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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:
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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:
|
PubmedQA64865
|
[
{
"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: Hypo- and hyperglycemia must be avoided to prevent additional brain damage following traumatic brain injury (TBI). However, the optimal blood glucose range requiring insulin remains unknown. Cerebral microdialysis is helpful in unmasking signs of metabolic impairment, thereby identifying deleterious blood glucose levels. A retrospective analysis of prospectively collected cerebral microdialysis samples obtained from 20 non-diabetic patients with severe TBI treated at the trauma surgical intensive care unit at the University Hospital Zürich, Switzerland. The impact of different arterial blood glucose values and concomitant insulin administration on cerebral interstitial glucose and lactate levels was investigated. In addition, energetic impairment was determined by calculating lactate-to-glucose ratios. Insulin administration was associated with significantly reduced cerebral glucose concentrations and significantly increased lactate-to-glucose ratios with arterial blood glucose levels <5 mM. At arterial blood glucose levels >7 mM, insulin administration was associated with significantly increased interstitial glucose values, significantly decreased lactate concentrations, and markedly diminished lactate-to-glucose ratios.\n Question: Does insulin differentially influence brain glucose and lactate in traumatic brain injured 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: Hypo- and hyperglycemia must be avoided to prevent additional brain damage following traumatic brain injury (TBI). However, the optimal blood glucose range requiring insulin remains unknown. Cerebral microdialysis is helpful in unmasking signs of metabolic impairment, thereby identifying deleterious blood glucose levels. A retrospective analysis of prospectively collected cerebral microdialysis samples obtained from 20 non-diabetic patients with severe TBI treated at the trauma surgical intensive care unit at the University Hospital Zürich, Switzerland. The impact of different arterial blood glucose values and concomitant insulin administration on cerebral interstitial glucose and lactate levels was investigated. In addition, energetic impairment was determined by calculating lactate-to-glucose ratios. Insulin administration was associated with significantly reduced cerebral glucose concentrations and significantly increased lactate-to-glucose ratios with arterial blood glucose levels <5 mM. At arterial blood glucose levels >7 mM, insulin administration was associated with significantly increased interstitial glucose values, significantly decreased lactate concentrations, and markedly diminished lactate-to-glucose ratios.
Question: Does insulin differentially influence brain glucose and lactate in traumatic brain injured patients?
Output:
|
PubmedQA116164
|
[
{
"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: Nephrotic syndrome is traditionally classified on the basis of the response to standard steroid treatment. Mutations in more than 24 genes have been associated with nephrotic syndrome in children, although the great majority of steroid-resistant cases have been attributed to mutations in three main genes: NPHS1, NPHS2 and WT1. The aims of this study were to identify mutations in these genes more frequently reported as mutated and to characterize each variation using different in silico prediction algorithms in order to understand their biological functions. We performed direct sequence analysis of exons 8 and 9 of WT1, 8 exons of NPHS2 and 29 exons of NPHS1, including NPHS2 and NPHS1 intron-exon boundary sequences, as well as 700 bp of the 5' UTR from both genes in 27 steroid-resistant patients aged between 3 months and 18 years. Analysis of the NPHS2 gene revealed four missense mutations, one frameshift mutation and three variations in the 5' UTR. Four patients presented compound heterozygosis, and four other patients presented one heterozygous alteration only. WT1 and NPHS1 gene analysis did not reveal any mutations.\n Question: Do nPHS2 mutations account for only 15 % of nephrotic syndrome cases?\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: Nephrotic syndrome is traditionally classified on the basis of the response to standard steroid treatment. Mutations in more than 24 genes have been associated with nephrotic syndrome in children, although the great majority of steroid-resistant cases have been attributed to mutations in three main genes: NPHS1, NPHS2 and WT1. The aims of this study were to identify mutations in these genes more frequently reported as mutated and to characterize each variation using different in silico prediction algorithms in order to understand their biological functions. We performed direct sequence analysis of exons 8 and 9 of WT1, 8 exons of NPHS2 and 29 exons of NPHS1, including NPHS2 and NPHS1 intron-exon boundary sequences, as well as 700 bp of the 5' UTR from both genes in 27 steroid-resistant patients aged between 3 months and 18 years. Analysis of the NPHS2 gene revealed four missense mutations, one frameshift mutation and three variations in the 5' UTR. Four patients presented compound heterozygosis, and four other patients presented one heterozygous alteration only. WT1 and NPHS1 gene analysis did not reveal any mutations.
Question: Do nPHS2 mutations account for only 15 % of nephrotic syndrome cases?
Output:
|
PubmedQA71124
|
[
{
"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: Although the prognosis is known to be poor in cirrhosis patients associated with sarcopenia, the relationships among skeletal muscle, visceral fat, and the liver have not yet been thoroughly investigated. Therefore, the prognosis and its associations with body composition and the severity of liver disease were examined in patients with cirrhosis. The skeletal muscle mass and visceral fat area were measured in 161 patients with cirrhosis, the effects of body composition on the prognosis were analyzed, and any factors that contribute to changes in body composition were assessed. During the mean observation period of 1,005 days, 73 patients died. Patients with sarcopenia or sarcopenic obesity had a poor prognosis, and this difference was pronounced in the subset of patients classified as Child-Pugh class A. A decreased skeletal muscle mass was strongly correlated with decreased serum albumin levels. Sarcopenia is a common feature of advanced cirrhosis, and transitions were observed from normal body composition to sarcopenia and from obese to sarcopenic obesity.\n Question: Do sarcopenia and Sarcopenic Obesity Are Prognostic Factors for Overall Survival in Patients with Cirrhosis?\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: Although the prognosis is known to be poor in cirrhosis patients associated with sarcopenia, the relationships among skeletal muscle, visceral fat, and the liver have not yet been thoroughly investigated. Therefore, the prognosis and its associations with body composition and the severity of liver disease were examined in patients with cirrhosis. The skeletal muscle mass and visceral fat area were measured in 161 patients with cirrhosis, the effects of body composition on the prognosis were analyzed, and any factors that contribute to changes in body composition were assessed. During the mean observation period of 1,005 days, 73 patients died. Patients with sarcopenia or sarcopenic obesity had a poor prognosis, and this difference was pronounced in the subset of patients classified as Child-Pugh class A. A decreased skeletal muscle mass was strongly correlated with decreased serum albumin levels. Sarcopenia is a common feature of advanced cirrhosis, and transitions were observed from normal body composition to sarcopenia and from obese to sarcopenic obesity.
Question: Do sarcopenia and Sarcopenic Obesity Are Prognostic Factors for Overall Survival in Patients with Cirrhosis?
Output:
|
PubmedQA145190
|
[
{
"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: : Mesenchymal stem cells (MSCs) have been extensively investigated as a promising approach to treat many autoimmune and inflammatory diseases. The stress condition would affect the therapeutic efficacy and induce autophagy of MSCs. However, whether autophagy would affect the immunosuppressive capacity of MSCs is largely unknown. The present study aimed to assess whether autophagy plays an important role in regulating the immunomodulation of MSCs and the undermechanisms. We successfully inhibited and induced autophagy of MSCs using 3-methyladenine (3-MA) and rapamycin, respectively. Our results demonstrated that rapamycin strengthened the capacity of MSCs to inhibit CD4\n Question: Does autophagy improve the Immunosuppression of CD4+ T Cells by Mesenchymal Stem Cells Through Transforming Growth Factor-β1?\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: : Mesenchymal stem cells (MSCs) have been extensively investigated as a promising approach to treat many autoimmune and inflammatory diseases. The stress condition would affect the therapeutic efficacy and induce autophagy of MSCs. However, whether autophagy would affect the immunosuppressive capacity of MSCs is largely unknown. The present study aimed to assess whether autophagy plays an important role in regulating the immunomodulation of MSCs and the undermechanisms. We successfully inhibited and induced autophagy of MSCs using 3-methyladenine (3-MA) and rapamycin, respectively. Our results demonstrated that rapamycin strengthened the capacity of MSCs to inhibit CD4
Question: Does autophagy improve the Immunosuppression of CD4+ T Cells by Mesenchymal Stem Cells Through Transforming Growth Factor-β1?
Output:
|
PubmedQA153079
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: In eukaryotic cells, nucleolar processing of preribosomal RNAs (prerRNAs) is assisted by a large number of small nucleolar RNAs (snoRNAs) that function in the 2'-O-methylation or the pseudouridylation of rRNAs. Most snoRNAs so far characterized are encoded and processed from introns of premRNAs. We found a novel intronic snoRNA gene, named U50HG, located on chromosome 6q15, at the breakpoint of chromosomal translocation t(3;6)(q27;q15). The U50HG gene is composed of six exons, whose spliced transcripts have little potential for coding a protein, and its introns produce both U50 and U50-like (U50') snoRNAs that are localized in nucleoli. It possesses an oligopyrimidine tract that is characteristic of the 5'-terminal oligopyrimidine (5'TOP) class of genes which have been shown to be coordinately regulated in response to cell growth.\n Question: Is intronic U50 small-nucleolar-RNA ( snoRNA ) host gene of no protein-coding potential mapped at the chromosome breakpoint t ( 3 ; 6 ) ( q27 ; q15 ) of human B-cell lymphoma?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: In eukaryotic cells, nucleolar processing of preribosomal RNAs (prerRNAs) is assisted by a large number of small nucleolar RNAs (snoRNAs) that function in the 2'-O-methylation or the pseudouridylation of rRNAs. Most snoRNAs so far characterized are encoded and processed from introns of premRNAs. We found a novel intronic snoRNA gene, named U50HG, located on chromosome 6q15, at the breakpoint of chromosomal translocation t(3;6)(q27;q15). The U50HG gene is composed of six exons, whose spliced transcripts have little potential for coding a protein, and its introns produce both U50 and U50-like (U50') snoRNAs that are localized in nucleoli. It possesses an oligopyrimidine tract that is characteristic of the 5'-terminal oligopyrimidine (5'TOP) class of genes which have been shown to be coordinately regulated in response to cell growth.
Question: Is intronic U50 small-nucleolar-RNA ( snoRNA ) host gene of no protein-coding potential mapped at the chromosome breakpoint t ( 3 ; 6 ) ( q27 ; q15 ) of human B-cell lymphoma?
Output:
|
PubmedQA162827
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To investigate the effect of synthetic retinoids on septic shock induced by lipopolysaccharide (LPS) in rats. Randomised study. University hospital laboratory, Sweden. 31 male Sprague Dawley rats randomised into four groups: controls, given vehicle alone (n = 6), LPS 6 mg/kg body weight alone (n = 12), and LPS 6 mg/kg but pretreated with the retinoic acid receptor-alpha (RAR-alpha) agonists CD336 (n = 6) and CD2081 (n = 7). Arterial blood pressure and heart rate measured hourly for four hours; mortality. LPS caused a pronounced fall in blood pressure within one hour of injection in all groups of rats. Of the 12 rats given LPS but not RAR-alpha agonists, 6 died before the end of the experiment. By contrast, all animal given either CD336 or CD2081 survived. The significantly improved survival was found despite no significant improvements in either mean arterial pressure or heart rate.\n Question: Do synthetic retinoids improve survival in rodent model of endotoxic shock?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To investigate the effect of synthetic retinoids on septic shock induced by lipopolysaccharide (LPS) in rats. Randomised study. University hospital laboratory, Sweden. 31 male Sprague Dawley rats randomised into four groups: controls, given vehicle alone (n = 6), LPS 6 mg/kg body weight alone (n = 12), and LPS 6 mg/kg but pretreated with the retinoic acid receptor-alpha (RAR-alpha) agonists CD336 (n = 6) and CD2081 (n = 7). Arterial blood pressure and heart rate measured hourly for four hours; mortality. LPS caused a pronounced fall in blood pressure within one hour of injection in all groups of rats. Of the 12 rats given LPS but not RAR-alpha agonists, 6 died before the end of the experiment. By contrast, all animal given either CD336 or CD2081 survived. The significantly improved survival was found despite no significant improvements in either mean arterial pressure or heart rate.
Question: Do synthetic retinoids improve survival in rodent model of endotoxic shock?
Output:
|
PubmedQA123607
|
[
{
"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: Although beneficial effects of potassium intake on blood pressure (BP) are well established, little is known about genetic factors that underlie interindividual variability in BP response to dietary potassium. In a previous study, we reported the first evidence for significant heritabilities for BP response in a dietary intervention study in rural Chinese. In this report, we extend our genetic studies to examine associations with polymorphisms in genes in vascular endothelial pathways. We genotyped study participants for 23 single nucleotide polymorphisms (SNPs) in endothelin 1 (EDN1), nitric oxide synthase 3, and E selectin (SELE). We tested 17 of these SNPs for associations with BP response to potassium supplementation in 1843 participants. Association tests used population-based [generalized estimation equation (GEE)] and family-based (quantitative transmission disequilibrium test) methods, as well as tests for gene-by-gene (GxG) interaction (generalized multifactor dimensionalilty reduction and GEE). Single SNP analysis identified significant associations for several SNPs in EDN1 with multiple measures of BP response to potassium supplementation. The cumulative effects of the minor EDN1 alleles that showed significant associations were to reduce measures of BP response by 0.5-0.9 mmHg. We found significant evidence for effects of GxG interactions between EDN1 and SELE, even in the absence of individual associations with SELE variants.\n Question: Is blood pressure response to potassium supplementation associated with genetic variation in endothelin 1 and interactions with E selectin in rural Chinese?\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: Although beneficial effects of potassium intake on blood pressure (BP) are well established, little is known about genetic factors that underlie interindividual variability in BP response to dietary potassium. In a previous study, we reported the first evidence for significant heritabilities for BP response in a dietary intervention study in rural Chinese. In this report, we extend our genetic studies to examine associations with polymorphisms in genes in vascular endothelial pathways. We genotyped study participants for 23 single nucleotide polymorphisms (SNPs) in endothelin 1 (EDN1), nitric oxide synthase 3, and E selectin (SELE). We tested 17 of these SNPs for associations with BP response to potassium supplementation in 1843 participants. Association tests used population-based [generalized estimation equation (GEE)] and family-based (quantitative transmission disequilibrium test) methods, as well as tests for gene-by-gene (GxG) interaction (generalized multifactor dimensionalilty reduction and GEE). Single SNP analysis identified significant associations for several SNPs in EDN1 with multiple measures of BP response to potassium supplementation. The cumulative effects of the minor EDN1 alleles that showed significant associations were to reduce measures of BP response by 0.5-0.9 mmHg. We found significant evidence for effects of GxG interactions between EDN1 and SELE, even in the absence of individual associations with SELE variants.
Question: Is blood pressure response to potassium supplementation associated with genetic variation in endothelin 1 and interactions with E selectin in rural Chinese?
Output:
|
PubmedQA200557
|
[
{
"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: Alcohol consumption has beneficial effects on mortality which are mainly due to reduction in cardiovascular disease. These are believed to be due, at least in part, to the increase in plasma high-density lipoprotein (HDL) which is associated with alcohol consumption. It has been proposed that ADH3 genotype modifies the relationships between alcohol intake and cardiovascular disease by altering the HDL response to alcohol. The aim of this paper was to test for effects of ADH2 and ADH3 genotypes on the response of HDL components to habitual alcohol consumption. Adult male and female subjects were genotyped for ADH2 and ADH3; and plasma HDL cholesterol, apolipoprotein A-I, and apolipoprotein A-II were measured. Nine hundred one subjects had both ADH2 and ADH3 genotypes and HDL cholesterol results, while 753 had both genotypes and all three lipid results. The effect of alcohol intake on the three measured HDL components, and a factor score derived from them, was estimated for each of the ADH2 and ADH3 genotype groups. All the measured components of HDL increased with increasing alcohol consumption over the range of intakes studied, 0-4 drinks per day. There were no significant interactions between alcohol consumption and ADH2 or ADH3 genotypes.\n Question: Does aDH genotype modify the effects of alcohol on high-density lipoprotein?\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: Alcohol consumption has beneficial effects on mortality which are mainly due to reduction in cardiovascular disease. These are believed to be due, at least in part, to the increase in plasma high-density lipoprotein (HDL) which is associated with alcohol consumption. It has been proposed that ADH3 genotype modifies the relationships between alcohol intake and cardiovascular disease by altering the HDL response to alcohol. The aim of this paper was to test for effects of ADH2 and ADH3 genotypes on the response of HDL components to habitual alcohol consumption. Adult male and female subjects were genotyped for ADH2 and ADH3; and plasma HDL cholesterol, apolipoprotein A-I, and apolipoprotein A-II were measured. Nine hundred one subjects had both ADH2 and ADH3 genotypes and HDL cholesterol results, while 753 had both genotypes and all three lipid results. The effect of alcohol intake on the three measured HDL components, and a factor score derived from them, was estimated for each of the ADH2 and ADH3 genotype groups. All the measured components of HDL increased with increasing alcohol consumption over the range of intakes studied, 0-4 drinks per day. There were no significant interactions between alcohol consumption and ADH2 or ADH3 genotypes.
Question: Does aDH genotype modify the effects of alcohol on high-density lipoprotein?
Output:
|
PubmedQA179854
|
[
{
"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: Platelet-activating factor (PAF), a potent proinflammatory phospholipid mediator, has been implicated in inducing intestinal inflammation in diseases such as inflammatory bowel disease (IBD) and necrotizing enterocolitis (NEC). However, its mechanisms of inducing inflammatory responses are not fully understood. Therefore, studies were designed to explore the mechanisms of PAF-induced inflammatory cascade in intestinal epithelial cells. Nuclear factor kappa B (NF-kappaB) activation was measured by luciferase assay and enzyme-linked immunosorbent assay (ELISA), and interleukin 8 (IL-8) production was determined by ELISA. B-cell lymphoma 10 (Bcl10), caspase recruitment domain-containing membrane-associated guanylate kinase protein 3 (CARMA3), and mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1) mRNA and protein levels were assessed by real-time reverse-transcription polymerase chain reaction (RT-PCR) and Western blot, respectively. siRNA silencing of Bcl10 was used to examine its role in PAF-induced NF-kappaB activation and IL-8 production. The promoter region of the Bcl10 gene was cloned with the PCR method and promoter activity measured by luciferase assay. The adaptor protein Bcl10 appeared to play an important role in the PAF-induced inflammatory pathway in human intestinal epithelial cells. Bcl10 was required for PAF-induced I kappaB alpha phosphorylation, NF-kappaB activation, and IL-8 production in NCM460, a cell line derived from normal human colon, and Caco-2, a transformed human intestinal cell line. PAF also stimulated Bcl10 interactions with CARMA3 and MALT1, and upregulated Bcl10 expression in these cells via transcriptional regulation.\n Question: Are platelet-activating factor-induced NF-kappaB activation and IL-8 production in intestinal epithelial cells Bcl10-dependent?\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: Platelet-activating factor (PAF), a potent proinflammatory phospholipid mediator, has been implicated in inducing intestinal inflammation in diseases such as inflammatory bowel disease (IBD) and necrotizing enterocolitis (NEC). However, its mechanisms of inducing inflammatory responses are not fully understood. Therefore, studies were designed to explore the mechanisms of PAF-induced inflammatory cascade in intestinal epithelial cells. Nuclear factor kappa B (NF-kappaB) activation was measured by luciferase assay and enzyme-linked immunosorbent assay (ELISA), and interleukin 8 (IL-8) production was determined by ELISA. B-cell lymphoma 10 (Bcl10), caspase recruitment domain-containing membrane-associated guanylate kinase protein 3 (CARMA3), and mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1) mRNA and protein levels were assessed by real-time reverse-transcription polymerase chain reaction (RT-PCR) and Western blot, respectively. siRNA silencing of Bcl10 was used to examine its role in PAF-induced NF-kappaB activation and IL-8 production. The promoter region of the Bcl10 gene was cloned with the PCR method and promoter activity measured by luciferase assay. The adaptor protein Bcl10 appeared to play an important role in the PAF-induced inflammatory pathway in human intestinal epithelial cells. Bcl10 was required for PAF-induced I kappaB alpha phosphorylation, NF-kappaB activation, and IL-8 production in NCM460, a cell line derived from normal human colon, and Caco-2, a transformed human intestinal cell line. PAF also stimulated Bcl10 interactions with CARMA3 and MALT1, and upregulated Bcl10 expression in these cells via transcriptional regulation.
Question: Are platelet-activating factor-induced NF-kappaB activation and IL-8 production in intestinal epithelial cells Bcl10-dependent?
Output:
|
PubmedQA77740
|
[
{
"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: WWOX, encoding WW domain-containing oxidoreductase, spans FRA16D, the second most common chromosomal fragile site frequently altered in cancers. It is therefore considered a tumor suppressor gene, but its direct implication in cancerogenesis remains controversial. By whole-exome sequencing, we identified a homozygous WWOX nonsense mutation, p.Arg54*, in a girl from a consanguineous family with a severe syndrome of growth retardation, microcephaly, epileptic seizures, retinopathy and early death, a phenotype highly similar to the abormalities reported in lde/lde rats with a spontaneous functional null mutation of Wwox. As in rats, no tumors were observed in the patient or heterozygous mutation carriers.\n Question: Is the supposed tumor suppressor gene WWOX mutated in an early lethal microcephaly syndrome with epilepsy , growth retardation and retinal degeneration?\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: WWOX, encoding WW domain-containing oxidoreductase, spans FRA16D, the second most common chromosomal fragile site frequently altered in cancers. It is therefore considered a tumor suppressor gene, but its direct implication in cancerogenesis remains controversial. By whole-exome sequencing, we identified a homozygous WWOX nonsense mutation, p.Arg54*, in a girl from a consanguineous family with a severe syndrome of growth retardation, microcephaly, epileptic seizures, retinopathy and early death, a phenotype highly similar to the abormalities reported in lde/lde rats with a spontaneous functional null mutation of Wwox. As in rats, no tumors were observed in the patient or heterozygous mutation carriers.
Question: Is the supposed tumor suppressor gene WWOX mutated in an early lethal microcephaly syndrome with epilepsy , growth retardation and retinal degeneration?
Output:
|
PubmedQA104969
|
[
{
"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: Previous studies on the insulin-like growth factor (IGF) system and mortality have shown ambiguous results. We investigated the association between IGF-I and insulin- like growth factor binding protein-1 (IGFBP-1) with all-cause mortality in an elderly female Swedish population. A prospective cohort study of elderly women (n=338) aged between 68 and 79 years (mean age 72 years) with a mean follow-up time of 9.9 years. Baseline data in the PRIMOS (Primary Health Care and Osteoporosis) study were collected between 1999 and 2001. Data of risk factors for cardiovascular disease were collected. Death rates were registered from the Swedish Cause of Death register for the period 1999-2009. Cox regression models were used to calculate hazard ratios. IGF-I and IGFBP-1 levels were separately divided into 3 groups (high, medium and low), with cut offs at the 30th and the 70th percentiles. In a fully adjusted Cox proportional hazard model, increased risk of mortality was shown for women with high serum levels of IGFBP-1, HR 3.03 (95% CI 1.64-5.63) and also with low serum levels of IGFBP-1, HR 1.98 (95% CI 1.03-3.81), compared to women with moderate levels. No significant association between IGF-I and mortality was observed.\n Question: Does iGFBP-1 predict all-cause mortality in elderly women independently of IGF-I?\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: Previous studies on the insulin-like growth factor (IGF) system and mortality have shown ambiguous results. We investigated the association between IGF-I and insulin- like growth factor binding protein-1 (IGFBP-1) with all-cause mortality in an elderly female Swedish population. A prospective cohort study of elderly women (n=338) aged between 68 and 79 years (mean age 72 years) with a mean follow-up time of 9.9 years. Baseline data in the PRIMOS (Primary Health Care and Osteoporosis) study were collected between 1999 and 2001. Data of risk factors for cardiovascular disease were collected. Death rates were registered from the Swedish Cause of Death register for the period 1999-2009. Cox regression models were used to calculate hazard ratios. IGF-I and IGFBP-1 levels were separately divided into 3 groups (high, medium and low), with cut offs at the 30th and the 70th percentiles. In a fully adjusted Cox proportional hazard model, increased risk of mortality was shown for women with high serum levels of IGFBP-1, HR 3.03 (95% CI 1.64-5.63) and also with low serum levels of IGFBP-1, HR 1.98 (95% CI 1.03-3.81), compared to women with moderate levels. No significant association between IGF-I and mortality was observed.
Question: Does iGFBP-1 predict all-cause mortality in elderly women independently of IGF-I?
Output:
|
PubmedQA132031
|
[
{
"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: Allergic diseases are more prevalent in affluent countries, which has been attributed to life-style factors. Life-style habits may also differ between socioeconomic (SES) classes. The objective of this paper therefore was to evaluate if SES had an impact on the development of atopic disorders. A total of 1314 German children were followed-up in an observational birth cohort study to 6 years of age. Parents filled in questionnaires, and had multi-allergen screening tests for sensitization. Indoor allergen concentrations were determined by ELISA. Children were examined regularly up to 6 years, specific serum IgE values were determined by CAP-Rast-Feia. The risk of aeroallergen sensitization (odds ratio 1.76; 95% CI 1.30-2.37), and the lifetime prevalence of hay fever (2.36; 1.76-3.17), and asthma (1.74; 1.08-2.80), but not of atopic dermatitis (AD: 0.90; 0. 54-1.51) was elevated in parents of high compared to low SES. With high SES the risk of smoking in pregnancy (0.35; 0.23-0.51), in the home (0.31; 0.21-0.46), pet ownership (0.37; 0.26-0.55), high mite (0.42; 0.25-0.74), and high cat (0.38; 0.18-0.82) allergen concentration in house dust was reduced, but elevated for breastfeeding over more than 6 months (4.67; 2.9-7.48). In children, even after controlling for other risk factors, only the risk of AD from 3 to 6 years (2.42; 1.42-4.14) was elevated in families with high SES, but not of AD in infancy or of any other atopic disorder.\n Question: Is socioeconomic status a risk factor for allergy in parents but not in their children?\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: Allergic diseases are more prevalent in affluent countries, which has been attributed to life-style factors. Life-style habits may also differ between socioeconomic (SES) classes. The objective of this paper therefore was to evaluate if SES had an impact on the development of atopic disorders. A total of 1314 German children were followed-up in an observational birth cohort study to 6 years of age. Parents filled in questionnaires, and had multi-allergen screening tests for sensitization. Indoor allergen concentrations were determined by ELISA. Children were examined regularly up to 6 years, specific serum IgE values were determined by CAP-Rast-Feia. The risk of aeroallergen sensitization (odds ratio 1.76; 95% CI 1.30-2.37), and the lifetime prevalence of hay fever (2.36; 1.76-3.17), and asthma (1.74; 1.08-2.80), but not of atopic dermatitis (AD: 0.90; 0. 54-1.51) was elevated in parents of high compared to low SES. With high SES the risk of smoking in pregnancy (0.35; 0.23-0.51), in the home (0.31; 0.21-0.46), pet ownership (0.37; 0.26-0.55), high mite (0.42; 0.25-0.74), and high cat (0.38; 0.18-0.82) allergen concentration in house dust was reduced, but elevated for breastfeeding over more than 6 months (4.67; 2.9-7.48). In children, even after controlling for other risk factors, only the risk of AD from 3 to 6 years (2.42; 1.42-4.14) was elevated in families with high SES, but not of AD in infancy or of any other atopic disorder.
Question: Is socioeconomic status a risk factor for allergy in parents but not in their children?
Output:
|
PubmedQA51451
|
[
{
"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: While there has been a great deal of literature describing the relationship between nutritional status and development of pressure ulcers, statistically rigorous studies analyzing the relationship between hypoalbuminemia and outcomes are lacking. The American College of Surgeons' multicenter, prospective, National Surgical Quality Improvement Program database was used to identify patients who underwent surgery for treatment of pressure ulcers between 2006 and 2011. Matched propensity-score analysis was performed to match experimental groups with regard to preoperative comorbidities. Outcomes of interest included overall/surgical/medical complications and 30-day mortality. Multivariable logistic regression models were used to assess the independent association between hypoalbuminemia and outcomes. Over the 6-year study period, 551 patients met criteria for study inclusion. Median albumin level was 2.8 g/dL. Before propensity matching, multiple adverse outcomes were significantly elevated in patients with albumin levels below the median value (very-low albumin, or VLA), compared to control patients. However, after matching preoperative comorbidities, the differences in 30-day outcomes were eliminated. In both analyses, there was no significant difference in 30-day surgical complications.\n Question: Is preoperative Albumin Alone a Predictor of 30-Day Outcomes in Pressure Ulcer Patients : A Matched Propensity-Score Analysis of the 2006-2011 NSQIP Datasets?\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: While there has been a great deal of literature describing the relationship between nutritional status and development of pressure ulcers, statistically rigorous studies analyzing the relationship between hypoalbuminemia and outcomes are lacking. The American College of Surgeons' multicenter, prospective, National Surgical Quality Improvement Program database was used to identify patients who underwent surgery for treatment of pressure ulcers between 2006 and 2011. Matched propensity-score analysis was performed to match experimental groups with regard to preoperative comorbidities. Outcomes of interest included overall/surgical/medical complications and 30-day mortality. Multivariable logistic regression models were used to assess the independent association between hypoalbuminemia and outcomes. Over the 6-year study period, 551 patients met criteria for study inclusion. Median albumin level was 2.8 g/dL. Before propensity matching, multiple adverse outcomes were significantly elevated in patients with albumin levels below the median value (very-low albumin, or VLA), compared to control patients. However, after matching preoperative comorbidities, the differences in 30-day outcomes were eliminated. In both analyses, there was no significant difference in 30-day surgical complications.
Question: Is preoperative Albumin Alone a Predictor of 30-Day Outcomes in Pressure Ulcer Patients : A Matched Propensity-Score Analysis of the 2006-2011 NSQIP Datasets?
Output:
|
PubmedQA142875
|
[
{
"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: High levels of homocysteine (Hcy) induce a sustained injury on arterial endothelial cells, which accelerates the development of thrombosis and atherosclerosis. Hcy specifically inhibits the growth of endothelial cells. The present study investigated the signaling pathways underlying this cell-cycle effect. Human umbilical venous endothelial cells were treated with Hcy, and/or LY294002, okadaic acid, peroxovanadate (PV), antisense Akt, phosphorylation of Akt and FKHRL1 proteins. p27(kip1) protein levels were measured with Western blotting, and Akt kinase activity and cell cycle were measured with immunoprecipitation and flow cytometry, respectively. We demonstrate that Hcy induces dephosphorylation of Akt and FKHRL1 and upregulates the cyclin-dependent kinase inhibitors p27(kip1) in a time- and dose-dependent manner. Phosphatidylinositol-3 kinase (PI3K) activator PV and phosphatase 2A inhibitor okadaic acid could reverse it, which suggests it was dependent on PI3K activity. Moreover, Hcy induces cell cycle G1 phase arrest prevented by pretreatment with PV and okadaic acid. Transfection with specific antisense oligonucleotides to Akt further proves the observations.\n Question: Does homocysteine induce cell cycle G1 arrest in endothelial cells through the PI3K/Akt/FOXO signaling pathway?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: High levels of homocysteine (Hcy) induce a sustained injury on arterial endothelial cells, which accelerates the development of thrombosis and atherosclerosis. Hcy specifically inhibits the growth of endothelial cells. The present study investigated the signaling pathways underlying this cell-cycle effect. Human umbilical venous endothelial cells were treated with Hcy, and/or LY294002, okadaic acid, peroxovanadate (PV), antisense Akt, phosphorylation of Akt and FKHRL1 proteins. p27(kip1) protein levels were measured with Western blotting, and Akt kinase activity and cell cycle were measured with immunoprecipitation and flow cytometry, respectively. We demonstrate that Hcy induces dephosphorylation of Akt and FKHRL1 and upregulates the cyclin-dependent kinase inhibitors p27(kip1) in a time- and dose-dependent manner. Phosphatidylinositol-3 kinase (PI3K) activator PV and phosphatase 2A inhibitor okadaic acid could reverse it, which suggests it was dependent on PI3K activity. Moreover, Hcy induces cell cycle G1 phase arrest prevented by pretreatment with PV and okadaic acid. Transfection with specific antisense oligonucleotides to Akt further proves the observations.
Question: Does homocysteine induce cell cycle G1 arrest in endothelial cells through the PI3K/Akt/FOXO signaling pathway?
Output:
|
PubmedQA15338
|
[
{
"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: Revision THA is associated with high blood loss and a high probability of blood transfusion in the perioperative period. In November 2003, government legislation established the Blood Utilization Program at our center to reduce the rate and risks associated with allogenic transfusion. The purposes of this study were to (1) determine whether the allogenic transfusion rate in patients undergoing revision THA decreased in those who were reviewed preoperatively by the Blood Utilization Program versus those who were not; (2) determine whether tranexamic acid reduced the rate of transfusion; and (3) identify potential perioperative clinical parameters that are associated with an increased risk of blood transfusion. We included all 159 patients who underwent revision THA from January 2006 to October 2008 having either a socket and/or femoral stem revision except those having only a liner exchange. One hundred and one patients attended the Blood Utilization Program preoperatively and 58 patients did not (ie, they required urgent/emergency surgery). The Blood Utilization Program referral made no difference in transfusion rate or transfusion amount; however, the transfusion rates and amount were decreased by 8% and one unit, respectively. In patients referred to the Blood Utilization Program, the intraoperative use of tranexamic acid (an antifibrinolytic) was associated with reduced transfusions, regardless of dosage; preoperative erythropoietin tended to reduce transfusions while preoperative oral iron supplements did not.\n Question: Does tranexamic acid reduce allogenic transfusion in revision hip arthroplasty?\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: Revision THA is associated with high blood loss and a high probability of blood transfusion in the perioperative period. In November 2003, government legislation established the Blood Utilization Program at our center to reduce the rate and risks associated with allogenic transfusion. The purposes of this study were to (1) determine whether the allogenic transfusion rate in patients undergoing revision THA decreased in those who were reviewed preoperatively by the Blood Utilization Program versus those who were not; (2) determine whether tranexamic acid reduced the rate of transfusion; and (3) identify potential perioperative clinical parameters that are associated with an increased risk of blood transfusion. We included all 159 patients who underwent revision THA from January 2006 to October 2008 having either a socket and/or femoral stem revision except those having only a liner exchange. One hundred and one patients attended the Blood Utilization Program preoperatively and 58 patients did not (ie, they required urgent/emergency surgery). The Blood Utilization Program referral made no difference in transfusion rate or transfusion amount; however, the transfusion rates and amount were decreased by 8% and one unit, respectively. In patients referred to the Blood Utilization Program, the intraoperative use of tranexamic acid (an antifibrinolytic) was associated with reduced transfusions, regardless of dosage; preoperative erythropoietin tended to reduce transfusions while preoperative oral iron supplements did not.
Question: Does tranexamic acid reduce allogenic transfusion in revision hip arthroplasty?
Output:
|
PubmedQA108927
|
[
{
"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: Type 2 amiodarone-induced thyrotoxicosis (AIT) is a destructive thyroiditis usually responsive to glucocorticoids; however, recent surveys showed that many expert thyroidologists worldwide use thionamides for type 2 AIT patients. The objective of the study was to compare the effectiveness of methimazole (MMI) or prednisone (GLU) in type 2 AIT patients who had a short cure time according to a published predictive model. This was a matched retrospective cohort study. The study was conducted at a university center. Forty-two untreated type 2 AIT patients with a predicted cure time < or = 40 d were divided into two groups (MMI and GLU groups). After matching for the predicted cure time, patients in the GLU group were selected in a 1:1 ratio to patients in the MMI group. Patients were treated with GLU or MMI for 40 d. Patients still thyrotoxic after 40 d continued glucocorticoids if in the GLU group or were switched to prednisone (MMI-GLU group) if in the MMI group. Time and rate of cure (healing) at 40 d were measured. Patients still thyrotoxic after 40 d were 23.8 +/- 9.3% in the GLU group and 85.7 +/- 7.6% in the MMI group (P = 0.000). The GLU and MMI-GLU groups did not significantly differ in the nonhealing rate at 40 d (P = 0.730). When patients in the MMI group were treated with glucocorticoids, 94.1% patients achieved euthyroidism within 40 d. However, the global median cure time (MMI period + prednisone period) was longer (60 d, 95% confidence interval 53.5-66.5 d) in the MMI-GLU group than the GLU group (21 d, 95% confidence interval 15.1-26.9 d).\n Question: Are glucocorticoids preferable to thionamides as first-line treatment for amiodarone-induced thyrotoxicosis due to destructive thyroiditis : a matched retrospective cohort study?\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: Type 2 amiodarone-induced thyrotoxicosis (AIT) is a destructive thyroiditis usually responsive to glucocorticoids; however, recent surveys showed that many expert thyroidologists worldwide use thionamides for type 2 AIT patients. The objective of the study was to compare the effectiveness of methimazole (MMI) or prednisone (GLU) in type 2 AIT patients who had a short cure time according to a published predictive model. This was a matched retrospective cohort study. The study was conducted at a university center. Forty-two untreated type 2 AIT patients with a predicted cure time < or = 40 d were divided into two groups (MMI and GLU groups). After matching for the predicted cure time, patients in the GLU group were selected in a 1:1 ratio to patients in the MMI group. Patients were treated with GLU or MMI for 40 d. Patients still thyrotoxic after 40 d continued glucocorticoids if in the GLU group or were switched to prednisone (MMI-GLU group) if in the MMI group. Time and rate of cure (healing) at 40 d were measured. Patients still thyrotoxic after 40 d were 23.8 +/- 9.3% in the GLU group and 85.7 +/- 7.6% in the MMI group (P = 0.000). The GLU and MMI-GLU groups did not significantly differ in the nonhealing rate at 40 d (P = 0.730). When patients in the MMI group were treated with glucocorticoids, 94.1% patients achieved euthyroidism within 40 d. However, the global median cure time (MMI period + prednisone period) was longer (60 d, 95% confidence interval 53.5-66.5 d) in the MMI-GLU group than the GLU group (21 d, 95% confidence interval 15.1-26.9 d).
Question: Are glucocorticoids preferable to thionamides as first-line treatment for amiodarone-induced thyrotoxicosis due to destructive thyroiditis : a matched retrospective cohort study?
Output:
|
PubmedQA100257
|
[
{
"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: Food-dependent exercise-induced anaphylaxis (FDEIA) is a serious food allergy in which anaphylaxis develops when exercise is performed within several hours after food intake. The precise mechanism underlying allergic sensitization in FDEIA has been an important issue but remains poorly understood. We aimed to elucidate the pathomechanism including the route of allergen sensitization involved in FDEIA. A Japanese family with wheat-dependent exercise-induced anaphylaxis (WDEIA), a specific form of FDEIA, were clinically examined. Mutation analysis of the gene encoding filaggrin (FLG) was also performed. Two of the family members were confirmed as WDEIA on the basis of their medical history and positive provocation test results. Notably, the two affected individuals in the family had concomitant ichthyosis vulgaris. Mutation analysis of FLG revealed that they carry one or more loss-of-function mutations that have not been described in the Japanese population.\n Question: Do loss-of-function mutations in the gene encoding filaggrin underlie a Japanese family with food-dependent exercise-induced anaphylaxis?\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: Food-dependent exercise-induced anaphylaxis (FDEIA) is a serious food allergy in which anaphylaxis develops when exercise is performed within several hours after food intake. The precise mechanism underlying allergic sensitization in FDEIA has been an important issue but remains poorly understood. We aimed to elucidate the pathomechanism including the route of allergen sensitization involved in FDEIA. A Japanese family with wheat-dependent exercise-induced anaphylaxis (WDEIA), a specific form of FDEIA, were clinically examined. Mutation analysis of the gene encoding filaggrin (FLG) was also performed. Two of the family members were confirmed as WDEIA on the basis of their medical history and positive provocation test results. Notably, the two affected individuals in the family had concomitant ichthyosis vulgaris. Mutation analysis of FLG revealed that they carry one or more loss-of-function mutations that have not been described in the Japanese population.
Question: Do loss-of-function mutations in the gene encoding filaggrin underlie a Japanese family with food-dependent exercise-induced anaphylaxis?
Output:
|
PubmedQA153875
|
[
{
"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: Chronic obstructive pulmonary disease (COPD) is characterized by a mixture of emphysema and airway disease. The forced oscillation technique (FOT) has been applied to COPD patients to clarify changes in respiratory mechanics; dynamic changes in respiratory resistance (Rrs) during breathing (within-breath changes in Rrs, ΔRrs) are characteristic of COPD. However, the pathophysiological significance of these changes is unknown. The aim of this study was to assess how emphysema and airway disease influence ΔRrs in COPD patients. In this cross-sectional study, stable COPD patients were recruited and underwent respiratory impedance measurements with a commercially available FOT device. Rrs was recorded during tidal breathing and then analyzed as whole-breath Rrs (Rrs at 5 Hz, R5; Rrs at 20 Hz, R20; and their difference, R5-R20) or as ΔRrs, the difference between the expiratory and inspiratory Rrs (ΔR5, ΔR20 and ΔR5-R20). The percentage of the low attenuation area (LAA%) and airway wall area (WA%) was quantified by computed tomography analysis, and their contributions to ΔRrs were examined. Seventy-five COPD patients were recruited. LAA% was negatively correlated with ΔR5 and ΔR5-R20 (P = 0.0002 and P = 0.0033, respectively); meanwhile, WA% in B(10) was positively correlated with ΔR5 and ΔR5-R20 (P = 0.0057 and P < 0.0001, respectively). Multivariate analysis revealed that the contribution of both LAA% and WA% in B(10) to ΔRrs was independent of the severity of airflow limitations.\n Question: Do emphysema and airway disease affect within-breath changes in respiratory resistance in COPD 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: Chronic obstructive pulmonary disease (COPD) is characterized by a mixture of emphysema and airway disease. The forced oscillation technique (FOT) has been applied to COPD patients to clarify changes in respiratory mechanics; dynamic changes in respiratory resistance (Rrs) during breathing (within-breath changes in Rrs, ΔRrs) are characteristic of COPD. However, the pathophysiological significance of these changes is unknown. The aim of this study was to assess how emphysema and airway disease influence ΔRrs in COPD patients. In this cross-sectional study, stable COPD patients were recruited and underwent respiratory impedance measurements with a commercially available FOT device. Rrs was recorded during tidal breathing and then analyzed as whole-breath Rrs (Rrs at 5 Hz, R5; Rrs at 20 Hz, R20; and their difference, R5-R20) or as ΔRrs, the difference between the expiratory and inspiratory Rrs (ΔR5, ΔR20 and ΔR5-R20). The percentage of the low attenuation area (LAA%) and airway wall area (WA%) was quantified by computed tomography analysis, and their contributions to ΔRrs were examined. Seventy-five COPD patients were recruited. LAA% was negatively correlated with ΔR5 and ΔR5-R20 (P = 0.0002 and P = 0.0033, respectively); meanwhile, WA% in B(10) was positively correlated with ΔR5 and ΔR5-R20 (P = 0.0057 and P < 0.0001, respectively). Multivariate analysis revealed that the contribution of both LAA% and WA% in B(10) to ΔRrs was independent of the severity of airflow limitations.
Question: Do emphysema and airway disease affect within-breath changes in respiratory resistance in COPD patients?
Output:
|
PubmedQA45062
|
[
{
"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: Genetic deletion or antagonism of the neurokinin 1 receptor (NK1R) decreases alcohol intake, alcohol reward, and stress-induced alcohol relapse in rodents, while TACR1 variation is associated with alcoholism in humans. We used L822429, a specific antagonist with high affinity for the rat NK1R, and examined whether sensitivity to NK1R blockade is altered in alcohol-preferring (P) rats. Operant alcohol self-administration and progressive ratio responding were analyzed in P-rats and their founder Wistar line. We also analyzed Tacr1 expression and binding and sequenced the Tacr1 promoter from both lines. Systemic L822429 decreased alcohol self-administration in P-rats but did not affect the lower rates of alcohol self-administration in Wistar rats. Tacr1 expression was elevated in the prefrontal cortex and the amygdala of P-rats. In central amygdala, elevated Tacr1 expression was accompanied by elevated NK1R binding. Central amygdala (but not prefrontal cortex) infusion of L822429 replicated the systemic antagonist effects on alcohol self-administration in P-rats. All P-rats, but only 18% of their founder Wistar population, were CC homozygous for a-1372G/C single nucleotide polymorphism. In silico analysis indicated that the Tacr1-1372 genotype could modulate binding of the transcription factors GATA-2 and E2F-1. Electromobility shift and luciferase reporter assays suggested that the-1372C allele confers increased transcription factor binding and transcription.\n Question: Is tacr1 gene variation and neurokinin 1 receptor expression associated with antagonist efficacy in genetically selected alcohol-preferring rats?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Genetic deletion or antagonism of the neurokinin 1 receptor (NK1R) decreases alcohol intake, alcohol reward, and stress-induced alcohol relapse in rodents, while TACR1 variation is associated with alcoholism in humans. We used L822429, a specific antagonist with high affinity for the rat NK1R, and examined whether sensitivity to NK1R blockade is altered in alcohol-preferring (P) rats. Operant alcohol self-administration and progressive ratio responding were analyzed in P-rats and their founder Wistar line. We also analyzed Tacr1 expression and binding and sequenced the Tacr1 promoter from both lines. Systemic L822429 decreased alcohol self-administration in P-rats but did not affect the lower rates of alcohol self-administration in Wistar rats. Tacr1 expression was elevated in the prefrontal cortex and the amygdala of P-rats. In central amygdala, elevated Tacr1 expression was accompanied by elevated NK1R binding. Central amygdala (but not prefrontal cortex) infusion of L822429 replicated the systemic antagonist effects on alcohol self-administration in P-rats. All P-rats, but only 18% of their founder Wistar population, were CC homozygous for a-1372G/C single nucleotide polymorphism. In silico analysis indicated that the Tacr1-1372 genotype could modulate binding of the transcription factors GATA-2 and E2F-1. Electromobility shift and luciferase reporter assays suggested that the-1372C allele confers increased transcription factor binding and transcription.
Question: Is tacr1 gene variation and neurokinin 1 receptor expression associated with antagonist efficacy in genetically selected alcohol-preferring rats?
Output:
|
PubmedQA33587
|
[
{
"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: Baseline severity and causal subtype are predictors of outcome in ischemic stroke. We used data from the Tinzaparin in Acute Ischemic Stroke Trial (TAIST) to further assess the relationship among stroke subtype, early recovery, and outcome. Patients with ischemic stroke (<48 hours ictus) and enrolled into TAIST were included. Severity was measured prospectively as the Scandinavian Neurological Stroke Scale (SNSS) at days 0, 4, 7, and 10. Causal subtype as large artery atherosclerosis (LAA), cardioembolism (CE), or small vessel occlusion (SVO) was assigned after standard investigations. The rate of recovery was calculated as the change in SNSS at each time point. Functional outcome was assessed using the modified Rankin Scale (mRS) and Barthel Index at day 90. Analyses were performed on the 1190 patients in TAIST who met criteria for LAA, CE, and SVO. The largest change in SNSS score occurred between baseline and day 4 and was greatest in SVO (median improvement 4 U), compared with LAA (median improvement 2 U) and CE (median improvement 2 U) (P < .0001). If no improvement in SNSS had occurred by day 4, irrespective of subgroup, then early recovery (median SNSS improvement by day 10: 2) and functional outcome (mRS 4) tended to be limited; patients who recovered early tended to continue to improve (median SNSS improvement by day 10: 11) and had a better outcome at day 90 (median, mRS 2).\n Question: Are early recovery and functional outcome related with causal stroke subtype : data from the tinzaparin in acute ischemic stroke trial?\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: Baseline severity and causal subtype are predictors of outcome in ischemic stroke. We used data from the Tinzaparin in Acute Ischemic Stroke Trial (TAIST) to further assess the relationship among stroke subtype, early recovery, and outcome. Patients with ischemic stroke (<48 hours ictus) and enrolled into TAIST were included. Severity was measured prospectively as the Scandinavian Neurological Stroke Scale (SNSS) at days 0, 4, 7, and 10. Causal subtype as large artery atherosclerosis (LAA), cardioembolism (CE), or small vessel occlusion (SVO) was assigned after standard investigations. The rate of recovery was calculated as the change in SNSS at each time point. Functional outcome was assessed using the modified Rankin Scale (mRS) and Barthel Index at day 90. Analyses were performed on the 1190 patients in TAIST who met criteria for LAA, CE, and SVO. The largest change in SNSS score occurred between baseline and day 4 and was greatest in SVO (median improvement 4 U), compared with LAA (median improvement 2 U) and CE (median improvement 2 U) (P < .0001). If no improvement in SNSS had occurred by day 4, irrespective of subgroup, then early recovery (median SNSS improvement by day 10: 2) and functional outcome (mRS 4) tended to be limited; patients who recovered early tended to continue to improve (median SNSS improvement by day 10: 11) and had a better outcome at day 90 (median, mRS 2).
Question: Are early recovery and functional outcome related with causal stroke subtype : data from the tinzaparin in acute ischemic stroke trial?
Output:
|
PubmedQA65723
|
[
{
"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: Sublobar resection of lung cancer may benefit patients with lung cancer presenting as ground-glass opacity (GGO) nodules. The purpose of this study was to evaluate the effect of margin width on recurrence after sublobar resection in patients with clinical N0 non-small cell lung cancer presenting as GGO-predominant nodule. We conducted a retrospective chart review of 91 patients treated for clinical N0 non-small cell lung cancer ≤3 cm by sublobar resection with clear resection margins. We assigned them to two groups: GGO-predominant tumor and solid-predominant tumor. Each group was subdivided into two groups according to the margin width: resection margin ≤5 mm and resection margin >5 mm. We analyzed the clinicopathological findings and survival among these four groups. There was no recurrence in GGO-predominant tumors after sublobar resection. Margin width did not influence the recurrence in GGO-predominant tumors. In the cases of solid-predominant tumor, 5-year recurrence-free survival after sublobar resection according to margin width ≤5 and >5 mm was 24.2 and 79.6 %, respectively (p < 0.001). Therefore, narrow margin width (resection margin ≤5 mm) was a significant risk factor for recurrence of solid-predominant tumors (hazard ratio 3.868, 95 % confidence interval 1.177-12.714, p = 0.026).\n Question: Does sublobar Resection Margin Width Affect Recurrence of Clinical N0 Non-small Cell Lung Cancer Presenting as GGO-Predominant Nodule of 3 cm or Less?\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: Sublobar resection of lung cancer may benefit patients with lung cancer presenting as ground-glass opacity (GGO) nodules. The purpose of this study was to evaluate the effect of margin width on recurrence after sublobar resection in patients with clinical N0 non-small cell lung cancer presenting as GGO-predominant nodule. We conducted a retrospective chart review of 91 patients treated for clinical N0 non-small cell lung cancer ≤3 cm by sublobar resection with clear resection margins. We assigned them to two groups: GGO-predominant tumor and solid-predominant tumor. Each group was subdivided into two groups according to the margin width: resection margin ≤5 mm and resection margin >5 mm. We analyzed the clinicopathological findings and survival among these four groups. There was no recurrence in GGO-predominant tumors after sublobar resection. Margin width did not influence the recurrence in GGO-predominant tumors. In the cases of solid-predominant tumor, 5-year recurrence-free survival after sublobar resection according to margin width ≤5 and >5 mm was 24.2 and 79.6 %, respectively (p < 0.001). Therefore, narrow margin width (resection margin ≤5 mm) was a significant risk factor for recurrence of solid-predominant tumors (hazard ratio 3.868, 95 % confidence interval 1.177-12.714, p = 0.026).
Question: Does sublobar Resection Margin Width Affect Recurrence of Clinical N0 Non-small Cell Lung Cancer Presenting as GGO-Predominant Nodule of 3 cm or Less?
Output:
|
PubmedQA186933
|
[
{
"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: Imprinted genes, which are monoallelically expressed by virtue of an epigenetic process initiated in the germline, are known to play key roles in regulating fetal growth and placental development. Numerous studies are investigating the expression of these imprinted genes in the human placenta in relation to common complications of pregnancy such as fetal growth restriction and preeclampsia. This study aimed to determine whether placental sampling protocols or other factors such as fetal sex, gestational age and mode of delivery may influence the expression of imprinted genes predicted to regulate placental signalling. Term placentas were collected from Caucasian women delivering at University Hospital of Wales or Royal Gwent Hospital within two hours of delivery. Expression of the imprinted genes PHLDA2, CDKN1C, PEG3 and PEG10 was assayed by quantitative real time PCR. Intraplacental gene expression was analysed (N = 5). Placental gene expression was compared between male (N = 11) and female (N = 11) infants, early term (N = 8) and late term (N = 10) deliveries and between labouring (N = 13) and non-labouring (N = 21) participants. The paternally expressed imprinted genes PEG3 and PEG10 were resilient to differences in sampling site, fetal sex, term gestational age and mode of delivery. The maternally expressed imprinted gene CDKN1C was elevated over 2-fold (p < 0.001) in placenta from labouring deliveries compared with elective caesarean sections. In addition, the maternally expressed imprinted gene PHLDA2 was elevated by 1.8 fold (p = 0.01) in samples taken at the distal edge of the placenta compared to the cord insertion site.\n Question: Does placental expression of imprinted genes vary with sampling site and mode of delivery?\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: Imprinted genes, which are monoallelically expressed by virtue of an epigenetic process initiated in the germline, are known to play key roles in regulating fetal growth and placental development. Numerous studies are investigating the expression of these imprinted genes in the human placenta in relation to common complications of pregnancy such as fetal growth restriction and preeclampsia. This study aimed to determine whether placental sampling protocols or other factors such as fetal sex, gestational age and mode of delivery may influence the expression of imprinted genes predicted to regulate placental signalling. Term placentas were collected from Caucasian women delivering at University Hospital of Wales or Royal Gwent Hospital within two hours of delivery. Expression of the imprinted genes PHLDA2, CDKN1C, PEG3 and PEG10 was assayed by quantitative real time PCR. Intraplacental gene expression was analysed (N = 5). Placental gene expression was compared between male (N = 11) and female (N = 11) infants, early term (N = 8) and late term (N = 10) deliveries and between labouring (N = 13) and non-labouring (N = 21) participants. The paternally expressed imprinted genes PEG3 and PEG10 were resilient to differences in sampling site, fetal sex, term gestational age and mode of delivery. The maternally expressed imprinted gene CDKN1C was elevated over 2-fold (p < 0.001) in placenta from labouring deliveries compared with elective caesarean sections. In addition, the maternally expressed imprinted gene PHLDA2 was elevated by 1.8 fold (p = 0.01) in samples taken at the distal edge of the placenta compared to the cord insertion site.
Question: Does placental expression of imprinted genes vary with sampling site and mode of delivery?
Output:
|
PubmedQA174270
|
[
{
"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: Leukoaraiosis (LA) is closely associated with aging, a major determinant of clinical outcome after ischemic stroke. In this study we sought to identify whether LA, independent of advancing age, affects outcome after acute ischemic stroke. LA volume was quantified in 240 patients with ischemic stroke and MRI within 24 hours of symptom onset. We explored the relationship between LA volume at admission and clinical outcome at 6 months, as assessed by the modified Rankin Scale (mRS). An ordinal logistic regression model was developed to analyze the independent effect of LA volume on clinical outcome. Bivariate analyses showed a significant correlation between LA volume and mRS at 6 months (r = 0.19, p = 0.003). Mean mRS was 1.7 +/- 1.8 among those in the lowest (< or =1.2 mL) and 2.5 +/- 1.9 in the highest (>9.9 mL) quartiles of LA volume (p = 0.01). The unfavorable prognostic effect of LA volume on clinical outcome was retained in the multivariable model (p = 0.002), which included age, gender, stroke risk factors (hypertension, diabetes mellitus, atrial fibrillation), previous history of brain infarction, admission plasma glucose level, admission NIH Stroke Scale score, IV rtPA treatment, and acute infarct volume on MRI as covariates.\n Question: Does severity of leukoaraiosis correlate with clinical outcome after 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: Leukoaraiosis (LA) is closely associated with aging, a major determinant of clinical outcome after ischemic stroke. In this study we sought to identify whether LA, independent of advancing age, affects outcome after acute ischemic stroke. LA volume was quantified in 240 patients with ischemic stroke and MRI within 24 hours of symptom onset. We explored the relationship between LA volume at admission and clinical outcome at 6 months, as assessed by the modified Rankin Scale (mRS). An ordinal logistic regression model was developed to analyze the independent effect of LA volume on clinical outcome. Bivariate analyses showed a significant correlation between LA volume and mRS at 6 months (r = 0.19, p = 0.003). Mean mRS was 1.7 +/- 1.8 among those in the lowest (< or =1.2 mL) and 2.5 +/- 1.9 in the highest (>9.9 mL) quartiles of LA volume (p = 0.01). The unfavorable prognostic effect of LA volume on clinical outcome was retained in the multivariable model (p = 0.002), which included age, gender, stroke risk factors (hypertension, diabetes mellitus, atrial fibrillation), previous history of brain infarction, admission plasma glucose level, admission NIH Stroke Scale score, IV rtPA treatment, and acute infarct volume on MRI as covariates.
Question: Does severity of leukoaraiosis correlate with clinical outcome after ischemic stroke?
Output:
|
PubmedQA123599
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To compare knowledge, attitudes and practice of standard methods in infection control by dentists in eight countries using a standardised questionnaire. Self-administered questionnaires on dental infection control and safety (IC&S) knowledge, attitudes and practice were distributed to a convenience sample of dentists in India, Pakistan, Thailand, Philippines, Taiwan, China, South Korea and the United States of America. Knowledge and practice of infection control among the Asian dentists lagged behind the levels of US dentists. Availability and affordability of equipment and materials were some of the reasons for the practice of infection control and safety. Attitude towards universal/standard precautions in controlling bloodborne pathogens was comparable between groups surveyed. Tested knowledge and practice of infection control was acceptable but the attitude and understanding of universal/standard precautions was ambiguous among both Asian and USA dental practitioners. Education in dental infection control should focus on improving the attitudes of practitioners towards universal precautions.\n Question: Does sample infection control need assessment survey data from eight countries?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To compare knowledge, attitudes and practice of standard methods in infection control by dentists in eight countries using a standardised questionnaire. Self-administered questionnaires on dental infection control and safety (IC&S) knowledge, attitudes and practice were distributed to a convenience sample of dentists in India, Pakistan, Thailand, Philippines, Taiwan, China, South Korea and the United States of America. Knowledge and practice of infection control among the Asian dentists lagged behind the levels of US dentists. Availability and affordability of equipment and materials were some of the reasons for the practice of infection control and safety. Attitude towards universal/standard precautions in controlling bloodborne pathogens was comparable between groups surveyed. Tested knowledge and practice of infection control was acceptable but the attitude and understanding of universal/standard precautions was ambiguous among both Asian and USA dental practitioners. Education in dental infection control should focus on improving the attitudes of practitioners towards universal precautions.
Question: Does sample infection control need assessment survey data from eight countries?
Output:
|
PubmedQA55411
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: We hypothesized that curcumin, a potent anti-oxidant, might be beneficial in ameliorating the development of diabetic nephropathy through inhibition of PKC-α and PKC-β1 activity-ERK1/2 pathway. Diabetes was induced by a single intraperitoneal injection of streptozotocin (STZ) (55 mg/kg) in rats. Three weeks after STZ injection, rats were divided into three groups, namely, normal, diabetic and diabetic treated with curcumin at 100 mg/kg/day, p.o., for 8 wk. At 11 wk after STZ injection, diabetic rats exhibited renal dysfunction, as evidenced by reduced creatinine clearance, increased blood urea nitrogen (BUN) and proteinuria, marked increases in lipid peroxidation, NOX4 and p67phox and decrease in anti-oxidant enzyme. All of these abnormalities were significantly reversed by curcumin. Furthermore, the high-glucose-induced PKC-α and PKC-β1 activities and phosphorylated ERK1/2 was significantly diminished by curcumin. Curcumin also attenuated the expression of TGF-β1, CTGF, osteopontin, p300 and ECM proteins such as fibronectin and type IV collagen. The high-glucose-induced expression of VEGF and its receptor VEGF receptor II (flk-1) was also ameliorated by curcumin.\n Question: Does curcumin attenuate diabetic nephropathy by inhibiting PKC-α and PKC-β1 activity in streptozotocin-induced type I diabetic rats?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: We hypothesized that curcumin, a potent anti-oxidant, might be beneficial in ameliorating the development of diabetic nephropathy through inhibition of PKC-α and PKC-β1 activity-ERK1/2 pathway. Diabetes was induced by a single intraperitoneal injection of streptozotocin (STZ) (55 mg/kg) in rats. Three weeks after STZ injection, rats were divided into three groups, namely, normal, diabetic and diabetic treated with curcumin at 100 mg/kg/day, p.o., for 8 wk. At 11 wk after STZ injection, diabetic rats exhibited renal dysfunction, as evidenced by reduced creatinine clearance, increased blood urea nitrogen (BUN) and proteinuria, marked increases in lipid peroxidation, NOX4 and p67phox and decrease in anti-oxidant enzyme. All of these abnormalities were significantly reversed by curcumin. Furthermore, the high-glucose-induced PKC-α and PKC-β1 activities and phosphorylated ERK1/2 was significantly diminished by curcumin. Curcumin also attenuated the expression of TGF-β1, CTGF, osteopontin, p300 and ECM proteins such as fibronectin and type IV collagen. The high-glucose-induced expression of VEGF and its receptor VEGF receptor II (flk-1) was also ameliorated by curcumin.
Question: Does curcumin attenuate diabetic nephropathy by inhibiting PKC-α and PKC-β1 activity in streptozotocin-induced type I diabetic rats?
Output:
|
PubmedQA194110
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: It has been suggested that perturbations in branched-chain amino acid (BCAA) catabolism are associated with insulin resistance and contribute to elevated systemic BCAAs. Evidence in rodents suggests dietary protein rich in BCAAs can increase BCAA catabolism, but there is limited evidence in humans. We hypothesize that a diet rich in BCAAs will increase BCAA catabolism, which will manifest in a reduction of fasting plasma BCAA concentrations. The metabolome of 27 obese women with metabolic syndrome before and after weight loss was investigated to identify changes in BCAA metabolism using GC-time-of-flight mass spectrometry. Subjects were enrolled in an 8-wk weight-loss study including either a 20-g/d whey (whey group, n = 16) or gelatin (gelatin group, n = 11) protein supplement. When matched for total protein by weight, whey protein has 3 times the amount of BCAAs compared with gelatin protein. Postintervention plasma abundances of Ile (gelatin group: 637 ± 18, quantifier ion peak height ÷ 100; whey group: 744 ± 65), Leu (gelatin group: 1210 ± 33; whey group: 1380 ± 79), and Val (gelatin group: 2080 ± 59; whey group: 2510 ± 230) did not differ between treatment groups. BCAAs were significantly correlated with homeostasis model assessment of insulin resistance at baseline (r = 0.52, 0.43, and 0.49 for Leu, Ile, and Val, respectively; all, P < 0.05), but correlations were no longer significant at postintervention. Pro- and Cys-related pathways were found discriminant of whey protein vs. gelatin protein supplementation in multivariate statistical analyses.\n Question: Does whey protein supplementation alter plasma branched-chained amino acid profiles but results in unique metabolomics patterns in obese women enrolled in an 8-week weight loss trial?\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: It has been suggested that perturbations in branched-chain amino acid (BCAA) catabolism are associated with insulin resistance and contribute to elevated systemic BCAAs. Evidence in rodents suggests dietary protein rich in BCAAs can increase BCAA catabolism, but there is limited evidence in humans. We hypothesize that a diet rich in BCAAs will increase BCAA catabolism, which will manifest in a reduction of fasting plasma BCAA concentrations. The metabolome of 27 obese women with metabolic syndrome before and after weight loss was investigated to identify changes in BCAA metabolism using GC-time-of-flight mass spectrometry. Subjects were enrolled in an 8-wk weight-loss study including either a 20-g/d whey (whey group, n = 16) or gelatin (gelatin group, n = 11) protein supplement. When matched for total protein by weight, whey protein has 3 times the amount of BCAAs compared with gelatin protein. Postintervention plasma abundances of Ile (gelatin group: 637 ± 18, quantifier ion peak height ÷ 100; whey group: 744 ± 65), Leu (gelatin group: 1210 ± 33; whey group: 1380 ± 79), and Val (gelatin group: 2080 ± 59; whey group: 2510 ± 230) did not differ between treatment groups. BCAAs were significantly correlated with homeostasis model assessment of insulin resistance at baseline (r = 0.52, 0.43, and 0.49 for Leu, Ile, and Val, respectively; all, P < 0.05), but correlations were no longer significant at postintervention. Pro- and Cys-related pathways were found discriminant of whey protein vs. gelatin protein supplementation in multivariate statistical analyses.
Question: Does whey protein supplementation alter plasma branched-chained amino acid profiles but results in unique metabolomics patterns in obese women enrolled in an 8-week weight loss trial?
Output:
|
PubmedQA31011
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The aim of this study was to investigate the changes in two of the enzymes involved in fluorouracil metabolism, thymidine phosphorylase (TP) and dihydropyrimidine dehydrogenase (DPD), in uterine cervical squamous cell cancer tissue after radiotherapy. Cervical tissue from 27 patients diagnosed with stage IIIB or IV uterine cervical squamous cell cancer was compared with normal cervical tissue from 33 patients with benign gynecologic diseases. Expression of TP and DPD in the cervical tissues was measured using enzyme-linked immunosorbent assays. TP and DPD expression before and after irradiation with 10 and 20 Gy was measured in 9 of the 27 patients with cervical cancer. Before irradiation, DPD expression in cancer tissue did not differ from that in normal tissue. TP expression and the TP/DPD ratio were significantly higher in cancer tissue than in normal tissue ( P<0.00001). TP and DPD expression and the TP/DPD ratio were not significantly changed by irradiation with 10 and 20 Gy. TP expression and the TP/DPD ratio after irradiation with 10 and 20 Gy were significantly higher than in normal tissue.\n Question: Is thymidine phosphorylase expression preserved after radiotherapy in patients with cervical squamous cell carcinoma?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: The aim of this study was to investigate the changes in two of the enzymes involved in fluorouracil metabolism, thymidine phosphorylase (TP) and dihydropyrimidine dehydrogenase (DPD), in uterine cervical squamous cell cancer tissue after radiotherapy. Cervical tissue from 27 patients diagnosed with stage IIIB or IV uterine cervical squamous cell cancer was compared with normal cervical tissue from 33 patients with benign gynecologic diseases. Expression of TP and DPD in the cervical tissues was measured using enzyme-linked immunosorbent assays. TP and DPD expression before and after irradiation with 10 and 20 Gy was measured in 9 of the 27 patients with cervical cancer. Before irradiation, DPD expression in cancer tissue did not differ from that in normal tissue. TP expression and the TP/DPD ratio were significantly higher in cancer tissue than in normal tissue ( P<0.00001). TP and DPD expression and the TP/DPD ratio were not significantly changed by irradiation with 10 and 20 Gy. TP expression and the TP/DPD ratio after irradiation with 10 and 20 Gy were significantly higher than in normal tissue.
Question: Is thymidine phosphorylase expression preserved after radiotherapy in patients with cervical squamous cell carcinoma?
Output:
|
PubmedQA91279
|
[
{
"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: Spinal cord stimulation (SCS) is commonly used for neuropathic pain; the optimal variables and mechanisms of action are unclear. We tested whether modulation of SCS variables improved analgesia in animals with neuropathic pain by comparing 6-hour vs 30-minute duration and 50%, 75%, or 90% motor threshold (MT) intensity (amplitude). Furthermore, we examined whether maximally effective SCS reduced glial activation in the spinal cord in neuropathic animals. Sprague-Dawley rats received the spared nerve injury model and were implanted with an epidural SCS lead. Animals were tested for mechanical withdrawal threshold of the paw before and 2 weeks after spared nerve injury, before and after SCS daily for 4 days, and 1, 4, and 9 days after SCS. Spinal cords were examined for the effects of SCS on glial cell activation. The mechanical withdrawal threshold decreased, and glial immunoreactivity increased 2 weeks after spared nerve injury. For duration, 6-hour SCS significantly increased the mechanical withdrawal threshold when compared with 30-minute SCS or sham SCS; 30-minute SCS was greater than sham SCS. For intensity (amplitude), 90% MT SCS significantly increased the withdrawal threshold when compared with 75% MT SCS, 50% MT SCS, and sham SCS. Both 4 and 60 Hz SCS decreased glial activation (GFAP, MCP-1, and OX-42) in the spinal cord dorsal horn when compared with sham.\n Question: Does spinal cord stimulation reduce mechanical hyperalgesia and glial cell activation in animals with neuropathic pain?\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: Spinal cord stimulation (SCS) is commonly used for neuropathic pain; the optimal variables and mechanisms of action are unclear. We tested whether modulation of SCS variables improved analgesia in animals with neuropathic pain by comparing 6-hour vs 30-minute duration and 50%, 75%, or 90% motor threshold (MT) intensity (amplitude). Furthermore, we examined whether maximally effective SCS reduced glial activation in the spinal cord in neuropathic animals. Sprague-Dawley rats received the spared nerve injury model and were implanted with an epidural SCS lead. Animals were tested for mechanical withdrawal threshold of the paw before and 2 weeks after spared nerve injury, before and after SCS daily for 4 days, and 1, 4, and 9 days after SCS. Spinal cords were examined for the effects of SCS on glial cell activation. The mechanical withdrawal threshold decreased, and glial immunoreactivity increased 2 weeks after spared nerve injury. For duration, 6-hour SCS significantly increased the mechanical withdrawal threshold when compared with 30-minute SCS or sham SCS; 30-minute SCS was greater than sham SCS. For intensity (amplitude), 90% MT SCS significantly increased the withdrawal threshold when compared with 75% MT SCS, 50% MT SCS, and sham SCS. Both 4 and 60 Hz SCS decreased glial activation (GFAP, MCP-1, and OX-42) in the spinal cord dorsal horn when compared with sham.
Question: Does spinal cord stimulation reduce mechanical hyperalgesia and glial cell activation in animals with neuropathic pain?
Output:
|
PubmedQA121596
|
[
{
"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: Angiotensin II (Ang II), the physiologically-active product of the renin-angiotensin system (RAS), has recently been found to be an adipokine secreted by adipocytes. Although Ang II is known to exert its effects via angiotensin II receptor type 1 (AT1R) or type 2 (AT2R), the roles of the two receptors in the adipose tissue are unclear. Apelin, another adipokine, has been found able to restore glucose tolerance in obese and insulin-resistant mice. Because they are both involved in metabolic disorders, there may be an interaction between the two adipokines. To observe the expression of RAS and apelin, 3T3-L1 adipocytes were harvested after 1, 2, 4, and 6 days of differentiation. The RAS blockers captopril (10(-4) M), perindopril (10(-3) M), losartan (10(-4) M), or PD123319 (10(-4) M) were added at day 2 of differentiation and harvested at day 4 and 6, when apelin expression was measured. Expressions of mRNAs were detected by real-time PCR. Production of Ang II and apelin was measured from culture media by ELISA. Cellular lipid droplets were detected by oil-red staining. Our study showed that the mRNA expressions of AGT, renin, ACE1, and AT2R were up-regulated while AT1R mRNA was down-regulated during adipogenesis. Apelin expression increased during adipogenesis, and this increase was further augmented by blocking RAS. RAS blockers also prevented excessive lipid accumulation and the generation of ROS (reactive oxygen species) in differentiating adipocytes.\n Question: Does blockade of the renin-angiotensin system ameliorate apelin production in 3T3-L1 adipocytes?\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: Angiotensin II (Ang II), the physiologically-active product of the renin-angiotensin system (RAS), has recently been found to be an adipokine secreted by adipocytes. Although Ang II is known to exert its effects via angiotensin II receptor type 1 (AT1R) or type 2 (AT2R), the roles of the two receptors in the adipose tissue are unclear. Apelin, another adipokine, has been found able to restore glucose tolerance in obese and insulin-resistant mice. Because they are both involved in metabolic disorders, there may be an interaction between the two adipokines. To observe the expression of RAS and apelin, 3T3-L1 adipocytes were harvested after 1, 2, 4, and 6 days of differentiation. The RAS blockers captopril (10(-4) M), perindopril (10(-3) M), losartan (10(-4) M), or PD123319 (10(-4) M) were added at day 2 of differentiation and harvested at day 4 and 6, when apelin expression was measured. Expressions of mRNAs were detected by real-time PCR. Production of Ang II and apelin was measured from culture media by ELISA. Cellular lipid droplets were detected by oil-red staining. Our study showed that the mRNA expressions of AGT, renin, ACE1, and AT2R were up-regulated while AT1R mRNA was down-regulated during adipogenesis. Apelin expression increased during adipogenesis, and this increase was further augmented by blocking RAS. RAS blockers also prevented excessive lipid accumulation and the generation of ROS (reactive oxygen species) in differentiating adipocytes.
Question: Does blockade of the renin-angiotensin system ameliorate apelin production in 3T3-L1 adipocytes?
Output:
|
PubmedQA44196
|
[
{
"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: Protein tyrosine kinase 6 (PTK6) is a non-receptor tyrosine kinase that is highly expressed in Human Epidermal Growth Factor 2(+) (Her2(+)) breast cancers. Overexpression of PTK6 enhances anchorage-independent survival, proliferation, and migration of breast cancer cells. We hypothesized that PTK6 inhibition is an effective strategy to inhibit growth and survival of Her2(+) breast cancer cells, including those that are relatively resistant to Lapatinib, a targeted therapy for Her2(+) breast cancer, either intrinsically or acquired after continuous drug exposure. To determine the effects of PTK6 inhibition on Lapatinib-resistant Her2(+) breast cancer cell lines (UACC893R1 and MDA-MB-453), we used short hairpin ribonucleic acid (shRNA) vectors to downregulate PTK6 expression. We determined the effects of PTK6 downregulation on growth and survival in vitro and in vivo, as well as the mechanisms responsible for these effects. Lapatinib treatment of \"sensitive\" Her2(+) cells induces apoptotic cell death and enhances transcript and protein levels of Bim, a pro-apoptotic Bcl2 family member. In contrast, treatment of relatively \"resistant\" Her2(+) cells fails to induce Bim or enhance levels of cleaved, poly-ADP ribose polymerase (PARP). Downregulation of PTK6 expression in these \"resistant\" cells enhances Bim expression, resulting in apoptotic cell death. PTK6 downregulation impairs growth of these cells in in vitro 3-D Matrigel(TM) cultures, and also inhibits growth of Her2(+) primary tumor xenografts. Bim expression is critical for apoptosis induced by PTK6 downregulation, as co-expression of Bim shRNA rescued these cells from PTK6 shRNA-induced death. The regulation of Bim by PTK6 is not via changes in Erk/MAPK or Akt signaling, two pathways known to regulate Bim expression. Rather, PTK6 downregulation activates p38, and pharmacological inhibition of p38 activity prevents PTK6 shRNA-induced Bim expression and partially rescues cells from apoptosis.\n Question: Does pTK6 inhibition promote apoptosis of Lapatinib-resistant Her2 ( + ) breast cancer cells by inducing Bim?\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: Protein tyrosine kinase 6 (PTK6) is a non-receptor tyrosine kinase that is highly expressed in Human Epidermal Growth Factor 2(+) (Her2(+)) breast cancers. Overexpression of PTK6 enhances anchorage-independent survival, proliferation, and migration of breast cancer cells. We hypothesized that PTK6 inhibition is an effective strategy to inhibit growth and survival of Her2(+) breast cancer cells, including those that are relatively resistant to Lapatinib, a targeted therapy for Her2(+) breast cancer, either intrinsically or acquired after continuous drug exposure. To determine the effects of PTK6 inhibition on Lapatinib-resistant Her2(+) breast cancer cell lines (UACC893R1 and MDA-MB-453), we used short hairpin ribonucleic acid (shRNA) vectors to downregulate PTK6 expression. We determined the effects of PTK6 downregulation on growth and survival in vitro and in vivo, as well as the mechanisms responsible for these effects. Lapatinib treatment of "sensitive" Her2(+) cells induces apoptotic cell death and enhances transcript and protein levels of Bim, a pro-apoptotic Bcl2 family member. In contrast, treatment of relatively "resistant" Her2(+) cells fails to induce Bim or enhance levels of cleaved, poly-ADP ribose polymerase (PARP). Downregulation of PTK6 expression in these "resistant" cells enhances Bim expression, resulting in apoptotic cell death. PTK6 downregulation impairs growth of these cells in in vitro 3-D Matrigel(TM) cultures, and also inhibits growth of Her2(+) primary tumor xenografts. Bim expression is critical for apoptosis induced by PTK6 downregulation, as co-expression of Bim shRNA rescued these cells from PTK6 shRNA-induced death. The regulation of Bim by PTK6 is not via changes in Erk/MAPK or Akt signaling, two pathways known to regulate Bim expression. Rather, PTK6 downregulation activates p38, and pharmacological inhibition of p38 activity prevents PTK6 shRNA-induced Bim expression and partially rescues cells from apoptosis.
Question: Does pTK6 inhibition promote apoptosis of Lapatinib-resistant Her2 ( + ) breast cancer cells by inducing Bim?
Output:
|
PubmedQA155861
|
[
{
"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: Magnesium sulfate (MgSO4) possesses potent anti-inflammation capacity. We sought to elucidate the effects of MgSO4 on mitigating acute lung injury induced by endotoxemia. MgSO4 is an antagonist of the L-type calcium channels and the N-methyl-D-aspartate (NMDA) receptor. The roles of the L-type calcium channels and NMDA receptor in this regard were also elucidated. Ninety-six adult male rats were randomized to receive normal saline, MgSO4 (100 mg/kg), lipopolysaccharide (LPS), LPS plus MgSO4 (10, 50, or 100 mg/kg), LPS plus MgSO4 (100 mg/kg) plus the L-type calcium channel activator BAY-K8644, or LPS plus MgSO4 (100 mg/kg) plus exogenous NMDA (n=12 in each group). Between-group differences in lung injury were evaluated. Histologic findings, in concert with assays of leukocyte infiltration (polymorphonuclear leukocytes/alveoli ratio and myeloperoxidase activity) and lung water content (wet/dry weight ratio), confirmed that LPS induced acute lung injury. LPS also caused significant inflammatory response (increases in chemokine, cytokine, and prostaglandin E2 concentrations) and imposed significant oxidative stress (increases in nitric oxide and malondialdehyde concentrations) in rat lungs. MgSO4 at the dosages of 50 mg/kg and 100 mg/kg, but not at 10 mg/kg, significantly mitigated the acute lung injury, lung inflammatory response, and oxidative stress caused by endotoxemia. Moreover, the protective effects of MgSO4 were counteracted by BAY-K8644 and exogenous NMDA.\n Question: Does magnesium sulfate mitigate acute lung injury in endotoxemia rats?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Magnesium sulfate (MgSO4) possesses potent anti-inflammation capacity. We sought to elucidate the effects of MgSO4 on mitigating acute lung injury induced by endotoxemia. MgSO4 is an antagonist of the L-type calcium channels and the N-methyl-D-aspartate (NMDA) receptor. The roles of the L-type calcium channels and NMDA receptor in this regard were also elucidated. Ninety-six adult male rats were randomized to receive normal saline, MgSO4 (100 mg/kg), lipopolysaccharide (LPS), LPS plus MgSO4 (10, 50, or 100 mg/kg), LPS plus MgSO4 (100 mg/kg) plus the L-type calcium channel activator BAY-K8644, or LPS plus MgSO4 (100 mg/kg) plus exogenous NMDA (n=12 in each group). Between-group differences in lung injury were evaluated. Histologic findings, in concert with assays of leukocyte infiltration (polymorphonuclear leukocytes/alveoli ratio and myeloperoxidase activity) and lung water content (wet/dry weight ratio), confirmed that LPS induced acute lung injury. LPS also caused significant inflammatory response (increases in chemokine, cytokine, and prostaglandin E2 concentrations) and imposed significant oxidative stress (increases in nitric oxide and malondialdehyde concentrations) in rat lungs. MgSO4 at the dosages of 50 mg/kg and 100 mg/kg, but not at 10 mg/kg, significantly mitigated the acute lung injury, lung inflammatory response, and oxidative stress caused by endotoxemia. Moreover, the protective effects of MgSO4 were counteracted by BAY-K8644 and exogenous NMDA.
Question: Does magnesium sulfate mitigate acute lung injury in endotoxemia rats?
Output:
|
PubmedQA37550
|
[
{
"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: Nutritional biochemical indexes are generally used as markers for critically ill patients. However, they are easily influenced by acute phase changes after injury and are difficult to use as common and practical biomarkers. The objective of this study was to determine the most valuable prognostic markers among 15 common laboratory tests in patients with sepsis. We included all sepsis patients who stayed in the intensive care unit for more than 2 weeks. We evaluated 15 biochemistry indexes including serum albumin, total protein, C-reactive protein, cholinesterase, total cholesterol (T-Cho), triglyceride, sodium, potassium, blood urea nitrogen, creatinine, aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, total bilirubin (T-Bil), and prothrombin time. The minimum and maximum values of these indexes during the first 14 days from admission were analyzed by classification and regression tree and multivariate logistic regression analyses. This study comprised 91 patients with sepsis. The primary split was the minimum value of serum T-Cho (T-Cho (Min)), and the cutoff value was 73.5 mg/dL by classification and regression tree analysis. The second split was the maximum value of T-Bil (T-Bil (Max)), and the cutoff value was 1.35 mg/dL. The rate of mortality was 63% (17/27) in the group with T-Cho (Min) less than 73.5 mg/dL and T-Bil (Max) greater than 1.35 mg/dL. Multivariate logistic regression revealed that T-Cho (Min) and T-Bil (Max) were the biomarkers most closely associated with prognosis.\n Question: Are low total cholesterol and high total bilirubin associated with prognosis in patients with prolonged sepsis?\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: Nutritional biochemical indexes are generally used as markers for critically ill patients. However, they are easily influenced by acute phase changes after injury and are difficult to use as common and practical biomarkers. The objective of this study was to determine the most valuable prognostic markers among 15 common laboratory tests in patients with sepsis. We included all sepsis patients who stayed in the intensive care unit for more than 2 weeks. We evaluated 15 biochemistry indexes including serum albumin, total protein, C-reactive protein, cholinesterase, total cholesterol (T-Cho), triglyceride, sodium, potassium, blood urea nitrogen, creatinine, aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, total bilirubin (T-Bil), and prothrombin time. The minimum and maximum values of these indexes during the first 14 days from admission were analyzed by classification and regression tree and multivariate logistic regression analyses. This study comprised 91 patients with sepsis. The primary split was the minimum value of serum T-Cho (T-Cho (Min)), and the cutoff value was 73.5 mg/dL by classification and regression tree analysis. The second split was the maximum value of T-Bil (T-Bil (Max)), and the cutoff value was 1.35 mg/dL. The rate of mortality was 63% (17/27) in the group with T-Cho (Min) less than 73.5 mg/dL and T-Bil (Max) greater than 1.35 mg/dL. Multivariate logistic regression revealed that T-Cho (Min) and T-Bil (Max) were the biomarkers most closely associated with prognosis.
Question: Are low total cholesterol and high total bilirubin associated with prognosis in patients with prolonged sepsis?
Output:
|
PubmedQA120666
|
[
{
"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: Eccentric exercise has become the treatment of choice for Achilles tendinopathy. However, little is known about the acute response of tendons to eccentric exercise or the mechanisms underlying its clinical benefit. This research evaluated the sonographic characteristics and acute anteroposterior (AP) strain response of control (healthy), asymptomatic, and symptomatic Achilles tendons to eccentric exercise. Eleven male adults with unilateral midportion Achilles tendinopathy and nine control male adults without tendinopathy participated in the research. Sagittal sonograms of the Achilles tendon were acquired immediately before and after completion of a common eccentric rehabilitation exercise protocol and again 24 h later. Tendon thickness, echogenicity, and AP strain were determined 40 mm proximal to the calcaneal insertion. Compared with the control tendon, both the asymptomatic and symptomatic tendons were thicker (P < 0.05) and hypoechoic (P < 0.05) at baseline. All tendons decreased in thickness immediately after eccentric exercise (P < 0.05). The symptomatic tendon was characterized by a significantly lower AP strain response to eccentric exercise compared with both the asymptomatic and control tendons (P < 0.05). AP strains did not differ in the control and asymptomatic tendons. For all tendons, preexercise thickness was restored 24 h after exercise completion.\n Question: Does achilles tendinopathy have an aberrant strain response to eccentric exercise?\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: Eccentric exercise has become the treatment of choice for Achilles tendinopathy. However, little is known about the acute response of tendons to eccentric exercise or the mechanisms underlying its clinical benefit. This research evaluated the sonographic characteristics and acute anteroposterior (AP) strain response of control (healthy), asymptomatic, and symptomatic Achilles tendons to eccentric exercise. Eleven male adults with unilateral midportion Achilles tendinopathy and nine control male adults without tendinopathy participated in the research. Sagittal sonograms of the Achilles tendon were acquired immediately before and after completion of a common eccentric rehabilitation exercise protocol and again 24 h later. Tendon thickness, echogenicity, and AP strain were determined 40 mm proximal to the calcaneal insertion. Compared with the control tendon, both the asymptomatic and symptomatic tendons were thicker (P < 0.05) and hypoechoic (P < 0.05) at baseline. All tendons decreased in thickness immediately after eccentric exercise (P < 0.05). The symptomatic tendon was characterized by a significantly lower AP strain response to eccentric exercise compared with both the asymptomatic and control tendons (P < 0.05). AP strains did not differ in the control and asymptomatic tendons. For all tendons, preexercise thickness was restored 24 h after exercise completion.
Question: Does achilles tendinopathy have an aberrant strain response to eccentric exercise?
Output:
|
PubmedQA98727
|
[
{
"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: Intravenous administration of the catecholamine epinephrine is known to have a stimulatory effect on aqueous humor flow in sleeping human subjects, an effect that is augmented by plasma corticosteroids. This study was performed to determine whether the closely related catecholamine norepinephrine has a similar effect on aqueous humor flow. Twenty normal subjects were studied. Aqueous flow was measured by fluorophotometry. At night during sleep, norepinephrine or placebo was infused intravenously (i.v.) between midnight and 6 AM. The rate of aqueous flow during the norepinephrine infusion was compared with the rate of flow during placebo infusion, with each subject serving as his/her own control. The urinary excretions of epinephrine and norepinephrine were measured at the end of each infusion period. The norepinephrine infusion caused an 8% increase in systolic blood pressure (P < 0.001), a 15% increase in diastolic blood pressure (P < 0.001), and a 9% decrease in heart rate (P=0.003) compared with the placebo. The rate of aqueous humor flow during sleep from 12 AM to 6 AM was unchanged by norepinephrine. The rate was 1.27+/-0.31 microl/min (mean+/-SD) during i.v. infusion of placebo and 1.30+/-0.27 microl/min during infusion of norepinephrine (P=0.63).\n Question: Is aqueous humor flow in sleeping humans unaffected by norepinephrine infusion?\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: Intravenous administration of the catecholamine epinephrine is known to have a stimulatory effect on aqueous humor flow in sleeping human subjects, an effect that is augmented by plasma corticosteroids. This study was performed to determine whether the closely related catecholamine norepinephrine has a similar effect on aqueous humor flow. Twenty normal subjects were studied. Aqueous flow was measured by fluorophotometry. At night during sleep, norepinephrine or placebo was infused intravenously (i.v.) between midnight and 6 AM. The rate of aqueous flow during the norepinephrine infusion was compared with the rate of flow during placebo infusion, with each subject serving as his/her own control. The urinary excretions of epinephrine and norepinephrine were measured at the end of each infusion period. The norepinephrine infusion caused an 8% increase in systolic blood pressure (P < 0.001), a 15% increase in diastolic blood pressure (P < 0.001), and a 9% decrease in heart rate (P=0.003) compared with the placebo. The rate of aqueous humor flow during sleep from 12 AM to 6 AM was unchanged by norepinephrine. The rate was 1.27+/-0.31 microl/min (mean+/-SD) during i.v. infusion of placebo and 1.30+/-0.27 microl/min during infusion of norepinephrine (P=0.63).
Question: Is aqueous humor flow in sleeping humans unaffected by norepinephrine infusion?
Output:
|
PubmedQA29970
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: In glomerulonephritides, dysmorphic red blood cells (RBCs) with membrane blebs can be found in the urine; this is referred to as glomerular hematuria. Glomerulonephritides are characterized by increased carbonyl stress and elevated methylglyoxal (MGO) levels. MGO causes oxidative stress and intracellular calcium accumulation. In the present study, we investigated whether the effect of MGO-induced calcium accumulation in RBCs develops through increased oxidative stress. Furthermore, we studied whether MGO can lead to RBC membrane blebbing. RBC suspensions from healthy volunteers were incubated with different concentrations of MGO at 37 degrees C. We measured oxidative stress and intracellular calcium level using fluorescent indicators. We determined the frequency of dysmorphic RBCs, and also performed scanning electron microscopy. MGO increased oxidative stress and caused accumulation of calcium in isolated RBCs. These effects could be prevented using antioxidants. In the presence of MGO, RBC membrane blebbing developed.\n Question: Is morphology of glomerular hematuria reproduced in vitro by carbonyl stress?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: In glomerulonephritides, dysmorphic red blood cells (RBCs) with membrane blebs can be found in the urine; this is referred to as glomerular hematuria. Glomerulonephritides are characterized by increased carbonyl stress and elevated methylglyoxal (MGO) levels. MGO causes oxidative stress and intracellular calcium accumulation. In the present study, we investigated whether the effect of MGO-induced calcium accumulation in RBCs develops through increased oxidative stress. Furthermore, we studied whether MGO can lead to RBC membrane blebbing. RBC suspensions from healthy volunteers were incubated with different concentrations of MGO at 37 degrees C. We measured oxidative stress and intracellular calcium level using fluorescent indicators. We determined the frequency of dysmorphic RBCs, and also performed scanning electron microscopy. MGO increased oxidative stress and caused accumulation of calcium in isolated RBCs. These effects could be prevented using antioxidants. In the presence of MGO, RBC membrane blebbing developed.
Question: Is morphology of glomerular hematuria reproduced in vitro by carbonyl stress?
Output:
|
PubmedQA162026
|
[
{
"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: Postanesthetic shivering develops in as many as one half of patients recovering from isoflurane anesthesia. Cholinergic stimulation of the hypothalamic-pituitary-adrenal axis and adrenal medulla by physostigmine enhances secretion of arginine vasopressin, epinephrine, and norepinephrine. Because the hypothalamus is the dominant thermoregulatory controller in mammals, and these neurotransmitters may be involved in body temperature control, physostigmine administration may influence the incidence of shivering. Accordingly, the authors tested the hypothesis that physostigmine administration inhibits postanesthetic shivering. Its efficacy was compared with that of saline (negative control) and meperidine and clonidine (positive controls). Sixty patients having surgery of the ear or nose were tested. General anesthesia was induced with 2 mg/kg propofol, 0.1 mg/kg vecuronium, and 1.5 microg/kg fentanyl and maintained with isoflurane (1.5 +/- 0.4%) in 70% nitrous oxide. At the end of surgery, the patients were randomly assigned to receive an intravenous bolus of 0.04 mg/kg physostigmine, isotonic saline, 0.5 mg/kg meperidine, or 1.5 microg/kg clonidine. Heart rate, mean arterial blood pressure, oxygen saturation, visual analog pain score, temperature, and postanesthetic shivering were measured during recovery. Postanesthetic shivering occurred in 6 of 15 (40%) patients given saline. In contrast, postanesthetic shivering was significantly reduced in physostigmine-treated patients (1 of 15, or 7%) and was absent in patients given clonidine or meperidine.\n Question: Does physostigmine prevent postanesthetic shivering as does meperidine or clonidine?\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: Postanesthetic shivering develops in as many as one half of patients recovering from isoflurane anesthesia. Cholinergic stimulation of the hypothalamic-pituitary-adrenal axis and adrenal medulla by physostigmine enhances secretion of arginine vasopressin, epinephrine, and norepinephrine. Because the hypothalamus is the dominant thermoregulatory controller in mammals, and these neurotransmitters may be involved in body temperature control, physostigmine administration may influence the incidence of shivering. Accordingly, the authors tested the hypothesis that physostigmine administration inhibits postanesthetic shivering. Its efficacy was compared with that of saline (negative control) and meperidine and clonidine (positive controls). Sixty patients having surgery of the ear or nose were tested. General anesthesia was induced with 2 mg/kg propofol, 0.1 mg/kg vecuronium, and 1.5 microg/kg fentanyl and maintained with isoflurane (1.5 +/- 0.4%) in 70% nitrous oxide. At the end of surgery, the patients were randomly assigned to receive an intravenous bolus of 0.04 mg/kg physostigmine, isotonic saline, 0.5 mg/kg meperidine, or 1.5 microg/kg clonidine. Heart rate, mean arterial blood pressure, oxygen saturation, visual analog pain score, temperature, and postanesthetic shivering were measured during recovery. Postanesthetic shivering occurred in 6 of 15 (40%) patients given saline. In contrast, postanesthetic shivering was significantly reduced in physostigmine-treated patients (1 of 15, or 7%) and was absent in patients given clonidine or meperidine.
Question: Does physostigmine prevent postanesthetic shivering as does meperidine or clonidine?
Output:
|
PubmedQA209814
|
[
{
"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: Nonylphenol (NP), an environmental organic compound, has been demonstrated to enhance reactive-oxygen species (ROS) synthesis. Chronic exposure to low-dose adenine (AD) has been reported to induce chronic kidney disease (CKD). In this study, we tested the hypothesis that chronic exposure to NP will aggravate AD-induced CKD through increasing generations of inflammation, ROS, and apoptosis that could be attenuated by rosuvastatin. Fifty male Wistar rats were equally divided into group 1 (control), group 2 (AD in fodder at a concentration of 0.25%), group 3 (NP: 2 mg/kg/day), group 4 (combined AD & NP), and group 5 (AD-NP + rosuvastatin: 20 mg/kg/day). Treatment was continued for 24 weeks for all animals before being sacrificed. By the end of 24 weeks, serum blood urea nitrogen (BUN) and creatinine levels were increased in group 4 than in groups 1-3, but significantly reduced in group 5 as compared with group 4 (all p < 0.05). Histopathology scorings of renal-parenchymal and tubular damages were significantly higher in group 4 than in groups 1-3, but remarkably lower in group 5 compared with group 4 (all p < 0.01). Both gene and protein levels of inflammation, oxidative stress, ROS, and cellular apoptosis were remarkably higher in group 4 compared with groups 1-3, but lowered in group 5 than in group 4 (all p < 0.001). Conversely, both gene and protein levels of anti-oxidants, anti-inflammation and anti-apoptosis were markedly increased in group 5 compared with group 4 (all p < 0.001).\n Question: Does continuing exposure to low-dose nonylphenol aggravate adenine-induced chronic renal dysfunction and role of rosuvastatin therapy?\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: Nonylphenol (NP), an environmental organic compound, has been demonstrated to enhance reactive-oxygen species (ROS) synthesis. Chronic exposure to low-dose adenine (AD) has been reported to induce chronic kidney disease (CKD). In this study, we tested the hypothesis that chronic exposure to NP will aggravate AD-induced CKD through increasing generations of inflammation, ROS, and apoptosis that could be attenuated by rosuvastatin. Fifty male Wistar rats were equally divided into group 1 (control), group 2 (AD in fodder at a concentration of 0.25%), group 3 (NP: 2 mg/kg/day), group 4 (combined AD & NP), and group 5 (AD-NP + rosuvastatin: 20 mg/kg/day). Treatment was continued for 24 weeks for all animals before being sacrificed. By the end of 24 weeks, serum blood urea nitrogen (BUN) and creatinine levels were increased in group 4 than in groups 1-3, but significantly reduced in group 5 as compared with group 4 (all p < 0.05). Histopathology scorings of renal-parenchymal and tubular damages were significantly higher in group 4 than in groups 1-3, but remarkably lower in group 5 compared with group 4 (all p < 0.01). Both gene and protein levels of inflammation, oxidative stress, ROS, and cellular apoptosis were remarkably higher in group 4 compared with groups 1-3, but lowered in group 5 than in group 4 (all p < 0.001). Conversely, both gene and protein levels of anti-oxidants, anti-inflammation and anti-apoptosis were markedly increased in group 5 compared with group 4 (all p < 0.001).
Question: Does continuing exposure to low-dose nonylphenol aggravate adenine-induced chronic renal dysfunction and role of rosuvastatin therapy?
Output:
|
PubmedQA152594
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To explore the role of inducible focal adhesion (FA) protein Hic-5 in actin cytoskeletal reorganization, FA formation, fibrogenic activity, and expression of myocilin in trabecular meshwork (TM) cells. Using primary cultures of human TM (HTM) cells, the effects of various external factors on Hic-5 protein levels, as well as the effects of recombinant Hic-5 and Hic-5 small interfering RNA (siRNA) on actin cytoskeleton, FAs, myocilin, α-smooth muscle actin (αSMA), and collagen-1 were determined by immunofluorescence and immunoblot analyses. Hic-5 distributes discretely to the FAs in HTM cells and throughout the TM and Schlemm's canal of the human aqueous humor (AH) outflow pathway. Transforming growth factor-β2 (TGF-β2), endothelin-1, lysophosphatidic acid, hydrogen peroxide, and RhoA significantly increased Hic-5 protein levels in HTM cells in association with reorganization of actin cytoskeleton and FAs. While recombinant Hic-5 induced actin stress fibers, FAs, αv integrin redistribution to the FAs, increased levels of αSMA, collagen-1, and myocilin, Hic-5 siRNA suppressed most of these responses in HTM cells. Hic-5 siRNA also suppressed TGF-β2-induced fibrogenic activity and dexamethasone-induced myocilin expression in HTM cells.\n Question: Does hic-5 regulate Actin Cytoskeletal Reorganization and Expression of Fibrogenic Markers and Myocilin in Trabecular Meshwork 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: To explore the role of inducible focal adhesion (FA) protein Hic-5 in actin cytoskeletal reorganization, FA formation, fibrogenic activity, and expression of myocilin in trabecular meshwork (TM) cells. Using primary cultures of human TM (HTM) cells, the effects of various external factors on Hic-5 protein levels, as well as the effects of recombinant Hic-5 and Hic-5 small interfering RNA (siRNA) on actin cytoskeleton, FAs, myocilin, α-smooth muscle actin (αSMA), and collagen-1 were determined by immunofluorescence and immunoblot analyses. Hic-5 distributes discretely to the FAs in HTM cells and throughout the TM and Schlemm's canal of the human aqueous humor (AH) outflow pathway. Transforming growth factor-β2 (TGF-β2), endothelin-1, lysophosphatidic acid, hydrogen peroxide, and RhoA significantly increased Hic-5 protein levels in HTM cells in association with reorganization of actin cytoskeleton and FAs. While recombinant Hic-5 induced actin stress fibers, FAs, αv integrin redistribution to the FAs, increased levels of αSMA, collagen-1, and myocilin, Hic-5 siRNA suppressed most of these responses in HTM cells. Hic-5 siRNA also suppressed TGF-β2-induced fibrogenic activity and dexamethasone-induced myocilin expression in HTM cells.
Question: Does hic-5 regulate Actin Cytoskeletal Reorganization and Expression of Fibrogenic Markers and Myocilin in Trabecular Meshwork Cells?
Output:
|
PubmedQA104754
|
[
{
"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 most common cause of hospitalization for children younger than age one is bronchiolitis. Several prenatal and environmental risk factors may affect the incidence of hospitalization for bronchiolitis. The aim of this study was to investigate the relation between exposure to vehicular traffic and the incidence of hospitalization for bronchiolitis in children during their first year of life in Italy. A multicenter prospective birth cohort study, where equal numbers of newborns of 33-34, 35-37 and ≥38 wGA were recruited at birth (1814 children) in 30 Italian neonatology units. Two interviewer-administered questionnaires were used to collect data. The first interview was carried out at the end of the Italian epidemic season. The second interview was carried out when the child was one year old. Data on possible prenatal, perinatal, and postnatal/environmental risk factors and on vehicular traffic density in the zone of residence were collected. On each interview, parents were also asked about any hospitalizations of the child. The outcome measure was the hospitalization for bronchiolitis (International Health Service ICD-9 code 466). Univariate analysis demonstrated that exposure to air pollution due to vehicular traffic, was significantly associated with an increased risk of hospitalization for bronchiolitis. The adjusted risk from logistic regression model confirmed that children exposed to air pollution due to vehicular traffic were at increased risk of hospitalization for bronchiolitis.\n Question: Is exposure to vehicular traffic associated to a higher risk of hospitalization for bronchiolitis during the first year of life?\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 most common cause of hospitalization for children younger than age one is bronchiolitis. Several prenatal and environmental risk factors may affect the incidence of hospitalization for bronchiolitis. The aim of this study was to investigate the relation between exposure to vehicular traffic and the incidence of hospitalization for bronchiolitis in children during their first year of life in Italy. A multicenter prospective birth cohort study, where equal numbers of newborns of 33-34, 35-37 and ≥38 wGA were recruited at birth (1814 children) in 30 Italian neonatology units. Two interviewer-administered questionnaires were used to collect data. The first interview was carried out at the end of the Italian epidemic season. The second interview was carried out when the child was one year old. Data on possible prenatal, perinatal, and postnatal/environmental risk factors and on vehicular traffic density in the zone of residence were collected. On each interview, parents were also asked about any hospitalizations of the child. The outcome measure was the hospitalization for bronchiolitis (International Health Service ICD-9 code 466). Univariate analysis demonstrated that exposure to air pollution due to vehicular traffic, was significantly associated with an increased risk of hospitalization for bronchiolitis. The adjusted risk from logistic regression model confirmed that children exposed to air pollution due to vehicular traffic were at increased risk of hospitalization for bronchiolitis.
Question: Is exposure to vehicular traffic associated to a higher risk of hospitalization for bronchiolitis during the first year of life?
Output:
|
PubmedQA28403
|
[
{
"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 accurate monitoring and evaluation of malaria vectors requires efficient sampling. The objective of this study was to compare methods for sampling outdoor-biting Anopheles mosquitoes in Cambodia. In the Cambodian provinces of Pursat, Preah Vihear, and Ratanakiri, six different mosquito trapping methods were evaluated: human landing collection (HLC), human-baited tent (HBT), cow-baited tent (CBT), CDC miniature light trap (LT), CDC miniature light trap baited with molasses and yeast (LT-M), and barrier fence (F) in a Latin square design during four or six consecutive nights at the height of the malaria transmission season. Using all traps, a total of 507, 1175, and 615 anophelines were collected in Pursat, Preah Vihear, and Ratanakiri, respectively. CBTs captured 10- to 20-fold more anophelines per night than the other five sampling methods. All 2297 Anopheles mosquitoes were morphologically identified and molecularly typed using standard morphological keys and sequencing the rDNA ITS2 region to distinguish cryptic species, respectively. Overall, an extremely diverse set of 27 known Anopheles species was sampled. CBTs captured the same molecular species that HLCs and the other four traps did, as well as additional species. Nine specimens representing five Anopheles species (Anopheles hyrcanus, Anopheles barbirostris sensu stricto, Anopheles barbirostris clade III, Anopheles nivipes, and Anopheles peditaeniatus) were infected with Plasmodium falciparum and were exclusively captured in CBTs.\n Question: Are cow-baited tents highly effective in sampling diverse Anopheles malaria vectors in Cambodia?\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 accurate monitoring and evaluation of malaria vectors requires efficient sampling. The objective of this study was to compare methods for sampling outdoor-biting Anopheles mosquitoes in Cambodia. In the Cambodian provinces of Pursat, Preah Vihear, and Ratanakiri, six different mosquito trapping methods were evaluated: human landing collection (HLC), human-baited tent (HBT), cow-baited tent (CBT), CDC miniature light trap (LT), CDC miniature light trap baited with molasses and yeast (LT-M), and barrier fence (F) in a Latin square design during four or six consecutive nights at the height of the malaria transmission season. Using all traps, a total of 507, 1175, and 615 anophelines were collected in Pursat, Preah Vihear, and Ratanakiri, respectively. CBTs captured 10- to 20-fold more anophelines per night than the other five sampling methods. All 2297 Anopheles mosquitoes were morphologically identified and molecularly typed using standard morphological keys and sequencing the rDNA ITS2 region to distinguish cryptic species, respectively. Overall, an extremely diverse set of 27 known Anopheles species was sampled. CBTs captured the same molecular species that HLCs and the other four traps did, as well as additional species. Nine specimens representing five Anopheles species (Anopheles hyrcanus, Anopheles barbirostris sensu stricto, Anopheles barbirostris clade III, Anopheles nivipes, and Anopheles peditaeniatus) were infected with Plasmodium falciparum and were exclusively captured in CBTs.
Question: Are cow-baited tents highly effective in sampling diverse Anopheles malaria vectors in Cambodia?
Output:
|
PubmedQA81095
|
[
{
"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: Sustained shortening of the atrial effective refractory period (AERP), probably due to reduction in the L-type calcium current, is a major factor in the initiation and maintenance of atrial fibrillation (AF). We investigated underlying molecular changes by studying the relation between gene expression of the L-type calcium channel and potassium channels and AERP in patients with AF. mRNA and protein expression were determined in the left and right atrial appendages of patients with paroxysmal (n=13) or persistent (n=16) AF and of 13 controls in sinus rhythm using reverse transcription polymerase chain reaction and slot-blot, respectively. The mRNA content of almost all investigated ion channel genes was reduced in persistent but not in paroxysmal AF. Protein levels for the L-type Ca(2+) channel and 5 potassium channels (Kv4.3, Kv1.5, HERG, minK, and Kir3.1) were significantly reduced in both persistent and paroxysmal AF. Furthermore, AERPs were determined intraoperatively at 5 basic cycle lengths between 250 and 600 ms. Patients with persistent and paroxysmal AF displayed significant shorter AERPs. Protein levels of all ion channels investigated correlated positively with the AERP and with the rate adaptation of AERP. Patients with reduced ion channel protein expression had a shorter AERP duration and poorer rate adaptation.\n Question: Is ion channel remodeling related to intraoperative atrial effective refractory periods in patients with paroxysmal and persistent atrial fibrillation?\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: Sustained shortening of the atrial effective refractory period (AERP), probably due to reduction in the L-type calcium current, is a major factor in the initiation and maintenance of atrial fibrillation (AF). We investigated underlying molecular changes by studying the relation between gene expression of the L-type calcium channel and potassium channels and AERP in patients with AF. mRNA and protein expression were determined in the left and right atrial appendages of patients with paroxysmal (n=13) or persistent (n=16) AF and of 13 controls in sinus rhythm using reverse transcription polymerase chain reaction and slot-blot, respectively. The mRNA content of almost all investigated ion channel genes was reduced in persistent but not in paroxysmal AF. Protein levels for the L-type Ca(2+) channel and 5 potassium channels (Kv4.3, Kv1.5, HERG, minK, and Kir3.1) were significantly reduced in both persistent and paroxysmal AF. Furthermore, AERPs were determined intraoperatively at 5 basic cycle lengths between 250 and 600 ms. Patients with persistent and paroxysmal AF displayed significant shorter AERPs. Protein levels of all ion channels investigated correlated positively with the AERP and with the rate adaptation of AERP. Patients with reduced ion channel protein expression had a shorter AERP duration and poorer rate adaptation.
Question: Is ion channel remodeling related to intraoperative atrial effective refractory periods in patients with paroxysmal and persistent atrial fibrillation?
Output:
|
PubmedQA181948
|
[
{
"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: XIAP-associated factor 1 (XAF1) is ubiquitously expressed in normal tissues, but its suppression in cancer cells is strongly associated with tumor progression. Although downregulation of XAF1 is observed in tumors, its expression profile in the peripheral blood of cancer patients has not yet been investigated. Here, we identified a novel XAF1 splice variant in cancer cells and then investigated the expression level of this variant in peripheral blood containing gastric cancer-derived circulating tumor cells (CTCs). To identify splice variants, RT-PCR and DNA sequencing were performed in mRNAs extracted from many cancer cells. We then carried out quantitative RT-PCR to investigate expression in peripheral blood from all 96 gastric cancer patients and 22 healthy volunteers. The XAF1 variant harbored a premature termination codon (PTC) and was differentially expressed in highly metastatic cancer cells versus the parental cells, and that nonsense-mediated mRNA decay (NMD) was suppressed in the variant-expressing cells. Furthermore, splice variants of XAF1 were upregulated in peripheral blood containing CTCs. In XAF1 variant-expressing patients, the expression levels of other NMD-targeted genes also increased, suggesting that the NMD pathway was suppressed in CTCs.\n Question: Is a novel splice variant of XIAP-associated factor 1 ( XAF1 ) expressed in peripheral blood containing gastric cancer-derived circulating tumor cells?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: XIAP-associated factor 1 (XAF1) is ubiquitously expressed in normal tissues, but its suppression in cancer cells is strongly associated with tumor progression. Although downregulation of XAF1 is observed in tumors, its expression profile in the peripheral blood of cancer patients has not yet been investigated. Here, we identified a novel XAF1 splice variant in cancer cells and then investigated the expression level of this variant in peripheral blood containing gastric cancer-derived circulating tumor cells (CTCs). To identify splice variants, RT-PCR and DNA sequencing were performed in mRNAs extracted from many cancer cells. We then carried out quantitative RT-PCR to investigate expression in peripheral blood from all 96 gastric cancer patients and 22 healthy volunteers. The XAF1 variant harbored a premature termination codon (PTC) and was differentially expressed in highly metastatic cancer cells versus the parental cells, and that nonsense-mediated mRNA decay (NMD) was suppressed in the variant-expressing cells. Furthermore, splice variants of XAF1 were upregulated in peripheral blood containing CTCs. In XAF1 variant-expressing patients, the expression levels of other NMD-targeted genes also increased, suggesting that the NMD pathway was suppressed in CTCs.
Question: Is a novel splice variant of XIAP-associated factor 1 ( XAF1 ) expressed in peripheral blood containing gastric cancer-derived circulating tumor cells?
Output:
|
PubmedQA166736
|
[
{
"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 purposes of this study were to characterize the direct effect of the C-terminal fragment of fibrinogen gamma chain (gammaC) on microvascular endothelial permeability and to examine its molecular mechanism of action. Intravital microscopy was performed to measure albumin extravasation in intact mesenteric microvasculature, followed by quantification of hydraulic conductivity in single perfused microvessels. Transendothelial electric resistance was measured in microvascular endothelial cells in combination with immunoblotting and immunocytochemistry. The results show that gammaC induced time- and concentration-dependent increases in protein transvascular flux and water permeability and decreases in endothelial barrier function, coupled with Rho GTPase activation, myosin light chain phosphorylation, and stress fiber formation. Depletion of RhoA via siRNA knockdown or pharmacological inhibition of RhoA signaling attenuated gammaC-induced barrier dysfunction. Imaging analyses demonstrated binding of gammaC to endothelial cells; the interaction was inhibited during blockage of the alphavbeta3 integrin. Furthermore, in vivo experiments showed that the microvascular leak response to gammaC was attenuated in integrin beta3(-/-) animals.\n Question: Do fibrinogen-gamma C-terminal fragments induce endothelial barrier dysfunction and microvascular leak via integrin-mediated and RhoA-dependent mechanism?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: The purposes of this study were to characterize the direct effect of the C-terminal fragment of fibrinogen gamma chain (gammaC) on microvascular endothelial permeability and to examine its molecular mechanism of action. Intravital microscopy was performed to measure albumin extravasation in intact mesenteric microvasculature, followed by quantification of hydraulic conductivity in single perfused microvessels. Transendothelial electric resistance was measured in microvascular endothelial cells in combination with immunoblotting and immunocytochemistry. The results show that gammaC induced time- and concentration-dependent increases in protein transvascular flux and water permeability and decreases in endothelial barrier function, coupled with Rho GTPase activation, myosin light chain phosphorylation, and stress fiber formation. Depletion of RhoA via siRNA knockdown or pharmacological inhibition of RhoA signaling attenuated gammaC-induced barrier dysfunction. Imaging analyses demonstrated binding of gammaC to endothelial cells; the interaction was inhibited during blockage of the alphavbeta3 integrin. Furthermore, in vivo experiments showed that the microvascular leak response to gammaC was attenuated in integrin beta3(-/-) animals.
Question: Do fibrinogen-gamma C-terminal fragments induce endothelial barrier dysfunction and microvascular leak via integrin-mediated and RhoA-dependent mechanism?
Output:
|
PubmedQA187150
|
[
{
"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: Endothelin (ET) receptor antagonism reduces neointimal lesion formation in animal models. This investigation addressed the hypothesis that the selective ETA receptor antagonist sitaxentan would be more effective than mixed ETA / B receptor antagonism at inhibiting neointimal proliferation in a mouse model of intraluminal injury. Antagonism of ETA receptors by sitaxentan (1-100 nM) was assessed in femoral arteries isolated from adult, male C57Bl6 mice using isometric wire myography. Neointimal lesion development was induced by intraluminal injury in mice receiving sitaxentan (ETA antagonist; 15 mg·kg(-1) ·day(-1) ), A192621 (ETB antagonist; 30 mg·kg(-1) ·day(-1) ), the combination of both antagonists or vehicle. Treatment began 1 week before, and continued for 28 days after, surgery. Femoral arteries were then harvested for analysis of lesion size and composition. Sitaxentan produced a selective, concentration-dependent parallel rightward shift of ET-1-mediated contraction in isolated femoral arteries. Sitaxentan reduced neointimal lesion size, whereas ETB and combined ETA / B receptor antagonism did not. Macrophage and α-smooth muscle actin content were unaltered by ET receptor antagonism but sitaxentan reduced the amount of collagen in lesions.\n Question: Does selective endothelin A receptor antagonism with sitaxentan reduce neointimal lesion size in a mouse model of intraluminal injury?\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: Endothelin (ET) receptor antagonism reduces neointimal lesion formation in animal models. This investigation addressed the hypothesis that the selective ETA receptor antagonist sitaxentan would be more effective than mixed ETA / B receptor antagonism at inhibiting neointimal proliferation in a mouse model of intraluminal injury. Antagonism of ETA receptors by sitaxentan (1-100 nM) was assessed in femoral arteries isolated from adult, male C57Bl6 mice using isometric wire myography. Neointimal lesion development was induced by intraluminal injury in mice receiving sitaxentan (ETA antagonist; 15 mg·kg(-1) ·day(-1) ), A192621 (ETB antagonist; 30 mg·kg(-1) ·day(-1) ), the combination of both antagonists or vehicle. Treatment began 1 week before, and continued for 28 days after, surgery. Femoral arteries were then harvested for analysis of lesion size and composition. Sitaxentan produced a selective, concentration-dependent parallel rightward shift of ET-1-mediated contraction in isolated femoral arteries. Sitaxentan reduced neointimal lesion size, whereas ETB and combined ETA / B receptor antagonism did not. Macrophage and α-smooth muscle actin content were unaltered by ET receptor antagonism but sitaxentan reduced the amount of collagen in lesions.
Question: Does selective endothelin A receptor antagonism with sitaxentan reduce neointimal lesion size in a mouse model of intraluminal injury?
Output:
|
PubmedQA143698
|
[
{
"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: Acutely ischemic limbs are often of uncertain viability. To assist operative management, this study determined prospectively which indicators on admission were the best predictors of major amputation and, conversely, limb preservation. Data were collected on admission. Presenting complaint, history, clinical assessment, and blood test results, including creatine kinase (CK), were recorded. Surgical procedures were noted-in particular, the presence or absence of major amputation by death or discharge. The setting was a tertiary vascular referral center in a university teaching hospital. Subjects included all patients referred as emergency cases to the vascular unit over an 18-month period who were admitted for inpatient management with acute lower limb ischemia. The main outcome measure was major amputation. A total of 97 patients with acute ischemia were studied prospectively (51 men and 46 women). Twenty-one patients (21.6%) underwent major amputation. Previous vascular surgery (P = .012), mottling (P = .001), sensory loss (P = .003), motor loss (P = .001), muscle tenderness (P < .001), absent ankle Doppler signals (P = .008), neutrophilia (P = .011), and increased CK (P < .001) were significantly associated with major amputation. If CK was normal, the risk of major amputation was 4.6% (95% confidence interval, 0.0%-9.7%). If CK was increased, the risk was 56.2% (95% CI, 39.1%-73.4%).\n Question: Does plasma creatine kinase indicate major amputation or limb preservation in acute lower limb ischemia?\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: Acutely ischemic limbs are often of uncertain viability. To assist operative management, this study determined prospectively which indicators on admission were the best predictors of major amputation and, conversely, limb preservation. Data were collected on admission. Presenting complaint, history, clinical assessment, and blood test results, including creatine kinase (CK), were recorded. Surgical procedures were noted-in particular, the presence or absence of major amputation by death or discharge. The setting was a tertiary vascular referral center in a university teaching hospital. Subjects included all patients referred as emergency cases to the vascular unit over an 18-month period who were admitted for inpatient management with acute lower limb ischemia. The main outcome measure was major amputation. A total of 97 patients with acute ischemia were studied prospectively (51 men and 46 women). Twenty-one patients (21.6%) underwent major amputation. Previous vascular surgery (P = .012), mottling (P = .001), sensory loss (P = .003), motor loss (P = .001), muscle tenderness (P < .001), absent ankle Doppler signals (P = .008), neutrophilia (P = .011), and increased CK (P < .001) were significantly associated with major amputation. If CK was normal, the risk of major amputation was 4.6% (95% confidence interval, 0.0%-9.7%). If CK was increased, the risk was 56.2% (95% CI, 39.1%-73.4%).
Question: Does plasma creatine kinase indicate major amputation or limb preservation in acute lower limb ischemia?
Output:
|
PubmedQA174896
|
[
{
"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: Neural stem cell (NSC) differentiation is a complex multistep process that persists in specific regions of the postnatal forebrain and requires tight regulation throughout life. The transcriptional control of NSC proliferation and specification involves Class II (proneural) and Class V (Id1-4) basic helix-loop-helix (bHLH) proteins. In this study, we analyzed the pattern of expression of their dimerization partners, Class I bHLH proteins (E-proteins), and explored their putative role in orchestrating postnatal subventricular zone (SVZ) neurogenesis. Overexpression of a dominant-negative form of the E-protein E47 (dnE47) confirmed a crucial role for bHLH transcriptional networks in postnatal neurogenesis by dramatically blocking SVZ NSC differentiation. In situ hybridization was used in combination with RT-qPCR to measure and compare the level of expression of E-protein transcripts (E2-2, E2A, and HEB) in the neonatal and adult SVZ as well as in magnetic affinity cell sorted progenitor cells and neuroblasts. Our results evidence that E-protein transcripts, in particular E2-2 and E2A, are enriched in the postnatal SVZ with expression levels increasing as cells engage towards neuronal differentiation. To investigate the role of E-proteins in orchestrating lineage progression, both in vitro and in vivo gain-of-function and loss-of-function experiments were performed for individual E-proteins. Overexpression of E2-2 and E2A promoted SVZ neurogenesis by enhancing not only radial glial cell differentiation but also cell cycle exit of their progeny. Conversely, knock-down by shRNA electroporation resulted in opposite effects. Manipulation of E-proteins and/or Ascl1 in SVZ NSC cultures indicated that those effects were Ascl1 dependent, although they could not solely be attributed to an Ascl1-induced switch from promoting cell proliferation to triggering cell cycle arrest and differentiation.\n Question: Do e-proteins orchestrate the progression of neural stem cell differentiation in the postnatal forebrain?\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: Neural stem cell (NSC) differentiation is a complex multistep process that persists in specific regions of the postnatal forebrain and requires tight regulation throughout life. The transcriptional control of NSC proliferation and specification involves Class II (proneural) and Class V (Id1-4) basic helix-loop-helix (bHLH) proteins. In this study, we analyzed the pattern of expression of their dimerization partners, Class I bHLH proteins (E-proteins), and explored their putative role in orchestrating postnatal subventricular zone (SVZ) neurogenesis. Overexpression of a dominant-negative form of the E-protein E47 (dnE47) confirmed a crucial role for bHLH transcriptional networks in postnatal neurogenesis by dramatically blocking SVZ NSC differentiation. In situ hybridization was used in combination with RT-qPCR to measure and compare the level of expression of E-protein transcripts (E2-2, E2A, and HEB) in the neonatal and adult SVZ as well as in magnetic affinity cell sorted progenitor cells and neuroblasts. Our results evidence that E-protein transcripts, in particular E2-2 and E2A, are enriched in the postnatal SVZ with expression levels increasing as cells engage towards neuronal differentiation. To investigate the role of E-proteins in orchestrating lineage progression, both in vitro and in vivo gain-of-function and loss-of-function experiments were performed for individual E-proteins. Overexpression of E2-2 and E2A promoted SVZ neurogenesis by enhancing not only radial glial cell differentiation but also cell cycle exit of their progeny. Conversely, knock-down by shRNA electroporation resulted in opposite effects. Manipulation of E-proteins and/or Ascl1 in SVZ NSC cultures indicated that those effects were Ascl1 dependent, although they could not solely be attributed to an Ascl1-induced switch from promoting cell proliferation to triggering cell cycle arrest and differentiation.
Question: Do e-proteins orchestrate the progression of neural stem cell differentiation in the postnatal forebrain?
Output:
|
PubmedQA169772
|
[
{
"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 tumor suppressor gene p53 has been shown to transcriptionally regulate expression of the cell cycle dependent kinase inhibitor p21. p53 is in turn regulated by the ubiquitin ligase mouse double minute-2 (mdm-2). We have set out to examine p21 expression in testicular germ cell tumors and its relationship with p53 and mdm-2 expression. Immunohistochemical analysis was performed on formalin-fixed paraffin-embedded tissue for p53, p21, and mdm-2 in 31 testicular germ cell tumors, which included 17 pure seminomas and 14 mixed germ cell tumors composed predominantly of embryonal carcinoma. Twenty-seven cases contained adjacent areas of intratubular germ cell neoplasia (ITGCN). 17 out of 17 seminomas and 14 out of 14 embryonal carcinomas expressed p53 in both ITGCN and the invasive tumor. In contrast, none of the 17 seminomas and only 2 of 14 embryonal carcinomas revealed positive staining for p21 protein. p21 expression was noted in 18 of 27 cases (67%) of ITGCN, and in 16 of these cases (89%) the corresponding invasive tumor had lost p21 expression. In nine additional cases p21 expression was absent in both the invasive and intratubular tumor. mdm-2 expression was present in 8 out of 17 (47%) seminomas and 13 out of 14 (93%) embryonal carcinomas but was present in only 2 out of 27 (7%) cases of ITGCN. Statistically significant associations for loss of p21 and gain of mdm-2 expression in invasive tumors were present (P < .0001).\n Question: Is transition from in situ to invasive testicular germ cell neoplasia associated with the loss of p21 and gain of mdm-2 expression?\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 tumor suppressor gene p53 has been shown to transcriptionally regulate expression of the cell cycle dependent kinase inhibitor p21. p53 is in turn regulated by the ubiquitin ligase mouse double minute-2 (mdm-2). We have set out to examine p21 expression in testicular germ cell tumors and its relationship with p53 and mdm-2 expression. Immunohistochemical analysis was performed on formalin-fixed paraffin-embedded tissue for p53, p21, and mdm-2 in 31 testicular germ cell tumors, which included 17 pure seminomas and 14 mixed germ cell tumors composed predominantly of embryonal carcinoma. Twenty-seven cases contained adjacent areas of intratubular germ cell neoplasia (ITGCN). 17 out of 17 seminomas and 14 out of 14 embryonal carcinomas expressed p53 in both ITGCN and the invasive tumor. In contrast, none of the 17 seminomas and only 2 of 14 embryonal carcinomas revealed positive staining for p21 protein. p21 expression was noted in 18 of 27 cases (67%) of ITGCN, and in 16 of these cases (89%) the corresponding invasive tumor had lost p21 expression. In nine additional cases p21 expression was absent in both the invasive and intratubular tumor. mdm-2 expression was present in 8 out of 17 (47%) seminomas and 13 out of 14 (93%) embryonal carcinomas but was present in only 2 out of 27 (7%) cases of ITGCN. Statistically significant associations for loss of p21 and gain of mdm-2 expression in invasive tumors were present (P < .0001).
Question: Is transition from in situ to invasive testicular germ cell neoplasia associated with the loss of p21 and gain of mdm-2 expression?
Output:
|
PubmedQA14913
|
[
{
"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 correlation between gait speed and strength in multiple sclerosis (MS) with particular regard to patients presenting with proprioceptive loss. Gait evaluation and isokinetic testing of muscular function were performed in 20 patients with unaided gait (expanded disability status scale < 6). Patients were separated into two groups in relation to the occurrence of somatosensory involvement: pyramidal group (8 patients) and sensory-pyramidal group (12 patients). Ten healthy subjects of similar age, sex, and height constituted a control group to evaluate gait parameters. In the whole patient group, gait speed was reduced and strongly related to hamstring peak torque but not with quadriceps peak torque. The gait speed and peak torques of quadriceps and hamstrings were similar in both groups of patients. However, in the patients with proprioceptive loss there was both a strong correlation between gait speed and hamstring torque and a significant correlation with quadriceps torque. In the pyramidal group there was poor or no correlation.\n Question: Is relation between walking speed and muscle strength affected by somatosensory loss in multiple sclerosis?\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 correlation between gait speed and strength in multiple sclerosis (MS) with particular regard to patients presenting with proprioceptive loss. Gait evaluation and isokinetic testing of muscular function were performed in 20 patients with unaided gait (expanded disability status scale < 6). Patients were separated into two groups in relation to the occurrence of somatosensory involvement: pyramidal group (8 patients) and sensory-pyramidal group (12 patients). Ten healthy subjects of similar age, sex, and height constituted a control group to evaluate gait parameters. In the whole patient group, gait speed was reduced and strongly related to hamstring peak torque but not with quadriceps peak torque. The gait speed and peak torques of quadriceps and hamstrings were similar in both groups of patients. However, in the patients with proprioceptive loss there was both a strong correlation between gait speed and hamstring torque and a significant correlation with quadriceps torque. In the pyramidal group there was poor or no correlation.
Question: Is relation between walking speed and muscle strength affected by somatosensory loss in multiple sclerosis?
Output:
|
PubmedQA94766
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: We investigated the risk of amnestic mild cognitive impairment (aMCI) in relation to serum bioavailable (BT) and total testosterone (TT) levels in older men. A cross-sectional study in an ambulatory setting, with older men aged 55-93 years with normal cognition, aMCI and Alzheimer's disease (AD). Morning serum BT and TT levels were determined. AD was diagnosed by the Neurological and Communicative Disorders and Stroke/Alzheimer's Disease and Related Disorders Association (NINCDS-ADRDA) criteria for probable AD and aMCI by the Petersen criteria. We recruited 203 Chinese older men (48 aMCI, 66 AD and 89 with normal cognition). Mean serum BT, but not TT, levels were significantly lower in the aMCI (mean BT +/- SEM 1.06 +/- 0.10 nmol/l) and AD (0.99 +/- 0.08 nmol/l) groups than in the normal controls (1.82 +/- 0.12 nmol/l) (P < 0.001, one-way anova) with no significant difference between the aMCI and AD groups. After adjustment for education, age and apolipoprotein E (apoE) genotype, logistic regression analyses showed that the serum BT level [adjusted odds ratio (OR) = 0.52, 95% confidence interval (CI) 0.32-0.85] was an independent protective factor for aMCI. For the combined outcome of aMCI and AD, the serum BT level was an independent protective factor but age and apoE epsilon4 were independent risk factors. There was no interaction between BT and age.\n Question: Is bioavailable testosterone associated with a reduced risk of amnestic mild cognitive impairment in older 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: We investigated the risk of amnestic mild cognitive impairment (aMCI) in relation to serum bioavailable (BT) and total testosterone (TT) levels in older men. A cross-sectional study in an ambulatory setting, with older men aged 55-93 years with normal cognition, aMCI and Alzheimer's disease (AD). Morning serum BT and TT levels were determined. AD was diagnosed by the Neurological and Communicative Disorders and Stroke/Alzheimer's Disease and Related Disorders Association (NINCDS-ADRDA) criteria for probable AD and aMCI by the Petersen criteria. We recruited 203 Chinese older men (48 aMCI, 66 AD and 89 with normal cognition). Mean serum BT, but not TT, levels were significantly lower in the aMCI (mean BT +/- SEM 1.06 +/- 0.10 nmol/l) and AD (0.99 +/- 0.08 nmol/l) groups than in the normal controls (1.82 +/- 0.12 nmol/l) (P < 0.001, one-way anova) with no significant difference between the aMCI and AD groups. After adjustment for education, age and apolipoprotein E (apoE) genotype, logistic regression analyses showed that the serum BT level [adjusted odds ratio (OR) = 0.52, 95% confidence interval (CI) 0.32-0.85] was an independent protective factor for aMCI. For the combined outcome of aMCI and AD, the serum BT level was an independent protective factor but age and apoE epsilon4 were independent risk factors. There was no interaction between BT and age.
Question: Is bioavailable testosterone associated with a reduced risk of amnestic mild cognitive impairment in older men?
Output:
|
PubmedQA63344
|
[
{
"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: Infection with hepatitis B virus (HBV) is the most common cause of liver disease worldwide. However, because the current interferon (IFN)-based treatments have toxic side effects and marginal efficacy, improved antivirals are essential. Here we report that unmethylated cytosine-phosphate-guanosine oligodeoxynucleotides (CpG ODNs) from the HBV genome (HBV-CpG) induced robust expression of IFN-α by plasmacytoid dendritic cells (pDCs) in a Toll-like receptor 9 (TLR9)-dependent manner. We also identified inhibitory guanosine-rich ODNs in the HBV genome (HBV-ODN) that are capable of inhibiting HBV-CpG-induced IFN-α production. Furthermore, nanoparticles containing HBV-CpG, termed NP(HBV-CpG), reversed the HBV-ODN-mediated suppression of IFN-α production and also exerted a strong immunostimulatory effect on lymphocytes. Our results suggest that NP(HBV-CpG) can enhance the immune response to hepatitis B surface antigen (HBsAg) and skew this response toward the Th1 pathway in mice immunized with rHBsAg and NP(HBV-CpG). Moreover, NP(HBV-CpG)-based therapy led to the efficient clearance of HBV and induced an anti-HBsAg response in HBV carrier mice.\n Question: Do nanoparticles encapsulating hepatitis B virus cytosine-phosphate-guanosine induce therapeutic immunity against HBV infection?\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: Infection with hepatitis B virus (HBV) is the most common cause of liver disease worldwide. However, because the current interferon (IFN)-based treatments have toxic side effects and marginal efficacy, improved antivirals are essential. Here we report that unmethylated cytosine-phosphate-guanosine oligodeoxynucleotides (CpG ODNs) from the HBV genome (HBV-CpG) induced robust expression of IFN-α by plasmacytoid dendritic cells (pDCs) in a Toll-like receptor 9 (TLR9)-dependent manner. We also identified inhibitory guanosine-rich ODNs in the HBV genome (HBV-ODN) that are capable of inhibiting HBV-CpG-induced IFN-α production. Furthermore, nanoparticles containing HBV-CpG, termed NP(HBV-CpG), reversed the HBV-ODN-mediated suppression of IFN-α production and also exerted a strong immunostimulatory effect on lymphocytes. Our results suggest that NP(HBV-CpG) can enhance the immune response to hepatitis B surface antigen (HBsAg) and skew this response toward the Th1 pathway in mice immunized with rHBsAg and NP(HBV-CpG). Moreover, NP(HBV-CpG)-based therapy led to the efficient clearance of HBV and induced an anti-HBsAg response in HBV carrier mice.
Question: Do nanoparticles encapsulating hepatitis B virus cytosine-phosphate-guanosine induce therapeutic immunity against HBV infection?
Output:
|
PubmedQA118051
|
[
{
"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: Resistin-like molecule alpha or found in inflammatory zone protein (Fizz1) is increased in pulmonary epithelial cells and also in limited amounts by other lung cells during various lung injuries and fibrosis. However, the direct role of Fizz1 produced in the pulmonary epithelium has not been determined. Fizz1 Transgenic mice (CCSP/Fizz1) were generated that overexpress Fizz1 in the lung epithelium under the control of a doxycycline (Dox) inducible lung epithelial cell specific promoter Scgb1a1 (Clara cell secretory protein, CCSP). Histology and FACS analysis of lung cells were used to identify the direct effects of Fizz1 in the transgenic mice (Dox treated) when compared with control (CCSP/-) mice. Intratracheal bleomycin sulfate or silica in saline and saline alone were used to study the role of Fizz1 during bleomycin- and silica-induced pulmonary fibrosis in CCSP/Fizz1 and CCSP/- mice. Weight change, pulmonary inflammation, and fibrosis were assessed 10 days post bleomycin or 28 days post silica challenge. When CCSP/Fizz1 mice were fed Dox food, elevated Fizz1 protein was detected in lung homogenates by western blot. Lungs of mice in which Fizz1 was induced in the epithelium contained increased lung cells staining for CD11c and F4/80 by FACS analysis consistent with increased dendritic cells however, no changes were observed in the percentage of interstitial macrophages compared to CCSP/- controls. No significant changes were found in the lung histology of CCSP/Fizz1 mice after up to 8 weeks of overexpression compared to CCSP/- controls. Overexpression of Fizz1 prior to challenge or following challenge with bleomycin or silica did not significantly alter airway inflammation or fibrosis compared to control mice.\n Question: Does resistin-like molecule α1 ( Fizz1 ) recruit lung dendritic cells without causing pulmonary fibrosis?\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: Resistin-like molecule alpha or found in inflammatory zone protein (Fizz1) is increased in pulmonary epithelial cells and also in limited amounts by other lung cells during various lung injuries and fibrosis. However, the direct role of Fizz1 produced in the pulmonary epithelium has not been determined. Fizz1 Transgenic mice (CCSP/Fizz1) were generated that overexpress Fizz1 in the lung epithelium under the control of a doxycycline (Dox) inducible lung epithelial cell specific promoter Scgb1a1 (Clara cell secretory protein, CCSP). Histology and FACS analysis of lung cells were used to identify the direct effects of Fizz1 in the transgenic mice (Dox treated) when compared with control (CCSP/-) mice. Intratracheal bleomycin sulfate or silica in saline and saline alone were used to study the role of Fizz1 during bleomycin- and silica-induced pulmonary fibrosis in CCSP/Fizz1 and CCSP/- mice. Weight change, pulmonary inflammation, and fibrosis were assessed 10 days post bleomycin or 28 days post silica challenge. When CCSP/Fizz1 mice were fed Dox food, elevated Fizz1 protein was detected in lung homogenates by western blot. Lungs of mice in which Fizz1 was induced in the epithelium contained increased lung cells staining for CD11c and F4/80 by FACS analysis consistent with increased dendritic cells however, no changes were observed in the percentage of interstitial macrophages compared to CCSP/- controls. No significant changes were found in the lung histology of CCSP/Fizz1 mice after up to 8 weeks of overexpression compared to CCSP/- controls. Overexpression of Fizz1 prior to challenge or following challenge with bleomycin or silica did not significantly alter airway inflammation or fibrosis compared to control mice.
Question: Does resistin-like molecule α1 ( Fizz1 ) recruit lung dendritic cells without causing pulmonary fibrosis?
Output:
|
PubmedQA109043
|
[
{
"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: Eosinophilic esophagitis (EE) is a clinical entity that is recognized increasingly in children. The treatment of EE has been debated since its identification as a clinical entity separate from reflux esophagitis. We hypothesize that the treatment with a high-dose proton pump inhibitor (HDPPI) helps differentiate EE from noneosinophilic esophagitis (NEE). Retrospective review of 2221 patients who underwent esophagogastroduodenoscopy (EGD) with biopsies was undertaken. Sixty-nine patients had more than or equal to 15 eosinophils/high-power field (eos/HPF) in 1 or more esophageal levels. Of those, 36 were initially treated with HDPPI for 3 months followed by repeat EGD. Patients who demonstrated histologic response were classified as NEE. Patients with no histologic response were diagnosed as having EE and treated with HDPPI+swallowed fluticasone for 3 months followed by repeat EGD. Of the 36 patients, histologic response was seen in 14 (39%) after treatment with HDPPI; 95% confidence interval (0.23-0.54). Swallowed fluticasone was added to the treatment of the 22 patients who did not show histologic response to HDPPI alone. Of those, 15 patients underwent repeat endoscopies. Seven patients were lost to follow-up or did not have repeated EGDs. Histologic response was observed in 9 of 15 (60%) patients. Of the nonresponders (6 of 15), 5 of 6 (83%) self-reported noncompliance with the swallowed fluticasone. Patients with more than or equal to 15 eos/HPF at all 3 levels (25 of 36) were less likely to respond to HDPPI alone and more likely to be categorized as EE (18 of 25), P=or<0.043. Symptomatically, 28 of 36 patients reported resolution of symptoms after HDPPI therapy alone, P=or<0.0001, regardless of histology. Visual endoscopic findings during the first and second EGDs did not show any significance in differentiating EE from NEE, P=0.625 and P=0.2405, respectively.\n Question: Does treatment with high-dose proton pump inhibitors help distinguish eosinophilic esophagitis from noneosinophilic esophagitis?\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: Eosinophilic esophagitis (EE) is a clinical entity that is recognized increasingly in children. The treatment of EE has been debated since its identification as a clinical entity separate from reflux esophagitis. We hypothesize that the treatment with a high-dose proton pump inhibitor (HDPPI) helps differentiate EE from noneosinophilic esophagitis (NEE). Retrospective review of 2221 patients who underwent esophagogastroduodenoscopy (EGD) with biopsies was undertaken. Sixty-nine patients had more than or equal to 15 eosinophils/high-power field (eos/HPF) in 1 or more esophageal levels. Of those, 36 were initially treated with HDPPI for 3 months followed by repeat EGD. Patients who demonstrated histologic response were classified as NEE. Patients with no histologic response were diagnosed as having EE and treated with HDPPI+swallowed fluticasone for 3 months followed by repeat EGD. Of the 36 patients, histologic response was seen in 14 (39%) after treatment with HDPPI; 95% confidence interval (0.23-0.54). Swallowed fluticasone was added to the treatment of the 22 patients who did not show histologic response to HDPPI alone. Of those, 15 patients underwent repeat endoscopies. Seven patients were lost to follow-up or did not have repeated EGDs. Histologic response was observed in 9 of 15 (60%) patients. Of the nonresponders (6 of 15), 5 of 6 (83%) self-reported noncompliance with the swallowed fluticasone. Patients with more than or equal to 15 eos/HPF at all 3 levels (25 of 36) were less likely to respond to HDPPI alone and more likely to be categorized as EE (18 of 25), P=or<0.043. Symptomatically, 28 of 36 patients reported resolution of symptoms after HDPPI therapy alone, P=or<0.0001, regardless of histology. Visual endoscopic findings during the first and second EGDs did not show any significance in differentiating EE from NEE, P=0.625 and P=0.2405, respectively.
Question: Does treatment with high-dose proton pump inhibitors help distinguish eosinophilic esophagitis from noneosinophilic esophagitis?
Output:
|
PubmedQA148884
|
[
{
"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: Insurers often seek to direct esophageal cancer patients to hospitals with high volumes of esophageal resection. However, controversy exists regarding the strength and validity of evidence for the volume-outcome association. The purpose of this study was to evaluate the volume-outcome relationship for esophageal cancer resection in a large population dataset and to compare 3alternative techniques for measuring the effect of volume. Esophageal cancer resection patients were identified in the 2007 Nationwide Inpatient Sample. Hospital volume was measured using a continuous linear function, a nonlinear function using restricted cubic splines, and using quintiles of volume. The statistical significance of the relationship between hospital volume and mortality risk was assessed, and adjusted for patient age, for comorbid disease, and for correlated events within hospitals. A total of 6,248 esophageal cancer resection patients from 217 hospitals were identified. All 3 models demonstrated excellent performance characteristics (C index=0.94, Nagelkerke R2=0.62). However, no significant association was demonstrated between hospital procedure volume and in-hospital mortality in any model. Important predictors of mortality included age, hypertension, weight loss, and peripheral vascular disease (p<0.001).\n Question: Does hospital esophageal cancer resection volume predict patient mortality risk?\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: Insurers often seek to direct esophageal cancer patients to hospitals with high volumes of esophageal resection. However, controversy exists regarding the strength and validity of evidence for the volume-outcome association. The purpose of this study was to evaluate the volume-outcome relationship for esophageal cancer resection in a large population dataset and to compare 3alternative techniques for measuring the effect of volume. Esophageal cancer resection patients were identified in the 2007 Nationwide Inpatient Sample. Hospital volume was measured using a continuous linear function, a nonlinear function using restricted cubic splines, and using quintiles of volume. The statistical significance of the relationship between hospital volume and mortality risk was assessed, and adjusted for patient age, for comorbid disease, and for correlated events within hospitals. A total of 6,248 esophageal cancer resection patients from 217 hospitals were identified. All 3 models demonstrated excellent performance characteristics (C index=0.94, Nagelkerke R2=0.62). However, no significant association was demonstrated between hospital procedure volume and in-hospital mortality in any model. Important predictors of mortality included age, hypertension, weight loss, and peripheral vascular disease (p<0.001).
Question: Does hospital esophageal cancer resection volume predict patient mortality risk?
Output:
|
PubmedQA141601
|
[
{
"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 degree and the determinants of peritoneal homocysteine (Hcy) clearance and to compare measured Hcy clearance with the Hcy clearance predicted based on molecular weight (MW). Cross-sectional observational analysis. Tertiary care institutional dialysis center. Sixty-five stable peritoneal dialysis (PD) patients. Fasting blood and 24-hour pooled dialysate effluents were collected for determination of peritoneal clearances of Hcy (CpHcy), urea (CpUr), and creatinine (CpCr). The dialysate-to-plasma creatinine ratio at 4 hours (D/P Cr 4 h) and levels of red cell folate, B12, ferritin, and C-reactive protein (CRP) were measured concurrently. Observed CpHcy was compared with predicted clearance, based on Hcy plasma protein binding and the relative molecular weights of Hcy, urea, and creatinine. Plasma concentrations of Hcy averaged 24.6 +/- 1.1 micromol/L and were elevated above the upper limit of normal in 59 (91%) patients. The mean dialysate concentration of Hcy was 2.9 +/- 0.3 micromol/L, equating to a daily peritoneal elimination of 34.6 +/- 3.6 micromol. Observed CpHcy was closely approximated by predicted CpHcy (8.7 +/- 0.6 L/week/1.73 m2 vs 9.0 +/- 0.3 L/week/1.73 m2 respectively, p = 0.55). Patients maintained on automated PD (n = 5) had a CpHcy similar to that of patients treated with continuous ambulatory peritoneal dialysis (8.9 +/- 1.0 L/week/1.73 m2 vs 8.7 +/- 0.6 L/week/1.73 m2, p = 0.92). The CpHcy was significantly correlated with C-reactive protein (CRP), D/P creatinine, CpUr, CpCr, and peritoneal protein loss, but not with plasma Hcy, albumin, B12, ferritin, age, dialysis duration, peritonitis episodes, or daily dialysate effluent volume. By multivariate analysis, the only variables that remained significant independent predictors of CpHcy were CRP and D/P Cr 4 h. High and high-average transporters had a higher CpHcy than low and low-average transporters (9.7 +/- 0.8 L/week/1.73 m2 vs 7.0 +/- 0.7 L/week/1.73 m2, p < 0.05), despite comparably elevated plasma Hcy concentrations [25.2 +/- 1.5 micromol/L vs 23.4 +/- 1.6 micromol/L, p = nonsignificant (NS)].\n Question: Is peritoneal homocysteine clearance inefficient in peritoneal dialysis 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: To investigate the degree and the determinants of peritoneal homocysteine (Hcy) clearance and to compare measured Hcy clearance with the Hcy clearance predicted based on molecular weight (MW). Cross-sectional observational analysis. Tertiary care institutional dialysis center. Sixty-five stable peritoneal dialysis (PD) patients. Fasting blood and 24-hour pooled dialysate effluents were collected for determination of peritoneal clearances of Hcy (CpHcy), urea (CpUr), and creatinine (CpCr). The dialysate-to-plasma creatinine ratio at 4 hours (D/P Cr 4 h) and levels of red cell folate, B12, ferritin, and C-reactive protein (CRP) were measured concurrently. Observed CpHcy was compared with predicted clearance, based on Hcy plasma protein binding and the relative molecular weights of Hcy, urea, and creatinine. Plasma concentrations of Hcy averaged 24.6 +/- 1.1 micromol/L and were elevated above the upper limit of normal in 59 (91%) patients. The mean dialysate concentration of Hcy was 2.9 +/- 0.3 micromol/L, equating to a daily peritoneal elimination of 34.6 +/- 3.6 micromol. Observed CpHcy was closely approximated by predicted CpHcy (8.7 +/- 0.6 L/week/1.73 m2 vs 9.0 +/- 0.3 L/week/1.73 m2 respectively, p = 0.55). Patients maintained on automated PD (n = 5) had a CpHcy similar to that of patients treated with continuous ambulatory peritoneal dialysis (8.9 +/- 1.0 L/week/1.73 m2 vs 8.7 +/- 0.6 L/week/1.73 m2, p = 0.92). The CpHcy was significantly correlated with C-reactive protein (CRP), D/P creatinine, CpUr, CpCr, and peritoneal protein loss, but not with plasma Hcy, albumin, B12, ferritin, age, dialysis duration, peritonitis episodes, or daily dialysate effluent volume. By multivariate analysis, the only variables that remained significant independent predictors of CpHcy were CRP and D/P Cr 4 h. High and high-average transporters had a higher CpHcy than low and low-average transporters (9.7 +/- 0.8 L/week/1.73 m2 vs 7.0 +/- 0.7 L/week/1.73 m2, p < 0.05), despite comparably elevated plasma Hcy concentrations [25.2 +/- 1.5 micromol/L vs 23.4 +/- 1.6 micromol/L, p = nonsignificant (NS)].
Question: Is peritoneal homocysteine clearance inefficient in peritoneal dialysis patients?
Output:
|
PubmedQA4677
|
[
{
"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 determine the sites of local recurrence following radical (R0) total mesorectal excision (TME) for rectal cancer in an effort to elucidate the reasons for recurrence. Thirty-seven patients with recurrence following curative resection for rectal cancer were identified from a population of 880 patients operated on by surgeons trained in the TME procedure. Two radiologists independently examined 33 available computed tomograms and magnetic resonance images taken when the recurrence was detected. Twenty-nine of the 33 recurrences were found in the lower two-thirds of the pelvis. Two recurrent tumours appeared to originate from lateral pelvic lymph nodes. Evidence of residual mesorectal fat was identified in 15 patients. Fourteen of the recurrent tumours originated from primary tumours in the upper rectum; all of these tumours recurred at the anastomosis and 12 of the 14 patients had evidence of residual mesorectal fat.\n Question: Do radiological findings support lateral residual tumour as a major cause of local recurrence of rectal cancer?\n Output: "
},
{
"role": "assistant",
"content": "no"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: The aim of this study was to determine the sites of local recurrence following radical (R0) total mesorectal excision (TME) for rectal cancer in an effort to elucidate the reasons for recurrence. Thirty-seven patients with recurrence following curative resection for rectal cancer were identified from a population of 880 patients operated on by surgeons trained in the TME procedure. Two radiologists independently examined 33 available computed tomograms and magnetic resonance images taken when the recurrence was detected. Twenty-nine of the 33 recurrences were found in the lower two-thirds of the pelvis. Two recurrent tumours appeared to originate from lateral pelvic lymph nodes. Evidence of residual mesorectal fat was identified in 15 patients. Fourteen of the recurrent tumours originated from primary tumours in the upper rectum; all of these tumours recurred at the anastomosis and 12 of the 14 patients had evidence of residual mesorectal fat.
Question: Do radiological findings support lateral residual tumour as a major cause of local recurrence of rectal cancer?
Output:
|
PubmedQA99814
|
[
{
"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: Although caffeine enhances respiratory control and decreases the need for mechanical ventilation and resultant bronchopulmonary dysplasia, it may also have anti-inflammatory properties in protecting lung function. We hypothesized that caffeine improves respiratory function via an anti-inflammatory effect in lungs of a lipopolysaccharide (LPS)-induced pro-inflammatory amnionitis rat pup model. Caffeine was given orally (10 mg/kg/day) from postnatal day (p)1 to p14 to pups exposed to intra-amniotic LPS or normal saline. Expression of IL-1β was assessed in lung homogenates at p8 and p14, and respiratory system resistance (Rrs) and compliance (Crs) as well as CD68 cell counts and radial alveolar counts were assessed at p8. In LPS-exposed rats, IL-1β and CD68 cell counts both increased at p8 compared to normal saline controls. These increases in pro-inflammatory markers were no longer present in caffeine-treated LPS-exposed pups. Rrs was higher in LPS-exposed pups (4.7 ± 0.9 cm H2O/ml·s) at p8 versus controls (1.6 ± 0.3 cm H2O/ml·s, p < 0.01). LPS-exposed pups no longer exhibited a significant increase in Rrs (2.8 ± 0.5 cm H2O/ml·s) after caffeine. Crs did not differ significantly between groups, although radial alveolar counts were lower in both groups of LPS-exposed pups.\n Question: Is anti-inflammatory effect of caffeine associated with improved lung function after lipopolysaccharide-induced amnionitis?\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: Although caffeine enhances respiratory control and decreases the need for mechanical ventilation and resultant bronchopulmonary dysplasia, it may also have anti-inflammatory properties in protecting lung function. We hypothesized that caffeine improves respiratory function via an anti-inflammatory effect in lungs of a lipopolysaccharide (LPS)-induced pro-inflammatory amnionitis rat pup model. Caffeine was given orally (10 mg/kg/day) from postnatal day (p)1 to p14 to pups exposed to intra-amniotic LPS or normal saline. Expression of IL-1β was assessed in lung homogenates at p8 and p14, and respiratory system resistance (Rrs) and compliance (Crs) as well as CD68 cell counts and radial alveolar counts were assessed at p8. In LPS-exposed rats, IL-1β and CD68 cell counts both increased at p8 compared to normal saline controls. These increases in pro-inflammatory markers were no longer present in caffeine-treated LPS-exposed pups. Rrs was higher in LPS-exposed pups (4.7 ± 0.9 cm H2O/ml·s) at p8 versus controls (1.6 ± 0.3 cm H2O/ml·s, p < 0.01). LPS-exposed pups no longer exhibited a significant increase in Rrs (2.8 ± 0.5 cm H2O/ml·s) after caffeine. Crs did not differ significantly between groups, although radial alveolar counts were lower in both groups of LPS-exposed pups.
Question: Is anti-inflammatory effect of caffeine associated with improved lung function after lipopolysaccharide-induced amnionitis?
Output:
|
PubmedQA179691
|
[
{
"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: Through maternal inheritance, to explore the genetic structures and relationships of Dong, Gelao, Tujia and Yi ethnic population in Guizhou of China. The mtDNA D-loop hypervariable segment I (HVS I ) in 108 samples of four ethnic populations were sequenced. Then, the nucleotide diversity was estimated and a phylogenetic tree was constructed by Neighbor-Joining method. In the detected 497 bp fragments, 86 polymorphic sites were found, and 82 different haplotypes were identified. The phylogenetic tree of four ethnic populations showed: Yi, Tujia and Gelao clustered more closely than Dong did.\n Question: Is [ The genetic relation of four ethnic populations in China 's Guizhou revealed by sequence variations of mtDNA D-loop ]?\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: Through maternal inheritance, to explore the genetic structures and relationships of Dong, Gelao, Tujia and Yi ethnic population in Guizhou of China. The mtDNA D-loop hypervariable segment I (HVS I ) in 108 samples of four ethnic populations were sequenced. Then, the nucleotide diversity was estimated and a phylogenetic tree was constructed by Neighbor-Joining method. In the detected 497 bp fragments, 86 polymorphic sites were found, and 82 different haplotypes were identified. The phylogenetic tree of four ethnic populations showed: Yi, Tujia and Gelao clustered more closely than Dong did.
Question: Is [ The genetic relation of four ethnic populations in China 's Guizhou revealed by sequence variations of mtDNA D-loop ]?
Output:
|
PubmedQA13724
|
[
{
"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 examined the prevalence and clinical correlates of Capgras syndrome (CS) in Alzheimer's disease. Cross-sectional study of elderly patients evaluated at an outpatient memory disorders clinic classified according to the presence or absence of CS. One hundred and fifty-one consecutive patients diagnosed with probable (N=110) or possible (N=48) Alzheimer's disease (AD) utilizing NINCDS-ADRDA diagnostic criteria. The Behavioral Pathology in Alzheimer's Disease Rating Scale (BEHAVE-AD), Mini-Mental State Examination (MMSE) and Blessed Dementia Scale (BDS). CS was observed in 10% of the sample (N=16). Associated factors included other delusions, lower MMSE scores and higher BDS scores. The relation between CS and both cognitive and functional status remained significant after controlling for other delusions.\n Question: Does prevalence and correlate of Capgras syndrome in 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: This study examined the prevalence and clinical correlates of Capgras syndrome (CS) in Alzheimer's disease. Cross-sectional study of elderly patients evaluated at an outpatient memory disorders clinic classified according to the presence or absence of CS. One hundred and fifty-one consecutive patients diagnosed with probable (N=110) or possible (N=48) Alzheimer's disease (AD) utilizing NINCDS-ADRDA diagnostic criteria. The Behavioral Pathology in Alzheimer's Disease Rating Scale (BEHAVE-AD), Mini-Mental State Examination (MMSE) and Blessed Dementia Scale (BDS). CS was observed in 10% of the sample (N=16). Associated factors included other delusions, lower MMSE scores and higher BDS scores. The relation between CS and both cognitive and functional status remained significant after controlling for other delusions.
Question: Does prevalence and correlate of Capgras syndrome in Alzheimer 's disease?
Output:
|
PubmedQA98505
|
[
{
"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 short-term efficacy, safety and tolerability of rosiglitazone were compared with placebo in patients with Type II (non-insulin-dependent) diabetes mellitus in a dose-ranging study. After a 2-week placebo run-in phase, 303 patients were randomly assigned to 8 weeks of treatment with twice-daily placebo or 2, 4 or 6 mg of rosiglitazone. All rosiglitazone doses significantly reduced fasting plasma glucose compared with baseline. All rosiglitazone treatment groups showed significantly reduced peak postprandial glucose concentrations compared with baseline (p < 0.001) and with placebo (p < 0.0001) and reduced postprandial glucose excursion, without an increase in the area under the postprandial insulin concentration-time curve. Rosiglitazone at 4 and 6 mg twice daily prevented the increase in HbA1c observed in the placebo group. C peptide and serum insulin concentrations were significantly reduced from baseline in all rosiglitazone treatment groups. In all rosiglitazone treatment groups, nonesterified fatty acids decreased significantly (p < 0.0001) and triglycerides did not change. Although total LDL and HDL cholesterol increased significantly in the rosiglitazone treatment groups, total cholesterol/HDL ratios did not change significantly. The proportion of patients with one or more adverse event was similar in all four treatment groups. No patient showed evidence of hepatotoxicity.\n Question: Does rosiglitazone short-term monotherapy lower fasting and post-prandial glucose in patients with type II diabetes?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: The short-term efficacy, safety and tolerability of rosiglitazone were compared with placebo in patients with Type II (non-insulin-dependent) diabetes mellitus in a dose-ranging study. After a 2-week placebo run-in phase, 303 patients were randomly assigned to 8 weeks of treatment with twice-daily placebo or 2, 4 or 6 mg of rosiglitazone. All rosiglitazone doses significantly reduced fasting plasma glucose compared with baseline. All rosiglitazone treatment groups showed significantly reduced peak postprandial glucose concentrations compared with baseline (p < 0.001) and with placebo (p < 0.0001) and reduced postprandial glucose excursion, without an increase in the area under the postprandial insulin concentration-time curve. Rosiglitazone at 4 and 6 mg twice daily prevented the increase in HbA1c observed in the placebo group. C peptide and serum insulin concentrations were significantly reduced from baseline in all rosiglitazone treatment groups. In all rosiglitazone treatment groups, nonesterified fatty acids decreased significantly (p < 0.0001) and triglycerides did not change. Although total LDL and HDL cholesterol increased significantly in the rosiglitazone treatment groups, total cholesterol/HDL ratios did not change significantly. The proportion of patients with one or more adverse event was similar in all four treatment groups. No patient showed evidence of hepatotoxicity.
Question: Does rosiglitazone short-term monotherapy lower fasting and post-prandial glucose in patients with type II diabetes?
Output:
|
PubmedQA96911
|
[
{
"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 receptor tyrosine kinase-like orphan receptors (ROR) family contains the atypical member ROR1, which plays an oncogenic role in several malignant tumors. However, the clinical potentials and underlying mechanisms of ROR1 in gastric cancer progression remain largely unknown. In this study, we validated the microRNA-mediated gene repression mechanism involved in the role of ROR1. Bioinformatic prediction, luciferase reporter assay, quantitative real-time PCR (qRT-PCR) and western blotting were used to reveal the regulatory relationship between miR-27b-3p and ROR1. The expression patterns of miR-27b-3p and ROR1 in human gastric cancer (GC) specimens and cell lines were determined by microRNA RT-PCR and western blotting. Cell proliferation, colony formation assay in soft agar in vitro and tumorigenicity in vivo were performed to observe the effects of downregulation and upregulation miR-27b-3p expression on GC cell phenotypes. miR-27b-3p suppressed ROR1 expression by binding to the 3'UTR of ROR1 mRNA in GC cells. miR-27b-3p was significantly downregulated and reversely correlated with ROR1 protein levels in clinical samples. Analysis of the clinicopathological significance showed that miR-27b-3p and ROR1 were closely correlated with GC characteristics. Ectopic miR-27b-3p expression suppressed cell proliferation, colony formation in soft agar, xenograft tumors of GC cells. By contrast, miR-27b-3p knockdown enhanced these malignant behaviors. Our studies further revealed that the c-Src/STAT3 signaling pathway was involved in miR-27b-3p-ROR1-mediated cell proliferation regulation.\n Question: Does miR-27b-3p suppress cell proliferation through targeting receptor tyrosine kinase like orphan receptor 1 in gastric 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: The receptor tyrosine kinase-like orphan receptors (ROR) family contains the atypical member ROR1, which plays an oncogenic role in several malignant tumors. However, the clinical potentials and underlying mechanisms of ROR1 in gastric cancer progression remain largely unknown. In this study, we validated the microRNA-mediated gene repression mechanism involved in the role of ROR1. Bioinformatic prediction, luciferase reporter assay, quantitative real-time PCR (qRT-PCR) and western blotting were used to reveal the regulatory relationship between miR-27b-3p and ROR1. The expression patterns of miR-27b-3p and ROR1 in human gastric cancer (GC) specimens and cell lines were determined by microRNA RT-PCR and western blotting. Cell proliferation, colony formation assay in soft agar in vitro and tumorigenicity in vivo were performed to observe the effects of downregulation and upregulation miR-27b-3p expression on GC cell phenotypes. miR-27b-3p suppressed ROR1 expression by binding to the 3'UTR of ROR1 mRNA in GC cells. miR-27b-3p was significantly downregulated and reversely correlated with ROR1 protein levels in clinical samples. Analysis of the clinicopathological significance showed that miR-27b-3p and ROR1 were closely correlated with GC characteristics. Ectopic miR-27b-3p expression suppressed cell proliferation, colony formation in soft agar, xenograft tumors of GC cells. By contrast, miR-27b-3p knockdown enhanced these malignant behaviors. Our studies further revealed that the c-Src/STAT3 signaling pathway was involved in miR-27b-3p-ROR1-mediated cell proliferation regulation.
Question: Does miR-27b-3p suppress cell proliferation through targeting receptor tyrosine kinase like orphan receptor 1 in gastric cancer?
Output:
|
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