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16,376,772 | Does planimetric assessment of anatomic valve area overestimate effective orifice area in bicuspid aortic stenosis? | {
"contexts": [
"Although the continuity equation remains the noninvasive standard, planimetry using transesophageal echocardiography is often used to assess valve area for patients with aortic stenosis (AS). Not uncommonly, however, anatomic valve area (AVAA) obtained by planimetry overestimates continuity-derived effective valve area (AVAE) in bicuspid AS.",
"Transthoracic Doppler and transesophageal echocardiography were performed to obtain AVAE and AVAA in 31 patients with bicuspid AS (age 61 +/- 11 years) and 22 patients with degenerative tricuspid AS (age 71 +/- 13 years). Aortic root and left ventricular outflow tract dimensions and the directional angle of the stenotic jet were assessed in all patients. Using these data, a computational fluid dynamics model was constructed to test the effect of these variables in determining the relationship between AVAE and AVAA.",
"For patients with tricuspid AS, the correlation between AVAA (1.15 +/- 0.36 cm2) and AVAE (1.13 +/- 0.46 cm2) was excellent (r = 0.91, P < .001, Delta = 0.02 +/- 0.21 cm2). However, AVAA was significantly larger (1.19 +/- 0.35 cm2) than AVAE (0.89 +/- 0.29 cm2) in the bicuspid AS group (r = 0.71, P < .001, Delta = 0.29 +/- 0.25 cm2). Computer simulation demonstrated that the observed discrepancy related to jet eccentricity."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Anatomy, Cross-Sectional",
"Aortic Valve Stenosis",
"Artifacts",
"Computer Simulation",
"Echocardiography, Doppler",
"Echocardiography, Transesophageal",
"Female",
"Humans",
"Image Enhancement",
"Image Interpretation, Computer-Assisted",
"Male",
"Mitral Valve",
"Models, Cardiovascular",
"Reproducibility of Results",
"Sensitivity and Specificity"
]
} | For a given anatomic orifice, functional severity tends to be greater in bicuspid AS than in tricuspid AS. This appears to be primarily related to greater jet eccentricity and less pressure recovery. | yes | [
{
"from": "human",
"value": "Question: Does planimetric assessment of anatomic valve area overestimate effective orifice area in bicuspid aortic stenosis?\nContext: {'contexts': ['Although the continuity equation remains the noninvasive standard, planimetry using transesophageal echocardiography is often used to assess valve area for patients with aortic stenosis (AS). Not uncommonly, however, anatomic valve area (AVAA) obtained by planimetry overestimates continuity-derived effective valve area (AVAE) in bicuspid AS.', 'Transthoracic Doppler and transesophageal echocardiography were performed to obtain AVAE and AVAA in 31 patients with bicuspid AS (age 61 +/- 11 years) and 22 patients with degenerative tricuspid AS (age 71 +/- 13 years). Aortic root and left ventricular outflow tract dimensions and the directional angle of the stenotic jet were assessed in all patients. Using these data, a computational fluid dynamics model was constructed to test the effect of these variables in determining the relationship between AVAE and AVAA.', 'For patients with tricuspid AS, the correlation between AVAA (1.15 +/- 0.36 cm2) and AVAE (1.13 +/- 0.46 cm2) was excellent (r = 0.91, P < .001, Delta = 0.02 +/- 0.21 cm2). However, AVAA was significantly larger (1.19 +/- 0.35 cm2) than AVAE (0.89 +/- 0.29 cm2) in the bicuspid AS group (r = 0.71, P < .001, Delta = 0.29 +/- 0.25 cm2). Computer simulation demonstrated that the observed discrepancy related to jet eccentricity.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Anatomy, Cross-Sectional', 'Aortic Valve Stenosis', 'Artifacts', 'Computer Simulation', 'Echocardiography, Doppler', 'Echocardiography, Transesophageal', 'Female', 'Humans', 'Image Enhancement', 'Image Interpretation, Computer-Assisted', 'Male', 'Mitral Valve', 'Models, Cardiovascular', 'Reproducibility of Results', 'Sensitivity and Specificity']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,388,505 | Is sprouty4 , a suppressor of tumor cell motility , down regulated by DNA methylation in human prostate cancer? | {
"contexts": [
"Alterations of fibroblast growth factors (FGFs) and their receptors contribute to prostate cancer progression by enhancing cellular proliferation, survival, and motility. The Sprouty gene family negatively regulates FGF signaling and may limit the ability of FGFs to enhance tumor progression. Sprouty1 is down regulated in human prostate cancers and Sprouty1 expression can markedly inhibit prostate cancer proliferation in vitro. Sprouty4 has been shown to negatively regulate both proliferation and cell migration in other systems. We therefore examined whether Sprouty4 expression was altered in prostate cancer.",
"Expression of Sprouty4 was examined by in situ hybridization and quantitative RT-PCR. Methylation of the Sprouty4 gene promoter was assessed using bisulfite modification and sequencing. The effect of Sprouty4 expression on cell migration was determined using an in vitro wounding assay.",
"By in situ hybridization Sprouty4 is expressed in normal prostatic epithelial cells and is decreased in a subset of prostate cancers. Quantitative RT-PCR confirms that Sprouty4 expression is decreased in approximately one half of prostate cancers. Analysis of the 5'-regulatory region revealed a CpG island approximately 1 kb upstream of the transcription initiation site, the proximal portion of which was preferentially methylated in prostate cancer tissues. More than one half of all prostate cancer DNAs were methylated in this region and methylation was significantly correlated with decreased Sprouty4 expression as determined by quantitative RT-PCR. When overexpressed in prostate cancer cell lines, Sprouty4 did not inhibit cell proliferation but did inhibit cell migration."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Cell Line, Tumor",
"Cell Movement",
"DNA Methylation",
"DNA Primers",
"Fibroblast Growth Factors",
"Gene Expression Regulation, Neoplastic",
"Humans",
"In Situ Hybridization",
"Intracellular Signaling Peptides and Proteins",
"Male",
"Nerve Tissue Proteins",
"Prostatic Neoplasms",
"Reverse Transcriptase Polymerase Chain Reaction",
"Transfection"
]
} | Sprouty4 expression is down regulated in human prostate cancer by DNA methylation and this decreased expression may contribute to increased cell migration. | yes | [
{
"from": "human",
"value": "Question: Is sprouty4 , a suppressor of tumor cell motility , down regulated by DNA methylation in human prostate cancer?\nContext: {'contexts': ['Alterations of fibroblast growth factors (FGFs) and their receptors contribute to prostate cancer progression by enhancing cellular proliferation, survival, and motility. The Sprouty gene family negatively regulates FGF signaling and may limit the ability of FGFs to enhance tumor progression. Sprouty1 is down regulated in human prostate cancers and Sprouty1 expression can markedly inhibit prostate cancer proliferation in vitro. Sprouty4 has been shown to negatively regulate both proliferation and cell migration in other systems. We therefore examined whether Sprouty4 expression was altered in prostate cancer.', 'Expression of Sprouty4 was examined by in situ hybridization and quantitative RT-PCR. Methylation of the Sprouty4 gene promoter was assessed using bisulfite modification and sequencing. The effect of Sprouty4 expression on cell migration was determined using an in vitro wounding assay.', \"By in situ hybridization Sprouty4 is expressed in normal prostatic epithelial cells and is decreased in a subset of prostate cancers. Quantitative RT-PCR confirms that Sprouty4 expression is decreased in approximately one half of prostate cancers. Analysis of the 5'-regulatory region revealed a CpG island approximately 1 kb upstream of the transcription initiation site, the proximal portion of which was preferentially methylated in prostate cancer tissues. More than one half of all prostate cancer DNAs were methylated in this region and methylation was significantly correlated with decreased Sprouty4 expression as determined by quantitative RT-PCR. When overexpressed in prostate cancer cell lines, Sprouty4 did not inhibit cell proliferation but did inhibit cell migration.\"], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Cell Line, Tumor', 'Cell Movement', 'DNA Methylation', 'DNA Primers', 'Fibroblast Growth Factors', 'Gene Expression Regulation, Neoplastic', 'Humans', 'In Situ Hybridization', 'Intracellular Signaling Peptides and Proteins', 'Male', 'Nerve Tissue Proteins', 'Prostatic Neoplasms', 'Reverse Transcriptase Polymerase Chain Reaction', 'Transfection']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,374,289 | Does topical becaplermin improve outcomes in work related fingertip injuries? | {
"contexts": [
"Fingertip injuries are common and bear significant costs associated with treatment, lost work, and functional impairment. This study compared these factors in occupationally related fingertip injuries treated with becaplermin, a recombinant human platelet-derived growth factor, and those treated with surgical reconstruction.",
"This was a prospective controlled trial involving occupationally related fingertip injuries. Fifty men (ages 23-51) with full thickness, single fingertip injuries > or =1.5 cm(2) with or without phalangeal exposure and distal to the distal interphalangeal (DIP) joint were evaluated. Group I (n = 25) underwent treatment with daily topical becaplermin. Group II (n = 25) underwent surgical reconstruction with a skin graft or local soft tissue flap. Time to wound healing, time to return to work, associated treatment costs, and calculated functional impairment were recorded.",
"Patients in Group I returned to work in significantly less time than those in Group II-10 days versus 38 days respectively). The average calculated functional impairment in Group I was 10% versus 22% in Group II. Associated treatment costs in group A were 1580 +/- 145 US Dollars compared with 6750 +/- 785 US Dollars in Group II. All differences were statistically significant at p < 0.05"
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Accidents, Occupational",
"Adult",
"Anticoagulants",
"Becaplermin",
"Finger Injuries",
"Humans",
"Male",
"Middle Aged",
"Occupational Diseases",
"Platelet-Derived Growth Factor",
"Proto-Oncogene Proteins c-sis",
"Time Factors",
"Wound Healing"
]
} | In this study, the functional and economic costs were significantly less when fingertip injuries were treated with topical becaplermin than when they were treated with surgical reconstruction. This information should allow emergency and acute care physicians to treat these injuries more efficaciously and conveniently. | yes | [
{
"from": "human",
"value": "Question: Does topical becaplermin improve outcomes in work related fingertip injuries?\nContext: {'contexts': ['Fingertip injuries are common and bear significant costs associated with treatment, lost work, and functional impairment. This study compared these factors in occupationally related fingertip injuries treated with becaplermin, a recombinant human platelet-derived growth factor, and those treated with surgical reconstruction.', 'This was a prospective controlled trial involving occupationally related fingertip injuries. Fifty men (ages 23-51) with full thickness, single fingertip injuries > or =1.5 cm(2) with or without phalangeal exposure and distal to the distal interphalangeal (DIP) joint were evaluated. Group I (n = 25) underwent treatment with daily topical becaplermin. Group II (n = 25) underwent surgical reconstruction with a skin graft or local soft tissue flap. Time to wound healing, time to return to work, associated treatment costs, and calculated functional impairment were recorded.', 'Patients in Group I returned to work in significantly less time than those in Group II-10 days versus 38 days respectively). The average calculated functional impairment in Group I was 10% versus 22% in Group II. Associated treatment costs in group A were 1580 +/- 145 US Dollars compared with 6750 +/- 785 US Dollars in Group II. All differences were statistically significant at p < 0.05'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Accidents, Occupational', 'Adult', 'Anticoagulants', 'Becaplermin', 'Finger Injuries', 'Humans', 'Male', 'Middle Aged', 'Occupational Diseases', 'Platelet-Derived Growth Factor', 'Proto-Oncogene Proteins c-sis', 'Time Factors', 'Wound Healing']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,389,573 | Does deficiency of regulatory B cells increase allergic airway inflammation? | {
"contexts": [
"To investigate the effect of the X-linked immunodeficiency (Xid) B cell defect on the response to the cockroach allergen in mice.",
"Two cockroach allergen immunization and challenge protocols were employed to sensitize CBA/J wild-type and CBA/CaHN-btk(-/-)xid/J (Xid) mice. Blood and tissue samples were collected 24 and 48 hrs after the last intratracheal antigen challenge and were analyzed for several parameters of allergic inflammation.",
"Nearly equivalent amounts of serum IgE were detected in Xid and CBA/J mice after short-term antigen challenge despite the B cell deficiency in Xid mice. A decreased concentration of IgE was detected in CBA/J mice after repeated allergen challenges but not in the Xid mice. Correlating with the discrepancy in serum IgE levels, higher levels of IL-13, IL-5, IL-10 and CCL5 were measured in whole lung homogenates from allergen-challenged Xid mice compared to CBA/J mice. In addition, draining lymph node cells from Xid mice expressed elevated levels of IL-4, IL-5, IL-10 and IFNgamma mRNA compared to cells from CBA/J mice after in vitro culture with cockroach antigen. An increase in lung inflammation, interstitial eosinophilia and mucus production was also observed in allergen-challenged Xid mice. CD95L expression increased on B-1a cells following allergen challenge, which was accompanied by an increase in lung CD4(+) Th cell apoptosis in wild-type CBA/J mice. In contrast, Xid mice did not have an increase in CD4(+) T cell apoptosis following allergen challenge."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Apoptosis",
"Asthma",
"B-Lymphocytes",
"CD4 Antigens",
"CD4 Lymphocyte Count",
"CD4-Positive T-Lymphocytes",
"CD5 Antigens",
"Chemokine CCL5",
"Cockroaches",
"Cytokines",
"Disease Models, Animal",
"Fas Ligand Protein",
"Female",
"Gene Expression Regulation",
"Hypersensitivity",
"Immunoglobulin E",
"Lung",
"Membrane Glycoproteins",
"Mice",
"Mice, Inbred CBA",
"Mice, Mutant Strains",
"Tumor Necrosis Factors"
]
} | These data suggest a regulatory role for B-1a cells in reducing cytokine production, pulmonary inflammation, and CD4(+) T cell survival during cockroach allergen-induced airway inflammation. | yes | [
{
"from": "human",
"value": "Question: Does deficiency of regulatory B cells increase allergic airway inflammation?\nContext: {'contexts': ['To investigate the effect of the X-linked immunodeficiency (Xid) B cell defect on the response to the cockroach allergen in mice.', 'Two cockroach allergen immunization and challenge protocols were employed to sensitize CBA/J wild-type and CBA/CaHN-btk(-/-)xid/J (Xid) mice. Blood and tissue samples were collected 24 and 48 hrs after the last intratracheal antigen challenge and were analyzed for several parameters of allergic inflammation.', 'Nearly equivalent amounts of serum IgE were detected in Xid and CBA/J mice after short-term antigen challenge despite the B cell deficiency in Xid mice. A decreased concentration of IgE was detected in CBA/J mice after repeated allergen challenges but not in the Xid mice. Correlating with the discrepancy in serum IgE levels, higher levels of IL-13, IL-5, IL-10 and CCL5 were measured in whole lung homogenates from allergen-challenged Xid mice compared to CBA/J mice. In addition, draining lymph node cells from Xid mice expressed elevated levels of IL-4, IL-5, IL-10 and IFNgamma mRNA compared to cells from CBA/J mice after in vitro culture with cockroach antigen. An increase in lung inflammation, interstitial eosinophilia and mucus production was also observed in allergen-challenged Xid mice. CD95L expression increased on B-1a cells following allergen challenge, which was accompanied by an increase in lung CD4(+) Th cell apoptosis in wild-type CBA/J mice. In contrast, Xid mice did not have an increase in CD4(+) T cell apoptosis following allergen challenge.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Apoptosis', 'Asthma', 'B-Lymphocytes', 'CD4 Antigens', 'CD4 Lymphocyte Count', 'CD4-Positive T-Lymphocytes', 'CD5 Antigens', 'Chemokine CCL5', 'Cockroaches', 'Cytokines', 'Disease Models, Animal', 'Fas Ligand Protein', 'Female', 'Gene Expression Regulation', 'Hypersensitivity', 'Immunoglobulin E', 'Lung', 'Membrane Glycoproteins', 'Mice', 'Mice, Inbred CBA', 'Mice, Mutant Strains', 'Tumor Necrosis Factors']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,397,039 | Does docetaxel followed by castration improve outcomes in LNCaP prostate cancer-bearing severe combined immunodeficient mice? | {
"contexts": [
"Androgen ablation is the standard initial treatment for advanced prostate cancer; however, tumors eventually develop androgen independence and become incurable. Chemotherapy is commonly used after hormone treatment fails but has not shown significant survival benefit. Studies suggest that androgen ablation can select for a population of hormone-independent cells that are also relatively chemotherapy resistant. Thus, it may be therapeutically advantageous to target prostate cancer with chemotherapy before hormone ablation. This study was undertaken to determine the relative efficacy of such an approach in a preclinical model of prostate cancer.",
"Severe combined immunodeficient mice bearing human LNCaP prostate tumors were treated with docetaxel and/or surgical castration applied singly, concurrently, or in different sequences. Treatment efficacy was determined by tumor volume and growth delay measurements. The extent of apoptosis in tumors in response to treatments was assessed via terminal deoxynucleotidyl transferase-mediated nick-end labeling (TUNEL) assays. In addition, Western blots were done to study the relative expression of Bcl-2 and Bax in the tumors.",
"Docetaxel followed by castration showed the most potent antitumor effects. In contrast, with the exception of castration alone, castration followed by docetaxel produced the least antitumor activity. TUNEL assays confirmed that the density of apoptotic tumor cells was significantly greater for docetaxel followed by castration than for any other treatment. In tumors of mice treated with single modality therapies, Bax to Bcl-2 ratios decreased significantly after castration, whereas this ratio remained high after docetaxel treatment."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Antineoplastic Agents, Phytogenic",
"Apoptosis",
"Blotting, Western",
"Castration",
"Cell Line, Tumor",
"Combined Modality Therapy",
"Disease Models, Animal",
"Docetaxel",
"Humans",
"In Situ Nick-End Labeling",
"Male",
"Mice",
"Mice, SCID",
"Neoplasm Transplantation",
"Prostatic Neoplasms",
"Proto-Oncogene Proteins c-bcl-2",
"Taxoids",
"bcl-2-Associated X Protein"
]
} | A treatment sequence of docetaxel followed by hormone ablation may be more effective in treating prostate cancer than concurrent docetaxel/hormone therapy or hormone ablation followed by docetaxel. | yes | [
{
"from": "human",
"value": "Question: Does docetaxel followed by castration improve outcomes in LNCaP prostate cancer-bearing severe combined immunodeficient mice?\nContext: {'contexts': ['Androgen ablation is the standard initial treatment for advanced prostate cancer; however, tumors eventually develop androgen independence and become incurable. Chemotherapy is commonly used after hormone treatment fails but has not shown significant survival benefit. Studies suggest that androgen ablation can select for a population of hormone-independent cells that are also relatively chemotherapy resistant. Thus, it may be therapeutically advantageous to target prostate cancer with chemotherapy before hormone ablation. This study was undertaken to determine the relative efficacy of such an approach in a preclinical model of prostate cancer.', 'Severe combined immunodeficient mice bearing human LNCaP prostate tumors were treated with docetaxel and/or surgical castration applied singly, concurrently, or in different sequences. Treatment efficacy was determined by tumor volume and growth delay measurements. The extent of apoptosis in tumors in response to treatments was assessed via terminal deoxynucleotidyl transferase-mediated nick-end labeling (TUNEL) assays. In addition, Western blots were done to study the relative expression of Bcl-2 and Bax in the tumors.', 'Docetaxel followed by castration showed the most potent antitumor effects. In contrast, with the exception of castration alone, castration followed by docetaxel produced the least antitumor activity. TUNEL assays confirmed that the density of apoptotic tumor cells was significantly greater for docetaxel followed by castration than for any other treatment. In tumors of mice treated with single modality therapies, Bax to Bcl-2 ratios decreased significantly after castration, whereas this ratio remained high after docetaxel treatment.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Antineoplastic Agents, Phytogenic', 'Apoptosis', 'Blotting, Western', 'Castration', 'Cell Line, Tumor', 'Combined Modality Therapy', 'Disease Models, Animal', 'Docetaxel', 'Humans', 'In Situ Nick-End Labeling', 'Male', 'Mice', 'Mice, SCID', 'Neoplasm Transplantation', 'Prostatic Neoplasms', 'Proto-Oncogene Proteins c-bcl-2', 'Taxoids', 'bcl-2-Associated X Protein']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,393,313 | Do the extent of oesophageal acid exposure overlap among the different gastro-oesophageal reflux disease groups? | {
"contexts": [
"Studies have demonstrated that patients with Barrett's oesophagus have the highest oesophageal acid exposure profile, followed by erosive oesophagitis and non-erosive reflux disease patients, but the exact extent of overlap remains unknown.",
"To determine the extent of overlap in oesophageal acid exposure among the different gastro-oesophageal reflux disease groups.",
"A total of 121 patients with gastro-oesophageal reflux disease underwent an upper endoscopy and were classified as having Barrett's oesophagus, erosive oesophagitis and non-erosive reflux disease-all (non-erosive reflux disease-positive and functional heartburn). Subsequently, patients underwent pH testing and overlap in oesophageal acid exposure among the different gastro-oesophageal reflux disease groups was determined.",
"Of those enrolled, 24 had Barrett's oesophagus, 30 erosive oesophagitis and 28 were non-erosive reflux disease-positive. Mean oesophageal acid exposure time was 224.8 +/- 35, 134.3 +/- 21.9 and 141.3 +/- 19.8 min for Barrett's oesophagus, erosive oesophagitis and non-erosive reflux disease-positive respectively. Per cent overlap for total, upright and supine time between non-erosive reflux disease-positive and erosive oesophagitis was 47.4%, 64.7% and 81.8%, between Barrett's oesophagus and erosive oesophagitis was 47.8%, 40.7% and 24%, and between Barrett's oesophagus and non-erosive reflux disease-positive was 31.6%, 37.5% and 20.8% respectively."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Aged, 80 and over",
"Barrett Esophagus",
"Esophagitis, Peptic",
"Esophagoscopy",
"Esophagus",
"Female",
"Gastric Acid",
"Gastroesophageal Reflux",
"Heartburn",
"Humans",
"Hydrogen-Ion Concentration",
"Male",
"Middle Aged",
"Time Factors"
]
} | Our study demonstrated a high oesophageal acid exposure overlap between patients with non-erosive reflux disease-positive and erosive oesophagitis, Barrett's oesophagus and erosive oesophagitis, as well as Barrett's oesophagus and non-erosive reflux disease-positive patients. | yes | [
{
"from": "human",
"value": "Question: Do the extent of oesophageal acid exposure overlap among the different gastro-oesophageal reflux disease groups?\nContext: {'contexts': [\"Studies have demonstrated that patients with Barrett's oesophagus have the highest oesophageal acid exposure profile, followed by erosive oesophagitis and non-erosive reflux disease patients, but the exact extent of overlap remains unknown.\", 'To determine the extent of overlap in oesophageal acid exposure among the different gastro-oesophageal reflux disease groups.', \"A total of 121 patients with gastro-oesophageal reflux disease underwent an upper endoscopy and were classified as having Barrett's oesophagus, erosive oesophagitis and non-erosive reflux disease-all (non-erosive reflux disease-positive and functional heartburn). Subsequently, patients underwent pH testing and overlap in oesophageal acid exposure among the different gastro-oesophageal reflux disease groups was determined.\", \"Of those enrolled, 24 had Barrett's oesophagus, 30 erosive oesophagitis and 28 were non-erosive reflux disease-positive. Mean oesophageal acid exposure time was 224.8 +/- 35, 134.3 +/- 21.9 and 141.3 +/- 19.8 min for Barrett's oesophagus, erosive oesophagitis and non-erosive reflux disease-positive respectively. Per cent overlap for total, upright and supine time between non-erosive reflux disease-positive and erosive oesophagitis was 47.4%, 64.7% and 81.8%, between Barrett's oesophagus and erosive oesophagitis was 47.8%, 40.7% and 24%, and between Barrett's oesophagus and non-erosive reflux disease-positive was 31.6%, 37.5% and 20.8% respectively.\"], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Aged, 80 and over', 'Barrett Esophagus', 'Esophagitis, Peptic', 'Esophagoscopy', 'Esophagus', 'Female', 'Gastric Acid', 'Gastroesophageal Reflux', 'Heartburn', 'Humans', 'Hydrogen-Ion Concentration', 'Male', 'Middle Aged', 'Time Factors']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,378,668 | Do spinal manipulation force and duration affect vertebral movement and neuromuscular responses? | {
"contexts": [
"Previous study in human subjects has documented biomechanical and neurophysiological responses to impulsive spinal manipulative thrusts, but very little is known about the neuromechanical effects of varying thrust force-time profiles.",
"Ten adolescent Merino sheep were anesthetized and posteroanterior mechanical thrusts were applied to the L3 spinous process using a computer-controlled, mechanical testing apparatus. Three variable pulse durations (10, 100, 200 ms, force = 80 N) and three variable force amplitudes (20, 40, 60 N, pulse duration = 100 ms) were examined for their effect on lumbar motion response (L3 displacement, L1, L2 acceleration) and normalized multifidus electromyographic response (L3, L4) using a repeated measures analysis of variance.",
"Increasing L3 posteroanterior force amplitude resulted in a fourfold linear increase in L3 posteroanterior vertebral displacement (p < 0.001) and adjacent segment (L1, L2) posteroanterior acceleration response (p < 0.001). L3 displacement was linearly correlated (p < 0.001) to the acceleration response over the 20-80 N force range (100 ms). At constant force, 10 ms thrusts resulted in nearly fivefold lower L3 displacements and significantly increased segmental (L2) acceleration responses compared to the 100 ms (19%, p = 0.005) and 200 ms (16%, p = 0.023) thrusts. Normalized electromyographic responses increased linearly with increasing force amplitude at higher amplitudes and were appreciably affected by mechanical excitation pulse duration."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Elasticity",
"Lumbar Vertebrae",
"Manipulation, Spinal",
"Movement",
"Muscle Contraction",
"Muscle, Skeletal",
"Physical Stimulation",
"Range of Motion, Articular",
"Reflex",
"Sheep",
"Stress, Mechanical",
"Weight-Bearing"
]
} | Changes in the biomechanical and neuromuscular response of the ovine lumbar spine were observed in response to changes in the force-time characteristics of the spinal manipulative thrusts and may be an underlying mechanism in related clinical outcomes. | yes | [
{
"from": "human",
"value": "Question: Do spinal manipulation force and duration affect vertebral movement and neuromuscular responses?\nContext: {'contexts': ['Previous study in human subjects has documented biomechanical and neurophysiological responses to impulsive spinal manipulative thrusts, but very little is known about the neuromechanical effects of varying thrust force-time profiles.', 'Ten adolescent Merino sheep were anesthetized and posteroanterior mechanical thrusts were applied to the L3 spinous process using a computer-controlled, mechanical testing apparatus. Three variable pulse durations (10, 100, 200 ms, force = 80 N) and three variable force amplitudes (20, 40, 60 N, pulse duration = 100 ms) were examined for their effect on lumbar motion response (L3 displacement, L1, L2 acceleration) and normalized multifidus electromyographic response (L3, L4) using a repeated measures analysis of variance.', 'Increasing L3 posteroanterior force amplitude resulted in a fourfold linear increase in L3 posteroanterior vertebral displacement (p < 0.001) and adjacent segment (L1, L2) posteroanterior acceleration response (p < 0.001). L3 displacement was linearly correlated (p < 0.001) to the acceleration response over the 20-80 N force range (100 ms). At constant force, 10 ms thrusts resulted in nearly fivefold lower L3 displacements and significantly increased segmental (L2) acceleration responses compared to the 100 ms (19%, p = 0.005) and 200 ms (16%, p = 0.023) thrusts. Normalized electromyographic responses increased linearly with increasing force amplitude at higher amplitudes and were appreciably affected by mechanical excitation pulse duration.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Elasticity', 'Lumbar Vertebrae', 'Manipulation, Spinal', 'Movement', 'Muscle Contraction', 'Muscle, Skeletal', 'Physical Stimulation', 'Range of Motion, Articular', 'Reflex', 'Sheep', 'Stress, Mechanical', 'Weight-Bearing']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,371,909 | Is balloon kyphoplasty effective in deformity correction of osteoporotic vertebral compression fractures? | {
"contexts": [
"A prospective radiographic analysis of deformity correction during the balloon kyphoplasty procedure.",
"To determine the spontaneous reduction of the deformity in prone position, the subsequent deformity correction by the inflatable bone tamp, and the overall deformity correction after deposition of the cement.",
"Fracture mobility has been shown to contribute to fracture reduction in vertebroplasty. Spontaneous reduction has not been taken into account in recently published series of balloon kyphoplasty, but it must be considered when performing vertebral augmentation and when reporting and interpreting the significance of vertebral height restoration.",
"A consecutive series of 39 osteoporotic vertebral compression fractures were treated in 30 patients. Lateral radiographs were taken and analyzed at six different time points: 1) Preoperative standing. During the kyphoplasty procedure, four consecutive radiographs were obtained: 2) after placing the patient in prone position on the operation table, 3) after inflation of the bone tamp (IBT), 4) after deflation and removal of the IBT, and 5) after deposition of the cement. 6) Standing lateral radiographs were taken after the procedure. All fractures were analyzed for improvement in sagittal alignment (Cobb angle, kyphotic angle, sagittal index, vertebral height), complications, and reduction of pain (VAS).",
"Placement of the patient in prone position displayed a significant spontaneous reduction in deformity of 6.5 degrees +/- 4.1 degrees Cobb angle. Inflation of the IBT demonstrated a further reduction of the fracture and a significant improvement of the Cobb angle of 3.4 degrees compared with baseline prone. After deflation and removal of the IBT and placement of the cement, no significant loss of fracture reduction was seen. Postoperative measurement of the Cobb angle by means of standing radiographs demonstrated a 3.1 degrees significant loss of reduction compared with the intraoperative measurement in prone position after cement application. Cement leaks occurred in 9 of 39 vertebral fractures. All patients subjectively reported immediate relief of their typical fracture pain. The VAS score significantly improved from 8.7 +/- 1.4 before surgery to 2.3 +/- 0.9."
],
"labels": [
"METHODS",
"OBJECTIVE",
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Aged, 80 and over",
"Female",
"Fracture Fixation",
"Humans",
"Kyphosis",
"Lumbar Vertebrae",
"Male",
"Middle Aged",
"Orthopedic Procedures",
"Prospective Studies",
"Spinal Cord Compression",
"Spinal Fractures",
"Thoracic Vertebrae"
]
} | The restoration of height in kyphoplasty is attributed to dynamic fracture mobility as well as to the expansion of the inserted balloon tamp. | yes | [
{
"from": "human",
"value": "Question: Is balloon kyphoplasty effective in deformity correction of osteoporotic vertebral compression fractures?\nContext: {'contexts': ['A prospective radiographic analysis of deformity correction during the balloon kyphoplasty procedure.', 'To determine the spontaneous reduction of the deformity in prone position, the subsequent deformity correction by the inflatable bone tamp, and the overall deformity correction after deposition of the cement.', 'Fracture mobility has been shown to contribute to fracture reduction in vertebroplasty. Spontaneous reduction has not been taken into account in recently published series of balloon kyphoplasty, but it must be considered when performing vertebral augmentation and when reporting and interpreting the significance of vertebral height restoration.', 'A consecutive series of 39 osteoporotic vertebral compression fractures were treated in 30 patients. Lateral radiographs were taken and analyzed at six different time points: 1) Preoperative standing. During the kyphoplasty procedure, four consecutive radiographs were obtained: 2) after placing the patient in prone position on the operation table, 3) after inflation of the bone tamp (IBT), 4) after deflation and removal of the IBT, and 5) after deposition of the cement. 6) Standing lateral radiographs were taken after the procedure. All fractures were analyzed for improvement in sagittal alignment (Cobb angle, kyphotic angle, sagittal index, vertebral height), complications, and reduction of pain (VAS).', 'Placement of the patient in prone position displayed a significant spontaneous reduction in deformity of 6.5 degrees +/- 4.1 degrees Cobb angle. Inflation of the IBT demonstrated a further reduction of the fracture and a significant improvement of the Cobb angle of 3.4 degrees compared with baseline prone. After deflation and removal of the IBT and placement of the cement, no significant loss of fracture reduction was seen. Postoperative measurement of the Cobb angle by means of standing radiographs demonstrated a 3.1 degrees significant loss of reduction compared with the intraoperative measurement in prone position after cement application. Cement leaks occurred in 9 of 39 vertebral fractures. All patients subjectively reported immediate relief of their typical fracture pain. The VAS score significantly improved from 8.7 +/- 1.4 before surgery to 2.3 +/- 0.9.'], 'labels': ['METHODS', 'OBJECTIVE', 'BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Aged, 80 and over', 'Female', 'Fracture Fixation', 'Humans', 'Kyphosis', 'Lumbar Vertebrae', 'Male', 'Middle Aged', 'Orthopedic Procedures', 'Prospective Studies', 'Spinal Cord Compression', 'Spinal Fractures', 'Thoracic Vertebrae']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,388,504 | Is t-cell recognition of a prostate specific antigen sufficient to induce prostate tissue destruction? | {
"contexts": [
"The ability of CD8(+) T-cells to induce prostate inflammation was examined using a prostate ovalbumin expressing transgenic mouse (POET) and/or adoptive transfer of T-cell receptor (TCR) transgenic T-cells (OT-I) that specifically recognize ovalbumin. Localization of inflammatory cells to prostate tissue was examined following T-cell activation via endogenous prostatic antigen, recombinant type 5 adenovirus carrying the gene coding ovalbumin (Ad5-mOVA), or adoptive transfer of in vitro antigen stimulated OT-I cells.",
"Ovalbumin specific OT-I cells were activated by autologous prostate antigen and trafficked to the prostate, but did not induce inflammation unless present in overwhelming numbers ( approximately 65% of CD8(+) T-cells). Activation of antigen specific CD8(+) T-cells in vitro (peptide pulsed antigen presenting cells) or in vivo (Ad5-mOVA) induced transitory prostate inflammation, without induction of prostate pathology, regardless of CD4(+) T-cell availability. Inflammation also was observed in OT-I x POET mice but again, pathological effects were not observed."
],
"labels": [
"METHODS",
"RESULTS"
],
"meshes": [
"Adoptive Transfer",
"Animals",
"CD8-Positive T-Lymphocytes",
"Cytokines",
"DNA Primers",
"Immunohistochemistry",
"Inflammation",
"Lymphocyte Activation",
"Lymphocyte Depletion",
"Male",
"Mice",
"Mice, Inbred C57BL",
"Mice, Transgenic",
"Ovalbumin",
"Prostate",
"Prostate-Specific Antigen",
"Reverse Transcriptase Polymerase Chain Reaction",
"Thymus Gland",
"Urinary Bladder"
]
} | T lymphocytes specific for a prostate antigen are capable of inducing inflammatory infiltration of prostatic tissue rapidly following activation, but do not produce pathological prostate injury. | no | [
{
"from": "human",
"value": "Question: Is t-cell recognition of a prostate specific antigen sufficient to induce prostate tissue destruction?\nContext: {'contexts': ['The ability of CD8(+) T-cells to induce prostate inflammation was examined using a prostate ovalbumin expressing transgenic mouse (POET) and/or adoptive transfer of T-cell receptor (TCR) transgenic T-cells (OT-I) that specifically recognize ovalbumin. Localization of inflammatory cells to prostate tissue was examined following T-cell activation via endogenous prostatic antigen, recombinant type 5 adenovirus carrying the gene coding ovalbumin (Ad5-mOVA), or adoptive transfer of in vitro antigen stimulated OT-I cells.', 'Ovalbumin specific OT-I cells were activated by autologous prostate antigen and trafficked to the prostate, but did not induce inflammation unless present in overwhelming numbers ( approximately 65% of CD8(+) T-cells). Activation of antigen specific CD8(+) T-cells in vitro (peptide pulsed antigen presenting cells) or in vivo (Ad5-mOVA) induced transitory prostate inflammation, without induction of prostate pathology, regardless of CD4(+) T-cell availability. Inflammation also was observed in OT-I x POET mice but again, pathological effects were not observed.'], 'labels': ['METHODS', 'RESULTS'], 'meshes': ['Adoptive Transfer', 'Animals', 'CD8-Positive T-Lymphocytes', 'Cytokines', 'DNA Primers', 'Immunohistochemistry', 'Inflammation', 'Lymphocyte Activation', 'Lymphocyte Depletion', 'Male', 'Mice', 'Mice, Inbred C57BL', 'Mice, Transgenic', 'Ovalbumin', 'Prostate', 'Prostate-Specific Antigen', 'Reverse Transcriptase Polymerase Chain Reaction', 'Thymus Gland', 'Urinary Bladder']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
16,385,250 | Are genetic polymorphisms of CD14 , toll-like receptor 4 , and caspase-recruitment domain 15 associated with necrotizing enterocolitis in very low birth weight infants? | {
"contexts": [
"Inadequate response of the innate immune system to bacterial antigens present in the intestinal flora may play a role in the development of necrotizing enterocolitis (NEC). Pattern recognition receptors such as CD14, toll-like receptor (TLR) 4, and caspase-recruitment domain (CARD) 15 bind bacterial lipopolysaccharide and peptidoglycan, and their activation leads to production of inflammatory cytokines. Our aim was to evaluate whether single nucleotide polymorphisms (SNPs) of CD14, TLR4, and CARD15 are associated with the risk of NEC in very low birth weight (VLBW) infants.",
"We determined the CD14 C-260T, TLR4 A +896G, C +1196T, and CARD15 G +2722C, C +2104T, 3020insC functional SNPs in dried blood samples from 118 VLBW infants (of those, 41 developed NEC) and from 146 healthy term newborns using polymerase chain reaction and restriction fragment length polymorphism methods. We tested the association between genotype and risk of NEC.",
"No significant differences were found in the prevalence of CD14 -260T, TLR4 +896G, +1196T, and CARD15 +2722C, +2104T, 3020insC alleles between VLBW infants and healthy term newborns (P = NS). The frequencies of investigated genotypes were similar in infants with and without NEC (P = NS). Furthermore, we did not find any association between genotype and prematurity or sepsis, which are important risk factors of NEC."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Enterocolitis, Necrotizing",
"Female",
"Gene Frequency",
"Genetic Predisposition to Disease",
"Genotype",
"Humans",
"Infant, Newborn",
"Infant, Very Low Birth Weight",
"Intracellular Signaling Peptides and Proteins",
"Lipopolysaccharide Receptors",
"Male",
"Nod2 Signaling Adaptor Protein",
"Polymerase Chain Reaction",
"Polymorphism, Genetic",
"Polymorphism, Restriction Fragment Length",
"Polymorphism, Single Nucleotide",
"Retrospective Studies",
"Toll-Like Receptor 4"
]
} | Carrier state of the tested CD14, TLR4, and CARD15 SNPs is not associated with NEC risk in VLBW infants. | no | [
{
"from": "human",
"value": "Question: Are genetic polymorphisms of CD14 , toll-like receptor 4 , and caspase-recruitment domain 15 associated with necrotizing enterocolitis in very low birth weight infants?\nContext: {'contexts': ['Inadequate response of the innate immune system to bacterial antigens present in the intestinal flora may play a role in the development of necrotizing enterocolitis (NEC). Pattern recognition receptors such as CD14, toll-like receptor (TLR) 4, and caspase-recruitment domain (CARD) 15 bind bacterial lipopolysaccharide and peptidoglycan, and their activation leads to production of inflammatory cytokines. Our aim was to evaluate whether single nucleotide polymorphisms (SNPs) of CD14, TLR4, and CARD15 are associated with the risk of NEC in very low birth weight (VLBW) infants.', 'We determined the CD14 C-260T, TLR4 A +896G, C +1196T, and CARD15 G +2722C, C +2104T, 3020insC functional SNPs in dried blood samples from 118 VLBW infants (of those, 41 developed NEC) and from 146 healthy term newborns using polymerase chain reaction and restriction fragment length polymorphism methods. We tested the association between genotype and risk of NEC.', 'No significant differences were found in the prevalence of CD14 -260T, TLR4 +896G, +1196T, and CARD15 +2722C, +2104T, 3020insC alleles between VLBW infants and healthy term newborns (P = NS). The frequencies of investigated genotypes were similar in infants with and without NEC (P = NS). Furthermore, we did not find any association between genotype and prematurity or sepsis, which are important risk factors of NEC.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Enterocolitis, Necrotizing', 'Female', 'Gene Frequency', 'Genetic Predisposition to Disease', 'Genotype', 'Humans', 'Infant, Newborn', 'Infant, Very Low Birth Weight', 'Intracellular Signaling Peptides and Proteins', 'Lipopolysaccharide Receptors', 'Male', 'Nod2 Signaling Adaptor Protein', 'Polymerase Chain Reaction', 'Polymorphism, Genetic', 'Polymorphism, Restriction Fragment Length', 'Polymorphism, Single Nucleotide', 'Retrospective Studies', 'Toll-Like Receptor 4']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
16,388,973 | Is spinal cord stimulation cost-effective for non-surgical management of critical limb ischaemia? | {
"contexts": [
"To quantify the costs of treatment in critical limb ischaemia (CLI) and to compare costs and effectiveness of two treatment strategies: spinal cord stimulation (SCS) and best medical treatment.",
"One hundred and twenty patients with CLI not suitable for vascular reconstruction were randomised to either SCS in addition to best medical treatment or best medical treatment alone. Primary outcomes were mortality, amputation and cost. Cost analysis was based on resources used by patients for 2 years after randomisation. Both medical and non-medical costs were included.",
"Patient and limb survival were similar in the two treatment groups. Costs of in-hospital-stay and institutional rehabilitation constituted the predominant part (+/-70%) of the total costs of medical care in CLI. Cost of SCS-implantation and complications (7950 euro per patient) exceeded by far cost due to amputation procedures (410 euro per patient). The total costs of treatment were 36,600 euro per patient over 2 years for the SCS-group vs. 28,700 euro for best medical treatment alone (28% higher for SCS-group, p=0.009)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Aged, 80 and over",
"Cost-Benefit Analysis",
"Electric Stimulation Therapy",
"Female",
"Follow-Up Studies",
"Health Care Costs",
"Humans",
"Ischemia",
"Leg",
"Male",
"Middle Aged",
"Spinal Cord",
"Survival Rate",
"Treatment Outcome"
]
} | Total costs of treatment in CLI are high. Major components are hospital and rehabilitation costs. In contrast to recent reviews, there were no long-term benefits of SCS-treatment. Therefore, cost-effectiveness is reduced to cost-minimisation and SCS-treatment is considerably more expensive than best medical treatment. | no | [
{
"from": "human",
"value": "Question: Is spinal cord stimulation cost-effective for non-surgical management of critical limb ischaemia?\nContext: {'contexts': ['To quantify the costs of treatment in critical limb ischaemia (CLI) and to compare costs and effectiveness of two treatment strategies: spinal cord stimulation (SCS) and best medical treatment.', 'One hundred and twenty patients with CLI not suitable for vascular reconstruction were randomised to either SCS in addition to best medical treatment or best medical treatment alone. Primary outcomes were mortality, amputation and cost. Cost analysis was based on resources used by patients for 2 years after randomisation. Both medical and non-medical costs were included.', 'Patient and limb survival were similar in the two treatment groups. Costs of in-hospital-stay and institutional rehabilitation constituted the predominant part (+/-70%) of the total costs of medical care in CLI. Cost of SCS-implantation and complications (7950 euro per patient) exceeded by far cost due to amputation procedures (410 euro per patient). The total costs of treatment were 36,600 euro per patient over 2 years for the SCS-group vs. 28,700 euro for best medical treatment alone (28% higher for SCS-group, p=0.009).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Aged, 80 and over', 'Cost-Benefit Analysis', 'Electric Stimulation Therapy', 'Female', 'Follow-Up Studies', 'Health Care Costs', 'Humans', 'Ischemia', 'Leg', 'Male', 'Middle Aged', 'Spinal Cord', 'Survival Rate', 'Treatment Outcome']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
16,393,221 | Does deep sedation occur frequently during elective endoscopy with meperidine and midazolam? | {
"contexts": [
"Although moderate (conscious) sedation is intended during elective gastrointestinal endoscopy, unintended levels of deep sedation occur. The aims of this study were to prospectively evaluate the incidence and risk factors of deep sedation during elective endoscopy with meperidine and midazolam intended to maintain a level of moderate sedation.",
"Eighty American Society of Anesthesiology class 1-2, outpatients presenting for elective esophagogastroduodenoscopy (EGD), colonoscopy, endoscopic retrograde cholangiopancreatography (ERCP), and endoscopic ultrasonography (EUS) were offered enrollment. Intravenous meperidine and midazolam were administered according to a standardized protocol. Hemodynamic parameters and levels of sedation were assessed and recorded by a single observer at 3-min intervals. The Modified Observer's Assessment of Alertness/Sedation (MOAA/S) scale (ranging 1-5) is a subjective sedation assessment scale used to assess sedation levels. Occurrence of deep sedation, defined by MOAA/S 1-2, was recorded. Univariable and multivariable analyses were used to assess predictors of deep sedation.",
"Deep sedation occurred in 54/80 (68%) patients for a total of 204/785 (26%) of total sedation assessments. The percentage of deep sedation episodes of all sedation-level observations by procedure was 26% for EGD, 11% for colonoscopy, 35% for ERCP, and 29% for EUS. Deep sedation occurred at least once in 60% of EGD, 45% of colonoscopy, 85% of ERCP, and 80% of EUS. Multivariable analysis showed that only ERCP and EUS were independent risk factors of deep sedation."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Cholangiopancreatography, Endoscopic Retrograde",
"Cohort Studies",
"Colonoscopy",
"Conscious Sedation",
"Dose-Response Relationship, Drug",
"Elective Surgical Procedures",
"Endoscopy, Digestive System",
"Endosonography",
"Esophagoscopy",
"Female",
"Follow-Up Studies",
"Gastroscopy",
"Humans",
"Hypnotics and Sedatives",
"Infusions, Intravenous",
"Male",
"Meperidine",
"Midazolam",
"Middle Aged",
"Pain Measurement",
"Patient Satisfaction",
"Prospective Studies",
"Risk Assessment"
]
} | Deep sedation occurs frequently during elective endoscopy with meperidine and midazolam used with the intent of moderate sedation. ERCP and EUS are risk factors for the occurrence of deep sedation, independent of sedation dose or length of procedure. | yes | [
{
"from": "human",
"value": "Question: Does deep sedation occur frequently during elective endoscopy with meperidine and midazolam?\nContext: {'contexts': ['Although moderate (conscious) sedation is intended during elective gastrointestinal endoscopy, unintended levels of deep sedation occur. The aims of this study were to prospectively evaluate the incidence and risk factors of deep sedation during elective endoscopy with meperidine and midazolam intended to maintain a level of moderate sedation.', \"Eighty American Society of Anesthesiology class 1-2, outpatients presenting for elective esophagogastroduodenoscopy (EGD), colonoscopy, endoscopic retrograde cholangiopancreatography (ERCP), and endoscopic ultrasonography (EUS) were offered enrollment. Intravenous meperidine and midazolam were administered according to a standardized protocol. Hemodynamic parameters and levels of sedation were assessed and recorded by a single observer at 3-min intervals. The Modified Observer's Assessment of Alertness/Sedation (MOAA/S) scale (ranging 1-5) is a subjective sedation assessment scale used to assess sedation levels. Occurrence of deep sedation, defined by MOAA/S 1-2, was recorded. Univariable and multivariable analyses were used to assess predictors of deep sedation.\", 'Deep sedation occurred in 54/80 (68%) patients for a total of 204/785 (26%) of total sedation assessments. The percentage of deep sedation episodes of all sedation-level observations by procedure was 26% for EGD, 11% for colonoscopy, 35% for ERCP, and 29% for EUS. Deep sedation occurred at least once in 60% of EGD, 45% of colonoscopy, 85% of ERCP, and 80% of EUS. Multivariable analysis showed that only ERCP and EUS were independent risk factors of deep sedation.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Cholangiopancreatography, Endoscopic Retrograde', 'Cohort Studies', 'Colonoscopy', 'Conscious Sedation', 'Dose-Response Relationship, Drug', 'Elective Surgical Procedures', 'Endoscopy, Digestive System', 'Endosonography', 'Esophagoscopy', 'Female', 'Follow-Up Studies', 'Gastroscopy', 'Humans', 'Hypnotics and Sedatives', 'Infusions, Intravenous', 'Male', 'Meperidine', 'Midazolam', 'Middle Aged', 'Pain Measurement', 'Patient Satisfaction', 'Prospective Studies', 'Risk Assessment']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,394,798 | Does overexpression of STAT-1 by adenoviral gene transfer inhibit hepatitis B virus replication? | {
"contexts": [
"Interferons are known to inhibit the replication of hepatitis B viruses (HBV) in several animal models in vitro and in vivo as well in humans. The STAT-1 protein plays a central role in the biological activity of both type I and type II interferons. The lack of functional STAT-1 renders cells and organisms susceptible to bacterial and viral infectious agents. We analysed whether the overexpression of STAT-1 protein enhances the biological interferon response and whether it elicits antiviral activity against HBV in vitro.",
"To achieve an efficient STAT-1 overexpression in primary liver cells and hepatoma cells, we generated a recombinant, replication-deficient adenovirus expressing human STAT-1 (Adv-STAT-1). We analysed whether the overexpression of STAT-1 inhibits the replication of duck HBV and human HBV in vitro using Western blot analysis, the immunofluorescence of viral proteins and quantification of HBV-DNA copies, respectively.",
"In the duck model of HBV infection the overexpression of STAT-1 neither inhibited an established infection nor prevented the establishment of duck HBV replication when administered simultaneously with Adv-STAT-1. These observations were confirmed in an in-vitro model of human HBV infection using the human hepatoma cell line HepG2.2.15, which continuously replicates HBV."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adenoviridae",
"Animals",
"Blotting, Western",
"Carcinoma, Hepatocellular",
"Cells, Cultured",
"DNA, Viral",
"Ducks",
"Gene Expression Regulation",
"Genetic Vectors",
"Hepatitis B virus",
"Hepatocytes",
"Humans",
"Liver Neoplasms",
"STAT1 Transcription Factor",
"Transfection",
"Tumor Cells, Cultured",
"Virus Replication"
]
} | These data demonstrate that the over-expression of STAT-1 alone is not sufficient to strengthen the biological response of interferon as an antiviral agent. | no | [
{
"from": "human",
"value": "Question: Does overexpression of STAT-1 by adenoviral gene transfer inhibit hepatitis B virus replication?\nContext: {'contexts': ['Interferons are known to inhibit the replication of hepatitis B viruses (HBV) in several animal models in vitro and in vivo as well in humans. The STAT-1 protein plays a central role in the biological activity of both type I and type II interferons. The lack of functional STAT-1 renders cells and organisms susceptible to bacterial and viral infectious agents. We analysed whether the overexpression of STAT-1 protein enhances the biological interferon response and whether it elicits antiviral activity against HBV in vitro.', 'To achieve an efficient STAT-1 overexpression in primary liver cells and hepatoma cells, we generated a recombinant, replication-deficient adenovirus expressing human STAT-1 (Adv-STAT-1). We analysed whether the overexpression of STAT-1 inhibits the replication of duck HBV and human HBV in vitro using Western blot analysis, the immunofluorescence of viral proteins and quantification of HBV-DNA copies, respectively.', 'In the duck model of HBV infection the overexpression of STAT-1 neither inhibited an established infection nor prevented the establishment of duck HBV replication when administered simultaneously with Adv-STAT-1. These observations were confirmed in an in-vitro model of human HBV infection using the human hepatoma cell line HepG2.2.15, which continuously replicates HBV.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adenoviridae', 'Animals', 'Blotting, Western', 'Carcinoma, Hepatocellular', 'Cells, Cultured', 'DNA, Viral', 'Ducks', 'Gene Expression Regulation', 'Genetic Vectors', 'Hepatitis B virus', 'Hepatocytes', 'Humans', 'Liver Neoplasms', 'STAT1 Transcription Factor', 'Transfection', 'Tumor Cells, Cultured', 'Virus Replication']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
16,372,494 | Does gleason scoring vary among pathologists and this affects clinical risk in patients with prostate cancer? | {
"contexts": [
"To investigate whether our practice of specialist review of all diagnostic biopsies was necessary to prevent misgrading of referred prostate cancer patients, and whether this misclassification, if any, would have resulted in misclassification of clinical risk grouping (Seattle Risk Grouping [SRG]) and subsequent treatment strategy and prognosis.",
"Important prognostic indicators for prostate cancer include the presenting prostate-specific antigen (PSA), clinical stage and Gleason sum of the tumour. These three variables are incorporated into the SRG cohorts to establish treatment strategy. Patients with prostate cancer referred for brachytherapy had their prostate biopsies reviewed by a reference pathologist (PD) with a special interest in prostate cancer. We compared the agreement between the scoring of the referring pathologists with that of PD, and evaluated if any differences changed the SRG and therefore the clinical risk and treatment strategy for the patients.",
"In only 52% (43/83) of cases, was there total agreement between the two sets of pathologists. The inter-rater agreement was statistically 'fair' (unweighted kappa statistic 0.27). In 90% (36/40) of cases with disagreement, PD assigned higher Gleason sums. In 40% (16/40) of cases with disagreement, the change in Gleason sum altered the SRG; in one out of 16 cases, the SRG was downgraded from 'intermediate' to 'low' risk disease; in six out of 16 cases, it was upgraded from 'low' to 'intermediate' risk, and, in nine out of 16, from 'intermediate' to 'high' risk."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Brachytherapy",
"Humans",
"Male",
"Neoplasm Staging",
"Prostatic Neoplasms"
]
} | Our findings confirm previous reports of only limited correlation between pathologists in reporting Gleason sums. In this study, 19% (16/83) of cases had their grading changed to a level that altered clinical risk, almost always (94%; 15/16) to one that worsened prognosis. This would have significantly affected treatment strategy for these patients, and thus we recommend that all centres ensure accurate Gleason grading by the use of pathologists with special interests in prostate cancer. | yes | [
{
"from": "human",
"value": "Question: Does gleason scoring vary among pathologists and this affects clinical risk in patients with prostate cancer?\nContext: {'contexts': ['To investigate whether our practice of specialist review of all diagnostic biopsies was necessary to prevent misgrading of referred prostate cancer patients, and whether this misclassification, if any, would have resulted in misclassification of clinical risk grouping (Seattle Risk Grouping [SRG]) and subsequent treatment strategy and prognosis.', 'Important prognostic indicators for prostate cancer include the presenting prostate-specific antigen (PSA), clinical stage and Gleason sum of the tumour. These three variables are incorporated into the SRG cohorts to establish treatment strategy. Patients with prostate cancer referred for brachytherapy had their prostate biopsies reviewed by a reference pathologist (PD) with a special interest in prostate cancer. We compared the agreement between the scoring of the referring pathologists with that of PD, and evaluated if any differences changed the SRG and therefore the clinical risk and treatment strategy for the patients.', \"In only 52% (43/83) of cases, was there total agreement between the two sets of pathologists. The inter-rater agreement was statistically 'fair' (unweighted kappa statistic 0.27). In 90% (36/40) of cases with disagreement, PD assigned higher Gleason sums. In 40% (16/40) of cases with disagreement, the change in Gleason sum altered the SRG; in one out of 16 cases, the SRG was downgraded from 'intermediate' to 'low' risk disease; in six out of 16 cases, it was upgraded from 'low' to 'intermediate' risk, and, in nine out of 16, from 'intermediate' to 'high' risk.\"], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Brachytherapy', 'Humans', 'Male', 'Neoplasm Staging', 'Prostatic Neoplasms']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,388,885 | Does addition of platelet transfusions to corticosteroids increase the recovery of severe HELLP syndrome? | {
"contexts": [
"The objective was to evaluate the effect of dexamethasone and platelet transfusion treatment on recovery in patients with class 1 hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome.",
"All women with class 1 HELLP syndrome (true HELLP syndrome) who were seen at the hospital Complejo Hospitalario de la Caja de Seguro Social de Panama, Panama between July 1996 and June 2004 took part in a retrospective, comparative study. They were divided into two groups. One group received dexamethasone and the other group received dexamethasone plus platelet transfusion. True HELLP syndrome was defined as hemolysis, elevated liver enzymes, and maternal platelet nadir < or =50,000 platelets/microl.",
"The primary endpoint was resolution of the HELLP syndrome as recognized by normalization of the platelet count (> or =150,000/microl) and the mean length (measured in days) of the postpartum stay in hospital.",
"Forty-six women with true HELLP syndrome were studied. Twenty-six patients received dexamethasone and 20 received dexamethasone plus platelet transfusion. The normalization of the platelet count was significantly more rapid in the dexamethasone group (p<0.004) and the postpartum hospital stay was significantly more prolonged in the dexamethasone plus platelet transfusion group (p<0.02). There was no maternal death."
],
"labels": [
"OBJECTIVE",
"METHODS",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Anti-Inflammatory Agents",
"Combined Modality Therapy",
"Dexamethasone",
"Dose-Response Relationship, Drug",
"Female",
"HELLP Syndrome",
"Humans",
"Platelet Count",
"Platelet Transfusion",
"Pregnancy",
"Pregnancy Maintenance",
"Retrospective Studies",
"Treatment Outcome"
]
} | The findings suggest the initiation of high-dose dexamethasone therapy in women with true HELLP syndrome, with the next step being delivery, and probably platelet count < or =50,000/microl alone is not always an indication for platelet transfusion. | no | [
{
"from": "human",
"value": "Question: Does addition of platelet transfusions to corticosteroids increase the recovery of severe HELLP syndrome?\nContext: {'contexts': ['The objective was to evaluate the effect of dexamethasone and platelet transfusion treatment on recovery in patients with class 1 hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome.', 'All women with class 1 HELLP syndrome (true HELLP syndrome) who were seen at the hospital Complejo Hospitalario de la Caja de Seguro Social de Panama, Panama between July 1996 and June 2004 took part in a retrospective, comparative study. They were divided into two groups. One group received dexamethasone and the other group received dexamethasone plus platelet transfusion. True HELLP syndrome was defined as hemolysis, elevated liver enzymes, and maternal platelet nadir < or =50,000 platelets/microl.', 'The primary endpoint was resolution of the HELLP syndrome as recognized by normalization of the platelet count (> or =150,000/microl) and the mean length (measured in days) of the postpartum stay in hospital.', 'Forty-six women with true HELLP syndrome were studied. Twenty-six patients received dexamethasone and 20 received dexamethasone plus platelet transfusion. The normalization of the platelet count was significantly more rapid in the dexamethasone group (p<0.004) and the postpartum hospital stay was significantly more prolonged in the dexamethasone plus platelet transfusion group (p<0.02). There was no maternal death.'], 'labels': ['OBJECTIVE', 'METHODS', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Anti-Inflammatory Agents', 'Combined Modality Therapy', 'Dexamethasone', 'Dose-Response Relationship, Drug', 'Female', 'HELLP Syndrome', 'Humans', 'Platelet Count', 'Platelet Transfusion', 'Pregnancy', 'Pregnancy Maintenance', 'Retrospective Studies', 'Treatment Outcome']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
16,386,676 | Are flow-dependent changes in Doppler-derived aortic valve effective orifice area real and not due to artifact? | {
"contexts": [
"We sought to determine whether the flow-dependent changes in Doppler-derived valve effective orifice area (EOA) are real or due to artifact.",
"It has frequently been reported that the EOA may vary with transvalvular flow in patients with aortic stenosis. However, the explanation of the flow dependence of EOA remains controversial and some studies have suggested that the EOA estimated by Doppler-echocardiography (EOA(Dop)) may underestimate the actual EOA at low flow rates.",
"One bioprosthetic valve and three rigid orifices were tested in a mock flow circulation model over a wide range of flow rates. The EOA(Dop) was compared with reference values obtained using particle image velocimetry (EOA(PIV)).",
"There was excellent agreement between EOA(Dop) and EOA(PIV) (r2 = 0.94). For rigid orifices of 0.5 and 1.0 cm2, no significant change in the EOA was observed with increasing flow rate. However, substantial increases of both EOA(Dop) and EOA(PIV) were observed when stroke volume increased from 20 to 70 ml both in the 1.5 cm2 rigid orifice (+52% for EOA(Dop) and +54% for EOA(PIV)) and the bioprosthetic valve (+62% for EOA(Dop) and +63% for EOA(PIV)); such changes are explained either by the presence of unsteady effects at low flow rates and/or by an increase in valve leaflet opening."
],
"labels": [
"OBJECTIVE",
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Aortic Valve",
"Aortic Valve Stenosis",
"Artifacts",
"Bioprosthesis",
"Blood Flow Velocity",
"Cardiac Catheterization",
"Echocardiography, Doppler",
"Heart Valve Prosthesis",
"Hemodynamics",
"Humans",
"Laser-Doppler Flowmetry",
"Models, Cardiovascular",
"Models, Structural"
]
} | The flow-dependent changes in EOA(Dop) are not artifacts but represent real changes in EOA attributable either to unsteady effects at low flow rates and/or to changes in valve leaflet opening. Such changes in EOA(Dop) can be relied on for clinical judgment making. | yes | [
{
"from": "human",
"value": "Question: Are flow-dependent changes in Doppler-derived aortic valve effective orifice area real and not due to artifact?\nContext: {'contexts': ['We sought to determine whether the flow-dependent changes in Doppler-derived valve effective orifice area (EOA) are real or due to artifact.', 'It has frequently been reported that the EOA may vary with transvalvular flow in patients with aortic stenosis. However, the explanation of the flow dependence of EOA remains controversial and some studies have suggested that the EOA estimated by Doppler-echocardiography (EOA(Dop)) may underestimate the actual EOA at low flow rates.', 'One bioprosthetic valve and three rigid orifices were tested in a mock flow circulation model over a wide range of flow rates. The EOA(Dop) was compared with reference values obtained using particle image velocimetry (EOA(PIV)).', 'There was excellent agreement between EOA(Dop) and EOA(PIV) (r2 = 0.94). For rigid orifices of 0.5 and 1.0 cm2, no significant change in the EOA was observed with increasing flow rate. However, substantial increases of both EOA(Dop) and EOA(PIV) were observed when stroke volume increased from 20 to 70 ml both in the 1.5 cm2 rigid orifice (+52% for EOA(Dop) and +54% for EOA(PIV)) and the bioprosthetic valve (+62% for EOA(Dop) and +63% for EOA(PIV)); such changes are explained either by the presence of unsteady effects at low flow rates and/or by an increase in valve leaflet opening.'], 'labels': ['OBJECTIVE', 'BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Aortic Valve', 'Aortic Valve Stenosis', 'Artifacts', 'Bioprosthesis', 'Blood Flow Velocity', 'Cardiac Catheterization', 'Echocardiography, Doppler', 'Heart Valve Prosthesis', 'Hemodynamics', 'Humans', 'Laser-Doppler Flowmetry', 'Models, Cardiovascular', 'Models, Structural']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,371,044 | Does cryopreservation of hematopoietic progenitor cells from apheresis at high cell concentrations impair the hematopoietic recovery after transplantation? | {
"contexts": [
"The high number of nuclear cells (NCs) from hematopoietic progenitor cells-apheresis (HPC-A) requires cryopreservation in large volumes or at high NC concentrations. The effect of NC concentration during cryopreservation has yet to be examined.",
"In the experimental arm (n = 610, Protocol B), the first HPC-A sample from the patient was cryopreserved in two cryobags and subsequent collections in one cryobag, resulting in high NC concentrations (>100 x 10(6) NCs/mL) in most cases. The effect of NC concentrations at freezing in NC recovery after thawing and engraftment kinetics was analyzed and compared with a group of HPC-A cryopreserved at standard NC concentrations (n = 455, Protocol A).",
"The mean (SD) NC concentration at freezing was 78 (28) x 10(6) per mL (median, 82 x 10(6)/mL; range, 12 x 10(6)-156 x 10(6)/mL) and 183 (108) x 10(6) per mL (median, 156 x 10(6)/mL; range, 16 x 10(6)-678 x 10(6)/mL), for HPC-A cryopreserved according to Protocols A and B, respectively. The NC viabilities of the test vials and HPC-A components after thawing were 88 percent versus 85 percent and 85 percent versus 82 percent, and the cloning efficiency was 49 percent versus 33 percent for Protocols A and B, respectively (p < 0.001). Significant differences were not observed in the recovery of NCs. Days to neutrophil and platelet engraftment were not different between patients transplanted in the standard- (n = 143) or high-cell-concentration group (n = 238)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Aged",
"Blood Component Removal",
"Blood Preservation",
"Cell Count",
"Cell Survival",
"Cryopreservation",
"Female",
"Freezing",
"Hematopoietic Stem Cell Transplantation",
"Hematopoietic Stem Cells",
"Humans",
"Male",
"Middle Aged"
]
} | The cryopreservation of HPC-A at higher than standard NC concentrations has no adverse impact on hematopoietic reconstitution after transplantation. | no | [
{
"from": "human",
"value": "Question: Does cryopreservation of hematopoietic progenitor cells from apheresis at high cell concentrations impair the hematopoietic recovery after transplantation?\nContext: {'contexts': ['The high number of nuclear cells (NCs) from hematopoietic progenitor cells-apheresis (HPC-A) requires cryopreservation in large volumes or at high NC concentrations. The effect of NC concentration during cryopreservation has yet to be examined.', 'In the experimental arm (n = 610, Protocol B), the first HPC-A sample from the patient was cryopreserved in two cryobags and subsequent collections in one cryobag, resulting in high NC concentrations (>100 x 10(6) NCs/mL) in most cases. The effect of NC concentrations at freezing in NC recovery after thawing and engraftment kinetics was analyzed and compared with a group of HPC-A cryopreserved at standard NC concentrations (n = 455, Protocol A).', 'The mean (SD) NC concentration at freezing was 78 (28) x 10(6) per mL (median, 82 x 10(6)/mL; range, 12 x 10(6)-156 x 10(6)/mL) and 183 (108) x 10(6) per mL (median, 156 x 10(6)/mL; range, 16 x 10(6)-678 x 10(6)/mL), for HPC-A cryopreserved according to Protocols A and B, respectively. The NC viabilities of the test vials and HPC-A components after thawing were 88 percent versus 85 percent and 85 percent versus 82 percent, and the cloning efficiency was 49 percent versus 33 percent for Protocols A and B, respectively (p < 0.001). Significant differences were not observed in the recovery of NCs. Days to neutrophil and platelet engraftment were not different between patients transplanted in the standard- (n = 143) or high-cell-concentration group (n = 238).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Aged', 'Blood Component Removal', 'Blood Preservation', 'Cell Count', 'Cell Survival', 'Cryopreservation', 'Female', 'Freezing', 'Hematopoietic Stem Cell Transplantation', 'Hematopoietic Stem Cells', 'Humans', 'Male', 'Middle Aged']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
16,370,258 | Does desensitization to strong vestibular stimuli improve tolerance to simulated aircraft motion? | {
"contexts": [
"The extent to which tolerance acquired in one motion environment can be transferred to another has not been fully elucidated. This study compares three provocative motion stimuli and whether tolerance acquired from cross-coupled motion and torso rotation can be transferred to simulated aircraft motion.",
"There were 18 healthy subjects (9 men and 9 women), 18-44 yr of age, who were divided into 3 groups. Each group was exposed to the following desensitization procedure in a pseudo-random repeated measures design. In condition D1, subjects were exposed to 4 consecutive days of cross-coupling and on the 5th d they were exposed to simulated aircraft motion. In D2, subjects were exposed to 4 consecutive days of torso rotation and on the 5th day they were exposed to the simulated aircraft motion as in D1. In D3, subjects were exposed to 5 consecutive days of simulated aircraft motion. Based on Graybiel's diagnostic criteria, severity of motion sickness on the 1st and 5th day in D1, D2, and D3 were compared.",
"Cross-coupled motion was the most provocative stimulus followed by torso rotation and simulated aircraft motion. Within each motion stimulus, there was evidence of desensitization (p < 0.001) within 4 d. There were no significant differences in the severity of motion sickness observed on the 5th day regardless of the desensitization stimuli."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adaptation, Physiological",
"Adolescent",
"Adult",
"Aircraft",
"Analysis of Variance",
"Disease Susceptibility",
"Female",
"Humans",
"Male",
"Motion Sickness",
"Rotation",
"Vestibule, Labyrinth"
]
} | Our results suggest that desensitization to one provocative motion could be transferred to a less severe motion stimulus. This result could be used in the refinement of desensitization programs for aircrew. | yes | [
{
"from": "human",
"value": "Question: Does desensitization to strong vestibular stimuli improve tolerance to simulated aircraft motion?\nContext: {'contexts': ['The extent to which tolerance acquired in one motion environment can be transferred to another has not been fully elucidated. This study compares three provocative motion stimuli and whether tolerance acquired from cross-coupled motion and torso rotation can be transferred to simulated aircraft motion.', \"There were 18 healthy subjects (9 men and 9 women), 18-44 yr of age, who were divided into 3 groups. Each group was exposed to the following desensitization procedure in a pseudo-random repeated measures design. In condition D1, subjects were exposed to 4 consecutive days of cross-coupling and on the 5th d they were exposed to simulated aircraft motion. In D2, subjects were exposed to 4 consecutive days of torso rotation and on the 5th day they were exposed to the simulated aircraft motion as in D1. In D3, subjects were exposed to 5 consecutive days of simulated aircraft motion. Based on Graybiel's diagnostic criteria, severity of motion sickness on the 1st and 5th day in D1, D2, and D3 were compared.\", 'Cross-coupled motion was the most provocative stimulus followed by torso rotation and simulated aircraft motion. Within each motion stimulus, there was evidence of desensitization (p < 0.001) within 4 d. There were no significant differences in the severity of motion sickness observed on the 5th day regardless of the desensitization stimuli.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adaptation, Physiological', 'Adolescent', 'Adult', 'Aircraft', 'Analysis of Variance', 'Disease Susceptibility', 'Female', 'Humans', 'Male', 'Motion Sickness', 'Rotation', 'Vestibule, Labyrinth']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,384,943 | Is h244R VSX1 associated with selective cone ON bipolar cell dysfunction and macular degeneration in a PPCD family? | {
"contexts": [
"To elucidate the retinal dysfunction and the molecular basis of posterior polymorphous corneal dystrophy (PPCD) associated with macular dystrophy, both inherited in a dominant manner through a three-generation family.",
"Ophthalmologic examinations including slit lamp examination, visual acuity tests, fundus visualization by scanning laser ophthalmoscopy, fluorescein angiography, color vision tests, electro-oculography, photopic and scotopic electroretinography (ERG) according to the International Society for Clinical Electrophysiology of Vision (ISCEV) protocols, and oscillatory potential (OP) recordings were conducted on affected family members. Corneal button from one affected patient was examined by transmission electron microscopy. All exons and intron-exon boundaries of the VSX1 and the COL8A2 genes were amplified by polymerase chain reaction and sequenced.",
"The presence of endothelial cells that have epithelial-like features with multiple layers, desmosomal junctions, and microvillous projections supports the diagnosis of PPCD. Sequence analysis indicated that the H244R variant in the VSX1 segregated with corneal and macular disease phenotypes in this family. Electrophysiologic studies indicated normal scotopic ERG findings, decreased amplitude of the photopic b-wave, photopic OP2 and OP3 barely recordable with a preserved OP4 amplitude, and variably decreased 30-Hz flicker amplitude."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Collagen Type VIII",
"Cornea",
"Corneal Dystrophies, Hereditary",
"Electrooculography",
"Electroretinography",
"Eye Proteins",
"Female",
"Fluorescein Angiography",
"Genes, Dominant",
"Homeodomain Proteins",
"Humans",
"Macular Degeneration",
"Male",
"Middle Aged",
"Mutation",
"Pedigree",
"Polymerase Chain Reaction",
"Retinal Bipolar Cells",
"Retinal Cone Photoreceptor Cells"
]
} | The human VSX1 is required for cone ON bipolar cell function but not for rod and cone OFF bipolar cells, giving a unique example of such a selective heritable retinal defect in humans. Furthermore, the authors provide the first clinical support for a new alternative role of VSX1 in cone biology, probably similar to that proposed for its goldfish ortholog during retinal differentiation. | yes | [
{
"from": "human",
"value": "Question: Is h244R VSX1 associated with selective cone ON bipolar cell dysfunction and macular degeneration in a PPCD family?\nContext: {'contexts': ['To elucidate the retinal dysfunction and the molecular basis of posterior polymorphous corneal dystrophy (PPCD) associated with macular dystrophy, both inherited in a dominant manner through a three-generation family.', 'Ophthalmologic examinations including slit lamp examination, visual acuity tests, fundus visualization by scanning laser ophthalmoscopy, fluorescein angiography, color vision tests, electro-oculography, photopic and scotopic electroretinography (ERG) according to the International Society for Clinical Electrophysiology of Vision (ISCEV) protocols, and oscillatory potential (OP) recordings were conducted on affected family members. Corneal button from one affected patient was examined by transmission electron microscopy. All exons and intron-exon boundaries of the VSX1 and the COL8A2 genes were amplified by polymerase chain reaction and sequenced.', 'The presence of endothelial cells that have epithelial-like features with multiple layers, desmosomal junctions, and microvillous projections supports the diagnosis of PPCD. Sequence analysis indicated that the H244R variant in the VSX1 segregated with corneal and macular disease phenotypes in this family. Electrophysiologic studies indicated normal scotopic ERG findings, decreased amplitude of the photopic b-wave, photopic OP2 and OP3 barely recordable with a preserved OP4 amplitude, and variably decreased 30-Hz flicker amplitude.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Collagen Type VIII', 'Cornea', 'Corneal Dystrophies, Hereditary', 'Electrooculography', 'Electroretinography', 'Eye Proteins', 'Female', 'Fluorescein Angiography', 'Genes, Dominant', 'Homeodomain Proteins', 'Humans', 'Macular Degeneration', 'Male', 'Middle Aged', 'Mutation', 'Pedigree', 'Polymerase Chain Reaction', 'Retinal Bipolar Cells', 'Retinal Cone Photoreceptor Cells']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,384,942 | Are globally , CYP1B1 mutations in primary congenital glaucoma strongly structured by geographic and haplotype backgrounds? | {
"contexts": [
"To obtain a global perspective on the distribution and evolution of CYP1B1 mutations in primary congenital glaucoma (PCG) worldwide.",
"Five intragenic single-nucleotide polymorphisms in CYP1B1-R48G, A119S, V432L, D449D, and N453S-were used to generate haplotype data from 138 Indian patients with PCG and 132 ethnically matched normal controls, which were then analyzed in conjunction with data from other populations. Maximum-likelihood estimates of haplotype frequencies were estimated from the genotype data. Subsets of patients and normal control subjects were also genotyped with respect to eight short tandem repeat (STR) markers around the CYP1B1 locus (D2S305, D2S165, D2S367, D2S2259, D2S391, D2S3337, D2S23678, and D2S286), to gain evolutionary insights.",
"Common mutations in CYP1B1 that are causal of PCG occurred on a uniform haplotype background among Indian patients, which is completely distinct from the modal haplotype background found among unaffected control subjects. Comparison of these data with data from other global regions reveals strong clustering of CYP1B1 mutations by geographic and haplotype backgrounds. The two distinct modal haplotypes found among Indian patients with PCG and control subjects are both ancient with ages of similar magnitudes, as indicated by large variances in the number of repeats at eight STR loci. Together with data from chimpanzee and normal control subjects from India and other global regions, it was possible to make a parsimonious reconstruction of the evolution of these haplotypes."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Africa",
"Age of Onset",
"Americas",
"Aryl Hydrocarbon Hydroxylases",
"Asia",
"Cytochrome P-450 CYP1B1",
"Cytochrome P-450 Enzyme System",
"Europe",
"Genetic Markers",
"Glaucoma",
"Haplotypes",
"Humans",
"Infant",
"Infant, Newborn",
"Likelihood Functions",
"Mutation",
"Polymorphism, Single Nucleotide"
]
} | The strong association of specific haplotypes with some predominant CYP1B1 mutations underlying PCG and the observed geographical clustering, probably due to founder effects, may be useful for predictive testing. | yes | [
{
"from": "human",
"value": "Question: Are globally , CYP1B1 mutations in primary congenital glaucoma strongly structured by geographic and haplotype backgrounds?\nContext: {'contexts': ['To obtain a global perspective on the distribution and evolution of CYP1B1 mutations in primary congenital glaucoma (PCG) worldwide.', 'Five intragenic single-nucleotide polymorphisms in CYP1B1-R48G, A119S, V432L, D449D, and N453S-were used to generate haplotype data from 138 Indian patients with PCG and 132 ethnically matched normal controls, which were then analyzed in conjunction with data from other populations. Maximum-likelihood estimates of haplotype frequencies were estimated from the genotype data. Subsets of patients and normal control subjects were also genotyped with respect to eight short tandem repeat (STR) markers around the CYP1B1 locus (D2S305, D2S165, D2S367, D2S2259, D2S391, D2S3337, D2S23678, and D2S286), to gain evolutionary insights.', 'Common mutations in CYP1B1 that are causal of PCG occurred on a uniform haplotype background among Indian patients, which is completely distinct from the modal haplotype background found among unaffected control subjects. Comparison of these data with data from other global regions reveals strong clustering of CYP1B1 mutations by geographic and haplotype backgrounds. The two distinct modal haplotypes found among Indian patients with PCG and control subjects are both ancient with ages of similar magnitudes, as indicated by large variances in the number of repeats at eight STR loci. Together with data from chimpanzee and normal control subjects from India and other global regions, it was possible to make a parsimonious reconstruction of the evolution of these haplotypes.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Africa', 'Age of Onset', 'Americas', 'Aryl Hydrocarbon Hydroxylases', 'Asia', 'Cytochrome P-450 CYP1B1', 'Cytochrome P-450 Enzyme System', 'Europe', 'Genetic Markers', 'Glaucoma', 'Haplotypes', 'Humans', 'Infant', 'Infant, Newborn', 'Likelihood Functions', 'Mutation', 'Polymorphism, Single Nucleotide']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,398,405 | Is pancreatic cancer cells invasiveness mainly affected by interleukin-1beta not by transforming growth factor-beta1? | {
"contexts": [
"We investigated in vitro whether IL-1beta and TGF-beta1 affect pancreatic cancer cell growth, adhesion to the extracellular matrix and Matrigel invasion.",
"Adhesion to fibronectin, laminin and type I collagen, and Matrigel invasion after stimulation with saline, IL-1beta and TGF-beta1 were evaluated using three primary and three metastatic pancreatic cancer cell lines.",
"Extracellular matrix adhesion of control cells varied independently of the metastatic characteristics of the studied cell lines, whereas Matrigel invasion of control cells was partly correlated with the in vivo metastatic potential. IL-1beta did not influence extracellular matrix adhesion, whereas it significantly enhanced the invasiveness of three of the six cell lines. TGF-beta1 affected the adhesion of one cell line, and exerted contrasting effects on Matrigel invasion of different cell lines."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Cell Adhesion",
"Cell Line, Tumor",
"Extracellular Matrix",
"Humans",
"Interleukin-1",
"Neoplasm Invasiveness",
"Pancreatic Neoplasms",
"Transforming Growth Factor beta",
"Transforming Growth Factor beta1"
]
} | IL-1beta enhances the invasive capacity of pancreatic cancer cells, whereas TGF-beta1 has paradoxical effects on pancreatic cancer cells; this makes it difficult to interfere with TGF-beta1 signaling in pancreatic cancer treatment. | yes | [
{
"from": "human",
"value": "Question: Is pancreatic cancer cells invasiveness mainly affected by interleukin-1beta not by transforming growth factor-beta1?\nContext: {'contexts': ['We investigated in vitro whether IL-1beta and TGF-beta1 affect pancreatic cancer cell growth, adhesion to the extracellular matrix and Matrigel invasion.', 'Adhesion to fibronectin, laminin and type I collagen, and Matrigel invasion after stimulation with saline, IL-1beta and TGF-beta1 were evaluated using three primary and three metastatic pancreatic cancer cell lines.', 'Extracellular matrix adhesion of control cells varied independently of the metastatic characteristics of the studied cell lines, whereas Matrigel invasion of control cells was partly correlated with the in vivo metastatic potential. IL-1beta did not influence extracellular matrix adhesion, whereas it significantly enhanced the invasiveness of three of the six cell lines. TGF-beta1 affected the adhesion of one cell line, and exerted contrasting effects on Matrigel invasion of different cell lines.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Cell Adhesion', 'Cell Line, Tumor', 'Extracellular Matrix', 'Humans', 'Interleukin-1', 'Neoplasm Invasiveness', 'Pancreatic Neoplasms', 'Transforming Growth Factor beta', 'Transforming Growth Factor beta1']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,386,511 | Is evolution of the renal function a better predictor of long-term survival than serum creatinine? | {
"contexts": [
"In recent years acute rejection has decreased to 10% to 20%. Therefore it is necessary to look for new endpoints in renal transplantation. Serum creatinine and changes in creatinine have been reported to be powerful predictors of long-term kidney transplant survival. Chronic renal allograft nephropathy is the primary cause of long-term graft failure but may appear at any stage in the evolution.",
"Data from 315 patients receiving cadaver donor renal transplants between February 1987 and March 2001 that functioned for 1 year were examined for the influence of demographic characteristics and transplant variables. Creatinine clearance was estimated using the Cockroft-Gault formula. Survival was assessed with the actuarial method. The multivariate analyses were performed using Cox proportional hazard models.",
"The 10-year graft survival showed a relative risk of 2.5 in the univariate analysis when there was more than 10% decrease in renal function at 3 months compared with nadir values. When the decrease was more than 25% of creatinine clearance at the third month, during the evolution and serum creatinine at 3 months introduced in the multivariate model, the latter was not significant, while the other variables had a RR of 4.4 and 10, respectively."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Creatinine",
"Female",
"Follow-Up Studies",
"Graft Survival",
"Humans",
"Kidney Function Tests",
"Kidney Transplantation",
"Male",
"Middle Aged",
"Multivariate Analysis",
"Predictive Value of Tests",
"Retrospective Studies",
"Time Factors"
]
} | The evolution of renal function at 3 months and throughout the evolution were better predictors of graft failure than an isolated serum creatinine value. | yes | [
{
"from": "human",
"value": "Question: Is evolution of the renal function a better predictor of long-term survival than serum creatinine?\nContext: {'contexts': ['In recent years acute rejection has decreased to 10% to 20%. Therefore it is necessary to look for new endpoints in renal transplantation. Serum creatinine and changes in creatinine have been reported to be powerful predictors of long-term kidney transplant survival. Chronic renal allograft nephropathy is the primary cause of long-term graft failure but may appear at any stage in the evolution.', 'Data from 315 patients receiving cadaver donor renal transplants between February 1987 and March 2001 that functioned for 1 year were examined for the influence of demographic characteristics and transplant variables. Creatinine clearance was estimated using the Cockroft-Gault formula. Survival was assessed with the actuarial method. The multivariate analyses were performed using Cox proportional hazard models.', 'The 10-year graft survival showed a relative risk of 2.5 in the univariate analysis when there was more than 10% decrease in renal function at 3 months compared with nadir values. When the decrease was more than 25% of creatinine clearance at the third month, during the evolution and serum creatinine at 3 months introduced in the multivariate model, the latter was not significant, while the other variables had a RR of 4.4 and 10, respectively.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Creatinine', 'Female', 'Follow-Up Studies', 'Graft Survival', 'Humans', 'Kidney Function Tests', 'Kidney Transplantation', 'Male', 'Middle Aged', 'Multivariate Analysis', 'Predictive Value of Tests', 'Retrospective Studies', 'Time Factors']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,378,111 | Does [ Lysophosphatidic acid activate L-arginine/nitric oxide pathway of platelets in rats ]? | {
"contexts": [
"To investigate the mechanism of platelet function caused by Lysophosphatidic acid (LPA), by observing the change of the L-arginine/nitric oxide synthase/nitric oxide (L-Arg/NOS/NO) pathway of platelet in rats.",
"LPA (10(-6), 10(-5) and 5x10(-5) mol/L) was administrated in rats and incubated for 30 and 60 minutes. The nitrite production was measured by Greiss assay; NOS activities and L-arginine transportation were detected by isotope tracer method and intracellular [Ca(2+)]i changes by fluorescent probe.",
"LPA increased NO release by 35% and 56%, after incubating for 30 and 60 minutes, respectively. LPA (10(-6), 10(-5)aand 5x10(-5) mol/L) enhanced the NO productions of platelets in a concentration-dependent manner (P<0.01). EC(50) was 17.8 micromol/L, and 95% CI was 13.3-24.2 micromol/L, involved in the physiological concentration of LPA in plasma (P<0.01). Simultaneously, different doses of LPA increased NOS activities and L-arginine uptake in a dose-dependent manner (P<0.01). In this study, LPA (50 micromol/L) increased the intracellular free calcium ion concentration ([Ca(2+)]i, P<0.01), after incubating for 30 and 60 minutes. Pre-treated with NOS inhibitor-L-NAME for 20 minutes, LPA obviously enhanced the effects by 20% and 32% respectively (P<0.01). On the contrary, pre-treated with L-arginine (200 micromol/L) for the same times obviously reduced the effects by 14% and 18% respectively (P<0.01)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Arginine",
"Blood Platelets",
"Dose-Response Relationship, Drug",
"Enzyme Inhibitors",
"Lysophospholipids",
"Male",
"NG-Nitroarginine Methyl Ester",
"Nitric Oxide",
"Nitric Oxide Synthase",
"Rats",
"Rats, Sprague-Dawley",
"Signal Transduction"
]
} | LPA increased NO release by enhancing L-arginine uptake and NOS activities, up-regulating L-arginine/NOS/NO pathway in platelets of rats. | yes | [
{
"from": "human",
"value": "Question: Does [ Lysophosphatidic acid activate L-arginine/nitric oxide pathway of platelets in rats ]?\nContext: {'contexts': ['To investigate the mechanism of platelet function caused by Lysophosphatidic acid (LPA), by observing the change of the L-arginine/nitric oxide synthase/nitric oxide (L-Arg/NOS/NO) pathway of platelet in rats.', 'LPA (10(-6), 10(-5) and 5x10(-5) mol/L) was administrated in rats and incubated for 30 and 60 minutes. The nitrite production was measured by Greiss assay; NOS activities and L-arginine transportation were detected by isotope tracer method and intracellular [Ca(2+)]i changes by fluorescent probe.', 'LPA increased NO release by 35% and 56%, after incubating for 30 and 60 minutes, respectively. LPA (10(-6), 10(-5)aand 5x10(-5) mol/L) enhanced the NO productions of platelets in a concentration-dependent manner (P<0.01). EC(50) was 17.8 micromol/L, and 95% CI was 13.3-24.2 micromol/L, involved in the physiological concentration of LPA in plasma (P<0.01). Simultaneously, different doses of LPA increased NOS activities and L-arginine uptake in a dose-dependent manner (P<0.01). In this study, LPA (50 micromol/L) increased the intracellular free calcium ion concentration ([Ca(2+)]i, P<0.01), after incubating for 30 and 60 minutes. Pre-treated with NOS inhibitor-L-NAME for 20 minutes, LPA obviously enhanced the effects by 20% and 32% respectively (P<0.01). On the contrary, pre-treated with L-arginine (200 micromol/L) for the same times obviously reduced the effects by 14% and 18% respectively (P<0.01).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Arginine', 'Blood Platelets', 'Dose-Response Relationship, Drug', 'Enzyme Inhibitors', 'Lysophospholipids', 'Male', 'NG-Nitroarginine Methyl Ester', 'Nitric Oxide', 'Nitric Oxide Synthase', 'Rats', 'Rats, Sprague-Dawley', 'Signal Transduction']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,378,112 | Is [ Cell-cycle negative regulatory gene ANA over-expressed in the brain tissues of patients with Down syndrome ]? | {
"contexts": [
"To investigate the expression level of genes located in chromosome 21 in the brain tissues of Down syndrome(DS).",
"An optimized semi-quantitative RT-PCR method was used to evaluate the expression levels of seven genes encoded in chromosome 21 in fetal cortex brain and cerebellum of DS and the control at the end of 20 weeks of gestation. B2M was used as internal reference to normalize cell loss.",
"The expression levels of 6 genes in cortex and cerebellum, including DYRK1A, SYNJ1, PCP4, C21orf5, C21orf2 and C21orf106, were comparable between DS and the control. ANA, a cell-cycle negative regulatory gene, was over-expressed dramatically in the cortex but not in the cerebellum of DS."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Brain",
"Cell Cycle Proteins",
"Cerebellum",
"Cerebral Cortex",
"Chromosomes, Human, Pair 21",
"Down Syndrome",
"Gene Expression Regulation, Developmental",
"Humans",
"RNA, Messenger",
"Reverse Transcriptase Polymerase Chain Reaction"
]
} | Over-expression of ANA may contribute to the reduction of neuronal density in DS brain. | yes | [
{
"from": "human",
"value": "Question: Is [ Cell-cycle negative regulatory gene ANA over-expressed in the brain tissues of patients with Down syndrome ]?\nContext: {'contexts': ['To investigate the expression level of genes located in chromosome 21 in the brain tissues of Down syndrome(DS).', 'An optimized semi-quantitative RT-PCR method was used to evaluate the expression levels of seven genes encoded in chromosome 21 in fetal cortex brain and cerebellum of DS and the control at the end of 20 weeks of gestation. B2M was used as internal reference to normalize cell loss.', 'The expression levels of 6 genes in cortex and cerebellum, including DYRK1A, SYNJ1, PCP4, C21orf5, C21orf2 and C21orf106, were comparable between DS and the control. ANA, a cell-cycle negative regulatory gene, was over-expressed dramatically in the cortex but not in the cerebellum of DS.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Brain', 'Cell Cycle Proteins', 'Cerebellum', 'Cerebral Cortex', 'Chromosomes, Human, Pair 21', 'Down Syndrome', 'Gene Expression Regulation, Developmental', 'Humans', 'RNA, Messenger', 'Reverse Transcriptase Polymerase Chain Reaction']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,386,307 | Is young age a risk factor for HIV among female sex workers -- an experience from India? | {
"contexts": [
"A cross-sectional community-based study was conducted among brothel-based sex workers of West Bengal, eastern India, to study the prevalence of HIV and associated risk factors.",
"Unlinked anonymous HIV testing was performed on 2076 sex workers. Of these, 558 were interviewed using a pre-tested questionnaire to study their risk factors.",
"Overall HIV sero-prevalence was 5.9%. All infections were HIV-1, except that four sex workers from Kolkata were infected with HIV-2. Surprisingly, HIV infection was much higher (12.5%) in younger sex workers (age < or =20 years) compared with older age groups (5.4%) (P=0.002; odds ratio 2.40, 95% CI: 1.29-4.38)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"AIDS Serodiagnosis",
"Adolescent",
"Adult",
"Age Distribution",
"Age Factors",
"Child",
"Female",
"HIV Antibodies",
"HIV Infections",
"HIV-1",
"HIV-2",
"Humans",
"India",
"Middle Aged",
"Risk Factors",
"Risk-Taking",
"Sex Work",
"Sexual Behavior",
"Sexually Transmitted Diseases",
"Surveys and Questionnaires"
]
} | This could be associated with larger areas of cervical ectopy of younger sex workers who are subjected to repeated trauma during sexual intercourse, facilitating higher HIV transmission. Behavioral factors may increase a young sex worker's risk of acquiring HIV infection, including professional immaturity with clients, which might lead to more unprotected sex. HIV status was associated with other sexually transmitted infection in the previous year but was not associated with literacy status, daily income, duration of sex work, number of clients entertained per day, entertaining clients outside a brothel (in a hotel), and reported condom use. | yes | [
{
"from": "human",
"value": "Question: Is young age a risk factor for HIV among female sex workers -- an experience from India?\nContext: {'contexts': ['A cross-sectional community-based study was conducted among brothel-based sex workers of West Bengal, eastern India, to study the prevalence of HIV and associated risk factors.', 'Unlinked anonymous HIV testing was performed on 2076 sex workers. Of these, 558 were interviewed using a pre-tested questionnaire to study their risk factors.', 'Overall HIV sero-prevalence was 5.9%. All infections were HIV-1, except that four sex workers from Kolkata were infected with HIV-2. Surprisingly, HIV infection was much higher (12.5%) in younger sex workers (age < or =20 years) compared with older age groups (5.4%) (P=0.002; odds ratio 2.40, 95% CI: 1.29-4.38).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['AIDS Serodiagnosis', 'Adolescent', 'Adult', 'Age Distribution', 'Age Factors', 'Child', 'Female', 'HIV Antibodies', 'HIV Infections', 'HIV-1', 'HIV-2', 'Humans', 'India', 'Middle Aged', 'Risk Factors', 'Risk-Taking', 'Sex Work', 'Sexual Behavior', 'Sexually Transmitted Diseases', 'Surveys and Questionnaires']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,385,498 | Does anti-tumor necrosis factor therapy increase synovial osteoprotegerin expression in rheumatoid arthritis? | {
"contexts": [
"Treatment of rheumatoid arthritis (RA) with tumor necrosis factor (TNF)-blocking agents, including etanercept and infliximab, has resulted in reductions in the radiographic progression of RA. However, the exact mechanism by which this protection occurs has not been determined. In order to add to such knowledge, we investigated the effect of anti-TNF therapy on the expression of osteoprotegerin (OPG) and receptor activator of NF-kappaB ligand (RANKL) in synovial tissue.",
"The expression of OPG and RANKL in synovial biopsy specimens was evaluated by immunohistochemistry. Serial synovial biopsy specimens were obtained from 18 patients with RA, before and after treatment with etanercept (9 patients) or infliximab (9 patients). Biopsy specimens were evaluated by double-blind semiquantitative analysis and image analysis. The in vitro effect of TNF antagonists on the RANKL/OPG expression in osteoblasts and endothelial cells was evaluated by Western blotting. Statistical analysis was performed using Wilcoxon's signed rank test, followed by the Bonferroni correction for multiple comparisons of paired samples. The results of in vitro experiments were evaluated by one-way analysis of variance, with Tukey's post hoc test.",
"Treatment with both infliximab and etanercept increased the expression of OPG in synovial tissue. After 8 weeks of treatment, neither infliximab nor etanercept influenced RANKL expression. In both groups of patients, the RANKL:OPG ratio decreased following therapy. In vitro, both of the TNF antagonists mimicked the in vivo effect, inducing a decrease in the RANKL:OPG ratio in TNF-primed osteoblasts and endothelial cells."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Antibodies, Monoclonal",
"Antirheumatic Agents",
"Arthritis, Rheumatoid",
"Carrier Proteins",
"Etanercept",
"Female",
"Glycoproteins",
"Humans",
"Immunoglobulin G",
"Infliximab",
"Male",
"Membrane Glycoproteins",
"Middle Aged",
"Osteoprotegerin",
"RANK Ligand",
"Receptor Activator of Nuclear Factor-kappa B",
"Receptors, Cytoplasmic and Nuclear",
"Receptors, Tumor Necrosis Factor",
"Synovial Membrane",
"Tumor Necrosis Factor-alpha"
]
} | Therapy with TNF antagonists in RA modulates the OPG/RANKL system, a potential mechanism that could explain the retardation of radiographic damage observed following anti-TNF therapy. | yes | [
{
"from": "human",
"value": "Question: Does anti-tumor necrosis factor therapy increase synovial osteoprotegerin expression in rheumatoid arthritis?\nContext: {'contexts': ['Treatment of rheumatoid arthritis (RA) with tumor necrosis factor (TNF)-blocking agents, including etanercept and infliximab, has resulted in reductions in the radiographic progression of RA. However, the exact mechanism by which this protection occurs has not been determined. In order to add to such knowledge, we investigated the effect of anti-TNF therapy on the expression of osteoprotegerin (OPG) and receptor activator of NF-kappaB ligand (RANKL) in synovial tissue.', \"The expression of OPG and RANKL in synovial biopsy specimens was evaluated by immunohistochemistry. Serial synovial biopsy specimens were obtained from 18 patients with RA, before and after treatment with etanercept (9 patients) or infliximab (9 patients). Biopsy specimens were evaluated by double-blind semiquantitative analysis and image analysis. The in vitro effect of TNF antagonists on the RANKL/OPG expression in osteoblasts and endothelial cells was evaluated by Western blotting. Statistical analysis was performed using Wilcoxon's signed rank test, followed by the Bonferroni correction for multiple comparisons of paired samples. The results of in vitro experiments were evaluated by one-way analysis of variance, with Tukey's post hoc test.\", 'Treatment with both infliximab and etanercept increased the expression of OPG in synovial tissue. After 8 weeks of treatment, neither infliximab nor etanercept influenced RANKL expression. In both groups of patients, the RANKL:OPG ratio decreased following therapy. In vitro, both of the TNF antagonists mimicked the in vivo effect, inducing a decrease in the RANKL:OPG ratio in TNF-primed osteoblasts and endothelial cells.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Antibodies, Monoclonal', 'Antirheumatic Agents', 'Arthritis, Rheumatoid', 'Carrier Proteins', 'Etanercept', 'Female', 'Glycoproteins', 'Humans', 'Immunoglobulin G', 'Infliximab', 'Male', 'Membrane Glycoproteins', 'Middle Aged', 'Osteoprotegerin', 'RANK Ligand', 'Receptor Activator of Nuclear Factor-kappa B', 'Receptors, Cytoplasmic and Nuclear', 'Receptors, Tumor Necrosis Factor', 'Synovial Membrane', 'Tumor Necrosis Factor-alpha']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,372,488 | Does postmastectomy radiotherapy reduce locoregional recurrence in elderly women with high-risk breast cancer? | {
"contexts": [
"Clinical trials of adjuvant radiotherapy after mastectomy have largely excluded women aged 70 years or over, even though they comprise 30% of the breast cancer population. This study examined outcomes in elderly women with high-risk breast cancer treated with or without postmastectomy radiotherapy (PMRT).",
"Data were analysed for 233 women aged 70 years or over with high-risk breast cancer (tumours > 5 cm or > or = 4 positive axillary nodes) treated with mastectomy and referred to the British Columbia Cancer Agency from 1989 to 1997. Tumour and treatment characteristics were compared between two cohorts: women treated with PMRT (n = 147) vs women treated without PMRT (n = 86). Univariate and multivariate analyses of 10-year Kaplan-Meier locoregional recurrence (LRR), distant recurrence, breast cancer-specific survival and overall survival were carried out.",
"Median follow-up time was 5.5 years. The distribution of tumour sizes was similar in the two groups. Compared with women treated without PMRT, higher proportions of women who underwent PMRT had four or more positive nodes (83% vs 67%, P = 0.01) and positive surgical margins (14% vs 4%, P = 0.02). Systemic therapy, used in 94% of women, was comparable in the two cohorts (P = 0.63). Elderly women treated with PMRT had significantly lower LRR compared with women treated without PMRT (16% vs 28%, P = 0.03). No differences in distant recurrence, breast cancer-specific survival or overall survival were observed in the two treatment groups (all P > 0.05). On multivariate analysis, the omission of PMRT and the presence of high-grade histology were significant predictors of LRR, whereas an increasing number of positive nodes was significantly associated with distant recurrence and overall survival."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Aged, 80 and over",
"Breast Neoplasms",
"Combined Modality Therapy",
"Female",
"Humans",
"Mastectomy",
"Multivariate Analysis",
"Neoplasm Recurrence, Local"
]
} | In women aged 70 years or over with tumours greater than 5 cm or four or more positive nodes, significantly lower LRR was observed in women treated with radiotherapy compared with women treated without radiotherapy. PMRT should be considered in the management of elderly women with these high-risk characteristics. | yes | [
{
"from": "human",
"value": "Question: Does postmastectomy radiotherapy reduce locoregional recurrence in elderly women with high-risk breast cancer?\nContext: {'contexts': ['Clinical trials of adjuvant radiotherapy after mastectomy have largely excluded women aged 70 years or over, even though they comprise 30% of the breast cancer population. This study examined outcomes in elderly women with high-risk breast cancer treated with or without postmastectomy radiotherapy (PMRT).', 'Data were analysed for 233 women aged 70 years or over with high-risk breast cancer (tumours > 5 cm or > or = 4 positive axillary nodes) treated with mastectomy and referred to the British Columbia Cancer Agency from 1989 to 1997. Tumour and treatment characteristics were compared between two cohorts: women treated with PMRT (n = 147) vs women treated without PMRT (n = 86). Univariate and multivariate analyses of 10-year Kaplan-Meier locoregional recurrence (LRR), distant recurrence, breast cancer-specific survival and overall survival were carried out.', 'Median follow-up time was 5.5 years. The distribution of tumour sizes was similar in the two groups. Compared with women treated without PMRT, higher proportions of women who underwent PMRT had four or more positive nodes (83% vs 67%, P = 0.01) and positive surgical margins (14% vs 4%, P = 0.02). Systemic therapy, used in 94% of women, was comparable in the two cohorts (P = 0.63). Elderly women treated with PMRT had significantly lower LRR compared with women treated without PMRT (16% vs 28%, P = 0.03). No differences in distant recurrence, breast cancer-specific survival or overall survival were observed in the two treatment groups (all P > 0.05). On multivariate analysis, the omission of PMRT and the presence of high-grade histology were significant predictors of LRR, whereas an increasing number of positive nodes was significantly associated with distant recurrence and overall survival.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Aged, 80 and over', 'Breast Neoplasms', 'Combined Modality Therapy', 'Female', 'Humans', 'Mastectomy', 'Multivariate Analysis', 'Neoplasm Recurrence, Local']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,387,179 | Does cyclosporine suppress cell growth and collagen production in hepatic stellate cells? | {
"contexts": [
"In HCV-related graft hepatitis, immunosuppression has been implicated in rapid progression to cirrhosis, a serious clinical issue. We investigated the effects of cyclosporine or tacrolimus on cell growth and collagen production by hepatic stellate cells (HSC), which play a role in hepatic fibrosis.",
"Cultured rat HSCs and human HSC-derived TWNT-4 cells were evaluated for proliferation, type I collagen, phosphorylation states of mitogen-activated protein kinases extracellular signal-regulated kinase 1/2; [MAPKs Erk1/2], c-Jun N-terminal kinase (JNK, p38), as well as the expression of collagen, matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) genes.",
"Cyclosporine suppressed cell growth and collagen production in a concentration-dependent manner. At clinically relevant concentrations of 0.125 micromol (150 ng/mL) cyclosporine significantly reduced collagen production per cell by more than 50%. Similarly, tacrolimus also reduced both collagen concentration and cell number; however, tacrolimus at a clinically relevant concentration of 12.5 nmol (10 ng/mL) did not significantly reduce collagen production. Treatment with cyclosporine reduced type I collagen and TIMP-1 expression and enhanced MMP-1 expression. Cyclosporine also inhibited phosphorylation strongly for JNK and p38, and weakly inhibited for Erk1/2."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Cells, Cultured",
"Collagen",
"Collagen Type I",
"Cyclosporine",
"Dose-Response Relationship, Drug",
"Hepatocytes",
"Humans",
"Immunosuppressive Agents",
"Mice",
"Tacrolimus",
"Tissue Inhibitor of Metalloproteinase-1"
]
} | These findings demonstrated that cyclosporine suppresses cell growth and collagen production, suggesting that it may have an antifibrogenic effect. | yes | [
{
"from": "human",
"value": "Question: Does cyclosporine suppress cell growth and collagen production in hepatic stellate cells?\nContext: {'contexts': ['In HCV-related graft hepatitis, immunosuppression has been implicated in rapid progression to cirrhosis, a serious clinical issue. We investigated the effects of cyclosporine or tacrolimus on cell growth and collagen production by hepatic stellate cells (HSC), which play a role in hepatic fibrosis.', 'Cultured rat HSCs and human HSC-derived TWNT-4 cells were evaluated for proliferation, type I collagen, phosphorylation states of mitogen-activated protein kinases extracellular signal-regulated kinase 1/2; [MAPKs Erk1/2], c-Jun N-terminal kinase (JNK, p38), as well as the expression of collagen, matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) genes.', 'Cyclosporine suppressed cell growth and collagen production in a concentration-dependent manner. At clinically relevant concentrations of 0.125 micromol (150 ng/mL) cyclosporine significantly reduced collagen production per cell by more than 50%. Similarly, tacrolimus also reduced both collagen concentration and cell number; however, tacrolimus at a clinically relevant concentration of 12.5 nmol (10 ng/mL) did not significantly reduce collagen production. Treatment with cyclosporine reduced type I collagen and TIMP-1 expression and enhanced MMP-1 expression. Cyclosporine also inhibited phosphorylation strongly for JNK and p38, and weakly inhibited for Erk1/2.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Cells, Cultured', 'Collagen', 'Collagen Type I', 'Cyclosporine', 'Dose-Response Relationship, Drug', 'Hepatocytes', 'Humans', 'Immunosuppressive Agents', 'Mice', 'Tacrolimus', 'Tissue Inhibitor of Metalloproteinase-1']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,384,883 | Are increased plasma markers of oxidative stress associated with coronary heart disease in males with diabetes mellitus and with 10-year risk in a prospective sample of males? | {
"contexts": [
"Increased oxidative stress is associated with coronary heart disease (CHD). We examined the association between plasma markers of oxidative stress and CHD in a cross-sectional sample of patients with diabetes and prospective CHD risk in a sample of men predominantly without diabetes.",
"Plasma total antioxidant status (TAOS) and the ratio of oxidized LDL (Ox-LDL) to LDL-cholesterol (LDL-C) were determined in a cross-section of 761 Caucasian individuals with diabetes (UDACS study). Plasma TAOS was also determined in 310 baseline samples from a 10-year prospective cohort of 3012 healthy males (NPHSII).",
"Within UDACS, males with CHD had lower mean (SD) plasma TAOS [no CHD, 43.4 (13.2)%; CHD, 40.3 (13.8)%; P = 0.04]. The prevalence of CHD was higher in the lowest compared with the upper quartiles (32.7% vs 19.7%; P = 0.004). We observed a significant association between plasma Ox-LDL:LDL-C and CHD status [no CHD vs CHD, 16.9 (3.1) vs 19.3 (5.0) units/mmol; P = 0.04], with the prevalence of CHD being higher among men in the upper compared with lower quartiles (18.4% vs 35.1%; P = 0.003). No association was observed in females. In NPHSII, TAOS was lower in those who developed CHD [35.1 (8.0)% vs 37.1 (7.9)%; P = 0.04]. The odds ratio for CHD in the lowest compared with the upper quartile was 1.91 (95% confidence interval, 0.99-3.70; P = 0.04). This remained unchanged after adjustment for classic risk factors."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Antioxidants",
"Biomarkers",
"Coronary Disease",
"Cross-Sectional Studies",
"Diabetes Complications",
"Female",
"Humans",
"Male",
"Middle Aged",
"Oxidative Stress",
"Prospective Studies",
"Risk",
"Risk Factors",
"Sex Factors"
]
} | A cross-sectional and prospective association exists between baseline plasma measures of oxidative stress and CHD risk. The association with prospective CHD risk remained after adjustment for "traditional" risk factors, implying an independent role for oxidative stress in CHD risk. | yes | [
{
"from": "human",
"value": "Question: Are increased plasma markers of oxidative stress associated with coronary heart disease in males with diabetes mellitus and with 10-year risk in a prospective sample of males?\nContext: {'contexts': ['Increased oxidative stress is associated with coronary heart disease (CHD). We examined the association between plasma markers of oxidative stress and CHD in a cross-sectional sample of patients with diabetes and prospective CHD risk in a sample of men predominantly without diabetes.', 'Plasma total antioxidant status (TAOS) and the ratio of oxidized LDL (Ox-LDL) to LDL-cholesterol (LDL-C) were determined in a cross-section of 761 Caucasian individuals with diabetes (UDACS study). Plasma TAOS was also determined in 310 baseline samples from a 10-year prospective cohort of 3012 healthy males (NPHSII).', 'Within UDACS, males with CHD had lower mean (SD) plasma TAOS [no CHD, 43.4 (13.2)%; CHD, 40.3 (13.8)%; P = 0.04]. The prevalence of CHD was higher in the lowest compared with the upper quartiles (32.7% vs 19.7%; P = 0.004). We observed a significant association between plasma Ox-LDL:LDL-C and CHD status [no CHD vs CHD, 16.9 (3.1) vs 19.3 (5.0) units/mmol; P = 0.04], with the prevalence of CHD being higher among men in the upper compared with lower quartiles (18.4% vs 35.1%; P = 0.003). No association was observed in females. In NPHSII, TAOS was lower in those who developed CHD [35.1 (8.0)% vs 37.1 (7.9)%; P = 0.04]. The odds ratio for CHD in the lowest compared with the upper quartile was 1.91 (95% confidence interval, 0.99-3.70; P = 0.04). This remained unchanged after adjustment for classic risk factors.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Antioxidants', 'Biomarkers', 'Coronary Disease', 'Cross-Sectional Studies', 'Diabetes Complications', 'Female', 'Humans', 'Male', 'Middle Aged', 'Oxidative Stress', 'Prospective Studies', 'Risk', 'Risk Factors', 'Sex Factors']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,401,472 | Do transient lower esophageal sphincter relaxations result from passive opening of the cardia by gastric distention? | {
"contexts": [
"Transient lower esophageal sphincter relaxation is the main mechanism for gastroesophageal reflux. Although there is evidence that transient lower esophageal sphincter relaxations are neurally mediated, another school of thought is that transient lower esophageal sphincter relaxations result from gastric distention, which shortens the sphincter to the point where it opens and the pressure decreases. We assessed the relationship of transient lower esophageal sphincter relaxation to gastroesophageal junction opening in an unsedated human model.",
"Seven healthy volunteers (6 men and 1 woman, aged 18-53 years) were studied while they were sitting. Manometry was performed by using a sleeve catheter passed through 1 nostril. A 5.3-mm endoscope was placed through the other nostril to obtain a retroflexed view of the cardia. The biopsy channel was connected to a barostat to distend the stomach with air at 15 mm Hg for 30 minutes. Manometric and endoscopic video-recording times were synchronized but scored independently.",
"The transient lower esophageal sphincter relaxation onset invariably preceded gastroesophageal junction opening (median, 5.0 seconds; range, 0.5-20.7 seconds; P < .001). The transient lower esophageal sphincter relaxation nadir also typically occurred before gastroesophageal junction opening (median, 2.1 seconds; range, -4.2 to +19.5 seconds; P < .001). Once open, the gastroesophageal junction moved proximally for the duration of the transient lower esophageal sphincter relaxation. Termination of transient lower esophageal sphincter relaxations occurred about the time the time of gastroesophageal junction closure."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Cardia",
"Endoscopy, Gastrointestinal",
"Esophageal Sphincter, Lower",
"Female",
"Gastroesophageal Reflux",
"Humans",
"Male",
"Manometry",
"Middle Aged",
"Pressure",
"Video Recording"
]
} | These data refute the hypothesis that transient lower esophageal sphincter relaxations result from passive mechanical distraction of the gastroesophageal junction. Rather, transient lower esophageal sphincter relaxations must occur before the gastroesophageal junction can open. | no | [
{
"from": "human",
"value": "Question: Do transient lower esophageal sphincter relaxations result from passive opening of the cardia by gastric distention?\nContext: {'contexts': ['Transient lower esophageal sphincter relaxation is the main mechanism for gastroesophageal reflux. Although there is evidence that transient lower esophageal sphincter relaxations are neurally mediated, another school of thought is that transient lower esophageal sphincter relaxations result from gastric distention, which shortens the sphincter to the point where it opens and the pressure decreases. We assessed the relationship of transient lower esophageal sphincter relaxation to gastroesophageal junction opening in an unsedated human model.', 'Seven healthy volunteers (6 men and 1 woman, aged 18-53 years) were studied while they were sitting. Manometry was performed by using a sleeve catheter passed through 1 nostril. A 5.3-mm endoscope was placed through the other nostril to obtain a retroflexed view of the cardia. The biopsy channel was connected to a barostat to distend the stomach with air at 15 mm Hg for 30 minutes. Manometric and endoscopic video-recording times were synchronized but scored independently.', 'The transient lower esophageal sphincter relaxation onset invariably preceded gastroesophageal junction opening (median, 5.0 seconds; range, 0.5-20.7 seconds; P < .001). The transient lower esophageal sphincter relaxation nadir also typically occurred before gastroesophageal junction opening (median, 2.1 seconds; range, -4.2 to +19.5 seconds; P < .001). Once open, the gastroesophageal junction moved proximally for the duration of the transient lower esophageal sphincter relaxation. Termination of transient lower esophageal sphincter relaxations occurred about the time the time of gastroesophageal junction closure.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Cardia', 'Endoscopy, Gastrointestinal', 'Esophageal Sphincter, Lower', 'Female', 'Gastroesophageal Reflux', 'Humans', 'Male', 'Manometry', 'Middle Aged', 'Pressure', 'Video Recording']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
16,401,477 | Does reg IV activate the epidermal growth factor receptor/Akt/AP-1 signaling pathway in colon adenocarcinomas? | {
"contexts": [
"Reg IV, a secreted protein and member of the Reg multigene family, is up-regulated in malignancies of the human gastrointestinal tract, including colorectal carcinoma (CRC). However, in vitro signal transduction pathway(s) utilized by Reg IV are not yet known.",
"To determine the signaling pathway(s) responsive to Reg IV, we examined the effects of purified recombinant human Reg IV (rhR4) on HCT116 and HT29 colon adenocarcinoma cells.",
"Addition of rhR4 to cultures led to a dose-dependent increase in cell number similar to that observed after treatment with epidermal growth factor (EGF). In addition, rhR4 treatment resulted in rapid phosphorylation of EGF receptor at Tyr992 and Tyr1068 and Akt at Thr308 and Ser473. Using luciferase reporter gene assays, we demonstrated that Reg IV signaling through EGF receptor and Akt results in increased activator protein-1 (AP-1) transcription factor activity. Real-time reverse-transcription polymerase chain reaction and Western blot analyses revealed quantitative increases in c-Jun, JunB, JunD, and FosB expression associated with increased AP-1 activity. Electrophoretic mobility shift assay further revealed significant increases in AP-1 binding activity in rhR4-treated cells, with increased supershift in the presence of antibodies to JunB, JunD, and FosB. Furthermore, rhR4 treatments led to the increased expression of Bcl-2, Bcl-XL, survivin, and matrilysin, genes associated with a poor prognosis in advanced CRC."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adenocarcinoma",
"Apoptosis",
"Colonic Neoplasms",
"ErbB Receptors",
"Humans",
"Lectins, C-Type",
"Neoplasm Metastasis",
"Pancreatitis-Associated Proteins",
"Phosphorylation",
"Proto-Oncogene Proteins c-akt",
"Signal Transduction",
"Transcription Factor AP-1",
"Tumor Cells, Cultured"
]
} | Reg IV is a potent activator of the EGF receptor/Akt/AP-1 signaling pathway in CRC. Disruption of Reg signaling may have utility as a therapeutic intervention for human gastrointestinal adenocarcinomas. | yes | [
{
"from": "human",
"value": "Question: Does reg IV activate the epidermal growth factor receptor/Akt/AP-1 signaling pathway in colon adenocarcinomas?\nContext: {'contexts': ['Reg IV, a secreted protein and member of the Reg multigene family, is up-regulated in malignancies of the human gastrointestinal tract, including colorectal carcinoma (CRC). However, in vitro signal transduction pathway(s) utilized by Reg IV are not yet known.', 'To determine the signaling pathway(s) responsive to Reg IV, we examined the effects of purified recombinant human Reg IV (rhR4) on HCT116 and HT29 colon adenocarcinoma cells.', 'Addition of rhR4 to cultures led to a dose-dependent increase in cell number similar to that observed after treatment with epidermal growth factor (EGF). In addition, rhR4 treatment resulted in rapid phosphorylation of EGF receptor at Tyr992 and Tyr1068 and Akt at Thr308 and Ser473. Using luciferase reporter gene assays, we demonstrated that Reg IV signaling through EGF receptor and Akt results in increased activator protein-1 (AP-1) transcription factor activity. Real-time reverse-transcription polymerase chain reaction and Western blot analyses revealed quantitative increases in c-Jun, JunB, JunD, and FosB expression associated with increased AP-1 activity. Electrophoretic mobility shift assay further revealed significant increases in AP-1 binding activity in rhR4-treated cells, with increased supershift in the presence of antibodies to JunB, JunD, and FosB. Furthermore, rhR4 treatments led to the increased expression of Bcl-2, Bcl-XL, survivin, and matrilysin, genes associated with a poor prognosis in advanced CRC.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adenocarcinoma', 'Apoptosis', 'Colonic Neoplasms', 'ErbB Receptors', 'Humans', 'Lectins, C-Type', 'Neoplasm Metastasis', 'Pancreatitis-Associated Proteins', 'Phosphorylation', 'Proto-Oncogene Proteins c-akt', 'Signal Transduction', 'Transcription Factor AP-1', 'Tumor Cells, Cultured']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,401,476 | Do myofibroblast matrix metalloproteinases activate the neutrophil chemoattractant CXCL7 from intestinal epithelial cells? | {
"contexts": [
"The up-regulation of matrix metalloproteinases (MMPs) in the inflamed gut has mainly been associated with mucosal degradation and ulceration. However, their in vitro capacity to specifically cleave inflammatory mediators indicates that MMPs may have a profound immunoregulatory impact. We hypothesized that MMPs proteolytically modify intestinal epithelial chemokine signaling.",
"Interleukin-1beta-stimulated Caco-2 cells were exposed basolaterally to nanomolar concentrations of activated MMP-3 or cocultured with interleukin-1beta-stimulated, MMP-producing, colonic myofibroblasts (CCD-18co). The conditioned media were subjected to chemotaxis assays. In addition, epithelial cells from patients with colitis were examined by real-time polymerase chain reaction, immunoblotting, and immunohistochemistry.",
"MMP-3 dose-dependently induced the neutrophil (up to 5-fold) but not monocyte chemoattractant capacity of Caco-2 cells. A similar Caco-2 chemotactic response was obtained in the Caco-2/CCD-18co cocultures. The principal mediator of these protease-related effects was identified as the potent neutrophil chemokine CXCL7 (neutrophil activating peptide 2), a proteolytic cleavage product of chemotactically inert platelet basic protein (PBP), not previously identified in the intestine. Antibodies against CXCL7 inhibited the MMP-induced chemotactic response by 84%, and PBP mRNA and protein were detected in stimulated Caco-2 but not in CCD-18co cells. Furthermore, PBP transcript and protein levels were low in the mucosa and in isolated epithelial cells from patients with Crohn's disease and from normal intestine but increased up to 13-fold in patients with ulcerative colitis."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Caco-2 Cells",
"Chemotaxis",
"Colitis, Ulcerative",
"Crohn Disease",
"Fibroblasts",
"Humans",
"Inflammation",
"Intestinal Mucosa",
"Leukocytes",
"Matrix Metalloproteinase 3",
"Matrix Metalloproteinases",
"Signal Transduction",
"Up-Regulation",
"beta-Thromboglobulin"
]
} | These findings identify a novel proinflammatory action of MMPs in inflammation and suggest that lamina propria myofibroblasts are required to achieve maximal intestinal epithelial immune activation. | yes | [
{
"from": "human",
"value": "Question: Do myofibroblast matrix metalloproteinases activate the neutrophil chemoattractant CXCL7 from intestinal epithelial cells?\nContext: {'contexts': ['The up-regulation of matrix metalloproteinases (MMPs) in the inflamed gut has mainly been associated with mucosal degradation and ulceration. However, their in vitro capacity to specifically cleave inflammatory mediators indicates that MMPs may have a profound immunoregulatory impact. We hypothesized that MMPs proteolytically modify intestinal epithelial chemokine signaling.', 'Interleukin-1beta-stimulated Caco-2 cells were exposed basolaterally to nanomolar concentrations of activated MMP-3 or cocultured with interleukin-1beta-stimulated, MMP-producing, colonic myofibroblasts (CCD-18co). The conditioned media were subjected to chemotaxis assays. In addition, epithelial cells from patients with colitis were examined by real-time polymerase chain reaction, immunoblotting, and immunohistochemistry.', \"MMP-3 dose-dependently induced the neutrophil (up to 5-fold) but not monocyte chemoattractant capacity of Caco-2 cells. A similar Caco-2 chemotactic response was obtained in the Caco-2/CCD-18co cocultures. The principal mediator of these protease-related effects was identified as the potent neutrophil chemokine CXCL7 (neutrophil activating peptide 2), a proteolytic cleavage product of chemotactically inert platelet basic protein (PBP), not previously identified in the intestine. Antibodies against CXCL7 inhibited the MMP-induced chemotactic response by 84%, and PBP mRNA and protein were detected in stimulated Caco-2 but not in CCD-18co cells. Furthermore, PBP transcript and protein levels were low in the mucosa and in isolated epithelial cells from patients with Crohn's disease and from normal intestine but increased up to 13-fold in patients with ulcerative colitis.\"], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Caco-2 Cells', 'Chemotaxis', 'Colitis, Ulcerative', 'Crohn Disease', 'Fibroblasts', 'Humans', 'Inflammation', 'Intestinal Mucosa', 'Leukocytes', 'Matrix Metalloproteinase 3', 'Matrix Metalloproteinases', 'Signal Transduction', 'Up-Regulation', 'beta-Thromboglobulin']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,375,765 | Is discontinuation of treatment of schizophrenic patients driven by poor symptom response : a pooled post-hoc analysis of four atypical antipsychotic drugs? | {
"contexts": [
"Stopping antipsychotic treatment can interrupt improvement and exacerbate the illness. The reasons for discontinuing treatment during controlled clinical trials were analyzed to explore this phenomenon.",
"A post-hoc, pooled analysis was made of 4 randomized, double-blind clinical trials, 24-28 weeks in duration, involving 1627 patients with schizophrenia or a related disorder. Analyses combined all the atypical antipsychotic treatment groups in the studies.",
"The majority of patients (53%) stopped their treatment at an early stage. Poor psychiatric response along with worsening symptoms was the most frequently given reason for discontinuing the course (36%), which was substantially more common than discontinuation due to poor tolerability of the medication (12%). This phenomenon was corroborated by less improvement in patients who discontinued treatment compared with those who completed, based on the PANSS total scores. Discontinuation due to poor response was, apparently, more predominantly linked to patient perception than to physicians' conclusions alone (80% vs. 20%). Discontinuation due to patient perception of poor response appeared to occur particularly early in the course of treatment. Patients who discontinued due to poor toleration of the medication responded in a more comparable manner with completers."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Analysis of Variance",
"Antipsychotic Agents",
"Benzodiazepines",
"Dibenzothiazepines",
"Female",
"Humans",
"Male",
"Middle Aged",
"Olanzapine",
"Patient Dropouts",
"Piperazines",
"Psychiatric Status Rating Scales",
"Quetiapine Fumarate",
"Randomized Controlled Trials as Topic",
"Risperidone",
"Schizophrenia",
"Schizophrenic Psychology",
"Thiazoles",
"Treatment Failure",
"Treatment Refusal"
]
} | Discontinuing treatment may lead to exacerbation of symptoms, undermining therapeutic progress. In these studies, poor response to treatment and worsening of underlying psychiatric symptoms, and to a lesser extent, intolerability to medication were the primary contributors to treatment being discontinued. Our findings suggest that adherence may be enhanced by effective symptom control, as objectively measured and as subjectively perceived. Such strategies may improve patients' willingness to undertake long-term therapy and increase the likelihood of a better prognosis. | yes | [
{
"from": "human",
"value": "Question: Is discontinuation of treatment of schizophrenic patients driven by poor symptom response : a pooled post-hoc analysis of four atypical antipsychotic drugs?\nContext: {'contexts': ['Stopping antipsychotic treatment can interrupt improvement and exacerbate the illness. The reasons for discontinuing treatment during controlled clinical trials were analyzed to explore this phenomenon.', 'A post-hoc, pooled analysis was made of 4 randomized, double-blind clinical trials, 24-28 weeks in duration, involving 1627 patients with schizophrenia or a related disorder. Analyses combined all the atypical antipsychotic treatment groups in the studies.', \"The majority of patients (53%) stopped their treatment at an early stage. Poor psychiatric response along with worsening symptoms was the most frequently given reason for discontinuing the course (36%), which was substantially more common than discontinuation due to poor tolerability of the medication (12%). This phenomenon was corroborated by less improvement in patients who discontinued treatment compared with those who completed, based on the PANSS total scores. Discontinuation due to poor response was, apparently, more predominantly linked to patient perception than to physicians' conclusions alone (80% vs. 20%). Discontinuation due to patient perception of poor response appeared to occur particularly early in the course of treatment. Patients who discontinued due to poor toleration of the medication responded in a more comparable manner with completers.\"], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Analysis of Variance', 'Antipsychotic Agents', 'Benzodiazepines', 'Dibenzothiazepines', 'Female', 'Humans', 'Male', 'Middle Aged', 'Olanzapine', 'Patient Dropouts', 'Piperazines', 'Psychiatric Status Rating Scales', 'Quetiapine Fumarate', 'Randomized Controlled Trials as Topic', 'Risperidone', 'Schizophrenia', 'Schizophrenic Psychology', 'Thiazoles', 'Treatment Failure', 'Treatment Refusal']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,388,493 | Does the receptor-binding region of human apolipoprotein E have direct anti-infective activity? | {
"contexts": [
"The APOE genotype has a uniquely strong influence on the outcome of viral infection. The mechanism is unknown, although one possibility is direct inhibition of viral entry into cells.",
"We have examined the direct anti-infective activity of a peptide analogue of the receptor-binding region of apolipoprotein E (apoE) that is known as \"apoE dimer tandem repeat peptide\" (apoEdp) and has previously been shown to mimic some of the biological effects of apoE and that recently was shown to bind low-density lipoprotein receptor-related protein.",
"apoEdp has activity against herpes simplex virus types 1 and 2, human immunodeficiency virus, Pseudomonas aeruginosa, and Staphylococcus aureus; concentrations in the range of 1-20 micromol/L inhibit infection by 50%. These biological actions depend on adoption of an alpha -helical structure, as has been found for other biological effects of apoE peptides. The peptide interferes with the earliest stages of viral infection, preventing viral attachment and exerting a mild virucidal action. In addition, an N-terminal fragment of apoE that also contains this binding domain has antiviral activity."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Anti-Infective Agents",
"Apolipoproteins E",
"Cell Line",
"Cercopithecus aethiops",
"HIV-1",
"Herpesvirus 1, Human",
"Herpesvirus 2, Human",
"Humans",
"Peptide Fragments",
"Pseudomonas aeruginosa",
"Receptors, Lipoprotein",
"Staphylococcus aureus",
"Vero Cells"
]
} | These data suggest that human apoE or fragments containing the receptor-binding domain may contribute to innate immunity to viral infection by direct disruption of viral particles and/or inhibition of viral attachment, thus reducing viral entry. | yes | [
{
"from": "human",
"value": "Question: Does the receptor-binding region of human apolipoprotein E have direct anti-infective activity?\nContext: {'contexts': ['The APOE genotype has a uniquely strong influence on the outcome of viral infection. The mechanism is unknown, although one possibility is direct inhibition of viral entry into cells.', 'We have examined the direct anti-infective activity of a peptide analogue of the receptor-binding region of apolipoprotein E (apoE) that is known as \"apoE dimer tandem repeat peptide\" (apoEdp) and has previously been shown to mimic some of the biological effects of apoE and that recently was shown to bind low-density lipoprotein receptor-related protein.', 'apoEdp has activity against herpes simplex virus types 1 and 2, human immunodeficiency virus, Pseudomonas aeruginosa, and Staphylococcus aureus; concentrations in the range of 1-20 micromol/L inhibit infection by 50%. These biological actions depend on adoption of an alpha -helical structure, as has been found for other biological effects of apoE peptides. The peptide interferes with the earliest stages of viral infection, preventing viral attachment and exerting a mild virucidal action. In addition, an N-terminal fragment of apoE that also contains this binding domain has antiviral activity.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Anti-Infective Agents', 'Apolipoproteins E', 'Cell Line', 'Cercopithecus aethiops', 'HIV-1', 'Herpesvirus 1, Human', 'Herpesvirus 2, Human', 'Humans', 'Peptide Fragments', 'Pseudomonas aeruginosa', 'Receptors, Lipoprotein', 'Staphylococcus aureus', 'Vero Cells']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,371,922 | Does low-dose radiation plus rapamycin promote long-term bone marrow chimerism? | {
"contexts": [
"The ability to achieve significant donor engraftment without fully myeloablative conditioning has revolutionized allogeneic stem cell transplantation. These nonmyeloablative approaches may allow extension of this potentially curative modality to an increasing number of patients including those with non-malignant diseases. Although a number of regimens have been explored, the optimal means of conditioning has not been determined.",
"We previously demonstrated that rapamycin (RAPA) has the ability to promote T-cell tolerance even in the presence of costimulation. In the current study, we examine the ability of rapamycin or the calcineurin inhibitor cyclosporine A (CSA) to promote chimerism in a murine haploidentical bone marrow transplantation model. Mice were conditioned with 300 cGy and received either RAPA at 3 mg/kg/day IP, CSA at 20 mg/kg/day IP, or no immunosuppression starting on the day before the transplant and continued for 4 weeks.",
"There was no apparent toxicity, and animals maintained normal blood counts throughout. More importantly, long-term macrochimerism was observed only in the RAPA-treated group."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Bone Marrow Transplantation",
"Female",
"Flow Cytometry",
"Immunosuppressive Agents",
"Mice",
"Mice, Inbred BALB C",
"Mice, Inbred C57BL",
"Models, Animal",
"Sirolimus",
"Transplantation Chimera",
"Transplantation Conditioning"
]
} | These results establish a simple, nontoxic, irradiation-based regimen that facilitates engraftment without ablation. This strategy may prove useful in nonmalignant disorders such as hemoglobinopathies in which moderate levels of donor chimerism could prove curative. | yes | [
{
"from": "human",
"value": "Question: Does low-dose radiation plus rapamycin promote long-term bone marrow chimerism?\nContext: {'contexts': ['The ability to achieve significant donor engraftment without fully myeloablative conditioning has revolutionized allogeneic stem cell transplantation. These nonmyeloablative approaches may allow extension of this potentially curative modality to an increasing number of patients including those with non-malignant diseases. Although a number of regimens have been explored, the optimal means of conditioning has not been determined.', 'We previously demonstrated that rapamycin (RAPA) has the ability to promote T-cell tolerance even in the presence of costimulation. In the current study, we examine the ability of rapamycin or the calcineurin inhibitor cyclosporine A (CSA) to promote chimerism in a murine haploidentical bone marrow transplantation model. Mice were conditioned with 300 cGy and received either RAPA at 3 mg/kg/day IP, CSA at 20 mg/kg/day IP, or no immunosuppression starting on the day before the transplant and continued for 4 weeks.', 'There was no apparent toxicity, and animals maintained normal blood counts throughout. More importantly, long-term macrochimerism was observed only in the RAPA-treated group.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Bone Marrow Transplantation', 'Female', 'Flow Cytometry', 'Immunosuppressive Agents', 'Mice', 'Mice, Inbred BALB C', 'Mice, Inbred C57BL', 'Models, Animal', 'Sirolimus', 'Transplantation Chimera', 'Transplantation Conditioning']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,389,649 | Is plasma apolipoprotein E concentration an important determinant of phospholipid transfer protein activity in type 2 diabetes mellitus? | {
"contexts": [
"Phospholipid transfer protein (PLTP) transfers phospholipids between lipoproteins and plays an important role in HDL metabolism. PLTP exists as a high-activity and a low-activity form in the circulation. In vitro studies have shown that apolipoprotein (apo) E is involved in maintaining PLTP in the active form, while the low-activity form is associated with apo AI. We have therefore investigated whether plasma apo AI, B and E concentrations are important determinants of plasma PLTP activity in type 2 diabetes, a condition associated with increased plasma PLTP activity.",
"Plasma PLTP activity was assayed by measuring the transfer of radiolabelled phosphatidylcholine from liposomes to HDL; apo AI and B by rate nephelometry and apo E by a 2-point turbidimetric assay.",
"Type 2 diabetic patients (n = 230) had higher PLTP activity than controls (n = 97) (2374 +/- 628 nmol/mL/h versus 1862 +/- 585 respectively, p < 0.01). They also had increased fasting triglyceride and low HDL. Plasma apo B (p < 0.01) and apo E (p < 0.05) were increased, whereas apo AI was reduced (p < 0.01). Univariate analysis showed that plasma PLTP activity correlated mainly with apolipoproteins AI and E. Stepwise regression analysis showed that apo E was the main determinant of plasma PLTP activity, accounting for 23% of its variability in the diabetic subjects and 8% in the controls respectively."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Apolipoproteins E",
"Diabetes Mellitus, Type 2",
"Female",
"Humans",
"Male",
"Middle Aged",
"Phospholipid Transfer Proteins",
"Reference Values",
"Regression Analysis"
]
} | The associations between plasma apo AI and E concentrations and PLTP activity suggest that these apolipoproteins are important regulators of PLTP activity in vivo. The increase in PLTP activity in type 2 diabetes is partly related to the changes in these apolipoproteins. | yes | [
{
"from": "human",
"value": "Question: Is plasma apolipoprotein E concentration an important determinant of phospholipid transfer protein activity in type 2 diabetes mellitus?\nContext: {'contexts': ['Phospholipid transfer protein (PLTP) transfers phospholipids between lipoproteins and plays an important role in HDL metabolism. PLTP exists as a high-activity and a low-activity form in the circulation. In vitro studies have shown that apolipoprotein (apo) E is involved in maintaining PLTP in the active form, while the low-activity form is associated with apo AI. We have therefore investigated whether plasma apo AI, B and E concentrations are important determinants of plasma PLTP activity in type 2 diabetes, a condition associated with increased plasma PLTP activity.', 'Plasma PLTP activity was assayed by measuring the transfer of radiolabelled phosphatidylcholine from liposomes to HDL; apo AI and B by rate nephelometry and apo E by a 2-point turbidimetric assay.', 'Type 2 diabetic patients (n = 230) had higher PLTP activity than controls (n = 97) (2374 +/- 628 nmol/mL/h versus 1862 +/- 585 respectively, p < 0.01). They also had increased fasting triglyceride and low HDL. Plasma apo B (p < 0.01) and apo E (p < 0.05) were increased, whereas apo AI was reduced (p < 0.01). Univariate analysis showed that plasma PLTP activity correlated mainly with apolipoproteins AI and E. Stepwise regression analysis showed that apo E was the main determinant of plasma PLTP activity, accounting for 23% of its variability in the diabetic subjects and 8% in the controls respectively.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Apolipoproteins E', 'Diabetes Mellitus, Type 2', 'Female', 'Humans', 'Male', 'Middle Aged', 'Phospholipid Transfer Proteins', 'Reference Values', 'Regression Analysis']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,376,769 | Is left atrial index a predictor of exercise capacity in patients with hypertrophic cardiomyopathy? | {
"contexts": [
"Left atrial (LA) enlargement is related to diastolic dysfunction and mitral regurgitation (MR), both of which are common in patients with hypertrophic cardiomyopathy (HCM). This study investigates the association between LA size and exercise capacity in patients with HCM.",
"All HCM patients who underwent a treadmill test with direct measurement of oxygen consumption (VO2) and a standard transthoracic echocardiography within 30 days in the years 2001-2003 were identified. Patients with significant comorbidities were excluded. Exercise capacity was defined as percentage of predicted peak VO2. Clinical and echocardiographic parameters were compared with those of a group of normal subjects.",
"Compared with normal subjects, HCM patients had increased left atrial (LA) volume index (36 vs 21 mL/m2; P < .0001) and mitral E/e' ratio (14 vs 9; P < .0001); 27% of the patients had at least moderate MR. LA volume index demonstrated borderline correlation with exercise capacity (r = -.20; P = .06) but was an independent predictor of exercise capacity in a multivariate linear analysis, together with body mass index, heart rate at rest, and left ventricular end-systolic diameter. Including the parameters E/e' ratio or moderate or severe MR did not add incremental value to the model."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Cardiomyopathy, Hypertrophic",
"Echocardiography",
"Exercise Test",
"Exercise Tolerance",
"Female",
"Heart Atria",
"Humans",
"Male",
"Middle Aged",
"Reproducibility of Results",
"Risk Assessment",
"Sensitivity and Specificity",
"Severity of Illness Index"
]
} | LA volume index, reflecting the combined influences of MR and diastolic dysfunction, was independently associated with objective measures of exercise capacity in patients with isolated HCM. | yes | [
{
"from": "human",
"value": "Question: Is left atrial index a predictor of exercise capacity in patients with hypertrophic cardiomyopathy?\nContext: {'contexts': ['Left atrial (LA) enlargement is related to diastolic dysfunction and mitral regurgitation (MR), both of which are common in patients with hypertrophic cardiomyopathy (HCM). This study investigates the association between LA size and exercise capacity in patients with HCM.', 'All HCM patients who underwent a treadmill test with direct measurement of oxygen consumption (VO2) and a standard transthoracic echocardiography within 30 days in the years 2001-2003 were identified. Patients with significant comorbidities were excluded. Exercise capacity was defined as percentage of predicted peak VO2. Clinical and echocardiographic parameters were compared with those of a group of normal subjects.', \"Compared with normal subjects, HCM patients had increased left atrial (LA) volume index (36 vs 21 mL/m2; P < .0001) and mitral E/e' ratio (14 vs 9; P < .0001); 27% of the patients had at least moderate MR. LA volume index demonstrated borderline correlation with exercise capacity (r = -.20; P = .06) but was an independent predictor of exercise capacity in a multivariate linear analysis, together with body mass index, heart rate at rest, and left ventricular end-systolic diameter. Including the parameters E/e' ratio or moderate or severe MR did not add incremental value to the model.\"], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Cardiomyopathy, Hypertrophic', 'Echocardiography', 'Exercise Test', 'Exercise Tolerance', 'Female', 'Heart Atria', 'Humans', 'Male', 'Middle Aged', 'Reproducibility of Results', 'Risk Assessment', 'Sensitivity and Specificity', 'Severity of Illness Index']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,374,292 | Is a low blood ethanol level associated with improved cytokine production in aged mice after traumatic injury? | {
"contexts": [
"Many trauma patients have been consuming alcohol at the time of injury. Although high concentrations of alcohol are correlated with poor outcome, few studies have examined the effects of low levels of alcohol. We examined the effects of low alcohol exposure after burn injury using a murine model.",
"Three- and 18-month-old mice were given ethanol or saline 30 minutes before a 15% total body surface area burn injury. Twenty-four hours after injury, cellular immune responses, including delayed-type hypersensitivity response and splenocyte proliferation were examined, along with production of interferon-gamma, interleukin (IL)-2, and IL-4.",
"Alcohol administration resulted in a significant increase in interferon-gamma in the aged, but not young, burn-injured mice. Likewise, slight increases in IL-2, IL-4, and the delayed-type hypersensitivity response were observed."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Aging",
"Animals",
"Burns",
"Central Nervous System Depressants",
"Ethanol",
"Female",
"Hypersensitivity, Delayed",
"Interferon-gamma",
"Interleukin-2",
"Interleukin-4",
"Mice",
"Mice, Inbred BALB C"
]
} | Low levels of ethanol at the time of injury are associated with partial restoration of immune responses in aged mice. | yes | [
{
"from": "human",
"value": "Question: Is a low blood ethanol level associated with improved cytokine production in aged mice after traumatic injury?\nContext: {'contexts': ['Many trauma patients have been consuming alcohol at the time of injury. Although high concentrations of alcohol are correlated with poor outcome, few studies have examined the effects of low levels of alcohol. We examined the effects of low alcohol exposure after burn injury using a murine model.', 'Three- and 18-month-old mice were given ethanol or saline 30 minutes before a 15% total body surface area burn injury. Twenty-four hours after injury, cellular immune responses, including delayed-type hypersensitivity response and splenocyte proliferation were examined, along with production of interferon-gamma, interleukin (IL)-2, and IL-4.', 'Alcohol administration resulted in a significant increase in interferon-gamma in the aged, but not young, burn-injured mice. Likewise, slight increases in IL-2, IL-4, and the delayed-type hypersensitivity response were observed.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Aging', 'Animals', 'Burns', 'Central Nervous System Depressants', 'Ethanol', 'Female', 'Hypersensitivity, Delayed', 'Interferon-gamma', 'Interleukin-2', 'Interleukin-4', 'Mice', 'Mice, Inbred BALB C']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,374,291 | Does tranexamic acid prevent rebleeding in an uncontrolled hemorrhage porcine model? | {
"contexts": [
"Fluid resuscitation after uncontrolled hemorrhage might promote rebleeding and irreversible shock. Tranexamic acid is a procoagulant drug that limits blood loss after surgery of the hip, knee, and heart. We hypothesized that pretreatment with tranexamic acid reduces the rebleeding in uncontrolled hemorrhage and thereby allows safe administration of crystalloid fluid resuscitation.",
"A 120-minute intravenous infusion of 100 mL/kg of Ringer's solution was given to 24 pigs (mean weight, 20 kg) 10 minutes after lacerating the infrarenal aorta. The animals were randomized to receive an intravenous injection of 15 mg/kg of tranexamic acid or placebo just before starting the resuscitation. Rebleeding events were monitored by two ultrasonic probes positioned proximal and distal to the laceration.",
"Tranexamic acid had no effect on the number of rebleeding events, bled volume, or mortality. The initial bleeding stopped within 4 minutes after the injury. The five animals that died suffered from 4.4 rebleeding events on average, which tripled the total blood loss, whereas the survivors had only 1.3 such events during fluid resuscitation (p < 0.02). At autopsy, death was associated with a larger total hemorrhage; the blood recovered from the abdomen weighed 1.4 kg (median) in nonsurvivors and 0.6 kg in survivors (p < 0.001), with the difference being attributable to rebleeding."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Antifibrinolytic Agents",
"Female",
"Fluid Therapy",
"Hemodynamics",
"Hemorrhage",
"Male",
"Secondary Prevention",
"Swine",
"Tranexamic Acid"
]
} | Rebleeding events increased the amount of blood lost and the mortality in uncontrolled aortic hemorrhage. Tranexamic acid offered no benefit. | no | [
{
"from": "human",
"value": "Question: Does tranexamic acid prevent rebleeding in an uncontrolled hemorrhage porcine model?\nContext: {'contexts': ['Fluid resuscitation after uncontrolled hemorrhage might promote rebleeding and irreversible shock. Tranexamic acid is a procoagulant drug that limits blood loss after surgery of the hip, knee, and heart. We hypothesized that pretreatment with tranexamic acid reduces the rebleeding in uncontrolled hemorrhage and thereby allows safe administration of crystalloid fluid resuscitation.', \"A 120-minute intravenous infusion of 100 mL/kg of Ringer's solution was given to 24 pigs (mean weight, 20 kg) 10 minutes after lacerating the infrarenal aorta. The animals were randomized to receive an intravenous injection of 15 mg/kg of tranexamic acid or placebo just before starting the resuscitation. Rebleeding events were monitored by two ultrasonic probes positioned proximal and distal to the laceration.\", 'Tranexamic acid had no effect on the number of rebleeding events, bled volume, or mortality. The initial bleeding stopped within 4 minutes after the injury. The five animals that died suffered from 4.4 rebleeding events on average, which tripled the total blood loss, whereas the survivors had only 1.3 such events during fluid resuscitation (p < 0.02). At autopsy, death was associated with a larger total hemorrhage; the blood recovered from the abdomen weighed 1.4 kg (median) in nonsurvivors and 0.6 kg in survivors (p < 0.001), with the difference being attributable to rebleeding.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Antifibrinolytic Agents', 'Female', 'Fluid Therapy', 'Hemodynamics', 'Hemorrhage', 'Male', 'Secondary Prevention', 'Swine', 'Tranexamic Acid']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
16,389,567 | Does alcohol consumption during gestation reduce the histamine and triiodothyronine content of rat immune cells? | {
"contexts": [
"Different factors acting during pregnancy can cause non-morphological alterations of cells which are manifested later, in adulthood. We studied the effect of maternal alcohol consumption for one day in early pregnancy on the hormone content of immune cells in the adult rat.",
"Lactating dams were given 15% ethanol in the drinking water for 24 h on the 3rd day post partum, exposing their pups to ethanol in the breast milk. Some of the same dams had been successfully mated on the day of delivery, so that they were also 3 days pregnant on the treatment day, exposing embryos to alcohol on the third day of pregnancy. In 4 month old pups histamine and triiodothyronine (T(3)) content of citrate elicited peritoneal immune cells (lymphocytes, monocyte-macrophage-granulocyte group, mast cells) as well as thymic cells were determined by flow cytometry and confocal microscopy using specific antibodies.",
"Alcohol treatment during pregnancy decreased highly significantly the content of both hormones in peritoneal cells of the 4 month old adult animals while it was ineffective by breast feeding after birth. Thymic cells did not show any changes."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Alcohol Drinking",
"Animals",
"Ethanol",
"Female",
"Flow Cytometry",
"Granulocytes",
"Histamine",
"Lactation",
"Leukocytes",
"Lymphocytes",
"Macrophages",
"Mast Cells",
"Microscopy, Confocal",
"Monocytes",
"Pregnancy",
"Prenatal Exposure Delayed Effects",
"Rats",
"Rats, Wistar",
"Thymus Gland",
"Triiodothyronine"
]
} | Since the immune system had not developed at the time of treatment (3rd day of pregnancy), stem cells were presumably imprinted. Our results indicate the deleterious effects of early maternal alcohol consumption on the hormone content of the immune system. | yes | [
{
"from": "human",
"value": "Question: Does alcohol consumption during gestation reduce the histamine and triiodothyronine content of rat immune cells?\nContext: {'contexts': ['Different factors acting during pregnancy can cause non-morphological alterations of cells which are manifested later, in adulthood. We studied the effect of maternal alcohol consumption for one day in early pregnancy on the hormone content of immune cells in the adult rat.', 'Lactating dams were given 15% ethanol in the drinking water for 24 h on the 3rd day post partum, exposing their pups to ethanol in the breast milk. Some of the same dams had been successfully mated on the day of delivery, so that they were also 3 days pregnant on the treatment day, exposing embryos to alcohol on the third day of pregnancy. In 4 month old pups histamine and triiodothyronine (T(3)) content of citrate elicited peritoneal immune cells (lymphocytes, monocyte-macrophage-granulocyte group, mast cells) as well as thymic cells were determined by flow cytometry and confocal microscopy using specific antibodies.', 'Alcohol treatment during pregnancy decreased highly significantly the content of both hormones in peritoneal cells of the 4 month old adult animals while it was ineffective by breast feeding after birth. Thymic cells did not show any changes.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Alcohol Drinking', 'Animals', 'Ethanol', 'Female', 'Flow Cytometry', 'Granulocytes', 'Histamine', 'Lactation', 'Leukocytes', 'Lymphocytes', 'Macrophages', 'Mast Cells', 'Microscopy, Confocal', 'Monocytes', 'Pregnancy', 'Prenatal Exposure Delayed Effects', 'Rats', 'Rats, Wistar', 'Thymus Gland', 'Triiodothyronine']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,380,413 | Are preoperative serum tissue factor levels an independent prognostic factor in patients with ovarian carcinoma? | {
"contexts": [
"Tissue factor (TF) is a procoagulant that plays an important part in tumor angiogenesis. We sought to determine the role of preoperative serum TF levels in predicting clinical outcome in patients with ovarian cancer.",
"TF expression was determined by reverse transcriptase polymerase chain reaction in ovarian cell lines. Using enzyme-linked immunosorbent assay, we assessed preoperative serum TF levels in 98 women with invasive epithelial ovarian carcinoma, 30 with low malignant potential (LMP) tumors, 16 with benign tumors, and a separate validation group of 39 women with adnexal masses. Clinical information was gathered from chart review.",
"TF was expressed in four of the five ovarian cancer cell lines, but absent in the nontransformed cells. Ovarian cancer patients had a median preoperative serum TF level of 85.2 pg/mL, which was significantly higher than in those with LMP tumors (12.8 pg/mL; P < .01) and benign adnexal disease (30.7 pg/mL; P < .01). TF >or= 190 pg/mL was significantly associated with decreased patient survival (P < .01). After adjusting for other clinical variables in a multivariate Cox regression model, TF >or= 190 pg/mL was an independent prognostic factor (P < .01). Analysis of serum TF levels from the validation set confirmed that high TF (>or=190 pg/mL) was associated with a 3.4-fold increase in risk of death from disease (P = .02) and shorter survival (P = .01)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Aged, 80 and over",
"Carcinoma",
"Cell Line, Tumor",
"Enzyme-Linked Immunosorbent Assay",
"Female",
"Gene Expression Profiling",
"Humans",
"Middle Aged",
"Neovascularization, Pathologic",
"Ovarian Neoplasms",
"Predictive Value of Tests",
"Prognosis",
"Reverse Transcriptase Polymerase Chain Reaction",
"Survival Analysis",
"Thromboplastin"
]
} | Preoperative serum TF levels are significantly elevated in patients with ovarian carcinoma. Elevated preoperative TF level is an independent prognostic factor for death from disease. | yes | [
{
"from": "human",
"value": "Question: Are preoperative serum tissue factor levels an independent prognostic factor in patients with ovarian carcinoma?\nContext: {'contexts': ['Tissue factor (TF) is a procoagulant that plays an important part in tumor angiogenesis. We sought to determine the role of preoperative serum TF levels in predicting clinical outcome in patients with ovarian cancer.', 'TF expression was determined by reverse transcriptase polymerase chain reaction in ovarian cell lines. Using enzyme-linked immunosorbent assay, we assessed preoperative serum TF levels in 98 women with invasive epithelial ovarian carcinoma, 30 with low malignant potential (LMP) tumors, 16 with benign tumors, and a separate validation group of 39 women with adnexal masses. Clinical information was gathered from chart review.', 'TF was expressed in four of the five ovarian cancer cell lines, but absent in the nontransformed cells. Ovarian cancer patients had a median preoperative serum TF level of 85.2 pg/mL, which was significantly higher than in those with LMP tumors (12.8 pg/mL; P < .01) and benign adnexal disease (30.7 pg/mL; P < .01). TF >or= 190 pg/mL was significantly associated with decreased patient survival (P < .01). After adjusting for other clinical variables in a multivariate Cox regression model, TF >or= 190 pg/mL was an independent prognostic factor (P < .01). Analysis of serum TF levels from the validation set confirmed that high TF (>or=190 pg/mL) was associated with a 3.4-fold increase in risk of death from disease (P = .02) and shorter survival (P = .01).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Aged, 80 and over', 'Carcinoma', 'Cell Line, Tumor', 'Enzyme-Linked Immunosorbent Assay', 'Female', 'Gene Expression Profiling', 'Humans', 'Middle Aged', 'Neovascularization, Pathologic', 'Ovarian Neoplasms', 'Predictive Value of Tests', 'Prognosis', 'Reverse Transcriptase Polymerase Chain Reaction', 'Survival Analysis', 'Thromboplastin']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,391,483 | Does [ Intravenous oxygen therapy increase the activity of the antioxidative and antiatherogenic serum enzyme paraoxonase 1 ]? | {
"contexts": [
"Intravenous oxygen infusions have been introduced in complementary medicine for treatment of atherosclerosis and inflammatory diseases. As atherosclerosis and inflammation are causally related to oxidative stress and as intravenous supply with oxygen causes oxidative stress, it was suggested that the clinical success of intravenous oxygen therapy is biochemically based on an enhancement of endogenous antioxidative mechanisms. The anti-atherogenic enzyme paraoxonase-1 (PON1) is is part of this system.",
"To evaluate the effect of repeated intravenous oxygen infusions on serum PON1 activity.",
"A total of 45 patients were treated with intravenous oxygen. During treatment oxygen dosage was increased from 15 to 50 ml (1-2 ml/min). Before treatments 1 and 10 blood was obtained for measurement of PON1 activities. From 20 patients blood was additionally obtained after 20 days of treatment and 2 weeks post treatment. Serum PON1 activity was measured spectrophotometrically using the synthetic substrates paraoxon, phenylacetate, and p-nitrophenyl-acetate.",
"Using the substrate paraoxon PON1 activity significantly increased by 38% above basal levels 24 hours after intravenous oxygen infusion 9 (p < 0.001). Adverse effects were not observed."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Aged, 80 and over",
"Aryldialkylphosphatase",
"Atherosclerosis",
"Dose-Response Relationship, Drug",
"Female",
"Humans",
"Inflammation",
"Infusions, Intravenous",
"Male",
"Middle Aged",
"Oxidative Stress",
"Oxygen"
]
} | Treatments with intravenous oxygen infusions evoke an adaptation to oxidative stress by an increase of serum PON1 activity. In this regard, a potential molecular mechanism has been found, that explains the protecting effects of intravenous oxygen therapy against oxidative stress and its consequences. PON1 activity is proposed to be an appropriate parameter for monitoring the success of this kind of oxygen therapy. | yes | [
{
"from": "human",
"value": "Question: Does [ Intravenous oxygen therapy increase the activity of the antioxidative and antiatherogenic serum enzyme paraoxonase 1 ]?\nContext: {'contexts': ['Intravenous oxygen infusions have been introduced in complementary medicine for treatment of atherosclerosis and inflammatory diseases. As atherosclerosis and inflammation are causally related to oxidative stress and as intravenous supply with oxygen causes oxidative stress, it was suggested that the clinical success of intravenous oxygen therapy is biochemically based on an enhancement of endogenous antioxidative mechanisms. The anti-atherogenic enzyme paraoxonase-1 (PON1) is is part of this system.', 'To evaluate the effect of repeated intravenous oxygen infusions on serum PON1 activity.', 'A total of 45 patients were treated with intravenous oxygen. During treatment oxygen dosage was increased from 15 to 50 ml (1-2 ml/min). Before treatments 1 and 10 blood was obtained for measurement of PON1 activities. From 20 patients blood was additionally obtained after 20 days of treatment and 2 weeks post treatment. Serum PON1 activity was measured spectrophotometrically using the synthetic substrates paraoxon, phenylacetate, and p-nitrophenyl-acetate.', 'Using the substrate paraoxon PON1 activity significantly increased by 38% above basal levels 24 hours after intravenous oxygen infusion 9 (p < 0.001). Adverse effects were not observed.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Aged, 80 and over', 'Aryldialkylphosphatase', 'Atherosclerosis', 'Dose-Response Relationship, Drug', 'Female', 'Humans', 'Inflammation', 'Infusions, Intravenous', 'Male', 'Middle Aged', 'Oxidative Stress', 'Oxygen']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,369,808 | Is tissue-type plasminogen activator activity in morphologically normal tissues adjacent to gastrointestinal carcinomas associated with the degree of tumor progression? | {
"contexts": [
"To investigate whether the level of plasminogen activator (PA) activity assayed in gastrointestinal carcinomas and the \"morphologically normal tissues\" adjacent to them is associated with the degree of tumor progression.",
"Tumor and \"normal tissues\" were obtained from gastrointestinal surgical samples to assess urokinase-type (u-PA) and tissue-type plasminogen activator (t-PA) activities by radial caseinolytic assay and the expression of PA inhibitor-1 (PAI-1) by ELISA. We compared the PA system between the tumor and \"normal tissues\" and we investigated the existence of correlations between: (a) PA production in the tumor and \"normal tissues\", (b) different components of the PA system, and (c) PA system and the degree of tumor progression.",
"(1) Total PA activity, u-PA activity and PAI-1 expression are significantly higher in tumor than in \"normal tissues\", whereas t-PA activity does not differ between them. (2) Total PA activity mainly correlates with u-PA activity in tumor tissues and similarly with u-PA and t-PA activities in \"normal tissues\". (3) There is a significant association between t-PA activity in tumor and \"normal tissues\" and the degree of tumor progression."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Aged, 80 and over",
"Carcinoma",
"Colon",
"Disease Progression",
"Female",
"Gastrointestinal Neoplasms",
"Humans",
"Male",
"Middle Aged",
"Plasminogen Activators",
"Rectum",
"Stomach",
"Tissue Plasminogen Activator",
"Urokinase-Type Plasminogen Activator"
]
} | "Morphologically normal tissues" adjacent to carcinomas present abnormal t-PA activity that is associated with the degree of tumor progression. Assaying of this activity could be useful as a predictive parameter. | yes | [
{
"from": "human",
"value": "Question: Is tissue-type plasminogen activator activity in morphologically normal tissues adjacent to gastrointestinal carcinomas associated with the degree of tumor progression?\nContext: {'contexts': ['To investigate whether the level of plasminogen activator (PA) activity assayed in gastrointestinal carcinomas and the \"morphologically normal tissues\" adjacent to them is associated with the degree of tumor progression.', 'Tumor and \"normal tissues\" were obtained from gastrointestinal surgical samples to assess urokinase-type (u-PA) and tissue-type plasminogen activator (t-PA) activities by radial caseinolytic assay and the expression of PA inhibitor-1 (PAI-1) by ELISA. We compared the PA system between the tumor and \"normal tissues\" and we investigated the existence of correlations between: (a) PA production in the tumor and \"normal tissues\", (b) different components of the PA system, and (c) PA system and the degree of tumor progression.', '(1) Total PA activity, u-PA activity and PAI-1 expression are significantly higher in tumor than in \"normal tissues\", whereas t-PA activity does not differ between them. (2) Total PA activity mainly correlates with u-PA activity in tumor tissues and similarly with u-PA and t-PA activities in \"normal tissues\". (3) There is a significant association between t-PA activity in tumor and \"normal tissues\" and the degree of tumor progression.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Aged, 80 and over', 'Carcinoma', 'Colon', 'Disease Progression', 'Female', 'Gastrointestinal Neoplasms', 'Humans', 'Male', 'Middle Aged', 'Plasminogen Activators', 'Rectum', 'Stomach', 'Tissue Plasminogen Activator', 'Urokinase-Type Plasminogen Activator']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,371,605 | Does bispectral index monitoring improve early recovery of geriatric outpatients undergoing brief surgical procedures? | {
"contexts": [
"To assess if titration of sevoflurane using the bispectral index (BIS) monitor improves the early and intermediate recovery in geriatric outpatients undergoing brief urologic procedures under general anesthesia without muscle relaxants.",
"After a standardized induction with propofol and fentanyl, a laryngeal mask airway was inserted and sevoflurane was administered in combination with 60% nitrous oxide in oxygen for maintenance of anesthesia in spontaneously breathing outpatients. In the Control group (n = 25), sevoflurane and fentanyl were titrated according to standard clinical practice. In the BIS-directed group (n = 25), sevoflurane was titrated to maintain a BIS value between 50 and 60, and supplemental fentanyl, 25 mug iv boluses were administered to treat tachypnea. The intraoperative anesthetic and analgesic requirements, as well as the times to eye opening, removal of the laryngeal mask airway device, response to simple commands, orientation to person and place, and postanesthesia care unit discharge eligibility (fast-track score of 14) were assessed at specific time intervals.",
"The minimum alveolar concentration-hour of sevoflurane (0.25 +/- 0.15 and 0.31 +/- 0.2) and end-tidal concentrations of sevoflurane at the end of surgery (0.3 +/- 0.3 and 0.4 +/- 0.20%) did not differ significantly between the Control and BIS-directed groups, respectively. Although the percentage of patients requiring supplemental boluses of fentanyl was reduced in the BIS-directed group (16 vs 48%, P <0.05), the intraoperative BIS values and recovery times were similar in the two groups."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Ambulatory Surgical Procedures",
"Anesthesia Recovery Period",
"Anesthesia, General",
"Anesthetics, Combined",
"Anesthetics, Inhalation",
"Anesthetics, Intravenous",
"Double-Blind Method",
"Electroencephalography",
"Female",
"Fentanyl",
"Humans",
"Male",
"Methyl Ethers",
"Monitoring, Intraoperative",
"Outpatients",
"Propofol",
"Prospective Studies",
"Sevoflurane",
"Time Factors",
"Urologic Surgical Procedures"
]
} | In this non-paralyzed elderly outpatient surgery population, the use of BIS monitoring for titrating the maintenance anesthetic (sevoflurane) failed to improve the early recovery process. | no | [
{
"from": "human",
"value": "Question: Does bispectral index monitoring improve early recovery of geriatric outpatients undergoing brief surgical procedures?\nContext: {'contexts': ['To assess if titration of sevoflurane using the bispectral index (BIS) monitor improves the early and intermediate recovery in geriatric outpatients undergoing brief urologic procedures under general anesthesia without muscle relaxants.', 'After a standardized induction with propofol and fentanyl, a laryngeal mask airway was inserted and sevoflurane was administered in combination with 60% nitrous oxide in oxygen for maintenance of anesthesia in spontaneously breathing outpatients. In the Control group (n = 25), sevoflurane and fentanyl were titrated according to standard clinical practice. In the BIS-directed group (n = 25), sevoflurane was titrated to maintain a BIS value between 50 and 60, and supplemental fentanyl, 25 mug iv boluses were administered to treat tachypnea. The intraoperative anesthetic and analgesic requirements, as well as the times to eye opening, removal of the laryngeal mask airway device, response to simple commands, orientation to person and place, and postanesthesia care unit discharge eligibility (fast-track score of 14) were assessed at specific time intervals.', 'The minimum alveolar concentration-hour of sevoflurane (0.25 +/- 0.15 and 0.31 +/- 0.2) and end-tidal concentrations of sevoflurane at the end of surgery (0.3 +/- 0.3 and 0.4 +/- 0.20%) did not differ significantly between the Control and BIS-directed groups, respectively. Although the percentage of patients requiring supplemental boluses of fentanyl was reduced in the BIS-directed group (16 vs 48%, P <0.05), the intraoperative BIS values and recovery times were similar in the two groups.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Ambulatory Surgical Procedures', 'Anesthesia Recovery Period', 'Anesthesia, General', 'Anesthetics, Combined', 'Anesthetics, Inhalation', 'Anesthetics, Intravenous', 'Double-Blind Method', 'Electroencephalography', 'Female', 'Fentanyl', 'Humans', 'Male', 'Methyl Ethers', 'Monitoring, Intraoperative', 'Outpatients', 'Propofol', 'Prospective Studies', 'Sevoflurane', 'Time Factors', 'Urologic Surgical Procedures']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
16,399,314 | Does chronic aspiration of gastric fluid accelerate pulmonary allograft dysfunction in a rat model of lung transplantation? | {
"contexts": [
"Emerging clinical evidence suggests that gastroesophageal reflux disease is associated with pulmonary allograft dysfunction. In this study, we used a model of rat lung transplantation to test the hypothesis that chronic aspiration of gastric contents accelerates pulmonary allograft dysfunction.",
"We evaluated the effects of chronic aspiration on pulmonary isografts (strain F344) and pulmonary allografts (strain WKY to strain F344). Chronic aspiration consisted of 0.5 mL/kg of filtered gastric contents injected weekly into the left lung for 4 to 8 weeks beginning 1 week after transplantation. Seven days after the last aspiration, animals were killed, and grafts were evaluated grossly and by histologic and immunochemical analyses, including Masson trichrome staining for collagen and immunostaining for CD68+ and CD8+ cells. Serum cytokine concentrations were determined by bead-based immunoassays or enzyme-linked immunosorbent assay.",
"Allografts without aspiration (n = 12) demonstrated a relatively normal architecture with diffuse International Society for Heart and Lung Transplantation grade 3 acute rejection; occasional grade 4 rejection was noted. In contrast, allografts with chronic aspiration (n = 7) demonstrated severe grade 4 acute rejection with significant monocyte infiltration, fibrosis, and loss of normal alveolar anatomy. Grossly, 8 (67%) of 12 allografts without aspiration seemed to inflate and perfuse normally, whereas all allografts exposed to chronic aspiration were firm and shrunken, without the ability to ventilate (P = .013; Fisher exact test). Aspiration was associated with increases in graft-infiltrating macrophages and CD8+ T cells and higher levels of serum transforming growth factor beta."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Chronic Disease",
"Disease Models, Animal",
"Lung Transplantation",
"Male",
"Pneumonia, Aspiration",
"Postoperative Complications",
"Rats",
"Rats, Inbred F344",
"Rats, Wistar"
]
} | Chronic aspiration of gastric contents promotes accelerated allograft failure and may promote a profibrotic environment. | yes | [
{
"from": "human",
"value": "Question: Does chronic aspiration of gastric fluid accelerate pulmonary allograft dysfunction in a rat model of lung transplantation?\nContext: {'contexts': ['Emerging clinical evidence suggests that gastroesophageal reflux disease is associated with pulmonary allograft dysfunction. In this study, we used a model of rat lung transplantation to test the hypothesis that chronic aspiration of gastric contents accelerates pulmonary allograft dysfunction.', 'We evaluated the effects of chronic aspiration on pulmonary isografts (strain F344) and pulmonary allografts (strain WKY to strain F344). Chronic aspiration consisted of 0.5 mL/kg of filtered gastric contents injected weekly into the left lung for 4 to 8 weeks beginning 1 week after transplantation. Seven days after the last aspiration, animals were killed, and grafts were evaluated grossly and by histologic and immunochemical analyses, including Masson trichrome staining for collagen and immunostaining for CD68+ and CD8+ cells. Serum cytokine concentrations were determined by bead-based immunoassays or enzyme-linked immunosorbent assay.', 'Allografts without aspiration (n = 12) demonstrated a relatively normal architecture with diffuse International Society for Heart and Lung Transplantation grade 3 acute rejection; occasional grade 4 rejection was noted. In contrast, allografts with chronic aspiration (n = 7) demonstrated severe grade 4 acute rejection with significant monocyte infiltration, fibrosis, and loss of normal alveolar anatomy. Grossly, 8 (67%) of 12 allografts without aspiration seemed to inflate and perfuse normally, whereas all allografts exposed to chronic aspiration were firm and shrunken, without the ability to ventilate (P = .013; Fisher exact test). Aspiration was associated with increases in graft-infiltrating macrophages and CD8+ T cells and higher levels of serum transforming growth factor beta.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Chronic Disease', 'Disease Models, Animal', 'Lung Transplantation', 'Male', 'Pneumonia, Aspiration', 'Postoperative Complications', 'Rats', 'Rats, Inbred F344', 'Rats, Wistar']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,373,300 | Does dexamethasone reduce reintubation rate due to postextubation stridor in a high-risk paediatric population? | {
"contexts": [
"To study the effect of dexamethasone on postextubation stridor (PS) incidence and reintubation rate due to PS in a high-risk paediatric intensive care population.",
"All children aged between 4 wk and 6 y, who were intubated for at least 24 h and extubated between August 1999 and May 2002, were retrospectively included (n=60). Medical records of the included patients were studied; records of patients treated with dexamethasone prior to and following extubation (n=23) were compared with control patients who had not received prophylactic medication (n=37).",
"Nine patients in the control group developed significant postextubation stridor, necessitating nebulized epinephrine or glucocorticosteroids. In six of these children, reintubation as a result of postextubation stridor was indicated. None of the patients treated with dexamethasone developed severe postextubation stridor or required reintubation."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Anti-Inflammatory Agents",
"Child, Preschool",
"Croup",
"Dexamethasone",
"Female",
"Humans",
"Infant",
"Intubation, Intratracheal",
"Male",
"Respiratory Sounds",
"Retrospective Studies"
]
} | The risk of postextubation stridor is relatively high in the group of children aged between 4 wk and 6 y with intubation exceeding 24 h. We found dexamethasone to be effective in preventing reintubation due to postextubation stridor in this paediatric high-risk group. | yes | [
{
"from": "human",
"value": "Question: Does dexamethasone reduce reintubation rate due to postextubation stridor in a high-risk paediatric population?\nContext: {'contexts': ['To study the effect of dexamethasone on postextubation stridor (PS) incidence and reintubation rate due to PS in a high-risk paediatric intensive care population.', 'All children aged between 4 wk and 6 y, who were intubated for at least 24 h and extubated between August 1999 and May 2002, were retrospectively included (n=60). Medical records of the included patients were studied; records of patients treated with dexamethasone prior to and following extubation (n=23) were compared with control patients who had not received prophylactic medication (n=37).', 'Nine patients in the control group developed significant postextubation stridor, necessitating nebulized epinephrine or glucocorticosteroids. In six of these children, reintubation as a result of postextubation stridor was indicated. None of the patients treated with dexamethasone developed severe postextubation stridor or required reintubation.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Anti-Inflammatory Agents', 'Child, Preschool', 'Croup', 'Dexamethasone', 'Female', 'Humans', 'Infant', 'Intubation, Intratracheal', 'Male', 'Respiratory Sounds', 'Retrospective Studies']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,374,168 | Do thermal injury-induced peroxynitrite production and pulmonary inducible nitric oxide synthase expression depend on JNK/AP-1 signaling? | {
"contexts": [
"To determine whether burn-induced peroxynitrite production and expression of lung inducible nitric oxide synthase (iNOS), intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1, CXCR2, macrophage inflammatory protein (MIP)-2, and neutrophil chemokine (KC) are mediated by the c-Jun NH2-terminal kinase (JNK).",
"Prospective, experimental study.",
"Research laboratory at a university hospital.",
"Thermal injury models in the mice.",
"In experiment 1, specific pathogen-free C57/BL6 mice were subjected to 30% total body surface area third-degree burn over shaved back. At 0 hr, 2 hrs, 4 hrs, and 6 hrs after burn, lung tissues of those mice were harvested for JNK activity assay, AP-1 DNA-binding activity, and pJNK immunohistochemistry. In experiment 2, a specific JNK inhibitor, SP600125, was given (30 mg/kg intraperitoneally) to mice immediately postburn to suppress the JNK activity. At 8 hrs after burn, blood was assayed for the peroxynitrite-mediated dihydrorhodamine (DHR) 123 oxidation. Lung tissues were harvested for myeloperoxidase (MPO) determination, ICAM-1, VCAM-1, CXCR2, KC, MIP-2, interleukin-1beta, and interleukin-6 messenger RNA expression; iNOS immunohistochemical staining; and histologic studies. Pulmonary microvascular dysfunction was quantified by measuring the extravasations of Evans blue dye.",
"The JNK activity and AP-1 DNA-binding activity of lung tissue significantly increased to a peak at 2 hrs and 4 hrs, respectively, after thermal injury. Immunohistochemical study demonstrated that the increase of the pJNK was mostly from the bronchiole epithelial cells. This increase of MPO activity in lung, blood DHR 123 oxidation level, and lung permeability increased six-fold, nine-fold, and four-fold after burn. SP600125 administration obliterated the thermal injury-induced JNK activity, AP-1 DNA-binding activity, and iNOS expression in lung tissue. SP600125 treatment also significantly decreased MPO activity, blood DHR 123 oxidation, and lung permeability by 54%, 8%, and 47%, respectively, and markedly decreased the thermal injury-induced perivascular and interstitial inflammatory cell infiltration and septum edema. Furthermore, SP600125 abolished thermal injury-induced ICAM-1, VCAM-1, CXCR2, MIP-2, and KC but not interleukin-1beta and interleukin-6 messenger RNA levels of lung tissues."
],
"labels": [
"OBJECTIVE",
"METHODS",
"METHODS",
"METHODS",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Base Sequence",
"Biopsy, Needle",
"Blotting, Western",
"Burns",
"Disease Models, Animal",
"Immunohistochemistry",
"Intercellular Adhesion Molecule-1",
"Lung",
"MAP Kinase Kinase 4",
"Male",
"Mice",
"Mice, Inbred C57BL",
"Molecular Sequence Data",
"Neutrophil Infiltration",
"Nitric Oxide Synthase",
"Peroxidase",
"Peroxynitrous Acid",
"Probability",
"RNA, Messenger",
"Random Allocation",
"Reference Values",
"Reverse Transcriptase Polymerase Chain Reaction",
"Sensitivity and Specificity",
"Signal Transduction",
"Transcription Factor AP-1",
"Vascular Cell Adhesion Molecule-1"
]
} | Thermal injury induces lung tissue JNK activation and AP-1 DNA-binding activity mainly from airway epithelial cells. Thermal injury-induced peroxynitrite production and lung iNOS, ICAM-1, and VCAM-1 expression are mediated by the JNK signaling. JNK inhibition decreases thermal injury-induced lung neutrophil infiltration and subsequently pulmonary hyperpermeability. | yes | [
{
"from": "human",
"value": "Question: Do thermal injury-induced peroxynitrite production and pulmonary inducible nitric oxide synthase expression depend on JNK/AP-1 signaling?\nContext: {'contexts': ['To determine whether burn-induced peroxynitrite production and expression of lung inducible nitric oxide synthase (iNOS), intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1, CXCR2, macrophage inflammatory protein (MIP)-2, and neutrophil chemokine (KC) are mediated by the c-Jun NH2-terminal kinase (JNK).', 'Prospective, experimental study.', 'Research laboratory at a university hospital.', 'Thermal injury models in the mice.', 'In experiment 1, specific pathogen-free C57/BL6 mice were subjected to 30% total body surface area third-degree burn over shaved back. At 0 hr, 2 hrs, 4 hrs, and 6 hrs after burn, lung tissues of those mice were harvested for JNK activity assay, AP-1 DNA-binding activity, and pJNK immunohistochemistry. In experiment 2, a specific JNK inhibitor, SP600125, was given (30 mg/kg intraperitoneally) to mice immediately postburn to suppress the JNK activity. At 8 hrs after burn, blood was assayed for the peroxynitrite-mediated dihydrorhodamine (DHR) 123 oxidation. Lung tissues were harvested for myeloperoxidase (MPO) determination, ICAM-1, VCAM-1, CXCR2, KC, MIP-2, interleukin-1beta, and interleukin-6 messenger RNA expression; iNOS immunohistochemical staining; and histologic studies. Pulmonary microvascular dysfunction was quantified by measuring the extravasations of Evans blue dye.', 'The JNK activity and AP-1 DNA-binding activity of lung tissue significantly increased to a peak at 2 hrs and 4 hrs, respectively, after thermal injury. Immunohistochemical study demonstrated that the increase of the pJNK was mostly from the bronchiole epithelial cells. This increase of MPO activity in lung, blood DHR 123 oxidation level, and lung permeability increased six-fold, nine-fold, and four-fold after burn. SP600125 administration obliterated the thermal injury-induced JNK activity, AP-1 DNA-binding activity, and iNOS expression in lung tissue. SP600125 treatment also significantly decreased MPO activity, blood DHR 123 oxidation, and lung permeability by 54%, 8%, and 47%, respectively, and markedly decreased the thermal injury-induced perivascular and interstitial inflammatory cell infiltration and septum edema. Furthermore, SP600125 abolished thermal injury-induced ICAM-1, VCAM-1, CXCR2, MIP-2, and KC but not interleukin-1beta and interleukin-6 messenger RNA levels of lung tissues.'], 'labels': ['OBJECTIVE', 'METHODS', 'METHODS', 'METHODS', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Base Sequence', 'Biopsy, Needle', 'Blotting, Western', 'Burns', 'Disease Models, Animal', 'Immunohistochemistry', 'Intercellular Adhesion Molecule-1', 'Lung', 'MAP Kinase Kinase 4', 'Male', 'Mice', 'Mice, Inbred C57BL', 'Molecular Sequence Data', 'Neutrophil Infiltration', 'Nitric Oxide Synthase', 'Peroxidase', 'Peroxynitrous Acid', 'Probability', 'RNA, Messenger', 'Random Allocation', 'Reference Values', 'Reverse Transcriptase Polymerase Chain Reaction', 'Sensitivity and Specificity', 'Signal Transduction', 'Transcription Factor AP-1', 'Vascular Cell Adhesion Molecule-1']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,376,212 | Does vascular endothelial growth factor naked DNA gene transfer enhance thrombus recanalization and resolution? | {
"contexts": [
"Enhancing thrombus resolution may reduce the long-term complications of venous thrombosis. The aim of this study was to examine whether a sustained release of vascular endothelial growth factor (VEGF) would further improve thrombus recanalization.",
"Inferior caval vein thrombosis was induced in a cohort of 21 male Wistar rats. A plasmid encoding the human VEGF gene (phVEGF) was injected directly into thrombus (30 to 50 microg) and the muscle adjacent to the inferior vena cava (300 to 400 microg). A plasmid containing the gene encoding beta-galactosidase (pCMVbeta) was injected into the same sites of a separate cohort of rats to act as a control. Tissues were harvested after 1 and 2 weeks, and beta-galactosidase activity was measured to estimate transfection efficiency. Muscle and serum VEGF were measured by enzyme-inked immunosorbent assay. Thrombus size, recanalization, and organization were determined by computer-assisted image analysis.",
"The efficiency of control plasmid transfection into muscle was about 1%. No serum hVEGF was detected in phVEGF- or pCMVbeta-treated animals. Significantly raised levels of hVEGF (P < .01) were detected in the muscle injected with phVEGF after 2 weeks compared with control muscle. There was a significant reduction in thrombus size of 23% (P < .05) and 48% (P < .001) in phVEGF-treated animals compared with pCMVbeta-treated controls after 1 and 2 weeks, respectively. Thrombus recanalization was a significantly greater in the phVEGF-treated group after 2 weeks (mean 19% +/- 2% [SEM]) compared with controls (mean 13% +/- 2%, P < .01). There were no differences in the thrombus organization score."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Disease Models, Animal",
"Gene Transfer Techniques",
"Genetic Therapy",
"Injections, Intralesional",
"Male",
"Plasmids",
"Rats",
"Rats, Wistar",
"Transfection",
"Treatment Outcome",
"Vaccines, DNA",
"Vascular Endothelial Growth Factor A",
"Vena Cava, Inferior",
"Venous Thrombosis"
]
} | VEGF gene therapy of venous thrombus resulted in smaller thrombi with greater recanalization. Angiogenic gene therapy may form the basis of a novel treatment that may improve the resolution of venous thrombi. | yes | [
{
"from": "human",
"value": "Question: Does vascular endothelial growth factor naked DNA gene transfer enhance thrombus recanalization and resolution?\nContext: {'contexts': ['Enhancing thrombus resolution may reduce the long-term complications of venous thrombosis. The aim of this study was to examine whether a sustained release of vascular endothelial growth factor (VEGF) would further improve thrombus recanalization.', 'Inferior caval vein thrombosis was induced in a cohort of 21 male Wistar rats. A plasmid encoding the human VEGF gene (phVEGF) was injected directly into thrombus (30 to 50 microg) and the muscle adjacent to the inferior vena cava (300 to 400 microg). A plasmid containing the gene encoding beta-galactosidase (pCMVbeta) was injected into the same sites of a separate cohort of rats to act as a control. Tissues were harvested after 1 and 2 weeks, and beta-galactosidase activity was measured to estimate transfection efficiency. Muscle and serum VEGF were measured by enzyme-inked immunosorbent assay. Thrombus size, recanalization, and organization were determined by computer-assisted image analysis.', 'The efficiency of control plasmid transfection into muscle was about 1%. No serum hVEGF was detected in phVEGF- or pCMVbeta-treated animals. Significantly raised levels of hVEGF (P < .01) were detected in the muscle injected with phVEGF after 2 weeks compared with control muscle. There was a significant reduction in thrombus size of 23% (P < .05) and 48% (P < .001) in phVEGF-treated animals compared with pCMVbeta-treated controls after 1 and 2 weeks, respectively. Thrombus recanalization was a significantly greater in the phVEGF-treated group after 2 weeks (mean 19% +/- 2% [SEM]) compared with controls (mean 13% +/- 2%, P < .01). There were no differences in the thrombus organization score.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Disease Models, Animal', 'Gene Transfer Techniques', 'Genetic Therapy', 'Injections, Intralesional', 'Male', 'Plasmids', 'Rats', 'Rats, Wistar', 'Transfection', 'Treatment Outcome', 'Vaccines, DNA', 'Vascular Endothelial Growth Factor A', 'Vena Cava, Inferior', 'Venous Thrombosis']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,401,338 | Does cytoregR inhibit growth and proliferation of human adenocarcinoma cells via induction of apoptosis? | {
"contexts": [
"Cancer is one of the devastating neovascular diseases that incapacitate so many people the world over. Recent reports from the National Cancer Institute indicate some significant gain therapy and cancer management as seen in the increase in the 5-year survival rate over the past two decades. Although near-perfect cure rate have been reported in the early-stage disease, these data reveal high recurrence rate and serious side effects including second malignancies and fatalities. Most of the currently used anticancer agents are only effective against proliferating cancer cells. Thus attention has been focused on potential anti-cancer agents capable of killing cancer cells independent of the cell cycle state, to ensure effective elimination of most cancer cells. The objective of this study was to test the chemosensitivity and potential mechanism of action of a novel cancer drug, CytoregR, in a panel of human cancer cells.",
"the study was performed using a series of bioassays including Trypan blue exclusion, MTS Growth inhibition, LDH-cytotoxicity, TUNEL-Terminal DNA fragmentation Apoptosis Assay, and the Caspase protease CPP32 activity assays.",
"CytoregR induced significant dose- and time-dependent inhibition of growth in all the cells; with significant differences in chemosensitivity (P < 0.05) between the target cells becoming more apparent at 48 hr exposure. CytoregR showed no significant effect on normal cells relative to the tumor cells. Growth inhibition in all the cells was due to induction of apoptosis at lower concentrations of cytoregR (> 1:300). CytoregR-induced caspase protease-3 (CPP32) activation significantly and positively correlated with apoptosis induction and growth inhibition; thus implicating CPP32 as the principal death pathway in cytoregR-induced apoptosis."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": []
} | CytoregR exerted a dose-and time-dependent growth inhibitory effect in all the target cells through induction of apoptosis via the CPP32 death pathway, independent of hormonal sensitivity of the cells. The present data indicate that not only could CPP32 provide a potential target for regulation of cytoregR-induced apoptosis but also that cytoregR could play a significant role in chemotherapeutic regimen in many human malignant tumors. | yes | [
{
"from": "human",
"value": "Question: Does cytoregR inhibit growth and proliferation of human adenocarcinoma cells via induction of apoptosis?\nContext: {'contexts': ['Cancer is one of the devastating neovascular diseases that incapacitate so many people the world over. Recent reports from the National Cancer Institute indicate some significant gain therapy and cancer management as seen in the increase in the 5-year survival rate over the past two decades. Although near-perfect cure rate have been reported in the early-stage disease, these data reveal high recurrence rate and serious side effects including second malignancies and fatalities. Most of the currently used anticancer agents are only effective against proliferating cancer cells. Thus attention has been focused on potential anti-cancer agents capable of killing cancer cells independent of the cell cycle state, to ensure effective elimination of most cancer cells. The objective of this study was to test the chemosensitivity and potential mechanism of action of a novel cancer drug, CytoregR, in a panel of human cancer cells.', 'the study was performed using a series of bioassays including Trypan blue exclusion, MTS Growth inhibition, LDH-cytotoxicity, TUNEL-Terminal DNA fragmentation Apoptosis Assay, and the Caspase protease CPP32 activity assays.', 'CytoregR induced significant dose- and time-dependent inhibition of growth in all the cells; with significant differences in chemosensitivity (P < 0.05) between the target cells becoming more apparent at 48 hr exposure. CytoregR showed no significant effect on normal cells relative to the tumor cells. Growth inhibition in all the cells was due to induction of apoptosis at lower concentrations of cytoregR (> 1:300). CytoregR-induced caspase protease-3 (CPP32) activation significantly and positively correlated with apoptosis induction and growth inhibition; thus implicating CPP32 as the principal death pathway in cytoregR-induced apoptosis.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,391,154 | Does activation of soluble guanylate cyclase reverse experimental pulmonary hypertension and vascular remodeling? | {
"contexts": [
"Severe pulmonary hypertension is a disabling disease with high mortality, characterized by pulmonary vascular remodeling and right heart hypertrophy. Using wild-type and homozygous endothelial nitric oxide synthase (NOS3(-/-)) knockout mice with pulmonary hypertension induced by chronic hypoxia and rats with monocrotaline-induced pulmonary hypertension, we examined whether the soluble guanylate cyclase (sGC) stimulator Bay41-2272 or the sGC activator Bay58-2667 could reverse pulmonary vascular remodeling.",
"Both Bay41-2272 and Bay58-2667 dose-dependently inhibited the pressor response of acute hypoxia in the isolated perfused lung system. When wild-type (NOS3(+/+)) or NOS3(-/-) mice were housed under 10% oxygen conditions for 21 or 35 days, both strains developed pulmonary hypertension, right heart hypertrophy, and pulmonary vascular remodeling, demonstrated by an increase in fully muscularized peripheral pulmonary arteries. Treatment of wild-type mice with the activator of sGC, Bay58-2667 (10 mg/kg per day), or the stimulator of sGC, Bay41-2272 (10 mg/kg per day), after full establishment of pulmonary hypertension from day 21 to day 35 significantly reduced pulmonary hypertension, right ventricular hypertrophy, and structural remodeling of the lung vasculature. In contrast, only minor efficacy of chronic sGC activator therapies was noted in NOS3(-/-) mice. In monocrotaline-injected rats with established severe pulmonary hypertension, both compounds significantly reversed hemodynamic and structural changes."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Animals",
"Benzoates",
"Cardiomegaly",
"Disease Models, Animal",
"Enzyme Activation",
"Guanylate Cyclase",
"Humans",
"Hypertension, Pulmonary",
"Hypertrophy, Right Ventricular",
"Hypoxia",
"Male",
"Mice",
"Mice, Knockout",
"Nitric Oxide Synthase Type II",
"Nitric Oxide Synthase Type III",
"Pulmonary Circulation",
"Pyrazoles",
"Pyridines",
"Rats",
"Rats, Sprague-Dawley",
"Solubility"
]
} | Activation of sGC reverses hemodynamic and structural changes associated with monocrotaline- and chronic hypoxia-induced experimental pulmonary hypertension. This effect is partially dependent on endogenous nitric oxide generated by NOS3. | yes | [
{
"from": "human",
"value": "Question: Does activation of soluble guanylate cyclase reverse experimental pulmonary hypertension and vascular remodeling?\nContext: {'contexts': ['Severe pulmonary hypertension is a disabling disease with high mortality, characterized by pulmonary vascular remodeling and right heart hypertrophy. Using wild-type and homozygous endothelial nitric oxide synthase (NOS3(-/-)) knockout mice with pulmonary hypertension induced by chronic hypoxia and rats with monocrotaline-induced pulmonary hypertension, we examined whether the soluble guanylate cyclase (sGC) stimulator Bay41-2272 or the sGC activator Bay58-2667 could reverse pulmonary vascular remodeling.', 'Both Bay41-2272 and Bay58-2667 dose-dependently inhibited the pressor response of acute hypoxia in the isolated perfused lung system. When wild-type (NOS3(+/+)) or NOS3(-/-) mice were housed under 10% oxygen conditions for 21 or 35 days, both strains developed pulmonary hypertension, right heart hypertrophy, and pulmonary vascular remodeling, demonstrated by an increase in fully muscularized peripheral pulmonary arteries. Treatment of wild-type mice with the activator of sGC, Bay58-2667 (10 mg/kg per day), or the stimulator of sGC, Bay41-2272 (10 mg/kg per day), after full establishment of pulmonary hypertension from day 21 to day 35 significantly reduced pulmonary hypertension, right ventricular hypertrophy, and structural remodeling of the lung vasculature. In contrast, only minor efficacy of chronic sGC activator therapies was noted in NOS3(-/-) mice. In monocrotaline-injected rats with established severe pulmonary hypertension, both compounds significantly reversed hemodynamic and structural changes.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Animals', 'Benzoates', 'Cardiomegaly', 'Disease Models, Animal', 'Enzyme Activation', 'Guanylate Cyclase', 'Humans', 'Hypertension, Pulmonary', 'Hypertrophy, Right Ventricular', 'Hypoxia', 'Male', 'Mice', 'Mice, Knockout', 'Nitric Oxide Synthase Type II', 'Nitric Oxide Synthase Type III', 'Pulmonary Circulation', 'Pyrazoles', 'Pyridines', 'Rats', 'Rats, Sprague-Dawley', 'Solubility']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,376,327 | Does autologous myoblast transplantation after myocardial infarction increase the inducibility of ventricular arrhythmias? | {
"contexts": [
"Small scale clinical trials suggested the feasibility and the efficacy of autologous myoblast transplantation to improve ventricular function after myocardial infarction. However, these trials were hampered by unexpected episodes of life-threatening ventricular tachyarrhythmias (VT). We investigated cardiac electrical stability after myoblast transplantation to the myocardium.",
"Seven days after coronary ligation, Wistar rats were randomized into 3 groups: a control group receiving no further treatment, a vehicle group injected with culture medium into the infarcted myocardium, and a myoblast group injected with autologous myoblasts. Holter monitoring did not discriminate the myoblast from the vehicle groups. Programmed Electrical Stimulation (PES) was performed to evaluate further a cardiac substrate for arrhythmia susceptibility. The occurrence of sustained VT during PES was similar in control and vehicle groups (5/17 and 4/19 rats, respectively; p=0.50). In contrast, 13/20 rats (65%) from the myoblast group showed at least one episode of sustained VT during PES (p<0.05 and p<0.005 versus control and vehicle groups). As a further control group, rats injected with autologous bone marrow mononuclear cells into the infarcted myocardium did not show increased susceptibility to PES."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Animals",
"Bone Marrow Transplantation",
"Cardiomegaly",
"Electric Stimulation",
"Electrocardiography, Ambulatory",
"Heart",
"Injections",
"Male",
"Myoblasts, Cardiac",
"Myocardial Infarction",
"Rats",
"Rats, Wistar",
"Reverse Transcriptase Polymerase Chain Reaction",
"Transplantation, Autologous",
"Ventricular Fibrillation"
]
} | In an infarcted rat model, myoblast transplantation but not bone marrow mononuclear cells or myocardial injection per se induces electrical ventricular instability. Because ventricular arrhythmias are life-threatening disorders, we suggest that such preclinical evaluation should be conducted for any new source of cells to be injected into the myocardium. | yes | [
{
"from": "human",
"value": "Question: Does autologous myoblast transplantation after myocardial infarction increase the inducibility of ventricular arrhythmias?\nContext: {'contexts': ['Small scale clinical trials suggested the feasibility and the efficacy of autologous myoblast transplantation to improve ventricular function after myocardial infarction. However, these trials were hampered by unexpected episodes of life-threatening ventricular tachyarrhythmias (VT). We investigated cardiac electrical stability after myoblast transplantation to the myocardium.', 'Seven days after coronary ligation, Wistar rats were randomized into 3 groups: a control group receiving no further treatment, a vehicle group injected with culture medium into the infarcted myocardium, and a myoblast group injected with autologous myoblasts. Holter monitoring did not discriminate the myoblast from the vehicle groups. Programmed Electrical Stimulation (PES) was performed to evaluate further a cardiac substrate for arrhythmia susceptibility. The occurrence of sustained VT during PES was similar in control and vehicle groups (5/17 and 4/19 rats, respectively; p=0.50). In contrast, 13/20 rats (65%) from the myoblast group showed at least one episode of sustained VT during PES (p<0.05 and p<0.005 versus control and vehicle groups). As a further control group, rats injected with autologous bone marrow mononuclear cells into the infarcted myocardium did not show increased susceptibility to PES.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Animals', 'Bone Marrow Transplantation', 'Cardiomegaly', 'Electric Stimulation', 'Electrocardiography, Ambulatory', 'Heart', 'Injections', 'Male', 'Myoblasts, Cardiac', 'Myocardial Infarction', 'Rats', 'Rats, Wistar', 'Reverse Transcriptase Polymerase Chain Reaction', 'Transplantation, Autologous', 'Ventricular Fibrillation']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,385,253 | Does eradication of small intestinal bacterial overgrowth in the cystic fibrosis mouse reduce mucus accumulation? | {
"contexts": [
"Mucus accumulation in cystic fibrosis (CF) is involved in blockage of the distal small intestine. Because expression of mucin genes and mucus secretion can be increased by infection and previous work indicated that small intestinal bacterial overgrowth occurs in CF, we tested whether reduction of bacterial load by antibiotic treatment would reduce mucin gene expression and mucus accumulation in the CF mouse small intestine.",
"CF transmembrane conductance regulator null (cftr (tm1UNC)) and wild type littermates were treated with ciprofloxacin and metronidazole for 3 weeks. Muc2 and Muc3 gene expression were measured by quantitative reverse-transcriptase polymerase chain reaction. Periodic acid Schiff (PAS) staining and morphometry were used to measure the size of mucus droplets within goblet cells and dilation of the intestinal crypt lumen, as estimates of mucus secretion and accumulation.",
"Antibiotic treatment did not significantly affect Muc2 and Muc3 gene expression in CF mice. In untreated CF mice, the crypt lumen was almost sevenfold wider than wild type. Antibiotic treatment of CF mice reduced the intensity of PAS crypt lumen staining, and the lumen width was decreased by approximately 25%. The area occupied by PAS-positive material in goblet cells was significantly greater in tissues from antibiotic treated mice."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Anti-Infective Agents",
"Bacteria",
"Ciprofloxacin",
"Cystic Fibrosis",
"Cystic Fibrosis Transmembrane Conductance Regulator",
"Disease Models, Animal",
"Female",
"Intestine, Small",
"Male",
"Metronidazole",
"Mice",
"Mice, Inbred C57BL",
"Mice, Inbred CFTR",
"Mucins",
"Mucus",
"Periodic Acid-Schiff Reaction",
"Reverse Transcriptase Polymerase Chain Reaction"
]
} | Eradication of bacterial overgrowth in CF mice significantly decreased mucus secretion and accumulation in intestinal crypts without an effect on mucin gene expression. It is proposed that bacterial overgrowth stimulates mucus secretion, which contributes to its accumulation in the small intestine. Control of bacterial overgrowth is expected to reduce mucus accumulation and may improve intestinal function and overall health in CF. | yes | [
{
"from": "human",
"value": "Question: Does eradication of small intestinal bacterial overgrowth in the cystic fibrosis mouse reduce mucus accumulation?\nContext: {'contexts': ['Mucus accumulation in cystic fibrosis (CF) is involved in blockage of the distal small intestine. Because expression of mucin genes and mucus secretion can be increased by infection and previous work indicated that small intestinal bacterial overgrowth occurs in CF, we tested whether reduction of bacterial load by antibiotic treatment would reduce mucin gene expression and mucus accumulation in the CF mouse small intestine.', 'CF transmembrane conductance regulator null (cftr (tm1UNC)) and wild type littermates were treated with ciprofloxacin and metronidazole for 3 weeks. Muc2 and Muc3 gene expression were measured by quantitative reverse-transcriptase polymerase chain reaction. Periodic acid Schiff (PAS) staining and morphometry were used to measure the size of mucus droplets within goblet cells and dilation of the intestinal crypt lumen, as estimates of mucus secretion and accumulation.', 'Antibiotic treatment did not significantly affect Muc2 and Muc3 gene expression in CF mice. In untreated CF mice, the crypt lumen was almost sevenfold wider than wild type. Antibiotic treatment of CF mice reduced the intensity of PAS crypt lumen staining, and the lumen width was decreased by approximately 25%. The area occupied by PAS-positive material in goblet cells was significantly greater in tissues from antibiotic treated mice.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Anti-Infective Agents', 'Bacteria', 'Ciprofloxacin', 'Cystic Fibrosis', 'Cystic Fibrosis Transmembrane Conductance Regulator', 'Disease Models, Animal', 'Female', 'Intestine, Small', 'Male', 'Metronidazole', 'Mice', 'Mice, Inbred C57BL', 'Mice, Inbred CFTR', 'Mucins', 'Mucus', 'Periodic Acid-Schiff Reaction', 'Reverse Transcriptase Polymerase Chain Reaction']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,385,255 | Do dietary gangliosides enhance in vitro lipid uptake in weanling rats? | {
"contexts": [
"The intestine adapts morphologically or functionally in response to environmental stimuli. Dietary lipids modify brush border membrane (BBM) permeability and nutrient transporter activities. Gangliosides (GANG) are glycolipids in human milk that are present only in low amounts in infant formula. Exogenous GANG are incorporated into cell membranes and increase their permeability. The objective of this study was to determine whether feeding a GANG-enriched diet alters in vitro intestinal lipid absorption.",
"Weanling rats were fed either (1) GANG-enriched diet; (2) diet enriched with polyunsaturated long-chain fatty acids; or (3) isocaloric control diet for 2 weeks, after which in vitro intestinal lipid uptake was measured.",
"Feeding GANG did not alter weight gain or intestinal morphology. Enhanced uptake of stearic acid (18:0) in the ileum and stearic and linoleic acid (18:2) in the jejunum was not associated with a change in the abundance of the ileal lipid binding protein (ILBP), the intestinal fatty acid binding protein (I-FABP), or the liver fatty acid binding protein (L-FABP)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adaptation, Physiological",
"Animals",
"Body Weight",
"Fatty Acid-Binding Proteins",
"Fatty Acids, Unsaturated",
"Gangliosides",
"Ileum",
"Intestinal Absorption",
"Intestine, Small",
"Jejunum",
"Lipid Metabolism",
"Male",
"Microvilli",
"Permeability",
"Rats",
"Rats, Sprague-Dawley",
"Weaning"
]
} | We speculate that the enhanced uptake of long-chain fatty acids in weanling rats fed GANG may be caused by a modification in physical properties of the BBM. | yes | [
{
"from": "human",
"value": "Question: Do dietary gangliosides enhance in vitro lipid uptake in weanling rats?\nContext: {'contexts': ['The intestine adapts morphologically or functionally in response to environmental stimuli. Dietary lipids modify brush border membrane (BBM) permeability and nutrient transporter activities. Gangliosides (GANG) are glycolipids in human milk that are present only in low amounts in infant formula. Exogenous GANG are incorporated into cell membranes and increase their permeability. The objective of this study was to determine whether feeding a GANG-enriched diet alters in vitro intestinal lipid absorption.', 'Weanling rats were fed either (1) GANG-enriched diet; (2) diet enriched with polyunsaturated long-chain fatty acids; or (3) isocaloric control diet for 2 weeks, after which in vitro intestinal lipid uptake was measured.', 'Feeding GANG did not alter weight gain or intestinal morphology. Enhanced uptake of stearic acid (18:0) in the ileum and stearic and linoleic acid (18:2) in the jejunum was not associated with a change in the abundance of the ileal lipid binding protein (ILBP), the intestinal fatty acid binding protein (I-FABP), or the liver fatty acid binding protein (L-FABP).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adaptation, Physiological', 'Animals', 'Body Weight', 'Fatty Acid-Binding Proteins', 'Fatty Acids, Unsaturated', 'Gangliosides', 'Ileum', 'Intestinal Absorption', 'Intestine, Small', 'Jejunum', 'Lipid Metabolism', 'Male', 'Microvilli', 'Permeability', 'Rats', 'Rats, Sprague-Dawley', 'Weaning']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,394,916 | Are small increases in extravascular lung water accurately detected by transpulmonary thermodilution? | {
"contexts": [
"Detection of small (10-20%) increases in lung water may be relevant to detect incipient pulmonary edema but no clinically usable method has demonstrated this capability to date.",
"In six pigs weighing 28 to 35 kg, we performed 18 determinations of extravascular lung water (EVLW; transpulmonary thermodilution method) before and immediately after the intratracheal introduction of 50 mL of saline solution. Six determinations were performed in normal lung and 12 in edematous lung.",
"In normal lung, the mean of EVLW increased from 245 +/- 18 mL to 288 +/- 19 mL (p < 0.001) after the intratracheal introduction of 50 mL of saline solution; therefore, 43 of the 50 mL (84%) were detected (range, 37-48 mL). In edematous lung, the EVLW increased from 491 +/- 106 mL to 530 +/- 108 mL after the introduction of 50 mL of saline solution; therefore, 39 of the 50 mL (77%) were detected (range, 15-67 mL)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Bronchoalveolar Lavage",
"Disease Models, Animal",
"Early Diagnosis",
"Extravascular Lung Water",
"Isotonic Solutions",
"Pulmonary Edema",
"Reproducibility of Results",
"Sodium Chloride",
"Swine",
"Thermodilution"
]
} | The transpulmonary thermodilution technique accurately detects small increases in extravascular lung water and may permit accurate diagnosis of incipient pulmonary edema. | yes | [
{
"from": "human",
"value": "Question: Are small increases in extravascular lung water accurately detected by transpulmonary thermodilution?\nContext: {'contexts': ['Detection of small (10-20%) increases in lung water may be relevant to detect incipient pulmonary edema but no clinically usable method has demonstrated this capability to date.', 'In six pigs weighing 28 to 35 kg, we performed 18 determinations of extravascular lung water (EVLW; transpulmonary thermodilution method) before and immediately after the intratracheal introduction of 50 mL of saline solution. Six determinations were performed in normal lung and 12 in edematous lung.', 'In normal lung, the mean of EVLW increased from 245 +/- 18 mL to 288 +/- 19 mL (p < 0.001) after the intratracheal introduction of 50 mL of saline solution; therefore, 43 of the 50 mL (84%) were detected (range, 37-48 mL). In edematous lung, the EVLW increased from 491 +/- 106 mL to 530 +/- 108 mL after the introduction of 50 mL of saline solution; therefore, 39 of the 50 mL (77%) were detected (range, 15-67 mL).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Bronchoalveolar Lavage', 'Disease Models, Animal', 'Early Diagnosis', 'Extravascular Lung Water', 'Isotonic Solutions', 'Pulmonary Edema', 'Reproducibility of Results', 'Sodium Chloride', 'Swine', 'Thermodilution']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,374,627 | Is elevated plasma phospholipid transfer protein activity a determinant of carotid intima-media thickness in type 2 diabetes mellitus? | {
"contexts": [
"The plasma activity of phospholipid transfer protein (PLTP), which has putative pro- and anti-atherogenic roles in lipoprotein metabolism, is increased in type 2 diabetes mellitus. We analysed the relationship between carotid artery intima-media thickness (IMT), an established marker of atherosclerosis, and PLTP activity in diabetic patients and control subjects.",
"The IMT (mean of three segments in both carotid arteries by ultrasonography), clinical variables, plasma PLTP activity (phospholipid vesicle-HDL system), lipoproteins, C-reactive protein and insulin were measured in 87 non-smoking men and women, who had type 2 diabetes mellitus, no cardiovascular disease, and were not on insulin or lipid-lowering medication, and in 83 age-matched control subjects.",
"In diabetic patients, carotid IMT (p=0.02), pulse pressure (p=0.003), plasma PLTP activity (p<0.001), triglycerides (p=0.01), C-reactive protein (p<0.01) and insulin (p<0.001) were higher, whereas HDL cholesterol was lower (p<0.001) than in control subjects. Multiple stepwise linear regression analysis demonstrated that in type 2 diabetic patients IMT was independently associated with age (p<0.001), sex (p=0.001), pulse pressure (p=0.003), plasma PLTP activity (p=0.03) and HDL cholesterol (p=0.03), but not with very low density lipoprotein+LDL cholesterol, triglycerides, C-reactive protein and insulin (all p>0.20). The relationship between plasma PLTP activity and IMT was not significant in control subjects."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Atherosclerosis",
"Biomarkers",
"C-Reactive Protein",
"Carotid Arteries",
"Case-Control Studies",
"Cholesterol, HDL",
"Diabetes Mellitus, Type 2",
"Diabetic Angiopathies",
"Female",
"Humans",
"Insulin",
"Lipoproteins",
"Male",
"Middle Aged",
"Phospholipid Transfer Proteins",
"Regression Analysis",
"Risk Factors",
"Tunica Intima",
"Tunica Media",
"Ultrasonography"
]
} | Plasma PLTP activity is a positive determinant of IMT in type 2 diabetes mellitus, suggesting that high PLTP activity is involved in accelerated atherosclerosis in this disease. | yes | [
{
"from": "human",
"value": "Question: Is elevated plasma phospholipid transfer protein activity a determinant of carotid intima-media thickness in type 2 diabetes mellitus?\nContext: {'contexts': ['The plasma activity of phospholipid transfer protein (PLTP), which has putative pro- and anti-atherogenic roles in lipoprotein metabolism, is increased in type 2 diabetes mellitus. We analysed the relationship between carotid artery intima-media thickness (IMT), an established marker of atherosclerosis, and PLTP activity in diabetic patients and control subjects.', 'The IMT (mean of three segments in both carotid arteries by ultrasonography), clinical variables, plasma PLTP activity (phospholipid vesicle-HDL system), lipoproteins, C-reactive protein and insulin were measured in 87 non-smoking men and women, who had type 2 diabetes mellitus, no cardiovascular disease, and were not on insulin or lipid-lowering medication, and in 83 age-matched control subjects.', 'In diabetic patients, carotid IMT (p=0.02), pulse pressure (p=0.003), plasma PLTP activity (p<0.001), triglycerides (p=0.01), C-reactive protein (p<0.01) and insulin (p<0.001) were higher, whereas HDL cholesterol was lower (p<0.001) than in control subjects. Multiple stepwise linear regression analysis demonstrated that in type 2 diabetic patients IMT was independently associated with age (p<0.001), sex (p=0.001), pulse pressure (p=0.003), plasma PLTP activity (p=0.03) and HDL cholesterol (p=0.03), but not with very low density lipoprotein+LDL cholesterol, triglycerides, C-reactive protein and insulin (all p>0.20). The relationship between plasma PLTP activity and IMT was not significant in control subjects.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Atherosclerosis', 'Biomarkers', 'C-Reactive Protein', 'Carotid Arteries', 'Case-Control Studies', 'Cholesterol, HDL', 'Diabetes Mellitus, Type 2', 'Diabetic Angiopathies', 'Female', 'Humans', 'Insulin', 'Lipoproteins', 'Male', 'Middle Aged', 'Phospholipid Transfer Proteins', 'Regression Analysis', 'Risk Factors', 'Tunica Intima', 'Tunica Media', 'Ultrasonography']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,385,920 | Is infection with Chlamydia pneumoniae but not Helicobacter pylori related to elevated apolipoprotein B levels? | {
"contexts": [
"Results of many studies show that apolipoprotein B (apo B) is a better marker of risk of vascular disease than other lipid markers including LDL and HDL-cholesterol and triglycerides. We investigated the association between two infectious agents: C. pneumoniae and H. pylori, known to have an atherogenic effect, and apo B, to evaluate the effects of chronic infections on apo B levels.",
"The study group consisted of 257 patients in whom diagnostic coronary angiography was performed. C. pneumoniae IgG and IgM and H. pylori IgG and IgA antibodies were measured by enzyme-linked immunosorbent assay and apo B levels were measured by the nephelometry method. Established risk factors of atherosclerosis were recorded. Of 257 patients recruited, 104 had normal vessels, 88 had 3 or more vessels obstructed and 65 had ectatic vessels without atherosclerosis. Mean apo B concentration was significantly higher in C. pneumoniae IgG and IgM positive healthy subjects compared with C. pneumoniae negatives (0.954 vs. 0.722 and 0.973 vs. 0.851, p < 0.001 and p = 0.007, respectively). Apo B levels were significantly higher in severe atherosclerotic patients (0.985 +/- 0.234 g/l) compared with control subjects (0.892 +/- 0.244 g/l) (p = 0.008), but the difference was not significant in ectatic subjects (0.946 +/- 0.272 g/l) when compared with controls (p = 0.18). Apo B levels were higher but not statistically significant in H. pylori antibody positive cases when compared with negatives."
],
"labels": [
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Age Distribution",
"Antibodies, Bacterial",
"Apolipoproteins B",
"Biomarkers",
"Case-Control Studies",
"Chlamydophila Infections",
"Chlamydophila pneumoniae",
"Coronary Angiography",
"Coronary Artery Disease",
"Enzyme-Linked Immunosorbent Assay",
"Female",
"Helicobacter Infections",
"Helicobacter pylori",
"Humans",
"Immunoglobulin A",
"Immunoglobulin M",
"Incidence",
"Linear Models",
"Logistic Models",
"Male",
"Multivariate Analysis",
"Probability",
"Reference Values",
"Risk Assessment",
"Severity of Illness Index",
"Sex Distribution",
"Survival Rate",
"Turkey"
]
} | Apo B levels increased with C. pneumoniae infection. This finding supports the hypothesis that lipid profiles change to atherogenic lipid profile in chronic infections. | yes | [
{
"from": "human",
"value": "Question: Is infection with Chlamydia pneumoniae but not Helicobacter pylori related to elevated apolipoprotein B levels?\nContext: {'contexts': ['Results of many studies show that apolipoprotein B (apo B) is a better marker of risk of vascular disease than other lipid markers including LDL and HDL-cholesterol and triglycerides. We investigated the association between two infectious agents: C. pneumoniae and H. pylori, known to have an atherogenic effect, and apo B, to evaluate the effects of chronic infections on apo B levels.', 'The study group consisted of 257 patients in whom diagnostic coronary angiography was performed. C. pneumoniae IgG and IgM and H. pylori IgG and IgA antibodies were measured by enzyme-linked immunosorbent assay and apo B levels were measured by the nephelometry method. Established risk factors of atherosclerosis were recorded. Of 257 patients recruited, 104 had normal vessels, 88 had 3 or more vessels obstructed and 65 had ectatic vessels without atherosclerosis. Mean apo B concentration was significantly higher in C. pneumoniae IgG and IgM positive healthy subjects compared with C. pneumoniae negatives (0.954 vs. 0.722 and 0.973 vs. 0.851, p < 0.001 and p = 0.007, respectively). Apo B levels were significantly higher in severe atherosclerotic patients (0.985 +/- 0.234 g/l) compared with control subjects (0.892 +/- 0.244 g/l) (p = 0.008), but the difference was not significant in ectatic subjects (0.946 +/- 0.272 g/l) when compared with controls (p = 0.18). Apo B levels were higher but not statistically significant in H. pylori antibody positive cases when compared with negatives.'], 'labels': ['OBJECTIVE', 'RESULTS'], 'meshes': ['Age Distribution', 'Antibodies, Bacterial', 'Apolipoproteins B', 'Biomarkers', 'Case-Control Studies', 'Chlamydophila Infections', 'Chlamydophila pneumoniae', 'Coronary Angiography', 'Coronary Artery Disease', 'Enzyme-Linked Immunosorbent Assay', 'Female', 'Helicobacter Infections', 'Helicobacter pylori', 'Humans', 'Immunoglobulin A', 'Immunoglobulin M', 'Incidence', 'Linear Models', 'Logistic Models', 'Male', 'Multivariate Analysis', 'Probability', 'Reference Values', 'Risk Assessment', 'Severity of Illness Index', 'Sex Distribution', 'Survival Rate', 'Turkey']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,380,156 | Does the PTEN tumor suppressor inhibit telomerase activity in endometrial cancer cells by decreasing hTERT mRNA levels? | {
"contexts": [
"Loss of PTEN expression is one of the most prevalent and earliest molecular abnormalities associated with endometrial carcinogenesis. Given that PTEN is often absent and telomerase is overexpressed by endometrial cancers, we hypothesize that PTEN signaling is important in telomerase regulation.",
"PTEN expression was reconstituted in the PTEN-null Ishikawa endometrial cancer cells by adenovirus-mediated gene transduction. Cell proliferation was evaluated 12-96 h after infection. Western blot analysis was performed to assess PTEN status and phosphorylated Akt expression. Telomerase activity was determined by the telomeric repeat amplification protocol (TRAP) assay. hTERT mRNA levels were assessed by real-time RT-PCR. Ishikawa cells were also treated with LY294002, a PI3-kinase inhibitor.",
"Infection of Ishikawa cells by replication-defective recombinant adenovirus expressing wild-type PTEN, but not control adenovirus or adenovirus expressing lipid phosphatase defective PTEN GE mutant, inhibited constitutive Akt activation and suppressed proliferation of Ishikawa cells. Infection by wild-type PTEN adenovirus, but not control adenovirus, inhibited telomerase activity 24 h after infection. This inhibition of telomerase activity was parallel to decreased hTERT mRNA levels. LY294002 treatment resulted in dose-dependent inhibition of Akt activation and cellular proliferation. LY294002 suppressed telomerase activity and decreased hTERT transcript levels in a dose-dependent manner."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adenoviridae",
"Cell Growth Processes",
"Chromones",
"DNA-Binding Proteins",
"Endometrial Neoplasms",
"Enzyme Inhibitors",
"Female",
"Humans",
"Morpholines",
"Oncogene Protein v-akt",
"PTEN Phosphohydrolase",
"Phosphorylation",
"RNA, Messenger",
"Signal Transduction",
"Telomerase",
"Transduction, Genetic"
]
} | Our data suggest that PTEN may regulate telomerase activity by a novel mechanism in which inhibition of Akt activation by PTEN leads to decreased hTERT mRNA levels. Thus, loss of PTEN may allow endometrial cells to continue to express high levels of telomerase activity, facilitating the neoplastic transformation of the endometrium. | yes | [
{
"from": "human",
"value": "Question: Does the PTEN tumor suppressor inhibit telomerase activity in endometrial cancer cells by decreasing hTERT mRNA levels?\nContext: {'contexts': ['Loss of PTEN expression is one of the most prevalent and earliest molecular abnormalities associated with endometrial carcinogenesis. Given that PTEN is often absent and telomerase is overexpressed by endometrial cancers, we hypothesize that PTEN signaling is important in telomerase regulation.', 'PTEN expression was reconstituted in the PTEN-null Ishikawa endometrial cancer cells by adenovirus-mediated gene transduction. Cell proliferation was evaluated 12-96 h after infection. Western blot analysis was performed to assess PTEN status and phosphorylated Akt expression. Telomerase activity was determined by the telomeric repeat amplification protocol (TRAP) assay. hTERT mRNA levels were assessed by real-time RT-PCR. Ishikawa cells were also treated with LY294002, a PI3-kinase inhibitor.', 'Infection of Ishikawa cells by replication-defective recombinant adenovirus expressing wild-type PTEN, but not control adenovirus or adenovirus expressing lipid phosphatase defective PTEN GE mutant, inhibited constitutive Akt activation and suppressed proliferation of Ishikawa cells. Infection by wild-type PTEN adenovirus, but not control adenovirus, inhibited telomerase activity 24 h after infection. This inhibition of telomerase activity was parallel to decreased hTERT mRNA levels. LY294002 treatment resulted in dose-dependent inhibition of Akt activation and cellular proliferation. LY294002 suppressed telomerase activity and decreased hTERT transcript levels in a dose-dependent manner.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adenoviridae', 'Cell Growth Processes', 'Chromones', 'DNA-Binding Proteins', 'Endometrial Neoplasms', 'Enzyme Inhibitors', 'Female', 'Humans', 'Morpholines', 'Oncogene Protein v-akt', 'PTEN Phosphohydrolase', 'Phosphorylation', 'RNA, Messenger', 'Signal Transduction', 'Telomerase', 'Transduction, Genetic']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,388,848 | Does effect of curing regime on the cytotoxicity of resin-modified glass-ionomer lining cement applied to an odontoblast-cell line? | {
"contexts": [
"The aim of this in vitro study was to evaluate the cytotoxicity of resin-modified glass-ionomer lining cements submitted to different curing regimes and applied to an immortalized odontoblast-cell line (MDPC-23).",
"Forty round-shaped specimens of each experimental material (Fuji Lining LC and Vitrebond) were prepared. They were light-cured for the manufacturers' recommended time (MRT = 30 s), under-cured (0.5 MRT = 15 s), over-cured (1.5 MRT = 45 s) or allowed to dark cure (0 MRT). Sterilized filter papers soaked with either 5 microL of PBS or HEMA were used as negative and positive control, respectively. After placing the specimens individually in wells of 24-well dishes, odontoblast-like cells MDPC-23 (30,000 cells/cm2) were plated in each well and incubated for 72 h in a humidified incubator at 37 degrees C with 5% CO2 and 95% air. The cytotoxicity was evaluated by the cell metabolism (MTT assay) and cell morphology (SEM).",
"Fuji Lining LC was less cytotoxic than Vitrebond (p < 0.05) in all the experimental conditions. However, the cytotoxicity of Fuji Lining LC was noticeably increased in the absence of light-curing while the same was not observed for Vitrebond. The length of light-curing (15, 30 or 45 s) did not influence the toxicity of both lining materials when they were applied on the odontoblast-cell line MDPC-23."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Cell Line, Transformed",
"Cell Shape",
"Coloring Agents",
"Dental Cavity Lining",
"Dentin-Bonding Agents",
"Glass Ionomer Cements",
"Light",
"Methacrylates",
"Mice",
"Microscopy, Electron, Scanning",
"Odontoblasts",
"Phase Transition",
"Resins, Synthetic",
"Tetrazolium Salts"
]
} | The light-activation plays an important role in reducing the cytotoxicity of Fuji Lining LC. Following the manufacturer' recommendation regarding the light-curing regime may prevent toxic effect to the pulp cells. | yes | [
{
"from": "human",
"value": "Question: Does effect of curing regime on the cytotoxicity of resin-modified glass-ionomer lining cement applied to an odontoblast-cell line?\nContext: {'contexts': ['The aim of this in vitro study was to evaluate the cytotoxicity of resin-modified glass-ionomer lining cements submitted to different curing regimes and applied to an immortalized odontoblast-cell line (MDPC-23).', \"Forty round-shaped specimens of each experimental material (Fuji Lining LC and Vitrebond) were prepared. They were light-cured for the manufacturers' recommended time (MRT = 30 s), under-cured (0.5 MRT = 15 s), over-cured (1.5 MRT = 45 s) or allowed to dark cure (0 MRT). Sterilized filter papers soaked with either 5 microL of PBS or HEMA were used as negative and positive control, respectively. After placing the specimens individually in wells of 24-well dishes, odontoblast-like cells MDPC-23 (30,000 cells/cm2) were plated in each well and incubated for 72 h in a humidified incubator at 37 degrees C with 5% CO2 and 95% air. The cytotoxicity was evaluated by the cell metabolism (MTT assay) and cell morphology (SEM).\", 'Fuji Lining LC was less cytotoxic than Vitrebond (p < 0.05) in all the experimental conditions. However, the cytotoxicity of Fuji Lining LC was noticeably increased in the absence of light-curing while the same was not observed for Vitrebond. The length of light-curing (15, 30 or 45 s) did not influence the toxicity of both lining materials when they were applied on the odontoblast-cell line MDPC-23.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Cell Line, Transformed', 'Cell Shape', 'Coloring Agents', 'Dental Cavity Lining', 'Dentin-Bonding Agents', 'Glass Ionomer Cements', 'Light', 'Methacrylates', 'Mice', 'Microscopy, Electron, Scanning', 'Odontoblasts', 'Phase Transition', 'Resins, Synthetic', 'Tetrazolium Salts']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,393,772 | Do aurothiomalate and hydroxychloroquine inhibit nitric oxide production in chondrocytes and in human osteoarthritic cartilage? | {
"contexts": [
"Nitric oxide (NO) is a destructive mediator produced by activated chondrocytes. The aim of the present study was to investigate the effect of disease-modifying anti-rheumatic drugs (DMARDs) on interleukin-1beta (IL-1beta)-induced NO production in chondrocyte cultures, and in human osteoarthritic cartilage.",
"Aurothiomalate, hydroxychloroquine, methotrexate and leflunomide inhibited IL-1beta-induced inducible NO synthase (iNOS) expression and NO production in immortalized H4 chondrocytes, while penicillamine and sulfasalazine had no effect. This can be explained by the fact that the four effective DMARDs also suppressed IL-1beta-induced activation of nuclear factor kappa B (NF-kappaB), which is a crucial transcription factor for iNOS. Aurothiomalate and hydroxychloroquine also inhibited IL-1beta-induced NO production in OA cartilage whereas methotrexate and leflunomide had no effect."
],
"labels": [
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Analysis of Variance",
"Animals",
"Antirheumatic Agents",
"Blotting, Western",
"Cartilage, Articular",
"Cells, Cultured",
"Chondrocytes",
"Gold Sodium Thiomalate",
"Humans",
"Hydroxychloroquine",
"Mice",
"Nitric Oxide",
"Nitric Oxide Synthase Type II",
"Osteoarthritis, Knee",
"RNA, Messenger"
]
} | Aurothiomalate and hydroxychloroquine suppressed IL-1beta-induced NO production in chondrocyte cultures and in OA cartilage. The results suggest an additional anti-inflammatory mechanism for aurothiomalate and hydroxychloroquine and indicates their possible therapeutic value in the treatment of osteoarthritis (OA). | yes | [
{
"from": "human",
"value": "Question: Do aurothiomalate and hydroxychloroquine inhibit nitric oxide production in chondrocytes and in human osteoarthritic cartilage?\nContext: {'contexts': ['Nitric oxide (NO) is a destructive mediator produced by activated chondrocytes. The aim of the present study was to investigate the effect of disease-modifying anti-rheumatic drugs (DMARDs) on interleukin-1beta (IL-1beta)-induced NO production in chondrocyte cultures, and in human osteoarthritic cartilage.', 'Aurothiomalate, hydroxychloroquine, methotrexate and leflunomide inhibited IL-1beta-induced inducible NO synthase (iNOS) expression and NO production in immortalized H4 chondrocytes, while penicillamine and sulfasalazine had no effect. This can be explained by the fact that the four effective DMARDs also suppressed IL-1beta-induced activation of nuclear factor kappa B (NF-kappaB), which is a crucial transcription factor for iNOS. Aurothiomalate and hydroxychloroquine also inhibited IL-1beta-induced NO production in OA cartilage whereas methotrexate and leflunomide had no effect.'], 'labels': ['OBJECTIVE', 'RESULTS'], 'meshes': ['Analysis of Variance', 'Animals', 'Antirheumatic Agents', 'Blotting, Western', 'Cartilage, Articular', 'Cells, Cultured', 'Chondrocytes', 'Gold Sodium Thiomalate', 'Humans', 'Hydroxychloroquine', 'Mice', 'Nitric Oxide', 'Nitric Oxide Synthase Type II', 'Osteoarthritis, Knee', 'RNA, Messenger']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,393,771 | Is syndecan-1 expression upregulated in degenerating articular cartilage in a transgenic mouse model for osteoarthritis? | {
"contexts": [
"Mice heterozygous for the Del1 transgene locus with a short deletion mutation in the type II collagen gene develop early-onset degenerative changes in the knee joints that progress to end-stage osteoarthritis by the age of 12-15 months. This study focuses on the expression and distribution of syndecan-1, a cell-surface heparan sulfate proteoglycan, during the development of osteoarthritic cartilage degeneration, to better understand its role in this disease.",
"Northern analyses of total RNA extracted from knee joints of transgenic Del1 mice and their nontransgenic controls were used to monitor changes in syndecan-1 mRNA levels during development, growth, ageing, and cartilage degeneration. Immunohistochemistry was used to study the distribution of syndecan-1 in the knee joints at different stages of cartilage degeneration.",
"Syndecan-1 mRNA was present in knee joints throughout life, with the highest mRNA levels in ageing knee joints. In Del1 mice, a transient upregulation of syndecan-1 mRNA synthesis was observed at the age of 6 months coinciding with early stages of cartilage degeneration and a period of attempted repair. Immunostaining for syndecan-1 was most intense in chondrocytes of superficial and intermediate zones of articular cartilage adjacent to defect areas. Chondrocyte clusters also stained strongly for syndecan-1."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Blotting, Northern",
"Cartilage, Articular",
"Immunohistochemistry",
"Knee Joint",
"Membrane Glycoproteins",
"Mice",
"Mice, Transgenic",
"Osteoarthritis, Knee",
"Proteoglycans",
"RNA, Messenger",
"Syndecan-1",
"Syndecans",
"Up-Regulation"
]
} | The present temporospatial expression data on upregulation of syndecan-1 in articular cartilage during early stages of cartilage degeneration suggest that this molecule is involved in the attempted repair of cartilage fibrillations. Combined with the known role of syndecan-1 during skeletal development and wound healing, this interesting finding warrants further validation. | yes | [
{
"from": "human",
"value": "Question: Is syndecan-1 expression upregulated in degenerating articular cartilage in a transgenic mouse model for osteoarthritis?\nContext: {'contexts': ['Mice heterozygous for the Del1 transgene locus with a short deletion mutation in the type II collagen gene develop early-onset degenerative changes in the knee joints that progress to end-stage osteoarthritis by the age of 12-15 months. This study focuses on the expression and distribution of syndecan-1, a cell-surface heparan sulfate proteoglycan, during the development of osteoarthritic cartilage degeneration, to better understand its role in this disease.', 'Northern analyses of total RNA extracted from knee joints of transgenic Del1 mice and their nontransgenic controls were used to monitor changes in syndecan-1 mRNA levels during development, growth, ageing, and cartilage degeneration. Immunohistochemistry was used to study the distribution of syndecan-1 in the knee joints at different stages of cartilage degeneration.', 'Syndecan-1 mRNA was present in knee joints throughout life, with the highest mRNA levels in ageing knee joints. In Del1 mice, a transient upregulation of syndecan-1 mRNA synthesis was observed at the age of 6 months coinciding with early stages of cartilage degeneration and a period of attempted repair. Immunostaining for syndecan-1 was most intense in chondrocytes of superficial and intermediate zones of articular cartilage adjacent to defect areas. Chondrocyte clusters also stained strongly for syndecan-1.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Blotting, Northern', 'Cartilage, Articular', 'Immunohistochemistry', 'Knee Joint', 'Membrane Glycoproteins', 'Mice', 'Mice, Transgenic', 'Osteoarthritis, Knee', 'Proteoglycans', 'RNA, Messenger', 'Syndecan-1', 'Syndecans', 'Up-Regulation']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,384,826 | Do urinary excretions of lipocalin-type prostaglandin D2 synthase predict the development of proteinuria and renal injury in OLETF rats? | {
"contexts": [
"Otsuka Long-Evans Tokushima Fatty (OLETF) rats genetically develop diabetes which is associated with hypertension. In preliminary studies, urinary excretions of L-PGDS (lipocaline-type prostaglandin D synthase) increase before diabetic nephropathy obviously develops, and this may predict progression of renal injury following diabetes. In the present study, we attempted to define whether urinary excretions of L-PGDS behave as the predictor of development of diabetic nephropathy in OLETF rats.",
"We investigated alterations of urinary L-PGDS excretions during the establishment of diabetes and assessed the relationship between the L-PGDS excretions and renal function in OLETF rats. Furthermore, we treated OLETF rats with troglitazone and analysed the effects on L-PGDS metabolisms. Urinary L-PGDS was measured by immunoenzyme assay and the occurrence of L-PGDS and its mRNA in the kidney was assessed by immunohistochemistry and a PCR method.",
"Urinary excretions of L-PGDS were significantly higher in OLETF rats than non-diabetic Long-Evans Tokushima Otsuka (LETO) rats. The excretions age-dependently increased in OLETF and this increase appeared to be due to increased glomerular permeability to L-PGDS. Messenger RNA and antigenicity of L-PGDS were demonstrated in renal tissue; however, the de novo synthesis of L-PGDS mRNA seemingly contributed to urinary L-PGDS excretions much less than glomerular filtration. Multiple regression analysis revealed that urinary L-PGDS was determined by urinary protein excretions, and not by high blood pressure per se. Conversely, urinary proteinuria in the established diabetic nephropathy was predicted by urinary L-PGDS excretions in the early stage of diabetes."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Chromans",
"Diabetes Mellitus, Type 2",
"Diabetic Nephropathies",
"Hypoglycemic Agents",
"Immunoenzyme Techniques",
"Intramolecular Oxidoreductases",
"Lipocalins",
"Proteinuria",
"RNA, Messenger",
"Rats",
"Rats, Inbred OLETF",
"Renal Insufficiency",
"Thiazolidinediones",
"Troglitazone"
]
} | Urinary excretions of L-PGDS are likely to reflect the underlying increase in glomerular permeability. This property may be useful to predict forthcoming glomerular damage following diabetes in OLETF rats. | yes | [
{
"from": "human",
"value": "Question: Do urinary excretions of lipocalin-type prostaglandin D2 synthase predict the development of proteinuria and renal injury in OLETF rats?\nContext: {'contexts': ['Otsuka Long-Evans Tokushima Fatty (OLETF) rats genetically develop diabetes which is associated with hypertension. In preliminary studies, urinary excretions of L-PGDS (lipocaline-type prostaglandin D synthase) increase before diabetic nephropathy obviously develops, and this may predict progression of renal injury following diabetes. In the present study, we attempted to define whether urinary excretions of L-PGDS behave as the predictor of development of diabetic nephropathy in OLETF rats.', 'We investigated alterations of urinary L-PGDS excretions during the establishment of diabetes and assessed the relationship between the L-PGDS excretions and renal function in OLETF rats. Furthermore, we treated OLETF rats with troglitazone and analysed the effects on L-PGDS metabolisms. Urinary L-PGDS was measured by immunoenzyme assay and the occurrence of L-PGDS and its mRNA in the kidney was assessed by immunohistochemistry and a PCR method.', 'Urinary excretions of L-PGDS were significantly higher in OLETF rats than non-diabetic Long-Evans Tokushima Otsuka (LETO) rats. The excretions age-dependently increased in OLETF and this increase appeared to be due to increased glomerular permeability to L-PGDS. Messenger RNA and antigenicity of L-PGDS were demonstrated in renal tissue; however, the de novo synthesis of L-PGDS mRNA seemingly contributed to urinary L-PGDS excretions much less than glomerular filtration. Multiple regression analysis revealed that urinary L-PGDS was determined by urinary protein excretions, and not by high blood pressure per se. Conversely, urinary proteinuria in the established diabetic nephropathy was predicted by urinary L-PGDS excretions in the early stage of diabetes.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Chromans', 'Diabetes Mellitus, Type 2', 'Diabetic Nephropathies', 'Hypoglycemic Agents', 'Immunoenzyme Techniques', 'Intramolecular Oxidoreductases', 'Lipocalins', 'Proteinuria', 'RNA, Messenger', 'Rats', 'Rats, Inbred OLETF', 'Renal Insufficiency', 'Thiazolidinediones', 'Troglitazone']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,384,989 | Does absence of chx10 cause neural progenitors to persist in the adult retina? | {
"contexts": [
"Mutation of the Chx10 homeobox gene in mice and humans causes congenital blindness and microphthalmia (small eyes). This study used Chx10-/- (ocular retardation) mice to investigate how lack of Chx10 affects progenitor/stem cell behavior in the retina and ciliary epithelium (CE).",
"The distribution of mitotic retinal progenitor cells (RPCs) during embryonic development was analyzed using phosphohistone 3 (H3)-labeling. DNA flow cytometry was used to measure DNA content. The distribution and phenotype of dividing cells in the postnatal retina and CE was analyzed by incorporation of the thymidine analogue BrdU and immunohistochemistry.",
"The Chx10-/- embryonic retina maintained a constantly sized population of mitotic RPCs during development, causing the mitotic index to increase markedly over time compared with the wild type. Also, the proportion of cells in the G1 phase of the cell cycle was increased compared with the wild type. Of interest, division of RPC-like cells with neurogenic properties persisted in the adult Chx10-/- retina. Colabeling for BrdU and the neural progenitor marker nestin or the neuronal markers beta3-tubulin, syntaxin, and VC1.1 showed that new amacrine-like neurons developed in the adult central retina. By contrast, cells with these characteristics were not observed in the mature wild-type retina. In the mature CE, BrdU-positive cells were observed in both wild-type and Chx10-/- mice. However, neurogenesis from this cell population was not evident."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Apoptosis",
"Biomarkers",
"Cell Cycle",
"Cell Proliferation",
"Ciliary Body",
"DNA Replication",
"Embryonic Development",
"Flow Cytometry",
"Fluorescent Antibody Technique, Indirect",
"Homeodomain Proteins",
"In Situ Nick-End Labeling",
"Mice",
"Mice, Mutant Strains",
"Nerve Tissue Proteins",
"Neurons",
"Pigment Epithelium of Eye",
"Retina",
"Stem Cells",
"Transcription Factors"
]
} | Without Chx10, proliferative expansion of the embryonic RPC pool is markedly reduced. In the adult retina, lack of Chx10 results in a population of dividing neural progenitor cells that persist and produce new neurons in the central retina. | yes | [
{
"from": "human",
"value": "Question: Does absence of chx10 cause neural progenitors to persist in the adult retina?\nContext: {'contexts': ['Mutation of the Chx10 homeobox gene in mice and humans causes congenital blindness and microphthalmia (small eyes). This study used Chx10-/- (ocular retardation) mice to investigate how lack of Chx10 affects progenitor/stem cell behavior in the retina and ciliary epithelium (CE).', 'The distribution of mitotic retinal progenitor cells (RPCs) during embryonic development was analyzed using phosphohistone 3 (H3)-labeling. DNA flow cytometry was used to measure DNA content. The distribution and phenotype of dividing cells in the postnatal retina and CE was analyzed by incorporation of the thymidine analogue BrdU and immunohistochemistry.', 'The Chx10-/- embryonic retina maintained a constantly sized population of mitotic RPCs during development, causing the mitotic index to increase markedly over time compared with the wild type. Also, the proportion of cells in the G1 phase of the cell cycle was increased compared with the wild type. Of interest, division of RPC-like cells with neurogenic properties persisted in the adult Chx10-/- retina. Colabeling for BrdU and the neural progenitor marker nestin or the neuronal markers beta3-tubulin, syntaxin, and VC1.1 showed that new amacrine-like neurons developed in the adult central retina. By contrast, cells with these characteristics were not observed in the mature wild-type retina. In the mature CE, BrdU-positive cells were observed in both wild-type and Chx10-/- mice. However, neurogenesis from this cell population was not evident.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Apoptosis', 'Biomarkers', 'Cell Cycle', 'Cell Proliferation', 'Ciliary Body', 'DNA Replication', 'Embryonic Development', 'Flow Cytometry', 'Fluorescent Antibody Technique, Indirect', 'Homeodomain Proteins', 'In Situ Nick-End Labeling', 'Mice', 'Mice, Mutant Strains', 'Nerve Tissue Proteins', 'Neurons', 'Pigment Epithelium of Eye', 'Retina', 'Stem Cells', 'Transcription Factors']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,387,212 | Does prevalence of negative chest radiography result in the emergency department patient with decompensated heart failure? | {
"contexts": [
"Although chest radiography is quick and inexpensive, previous research suggests that it is often misleading in emergency department (ED) patients with decompensated heart failure, resulting in misdiagnosis and inappropriate treatment. This study determines the rate of negative chest radiography results in patients found to have disease and the potential contribution of negative findings to a diagnosis discordant with heart failure by an emergency physician.",
"We used data from the Acute Decompensated Heart Failure National Registry (ADHERE), a registry of patients with a primary hospital discharge diagnosis of heart failure. We compared initial ED admitting diagnosis to the criterion standard of a hospital discharge diagnosis of heart failure and related these to radiographic findings of heart failure (interstitial edema, pulmonary edema, or vascular congestion, as determined by a staff radiologist) for patients first treated in the ED. The proportion of patients with a non-heart failure ED diagnosis and the diagnostic sensitivity of radiographic findings of heart failure are calculated.",
"There were 85,376 patients with chest radiograph results and an ED admitting diagnosis. Overall, there were 15,937 patients with no signs of congestion on ED chest radiography, giving a negative rate of 18.7% (95% confidence interval [CI] 18.4% to 18.9%). The proportion of patients with an ED non-heart failure admitting diagnosis was higher in patients with a negative chest radiograph result (23.3%; 95% CI 22.6% to 23.9%) than in patients with a positive chest radiograph result (13.0%; 95% CI 12.7% to 13.2%)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Cohort Studies",
"Emergency Medicine",
"Emergency Service, Hospital",
"False Negative Reactions",
"Female",
"Heart Failure",
"Humans",
"Male",
"Outcome and Process Assessment (Health Care)",
"Prevalence",
"Radiography",
"Registries",
"Retrospective Studies",
"Sensitivity and Specificity",
"United States"
]
} | Approximately 1 of every 5 patients admitted from the ED with acute decompensated heart failure had no signs of congestion on chest radiography. Patients lacking signs of congestion on ED chest radiography were more likely to have an ED non-heart failure diagnosis than patients with signs of congestion. Clinicians should not rule out heart failure in patients with no radiographic signs of congestion. | yes | [
{
"from": "human",
"value": "Question: Does prevalence of negative chest radiography result in the emergency department patient with decompensated heart failure?\nContext: {'contexts': ['Although chest radiography is quick and inexpensive, previous research suggests that it is often misleading in emergency department (ED) patients with decompensated heart failure, resulting in misdiagnosis and inappropriate treatment. This study determines the rate of negative chest radiography results in patients found to have disease and the potential contribution of negative findings to a diagnosis discordant with heart failure by an emergency physician.', 'We used data from the Acute Decompensated Heart Failure National Registry (ADHERE), a registry of patients with a primary hospital discharge diagnosis of heart failure. We compared initial ED admitting diagnosis to the criterion standard of a hospital discharge diagnosis of heart failure and related these to radiographic findings of heart failure (interstitial edema, pulmonary edema, or vascular congestion, as determined by a staff radiologist) for patients first treated in the ED. The proportion of patients with a non-heart failure ED diagnosis and the diagnostic sensitivity of radiographic findings of heart failure are calculated.', 'There were 85,376 patients with chest radiograph results and an ED admitting diagnosis. Overall, there were 15,937 patients with no signs of congestion on ED chest radiography, giving a negative rate of 18.7% (95% confidence interval [CI] 18.4% to 18.9%). The proportion of patients with an ED non-heart failure admitting diagnosis was higher in patients with a negative chest radiograph result (23.3%; 95% CI 22.6% to 23.9%) than in patients with a positive chest radiograph result (13.0%; 95% CI 12.7% to 13.2%).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Cohort Studies', 'Emergency Medicine', 'Emergency Service, Hospital', 'False Negative Reactions', 'Female', 'Heart Failure', 'Humans', 'Male', 'Outcome and Process Assessment (Health Care)', 'Prevalence', 'Radiography', 'Registries', 'Retrospective Studies', 'Sensitivity and Specificity', 'United States']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,399,290 | Does aprotinin inhibit proinflammatory activation of endothelial cells by thrombin through the protease-activated receptor 1? | {
"contexts": [
"Thrombin is generated in significant quantities during cardiopulmonary bypass and mediates adverse events, such as platelet aggregation and proinflammatory responses, through activation of the high-affinity thrombin receptor protease-activated receptor 1, which is expressed on platelets and endothelium. Thus antagonism of protease-activated receptor 1 might have broad therapeutic significance. Aprotinin, used clinically to reduce transfusion requirements and the inflammatory response to bypass, has been shown to inhibit protease-activated receptor 1 on platelets in vitro and in vivo. Here we have examined whether aprotinin inhibits endothelial protease-activated receptor 1 activation and resulting proinflammatory responses induced by thrombin.",
"Protease-activated receptor 1 expression and function were examined in cultured human umbilical vein endothelial cells after treatment with alpha-thrombin at 0.02 to 0.15 U/mL in the presence or absence of aprotinin (200-1600 kallikrein inhibitory units/mL). Protease-activated receptor 1 activation was assessed by using an antibody, SPAN-12, which detects only the unactivated receptor, and thrombin-mediated calcium fluxes. Other thrombin-dependent inflammatory pathways investigated were phosphorylation of the p42/44 mitogen-activated protein kinase, upregulation of the early growth response 1 transcription factor, and production of the proinflammatory cytokine interleukin 6.",
"Pretreatment of cultured endothelial cells with aprotinin significantly spared protease-activated receptor 1 receptor cleavage (P < .0001) and abrogated calcium fluxes caused by thrombin. Aprotinin inhibited intracellular signaling through p42/44 mitogen-activated protein kinase (P < .05) and early growth response 1 transcription factor (P < .05), as well as interleukin 6 secretion caused by thrombin (P < .005)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aprotinin",
"Cells, Cultured",
"Endothelial Cells",
"Humans",
"Inflammation",
"Receptor, PAR-1",
"Thrombin"
]
} | This study demonstrates that endothelial cell activation by thrombin and downstream inflammatory responses can be inhibited by aprotinin in vitro through blockade of protease-activated receptor 1. Our results provide a new molecular basis to help explain the anti-inflammatory properties of aprotinin reported clinically. | yes | [
{
"from": "human",
"value": "Question: Does aprotinin inhibit proinflammatory activation of endothelial cells by thrombin through the protease-activated receptor 1?\nContext: {'contexts': ['Thrombin is generated in significant quantities during cardiopulmonary bypass and mediates adverse events, such as platelet aggregation and proinflammatory responses, through activation of the high-affinity thrombin receptor protease-activated receptor 1, which is expressed on platelets and endothelium. Thus antagonism of protease-activated receptor 1 might have broad therapeutic significance. Aprotinin, used clinically to reduce transfusion requirements and the inflammatory response to bypass, has been shown to inhibit protease-activated receptor 1 on platelets in vitro and in vivo. Here we have examined whether aprotinin inhibits endothelial protease-activated receptor 1 activation and resulting proinflammatory responses induced by thrombin.', 'Protease-activated receptor 1 expression and function were examined in cultured human umbilical vein endothelial cells after treatment with alpha-thrombin at 0.02 to 0.15 U/mL in the presence or absence of aprotinin (200-1600 kallikrein inhibitory units/mL). Protease-activated receptor 1 activation was assessed by using an antibody, SPAN-12, which detects only the unactivated receptor, and thrombin-mediated calcium fluxes. Other thrombin-dependent inflammatory pathways investigated were phosphorylation of the p42/44 mitogen-activated protein kinase, upregulation of the early growth response 1 transcription factor, and production of the proinflammatory cytokine interleukin 6.', 'Pretreatment of cultured endothelial cells with aprotinin significantly spared protease-activated receptor 1 receptor cleavage (P < .0001) and abrogated calcium fluxes caused by thrombin. Aprotinin inhibited intracellular signaling through p42/44 mitogen-activated protein kinase (P < .05) and early growth response 1 transcription factor (P < .05), as well as interleukin 6 secretion caused by thrombin (P < .005).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aprotinin', 'Cells, Cultured', 'Endothelial Cells', 'Humans', 'Inflammation', 'Receptor, PAR-1', 'Thrombin']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,399,296 | Does endoscopic ultrasonography-identified celiac adenopathy remain a poor prognostic factor despite preoperative chemoradiotherapy in esophageal adenocarcinoma? | {
"contexts": [
"We reviewed our experience with preoperative chemoradiotherapy in patients with adenocarcinoma of the distal esophagus and pretreatment endoscopic ultrasonography-identified celiac adenopathy.",
"One hundred eighty-six patients with adenocarcinoma of the distal esophagus were staged with endoscopic ultrasonography before treatment from 1997 through 2004. All patients were treated with concurrent chemoradiotherapy (CRT group) and surgical intervention or induction chemotherapy followed by concurrent chemoradiotherapy (C-->CRT group) and surgical intervention. Survival analysis (excluding operative mortality) evaluated various pretreatment factors.",
"Multivariable Cox regression analysis showed that pretreatment endoscopic ultrasonography-identified celiac adenopathy was a significant predictor of decreased long-term survival (P = .03). Median and 3-year survivals were 49 months and 54% in the endoscopic ultrasonography-identified cN0 M0 group (n = 65), 45 months and 56% in the endoscopic ultrasonography-identified cN1 M0 group (n = 96), and 19 months and 12% in the endoscopic ultrasonography-identified celiac adenopathy (cM1a) group (n = 18; P = .03). Increased systemic relapse was noted in the endoscopic ultrasonography-identified cM1a group (44% vs 22%, P = .07). The only factor associated with increased survival in the endoscopic ultrasonography-identified cM1a group (27 vs 15 months, P = .02) was the addition of induction chemotherapy before concurrent chemoradiotherapy and surgical intervention."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Abdomen",
"Adenocarcinoma",
"Adult",
"Aged",
"Combined Modality Therapy",
"Endosonography",
"Esophageal Neoplasms",
"Esophagoscopy",
"Female",
"Follow-Up Studies",
"Humans",
"Lymphatic Metastasis",
"Male",
"Middle Aged",
"Preoperative Care",
"Prognosis"
]
} | Endoscopic ultrasonography-identified celiac adenopathy in patients with adenocarcinoma of the distal esophagus conveys a poor prognosis despite preoperative chemoradiotherapy. These patients should be stratified in future multimodality trials. The investigation of induction chemotherapy before concurrent chemoradiotherapy might be warranted in this high-risk group of patients. | yes | [
{
"from": "human",
"value": "Question: Does endoscopic ultrasonography-identified celiac adenopathy remain a poor prognostic factor despite preoperative chemoradiotherapy in esophageal adenocarcinoma?\nContext: {'contexts': ['We reviewed our experience with preoperative chemoradiotherapy in patients with adenocarcinoma of the distal esophagus and pretreatment endoscopic ultrasonography-identified celiac adenopathy.', 'One hundred eighty-six patients with adenocarcinoma of the distal esophagus were staged with endoscopic ultrasonography before treatment from 1997 through 2004. All patients were treated with concurrent chemoradiotherapy (CRT group) and surgical intervention or induction chemotherapy followed by concurrent chemoradiotherapy (C-->CRT group) and surgical intervention. Survival analysis (excluding operative mortality) evaluated various pretreatment factors.', 'Multivariable Cox regression analysis showed that pretreatment endoscopic ultrasonography-identified celiac adenopathy was a significant predictor of decreased long-term survival (P = .03). Median and 3-year survivals were 49 months and 54% in the endoscopic ultrasonography-identified cN0 M0 group (n = 65), 45 months and 56% in the endoscopic ultrasonography-identified cN1 M0 group (n = 96), and 19 months and 12% in the endoscopic ultrasonography-identified celiac adenopathy (cM1a) group (n = 18; P = .03). Increased systemic relapse was noted in the endoscopic ultrasonography-identified cM1a group (44% vs 22%, P = .07). The only factor associated with increased survival in the endoscopic ultrasonography-identified cM1a group (27 vs 15 months, P = .02) was the addition of induction chemotherapy before concurrent chemoradiotherapy and surgical intervention.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Abdomen', 'Adenocarcinoma', 'Adult', 'Aged', 'Combined Modality Therapy', 'Endosonography', 'Esophageal Neoplasms', 'Esophagoscopy', 'Female', 'Follow-Up Studies', 'Humans', 'Lymphatic Metastasis', 'Male', 'Middle Aged', 'Preoperative Care', 'Prognosis']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,397,889 | Are connexin43 levels increased in mouse neural crest cells exposed to homocysteine? | {
"contexts": [
"Elevated homocysteine levels during embryonic development can result in neural tube and cardiovascular defects. The mechanisms that underlie the toxic effect of homocysteine are largely unknown.",
"We cultured mouse neural tube explants to study the effects of homocysteine on the migratory behavior of neural crest cells and on the levels of the gap junction protein Connexin43 (Cx43) and the actin- and Cx43-interacting protein ZO-1.",
"Homocysteine exposure resulted in a significantly augmented maximal migration distance (MMD). The level of Cx43 immunolabeling was 2 times higher in the cytoplasm and cell protrusions of neural crest cells in homocysteine-treated cultures than in control cultures. Furthermore, colocalization of Cx43 and ZO-1 was increased in neural crest cell protrusions by this treatment."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Cell Movement",
"Connexin 43",
"Homocysteine",
"Immunohistochemistry",
"Membrane Proteins",
"Mice",
"Neural Crest",
"Organ Culture Techniques",
"Phosphoproteins",
"Up-Regulation",
"Zonula Occludens-1 Protein"
]
} | Increased Cx43 levels were previously shown to result in abnormal embryonic development. Our data raises the hypothesis that the embryotoxic effects of homocysteine may be mediated in part by its effects on Cx43 expression level and gap junction function in neural crest cells. | yes | [
{
"from": "human",
"value": "Question: Are connexin43 levels increased in mouse neural crest cells exposed to homocysteine?\nContext: {'contexts': ['Elevated homocysteine levels during embryonic development can result in neural tube and cardiovascular defects. The mechanisms that underlie the toxic effect of homocysteine are largely unknown.', 'We cultured mouse neural tube explants to study the effects of homocysteine on the migratory behavior of neural crest cells and on the levels of the gap junction protein Connexin43 (Cx43) and the actin- and Cx43-interacting protein ZO-1.', 'Homocysteine exposure resulted in a significantly augmented maximal migration distance (MMD). The level of Cx43 immunolabeling was 2 times higher in the cytoplasm and cell protrusions of neural crest cells in homocysteine-treated cultures than in control cultures. Furthermore, colocalization of Cx43 and ZO-1 was increased in neural crest cell protrusions by this treatment.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Cell Movement', 'Connexin 43', 'Homocysteine', 'Immunohistochemistry', 'Membrane Proteins', 'Mice', 'Neural Crest', 'Organ Culture Techniques', 'Phosphoproteins', 'Up-Regulation', 'Zonula Occludens-1 Protein']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,374,171 | Does beta2-adrenergic agonist protect human endothelial cells from hypoxia/reoxygenation injury in vitro? | {
"contexts": [
"Circulatory shock results in hypoxia/reoxygenation processes that lead to the release of reactive oxygen species, endothelial injury, and multiple organ failure. Previous data suggest that beta2-adrenergic agonists prevent endothelial dysfunction. The study aimed at determining whether the beta2-adrenergic agonist formoterol protects endothelial cells against hypoxia/reoxygenation injury in vitro.",
"Prospective controlled trial.",
"University hospital research laboratory.",
"Cultured human umbilical vein endothelial cells (HUVECs).",
"Confluent HUVECs were sealed in a flow-through chamber mounted on an inverted microscope and perfused with a constant flow of Krebs medium. After 1 hr of equilibration, HUVECs underwent 2 hrs of hypoxia and 1 hr of reoxygenation. Cell death at the end of reoxygenation and reactive oxygen species formation were assessed with fluorescent probes propidium iodide and 2',7'-dichlorodihydrofluorescein diacetate, respectively. The effects of the beta2-adrenergic agonist formoterol, the beta2-adrenergic antagonist ICI 118,551 and the nitric oxide synthase inhibitor L-NNA were investigated. Statistical analysis was performed with analysis of variance followed by post hoc Fisher's test.",
"Hypoxia/reoxygenation increased cell death (hypoxia/reoxygenation 29 +/- 4% vs. control 1 +/- 5%, p < .05) and endothelial reactive oxygen species production (hypoxia/reoxygenation 126 +/- 4% vs. control 108 +/- 4%, p < .05). Formoterol reduced cell death in a concentration-dependent manner (EC95 = 10 mol/L) and reduced endothelial reactive oxygen species production (hypoxia/reoxygenation + formoterol EC95 109 +/- 4% vs. hypoxia/reoxygenation 126 +/- 4%, p < .05). When added to formoterol EC95, ICI 118,551 and L-NNA abolished the formoterol-induced cell protection and reduced reactive oxygen species production."
],
"labels": [
"OBJECTIVE",
"METHODS",
"METHODS",
"METHODS",
"METHODS",
"RESULTS"
],
"meshes": [
"Adrenergic beta-Agonists",
"Cell Death",
"Cell Hypoxia",
"Cells, Cultured",
"Endothelial Cells",
"Ethanolamines",
"Formoterol Fumarate",
"Humans",
"In Vitro Techniques",
"Nitric Oxide Synthase",
"Perfusion",
"Reactive Oxygen Species",
"Reference Values",
"Reperfusion Injury",
"Sensitivity and Specificity"
]
} | These results indicate that formoterol reduces endothelial cell death and reactive oxygen species production in this in vitro hypoxia/reoxygenation model. These effects are beta2-adrenergic specific and are partially mediated by nitric oxide synthase. | yes | [
{
"from": "human",
"value": "Question: Does beta2-adrenergic agonist protect human endothelial cells from hypoxia/reoxygenation injury in vitro?\nContext: {'contexts': ['Circulatory shock results in hypoxia/reoxygenation processes that lead to the release of reactive oxygen species, endothelial injury, and multiple organ failure. Previous data suggest that beta2-adrenergic agonists prevent endothelial dysfunction. The study aimed at determining whether the beta2-adrenergic agonist formoterol protects endothelial cells against hypoxia/reoxygenation injury in vitro.', 'Prospective controlled trial.', 'University hospital research laboratory.', 'Cultured human umbilical vein endothelial cells (HUVECs).', \"Confluent HUVECs were sealed in a flow-through chamber mounted on an inverted microscope and perfused with a constant flow of Krebs medium. After 1 hr of equilibration, HUVECs underwent 2 hrs of hypoxia and 1 hr of reoxygenation. Cell death at the end of reoxygenation and reactive oxygen species formation were assessed with fluorescent probes propidium iodide and 2',7'-dichlorodihydrofluorescein diacetate, respectively. The effects of the beta2-adrenergic agonist formoterol, the beta2-adrenergic antagonist ICI 118,551 and the nitric oxide synthase inhibitor L-NNA were investigated. Statistical analysis was performed with analysis of variance followed by post hoc Fisher's test.\", 'Hypoxia/reoxygenation increased cell death (hypoxia/reoxygenation 29 +/- 4% vs. control 1 +/- 5%, p < .05) and endothelial reactive oxygen species production (hypoxia/reoxygenation 126 +/- 4% vs. control 108 +/- 4%, p < .05). Formoterol reduced cell death in a concentration-dependent manner (EC95 = 10 mol/L) and reduced endothelial reactive oxygen species production (hypoxia/reoxygenation + formoterol EC95 109 +/- 4% vs. hypoxia/reoxygenation 126 +/- 4%, p < .05). When added to formoterol EC95, ICI 118,551 and L-NNA abolished the formoterol-induced cell protection and reduced reactive oxygen species production.'], 'labels': ['OBJECTIVE', 'METHODS', 'METHODS', 'METHODS', 'METHODS', 'RESULTS'], 'meshes': ['Adrenergic beta-Agonists', 'Cell Death', 'Cell Hypoxia', 'Cells, Cultured', 'Endothelial Cells', 'Ethanolamines', 'Formoterol Fumarate', 'Humans', 'In Vitro Techniques', 'Nitric Oxide Synthase', 'Perfusion', 'Reactive Oxygen Species', 'Reference Values', 'Reperfusion Injury', 'Sensitivity and Specificity']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,385,086 | Does thromboxane A2/prostaglandin H2 receptor activation mediate angiotensin II-induced postischemic neovascularization? | {
"contexts": [
"We analyzed the involvement of thromboxane (TX) A2/prostaglandin (PG) H2 (TP) receptor in ischemia-induced neovascularization in mice.",
"Unilateral hindlimb ischemia was induced by right femoral artery ligature in male C57BL/6J mice (n=7 per group). Animals were then treated with or without TP receptor antagonist (S18886, 5 or 10 mg/kg per day; ramatroban, 10 mg/kg per day) or aspirin (30 mg/kg per day) in drinking water for 21 days. Hindlimb ischemia raised plasma level of TXB2, the stable metabolite of TXA2, by 4.7-fold. This increase was blocked by aspirin treatment whereas S18886 (5 or 10 mg/kg per day) had no effect. However, neither S 18886 nor aspirin affected postischemic neovascularization. We next assessed the putative involvement of TXA2 signaling in angiotensin II (Ang II) proangiogenic pathway. Ang II (0.3 mg/kg per day) enhanced TXB2 plasma levels by 2.6-fold over that of control (P<0.01). Ang II-induced TXB2 upregulation was reduced by cotreatment with Ang II type I receptor antagonist (candesartan, 20 mg/kg per day). Angiographic score, capillary number, and foot perfusion were improved by 1.7-, 1.7-, and 1.4-fold, respectively, in Ang II-treated mice compared with controls (P<0.05). Ang II proangiogenic effect was associated with a 1.6-fold increase in VEGF-A protein content (P<0.05) and a 1.4-fold increase in the number of Mac-3-positive cells (ie, macrophages) in ischemic areas (P<0.05). Interestingly, treatments with TP receptor antagonists or aspirin hampered the proangiogenic effects of Ang II."
],
"labels": [
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Angiotensin II",
"Animals",
"Capillaries",
"Hindlimb",
"Ischemia",
"Male",
"Mice",
"Mice, Inbred C57BL",
"Naphthalenes",
"Neovascularization, Physiologic",
"Propionates",
"Receptors, Thromboxane A2, Prostaglandin H2",
"Signal Transduction",
"Thromboxane A2",
"Thromboxane B2",
"Vasculitis",
"Vasoconstrictor Agents"
]
} | Endogenous activation of TXA2 receptor by eicosanoids did not modulate spontaneous neovascularization in the setting of ischemia. Conversely, TXA2 signaling is involved in Ang II-induced AT1-dependent vessel growth. | yes | [
{
"from": "human",
"value": "Question: Does thromboxane A2/prostaglandin H2 receptor activation mediate angiotensin II-induced postischemic neovascularization?\nContext: {'contexts': ['We analyzed the involvement of thromboxane (TX) A2/prostaglandin (PG) H2 (TP) receptor in ischemia-induced neovascularization in mice.', 'Unilateral hindlimb ischemia was induced by right femoral artery ligature in male C57BL/6J mice (n=7 per group). Animals were then treated with or without TP receptor antagonist (S18886, 5 or 10 mg/kg per day; ramatroban, 10 mg/kg per day) or aspirin (30 mg/kg per day) in drinking water for 21 days. Hindlimb ischemia raised plasma level of TXB2, the stable metabolite of TXA2, by 4.7-fold. This increase was blocked by aspirin treatment whereas S18886 (5 or 10 mg/kg per day) had no effect. However, neither S 18886 nor aspirin affected postischemic neovascularization. We next assessed the putative involvement of TXA2 signaling in angiotensin II (Ang II) proangiogenic pathway. Ang II (0.3 mg/kg per day) enhanced TXB2 plasma levels by 2.6-fold over that of control (P<0.01). Ang II-induced TXB2 upregulation was reduced by cotreatment with Ang II type I receptor antagonist (candesartan, 20 mg/kg per day). Angiographic score, capillary number, and foot perfusion were improved by 1.7-, 1.7-, and 1.4-fold, respectively, in Ang II-treated mice compared with controls (P<0.05). Ang II proangiogenic effect was associated with a 1.6-fold increase in VEGF-A protein content (P<0.05) and a 1.4-fold increase in the number of Mac-3-positive cells (ie, macrophages) in ischemic areas (P<0.05). Interestingly, treatments with TP receptor antagonists or aspirin hampered the proangiogenic effects of Ang II.'], 'labels': ['OBJECTIVE', 'RESULTS'], 'meshes': ['Angiotensin II', 'Animals', 'Capillaries', 'Hindlimb', 'Ischemia', 'Male', 'Mice', 'Mice, Inbred C57BL', 'Naphthalenes', 'Neovascularization, Physiologic', 'Propionates', 'Receptors, Thromboxane A2, Prostaglandin H2', 'Signal Transduction', 'Thromboxane A2', 'Thromboxane B2', 'Vasculitis', 'Vasoconstrictor Agents']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,385,085 | Is atherosclerosis in mice affected by a reduction in tissue factor expression? | {
"contexts": [
"To determine whether tissue factor (TF) contributes to the progression of atherosclerotic lesions in mice.",
"We determined the effect of a 50% reduction of TF levels in all cells on atherosclerosis in apolipoprotein E-deficient (apoE(-/-)) mice. No differences were observed in the extent of atherosclerosis in apoE(-/-)/TF(+/+) and apoE(-/-)/TF(+/-) mice fed regular chow for 34 weeks. Atherosclerosis could not be analyzed in apoE(-/-) mice expressing low levels of TF because of premature death of these mice. Macrophages are a major source of TF in atherosclerotic plaques. Therefore, in a second series of experiments, we investigated the effect on atherosclerosis of selectively reducing hematopoietic cell-derived TF by transplanting bone marrow from mice expressing low levels of TF into low-density lipoprotein receptor deficient (LDLR(-/-)) mice. Atherosclerosis within the arterial tree and aortic root were similar in LDLR(-/-) mice with low-TF bone marrow compared with control bone marrow (TF(+/+) or TF(+/-)) after 4 and 16 weeks on an atherogenic diet. Furthermore, the cellular composition of the aortic root lesions was similar between the 2 groups."
],
"labels": [
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Animals",
"Aorta",
"Apolipoproteins E",
"Atherosclerosis",
"Bone Marrow Transplantation",
"Gene Expression",
"Hematopoietic Stem Cells",
"Mice",
"Mice, Inbred C57BL",
"Mice, Mutant Strains",
"Receptors, LDL",
"Thromboplastin"
]
} | Our data indicate that either a 50% reduction of TF in all cells or a selective reduction in hematopoietic cell-derived TF does not affect the development of atherosclerotic lesions in mice. | no | [
{
"from": "human",
"value": "Question: Is atherosclerosis in mice affected by a reduction in tissue factor expression?\nContext: {'contexts': ['To determine whether tissue factor (TF) contributes to the progression of atherosclerotic lesions in mice.', 'We determined the effect of a 50% reduction of TF levels in all cells on atherosclerosis in apolipoprotein E-deficient (apoE(-/-)) mice. No differences were observed in the extent of atherosclerosis in apoE(-/-)/TF(+/+) and apoE(-/-)/TF(+/-) mice fed regular chow for 34 weeks. Atherosclerosis could not be analyzed in apoE(-/-) mice expressing low levels of TF because of premature death of these mice. Macrophages are a major source of TF in atherosclerotic plaques. Therefore, in a second series of experiments, we investigated the effect on atherosclerosis of selectively reducing hematopoietic cell-derived TF by transplanting bone marrow from mice expressing low levels of TF into low-density lipoprotein receptor deficient (LDLR(-/-)) mice. Atherosclerosis within the arterial tree and aortic root were similar in LDLR(-/-) mice with low-TF bone marrow compared with control bone marrow (TF(+/+) or TF(+/-)) after 4 and 16 weeks on an atherogenic diet. Furthermore, the cellular composition of the aortic root lesions was similar between the 2 groups.'], 'labels': ['OBJECTIVE', 'RESULTS'], 'meshes': ['Animals', 'Aorta', 'Apolipoproteins E', 'Atherosclerosis', 'Bone Marrow Transplantation', 'Gene Expression', 'Hematopoietic Stem Cells', 'Mice', 'Mice, Inbred C57BL', 'Mice, Mutant Strains', 'Receptors, LDL', 'Thromboplastin']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
16,378,215 | Does 3,4-Methylenedioxymethamphetamine enhance the release of acetylcholine in the prefrontal cortex and dorsal hippocampus of the rat? | {
"contexts": [
"The neurochemical effects produced by acute administration of 3,4-methylenedioxymethamphetamine (MDMA) on the monoaminergic systems in the brain are well documented; however, there has been little consideration of the potential effects of MDMA on other neurotransmitter systems.",
"The present study was designed to investigate the acute effect of MDMA on cholinergic neurons by measuring acetylcholine (ACh) release in the medial prefrontal cortex (PFC) and dorsal hippocampus, terminal regions of cholinergic projection neurons originating in the basal forebrain.",
"In vivo microdialysis and high-performance liquid chromatography with electrochemical detection (HPLC-ED) were used to assess the effects of MDMA on the extracellular concentration of ACh in the PFC and dorsal hippocampus of the rat.",
"The systemic administration of MDMA (3-20 mg/kg, i.p.) resulted in an increased extracellular concentration of ACh in the PFC and dorsal hippocampus. Reverse dialysis of MDMA (100 microM) into the PFC and hippocampus also increased ACh release in these brain regions. Treatment with parachlorophenylalanine and alpha-methyl-para-tyrosine, inhibitors of serotonin (5-HT) and dopamine (DA) synthesis, respectively, significantly attenuated the release of ACh stimulated by MDMA in the PFC, but not in the dorsal hippocampus."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Acetylcholine",
"Amphetamine",
"Animals",
"Chromatography, High Pressure Liquid",
"Dopamine Uptake Inhibitors",
"Electrochemistry",
"Extracellular Space",
"Hallucinogens",
"Hippocampus",
"Male",
"Microdialysis",
"N-Methyl-3,4-methylenedioxyamphetamine",
"Prefrontal Cortex",
"Rats",
"Rats, Sprague-Dawley"
]
} | MDMA exerts a stimulatory effect on the release of ACh in the PFC and dorsal hippocampus in vivo, possibly by mechanisms localized within these brain regions. In addition, these results suggest that the MDMA-induced release of ACh in the PFC involves both serotonergic and dopaminergic mechanisms. | yes | [
{
"from": "human",
"value": "Question: Does 3,4-Methylenedioxymethamphetamine enhance the release of acetylcholine in the prefrontal cortex and dorsal hippocampus of the rat?\nContext: {'contexts': ['The neurochemical effects produced by acute administration of 3,4-methylenedioxymethamphetamine (MDMA) on the monoaminergic systems in the brain are well documented; however, there has been little consideration of the potential effects of MDMA on other neurotransmitter systems.', 'The present study was designed to investigate the acute effect of MDMA on cholinergic neurons by measuring acetylcholine (ACh) release in the medial prefrontal cortex (PFC) and dorsal hippocampus, terminal regions of cholinergic projection neurons originating in the basal forebrain.', 'In vivo microdialysis and high-performance liquid chromatography with electrochemical detection (HPLC-ED) were used to assess the effects of MDMA on the extracellular concentration of ACh in the PFC and dorsal hippocampus of the rat.', 'The systemic administration of MDMA (3-20 mg/kg, i.p.) resulted in an increased extracellular concentration of ACh in the PFC and dorsal hippocampus. Reverse dialysis of MDMA (100 microM) into the PFC and hippocampus also increased ACh release in these brain regions. Treatment with parachlorophenylalanine and alpha-methyl-para-tyrosine, inhibitors of serotonin (5-HT) and dopamine (DA) synthesis, respectively, significantly attenuated the release of ACh stimulated by MDMA in the PFC, but not in the dorsal hippocampus.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Acetylcholine', 'Amphetamine', 'Animals', 'Chromatography, High Pressure Liquid', 'Dopamine Uptake Inhibitors', 'Electrochemistry', 'Extracellular Space', 'Hallucinogens', 'Hippocampus', 'Male', 'Microdialysis', 'N-Methyl-3,4-methylenedioxyamphetamine', 'Prefrontal Cortex', 'Rats', 'Rats, Sprague-Dawley']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,371,871 | Does age influence the emm type distribution of pediatric group A streptococcal pharyngeal isolates? | {
"contexts": [
"emm types 12, 1, 28, 3, 4, 2 and 6 (in that order) are the types most commonly associated with uncomplicated group A streptococcal (GAS) pharyngitis in the United States, together accounting for approximately 78% of isolates.",
"To determine whether the distribution of common pharyngeal group A streptococcal GAS types differs at various ages throughout childhood.",
"We emm typed 3356 GAS isolates collected from the United States and Canada during 3 streptococcal seasons (2000-2003). Variations in prevalence by age for the 7 most prevalent emm types and the \"uncommon\" category (all types accounting for <5% of the total number of isolates) were analyzed and assessed for significance by chi2.",
"The proportion of uncommon isolates increased significantly with increasing age from 18% in group 1 to 37% in group 4 (P = 0.001). We found a significant decrease in the proportion of the common pharyngeal emm types, specifically emm 12 and emm 4 type isolates, with increasing age (P = 0.001 and P = 0.003, respectively); there was no significant decline in the prevalence of other common pharyngeal types (emm 1, 2, 3, 6 and 28) with increasing age."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Age Distribution",
"Aging",
"Antigens, Bacterial",
"Bacterial Outer Membrane Proteins",
"Carrier Proteins",
"Child",
"Child, Preschool",
"Humans",
"Pharyngitis",
"Pharynx",
"Population Surveillance",
"Prevalence",
"Streptococcal Infections",
"Streptococcus pyogenes"
]
} | Age-related changes in emm type distribution of pharyngeal GAS are present in childhood; these changes may reflect acquisition of immunity to more common types as a consequence of exposure early in life, but this remains to be demonstrated. | yes | [
{
"from": "human",
"value": "Question: Does age influence the emm type distribution of pediatric group A streptococcal pharyngeal isolates?\nContext: {'contexts': ['emm types 12, 1, 28, 3, 4, 2 and 6 (in that order) are the types most commonly associated with uncomplicated group A streptococcal (GAS) pharyngitis in the United States, together accounting for approximately 78% of isolates.', 'To determine whether the distribution of common pharyngeal group A streptococcal GAS types differs at various ages throughout childhood.', 'We emm typed 3356 GAS isolates collected from the United States and Canada during 3 streptococcal seasons (2000-2003). Variations in prevalence by age for the 7 most prevalent emm types and the \"uncommon\" category (all types accounting for <5% of the total number of isolates) were analyzed and assessed for significance by chi2.', 'The proportion of uncommon isolates increased significantly with increasing age from 18% in group 1 to 37% in group 4 (P = 0.001). We found a significant decrease in the proportion of the common pharyngeal emm types, specifically emm 12 and emm 4 type isolates, with increasing age (P = 0.001 and P = 0.003, respectively); there was no significant decline in the prevalence of other common pharyngeal types (emm 1, 2, 3, 6 and 28) with increasing age.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Age Distribution', 'Aging', 'Antigens, Bacterial', 'Bacterial Outer Membrane Proteins', 'Carrier Proteins', 'Child', 'Child, Preschool', 'Humans', 'Pharyngitis', 'Pharynx', 'Population Surveillance', 'Prevalence', 'Streptococcal Infections', 'Streptococcus pyogenes']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,375,772 | Are parkin-deficient mice more sensitive to 6-hydroxydopamine or methamphetamine neurotoxicity? | {
"contexts": [
"Autosomal recessive juvenile parkinsonism (AR-JP) is caused by mutations in the parkin gene which encodes an E3 ubiquitin-protein ligase. Parkin is thought to be critical for protecting dopaminergic neurons from toxic insults by targeting misfolded or oxidatively damaged proteins for proteasomal degradation. Surprisingly, mice with targeted deletions of parkin do not recapitulate robust behavioral or pathological signs of parkinsonism. Since Parkin is thought to protect against neurotoxic insults, we hypothesized that the reason Parkin-deficient mice do not develop parkinsonism is because they are not exposed to appropriate environmental triggers. To test this possibility, we challenged Parkin-deficient mice with neurotoxic regimens of either methamphetamine (METH) or 6-hydroxydopamine (6-OHDA). Because Parkin function has been linked to many of the pathways involved in METH and 6-OHDA toxicity, we predicted that Parkin-deficient mice would be more sensitive to the neurotoxic effects of these agents.",
"We found no signs consistent with oxidative stress, ubiquitin dysfunction, or degeneration of striatal dopamine neuron terminals in aged Parkin-deficient mice. Moreover, results from behavioral, neurochemical, and immunoblot analyses indicate that Parkin-deficient mice are not more sensitive to dopaminergic neurotoxicity following treatment with METH or 6-OHDA."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Aging",
"Animals",
"Dopamine",
"Drug Resistance",
"Methamphetamine",
"Mice",
"Mice, Knockout",
"Nerve Degeneration",
"Neurons",
"Neurotoxins",
"Oxidative Stress",
"Oxidopamine",
"Ubiquitin",
"Ubiquitin-Protein Ligases"
]
} | Our results suggest that the absence of a robust parkinsonian phenotype in Parkin-deficient mice is not due to the lack of exposure to environmental triggers with mechanisms of action similar to METH or 6-OHDA. Nevertheless, Parkin-deficient mice could be more sensitive to other neurotoxins, such as rotenone or MPTP, which have different mechanisms of action; therefore, identifying conditions that precipitate parkinsonism specifically in Parkin-deficient mice would increase the utility of this model and could provide insight into the mechanism of AR-JP. Alternatively, it remains possible that the absence of parkinsonism in Parkin-deficient mice could reflect fundamental differences between the function of human and mouse Parkin, or the existence of a redundant E3 ubiquitin-protein ligase in mouse that is not found in humans. Therefore, additional studies are necessary to understand why Parkin-deficient mice do not display robust signs of parkinsonism. | no | [
{
"from": "human",
"value": "Question: Are parkin-deficient mice more sensitive to 6-hydroxydopamine or methamphetamine neurotoxicity?\nContext: {'contexts': ['Autosomal recessive juvenile parkinsonism (AR-JP) is caused by mutations in the parkin gene which encodes an E3 ubiquitin-protein ligase. Parkin is thought to be critical for protecting dopaminergic neurons from toxic insults by targeting misfolded or oxidatively damaged proteins for proteasomal degradation. Surprisingly, mice with targeted deletions of parkin do not recapitulate robust behavioral or pathological signs of parkinsonism. Since Parkin is thought to protect against neurotoxic insults, we hypothesized that the reason Parkin-deficient mice do not develop parkinsonism is because they are not exposed to appropriate environmental triggers. To test this possibility, we challenged Parkin-deficient mice with neurotoxic regimens of either methamphetamine (METH) or 6-hydroxydopamine (6-OHDA). Because Parkin function has been linked to many of the pathways involved in METH and 6-OHDA toxicity, we predicted that Parkin-deficient mice would be more sensitive to the neurotoxic effects of these agents.', 'We found no signs consistent with oxidative stress, ubiquitin dysfunction, or degeneration of striatal dopamine neuron terminals in aged Parkin-deficient mice. Moreover, results from behavioral, neurochemical, and immunoblot analyses indicate that Parkin-deficient mice are not more sensitive to dopaminergic neurotoxicity following treatment with METH or 6-OHDA.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Aging', 'Animals', 'Dopamine', 'Drug Resistance', 'Methamphetamine', 'Mice', 'Mice, Knockout', 'Nerve Degeneration', 'Neurons', 'Neurotoxins', 'Oxidative Stress', 'Oxidopamine', 'Ubiquitin', 'Ubiquitin-Protein Ligases']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
16,388,481 | Are physical distance , genetic relationship , age , and leprosy classification independent risk factors for leprosy in contacts of patients with leprosy? | {
"contexts": [
"Close contacts of patients with leprosy have a higher risk of developing leprosy. Several risk factors have been identified, including genetic relationship and physical distance. Their independent contributions to the risk of developing leprosy, however, have never been sufficiently quantified.",
"Logistic-regression analysis was performed on intake data from a prospective cohort study of 1037 patients newly diagnosed as having leprosy and their 21,870 contacts.",
"Higher age showed an increased risk, with a bimodal distribution. Contacts of patients with paucibacillary (PB) leprosy with 2-5 lesions (PB2-5) and those with multibacillary (MB) leprosy had a higher risk than did contacts of patients with single-lesion PB leprosy. The core household group had a higher risk than other contacts living under the same roof and next-door neighbors, who again had a higher risk than neighbors of neighbors. A close genetic relationship indicated an increased risk when blood-related children, parents, and siblings were pooled together."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Age Distribution",
"Bangladesh",
"Child",
"Child, Preschool",
"Cohort Studies",
"Contact Tracing",
"Family Characteristics",
"Female",
"Humans",
"Leprosy",
"Logistic Models",
"Male",
"Middle Aged",
"Prospective Studies",
"Risk Factors",
"Sex Distribution"
]
} | Age of the contact, the disease classification of the index patient, and physical and genetic distance were independently associated with the risk of a contact acquiring leprosy. Contact surveys in leprosy should be not only focused on household contacts but also extended to neighbors and consanguineous relatives, especially when the patient has PB2-5 or MB leprosy. | yes | [
{
"from": "human",
"value": "Question: Are physical distance , genetic relationship , age , and leprosy classification independent risk factors for leprosy in contacts of patients with leprosy?\nContext: {'contexts': ['Close contacts of patients with leprosy have a higher risk of developing leprosy. Several risk factors have been identified, including genetic relationship and physical distance. Their independent contributions to the risk of developing leprosy, however, have never been sufficiently quantified.', 'Logistic-regression analysis was performed on intake data from a prospective cohort study of 1037 patients newly diagnosed as having leprosy and their 21,870 contacts.', 'Higher age showed an increased risk, with a bimodal distribution. Contacts of patients with paucibacillary (PB) leprosy with 2-5 lesions (PB2-5) and those with multibacillary (MB) leprosy had a higher risk than did contacts of patients with single-lesion PB leprosy. The core household group had a higher risk than other contacts living under the same roof and next-door neighbors, who again had a higher risk than neighbors of neighbors. A close genetic relationship indicated an increased risk when blood-related children, parents, and siblings were pooled together.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Age Distribution', 'Bangladesh', 'Child', 'Child, Preschool', 'Cohort Studies', 'Contact Tracing', 'Family Characteristics', 'Female', 'Humans', 'Leprosy', 'Logistic Models', 'Male', 'Middle Aged', 'Prospective Studies', 'Risk Factors', 'Sex Distribution']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,371,932 | Does sex steroid ablation enhance lymphoid recovery following autologous hematopoietic stem cell transplantation? | {
"contexts": [
"Autologous hematopoietic stem cell transplantation (auto-HSCT) patients experience long-term immunosuppression, which increases susceptibility to infection and relapse rates due to minimal residual disease (MRD). Sex steroid (SS) ablation is known to reverse age-related thymic atrophy and decline in B-cell production",
"This study used a congenic HSCT mouse model to analyze the effects of SS ablation (through surgical castration) on immune reconstitution and growth factor production following auto-HSCT. Bone marrow (BM) and thymic stromal cell (TSCs) populations were analyzed using RT-PCR and were tested for the production of growth factors previously implicated in immune reconstitution or age-relate immune degeneration",
"Castration increased bone marrow (BM), thymic, and splenic cellularity following auto-HSCT. HSC number and common lymphoid precursor (CLP) frequency and number were increased in castrated mice. B cell precursor numbers were also significantly increased in the BM of these mice. Triple negative, double positive and single positive thymocytes were increased following HSCT and castration, as were thymic dendritic cells and natural killer T (NKT) cells. This enhanced lymphoid reconstitution of the primary immune organs leads to a significant increase in splenic T and B cells 42 days after HSCT. The molecular mechanisms behind the enhanced reconstitution were also studied. TGF-beta1 was decreased in castrated mice compared to sham-castrated controls in TSCs and BM cells. TSC production of IL-6 was also decreased in castrated mice"
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Androgens",
"Animals",
"B-Lymphocytes",
"Bone Marrow Cells",
"Male",
"Mice",
"Mice, Inbred C57BL",
"Models, Animal",
"Orchiectomy",
"Stem Cell Transplantation",
"Thymus Gland",
"Transplantation, Autologous"
]
} | These data suggest that sex steroid ablation significantly enhances lymphopoiesis following auto-HSCT providing a new strategy for posttransplant immune reconstitution. | yes | [
{
"from": "human",
"value": "Question: Does sex steroid ablation enhance lymphoid recovery following autologous hematopoietic stem cell transplantation?\nContext: {'contexts': ['Autologous hematopoietic stem cell transplantation (auto-HSCT) patients experience long-term immunosuppression, which increases susceptibility to infection and relapse rates due to minimal residual disease (MRD). Sex steroid (SS) ablation is known to reverse age-related thymic atrophy and decline in B-cell production', 'This study used a congenic HSCT mouse model to analyze the effects of SS ablation (through surgical castration) on immune reconstitution and growth factor production following auto-HSCT. Bone marrow (BM) and thymic stromal cell (TSCs) populations were analyzed using RT-PCR and were tested for the production of growth factors previously implicated in immune reconstitution or age-relate immune degeneration', 'Castration increased bone marrow (BM), thymic, and splenic cellularity following auto-HSCT. HSC number and common lymphoid precursor (CLP) frequency and number were increased in castrated mice. B cell precursor numbers were also significantly increased in the BM of these mice. Triple negative, double positive and single positive thymocytes were increased following HSCT and castration, as were thymic dendritic cells and natural killer T (NKT) cells. This enhanced lymphoid reconstitution of the primary immune organs leads to a significant increase in splenic T and B cells 42 days after HSCT. The molecular mechanisms behind the enhanced reconstitution were also studied. TGF-beta1 was decreased in castrated mice compared to sham-castrated controls in TSCs and BM cells. TSC production of IL-6 was also decreased in castrated mice'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Androgens', 'Animals', 'B-Lymphocytes', 'Bone Marrow Cells', 'Male', 'Mice', 'Mice, Inbred C57BL', 'Models, Animal', 'Orchiectomy', 'Stem Cell Transplantation', 'Thymus Gland', 'Transplantation, Autologous']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,401,538 | Does perivascular treatment with azathioprine reduce neointimal hyperplasia in experimental vein grafts? | {
"contexts": [
"Azathioprine is an immunosuppressive and anti-inflammatory drug, and it has been shown to induce apoptosis in human T-lymphocytes. We investigated whether local treatment with azathioprine can inhibit neointimal hyperplasia in experimental vein grafts.",
"C57BL/6J mice underwent interposition of the inferior vena cava from isogenic donor mice into the common carotid artery using a cuff technique. In the treatment group azathioprine was perivascularly applied. The control group did not receive local treatment. Vein grafts were harvested at 1 and 2 weeks postoperatively and underwent morphometric analysis as well as immunohistochemical analysis for apoptosis (TUNEL).",
"In grafted veins without treatment (controls), neointimal thickness was 10 microm (range, 6-29 microm), and 12 microm (range, 8-40 microm) at 1 and 2 weeks postoperatively, respectively. In azathioprine-treated grafts, the neointimal thickness was 2 microm (range, 1-5 microm) and 4 microm (range, 3-11 microm) at 1 and 2 weeks postoperatively, respectively. This reduction of neointimal thickness was significant at 1 week (P = .001) and 2 weeks (P = .016) postoperatively. Azathioprine-treated vein grafts showed an increased rate of apoptosis in the vascular wall as compared with controls (593 [range, 26-783] versus 45 [range, 0-106] apoptotic cells/mm(2) at 1 week, P = .063; and 656 [range, 327-1270] versus 19 [range, 0-79] apoptotic cells/mm(2) at 2 weeks, P = .016)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Apoptosis",
"Azathioprine",
"Carotid Artery, Common",
"Hyperplasia",
"Immunosuppressive Agents",
"In Situ Nick-End Labeling",
"Mice",
"Mice, Inbred C57BL",
"Tunica Intima",
"Vascular Surgical Procedures",
"Vena Cava, Inferior"
]
} | We conclude that treatment of experimental vein grafts with azathioprine is associated with a reduction of neointimal hyperplasia and an increased apoptosis rate in the vascular wall. These results suggest that azathioprine may be useful for the prevention of vein graft disease after coronary artery bypass grafting. | yes | [
{
"from": "human",
"value": "Question: Does perivascular treatment with azathioprine reduce neointimal hyperplasia in experimental vein grafts?\nContext: {'contexts': ['Azathioprine is an immunosuppressive and anti-inflammatory drug, and it has been shown to induce apoptosis in human T-lymphocytes. We investigated whether local treatment with azathioprine can inhibit neointimal hyperplasia in experimental vein grafts.', 'C57BL/6J mice underwent interposition of the inferior vena cava from isogenic donor mice into the common carotid artery using a cuff technique. In the treatment group azathioprine was perivascularly applied. The control group did not receive local treatment. Vein grafts were harvested at 1 and 2 weeks postoperatively and underwent morphometric analysis as well as immunohistochemical analysis for apoptosis (TUNEL).', 'In grafted veins without treatment (controls), neointimal thickness was 10 microm (range, 6-29 microm), and 12 microm (range, 8-40 microm) at 1 and 2 weeks postoperatively, respectively. In azathioprine-treated grafts, the neointimal thickness was 2 microm (range, 1-5 microm) and 4 microm (range, 3-11 microm) at 1 and 2 weeks postoperatively, respectively. This reduction of neointimal thickness was significant at 1 week (P = .001) and 2 weeks (P = .016) postoperatively. Azathioprine-treated vein grafts showed an increased rate of apoptosis in the vascular wall as compared with controls (593 [range, 26-783] versus 45 [range, 0-106] apoptotic cells/mm(2) at 1 week, P = .063; and 656 [range, 327-1270] versus 19 [range, 0-79] apoptotic cells/mm(2) at 2 weeks, P = .016).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Apoptosis', 'Azathioprine', 'Carotid Artery, Common', 'Hyperplasia', 'Immunosuppressive Agents', 'In Situ Nick-End Labeling', 'Mice', 'Mice, Inbred C57BL', 'Tunica Intima', 'Vascular Surgical Procedures', 'Vena Cava, Inferior']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,388,520 | Are elevated serum heparanase-1 levels in patients with pancreatic carcinoma associated with poor survival? | {
"contexts": [
"It has previously been shown that heparanase-1 (HPR1), an endoglycosidase, is up-regulated in pancreatic carcinoma. The purpose of this study was to test whether serum HPR1 levels in pancreatic carcinoma patients are elevated, and whether higher serum HPR1 levels are associated with a shortened survival.",
"Serum HPR1 levels in 40 healthy donors, 31 pancreatic carcinoma patients, and 11 patients treated with gemcitabine were measured by a novel enzyme-linked immunoadsorbent assay. HPR1 expression in tumors was analyzed by immunohistochemical staining. Patient overall survival time was determined according to the Kaplan-Meier method, and their difference was evaluated by the log-rank test. A P value<0.05 was considered statistically significant.",
"The mean serum HPR1 activity in pancreatic carcinoma patients was 439+/-14 units/mL, compared with 190+/-4 units/mL in the control serum samples from healthy donors. Serum HPR1 levels were significantly higher in patients with HPR1-positive tumors (660+/-62 units/mL) compared with those with HPR1-negative tumors (241+/-14 units/mL). The mean survival of 19 pancreatic carcinoma patients with serum HPR1 activity>300 units/mL was 7.9+/-0.2 months, whereas the mean survival of 12 patients with serum HPR1 activity<300 units/mL was 13.3+/-0.6 months. A Kaplan-Meier plot of the patient survival curve followed by log-rank test revealed that patients in the high serum HPR1 group had a significantly shorter survival compared with those in the low serum HPR1 group. Mean serum HPR1 activity decreased by 64% in 11 pancreatic carcinoma patients after 2 weeks of treatment with gemcitabine."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Aged, 80 and over",
"Carcinoma",
"Case-Control Studies",
"Enzyme-Linked Immunosorbent Assay",
"Female",
"Gene Expression Profiling",
"Glucuronidase",
"Humans",
"Immunohistochemistry",
"Male",
"Middle Aged",
"Pancreatic Neoplasms",
"Prognosis",
"Survival Analysis",
"Up-Regulation"
]
} | Serum HPR1 activity in pancreatic carcinoma patients was found to be significantly elevated, in particular in those with HPR1-positive tumors. Increased serum HPR1 activity was associated with a shorter survival in patients with pancreatic carcinoma patients. | yes | [
{
"from": "human",
"value": "Question: Are elevated serum heparanase-1 levels in patients with pancreatic carcinoma associated with poor survival?\nContext: {'contexts': ['It has previously been shown that heparanase-1 (HPR1), an endoglycosidase, is up-regulated in pancreatic carcinoma. The purpose of this study was to test whether serum HPR1 levels in pancreatic carcinoma patients are elevated, and whether higher serum HPR1 levels are associated with a shortened survival.', 'Serum HPR1 levels in 40 healthy donors, 31 pancreatic carcinoma patients, and 11 patients treated with gemcitabine were measured by a novel enzyme-linked immunoadsorbent assay. HPR1 expression in tumors was analyzed by immunohistochemical staining. Patient overall survival time was determined according to the Kaplan-Meier method, and their difference was evaluated by the log-rank test. A P value<0.05 was considered statistically significant.', 'The mean serum HPR1 activity in pancreatic carcinoma patients was 439+/-14 units/mL, compared with 190+/-4 units/mL in the control serum samples from healthy donors. Serum HPR1 levels were significantly higher in patients with HPR1-positive tumors (660+/-62 units/mL) compared with those with HPR1-negative tumors (241+/-14 units/mL). The mean survival of 19 pancreatic carcinoma patients with serum HPR1 activity>300 units/mL was 7.9+/-0.2 months, whereas the mean survival of 12 patients with serum HPR1 activity<300 units/mL was 13.3+/-0.6 months. A Kaplan-Meier plot of the patient survival curve followed by log-rank test revealed that patients in the high serum HPR1 group had a significantly shorter survival compared with those in the low serum HPR1 group. Mean serum HPR1 activity decreased by 64% in 11 pancreatic carcinoma patients after 2 weeks of treatment with gemcitabine.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Aged, 80 and over', 'Carcinoma', 'Case-Control Studies', 'Enzyme-Linked Immunosorbent Assay', 'Female', 'Gene Expression Profiling', 'Glucuronidase', 'Humans', 'Immunohistochemistry', 'Male', 'Middle Aged', 'Pancreatic Neoplasms', 'Prognosis', 'Survival Analysis', 'Up-Regulation']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,374,022 | Does encasement of bedding improve asthma in atopic adult asthmatics? | {
"contexts": [
"We evaluated the impact of impermeable bed covers on asthma in asthmatics with clinically relevant house dust mite (HDM) sensitization.",
"The study included 32 HDM-sensitized asthmatics in whom HDM allergy was considered as a significant factor in their asthma. They were randomized into either an intervention group whose bedding was encased with impermeable covers, or a control group who received cotton covers. Before and 3 and 6 months after encasement, dust samples were collected from the bedding and assayed for Der p 1. Clinical outcomes included quality of life, lung function, bronchial reactivity to methacholine, symptoms, medications and peak flow rates.",
"Baseline Der p 1 levels in both the active and the placebo groups were comparable and high (19.2 vs 18.9 microg/g of dust). There was a significant reduction in Der p 1 levels in the active group after 6 months, but not in the placebo group (7.3 vs 21.9 microg/g of dust). Quality of life improved significantly in both the intervention and control groups, but there was no significant difference in the improvements between the groups. There was no significant change in lung function, symptoms, and requirements for medications."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Antigens, Dermatophagoides",
"Arthropod Proteins",
"Asthma",
"Beds",
"Cysteine Endopeptidases",
"Dermatophagoides pteronyssinus",
"Dust",
"Female",
"Humans",
"Male",
"Quality of Life"
]
} | Encasement of bedding significantly reduced the Der p 1 levels. However, this was not sufficient to produce worthwhile clinical improvement in those in whom dust mite avoidance might well have been recommended as part of their clinical management. | no | [
{
"from": "human",
"value": "Question: Does encasement of bedding improve asthma in atopic adult asthmatics?\nContext: {'contexts': ['We evaluated the impact of impermeable bed covers on asthma in asthmatics with clinically relevant house dust mite (HDM) sensitization.', 'The study included 32 HDM-sensitized asthmatics in whom HDM allergy was considered as a significant factor in their asthma. They were randomized into either an intervention group whose bedding was encased with impermeable covers, or a control group who received cotton covers. Before and 3 and 6 months after encasement, dust samples were collected from the bedding and assayed for Der p 1. Clinical outcomes included quality of life, lung function, bronchial reactivity to methacholine, symptoms, medications and peak flow rates.', 'Baseline Der p 1 levels in both the active and the placebo groups were comparable and high (19.2 vs 18.9 microg/g of dust). There was a significant reduction in Der p 1 levels in the active group after 6 months, but not in the placebo group (7.3 vs 21.9 microg/g of dust). Quality of life improved significantly in both the intervention and control groups, but there was no significant difference in the improvements between the groups. There was no significant change in lung function, symptoms, and requirements for medications.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Antigens, Dermatophagoides', 'Arthropod Proteins', 'Asthma', 'Beds', 'Cysteine Endopeptidases', 'Dermatophagoides pteronyssinus', 'Dust', 'Female', 'Humans', 'Male', 'Quality of Life']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
16,385,089 | Does family history of stroke predict risk of stroke after transient ischemic attack? | {
"contexts": [
"Animal models suggest a genetic contribution to cerebral susceptibility to ischemia. Family history of stroke (FHxstroke) is a risk factor for ischemic stroke, but there is significant confounding by heritability of hypertension and other intermediate phenotypes, and it is uncertain whether genetic factors have a direct independent influence on cerebral susceptibility to ischemia in man.",
"We related detailed FHxstroke to baseline characteristics and subsequent risk of stroke in 2 population-based incidence studies and a consecutive hospital-referred series of patients with recent transient ischemic attack (TIA).",
"In none of the cohorts or the pooled data (757 patients; 5515 patient years follow-up; 200 ischemic strokes; 126 myocardial infarctions [MIs]) did FHxstroke predict ischemic stroke (odds ratio [OR], 0.87; 95% CI, 0.57 to 1.32). No associations were revealed by analyses stratified by age or hypertension in the proband, FHx(stroke) in parents versus siblings, number of affected relatives, or their age at stroke. FHxstroke was unrelated to presence of ischemic lesions on baseline computed tomography (OR, 0.96; 0.52 to 1.76) or risk of MI during follow-up. There was no bias attributable to any relationship between FHxstroke and risk factor control or medication."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Brain Ischemia",
"Cohort Studies",
"Disease-Free Survival",
"Family Health",
"Female",
"Humans",
"Ischemic Attack, Transient",
"Male",
"Middle Aged",
"Myocardial Infarction",
"Odds Ratio",
"Phenotype",
"Prognosis",
"Risk",
"Risk Factors",
"Stroke",
"Time Factors",
"Tomography, X-Ray Computed"
]
} | Family history of stroke does not predict risk of ischemic stroke after TIA. | no | [
{
"from": "human",
"value": "Question: Does family history of stroke predict risk of stroke after transient ischemic attack?\nContext: {'contexts': ['Animal models suggest a genetic contribution to cerebral susceptibility to ischemia. Family history of stroke (FHxstroke) is a risk factor for ischemic stroke, but there is significant confounding by heritability of hypertension and other intermediate phenotypes, and it is uncertain whether genetic factors have a direct independent influence on cerebral susceptibility to ischemia in man.', 'We related detailed FHxstroke to baseline characteristics and subsequent risk of stroke in 2 population-based incidence studies and a consecutive hospital-referred series of patients with recent transient ischemic attack (TIA).', 'In none of the cohorts or the pooled data (757 patients; 5515 patient years follow-up; 200 ischemic strokes; 126 myocardial infarctions [MIs]) did FHxstroke predict ischemic stroke (odds ratio [OR], 0.87; 95% CI, 0.57 to 1.32). No associations were revealed by analyses stratified by age or hypertension in the proband, FHx(stroke) in parents versus siblings, number of affected relatives, or their age at stroke. FHxstroke was unrelated to presence of ischemic lesions on baseline computed tomography (OR, 0.96; 0.52 to 1.76) or risk of MI during follow-up. There was no bias attributable to any relationship between FHxstroke and risk factor control or medication.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Brain Ischemia', 'Cohort Studies', 'Disease-Free Survival', 'Family Health', 'Female', 'Humans', 'Ischemic Attack, Transient', 'Male', 'Middle Aged', 'Myocardial Infarction', 'Odds Ratio', 'Phenotype', 'Prognosis', 'Risk', 'Risk Factors', 'Stroke', 'Time Factors', 'Tomography, X-Ray Computed']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
16,369,812 | Is macrophage migration inhibition factor elevated in pregnancy , but not to a greater extent in preeclampsia? | {
"contexts": [
"Maternal serum concentrations of macrophage migration inhibitory factor (MIF) have recently been reported to be elevated in cases with preeclampsia. These findings may be important in increasing our understanding of the underlying events leading to the development of preeclampsia, as this cytokine is also expressed in the placenta, where it has been shown to possess immunemodulatory activities. For this reason we attempted to independently verify this report.",
"Plasma levels of MIF were assessed by ELISA in plasma samples collected from normal healthy male and female blood donors (n=20 per group), as well as healthy normal pregnant women in all three trimesters of pregnancy (n=60). In addition, MIF levels were examined from cases with mild and severe preeclampsia (n=20 per study cohort) and matched normotensive pregnancies (n=20).",
"MIF levels were found to be elevated in pregnancy (median=10.1 ng/ml) when compared to non-pregnant controls (median=1.7 ng/ml). A moderate, but not significant, elevation was found to occur from the first to the third trimester of pregnancy. No significant difference was found to occur between the two preeclampsia study groups when compared to the normotensive control group."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Blood Donors",
"Case-Control Studies",
"Female",
"HELLP Syndrome",
"Humans",
"Macrophage Migration-Inhibitory Factors",
"Male",
"Pre-Eclampsia",
"Pregnancy"
]
} | Our data suggest that circulatory MIF concentrations are elevated throughout pregnancy, but are not further increased in preeclampsia. | yes | [
{
"from": "human",
"value": "Question: Is macrophage migration inhibition factor elevated in pregnancy , but not to a greater extent in preeclampsia?\nContext: {'contexts': ['Maternal serum concentrations of macrophage migration inhibitory factor (MIF) have recently been reported to be elevated in cases with preeclampsia. These findings may be important in increasing our understanding of the underlying events leading to the development of preeclampsia, as this cytokine is also expressed in the placenta, where it has been shown to possess immunemodulatory activities. For this reason we attempted to independently verify this report.', 'Plasma levels of MIF were assessed by ELISA in plasma samples collected from normal healthy male and female blood donors (n=20 per group), as well as healthy normal pregnant women in all three trimesters of pregnancy (n=60). In addition, MIF levels were examined from cases with mild and severe preeclampsia (n=20 per study cohort) and matched normotensive pregnancies (n=20).', 'MIF levels were found to be elevated in pregnancy (median=10.1 ng/ml) when compared to non-pregnant controls (median=1.7 ng/ml). A moderate, but not significant, elevation was found to occur from the first to the third trimester of pregnancy. No significant difference was found to occur between the two preeclampsia study groups when compared to the normotensive control group.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Blood Donors', 'Case-Control Studies', 'Female', 'HELLP Syndrome', 'Humans', 'Macrophage Migration-Inhibitory Factors', 'Male', 'Pre-Eclampsia', 'Pregnancy']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,392,028 | Is ileum resection the most predictive factor for osteoporosis in patients with Crohn 's disease? | {
"contexts": [
"Crohn's disease is associated with a host of factors potentially increasing the risk for osteoporosis and fractures. The aim of our study was to identify the most predictive factors for skeletal pathology in this patients.",
"Using a cross-sectional study design, 146 randomly selected patients with Crohn's disease of variable disease activity who were given standard therapy to control disease activity, including glucocorticoids, and who attended the outpatient clinic of the Gastroenterology Unit on regular follow-up visits were studied. Bone mineral density (BMD) measurements and lateral X-rays of the spine were performed, and biochemical parameters of bone turnover, gonadal hormones and C-reactive protein (CRP) as markers of disease activity were measured in all patients.",
"There were 61 men and 85 women, with a mean age of 43 years and mean disease duration of 20 years. The majority of patients (86%) had been treated with glucocorticoids at some stage during their illness at a median dose of 7.5 mg/day, 43% were currently using these agents and 66% had undergone an intestinal resection. Twenty-one percent of patients had below-normal 25-hydroxy vitamin D levels. Osteoporosis was documented in 26% of patients, predominantly at the femoral neck, but also at the lumbar spine or at both sites; osteopenia was documented in 45% of patients. Prevalence of vertebral and non-vertebral fractures was, respectively, 6% and 12%. Ileum resection was the most predictive factor for osteoporosis: RR 3.84 (CI 1.24-9.77, p=0.018), followed by age: RR 1.05 (CI 1.02-1.08, p<0.001) and current or past glucocorticoid use: RR 1.94 (CI 0.92-4.10, p=0.08)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Aged",
"Biomarkers",
"Bone Density",
"Bone Remodeling",
"C-Reactive Protein",
"Crohn Disease",
"Cross-Sectional Studies",
"Female",
"Femur Neck",
"Fractures, Bone",
"Glucocorticoids",
"Gonadal Hormones",
"Humans",
"Ileum",
"Lumbar Vertebrae",
"Male",
"Middle Aged",
"Netherlands",
"Osteoporosis",
"Prevalence",
"Radiography",
"Risk Factors",
"Vitamin D Deficiency"
]
} | Our data suggest that in patients with Crohn's disease, the risk of osteoporosis is best predicted by a history of ileum resection. | yes | [
{
"from": "human",
"value": "Question: Is ileum resection the most predictive factor for osteoporosis in patients with Crohn 's disease?\nContext: {'contexts': [\"Crohn's disease is associated with a host of factors potentially increasing the risk for osteoporosis and fractures. The aim of our study was to identify the most predictive factors for skeletal pathology in this patients.\", \"Using a cross-sectional study design, 146 randomly selected patients with Crohn's disease of variable disease activity who were given standard therapy to control disease activity, including glucocorticoids, and who attended the outpatient clinic of the Gastroenterology Unit on regular follow-up visits were studied. Bone mineral density (BMD) measurements and lateral X-rays of the spine were performed, and biochemical parameters of bone turnover, gonadal hormones and C-reactive protein (CRP) as markers of disease activity were measured in all patients.\", 'There were 61 men and 85 women, with a mean age of 43 years and mean disease duration of 20 years. The majority of patients (86%) had been treated with glucocorticoids at some stage during their illness at a median dose of 7.5 mg/day, 43% were currently using these agents and 66% had undergone an intestinal resection. Twenty-one percent of patients had below-normal 25-hydroxy vitamin D levels. Osteoporosis was documented in 26% of patients, predominantly at the femoral neck, but also at the lumbar spine or at both sites; osteopenia was documented in 45% of patients. Prevalence of vertebral and non-vertebral fractures was, respectively, 6% and 12%. Ileum resection was the most predictive factor for osteoporosis: RR 3.84 (CI 1.24-9.77, p=0.018), followed by age: RR 1.05 (CI 1.02-1.08, p<0.001) and current or past glucocorticoid use: RR 1.94 (CI 0.92-4.10, p=0.08).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Aged', 'Biomarkers', 'Bone Density', 'Bone Remodeling', 'C-Reactive Protein', 'Crohn Disease', 'Cross-Sectional Studies', 'Female', 'Femur Neck', 'Fractures, Bone', 'Glucocorticoids', 'Gonadal Hormones', 'Humans', 'Ileum', 'Lumbar Vertebrae', 'Male', 'Middle Aged', 'Netherlands', 'Osteoporosis', 'Prevalence', 'Radiography', 'Risk Factors', 'Vitamin D Deficiency']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,394,685 | Is lorazepam an independent risk factor for transitioning to delirium in intensive care unit patients? | {
"contexts": [
"Delirium has recently been shown as a predictor of death, increased cost, and longer duration of stay in ventilated patients. Sedative and analgesic medications relieve anxiety and pain but may contribute to patients' transitioning into delirium.",
"In this cohort study, the authors designed a priori an investigation to determine whether sedative and analgesic medications independently increased the probability of daily transition to delirium. Markov regression modeling (adjusting for 11 covariates) was used in the evaluation of 198 mechanically ventilated patients to determine the probability of daily transition to delirium as a function of sedative and analgesic dose administration during the previous 24 h.",
"Lorazepam was an independent risk factor for daily transition to delirium (odds ratio, 1.2 [95% confidence interval, 1.1-1.4]; P = 0.003), whereas fentanyl, morphine, and propofol were associated with higher but not statistically significant odds ratios. Increasing age and Acute Physiology and Chronic Health Evaluation II scores were also independent predictors of transitioning to delirium (multivariable P values < 0.05)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"APACHE",
"Age Factors",
"Aged",
"Analgesics, Opioid",
"Antipsychotic Agents",
"Coma",
"Critical Care",
"Delirium",
"Female",
"Humans",
"Hypnotics and Sedatives",
"Length of Stay",
"Lorazepam",
"Male",
"Markov Chains",
"Middle Aged",
"Risk Factors",
"Sex Factors",
"Treatment Outcome"
]
} | Lorazepam administration is an important and potentially modifiable risk factor for transitioning into delirium even after adjusting for relevant covariates. | yes | [
{
"from": "human",
"value": "Question: Is lorazepam an independent risk factor for transitioning to delirium in intensive care unit patients?\nContext: {'contexts': [\"Delirium has recently been shown as a predictor of death, increased cost, and longer duration of stay in ventilated patients. Sedative and analgesic medications relieve anxiety and pain but may contribute to patients' transitioning into delirium.\", 'In this cohort study, the authors designed a priori an investigation to determine whether sedative and analgesic medications independently increased the probability of daily transition to delirium. Markov regression modeling (adjusting for 11 covariates) was used in the evaluation of 198 mechanically ventilated patients to determine the probability of daily transition to delirium as a function of sedative and analgesic dose administration during the previous 24 h.', 'Lorazepam was an independent risk factor for daily transition to delirium (odds ratio, 1.2 [95% confidence interval, 1.1-1.4]; P = 0.003), whereas fentanyl, morphine, and propofol were associated with higher but not statistically significant odds ratios. Increasing age and Acute Physiology and Chronic Health Evaluation II scores were also independent predictors of transitioning to delirium (multivariable P values < 0.05).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['APACHE', 'Age Factors', 'Aged', 'Analgesics, Opioid', 'Antipsychotic Agents', 'Coma', 'Critical Care', 'Delirium', 'Female', 'Humans', 'Hypnotics and Sedatives', 'Length of Stay', 'Lorazepam', 'Male', 'Markov Chains', 'Middle Aged', 'Risk Factors', 'Sex Factors', 'Treatment Outcome']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,372,334 | Do e-cadherin polymorphisms and haplotypes influence risk for prostate cancer? | {
"contexts": [
"The E-cadherin (CDH1) gene has been implicated in prostate cancer (PCA) risk, however, the exact mechanism is unknown. Several polymorphisms, such as the C/A variant -160 base pairs from the transcription start site, in the CDH1 gene promoter region have been associated with cancer risk, mainly in European descent populations.",
"We screened the entire coding region and 3.0 kilobases of the CDH1 promoter for polymorphisms in 48 African Americans using dHPLC. Twenty-one (21) polymorphisms were observed. Four polymorphisms, including -160C/A, were genotyped in a genetic association study using incident PCA cases (N = 427) and unaffected controls (N = 337) of similar age from three different ethnic groups consisting of African Americans, Jamaicans, and European Americans.",
"We observed a significantly higher frequency of the -160A allele among European American PCA patients (27.5%) compared to the control group (19.7%) (P = 0.04). More importantly, among men of European ancestry under the age of 65 who possess the -160 A allele there was over three times increased risk for prostate cancer (P = 0.05). Also, the AACT haplotype bearing the -160A allele was significantly associated with PCA in European Americans (P = 0.04)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"African Americans",
"Aged",
"Cadherins",
"Exons",
"Genetic Predisposition to Disease",
"Humans",
"Introns",
"Male",
"Middle Aged",
"Polymorphism, Genetic",
"Promoter Regions, Genetic",
"Prostate-Specific Antigen",
"Prostatic Neoplasms",
"Risk Factors",
"Sequence Deletion",
"United States"
]
} | Our data indicate that CDH1 likely is a low-penetrant PCA susceptibility gene, however, population differences in linkage disequilibrium within the CDH1 gene region may influence the effect of susceptibility alleles such as -160A. | yes | [
{
"from": "human",
"value": "Question: Do e-cadherin polymorphisms and haplotypes influence risk for prostate cancer?\nContext: {'contexts': ['The E-cadherin (CDH1) gene has been implicated in prostate cancer (PCA) risk, however, the exact mechanism is unknown. Several polymorphisms, such as the C/A variant -160 base pairs from the transcription start site, in the CDH1 gene promoter region have been associated with cancer risk, mainly in European descent populations.', 'We screened the entire coding region and 3.0 kilobases of the CDH1 promoter for polymorphisms in 48 African Americans using dHPLC. Twenty-one (21) polymorphisms were observed. Four polymorphisms, including -160C/A, were genotyped in a genetic association study using incident PCA cases (N = 427) and unaffected controls (N = 337) of similar age from three different ethnic groups consisting of African Americans, Jamaicans, and European Americans.', 'We observed a significantly higher frequency of the -160A allele among European American PCA patients (27.5%) compared to the control group (19.7%) (P = 0.04). More importantly, among men of European ancestry under the age of 65 who possess the -160 A allele there was over three times increased risk for prostate cancer (P = 0.05). Also, the AACT haplotype bearing the -160A allele was significantly associated with PCA in European Americans (P = 0.04).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['African Americans', 'Aged', 'Cadherins', 'Exons', 'Genetic Predisposition to Disease', 'Humans', 'Introns', 'Male', 'Middle Aged', 'Polymorphism, Genetic', 'Promoter Regions, Genetic', 'Prostate-Specific Antigen', 'Prostatic Neoplasms', 'Risk Factors', 'Sequence Deletion', 'United States']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,400,048 | Do body mass index and waist circumference both contribute to differences in insulin-mediated glucose disposal in nondiabetic adults? | {
"contexts": [
"Overweight and obese individuals are more likely to be insulin resistant and at increased risk of adverse clinical outcomes. Questions remain as to whether waist circumference (WC) or body mass index (BMI) most effectively identifies insulin-resistant individuals.",
"This study quantified insulin-mediated glucose uptake (IMGU) in 330 apparently healthy volunteers and compared the relation between this value and measurements of WC and BMI.",
"IMGU was quantified via determination of the steady-state plasma glucose (SSPG) concentration during the insulin-suppression test. Differences in SSPG concentrations due to variations in WC within a given BMI category, as well as those due to differences in BMI within a given WC classification, were then compared.",
"BMI and WC correlated with each other (r = 0.78, P < 0.001) and equally with SSPG concentrations (r = 0.58 and 0.57, respectively; P < 0.001). When stratified by BMI, abdominally obese subjects within the overweight BMI category had higher SSPG concentrations than did those with a normal WC (P < 0.05). When classified by WC, subjects in the overweight BMI category had greater SSPG concentrations than did subjects in the normal BMI category within the normal WC category (P < 0.01), as did subjects in the obese BMI category in comparison with subjects in the overweight BMI category within the obese WC category (P < 0.01)."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Abdominal Fat",
"Blood Glucose",
"Body Mass Index",
"Female",
"Glucose",
"Health Surveys",
"Humans",
"Insulin",
"Insulin Resistance",
"Male",
"Middle Aged",
"Obesity",
"Risk Factors",
"Waist-Hip Ratio"
]
} | The more overweight or obese a person, the greater the degree of insulin resistance; differences in adiposity accounted for approximately one-third of the variation in IMGU, irrespective of the index used. Furthermore, there was no difference in the relation between the degree of insulin resistance and either index of adiposity. | yes | [
{
"from": "human",
"value": "Question: Do body mass index and waist circumference both contribute to differences in insulin-mediated glucose disposal in nondiabetic adults?\nContext: {'contexts': ['Overweight and obese individuals are more likely to be insulin resistant and at increased risk of adverse clinical outcomes. Questions remain as to whether waist circumference (WC) or body mass index (BMI) most effectively identifies insulin-resistant individuals.', 'This study quantified insulin-mediated glucose uptake (IMGU) in 330 apparently healthy volunteers and compared the relation between this value and measurements of WC and BMI.', 'IMGU was quantified via determination of the steady-state plasma glucose (SSPG) concentration during the insulin-suppression test. Differences in SSPG concentrations due to variations in WC within a given BMI category, as well as those due to differences in BMI within a given WC classification, were then compared.', 'BMI and WC correlated with each other (r = 0.78, P < 0.001) and equally with SSPG concentrations (r = 0.58 and 0.57, respectively; P < 0.001). When stratified by BMI, abdominally obese subjects within the overweight BMI category had higher SSPG concentrations than did those with a normal WC (P < 0.05). When classified by WC, subjects in the overweight BMI category had greater SSPG concentrations than did subjects in the normal BMI category within the normal WC category (P < 0.01), as did subjects in the obese BMI category in comparison with subjects in the overweight BMI category within the obese WC category (P < 0.01).'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Abdominal Fat', 'Blood Glucose', 'Body Mass Index', 'Female', 'Glucose', 'Health Surveys', 'Humans', 'Insulin', 'Insulin Resistance', 'Male', 'Middle Aged', 'Obesity', 'Risk Factors', 'Waist-Hip Ratio']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,385,301 | Do cTLA4Ig introduced by adenovirus vector locally to prolong the survival of xenogeneic skin grafts on rat burn wounds? | {
"contexts": [
"The purpose of this study was to explore an applicable approach for prolonging the survival of heterogenetic skin grafts on burn wounds with CTLA4Ig.",
"An adenovirus vector named Ad-CTLA4Ig, which could express human CTLA4Ig fusion protein, was constructed. Infecting and replicating in 293 cells, more Ad-CTLA4Ig and recombinant human CTLA4Ig (rhCTLA4Ig) were prepared, respectively. In a rat flame thermal injury model, the effect of rhCTLA4Ig on survival time of human skin graft on the eschar-excised rat burn wound was observed. Meanwhile, the efficiency of Ad-CTLA4Ig infecting cultured skin fibroblasts, keratinocytes, and partial-thickness skin samples were checked by CTLA4Ig expression essay. Then, the Ad-CTLA4Ig was administered locally on the eschar-excised wound and dermis of the skin graft, and the survival time of the human skin graft on burn wound was measured. The influence of the systemic immune function by rhCTLA4Ig and Ad-CTLA4Ig were also determined.",
"The prepared rhCTLA4Ig from the supernatant of Ad-CTLA4Ig-infected 293 cells was verified by sodium dodecyl sulfate polyacrylamide gel electrophoresis sodium dodecyl sulfate poly-acrylamide gel electrophoresis and Western blot. It was found that CTLA4Ig could significantly prolong the xenogeneic skin graft survival in a dosage-dependent manner. Interestingly, the survival time was longer when CTLA4Ig was used 24 hours posttransplantation than that at hour 0. The expression of CTLA4Ig could be observed in the cultured skin fibroblasts, keratinocytes, and skin pieces soon after Ad-CTLA4Ig transfection, as demonstrated by either immunocellular chemistry or immunohistochemistry assay. When Ad-CTLA4Ig was locally administered during skin transplantation on burn wound, the survival time was increased from 7.9 days of control group to 21.6 days, whereas the systemic immune function was not affected."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Abatacept",
"Adenoviridae",
"Animals",
"Burns",
"Cells, Cultured",
"Genetic Vectors",
"Graft Rejection",
"Graft Survival",
"Humans",
"Immunoconjugates",
"Immunohistochemistry",
"Immunologic Factors",
"Keratinocytes",
"Rats",
"Rats, Wistar",
"Recombinant Proteins",
"Skin Transplantation",
"Transfection",
"Transplantation, Heterologous"
]
} | Administration of Ad-CTLA4Ig locally could prolong the survival time of xenogeneic skin graft on burn wound without significantly influencing the systemic immune function. | yes | [
{
"from": "human",
"value": "Question: Do cTLA4Ig introduced by adenovirus vector locally to prolong the survival of xenogeneic skin grafts on rat burn wounds?\nContext: {'contexts': ['The purpose of this study was to explore an applicable approach for prolonging the survival of heterogenetic skin grafts on burn wounds with CTLA4Ig.', 'An adenovirus vector named Ad-CTLA4Ig, which could express human CTLA4Ig fusion protein, was constructed. Infecting and replicating in 293 cells, more Ad-CTLA4Ig and recombinant human CTLA4Ig (rhCTLA4Ig) were prepared, respectively. In a rat flame thermal injury model, the effect of rhCTLA4Ig on survival time of human skin graft on the eschar-excised rat burn wound was observed. Meanwhile, the efficiency of Ad-CTLA4Ig infecting cultured skin fibroblasts, keratinocytes, and partial-thickness skin samples were checked by CTLA4Ig expression essay. Then, the Ad-CTLA4Ig was administered locally on the eschar-excised wound and dermis of the skin graft, and the survival time of the human skin graft on burn wound was measured. The influence of the systemic immune function by rhCTLA4Ig and Ad-CTLA4Ig were also determined.', 'The prepared rhCTLA4Ig from the supernatant of Ad-CTLA4Ig-infected 293 cells was verified by sodium dodecyl sulfate polyacrylamide gel electrophoresis sodium dodecyl sulfate poly-acrylamide gel electrophoresis and Western blot. It was found that CTLA4Ig could significantly prolong the xenogeneic skin graft survival in a dosage-dependent manner. Interestingly, the survival time was longer when CTLA4Ig was used 24 hours posttransplantation than that at hour 0. The expression of CTLA4Ig could be observed in the cultured skin fibroblasts, keratinocytes, and skin pieces soon after Ad-CTLA4Ig transfection, as demonstrated by either immunocellular chemistry or immunohistochemistry assay. When Ad-CTLA4Ig was locally administered during skin transplantation on burn wound, the survival time was increased from 7.9 days of control group to 21.6 days, whereas the systemic immune function was not affected.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Abatacept', 'Adenoviridae', 'Animals', 'Burns', 'Cells, Cultured', 'Genetic Vectors', 'Graft Rejection', 'Graft Survival', 'Humans', 'Immunoconjugates', 'Immunohistochemistry', 'Immunologic Factors', 'Keratinocytes', 'Rats', 'Rats, Wistar', 'Recombinant Proteins', 'Skin Transplantation', 'Transfection', 'Transplantation, Heterologous']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,378,715 | Are beta-Catenin mutation and its nuclear localization confirmed to be frequent causes of Wnt signaling pathway activation in pilomatricomas? | {
"contexts": [
"beta-Catenin has been shown to play an important role in the formation of hair follicle-related tumors, including pilomatricomas. Several investigators have shown that beta-catenin gene mutation is observed in pilomatricomas. However, the relationship between the pattern of beta-catenin localization in the cell and beta-catenin gene mutation is still controversial.",
"This work was performed to determine the frequency of beta-catenin nuclear localization in pilomatricoma, the relationship between the pattern of beta-catenin localization and beta-catenin mutation, and the involvement of APC mutation.",
"Typical 32 pilomatricomas were examined for beta-catenin expression by immunostaining. Genomic DNA was extracted, amplified and sequenced from 23 pilomaticomas with nuclear beta-catenin staining and 4 pilomaticomas without nuclear beta-catenin staining. Mutations of beta-catenin gene were confirmed by subcloning assay and restriction endonuclease assay.",
"Using immunostaining, we found that 81% (26/32) of pilomatricomas displayed nuclear beta-catenin staining in basophilic cells. Sequence analysis revealed that 61% (14/23) contained mutations in exon 3 of beta-catenin. However, no mutations were detected in 4 pilomaticomas without beta-catenin nuclear staining. Detected mutations were adjacent to or abolished well-known regulatory phosphorylation sites of beta-catenin. APC gene mutations were not detected in 27 pilomatricomas with/without beta-catenin nuclear staining."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Amino Acid Sequence",
"Cell Nucleus",
"Child",
"Child, Preschool",
"Exons",
"Female",
"Genes, APC",
"Hair Follicle",
"Humans",
"Male",
"Middle Aged",
"Molecular Sequence Data",
"Pilomatrixoma",
"Point Mutation",
"Signal Transduction",
"Skin Neoplasms",
"Wnt Proteins",
"beta Catenin"
]
} | These results confirmed that beta-catenin mutation and its nuclear localization are frequent causes of Wnt signaling pathway activation and suggested that beta-catenin activation mutations contribute to tumorigenesis of pilomatricomas. | yes | [
{
"from": "human",
"value": "Question: Are beta-Catenin mutation and its nuclear localization confirmed to be frequent causes of Wnt signaling pathway activation in pilomatricomas?\nContext: {'contexts': ['beta-Catenin has been shown to play an important role in the formation of hair follicle-related tumors, including pilomatricomas. Several investigators have shown that beta-catenin gene mutation is observed in pilomatricomas. However, the relationship between the pattern of beta-catenin localization in the cell and beta-catenin gene mutation is still controversial.', 'This work was performed to determine the frequency of beta-catenin nuclear localization in pilomatricoma, the relationship between the pattern of beta-catenin localization and beta-catenin mutation, and the involvement of APC mutation.', 'Typical 32 pilomatricomas were examined for beta-catenin expression by immunostaining. Genomic DNA was extracted, amplified and sequenced from 23 pilomaticomas with nuclear beta-catenin staining and 4 pilomaticomas without nuclear beta-catenin staining. Mutations of beta-catenin gene were confirmed by subcloning assay and restriction endonuclease assay.', 'Using immunostaining, we found that 81% (26/32) of pilomatricomas displayed nuclear beta-catenin staining in basophilic cells. Sequence analysis revealed that 61% (14/23) contained mutations in exon 3 of beta-catenin. However, no mutations were detected in 4 pilomaticomas without beta-catenin nuclear staining. Detected mutations were adjacent to or abolished well-known regulatory phosphorylation sites of beta-catenin. APC gene mutations were not detected in 27 pilomatricomas with/without beta-catenin nuclear staining.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Amino Acid Sequence', 'Cell Nucleus', 'Child', 'Child, Preschool', 'Exons', 'Female', 'Genes, APC', 'Hair Follicle', 'Humans', 'Male', 'Middle Aged', 'Molecular Sequence Data', 'Pilomatrixoma', 'Point Mutation', 'Signal Transduction', 'Skin Neoplasms', 'Wnt Proteins', 'beta Catenin']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,398,736 | Does taiwan experience suggest that RhD typing for blood transfusion is unnecessary in southeast Asian populations? | {
"contexts": [
"The high frequency of RhD (D) antigen among Taiwanese persons (99.67%) often imposes unnecessary risks of under-transfusion on D- patients awaiting D- blood. Also because of the rare occurrence of anti-D among Taiwanese persons, routine pretransfusion D typing has been discontinued in the Mackay Memorial Hospital since 1988. This report is the retrospective evaluation of the outcome of abolishing RhD typing for Taiwanese.",
"More than 10 years of alloantibody data at Mackay Memorial Hospital Blood Bank were reviewed. The cases with anti-D were further used to analyze the potency of D antigen and to observe whether there were differences in the incidence of anti-D before and after discontinuation of routine D typing among Taiwanese individuals.",
"The incidence of anti-D before and after discontinuation of routine pretransfusion D typing has remained unchanged. The immunogenicity of D and \"Mi(a)\" in Taiwanese persons is found to be similar. In terms of opportunity for immunization, however, the \"Mi(a)\" antigen (phenotype frequency 7.3% in Taiwanese persons) has become the most important blood group antigen in Taiwan."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Asian Continental Ancestry Group",
"Blood Group Incompatibility",
"Blood Grouping and Crossmatching",
"Humans",
"Incidence",
"Isoantibodies",
"Retrospective Studies",
"Rh-Hr Blood-Group System",
"Rho(D) Immune Globulin",
"Taiwan"
]
} | The results strongly support the exclusion of D typing from routine compatibility testing for individuals of Taiwanese origin. Because the low incidence of D- and relatively high incidence of "Mi(a)"+ phenotypes are common findings throughout southeast Asia, and because a population genetic study revealed that the Taiwanese people are genetically related to southern Asian populations, it is suggested that RhD typing for blood transfusion is unnecessary among southeast Asian populations. | yes | [
{
"from": "human",
"value": "Question: Does taiwan experience suggest that RhD typing for blood transfusion is unnecessary in southeast Asian populations?\nContext: {'contexts': ['The high frequency of RhD (D) antigen among Taiwanese persons (99.67%) often imposes unnecessary risks of under-transfusion on D- patients awaiting D- blood. Also because of the rare occurrence of anti-D among Taiwanese persons, routine pretransfusion D typing has been discontinued in the Mackay Memorial Hospital since 1988. This report is the retrospective evaluation of the outcome of abolishing RhD typing for Taiwanese.', 'More than 10 years of alloantibody data at Mackay Memorial Hospital Blood Bank were reviewed. The cases with anti-D were further used to analyze the potency of D antigen and to observe whether there were differences in the incidence of anti-D before and after discontinuation of routine D typing among Taiwanese individuals.', 'The incidence of anti-D before and after discontinuation of routine pretransfusion D typing has remained unchanged. The immunogenicity of D and \"Mi(a)\" in Taiwanese persons is found to be similar. In terms of opportunity for immunization, however, the \"Mi(a)\" antigen (phenotype frequency 7.3% in Taiwanese persons) has become the most important blood group antigen in Taiwan.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Asian Continental Ancestry Group', 'Blood Group Incompatibility', 'Blood Grouping and Crossmatching', 'Humans', 'Incidence', 'Isoantibodies', 'Retrospective Studies', 'Rh-Hr Blood-Group System', 'Rho(D) Immune Globulin', 'Taiwan']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,387,801 | Does leflunomide prevent alveolar fluid clearance inhibition by respiratory syncytial virus? | {
"contexts": [
"Previously, we demonstrated that intranasal infection of BALB/c mice with respiratory syncytial virus (RSV) resulted in an early 40% reduction in alveolar fluid clearance (AFC), an effect mediated via P2Y purinergic receptors.",
"To confirm that RSV-induced inhibition of AFC is mediated by uridine triphosphate (UTP), and to demonstrate that inhibition of de novo pyrimidine synthesis with leflunomide prevents increased UTP release after RSV infection, and thereby also prevents inhibition of AFC by RSV.",
"BALB/c mice were infected intranasally with RSV strain A2. AFC was measured in anesthetized, ventilated mice by instillation of 5% bovine serum albumin into the dependent lung. Some mice were pretreated with leflunomide or 6-mercaptopurine.",
"RSV-mediated inhibition of AFC is associated temporally with a 20-nM increase in UTP and ATP content of bronchoalveolar lavage fluid, hypoxemia, and altered nasal potential difference. RSV-mediated nucleotide release, AFC inhibition, and physiologic sequelae thereof can be prevented by pretreatment of mice with the de novo pyrimidine synthesis inhibitor leflunomide, which is not toxic to the mice, and which does not affect RSV replication in the lungs. In contrast, pretreatment of mice with 6-mercaptopurine, an inhibitor of de novo purine synthesis, has no beneficial effect on AFC or other indicators of disease progression. Finally, RSV-mediated inhibition of AFC is prevented by volume-regulated anion channel inhibitors."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Antiviral Agents",
"Bronchoalveolar Lavage Fluid",
"Disease Models, Animal",
"Disease Progression",
"Female",
"Isoxazoles",
"Leflunomide",
"Lung",
"Male",
"Mice",
"Mice, Inbred BALB C",
"Nucleotidases",
"Pneumonia, Viral",
"Respiratory Syncytial Virus Infections",
"Respiratory Syncytial Viruses",
"Severity of Illness Index"
]
} | Pyrimidine synthesis or release pathways may provide novel therapeutic targets to counter the pathophysiologic sequelae of impaired AFC in RSV disease. | yes | [
{
"from": "human",
"value": "Question: Does leflunomide prevent alveolar fluid clearance inhibition by respiratory syncytial virus?\nContext: {'contexts': ['Previously, we demonstrated that intranasal infection of BALB/c mice with respiratory syncytial virus (RSV) resulted in an early 40% reduction in alveolar fluid clearance (AFC), an effect mediated via P2Y purinergic receptors.', 'To confirm that RSV-induced inhibition of AFC is mediated by uridine triphosphate (UTP), and to demonstrate that inhibition of de novo pyrimidine synthesis with leflunomide prevents increased UTP release after RSV infection, and thereby also prevents inhibition of AFC by RSV.', 'BALB/c mice were infected intranasally with RSV strain A2. AFC was measured in anesthetized, ventilated mice by instillation of 5% bovine serum albumin into the dependent lung. Some mice were pretreated with leflunomide or 6-mercaptopurine.', 'RSV-mediated inhibition of AFC is associated temporally with a 20-nM increase in UTP and ATP content of bronchoalveolar lavage fluid, hypoxemia, and altered nasal potential difference. RSV-mediated nucleotide release, AFC inhibition, and physiologic sequelae thereof can be prevented by pretreatment of mice with the de novo pyrimidine synthesis inhibitor leflunomide, which is not toxic to the mice, and which does not affect RSV replication in the lungs. In contrast, pretreatment of mice with 6-mercaptopurine, an inhibitor of de novo purine synthesis, has no beneficial effect on AFC or other indicators of disease progression. Finally, RSV-mediated inhibition of AFC is prevented by volume-regulated anion channel inhibitors.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Antiviral Agents', 'Bronchoalveolar Lavage Fluid', 'Disease Models, Animal', 'Disease Progression', 'Female', 'Isoxazoles', 'Leflunomide', 'Lung', 'Male', 'Mice', 'Mice, Inbred BALB C', 'Nucleotidases', 'Pneumonia, Viral', 'Respiratory Syncytial Virus Infections', 'Respiratory Syncytial Viruses', 'Severity of Illness Index']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,387,802 | Does increased glucocorticoid receptor beta alter steroid response in glucocorticoid-insensitive asthma? | {
"contexts": [
"Glucocorticoids (GCs) are highly effective in the treatment of asthma. However, some individuals have GC-insensitive asthma.",
"To evaluate the functional response to steroids of bronchoalveolar lavage (BAL) cells from sites of airway inflammation from patients with GC-insensitive versus GC-sensitive asthma. As well, to attempt to define the functional role of glucocorticoid receptor (GCR)beta (a splicing variant, and dominant negative inhibitor of, the classic GCRalpha) in controlling GCRalpha nuclear translocation and transactivation at a molecular level.",
"Fiberoptic bronchoscopy with collection of BAL fluid was performed on seven patients with GC-sensitive asthma and eight patients with GC-insensitive asthma. GCRalpha cellular shuttling in response to 10(-6) M dexamethasone treatment and GCRbeta expression were analyzed in BAL cells by immunofluorescence staining. The effects of overexpression and silencing of GCRbeta mRNA on GCRalpha function were assessed.",
"Significantly reduced nuclear translocation of GCRalpha in response to steroids was found in BAL cells from patients with GC-insensitive asthma. BAL macrophages from patients with GC-insensitive asthma had significantly increased levels of cytoplasmic and nuclear GCRbeta. It was demonstrated that GCRalpha nuclear translocation and its transactivation properties were proportionately reduced by level of viral transduction of the GCRbeta gene into the DO-11.10 cell line. RNA silencing of GCRbeta mRNA in human BAL macrophages from patients with GC-insensitive asthma resulted in enhanced dexamethasone-induced GCRalpha transactivation."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Animals",
"Asthma",
"Blotting, Western",
"Bronchoalveolar Lavage Fluid",
"Bronchoscopy",
"Female",
"Fiber Optic Technology",
"Gene Expression",
"Glucocorticoids",
"Humans",
"Macrophages, Alveolar",
"Male",
"Mice",
"Polymerase Chain Reaction",
"Prognosis",
"RNA, Messenger",
"Receptors, Glucocorticoid"
]
} | GC insensitivity is associated with loss of GCRalpha nuclear translocation in BAL cells and elevated GCRbeta, which may inhibit GCRalpha transactivation in response to steroids. | yes | [
{
"from": "human",
"value": "Question: Does increased glucocorticoid receptor beta alter steroid response in glucocorticoid-insensitive asthma?\nContext: {'contexts': ['Glucocorticoids (GCs) are highly effective in the treatment of asthma. However, some individuals have GC-insensitive asthma.', 'To evaluate the functional response to steroids of bronchoalveolar lavage (BAL) cells from sites of airway inflammation from patients with GC-insensitive versus GC-sensitive asthma. As well, to attempt to define the functional role of glucocorticoid receptor (GCR)beta (a splicing variant, and dominant negative inhibitor of, the classic GCRalpha) in controlling GCRalpha nuclear translocation and transactivation at a molecular level.', 'Fiberoptic bronchoscopy with collection of BAL fluid was performed on seven patients with GC-sensitive asthma and eight patients with GC-insensitive asthma. GCRalpha cellular shuttling in response to 10(-6) M dexamethasone treatment and GCRbeta expression were analyzed in BAL cells by immunofluorescence staining. The effects of overexpression and silencing of GCRbeta mRNA on GCRalpha function were assessed.', 'Significantly reduced nuclear translocation of GCRalpha in response to steroids was found in BAL cells from patients with GC-insensitive asthma. BAL macrophages from patients with GC-insensitive asthma had significantly increased levels of cytoplasmic and nuclear GCRbeta. It was demonstrated that GCRalpha nuclear translocation and its transactivation properties were proportionately reduced by level of viral transduction of the GCRbeta gene into the DO-11.10 cell line. RNA silencing of GCRbeta mRNA in human BAL macrophages from patients with GC-insensitive asthma resulted in enhanced dexamethasone-induced GCRalpha transactivation.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Animals', 'Asthma', 'Blotting, Western', 'Bronchoalveolar Lavage Fluid', 'Bronchoscopy', 'Female', 'Fiber Optic Technology', 'Gene Expression', 'Glucocorticoids', 'Humans', 'Macrophages, Alveolar', 'Male', 'Mice', 'Polymerase Chain Reaction', 'Prognosis', 'RNA, Messenger', 'Receptors, Glucocorticoid']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,387,807 | Does a novel low molecular weight inhibitor of dendritic cells and B cells block allergic inflammation? | {
"contexts": [
"During allergic lung inflammation dendritic cells (DCs) direct the generation and function of effector T-helper type 2 cells. T-helper type 2 cells not only orchestrate the inflammatory processes in the tissue by inducing the accumulation and activation of proinflammatory cells but also induce IgE production by B cells. Thus, inhibitors of DC function should have therapeutic benefits in patients with allergies.",
"VAF347, a novel low molecular weight immunomodulator, is described and acts as an antiinflammatory compound by a dual mode of action.",
"VAF347 inhibited the function of human monocyte-derived DCs to induce T-cell proliferation and cytokine production. Mechanistically, this effect may be due to reduced expression of CD86, HLA-DR, and interleukin 6 by DCs. In addition, the compound inhibited IgE synthesis in an isotype-specific fashion by human B lymphocytes. In a mouse model of antigen-induced eosinophilic inflammation, VAF347 blocked lung eosinophilia, mucus hyperplasia, and serum IgE levels, representing the hallmarks of allergic lung inflammation. The biological effects in vivo are most likely mediated by the immunoregulatory role of VAF347 on DCs because allergic lung inflammation was also inhibited in B-cell-deficient mice."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Anti-Inflammatory Agents, Non-Steroidal",
"B-Lymphocytes",
"B7-2 Antigen",
"Cell Proliferation",
"Dendritic Cells",
"Disease Models, Animal",
"HLA-DR Antigens",
"Humans",
"Immunoglobulin E",
"In Vitro Techniques",
"Interleukin-6",
"Lymphocyte Activation",
"Mice",
"Mice, Inbred C57BL",
"Molecular Weight",
"Pyrimidines",
"Respiratory Hypersensitivity",
"Th2 Cells"
]
} | VAF347 represents a novel type of immunomodulator by affecting two major pathways in allergic airway pathogenesis: dendritic cell-mediated T-helper-cell activation and induction of IgE production by human B lymphocytes. | yes | [
{
"from": "human",
"value": "Question: Does a novel low molecular weight inhibitor of dendritic cells and B cells block allergic inflammation?\nContext: {'contexts': ['During allergic lung inflammation dendritic cells (DCs) direct the generation and function of effector T-helper type 2 cells. T-helper type 2 cells not only orchestrate the inflammatory processes in the tissue by inducing the accumulation and activation of proinflammatory cells but also induce IgE production by B cells. Thus, inhibitors of DC function should have therapeutic benefits in patients with allergies.', 'VAF347, a novel low molecular weight immunomodulator, is described and acts as an antiinflammatory compound by a dual mode of action.', 'VAF347 inhibited the function of human monocyte-derived DCs to induce T-cell proliferation and cytokine production. Mechanistically, this effect may be due to reduced expression of CD86, HLA-DR, and interleukin 6 by DCs. In addition, the compound inhibited IgE synthesis in an isotype-specific fashion by human B lymphocytes. In a mouse model of antigen-induced eosinophilic inflammation, VAF347 blocked lung eosinophilia, mucus hyperplasia, and serum IgE levels, representing the hallmarks of allergic lung inflammation. The biological effects in vivo are most likely mediated by the immunoregulatory role of VAF347 on DCs because allergic lung inflammation was also inhibited in B-cell-deficient mice.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Anti-Inflammatory Agents, Non-Steroidal', 'B-Lymphocytes', 'B7-2 Antigen', 'Cell Proliferation', 'Dendritic Cells', 'Disease Models, Animal', 'HLA-DR Antigens', 'Humans', 'Immunoglobulin E', 'In Vitro Techniques', 'Interleukin-6', 'Lymphocyte Activation', 'Mice', 'Mice, Inbred C57BL', 'Molecular Weight', 'Pyrimidines', 'Respiratory Hypersensitivity', 'Th2 Cells']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,387,809 | Does metalworking fluid with mycobacteria and endotoxin induce hypersensitivity pneumonitis in mice? | {
"contexts": [
"Human cases of hypersensitivity pneumonitis (HP) have been reported among machinists for over 10 yr. Although mycobacteria have been implicated as causal agents, this has not been established in experimental studies and the mechanisms remain unclear. Other constituents of in-use metalworking fluids (MWFs) may also contribute to the development of lung disease. We investigated the potential for Mycobacterium immunogenum (MI) in MWFs to induce HP.",
"Mice were exposed intranasally for 3 wk to MI (isolated from MWFs), Saccharopolyspora rectivirgula (positive control), saline, endotoxin, MWFs spiked with endotoxin and/or MI, used MWFs, and particulate-fortified used MWFs. Responses were assessed 96 h after the last exposure.",
"Mice exposed to MI in MWFs developed lung pathology consistent with HP along with significantly more monocytes and neutrophils in lung lavage, increased CD4+/CD8+ T-lymphocyte ratio, and marked pulmonary lymphocytosis on histologic examination when compared with saline-treated control mice. Mice with Grade 2 or higher pathology (0-4 point scale) exhibited significantly elevated macrophage inflammatory protein-1alpha and IL-10 and a trend toward higher RANTES 96 h after the final dose. Endotoxin coexposure augmented lung pathology."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Aerosols",
"Air Pollutants",
"Alveolitis, Extrinsic Allergic",
"Animals",
"Bronchoalveolar Lavage Fluid",
"CD4-CD8 Ratio",
"Disease Models, Animal",
"Endotoxins",
"Female",
"Inhalation Exposure",
"Lung",
"Metallurgy",
"Mice",
"Mice, Inbred C57BL",
"Mycobacterium",
"T-Lymphocytes"
]
} | MWFs containing mycobacteria induced granulomatous lung lesions, peribronchiolar lymphocytosis, increased cell concentrations in lavage, and up-regulation of several cytokines. These findings are consistent with HP. | yes | [
{
"from": "human",
"value": "Question: Does metalworking fluid with mycobacteria and endotoxin induce hypersensitivity pneumonitis in mice?\nContext: {'contexts': ['Human cases of hypersensitivity pneumonitis (HP) have been reported among machinists for over 10 yr. Although mycobacteria have been implicated as causal agents, this has not been established in experimental studies and the mechanisms remain unclear. Other constituents of in-use metalworking fluids (MWFs) may also contribute to the development of lung disease. We investigated the potential for Mycobacterium immunogenum (MI) in MWFs to induce HP.', 'Mice were exposed intranasally for 3 wk to MI (isolated from MWFs), Saccharopolyspora rectivirgula (positive control), saline, endotoxin, MWFs spiked with endotoxin and/or MI, used MWFs, and particulate-fortified used MWFs. Responses were assessed 96 h after the last exposure.', 'Mice exposed to MI in MWFs developed lung pathology consistent with HP along with significantly more monocytes and neutrophils in lung lavage, increased CD4+/CD8+ T-lymphocyte ratio, and marked pulmonary lymphocytosis on histologic examination when compared with saline-treated control mice. Mice with Grade 2 or higher pathology (0-4 point scale) exhibited significantly elevated macrophage inflammatory protein-1alpha and IL-10 and a trend toward higher RANTES 96 h after the final dose. Endotoxin coexposure augmented lung pathology.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Aerosols', 'Air Pollutants', 'Alveolitis, Extrinsic Allergic', 'Animals', 'Bronchoalveolar Lavage Fluid', 'CD4-CD8 Ratio', 'Disease Models, Animal', 'Endotoxins', 'Female', 'Inhalation Exposure', 'Lung', 'Metallurgy', 'Mice', 'Mice, Inbred C57BL', 'Mycobacterium', 'T-Lymphocytes']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,394,901 | Does abdominal insufflation decrease blood loss and mortality after porcine liver injury? | {
"contexts": [
"Uncontrolled intra-abdominal bleeding is a common cause of death in trauma patients in the prehospital and perioperative settings. The detrimental effects of abdominal hypertension are well studied, but the potential therapeutic use of abdominal insufflation for hemostasis has not been fully explored. We measured the effect of abdominal insufflation on blood loss and physiologic outcomes in a swine model of blunt liver injury.",
"Twenty-one anticoagulated swine (32 +/- 3 kg) were anesthesized; laparotomy was performed to localize liver anatomy and to place loose tourniquettes isolating the porta hepatis and supra/infrahepatic vena cava. A captive bolt gun was used to create a grade V hepatic laceration, producing massive parenchymal injury as well as complex tears of the middle and right hepatic veins. Animals were randomized into either control (n = 10) or abdominal insufflation at 20 cm H(2)O pressure (n = 11) groups. Crystalloid was used to maintain a mean arterial pressure of 30 mm Hg. Arterial pressure and other physiologic variables were recorded for 20 minutes. Animals were then sacrificed and blood loss measured.",
"Blood loss was 69% lower in insufflated animals compared with controls (384 +/- 51 versus 1252 +/- 88 cc, p < 0.001). After 20 minutes, insufflated animals had significantly higher mean arterial blood pressure (32.2 +/- 4.2 versus 21.2 +/- 4.0 mm Hg) and lower total resuscitation volume (195 +/- 83 versus 1356 +/- 95 cc). Three pigs died in the control group (30%), whereas no insufflated animals died (p < 0.05)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Abdomen",
"Animals",
"Blood Pressure",
"Blood Volume",
"Disease Models, Animal",
"Gastrointestinal Hemorrhage",
"Heart Rate",
"Insufflation",
"Liver",
"Swine",
"Wounds, Nonpenetrating"
]
} | In a swine model of catastrophic blunt hepatic injury, abdominal insufflation significantly decreased blood loss and mortality. | yes | [
{
"from": "human",
"value": "Question: Does abdominal insufflation decrease blood loss and mortality after porcine liver injury?\nContext: {'contexts': ['Uncontrolled intra-abdominal bleeding is a common cause of death in trauma patients in the prehospital and perioperative settings. The detrimental effects of abdominal hypertension are well studied, but the potential therapeutic use of abdominal insufflation for hemostasis has not been fully explored. We measured the effect of abdominal insufflation on blood loss and physiologic outcomes in a swine model of blunt liver injury.', 'Twenty-one anticoagulated swine (32 +/- 3 kg) were anesthesized; laparotomy was performed to localize liver anatomy and to place loose tourniquettes isolating the porta hepatis and supra/infrahepatic vena cava. A captive bolt gun was used to create a grade V hepatic laceration, producing massive parenchymal injury as well as complex tears of the middle and right hepatic veins. Animals were randomized into either control (n = 10) or abdominal insufflation at 20 cm H(2)O pressure (n = 11) groups. Crystalloid was used to maintain a mean arterial pressure of 30 mm Hg. Arterial pressure and other physiologic variables were recorded for 20 minutes. Animals were then sacrificed and blood loss measured.', 'Blood loss was 69% lower in insufflated animals compared with controls (384 +/- 51 versus 1252 +/- 88 cc, p < 0.001). After 20 minutes, insufflated animals had significantly higher mean arterial blood pressure (32.2 +/- 4.2 versus 21.2 +/- 4.0 mm Hg) and lower total resuscitation volume (195 +/- 83 versus 1356 +/- 95 cc). Three pigs died in the control group (30%), whereas no insufflated animals died (p < 0.05).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Abdomen', 'Animals', 'Blood Pressure', 'Blood Volume', 'Disease Models, Animal', 'Gastrointestinal Hemorrhage', 'Heart Rate', 'Insufflation', 'Liver', 'Swine', 'Wounds, Nonpenetrating']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,378,863 | Does surgery for spontaneous intracerebral hemorrhage have greater remedial value than conservative therapy? | {
"contexts": [
"The aim of this study was to compare the efficacy of surgery for spontaneous intracerebral hemorrhage with that of medical treatment, based on data from the Japan Stroke Registry Study.",
"From 1999 to 2001, 1010 patients with spontaneous intracerebral hemorrhage were registered in the Japan Standard Stroke Registry Study from 45 stroke center hospitals in Japan. The National Institutes of Health Stroke Scale (NIHSS), Japan Stroke Scale (JSS), and modified Rankin Scale scores were used to compare severity and improvement in patients given surgical and medical treatment."
],
"labels": [
"BACKGROUND",
"METHODS"
],
"meshes": [
"Adult",
"Aged",
"Aged, 80 and over",
"Cerebral Hemorrhage",
"Craniotomy",
"Female",
"Hematoma",
"Humans",
"Japan",
"Logistic Models",
"Male",
"Middle Aged",
"Recovery of Function",
"Registries",
"Severity of Illness Index",
"Stereotaxic Techniques",
"Suction",
"Treatment Outcome"
]
} | Surgically treated patients, especially those with cerebellar hemorrhage, had significantly greater improvement in NIHSS or JSS score compared with medically treated patients. Our findings indicated that the patients who underwent surgery appeared to have better outcomes. But, because the study was not randomized, this observation cannot be interpreted as indicating that surgery is advantageous. | yes | [
{
"from": "human",
"value": "Question: Does surgery for spontaneous intracerebral hemorrhage have greater remedial value than conservative therapy?\nContext: {'contexts': ['The aim of this study was to compare the efficacy of surgery for spontaneous intracerebral hemorrhage with that of medical treatment, based on data from the Japan Stroke Registry Study.', 'From 1999 to 2001, 1010 patients with spontaneous intracerebral hemorrhage were registered in the Japan Standard Stroke Registry Study from 45 stroke center hospitals in Japan. The National Institutes of Health Stroke Scale (NIHSS), Japan Stroke Scale (JSS), and modified Rankin Scale scores were used to compare severity and improvement in patients given surgical and medical treatment.'], 'labels': ['BACKGROUND', 'METHODS'], 'meshes': ['Adult', 'Aged', 'Aged, 80 and over', 'Cerebral Hemorrhage', 'Craniotomy', 'Female', 'Hematoma', 'Humans', 'Japan', 'Logistic Models', 'Male', 'Middle Aged', 'Recovery of Function', 'Registries', 'Severity of Illness Index', 'Stereotaxic Techniques', 'Suction', 'Treatment Outcome']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,384,965 | Does perfusion of his-tagged eukaryotic myocilin increase outflow resistance in human anterior segments in the presence of aqueous humor? | {
"contexts": [
"A previous study by the authors has shown that recombinant myocilin purified from a prokaryotic expression system increases outflow resistance in cultured human anterior segments. The present study was performed to determine whether full-length myocilin purified from a human trabecular meshwork cell expression system alters outflow resistance after infusion into human anterior segments.",
"A feline immunodeficiency virus vector encoding both full-length myocilin (amino acids 1-503 fused to C-terminal V5 and six-histidine epitopes) and puromycin resistance was used to transduce a transformed trabecular meshwork cell line (TM5). Stably expressing cells were selected with puromycin. Recombinant myocilin was purified from the media using nickel ion affinity chromatography. Control purifications were performed on media from parental TM5 cells. Anterior segments of human eyes were placed in organ culture and perfused with either Dulbecco's modified Eagle's medium (DMEM) or DMEM supplemented with 50% porcine aqueous humor. One eye received an anterior chamber exchange with recombinant myocilin (2 microg/mL), whereas the fellow eye received an equal volume of control. Immunohistochemistry was performed with anti-myocilin and anti-V5 antibodies. Native polyacrylamide gel electrophoresis was used to analyze myocilin complex formation in porcine aqueous humor.",
"Recombinant myocilin in porcine aqueous humor increased outflow resistance in cultured human anterior segments (91% +/- 68% [mean +/- SD] versus 18% +/- 31% in fellow control eye; n = 9, P = 0.004). Maximum outflow resistance was obtained 5 to 17 hours after infusion and remained above baseline for >3 days. Recombinant myocilin also increased outflow resistance in eyes incubated in DMEM, but only if myocilin was preincubated with porcine aqueous humor (78% +/- 77% when preincubated in DMEM containing porcine aqueous humor versus 13% +/- 15% when preincubated with DMEM alone, n = 6, P = 0.03). Recombinant myocilin appears to form a complex in porcine aqueous humor with a heat-labile protein(s). Immunohistochemistry revealed the presence of myocilin in the juxtacanalicular region of the trabecular meshwork."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Aged, 80 and over",
"Animals",
"Aqueous Humor",
"Cell Line",
"Cytoskeletal Proteins",
"Eye Proteins",
"Female",
"Gene Expression",
"Genetic Vectors",
"Glycoproteins",
"Histidine",
"Humans",
"Male",
"Middle Aged",
"Organ Culture Techniques",
"Recombinant Fusion Proteins",
"Swine",
"Trabecular Meshwork",
"Transfection"
]
} | Myocilin purified from human trabecular meshwork cells increased outflow resistance in cultured human anterior segments, but only after incubation with porcine aqueous humor. Recombinant myocilin appears to form a complex in porcine aqueous humor that enables it to bind specifically within the trabecular meshwork. | yes | [
{
"from": "human",
"value": "Question: Does perfusion of his-tagged eukaryotic myocilin increase outflow resistance in human anterior segments in the presence of aqueous humor?\nContext: {'contexts': ['A previous study by the authors has shown that recombinant myocilin purified from a prokaryotic expression system increases outflow resistance in cultured human anterior segments. The present study was performed to determine whether full-length myocilin purified from a human trabecular meshwork cell expression system alters outflow resistance after infusion into human anterior segments.', \"A feline immunodeficiency virus vector encoding both full-length myocilin (amino acids 1-503 fused to C-terminal V5 and six-histidine epitopes) and puromycin resistance was used to transduce a transformed trabecular meshwork cell line (TM5). Stably expressing cells were selected with puromycin. Recombinant myocilin was purified from the media using nickel ion affinity chromatography. Control purifications were performed on media from parental TM5 cells. Anterior segments of human eyes were placed in organ culture and perfused with either Dulbecco's modified Eagle's medium (DMEM) or DMEM supplemented with 50% porcine aqueous humor. One eye received an anterior chamber exchange with recombinant myocilin (2 microg/mL), whereas the fellow eye received an equal volume of control. Immunohistochemistry was performed with anti-myocilin and anti-V5 antibodies. Native polyacrylamide gel electrophoresis was used to analyze myocilin complex formation in porcine aqueous humor.\", 'Recombinant myocilin in porcine aqueous humor increased outflow resistance in cultured human anterior segments (91% +/- 68% [mean +/- SD] versus 18% +/- 31% in fellow control eye; n = 9, P = 0.004). Maximum outflow resistance was obtained 5 to 17 hours after infusion and remained above baseline for >3 days. Recombinant myocilin also increased outflow resistance in eyes incubated in DMEM, but only if myocilin was preincubated with porcine aqueous humor (78% +/- 77% when preincubated in DMEM containing porcine aqueous humor versus 13% +/- 15% when preincubated with DMEM alone, n = 6, P = 0.03). Recombinant myocilin appears to form a complex in porcine aqueous humor with a heat-labile protein(s). Immunohistochemistry revealed the presence of myocilin in the juxtacanalicular region of the trabecular meshwork.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Aged, 80 and over', 'Animals', 'Aqueous Humor', 'Cell Line', 'Cytoskeletal Proteins', 'Eye Proteins', 'Female', 'Gene Expression', 'Genetic Vectors', 'Glycoproteins', 'Histidine', 'Humans', 'Male', 'Middle Aged', 'Organ Culture Techniques', 'Recombinant Fusion Proteins', 'Swine', 'Trabecular Meshwork', 'Transfection']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,390,788 | Is third trimester nonrecurrent fetal loss associated with factor V Leiden and prothrombin gene mutations? | {
"contexts": [
"To determine the role of factor V Leiden and prothrombin gene mutation in the pathogenesis of unexplained second and third trimester nonrecurrent fetal loss.",
"One hundred and fourteen women with unexplained nonrecurrent late fetal loss made up the study group, and 106 normal pregnant women with a history of delivery of at least one healthy fetus and no history of late fetal loss made up the control group. The study group was further divided into two subgroups: second (n = 36) and third (n = 78) trimester fetal loss. All women were tested for factor V Leiden and G20210A prothrombin gene mutations.",
"Twenty-one (18.4%) of the women in the study group and seven (6.6%) of the women in the control group were heterozygous carriers of factor V Leiden mutation (OR = 3.19). Eleven (9.6%) of the women in the study group and three (2.8%) of the women in the control group were heterozygous carriers of prothrombin gene mutation (OR = 3.66). In assessing with regard to trimesters, 18 (23%) factor V Leiden and 10 (12.8%) prothrombin gene mutations were present in the group of third trimester fetal loss (OR = 4.24 and OR = 5.04, respectively). Three (8.3%) factor V Leiden and one (2.7%) prothrombin gene mutation were detected in women with second trimester fetal loss (OR = 1.28 and OR = 0.40, respectively)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Abortion, Spontaneous",
"Adult",
"Case-Control Studies",
"Factor V",
"Female",
"Heterozygote",
"Humans",
"Mutation",
"Pregnancy",
"Pregnancy Trimester, Second",
"Pregnancy Trimester, Third",
"Prothrombin"
]
} | Factor V Leiden and prothrombin gene mutations were associated with third trimester nonrecurrent fetal loss. These mutations should be screened in women with third trimester but not second trimester unexplained nonrecurrent late fetal loss. | yes | [
{
"from": "human",
"value": "Question: Is third trimester nonrecurrent fetal loss associated with factor V Leiden and prothrombin gene mutations?\nContext: {'contexts': ['To determine the role of factor V Leiden and prothrombin gene mutation in the pathogenesis of unexplained second and third trimester nonrecurrent fetal loss.', 'One hundred and fourteen women with unexplained nonrecurrent late fetal loss made up the study group, and 106 normal pregnant women with a history of delivery of at least one healthy fetus and no history of late fetal loss made up the control group. The study group was further divided into two subgroups: second (n = 36) and third (n = 78) trimester fetal loss. All women were tested for factor V Leiden and G20210A prothrombin gene mutations.', 'Twenty-one (18.4%) of the women in the study group and seven (6.6%) of the women in the control group were heterozygous carriers of factor V Leiden mutation (OR = 3.19). Eleven (9.6%) of the women in the study group and three (2.8%) of the women in the control group were heterozygous carriers of prothrombin gene mutation (OR = 3.66). In assessing with regard to trimesters, 18 (23%) factor V Leiden and 10 (12.8%) prothrombin gene mutations were present in the group of third trimester fetal loss (OR = 4.24 and OR = 5.04, respectively). Three (8.3%) factor V Leiden and one (2.7%) prothrombin gene mutation were detected in women with second trimester fetal loss (OR = 1.28 and OR = 0.40, respectively).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Abortion, Spontaneous', 'Adult', 'Case-Control Studies', 'Factor V', 'Female', 'Heterozygote', 'Humans', 'Mutation', 'Pregnancy', 'Pregnancy Trimester, Second', 'Pregnancy Trimester, Third', 'Prothrombin']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,377,839 | Does magnetic resonance restricted diffusion resolution correlate with clinical improvement and response to treatment in herpes simplex encephalitis? | {
"contexts": [
"A 34-year-old man presented with herpes simplex encephalitis (HSE), with magnetic resonance imaging (MRI) showing dense foci of restricted diffusion in the temporal lobe.",
"With treatment and clinical improvement, follow-up MRI done 8 days later showed complete resolution of the restricted diffusion abnormalities, whereas other MRI sequences suggested interval progression."
],
"labels": [
"BACKGROUND",
"METHODS"
],
"meshes": [
"Adult",
"Diffusion Magnetic Resonance Imaging",
"Disease Progression",
"Encephalitis, Herpes Simplex",
"Humans",
"Male",
"Sensitivity and Specificity",
"Treatment Outcome"
]
} | Restricted diffusion abnormalities on MRI in patients with HSE may be more sensitive to and correlate better with disease activity in HSE. | yes | [
{
"from": "human",
"value": "Question: Does magnetic resonance restricted diffusion resolution correlate with clinical improvement and response to treatment in herpes simplex encephalitis?\nContext: {'contexts': ['A 34-year-old man presented with herpes simplex encephalitis (HSE), with magnetic resonance imaging (MRI) showing dense foci of restricted diffusion in the temporal lobe.', 'With treatment and clinical improvement, follow-up MRI done 8 days later showed complete resolution of the restricted diffusion abnormalities, whereas other MRI sequences suggested interval progression.'], 'labels': ['BACKGROUND', 'METHODS'], 'meshes': ['Adult', 'Diffusion Magnetic Resonance Imaging', 'Disease Progression', 'Encephalitis, Herpes Simplex', 'Humans', 'Male', 'Sensitivity and Specificity', 'Treatment Outcome']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,380,569 | Does epidemiology and correlate of daily smoking and nicotine dependence among young adults in the United States? | {
"contexts": [
"We describe the epidemiology of smoking behaviors in a national young adult sample and identify common and unique demographic, social, and psychological correlates of daily smoking and lifetime and current nicotine dependence by race/ethnicity.",
"Data are from the National Longitudinal Survey of Adolescent Health, wave III. Dependence was measured by the Revised Fagerström Test for Nicotine Dependence. Logistic regressions were estimated.",
"Hispanic ethnicity, low education, parental and peer smoking, novelty seeking, early age of smoking onset, and pleasurable initial smoking experiences are significantly correlated with daily smoking and lifetime nicotine dependence. Depressive symptoms are uniquely associated with lifetime and current dependence. Few factors are highly associated with current dependence. Initial sensitivity to smoking has a significantly greater impact on daily smoking than on dependence. Correlates of smoking behaviors are mostly common across racial/ethnic groups, although parental and peer smoking are significant for Whites and Hispanics but not for African Americans."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adolescent Behavior",
"Adult",
"Depression",
"Female",
"Humans",
"Logistic Models",
"Longitudinal Studies",
"Male",
"Prevalence",
"Risk Factors",
"Sex Factors",
"Smoking",
"Tobacco Use Disorder",
"United States"
]
} | There are more common than unique correlates of each smoking stage and across racial/ethnic groups. Primary prevention and interventions addressing the factors tested could be uniform for most chronic smokers irrespective of dependence status and race/ethnicity. | yes | [
{
"from": "human",
"value": "Question: Does epidemiology and correlate of daily smoking and nicotine dependence among young adults in the United States?\nContext: {'contexts': ['We describe the epidemiology of smoking behaviors in a national young adult sample and identify common and unique demographic, social, and psychological correlates of daily smoking and lifetime and current nicotine dependence by race/ethnicity.', 'Data are from the National Longitudinal Survey of Adolescent Health, wave III. Dependence was measured by the Revised Fagerström Test for Nicotine Dependence. Logistic regressions were estimated.', 'Hispanic ethnicity, low education, parental and peer smoking, novelty seeking, early age of smoking onset, and pleasurable initial smoking experiences are significantly correlated with daily smoking and lifetime nicotine dependence. Depressive symptoms are uniquely associated with lifetime and current dependence. Few factors are highly associated with current dependence. Initial sensitivity to smoking has a significantly greater impact on daily smoking than on dependence. Correlates of smoking behaviors are mostly common across racial/ethnic groups, although parental and peer smoking are significant for Whites and Hispanics but not for African Americans.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adolescent Behavior', 'Adult', 'Depression', 'Female', 'Humans', 'Logistic Models', 'Longitudinal Studies', 'Male', 'Prevalence', 'Risk Factors', 'Sex Factors', 'Smoking', 'Tobacco Use Disorder', 'United States']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,386,082 | Does retinoic acid induce VEGF gene expression in human retinal pigment epithelial cells ( ARPE-19 )? | {
"contexts": [
"The aim of this study was to evaluate the expression of vascular endothelial growth factor (VEGF) in response to retinoic acid (RA) in human retinal pigment epithelial cells.",
"Expression of VEGF in human ARPE-19 cells was determined by a semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). mRNA stability was assessed after the administration of actinomycin D. The induction of the VEGF gene by various RAs was also determined by semiquantitative RT-PCR.",
"All-trans retinoic acid (atRA) time-dependently increased VEGF mRNA levels. The effect of atRA was dose-dependent in a range between 10(-7) M and 10(-6) M. Treatment with actinomycin D revealed that atRA induces the VEGF gene at the transcriptional level. Of the various RAs tested, atRA was the most potent inducer of the VEGF gene."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Cell Line",
"Dactinomycin",
"Dose-Response Relationship, Drug",
"Epithelial Cells",
"Gene Expression",
"Humans",
"Pigment Epithelium of Eye",
"Time Factors",
"Transcription, Genetic",
"Tretinoin",
"Vascular Endothelial Growth Factor A"
]
} | We demonstrated that atRA stimulates the induction of the VEGF gene in ARPE-19 cells, suggesting a novel pathway for the development of age-related macular degeneration. | yes | [
{
"from": "human",
"value": "Question: Does retinoic acid induce VEGF gene expression in human retinal pigment epithelial cells ( ARPE-19 )?\nContext: {'contexts': ['The aim of this study was to evaluate the expression of vascular endothelial growth factor (VEGF) in response to retinoic acid (RA) in human retinal pigment epithelial cells.', 'Expression of VEGF in human ARPE-19 cells was determined by a semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). mRNA stability was assessed after the administration of actinomycin D. The induction of the VEGF gene by various RAs was also determined by semiquantitative RT-PCR.', 'All-trans retinoic acid (atRA) time-dependently increased VEGF mRNA levels. The effect of atRA was dose-dependent in a range between 10(-7) M and 10(-6) M. Treatment with actinomycin D revealed that atRA induces the VEGF gene at the transcriptional level. Of the various RAs tested, atRA was the most potent inducer of the VEGF gene.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Cell Line', 'Dactinomycin', 'Dose-Response Relationship, Drug', 'Epithelial Cells', 'Gene Expression', 'Humans', 'Pigment Epithelium of Eye', 'Time Factors', 'Transcription, Genetic', 'Tretinoin', 'Vascular Endothelial Growth Factor A']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,384,994 | Does superior cervical ganglionectomy induce changes in growth factor expression in the rat retina? | {
"contexts": [
"To determine whether sympathetic nerves regulate expression of known angiogenic growth factors.",
"Surgical sympathectomy (SNX) was used to remove sympathetic innervation to the eye. Real-time PCR was used to measure steady state mRNA expression of VEGF, VEGFR-2, angiopoietin-1, and Tie2. Western blot analysis was performed to assess protein expression. Blood-retinal barrier (BRB) permeability surface area product (PS) was measured using enhanced MRI on a separate group of control and SNX rats.",
"mRNA of both VEGF and VEGFR-2 decreased significantly at 6 weeks after SNX. VEGF protein expression also decreased significantly. VEGFR-2 protein was unchanged. Both angiopoietin-1 and Tie2 mRNA expression increased significantly after SNX. Immunoblot analysis showed that angiopoietin-1 protein expression coincided with its mRNA expression. Tie2 protein expression was unaffected. Sympathetic denervation did not significantly increase BRB PS."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Angiopoietin-1",
"Animals",
"Blood-Retinal Barrier",
"Blotting, Western",
"Female",
"Ganglionectomy",
"Gene Expression Regulation",
"Magnetic Resonance Imaging",
"RNA, Messenger",
"Rats",
"Rats, Sprague-Dawley",
"Receptor, TIE-2",
"Reverse Transcriptase Polymerase Chain Reaction",
"Superior Cervical Ganglion",
"Time Factors",
"Vascular Endothelial Growth Factor A",
"Vascular Endothelial Growth Factor Receptor-2"
]
} | Surgical SNX results in a reduction in VEGF gene and protein expression, while increasing protein expression of Ang-1. These findings suggest that sympathetic nerves regulate the expression of angiogenic growth factors in rat retina. | yes | [
{
"from": "human",
"value": "Question: Does superior cervical ganglionectomy induce changes in growth factor expression in the rat retina?\nContext: {'contexts': ['To determine whether sympathetic nerves regulate expression of known angiogenic growth factors.', 'Surgical sympathectomy (SNX) was used to remove sympathetic innervation to the eye. Real-time PCR was used to measure steady state mRNA expression of VEGF, VEGFR-2, angiopoietin-1, and Tie2. Western blot analysis was performed to assess protein expression. Blood-retinal barrier (BRB) permeability surface area product (PS) was measured using enhanced MRI on a separate group of control and SNX rats.', 'mRNA of both VEGF and VEGFR-2 decreased significantly at 6 weeks after SNX. VEGF protein expression also decreased significantly. VEGFR-2 protein was unchanged. Both angiopoietin-1 and Tie2 mRNA expression increased significantly after SNX. Immunoblot analysis showed that angiopoietin-1 protein expression coincided with its mRNA expression. Tie2 protein expression was unaffected. Sympathetic denervation did not significantly increase BRB PS.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Angiopoietin-1', 'Animals', 'Blood-Retinal Barrier', 'Blotting, Western', 'Female', 'Ganglionectomy', 'Gene Expression Regulation', 'Magnetic Resonance Imaging', 'RNA, Messenger', 'Rats', 'Rats, Sprague-Dawley', 'Receptor, TIE-2', 'Reverse Transcriptase Polymerase Chain Reaction', 'Superior Cervical Ganglion', 'Time Factors', 'Vascular Endothelial Growth Factor A', 'Vascular Endothelial Growth Factor Receptor-2']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,390,758 | Are serum C-reactive protein and plasma homocysteine levels associated with hormone therapy use and other factors : a population-based study of middle-aged Australian-born women? | {
"contexts": [
"To investigate the associations between C-reactive protein (CRP), homocysteine levels, use of hormone therapy (HT) and other factors.",
"A 12-year prospective study of 438 Australian-born women (Melbourne Women's Midlife Health Project), who at baseline were aged 45-55 years, had menstruated in the previous 3 months and were not taking HT. Fasting blood was collected in the 11th follow-up year for CRP, homocysteine, estradiol and follicle stimulating hormone (FSH) levels. Physical measurements and face-to-face interviews obtained information on health and lifestyle variables.",
"A total of 258 women (mean age 60 years) participated in the 11th follow-up year. Multiple regression analysis found that CRP levels were positively associated with body mass index (p < 0.001), HT use (p < 0.01), and negatively associated with statin use (p < 0.005) and exercising (p < 0.05). In postmenopausal women currently not using HT (n = 173) and after adjusting for body mass index, exercise and smoking, CRP was negatively associated with FSH levels (beta = -0.32, p < 0.05). Homocysteine levels were positively associated with smoking (p < 0.001) and negatively associated with HT use (p < 0.05)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Australia",
"Body Mass Index",
"C-Reactive Protein",
"Cholesterol, HDL",
"Exercise",
"Female",
"Follicle Stimulating Hormone",
"Follow-Up Studies",
"Homocysteine",
"Hormone Replacement Therapy",
"Humans",
"Hydroxymethylglutaryl-CoA Reductase Inhibitors",
"Middle Aged",
"Prospective Studies",
"Regression Analysis",
"Smoking"
]
} | In middle-aged Australian-born women, HT use was associated with increased CRP and decreased homocysteine levels. High CRP levels were also associated with high relative weight, low exercise levels and no statin medication. | yes | [
{
"from": "human",
"value": "Question: Are serum C-reactive protein and plasma homocysteine levels associated with hormone therapy use and other factors : a population-based study of middle-aged Australian-born women?\nContext: {'contexts': ['To investigate the associations between C-reactive protein (CRP), homocysteine levels, use of hormone therapy (HT) and other factors.', \"A 12-year prospective study of 438 Australian-born women (Melbourne Women's Midlife Health Project), who at baseline were aged 45-55 years, had menstruated in the previous 3 months and were not taking HT. Fasting blood was collected in the 11th follow-up year for CRP, homocysteine, estradiol and follicle stimulating hormone (FSH) levels. Physical measurements and face-to-face interviews obtained information on health and lifestyle variables.\", 'A total of 258 women (mean age 60 years) participated in the 11th follow-up year. Multiple regression analysis found that CRP levels were positively associated with body mass index (p < 0.001), HT use (p < 0.01), and negatively associated with statin use (p < 0.005) and exercising (p < 0.05). In postmenopausal women currently not using HT (n = 173) and after adjusting for body mass index, exercise and smoking, CRP was negatively associated with FSH levels (beta = -0.32, p < 0.05). Homocysteine levels were positively associated with smoking (p < 0.001) and negatively associated with HT use (p < 0.05).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Australia', 'Body Mass Index', 'C-Reactive Protein', 'Cholesterol, HDL', 'Exercise', 'Female', 'Follicle Stimulating Hormone', 'Follow-Up Studies', 'Homocysteine', 'Hormone Replacement Therapy', 'Humans', 'Hydroxymethylglutaryl-CoA Reductase Inhibitors', 'Middle Aged', 'Prospective Studies', 'Regression Analysis', 'Smoking']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
16,373,905 | Is impaired coronary endothelium-dependent vasodilation associated with microalbuminuria in patients with type 2 diabetes and angiographically normal coronary arteries? | {
"contexts": [
"Microalbuminuria and impaired endothelium-dependent vasodilation are both predictors for cardiac events in patients with type 2 diabetes. The aim of the study was to evaluate whether microalbuminuria correlated with coronary endothelium-dependent vasodilation.",
"We evaluated 84 patients (47 men, mean age 50.5 +/- 5.9 years) with type 2 diabetes for 9.4 +/- 3.4 years, without angiographic coronary stenosis and without major cardiovascular risk factors or other confounding factors, for endothelium investigation. Quantitative coronary angiography was used to assess coronary artery response to cold pressor testing, used to assess endothelium-dependent vasodilation, and to isosorbide dinitrate (endothelium-independent vasodilation).",
"Endothelium-dependent vasodilation differed in the patients with and without microalbuminuria (changes in coronary artery diameter during cold pressor testing: -15.0 +/- 1.9% vs. -10.2 +/- 1.3%, respectively, P < 0.05) and correlated with urinary albumin excretion rate (r = -0.39, P = 0.003), diastolic blood pressure (r = 0.29, P < 0.01), and left ventricular mass index (r = -0.24, P < 0.05). Independent predictors for endothelium-dependent vasodilation were urinary albumin excretion rate (beta -0.04 [95% CI -0.07 to -0.01], P < 0.005) and left ventricular mass index (-0.26 [-0.49 to -0.05], P < 0.05). Endothelium-independent vasodilation was similar in both groups."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Albuminuria",
"Coronary Angiography",
"Coronary Vessels",
"Diabetes Mellitus, Type 2",
"Diabetic Nephropathies",
"Endothelium, Vascular",
"Female",
"Follow-Up Studies",
"Humans",
"Male",
"Middle Aged",
"Vasodilation"
]
} | Type 2 diabetic patients with microalbuminuria have a more severely impaired coronary endothelium-dependent vasodilation than those with normoalbuminuria. These data suggest a common pathophysiological process for both coronary vasomotor abnormalities and microalbuminuria. | yes | [
{
"from": "human",
"value": "Question: Is impaired coronary endothelium-dependent vasodilation associated with microalbuminuria in patients with type 2 diabetes and angiographically normal coronary arteries?\nContext: {'contexts': ['Microalbuminuria and impaired endothelium-dependent vasodilation are both predictors for cardiac events in patients with type 2 diabetes. The aim of the study was to evaluate whether microalbuminuria correlated with coronary endothelium-dependent vasodilation.', 'We evaluated 84 patients (47 men, mean age 50.5 +/- 5.9 years) with type 2 diabetes for 9.4 +/- 3.4 years, without angiographic coronary stenosis and without major cardiovascular risk factors or other confounding factors, for endothelium investigation. Quantitative coronary angiography was used to assess coronary artery response to cold pressor testing, used to assess endothelium-dependent vasodilation, and to isosorbide dinitrate (endothelium-independent vasodilation).', 'Endothelium-dependent vasodilation differed in the patients with and without microalbuminuria (changes in coronary artery diameter during cold pressor testing: -15.0 +/- 1.9% vs. -10.2 +/- 1.3%, respectively, P < 0.05) and correlated with urinary albumin excretion rate (r = -0.39, P = 0.003), diastolic blood pressure (r = 0.29, P < 0.01), and left ventricular mass index (r = -0.24, P < 0.05). Independent predictors for endothelium-dependent vasodilation were urinary albumin excretion rate (beta -0.04 [95% CI -0.07 to -0.01], P < 0.005) and left ventricular mass index (-0.26 [-0.49 to -0.05], P < 0.05). Endothelium-independent vasodilation was similar in both groups.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Albuminuria', 'Coronary Angiography', 'Coronary Vessels', 'Diabetes Mellitus, Type 2', 'Diabetic Nephropathies', 'Endothelium, Vascular', 'Female', 'Follow-Up Studies', 'Humans', 'Male', 'Middle Aged', 'Vasodilation']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
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