inflammatory infiltrates, airway hyper-responsiveness, goblet cell hyperplasia and subepithelial thickening are characteristic of chronic asthma. Current animal models of allergen-induced airway inflammation generally concentrate on the acute inflammation following allergen exposure and fail to mimic all of these features. The aim of this study was to use a murine model of prolonged allergen-induced airway inflammation in order to characterize the cells and molecules involved in the ensuing airway remodelling. Moreover, we investigated whether remodelling persists in the absence of continued allergen challenge. Acute pulmonary eosinophilia and airways hyper-reactivity were induced after six serial allergen challenges in sensitized mice (acute phase). Mice were subsequently challenged three times a week with ovalbumin (OVA) (chronic phase) up to day 55. To investigate the persistence of pathology, one group of mice were left for another 4 weeks without further allergen challenge (day 80). The extended OVA challenge protocol caused significant airway remodelling, which was absent in the acute phase. Specifically, remodelling was characterized by deposition of collagen as well as airway smooth muscle and goblet cell hyperplasia. Importantly, these airway changes, together with tissue eosinophilia were sustained in the absence of further allergen challenge. Examination of cytokines revealed a dramatic up-regulation of IL-4 and tumour growth factor-beta1 during the chronic phase. Interestingly, while IL-4 levels were significantly increased during the chronic phase, levels of IL-13 fell. Levels of the Th1-associated cytokine IFN-gamma also increased during the chronic phase.\n Question: Does prolonged allergen challenge in mice lead to persistent airway remodelling?\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: Inflammatory infiltrates, airway hyper-responsiveness, goblet cell hyperplasia and subepithelial thickening are characteristic of chronic asthma. Current animal models of allergen-induced airway inflammation generally concentrate on the acute inflammation following allergen exposure and fail to mimic all of these features. The aim of this study was to use a murine model of prolonged allergen-induced airway inflammation in order to characterize the cells and molecules involved in the ensuing airway remodelling. Moreover, we investigated whether remodelling persists in the absence of continued allergen challenge. Acute pulmonary eosinophilia and airways hyper-reactivity were induced after six serial allergen challenges in sensitized mice (acute phase). Mice were subsequently challenged three times a week with ovalbumin (OVA) (chronic phase) up to day 55. To investigate the persistence of pathology, one group of mice were left for another 4 weeks without further allergen challenge (day 80). The extended OVA challenge protocol caused significant airway remodelling, which was absent in the acute phase. Specifically, remodelling was characterized by deposition of collagen as well as airway smooth muscle and goblet cell hyperplasia. Importantly, these airway changes, together with tissue eosinophilia were sustained in the absence of further allergen challenge. Examination of cytokines revealed a dramatic up-regulation of IL-4 and tumour growth factor-beta1 during the chronic phase. Interestingly, while IL-4 levels were significantly increased during the chronic phase, levels of IL-13 fell. Levels of the Th1-associated cytokine IFN-gamma also increased during the chronic phase. Question: Does prolonged allergen challenge in mice lead to persistent airway remodelling? Output:
PubmedQA45790	[ { "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: Live, attenuated measles virus (MeV) vaccine strains were generated by adaptation to cell culture. The genetic basis for the attenuation of the vaccine strains is unknown. We previously reported that adaptation of a pathogenic, wild-type MeV to Vero cells or primary chicken embryo fibroblasts (CEFs) resulted in a loss of pathogenicity in rhesus macaques. The CEF-adapted virus (D-CEF) contained single amino acid changes in the C and matrix (M) proteins and two substitutions in the shared amino terminal domain of the phosphoprotein (P) and V protein. The Vero-adapted virus (D-VI) had a mutation in the cytoplasmic tail of the hemagglutinin (H) protein. In vitro assays were used to test the functions of the wild-type and mutant proteins. The substitution in the C protein of D-CEF decreased its ability to inhibit mini-genome replication, while the wild-type and mutant M proteins inhibited replication to the same extent. The substitution in the cytoplasmic tail of the D-VI H protein resulted in reduced fusion in a quantitative fusion assay. Co-expression of M proteins with wild-type fusion and H proteins decreased fusion activity, but the mutation in the M protein of D-CEF did not affect this function. Both mutations in the P and V proteins of D-CEF reduced the ability of these proteins to inhibit type I and II interferon signaling.\n Question: Does adaptation to cell culture induce functional differences in measles virus proteins?\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: Live, attenuated measles virus (MeV) vaccine strains were generated by adaptation to cell culture. The genetic basis for the attenuation of the vaccine strains is unknown. We previously reported that adaptation of a pathogenic, wild-type MeV to Vero cells or primary chicken embryo fibroblasts (CEFs) resulted in a loss of pathogenicity in rhesus macaques. The CEF-adapted virus (D-CEF) contained single amino acid changes in the C and matrix (M) proteins and two substitutions in the shared amino terminal domain of the phosphoprotein (P) and V protein. The Vero-adapted virus (D-VI) had a mutation in the cytoplasmic tail of the hemagglutinin (H) protein. In vitro assays were used to test the functions of the wild-type and mutant proteins. The substitution in the C protein of D-CEF decreased its ability to inhibit mini-genome replication, while the wild-type and mutant M proteins inhibited replication to the same extent. The substitution in the cytoplasmic tail of the D-VI H protein resulted in reduced fusion in a quantitative fusion assay. Co-expression of M proteins with wild-type fusion and H proteins decreased fusion activity, but the mutation in the M protein of D-CEF did not affect this function. Both mutations in the P and V proteins of D-CEF reduced the ability of these proteins to inhibit type I and II interferon signaling. Question: Does adaptation to cell culture induce functional differences in measles virus proteins? Output:
PubmedQA103241	[ { "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: Parenchymal hematoma (PH) may worsen the outcome of patients with stroke. The aim of our study was to confirm the relationship between the volume of very low cerebral blood volume (CBV) and PH using a European multicenter database (I-KNOW). A secondary objective was to explore the impact of early reperfusion and recanalization. The volume of cerebral tissue with CBV≤2.5th percentile of the normal hemisphere was calculated within the acute diffusion-weighted imaging lesion. Hemorrhagic transformation was assessed on day 2 MRI according to the European Cooperative Acute Stroke Study II criteria. Recanalization and reperfusion were assessed on 3-hour follow-up MRI. Of the 110 patients, hemorrhagic transformation occurred in 59 patients, including 7 PH. In univariate analysis, the acute National Institutes of Health Stroke Scale score (P=0.002), acute diffusion-weighted imaging lesion volume (P=0.02), and thrombolysis (P=0.03), but not very low CBV (P=0.52), were associated with hemorrhagic transformation. The volume of very low CBV was the only predictor of PH (P=0.007). Early reperfusion and recanalization had no influence on either hemorrhagic transformation or PH.\n Question: Does very low cerebral blood volume predict parenchymal hematoma in acute ischemic 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: Parenchymal hematoma (PH) may worsen the outcome of patients with stroke. The aim of our study was to confirm the relationship between the volume of very low cerebral blood volume (CBV) and PH using a European multicenter database (I-KNOW). A secondary objective was to explore the impact of early reperfusion and recanalization. The volume of cerebral tissue with CBV≤2.5th percentile of the normal hemisphere was calculated within the acute diffusion-weighted imaging lesion. Hemorrhagic transformation was assessed on day 2 MRI according to the European Cooperative Acute Stroke Study II criteria. Recanalization and reperfusion were assessed on 3-hour follow-up MRI. Of the 110 patients, hemorrhagic transformation occurred in 59 patients, including 7 PH. In univariate analysis, the acute National Institutes of Health Stroke Scale score (P=0.002), acute diffusion-weighted imaging lesion volume (P=0.02), and thrombolysis (P=0.03), but not very low CBV (P=0.52), were associated with hemorrhagic transformation. The volume of very low CBV was the only predictor of PH (P=0.007). Early reperfusion and recanalization had no influence on either hemorrhagic transformation or PH. Question: Does very low cerebral blood volume predict parenchymal hematoma in acute ischemic stroke? Output:
PubmedQA188141	[ { "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: Mixed cannabinoid receptor 1 and 2 (CB1 and CB2) agonists such as Δ(9)-tetrahydrocannabinol (Δ(9)-THC) can produce tolerance, physical withdrawal, and unwanted CB1-mediated central nervous system side effects. Whether repeated systemic administration of a CB2-preferring agonist engages CB1 receptors or produces CB1-mediated side effects is unknown. We evaluated antiallodynic efficacy, possible tolerance, and cannabimimetic side effects of repeated dosing with a CB2-preferring agonist AM1710 in a model of chemotherapy-induced neuropathy produced by paclitaxel using CB1 knockout (CB1KO), CB2 knockout (CB2KO), and wild-type (WT) mice. Comparisons were made with the prototypic classic cannabinoid Δ(9)-THC. We also explored the site and possible mechanism of action of AM1710. Paclitaxel-induced mechanical and cold allodynia developed to an equivalent degree in CB1KO, CB2KO, and WT mice. Both AM1710 and Δ(9)-THC suppressed established paclitaxel-induced allodynia in WT mice. In contrast to Δ(9)-THC, chronic administration of AM1710 did not engage CB1 activity or produce antinociceptive tolerance, CB1-mediated cannabinoid withdrawal, hypothermia, or motor dysfunction. Antiallodynic efficacy of systemic administration of AM1710 was absent in CB2KO mice and WT mice receiving the CB2 antagonist AM630, administered either systemically or intrathecally. Intrathecal administration of AM1710 also attenuated paclitaxel-induced allodynia in WT mice, but not CB2KO mice, implicating a possible role for spinal CB2 receptors in AM1710 antiallodynic efficacy. Finally, both acute and chronic administration of AM1710 decreased messenger RNA levels of tumor necrosis factor-α and monocyte chemoattractant protein 1 in lumbar spinal cord of paclitaxel-treated WT mice.\n Question: Does chronic cannabinoid receptor 2 activation reverse paclitaxel neuropathy without tolerance or cannabinoid receptor 1-dependent withdrawal?\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: Mixed cannabinoid receptor 1 and 2 (CB1 and CB2) agonists such as Δ(9)-tetrahydrocannabinol (Δ(9)-THC) can produce tolerance, physical withdrawal, and unwanted CB1-mediated central nervous system side effects. Whether repeated systemic administration of a CB2-preferring agonist engages CB1 receptors or produces CB1-mediated side effects is unknown. We evaluated antiallodynic efficacy, possible tolerance, and cannabimimetic side effects of repeated dosing with a CB2-preferring agonist AM1710 in a model of chemotherapy-induced neuropathy produced by paclitaxel using CB1 knockout (CB1KO), CB2 knockout (CB2KO), and wild-type (WT) mice. Comparisons were made with the prototypic classic cannabinoid Δ(9)-THC. We also explored the site and possible mechanism of action of AM1710. Paclitaxel-induced mechanical and cold allodynia developed to an equivalent degree in CB1KO, CB2KO, and WT mice. Both AM1710 and Δ(9)-THC suppressed established paclitaxel-induced allodynia in WT mice. In contrast to Δ(9)-THC, chronic administration of AM1710 did not engage CB1 activity or produce antinociceptive tolerance, CB1-mediated cannabinoid withdrawal, hypothermia, or motor dysfunction. Antiallodynic efficacy of systemic administration of AM1710 was absent in CB2KO mice and WT mice receiving the CB2 antagonist AM630, administered either systemically or intrathecally. Intrathecal administration of AM1710 also attenuated paclitaxel-induced allodynia in WT mice, but not CB2KO mice, implicating a possible role for spinal CB2 receptors in AM1710 antiallodynic efficacy. Finally, both acute and chronic administration of AM1710 decreased messenger RNA levels of tumor necrosis factor-α and monocyte chemoattractant protein 1 in lumbar spinal cord of paclitaxel-treated WT mice. Question: Does chronic cannabinoid receptor 2 activation reverse paclitaxel neuropathy without tolerance or cannabinoid receptor 1-dependent withdrawal? Output:
PubmedQA113293	[ { "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: Glycoproteins encoded by the major histocompatibility complex class I region (MHC class I) present peptide antigens to cytotoxic T cells (CTLs). Peptides are delivered to the site of MHC class I assembly by the transporter associated with antigen processing (TAP), and cell lines that lack this transporter are unable to present endogenous antigens to CTLs. Although it has been shown that a fraction of newly synthesized class I molecules are in physical association with TAP, it is not known whether this interaction is functionally relevant, or where on the class I molecule the TAP binding site might be. C1R cells transfected with a mutant HLA-A2.1 heavy chain (HC), where threonine at position 134 in the alpha 2 domain is changed to lysine (T134K), are unable to present endogenous antigens to CTLs. We have studied the biochemistry of this mutant in C1R cells, and found that a large pool of unstable empty class I HC-beta 2m (beta-2 microglobulin) heterodimers exist that are rapidly transported to the cell surface. The T134K mutant seemed to bind peptide antigens and assemble with beta 2m as efficiently as wild-type HLA-A2.1. However, we show here that the inefficiency with which T134K presents intracellular antigen is associated with its inability to interact with the TAP heterodimer.\n Question: Do point mutations in the alpha 2 domain of HLA-A2.1 define a functionally relevant interaction with TAP?\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: Glycoproteins encoded by the major histocompatibility complex class I region (MHC class I) present peptide antigens to cytotoxic T cells (CTLs). Peptides are delivered to the site of MHC class I assembly by the transporter associated with antigen processing (TAP), and cell lines that lack this transporter are unable to present endogenous antigens to CTLs. Although it has been shown that a fraction of newly synthesized class I molecules are in physical association with TAP, it is not known whether this interaction is functionally relevant, or where on the class I molecule the TAP binding site might be. C1R cells transfected with a mutant HLA-A2.1 heavy chain (HC), where threonine at position 134 in the alpha 2 domain is changed to lysine (T134K), are unable to present endogenous antigens to CTLs. We have studied the biochemistry of this mutant in C1R cells, and found that a large pool of unstable empty class I HC-beta 2m (beta-2 microglobulin) heterodimers exist that are rapidly transported to the cell surface. The T134K mutant seemed to bind peptide antigens and assemble with beta 2m as efficiently as wild-type HLA-A2.1. However, we show here that the inefficiency with which T134K presents intracellular antigen is associated with its inability to interact with the TAP heterodimer. Question: Do point mutations in the alpha 2 domain of HLA-A2.1 define a functionally relevant interaction with TAP? Output:
PubmedQA191697	[ { "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 objective of this study was to determine whether baseline albuminuria predicts coronary artery calcification (CAC) progression in subjects with type 1 diabetes and whether angiotensin-converting enzyme inhibitor (ACE-I) or angiotensin II type I receptor blocker (ARB) treatment is associated with lower odds of CAC progression. In 2000-2002, the Coronary Artery Calcification in Type 1 Diabetes study enrolled 652 subjects with type 1 diabetes who were between 19 and 56 years old and had no known history of coronary artery disease (CAD). In this analysis, CAC progression over 2.5+/-0.4 years was evaluated in 478 subjects (age=37+/-9 years; male=45%; diabetes duration=23+/-9 years) at a follow-up visit. Albuminuria was defined by American Diabetes Association criteria, and microalbuminuria and macroalbuminuria were combined for the analysis. Logistic regression was used to evaluate the relationship between baseline categorical presence of albuminuria and CAC progression. At baseline, of the 478 subjects, 157 (33%) were on ACE-I/ARB treatment and 83 (17%) had albuminuria, with 114 (24%) having CAC progression at follow-up. In backward logistic regression, presence of albuminuria at baseline predicted progression of CAC among subjects not treated with ACE-I/ARB [odds ratio=4.06; 95% confidence interval (CI)=1.45-11.35; P=.008]. Among the subjects with albuminuria, the odds of progression was 62% lower (95% CI=88% decrease to 23% increase; P=.106) in those treated with ACE-I/ARB.\n Question: Is aCE-I/ARB treatment in type 1 diabetes patients with albuminuria associated with lower odds of progression of coronary artery calcification?\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 objective of this study was to determine whether baseline albuminuria predicts coronary artery calcification (CAC) progression in subjects with type 1 diabetes and whether angiotensin-converting enzyme inhibitor (ACE-I) or angiotensin II type I receptor blocker (ARB) treatment is associated with lower odds of CAC progression. In 2000-2002, the Coronary Artery Calcification in Type 1 Diabetes study enrolled 652 subjects with type 1 diabetes who were between 19 and 56 years old and had no known history of coronary artery disease (CAD). In this analysis, CAC progression over 2.5+/-0.4 years was evaluated in 478 subjects (age=37+/-9 years; male=45%; diabetes duration=23+/-9 years) at a follow-up visit. Albuminuria was defined by American Diabetes Association criteria, and microalbuminuria and macroalbuminuria were combined for the analysis. Logistic regression was used to evaluate the relationship between baseline categorical presence of albuminuria and CAC progression. At baseline, of the 478 subjects, 157 (33%) were on ACE-I/ARB treatment and 83 (17%) had albuminuria, with 114 (24%) having CAC progression at follow-up. In backward logistic regression, presence of albuminuria at baseline predicted progression of CAC among subjects not treated with ACE-I/ARB [odds ratio=4.06; 95% confidence interval (CI)=1.45-11.35; P=.008]. Among the subjects with albuminuria, the odds of progression was 62% lower (95% CI=88% decrease to 23% increase; P=.106) in those treated with ACE-I/ARB. Question: Is aCE-I/ARB treatment in type 1 diabetes patients with albuminuria associated with lower odds of progression of coronary artery calcification? Output:
PubmedQA23048	[ { "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 systematic review was to compare the long-term results of stapled hemorrhoidopexy with conventional excisional hemorrhoidectomy in patients with internal hemorrhoids. A systematic review of all randomized, controlled trials comparing stapled hemorrhoidopexy and conventional hemorrhoidectomy with long-term results was performed by using the Cochrane methodology. The minimum follow-up was six months. Primary outcomes were hemorrhoid recurrence, hemorrhoid symptom recurrence, complications, and pain. Twelve trials were included. Follow-up varied from six months to four years. Conventional hemorrhoidectomy was more effective in preventing long-term recurrence of hemorrhoids (odds ratio (OR), 3.85; 95 percent confidence interval (CI), 1.47-10.07; P < 0.006). Conventional hemorrhoidectomy also prevents hemorrhoids in studies with follow-up of one year or more (OR, 3.6; 95 percent CI, 1.24-10.49; P < 0.02). Conventional hemorrhoidectomy is superior in preventing the symptom of prolapse (OR, 2.96; 95 percent CI, 1.33-6.58; P < 0.008). Conventional hemorrhoidectomy also is more effective at preventing prolapse in studies with follow-up of one year or more (OR, 2.68; 95 percent CI, 0.98-7.34; P < 0.05). Nonsignificant trends in favor of conventional hemorrhoidectomy were seen in the proportion of asymptomatic patients, bleeding, soiling/difficultly with hygiene/incontinence, the presence of perianal skin tags, and the need for further surgery. Nonsignificant trends in favor of stapled hemorrhoidopexy were seen in pain, pruritus ani, and symptoms of anal obstruction/stenosis.\n Question: Is stapled hemorrhoidopexy associated with a higher long-term recurrence rate of internal hemorrhoids compared with conventional excisional hemorrhoid 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: The purpose of this systematic review was to compare the long-term results of stapled hemorrhoidopexy with conventional excisional hemorrhoidectomy in patients with internal hemorrhoids. A systematic review of all randomized, controlled trials comparing stapled hemorrhoidopexy and conventional hemorrhoidectomy with long-term results was performed by using the Cochrane methodology. The minimum follow-up was six months. Primary outcomes were hemorrhoid recurrence, hemorrhoid symptom recurrence, complications, and pain. Twelve trials were included. Follow-up varied from six months to four years. Conventional hemorrhoidectomy was more effective in preventing long-term recurrence of hemorrhoids (odds ratio (OR), 3.85; 95 percent confidence interval (CI), 1.47-10.07; P < 0.006). Conventional hemorrhoidectomy also prevents hemorrhoids in studies with follow-up of one year or more (OR, 3.6; 95 percent CI, 1.24-10.49; P < 0.02). Conventional hemorrhoidectomy is superior in preventing the symptom of prolapse (OR, 2.96; 95 percent CI, 1.33-6.58; P < 0.008). Conventional hemorrhoidectomy also is more effective at preventing prolapse in studies with follow-up of one year or more (OR, 2.68; 95 percent CI, 0.98-7.34; P < 0.05). Nonsignificant trends in favor of conventional hemorrhoidectomy were seen in the proportion of asymptomatic patients, bleeding, soiling/difficultly with hygiene/incontinence, the presence of perianal skin tags, and the need for further surgery. Nonsignificant trends in favor of stapled hemorrhoidopexy were seen in pain, pruritus ani, and symptoms of anal obstruction/stenosis. Question: Is stapled hemorrhoidopexy associated with a higher long-term recurrence rate of internal hemorrhoids compared with conventional excisional hemorrhoid surgery? Output:
PubmedQA179212	[ { "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 relationship between the posterior vitreous cortex and the posterior retina in eyes with early stages of idiopathic macular hole formation. Twenty-six eyes of 26 consecutive patients with stage 1 or stage 2 idiopathic macular hole underwent complete ophthalmologic examination, contact lens biomicroscopy, and B-scan ultrasonography or vitreoretinal surgery or both. In eyes that were operated on, the posterior cortical vitreous layer was meticulously examined with a silicone-tipped cannula prior to inducing a posterior vitreous detachment. In 25 (96%) of 26 eyes, one or more examination techniques revealed a shallow, localized detachment of the perifoveal vitreous, typically extending to the level of the vascular arcades. Among these 25 eyes, the posterior hyaloid membrane separation was detectable biomicroscopically in 4 (16%) of 25 eyes, ultrasonographically in 17 (74%) of 23 eyes, and intraoperatively in 23 (100%) of 23 eyes. Persistent vitreous adherence to the foveola was evident in 6 (100%) of 6 eyes with a stage 1 hole and in 12 (92%) of 13 eyes with a stage 2 hole but no operculum.\n Question: Is perifoveal vitreous detachment the primary pathogenic event in idiopathic macular hole formation?\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 relationship between the posterior vitreous cortex and the posterior retina in eyes with early stages of idiopathic macular hole formation. Twenty-six eyes of 26 consecutive patients with stage 1 or stage 2 idiopathic macular hole underwent complete ophthalmologic examination, contact lens biomicroscopy, and B-scan ultrasonography or vitreoretinal surgery or both. In eyes that were operated on, the posterior cortical vitreous layer was meticulously examined with a silicone-tipped cannula prior to inducing a posterior vitreous detachment. In 25 (96%) of 26 eyes, one or more examination techniques revealed a shallow, localized detachment of the perifoveal vitreous, typically extending to the level of the vascular arcades. Among these 25 eyes, the posterior hyaloid membrane separation was detectable biomicroscopically in 4 (16%) of 25 eyes, ultrasonographically in 17 (74%) of 23 eyes, and intraoperatively in 23 (100%) of 23 eyes. Persistent vitreous adherence to the foveola was evident in 6 (100%) of 6 eyes with a stage 1 hole and in 12 (92%) of 13 eyes with a stage 2 hole but no operculum. Question: Is perifoveal vitreous detachment the primary pathogenic event in idiopathic macular hole formation? Output:
PubmedQA195277	[ { "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: Adjuvant radiotherapy (RT) for left-sided breast cancer has a negative impact on cardiac health. The concurrent use of aromatase inhibitors (AIs) during RT was found to increase the anticancer efficacy of radiation in pre-clinical models. We evaluated whether the acute effects of RT on cardiac functions are augmented by the concurrent use of AIs. Sixty patients with early-stage left-sided breast cancer underwent a 2D echocardiography, electrocardiogram and cardiac biomarker measurements before and after adjuvant breast RT. Data were analyzed in two groups according to AI use. We observed a significant (p<0.05) decrease in right ventricular systolic function during RT in tricuspid annular plane systolic excursion (TAPSE). TAPSE decreased by 3.0 mm [95% confidence interval (CI)=1.9-4.1 mm] in the AI group and 1.4 mm (95% CI=0.3-2.4 mm) in the non-AI group. In addition, left ventricular diastolic function decreased among patients using AI, as the mitral inflow E-wave decreased 5.8 cm/s (95% CI=1.8-9.7 cm/s) (p=0.006).\n Question: Does the concurrent use of aromatase inhibitors and radiotherapy induce echocardiographic changes in patients with breast 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: Adjuvant radiotherapy (RT) for left-sided breast cancer has a negative impact on cardiac health. The concurrent use of aromatase inhibitors (AIs) during RT was found to increase the anticancer efficacy of radiation in pre-clinical models. We evaluated whether the acute effects of RT on cardiac functions are augmented by the concurrent use of AIs. Sixty patients with early-stage left-sided breast cancer underwent a 2D echocardiography, electrocardiogram and cardiac biomarker measurements before and after adjuvant breast RT. Data were analyzed in two groups according to AI use. We observed a significant (p<0.05) decrease in right ventricular systolic function during RT in tricuspid annular plane systolic excursion (TAPSE). TAPSE decreased by 3.0 mm [95% confidence interval (CI)=1.9-4.1 mm] in the AI group and 1.4 mm (95% CI=0.3-2.4 mm) in the non-AI group. In addition, left ventricular diastolic function decreased among patients using AI, as the mitral inflow E-wave decreased 5.8 cm/s (95% CI=1.8-9.7 cm/s) (p=0.006). Question: Does the concurrent use of aromatase inhibitors and radiotherapy induce echocardiographic changes in patients with breast cancer? Output:
PubmedQA180586	[ { "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 assess the risk associated with microbial contamination in the hub-fluid in Luer-lock syringes to the end-product, and ultimately patients. The hub-fluid of 48 sterile syringes prefilled with broth was contaminated with a low number of Staphylococcus epidermidis or spores of Bacillus subtilis. After incubation for three weeks, the syringe fills were tested for the presence of bacterial contaminants and some syringes were used to inoculate an end product broth that was then investigated for the presence of microorganisms. After three weeks of incubation only 20.8% of syringe fills showed turbidity, although following further investigation 70.8% were positive for the presence of viable bacteria, whereas 95.6% of end products became contaminated following injection of the syringe fill.\n Question: Does low-level microbial contamination of liquid in syringe hubs lead to an unacceptable risk to the end product?\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 assess the risk associated with microbial contamination in the hub-fluid in Luer-lock syringes to the end-product, and ultimately patients. The hub-fluid of 48 sterile syringes prefilled with broth was contaminated with a low number of Staphylococcus epidermidis or spores of Bacillus subtilis. After incubation for three weeks, the syringe fills were tested for the presence of bacterial contaminants and some syringes were used to inoculate an end product broth that was then investigated for the presence of microorganisms. After three weeks of incubation only 20.8% of syringe fills showed turbidity, although following further investigation 70.8% were positive for the presence of viable bacteria, whereas 95.6% of end products became contaminated following injection of the syringe fill. Question: Does low-level microbial contamination of liquid in syringe hubs lead to an unacceptable risk to the end product? Output:
PubmedQA78959	[ { "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: Vincristine sulfate liposome injection (VSLI) facilitates vincristine dose intensification and densification, is active in untreated and relapsed lymphoma, and has been approved in the United States for relapsed and refractory acute lymphoblastic leukemia. Cancer- and concomitant chemotherapy-related anemia, neutropenia, and thrombocytopenia in patients with hematologic malignancy have complicated the evaluation of hematologic toxicity related to new drugs. We assessed the hematologic toxicity of VSLI 2.25 mg/m(2) administered every 14 (cohort 1) or 7 (cohort 2) days in 54 patients with metastatic uveal melanoma, a cancer not known to involve the bone marrow. Cohort 2 received a greater median number of VSLI doses (6 vs. 4) within a shorter median period (5.7 vs. 8.7 weeks), resulting in a larger median cumulative exposure (22.6 vs. 17.7 mg) and near doubling of the median dose density (2.2 vs. 4.0 mg/wk) compared with cohort 1. Despite greater VSLI exposure and dose density, cohort 2 had a lower median decrease from baseline in the neutrophil count and a greater increase from baseline in the platelet count compared with cohort 1. Hematologic adverse events (AEs) were uncommon and mostly grade 1 or 2 in severity. No grade 4 hematologic AEs developed.\n Question: Is high-dose vincristine sulfate liposome injection ( Marqibo ) associated with clinically meaningful hematologic toxicity?\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: Vincristine sulfate liposome injection (VSLI) facilitates vincristine dose intensification and densification, is active in untreated and relapsed lymphoma, and has been approved in the United States for relapsed and refractory acute lymphoblastic leukemia. Cancer- and concomitant chemotherapy-related anemia, neutropenia, and thrombocytopenia in patients with hematologic malignancy have complicated the evaluation of hematologic toxicity related to new drugs. We assessed the hematologic toxicity of VSLI 2.25 mg/m(2) administered every 14 (cohort 1) or 7 (cohort 2) days in 54 patients with metastatic uveal melanoma, a cancer not known to involve the bone marrow. Cohort 2 received a greater median number of VSLI doses (6 vs. 4) within a shorter median period (5.7 vs. 8.7 weeks), resulting in a larger median cumulative exposure (22.6 vs. 17.7 mg) and near doubling of the median dose density (2.2 vs. 4.0 mg/wk) compared with cohort 1. Despite greater VSLI exposure and dose density, cohort 2 had a lower median decrease from baseline in the neutrophil count and a greater increase from baseline in the platelet count compared with cohort 1. Hematologic adverse events (AEs) were uncommon and mostly grade 1 or 2 in severity. No grade 4 hematologic AEs developed. Question: Is high-dose vincristine sulfate liposome injection ( Marqibo ) associated with clinically meaningful hematologic toxicity? Output:
PubmedQA200549	[ { "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: Different routes of administration of CCK-33 and blockage of CCK-A and muscarinic (m3) receptors are used in this study to evaluate the mechanisms by which cholecystokinin can stimulate the exocrine pancreas. The experiment was performed on eight anaesthetized pigs during control conditions and after administration of the CCK-A and m3 receptor antagonists, Tarazepide and 4-DAMP, respectively. Catheters were surgically implanted in the pancreatic duct for juice collection and in the gastric and right gastro-epipoic arteries and in the jugular vein, so that infusions of CCK-33 could be made exclusively to the duodenum/stomach, duodenum/pancreas or general circulation, respectively. Infusion of a low dose of CCK-33 (13 pmol kg(-1)) to the general circulation did not affect pancreatic protein or trypsin output. When the same dose was given directly to the duodenum/stomach or the duodenum/pancreas, pancreatic output increased during both control conditions and after Tarazepide and/or 4-DAMP treatment, though the increase in trypsin output was lower after Tarazepide and/or 4-DAMP blockade. A high dose of CCK-33 (130 pmol kg(-1)) given peripherally stimulated the pancreatic secretion, but this response was totally abolished in Tarazepide and 4-Damp treated animals.\n Question: Does cCK regulate pancreatic enzyme secretion via short duodenal-pancreatic reflexes in pigs?\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: Different routes of administration of CCK-33 and blockage of CCK-A and muscarinic (m3) receptors are used in this study to evaluate the mechanisms by which cholecystokinin can stimulate the exocrine pancreas. The experiment was performed on eight anaesthetized pigs during control conditions and after administration of the CCK-A and m3 receptor antagonists, Tarazepide and 4-DAMP, respectively. Catheters were surgically implanted in the pancreatic duct for juice collection and in the gastric and right gastro-epipoic arteries and in the jugular vein, so that infusions of CCK-33 could be made exclusively to the duodenum/stomach, duodenum/pancreas or general circulation, respectively. Infusion of a low dose of CCK-33 (13 pmol kg(-1)) to the general circulation did not affect pancreatic protein or trypsin output. When the same dose was given directly to the duodenum/stomach or the duodenum/pancreas, pancreatic output increased during both control conditions and after Tarazepide and/or 4-DAMP treatment, though the increase in trypsin output was lower after Tarazepide and/or 4-DAMP blockade. A high dose of CCK-33 (130 pmol kg(-1)) given peripherally stimulated the pancreatic secretion, but this response was totally abolished in Tarazepide and 4-Damp treated animals. Question: Does cCK regulate pancreatic enzyme secretion via short duodenal-pancreatic reflexes in pigs? Output:
PubmedQA153450	[ { "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: Coagulation proteins promote neointimal hyperplasia and vascular remodelling after vessel injury, but the precise mechanisms by which they act in vivo remain undetermined. This study, using an injury model in which the neointima is derived from bone marrow (BM)-derived cells, compared inhibition of tissue factor or thrombin on either BM-derived or existing vascular smooth muscle cells. Two transgenic (Tg) mouse strains expressing membrane-tethered tissue factor pathway inhibitor (TFPI) or hirudin (Hir) fusion proteins driven by an alpha smooth muscle actin (SMA) promoter were generated (alpha-TFPI-Tg and alpha-Hir-Tg) and the phenotype after wire-induced endovascular injury was compared with that in wild-type (WT) controls. WT mice developed progressive neointimal expansion, whereas injury in either Tg was followed by repair back to a preinjured state. This was also seen when WT mice were reconstituted with BM from Tg mice but not when Tgs were reconstituted with WT BM, in which injury was followed by slowly progressive neointimal expansion. Injection of CD34+ cells from Tg mice into injured WT mice resulted in the accumulation of fusion protein-expressing cells from day 3 onwards and an absence of neointimal hyperplasia in those areas.\n Question: Is postinjury vascular intimal hyperplasia in mice completely inhibited by CD34+ bone marrow-derived progenitor cells expressing membrane-tethered anticoagulant fusion proteins?\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: Coagulation proteins promote neointimal hyperplasia and vascular remodelling after vessel injury, but the precise mechanisms by which they act in vivo remain undetermined. This study, using an injury model in which the neointima is derived from bone marrow (BM)-derived cells, compared inhibition of tissue factor or thrombin on either BM-derived or existing vascular smooth muscle cells. Two transgenic (Tg) mouse strains expressing membrane-tethered tissue factor pathway inhibitor (TFPI) or hirudin (Hir) fusion proteins driven by an alpha smooth muscle actin (SMA) promoter were generated (alpha-TFPI-Tg and alpha-Hir-Tg) and the phenotype after wire-induced endovascular injury was compared with that in wild-type (WT) controls. WT mice developed progressive neointimal expansion, whereas injury in either Tg was followed by repair back to a preinjured state. This was also seen when WT mice were reconstituted with BM from Tg mice but not when Tgs were reconstituted with WT BM, in which injury was followed by slowly progressive neointimal expansion. Injection of CD34+ cells from Tg mice into injured WT mice resulted in the accumulation of fusion protein-expressing cells from day 3 onwards and an absence of neointimal hyperplasia in those areas. Question: Is postinjury vascular intimal hyperplasia in mice completely inhibited by CD34+ bone marrow-derived progenitor cells expressing membrane-tethered anticoagulant fusion proteins? Output:
PubmedQA136327	[ { "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 serum sex hormone levels and lower urinary tract symptoms in men aged 40-79 years. A cross-sectional study was conducted in 509 men (mean age 58 years). The serum total testosterone (TT), dihydrotestosterone, and estradiol levels were measured. The total prostate volume measured by transrectal ultrasonography and International Prostate Symptom Score (IPSS) questionnaire were obtained. Correlations were determined using univariate and multivariate regression analysis. The subjects with moderate to severe lower urinary tract symptoms (total IPSS≥8) were older, with a greater incidence of hypertension and diabetes, a larger prostate, and had lower serum TT levels. On the univariate analysis, the serum TT levels were negatively associated with the total IPSS, IPSS storage subscore, weak stream, and nocturia. After adjusting for age, hypertension, diabetes, and total prostate volume, only the serum TT level was significantly associated with nocturia (>2 times/night; P=.042), and men with serum TT levels in the greatest quartile had a 44% reduced risk of nocturia than in the lowest quartile (P=.037).\n Question: Do serum testosterone levels significantly correlate with nocturia in men aged 40-79 years?\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 serum sex hormone levels and lower urinary tract symptoms in men aged 40-79 years. A cross-sectional study was conducted in 509 men (mean age 58 years). The serum total testosterone (TT), dihydrotestosterone, and estradiol levels were measured. The total prostate volume measured by transrectal ultrasonography and International Prostate Symptom Score (IPSS) questionnaire were obtained. Correlations were determined using univariate and multivariate regression analysis. The subjects with moderate to severe lower urinary tract symptoms (total IPSS≥8) were older, with a greater incidence of hypertension and diabetes, a larger prostate, and had lower serum TT levels. On the univariate analysis, the serum TT levels were negatively associated with the total IPSS, IPSS storage subscore, weak stream, and nocturia. After adjusting for age, hypertension, diabetes, and total prostate volume, only the serum TT level was significantly associated with nocturia (>2 times/night; P=.042), and men with serum TT levels in the greatest quartile had a 44% reduced risk of nocturia than in the lowest quartile (P=.037). Question: Do serum testosterone levels significantly correlate with nocturia in men aged 40-79 years? Output:
PubmedQA54462	[ { "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 persistence of circulating tumor cells (CTC) in breast cancer patients might be associated with stem cell like tumor cells which have been suggested to be the active source of metastatic spread in primary tumors. Furthermore, these cells also may undergo phenotypic changes, known as epithelial-mesenchymal transition (EMT), which allows them to travel to the site of metastasis formation without getting affected by conventional treatment. Here we evaluated 226 blood samples of 39 metastatic breast cancer patients during a follow-up of palliative chemo-, antibody - or hormonal therapy for the expression of the stem cell marker ALDH1 and markers for EMT and correlated these findings with the presence of CTC and response to therapy. 2 x 5 ml blood was analyzed for CTC with the AdnaTest BreastCancer (AdnaGen AG) for the detection of EpCAM, MUC-1 and HER2 transcripts. The recovered c-DNA was additionally multiplex tested for three EMT markers [Twist1, Akt2, PI3Kalpha] and separately for the tumor stem-cell markers ALDH1. The identification of EMT markers was considered positive if at least one marker was detected in the sample. 97% of 30 healthy donor samples investigated were negative for EMT and 95% for ALDH1 transcripts. CTC were detected in 69/226 (31%) cancer samples. In the CTC (+) group, 62% were positive for at least one of the EMT markers and 69% for ALDH1, respectively. In the CTC (-) group the percentages were 7% and 14%, respectively. In non-responders, EMT and ALDH1 expression was found in 62% and 44% of patients, in responders the rates were 10% and 5%, respectively.\n Question: Are stem cell and epithelial-mesenchymal transition markers frequently overexpressed in circulating tumor cells of metastatic breast cancer 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 persistence of circulating tumor cells (CTC) in breast cancer patients might be associated with stem cell like tumor cells which have been suggested to be the active source of metastatic spread in primary tumors. Furthermore, these cells also may undergo phenotypic changes, known as epithelial-mesenchymal transition (EMT), which allows them to travel to the site of metastasis formation without getting affected by conventional treatment. Here we evaluated 226 blood samples of 39 metastatic breast cancer patients during a follow-up of palliative chemo-, antibody - or hormonal therapy for the expression of the stem cell marker ALDH1 and markers for EMT and correlated these findings with the presence of CTC and response to therapy. 2 x 5 ml blood was analyzed for CTC with the AdnaTest BreastCancer (AdnaGen AG) for the detection of EpCAM, MUC-1 and HER2 transcripts. The recovered c-DNA was additionally multiplex tested for three EMT markers [Twist1, Akt2, PI3Kalpha] and separately for the tumor stem-cell markers ALDH1. The identification of EMT markers was considered positive if at least one marker was detected in the sample. 97% of 30 healthy donor samples investigated were negative for EMT and 95% for ALDH1 transcripts. CTC were detected in 69/226 (31%) cancer samples. In the CTC (+) group, 62% were positive for at least one of the EMT markers and 69% for ALDH1, respectively. In the CTC (-) group the percentages were 7% and 14%, respectively. In non-responders, EMT and ALDH1 expression was found in 62% and 44% of patients, in responders the rates were 10% and 5%, respectively. Question: Are stem cell and epithelial-mesenchymal transition markers frequently overexpressed in circulating tumor cells of metastatic breast cancer patients? Output:
PubmedQA207521	[ { "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: Neutropenia is a major dose-limiting side effect of chemotherapy and is closely related to febrile neutropenia which mainly occurs during the first cycle. Our objectives were to establish model-based decision rules from early absolute neutrophil counts (ANC) to anticipate prolonged high grade neutropenia at cycle 1 and to prevent it through delayed granulocyte colony stimulating factor (G-CSF) administration in carboplatin-treated patients. The decision rules were built from Monte Carlo simulations performed with a previously published semi-mechanistic model describing ANC time-course in carboplatin-treated patients with or without concomitant G-CSF therapy. ANC measured at day 0 (D0, baseline), D4 and D5 were good predictors of prolonged high grade neutropenia at cycle 1. Pegfilgrastim administration on D5 was as effective as the conventional pegfilgrastim administration on D1 but none avoided prolonged high grade neutropenia in all patients. Additional decision rules were thus derived, using the same ANC combination, to identify patients for whom G-CSF was beneficial. All decision rules showed good performances (sensitivity/specificity).\n Question: Do model-based approach to early predict prolonged high grade neutropenia in carboplatin-treated patients and guide G-CSF prophylactic treatment?\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: Neutropenia is a major dose-limiting side effect of chemotherapy and is closely related to febrile neutropenia which mainly occurs during the first cycle. Our objectives were to establish model-based decision rules from early absolute neutrophil counts (ANC) to anticipate prolonged high grade neutropenia at cycle 1 and to prevent it through delayed granulocyte colony stimulating factor (G-CSF) administration in carboplatin-treated patients. The decision rules were built from Monte Carlo simulations performed with a previously published semi-mechanistic model describing ANC time-course in carboplatin-treated patients with or without concomitant G-CSF therapy. ANC measured at day 0 (D0, baseline), D4 and D5 were good predictors of prolonged high grade neutropenia at cycle 1. Pegfilgrastim administration on D5 was as effective as the conventional pegfilgrastim administration on D1 but none avoided prolonged high grade neutropenia in all patients. Additional decision rules were thus derived, using the same ANC combination, to identify patients for whom G-CSF was beneficial. All decision rules showed good performances (sensitivity/specificity). Question: Do model-based approach to early predict prolonged high grade neutropenia in carboplatin-treated patients and guide G-CSF prophylactic treatment? Output:
PubmedQA140181	[ { "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 distressed (Type D) personality is associated with adverse coronary heart disease outcomes, but the mechanisms accounting for this association remain to be elucidated. We examined whether myocardial and hemodynamic responses to mental stress are disrupted in Type D patients with chronic heart failure (HF). Ninety-nine HF patients (mean age 65±12years; 75% men) underwent a public speech task, during which heart rate (HR) and blood pressure (BP) were recorded. Type D personality and its components negative affectivity (NA) and social inhibition (SI) were assessed with the DS14. General linear models with repeated measures and logistic regression were used to assess differences in stress response and recovery. Type D personality was associated with a reduced HR response (F1,93=4.31, p<.05) independent of the use of beta adrenergic blocking agents and the presence of atrial fibrillation. There were no differences between HF patients with and without a Type D personality with respect to the BP response. Examining continuous NA and SI scores and their interaction (NA∗SI), revealed a significant association of NA∗SI with the SBP response (F1,93=4.11, p<.05), independent of BP covariates. Results with respect to HR and DBP responses were comparable to the findings using the dichotomous Type D measure. No significant associations between Type D and recovery patterns were found.\n Question: Is type D personality associated with low cardiovascular reactivity to acute mental stress 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 distressed (Type D) personality is associated with adverse coronary heart disease outcomes, but the mechanisms accounting for this association remain to be elucidated. We examined whether myocardial and hemodynamic responses to mental stress are disrupted in Type D patients with chronic heart failure (HF). Ninety-nine HF patients (mean age 65±12years; 75% men) underwent a public speech task, during which heart rate (HR) and blood pressure (BP) were recorded. Type D personality and its components negative affectivity (NA) and social inhibition (SI) were assessed with the DS14. General linear models with repeated measures and logistic regression were used to assess differences in stress response and recovery. Type D personality was associated with a reduced HR response (F1,93=4.31, p<.05) independent of the use of beta adrenergic blocking agents and the presence of atrial fibrillation. There were no differences between HF patients with and without a Type D personality with respect to the BP response. Examining continuous NA and SI scores and their interaction (NA∗SI), revealed a significant association of NA∗SI with the SBP response (F1,93=4.11, p<.05), independent of BP covariates. Results with respect to HR and DBP responses were comparable to the findings using the dichotomous Type D measure. No significant associations between Type D and recovery patterns were found. Question: Is type D personality associated with low cardiovascular reactivity to acute mental stress in heart failure patients? Output:
PubmedQA30135	[ { "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: Primary congenital glaucoma (PCG) is an autosomal recessive disorder that has been linked to CYP1B1 mutations. This study was conducted to explore the role of FOXC1, which is involved in anterior segment dysgenesis, in PCG. An earlier screening for CYP1B1 in a clinically well-characterized PCG cohort (n = 301) revealed cases that were either homozygous (n = 73), compound heterozygous (n = 18), or heterozygous (n = 41) for the mutant allele, whereas the remaining (n = 169) did not harbor any mutation. Hence, FOXC1 was screened in 210 PCG cases who were either heterozygous (n = 41) or did not harbor any CYP1B1 mutation (n = 169), along with ethnically matched normal control subjects (n = 157) by resequencing the entire coding region. Two heterozygous missense (H128R and C135Y) and three frame shift mutations (g.1086delC, g.1155del9bp, and g.1947dup25bp) were observed in FOXC1 in 5 (2.38%) of 210 cases. The missense mutations had a de novo origin in two sporadic cases, whereas the FOXC1 deletions were seen in two cases that were also heterozygous for the CYP1B1 allele (R368H). The parents of the proband with g.1086delC were heterozygous for either the FOXC1 or CYP1B1 alleles. The unaffected mother of the proband with the g.1155del9bp was heterozygous for both the FOXC1 and CYP1B1 alleles; the father harbored only the FOXC1 allele. Familial segregation of the g.1947dup25bp could not be performed because of the unavailability of DNA from one parent. Except for the g.1155del9bp (0.95% normal chromosomes), all the other variations were absent in the control subjects.\n Question: Does the transcription factor gene FOXC1 exhibit a limited role in primary congenital glaucoma?\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: Primary congenital glaucoma (PCG) is an autosomal recessive disorder that has been linked to CYP1B1 mutations. This study was conducted to explore the role of FOXC1, which is involved in anterior segment dysgenesis, in PCG. An earlier screening for CYP1B1 in a clinically well-characterized PCG cohort (n = 301) revealed cases that were either homozygous (n = 73), compound heterozygous (n = 18), or heterozygous (n = 41) for the mutant allele, whereas the remaining (n = 169) did not harbor any mutation. Hence, FOXC1 was screened in 210 PCG cases who were either heterozygous (n = 41) or did not harbor any CYP1B1 mutation (n = 169), along with ethnically matched normal control subjects (n = 157) by resequencing the entire coding region. Two heterozygous missense (H128R and C135Y) and three frame shift mutations (g.1086delC, g.1155del9bp, and g.1947dup25bp) were observed in FOXC1 in 5 (2.38%) of 210 cases. The missense mutations had a de novo origin in two sporadic cases, whereas the FOXC1 deletions were seen in two cases that were also heterozygous for the CYP1B1 allele (R368H). The parents of the proband with g.1086delC were heterozygous for either the FOXC1 or CYP1B1 alleles. The unaffected mother of the proband with the g.1155del9bp was heterozygous for both the FOXC1 and CYP1B1 alleles; the father harbored only the FOXC1 allele. Familial segregation of the g.1947dup25bp could not be performed because of the unavailability of DNA from one parent. Except for the g.1155del9bp (0.95% normal chromosomes), all the other variations were absent in the control subjects. Question: Does the transcription factor gene FOXC1 exhibit a limited role in primary congenital glaucoma? Output:
PubmedQA189675	[ { "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: Insights into the diurnal patterns of sedentary behavior and the identification of subgroups that are at increased risk for engaging in high levels of sedentary behavior are needed to inform potential interventions for reducing older adults' sedentary time. Therefore, we examined the diurnal patterns and sociodemographic correlates of older adults' sedentary behavior(s). Stratified cluster sampling was used to recruit 508 non-institutionalized Belgian older adults (≥ 65 years). Morning, afternoon, evening and total sedentary time was assessed objectively using accelerometers. Specific sedentary behaviors, total sitting time and sociodemographic attributes were assessed using an interviewer-administered questionnaire. Participants self-reported a median of 475 (Q1-Q3 = 383-599) minutes/day of total sitting time and they accumulated a mean of 580 ± 98 minutes/day of accelerometer-derived sedentary time. Sedentary time was lowest during the morning and highest during the evening. Older participants were as sedentary as younger participants during the evening, but they were more sedentary during daytime. Compared to married participants, widowers were more sedentary during daytime. Younger participants (< 75 years), men and the higher educated were more likely to engage in (high levels of) sitting while driving a car and using the computer. Those with tertiary education viewed 29% and 22% minutes/day less television compared to those with primary or secondary education, respectively. Older participants accumulated 35 sedentary minutes/day more than did younger participants and men accumulated 32 sedentary minutes/day more than did women.\n Question: Does diurnal Patterns and correlate of Older Adults ' Sedentary 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: Insights into the diurnal patterns of sedentary behavior and the identification of subgroups that are at increased risk for engaging in high levels of sedentary behavior are needed to inform potential interventions for reducing older adults' sedentary time. Therefore, we examined the diurnal patterns and sociodemographic correlates of older adults' sedentary behavior(s). Stratified cluster sampling was used to recruit 508 non-institutionalized Belgian older adults (≥ 65 years). Morning, afternoon, evening and total sedentary time was assessed objectively using accelerometers. Specific sedentary behaviors, total sitting time and sociodemographic attributes were assessed using an interviewer-administered questionnaire. Participants self-reported a median of 475 (Q1-Q3 = 383-599) minutes/day of total sitting time and they accumulated a mean of 580 ± 98 minutes/day of accelerometer-derived sedentary time. Sedentary time was lowest during the morning and highest during the evening. Older participants were as sedentary as younger participants during the evening, but they were more sedentary during daytime. Compared to married participants, widowers were more sedentary during daytime. Younger participants (< 75 years), men and the higher educated were more likely to engage in (high levels of) sitting while driving a car and using the computer. Those with tertiary education viewed 29% and 22% minutes/day less television compared to those with primary or secondary education, respectively. Older participants accumulated 35 sedentary minutes/day more than did younger participants and men accumulated 32 sedentary minutes/day more than did women. Question: Does diurnal Patterns and correlate of Older Adults ' Sedentary Behavior? Output:
PubmedQA201897	[ { "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 molecular basis for spontaneous resolution of acute gouty arthritis (GA) remains unclear. The hypothesis that extracellular and intracellular mechanisms play roles in resolving acute GA was tested. Synovial fluid (SF) levels of transforming growth factor β1 (TGFβ1), interleukin 1 (IL-1) receptor antagonist (IL-1ra), IL-10 and soluble tumour necrosis factor (TNF) receptor I (sTNFRI) and II (sTNFRII) were measured by ELISA in patients with acute GA and osteoarthritis (OA). Monosodium urate (MSU) crystal-stimulated RAW264.7 mouse macrophages were analysed for cytokine inducible SH2-containing protein (CIS) and suppressors of cytokine signalling (SOCS)1-7 mRNA expression by reverse transcription (RT)-PCR. Immunohistochemical analysis, quantitative PCR and immunoblotting were performed to detect CIS and SOCS3 expression in synovial tissue, SF mononuclear cells (SFMCs) from patients with GA and MSU crystal-stimulated monocyte-derived macrophages from healthy donors. CIS overexpression and small interfering RNA-mediated knockdown in RAW264.7 cells were used to investigate the role of CIS in resolving MSU crystal-induced acute inflammation. SF levels of anti-inflammatory molecules TGFβ1, IL-1ra, IL-10 and sTNFR-I/II were significantly elevated in GA compared to OA. CIS and SOCS3 were upregulated in the synovium and SFMCs from acute GA and MSU crystal-stimulated monocyte-derived macrophages and RAW264.7 cells. CIS overexpression in RAW264.7 cells attenuated MSU crystal-induced IL-1β and TNFα but enhanced TGFβ1 production via increased binding of signal transducer and activator of transcription 3 (STAT3) to the TGFβ1 promoter. Conversely, CIS knockdown reversed the effect of CIS overexpression, resulting in enhanced IL-1β and TNFα but reduced TGFβ1 production in MSU crystal-stimulated RAW264.7 cells.\n Question: Is spontaneous resolution of acute gouty arthritis associated with rapid induction of the anti-inflammatory factors TGFβ1 , IL-10 and soluble TNF receptors and the intracellular cytokine negative regulators CIS and SOCS3?\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 molecular basis for spontaneous resolution of acute gouty arthritis (GA) remains unclear. The hypothesis that extracellular and intracellular mechanisms play roles in resolving acute GA was tested. Synovial fluid (SF) levels of transforming growth factor β1 (TGFβ1), interleukin 1 (IL-1) receptor antagonist (IL-1ra), IL-10 and soluble tumour necrosis factor (TNF) receptor I (sTNFRI) and II (sTNFRII) were measured by ELISA in patients with acute GA and osteoarthritis (OA). Monosodium urate (MSU) crystal-stimulated RAW264.7 mouse macrophages were analysed for cytokine inducible SH2-containing protein (CIS) and suppressors of cytokine signalling (SOCS)1-7 mRNA expression by reverse transcription (RT)-PCR. Immunohistochemical analysis, quantitative PCR and immunoblotting were performed to detect CIS and SOCS3 expression in synovial tissue, SF mononuclear cells (SFMCs) from patients with GA and MSU crystal-stimulated monocyte-derived macrophages from healthy donors. CIS overexpression and small interfering RNA-mediated knockdown in RAW264.7 cells were used to investigate the role of CIS in resolving MSU crystal-induced acute inflammation. SF levels of anti-inflammatory molecules TGFβ1, IL-1ra, IL-10 and sTNFR-I/II were significantly elevated in GA compared to OA. CIS and SOCS3 were upregulated in the synovium and SFMCs from acute GA and MSU crystal-stimulated monocyte-derived macrophages and RAW264.7 cells. CIS overexpression in RAW264.7 cells attenuated MSU crystal-induced IL-1β and TNFα but enhanced TGFβ1 production via increased binding of signal transducer and activator of transcription 3 (STAT3) to the TGFβ1 promoter. Conversely, CIS knockdown reversed the effect of CIS overexpression, resulting in enhanced IL-1β and TNFα but reduced TGFβ1 production in MSU crystal-stimulated RAW264.7 cells. Question: Is spontaneous resolution of acute gouty arthritis associated with rapid induction of the anti-inflammatory factors TGFβ1 , IL-10 and soluble TNF receptors and the intracellular cytokine negative regulators CIS and SOCS3? Output: