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10,733,771 | Does preservation of the right atrial appendage improve reduced plasma atrial natriuretic peptide levels after the maze procedure? | {
"contexts": [
"The present study was conducted to determine whether preservation of the right atrial appendage lessens the decrease of plasma atrial natriuretic peptide levels after the maze procedure and whether the increase of plasma atrial natriuretic peptides improves the ability of the kidneys to excrete the fluid load after the operation.",
"We evaluated 42 patients who underwent the maze procedure. The right atrial appendage was preserved in 22 patients but not in 20. Blood samples were obtained before and after the operation for measurement of atrial natriuretic peptides. To evaluate the influence of atrial natriuretic peptides on the ability of the kidneys, we also measured body weight, fluid balance, and the doses of furosemide and dopamine administered after the operation.",
"The restoration to sinus rhythm at 1 month after was comparable in the two groups. Plasma atrial natriuretic peptide levels significantly increased after the operation in patients in whom the right atrial appendage was preserved (1 day after: 23.4 +/- 17.8 vs 3 days after: 42.7 +/- 23.6 and 7 days after: 36.3 +/- 23.7 pg/mL, P <.05) but not in patients in whom the right atrial appendage was not preserved (1 day after: 20.0 +/- 19.6, 3 days after: 28.5 +/- 19.3, and 7 days after: 23.0 +/- 16.1 pg/mL). Furthermore, plasma atrial natriuretic peptide levels were significantly lower in patients in whom the right atrial appendage was not preserved than in patients in whom the right atrial appendage was preserved at 3 and 7 days after the operation. The fluid balance during the first 7 days of the postoperative period was comparable in the two groups, although the total dose of dopamine used in the same period was significantly smaller in patients in whom the right atrial appendage was preserved than in patients in whom the right atrial appendage was not preserved (155.3 +/- 119.0 vs 244.9 +/- 129.0 microg/kg, P <.05)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Atrial Appendage",
"Atrial Fibrillation",
"Atrial Natriuretic Factor",
"Body Weight",
"Cardiac Surgical Procedures",
"Cardiotonic Agents",
"Diuretics",
"Dopamine",
"Female",
"Furosemide",
"Humans",
"Kidney",
"Male",
"Middle Aged",
"Urine",
"Water-Electrolyte Balance"
]
} | The present study showed that preservation of the right atrial appendage lessens the decrease of plasma atrial natriuretic peptide levels after the maze procedure and that increased plasma atrial natriuretic peptides may improve the ability of the kidneys to excrete the fluid load after the operation. | yes | [
{
"from": "human",
"value": "Question: Does preservation of the right atrial appendage improve reduced plasma atrial natriuretic peptide levels after the maze procedure?\nContext: {'contexts': ['The present study was conducted to determine whether preservation of the right atrial appendage lessens the decrease of plasma atrial natriuretic peptide levels after the maze procedure and whether the increase of plasma atrial natriuretic peptides improves the ability of the kidneys to excrete the fluid load after the operation.', 'We evaluated 42 patients who underwent the maze procedure. The right atrial appendage was preserved in 22 patients but not in 20. Blood samples were obtained before and after the operation for measurement of atrial natriuretic peptides. To evaluate the influence of atrial natriuretic peptides on the ability of the kidneys, we also measured body weight, fluid balance, and the doses of furosemide and dopamine administered after the operation.', 'The restoration to sinus rhythm at 1 month after was comparable in the two groups. Plasma atrial natriuretic peptide levels significantly increased after the operation in patients in whom the right atrial appendage was preserved (1 day after: 23.4 +/- 17.8 vs 3 days after: 42.7 +/- 23.6 and 7 days after: 36.3 +/- 23.7 pg/mL, P <.05) but not in patients in whom the right atrial appendage was not preserved (1 day after: 20.0 +/- 19.6, 3 days after: 28.5 +/- 19.3, and 7 days after: 23.0 +/- 16.1 pg/mL). Furthermore, plasma atrial natriuretic peptide levels were significantly lower in patients in whom the right atrial appendage was not preserved than in patients in whom the right atrial appendage was preserved at 3 and 7 days after the operation. The fluid balance during the first 7 days of the postoperative period was comparable in the two groups, although the total dose of dopamine used in the same period was significantly smaller in patients in whom the right atrial appendage was preserved than in patients in whom the right atrial appendage was not preserved (155.3 +/- 119.0 vs 244.9 +/- 129.0 microg/kg, P <.05).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Atrial Appendage', 'Atrial Fibrillation', 'Atrial Natriuretic Factor', 'Body Weight', 'Cardiac Surgical Procedures', 'Cardiotonic Agents', 'Diuretics', 'Dopamine', 'Female', 'Furosemide', 'Humans', 'Kidney', 'Male', 'Middle Aged', 'Urine', 'Water-Electrolyte Balance']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,735,605 | Are cholangiocarcinoma in primary sclerosing cholangitis : K-ras mutations and Tp53 dysfunction implicated in the neoplastic development? | {
"contexts": [
"Cholangiocarcinoma is a feared complication of primary sclerosing cholangitis (PSC). Neoplastic bile duct strictures may be difficult to differentiate cholangiographically from the non-neoplastic bile duct irregularities characteristic of this disorder, and the diagnosis of cholangiocarcinoma may be difficult to establish with certainty, even in tissue samples. Thus, new methods which can improve the diagnostic accuracy of cholangiocarcinoma in PSC are needed.",
"We investigated the occurrence of K-ras codon 12 and 13 mutations, p53 protein accumulation, and Ki-67 expression in tumor tissue from PSC patients (n=33) who had developed cholangiocarcinoma, using bile duct specimens exised at liver transplantation of PSC patients without cholangiocarcinoma (n=15) as controls",
"K-ras mutations were present in 11 (33%) of the cholangiocarcinoma samples and significantly more frequent in females. Nine tumors carried a codon 12 mutation, and 2 had a codon 13 mutation. The most frequent substitutions in codon 12 were GGT-->GAT (n=5) and GGT-->TGT (n=3). None of the control bile ducts had K-ras mutations. p53 protein was accumulated in 10 (31%) of the tumors, as opposed to negative findings in all the control samples. Sixteen (48%) tumors revealed either K-ras mutation or p53 accumulation. Ki-67 positivity was significantly higher in cholangiocarcinomas than in the non-neoplastic bile ducts (median 29% vs 12%, respectively; p=0.011)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Bile Duct Neoplasms",
"Cholangiocarcinoma",
"Cholangitis, Sclerosing",
"Disease Progression",
"Female",
"Genes, ras",
"Humans",
"Immunohistochemistry",
"Ki-67 Antigen",
"Male",
"Middle Aged",
"Mutation",
"Tumor Suppressor Protein p53"
]
} | We conclude that K-ras mutations and p53 dysfunction are implicated in tumorigenesis of cholangiocarcinomas arising in PSC patients and that these abnormalities together with increased Ki-67 index may indicate neoplastic progression of bile ducts in these patients. | yes | [
{
"from": "human",
"value": "Question: Are cholangiocarcinoma in primary sclerosing cholangitis : K-ras mutations and Tp53 dysfunction implicated in the neoplastic development?\nContext: {'contexts': ['Cholangiocarcinoma is a feared complication of primary sclerosing cholangitis (PSC). Neoplastic bile duct strictures may be difficult to differentiate cholangiographically from the non-neoplastic bile duct irregularities characteristic of this disorder, and the diagnosis of cholangiocarcinoma may be difficult to establish with certainty, even in tissue samples. Thus, new methods which can improve the diagnostic accuracy of cholangiocarcinoma in PSC are needed.', 'We investigated the occurrence of K-ras codon 12 and 13 mutations, p53 protein accumulation, and Ki-67 expression in tumor tissue from PSC patients (n=33) who had developed cholangiocarcinoma, using bile duct specimens exised at liver transplantation of PSC patients without cholangiocarcinoma (n=15) as controls', 'K-ras mutations were present in 11 (33%) of the cholangiocarcinoma samples and significantly more frequent in females. Nine tumors carried a codon 12 mutation, and 2 had a codon 13 mutation. The most frequent substitutions in codon 12 were GGT-->GAT (n=5) and GGT-->TGT (n=3). None of the control bile ducts had K-ras mutations. p53 protein was accumulated in 10 (31%) of the tumors, as opposed to negative findings in all the control samples. Sixteen (48%) tumors revealed either K-ras mutation or p53 accumulation. Ki-67 positivity was significantly higher in cholangiocarcinomas than in the non-neoplastic bile ducts (median 29% vs 12%, respectively; p=0.011).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Bile Duct Neoplasms', 'Cholangiocarcinoma', 'Cholangitis, Sclerosing', 'Disease Progression', 'Female', 'Genes, ras', 'Humans', 'Immunohistochemistry', 'Ki-67 Antigen', 'Male', 'Middle Aged', 'Mutation', 'Tumor Suppressor Protein p53']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,752,946 | Does aqueous humor stimulate the migration of human trabecular meshwork cells in vitro? | {
"contexts": [
"Depletion of trabecular meshwork cell numbers is a feature of the outflow system in aging and in primary open-angle glaucoma. It is possible that migration stimulated by factors present in aqueous humor may contribute to the cell loss. This investigation assessed the chemoattractant potential of glaucomatous and nonglaucomatous human aqueous humor and fibronectin, one of its constituents, on a range of cultured trabecular meshwork cell lines.",
"Migration was assessed in 48-well modified Boyden chambers. The potential migratory stimulants were soluble fibronectin and glaucomatous and nonglaucomatous aqueous humor. The glaucomatous aqueous samples were collected from patients undergoing trabeculotomy for primary open-angle glaucoma and the normal aqueous from normal bovine eyes and patients undergoing cataract surgery. The target cell types were normal human and bovine meshwork cells grown from explants and two human transformed meshwork cell lines from a normal (HTM-5) and a glaucomatous (HTM-3) source.",
"Soluble fibronectin stimulated all the target cells to migrate with an optimal concentration ranging from 1 to 30 microg/ml, and Zigmond Hirsch checkerboard analysis indicated that both chemotaxis and chemokinesis took place. All the aqueous humor samples stimulated migration of the meshwork cell lines at an optimal concentration of 200 microl/ml. Glaucomatous aqueous humor stimulated a greater migratory response than nonglaucomatous aqueous for two of the four target cell types (P < or = 0.03). Neutralization of the fibronectin content of nonglaucomatous and glaucomatous aqueous by addition of excess anti-fibronectin antibody indicated that fibronectin could account for 35% to 80% of the migratory activity of the aqueous."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Aged",
"Aged, 80 and over",
"Animals",
"Aqueous Humor",
"Cattle",
"Cell Line, Transformed",
"Cell Movement",
"Cells, Cultured",
"Child",
"Child, Preschool",
"Dose-Response Relationship, Drug",
"Fibronectins",
"Glaucoma, Open-Angle",
"Humans",
"Middle Aged",
"Trabecular Meshwork"
]
} | Aqueous humor contains potentially powerful chemoattractants for trabecular meshwork cells. The activity of one of these constituents, fibronectin, has been accounted for by this study. Glaucomatous aqueous appears to be as good and in some cases a better migratory stimulant than nonglaucomatous aqueous in vitro. The migratory evidence points to a trend that may help to explain cell loss in the aging meshwork and possibly some of the extra loss in primary open-angle glaucoma. | yes | [
{
"from": "human",
"value": "Question: Does aqueous humor stimulate the migration of human trabecular meshwork cells in vitro?\nContext: {'contexts': ['Depletion of trabecular meshwork cell numbers is a feature of the outflow system in aging and in primary open-angle glaucoma. It is possible that migration stimulated by factors present in aqueous humor may contribute to the cell loss. This investigation assessed the chemoattractant potential of glaucomatous and nonglaucomatous human aqueous humor and fibronectin, one of its constituents, on a range of cultured trabecular meshwork cell lines.', 'Migration was assessed in 48-well modified Boyden chambers. The potential migratory stimulants were soluble fibronectin and glaucomatous and nonglaucomatous aqueous humor. The glaucomatous aqueous samples were collected from patients undergoing trabeculotomy for primary open-angle glaucoma and the normal aqueous from normal bovine eyes and patients undergoing cataract surgery. The target cell types were normal human and bovine meshwork cells grown from explants and two human transformed meshwork cell lines from a normal (HTM-5) and a glaucomatous (HTM-3) source.', 'Soluble fibronectin stimulated all the target cells to migrate with an optimal concentration ranging from 1 to 30 microg/ml, and Zigmond Hirsch checkerboard analysis indicated that both chemotaxis and chemokinesis took place. All the aqueous humor samples stimulated migration of the meshwork cell lines at an optimal concentration of 200 microl/ml. Glaucomatous aqueous humor stimulated a greater migratory response than nonglaucomatous aqueous for two of the four target cell types (P < or = 0.03). Neutralization of the fibronectin content of nonglaucomatous and glaucomatous aqueous by addition of excess anti-fibronectin antibody indicated that fibronectin could account for 35% to 80% of the migratory activity of the aqueous.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Aged', 'Aged, 80 and over', 'Animals', 'Aqueous Humor', 'Cattle', 'Cell Line, Transformed', 'Cell Movement', 'Cells, Cultured', 'Child', 'Child, Preschool', 'Dose-Response Relationship, Drug', 'Fibronectins', 'Glaucoma, Open-Angle', 'Humans', 'Middle Aged', 'Trabecular Meshwork']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,754,522 | Does synthetic inhibitor of matrix metalloproteinases ( batimastat ) reduce prostate cancer growth in an orthotopic rat model? | {
"contexts": [
"Increased concentrations of metalloproteinases are associated with the invasive and metastatic behavior of several human malignant tumors. Normally, enzymatic activity is tightly regulated by nonspecific mechanisms and specific inhibitors. The aim of the study was to determine the potential of a synthetic metalloproteinase inhibitor, batimastat, to show its in vitro effect on MatLyLu cancer cells and its in vivo effect on tumor growth in orthotopic cancer (R3327 Dunning tumor) in rats.",
"In vitro, a dose response curve of batimastat was generated over 4 days using the MTT assay. Prostate cancer was injected in vivo in male Copenhagen rats by inoculating R3327 Dunning tumor cells (MatLyLu) into the ventral prostatic lobe of 30 rats. Each of 10 rats received batimastat (30 mg/kg body weight) or vehicle administered once a day by i.p. application beginning the day of cell inoculation. Ten rats remained untreated. The effect on local tumor growth was evaluated by measuring tumor weights 20 days after tumor cell inoculation.",
"Significant inhibition of tumor cell proliferation in vitro occurred at 400 and 4,000 ng/ml batimastat. After orthotopic cell inoculation, tumors grew to mean weights of 18.9 g in the control group without treatment, to 22.3 g in the vehicle group, and to 11.1 g in the treated group. In comparison to the control group and to the vehicle group, tumor weights increased significantly less under treatment with batimastat."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Antineoplastic Agents",
"Cell Division",
"Dose-Response Relationship, Drug",
"Male",
"Neoplasm Transplantation",
"Phenylalanine",
"Prostatic Neoplasms",
"Rats",
"Thiophenes",
"Tumor Cells, Cultured"
]
} | Batimastat is able to reduce tumor growth in the standard prostate cancer model. Using this model, activity against cancer progression of future inhibitory agents can be reliably assessed. | yes | [
{
"from": "human",
"value": "Question: Does synthetic inhibitor of matrix metalloproteinases ( batimastat ) reduce prostate cancer growth in an orthotopic rat model?\nContext: {'contexts': ['Increased concentrations of metalloproteinases are associated with the invasive and metastatic behavior of several human malignant tumors. Normally, enzymatic activity is tightly regulated by nonspecific mechanisms and specific inhibitors. The aim of the study was to determine the potential of a synthetic metalloproteinase inhibitor, batimastat, to show its in vitro effect on MatLyLu cancer cells and its in vivo effect on tumor growth in orthotopic cancer (R3327 Dunning tumor) in rats.', 'In vitro, a dose response curve of batimastat was generated over 4 days using the MTT assay. Prostate cancer was injected in vivo in male Copenhagen rats by inoculating R3327 Dunning tumor cells (MatLyLu) into the ventral prostatic lobe of 30 rats. Each of 10 rats received batimastat (30 mg/kg body weight) or vehicle administered once a day by i.p. application beginning the day of cell inoculation. Ten rats remained untreated. The effect on local tumor growth was evaluated by measuring tumor weights 20 days after tumor cell inoculation.', 'Significant inhibition of tumor cell proliferation in vitro occurred at 400 and 4,000 ng/ml batimastat. After orthotopic cell inoculation, tumors grew to mean weights of 18.9 g in the control group without treatment, to 22.3 g in the vehicle group, and to 11.1 g in the treated group. In comparison to the control group and to the vehicle group, tumor weights increased significantly less under treatment with batimastat.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Antineoplastic Agents', 'Cell Division', 'Dose-Response Relationship, Drug', 'Male', 'Neoplasm Transplantation', 'Phenylalanine', 'Prostatic Neoplasms', 'Rats', 'Thiophenes', 'Tumor Cells, Cultured']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,754,523 | Are ornithine decarboxylase activity and its gene expression increased in benign hyperplastic prostate? | {
"contexts": [
"Ornithine decarboxylase (ODC) is the first key enzyme in the polyamine biosynthesis pathway. Polyamine is believed to participate in cellular proliferation and differentiation. To study the relationship between ODC and the pathogenesis of benign prostatic hyperplasia (BPH), the polyamine levels, ODC activities, and expression of ODC mRNA in benign hyperplastic and normal human prostates were assayed.",
"Polyamine contents and ODC activities in tissue extracts were determined by reverse-phase high-performance liquid chromatography and spectrophotometric procedures, respectively. The ODC mRNA levels were assayed by Northern blot analysis.",
"The contents of putrescine, spermidine, and spermine in BPH tissues were 2.2, 3.4, and 6.0 times higher than those in normal tissues, respectively; the ODC activity of BPH tissue was about 3.2 times higher than in normal tissue; the expression level of ODC mRNA in the BPH tissues was greater than that of normal tissues."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Blotting, Northern",
"Gene Expression",
"Humans",
"Male",
"Ornithine Decarboxylase",
"Polyamines",
"Prostatic Hyperplasia",
"Reference Values"
]
} | The findings imply that 1) the increased ODC activity and polyamine content in prostatic tissue may correlate with the pathogenesis of BPH, and 2) the high level of ODC activity is induced by the overexpression of ODC mRNA. | yes | [
{
"from": "human",
"value": "Question: Are ornithine decarboxylase activity and its gene expression increased in benign hyperplastic prostate?\nContext: {'contexts': ['Ornithine decarboxylase (ODC) is the first key enzyme in the polyamine biosynthesis pathway. Polyamine is believed to participate in cellular proliferation and differentiation. To study the relationship between ODC and the pathogenesis of benign prostatic hyperplasia (BPH), the polyamine levels, ODC activities, and expression of ODC mRNA in benign hyperplastic and normal human prostates were assayed.', 'Polyamine contents and ODC activities in tissue extracts were determined by reverse-phase high-performance liquid chromatography and spectrophotometric procedures, respectively. The ODC mRNA levels were assayed by Northern blot analysis.', 'The contents of putrescine, spermidine, and spermine in BPH tissues were 2.2, 3.4, and 6.0 times higher than those in normal tissues, respectively; the ODC activity of BPH tissue was about 3.2 times higher than in normal tissue; the expression level of ODC mRNA in the BPH tissues was greater than that of normal tissues.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Blotting, Northern', 'Gene Expression', 'Humans', 'Male', 'Ornithine Decarboxylase', 'Polyamines', 'Prostatic Hyperplasia', 'Reference Values']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,746,605 | Do line bisection judgments implicate right parietal cortex and cerebellum as assessed by fMRI? | {
"contexts": [
"To use functional MRI (fMRI) to determine which brain regions are implicated when normal volunteers judge whether pretransected horizontal lines are correctly bisected (the Landmark test).",
"Manual line bisection and a variant thereof involving perceptual judgments of pretransected lines (the Landmark test) are widely used to assess unilateral visuospatial neglect in patients with neurologic disease. Although unilateral (left) neglect most often results from lesions to right temporoparietal cortex, the normal functional anatomy of the Landmark test has not been convincingly demonstrated.",
"fMRI was carried out in 12 healthy right-handed male volunteers who judged whether horizontal lines were correctly prebisected. In the control task, subjects detected whether the horizontal lines contained a transection mark irrespective of the position of that mark. Response was by two-choice key press: on half the trials, subjects used the right, and on half, the left hand. Statistical analysis of evoked blood oxygenation level-dependent responses, measured with echoplanar imaging, employed statistical parametric mapping.",
"Performing the Landmark task showed neural activity (p < 0.05, corrected) in the right superior posterior and right inferior parietal lobe, early visual processing areas bilaterally, the cerebellar vermis, and the left cerebellar hemisphere. Only the latter area showed a significant interaction with hand used."
],
"labels": [
"OBJECTIVE",
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Brain Mapping",
"Cerebellum",
"Eye Movements",
"Functional Laterality",
"Humans",
"Image Processing, Computer-Assisted",
"Magnetic Resonance Imaging",
"Male",
"Parietal Lobe",
"Reaction Time",
"Task Performance and Analysis",
"Visual Perception"
]
} | The right hemispheric dominance observed in inferior parietal cortex is consistent with the results of lesion studies. Right superior parietal cortex, vermis, and left cerebellar hemisphere have not been implicated in neglect, but all appear to play a cognitive role in the Landmark task. | yes | [
{
"from": "human",
"value": "Question: Do line bisection judgments implicate right parietal cortex and cerebellum as assessed by fMRI?\nContext: {'contexts': ['To use functional MRI (fMRI) to determine which brain regions are implicated when normal volunteers judge whether pretransected horizontal lines are correctly bisected (the Landmark test).', 'Manual line bisection and a variant thereof involving perceptual judgments of pretransected lines (the Landmark test) are widely used to assess unilateral visuospatial neglect in patients with neurologic disease. Although unilateral (left) neglect most often results from lesions to right temporoparietal cortex, the normal functional anatomy of the Landmark test has not been convincingly demonstrated.', 'fMRI was carried out in 12 healthy right-handed male volunteers who judged whether horizontal lines were correctly prebisected. In the control task, subjects detected whether the horizontal lines contained a transection mark irrespective of the position of that mark. Response was by two-choice key press: on half the trials, subjects used the right, and on half, the left hand. Statistical analysis of evoked blood oxygenation level-dependent responses, measured with echoplanar imaging, employed statistical parametric mapping.', 'Performing the Landmark task showed neural activity (p < 0.05, corrected) in the right superior posterior and right inferior parietal lobe, early visual processing areas bilaterally, the cerebellar vermis, and the left cerebellar hemisphere. Only the latter area showed a significant interaction with hand used.'], 'labels': ['OBJECTIVE', 'BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Brain Mapping', 'Cerebellum', 'Eye Movements', 'Functional Laterality', 'Humans', 'Image Processing, Computer-Assisted', 'Magnetic Resonance Imaging', 'Male', 'Parietal Lobe', 'Reaction Time', 'Task Performance and Analysis', 'Visual Perception']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,755,109 | Is retinal maturation delayed by repeated , but not single , maternal injections of betamethasone in sheep? | {
"contexts": [
"The safety and efficacy of prescribing a single maternal course of corticosteroid during pregnancy has been documented in human trials. However, the current trend is to prescribe repeated courses of corticosteroid. We investigated an aspect of the safety of this practice in an animal model.",
"Date-mated ewes received saline, single or four corticosteroid injections between days 104 and 124 of gestation (term = 150). Lambs were delivered on day 125 or 145 by caesarian section after spinal anaesthesia. Eye diameters were measured and semi-thin toluidine-blue-stained transverse sections of retinae were analysed using an Optimus Image Analysis program.",
"At 125 days, retinal measures in the ventral periphery and area centralis were significantly thinner than control (p = 0.0001). At 145 days, total eye size was significantly reduced compared with control (p = 0.03), and retinal measures in the ventral periphery (p = 0.0001), but not the area centralis (p = 0.19), remained significantly different from control."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Betamethasone",
"Drug Administration Schedule",
"Embryonic and Fetal Development",
"Eye",
"Female",
"Glucocorticoids",
"Maternal-Fetal Exchange",
"Pregnancy",
"Prenatal Exposure Delayed Effects",
"Retina",
"Sheep"
]
} | Repeated maternal administration of corticosteroid may affect retinal maturation in the fetus. | yes | [
{
"from": "human",
"value": "Question: Is retinal maturation delayed by repeated , but not single , maternal injections of betamethasone in sheep?\nContext: {'contexts': ['The safety and efficacy of prescribing a single maternal course of corticosteroid during pregnancy has been documented in human trials. However, the current trend is to prescribe repeated courses of corticosteroid. We investigated an aspect of the safety of this practice in an animal model.', 'Date-mated ewes received saline, single or four corticosteroid injections between days 104 and 124 of gestation (term = 150). Lambs were delivered on day 125 or 145 by caesarian section after spinal anaesthesia. Eye diameters were measured and semi-thin toluidine-blue-stained transverse sections of retinae were analysed using an Optimus Image Analysis program.', 'At 125 days, retinal measures in the ventral periphery and area centralis were significantly thinner than control (p = 0.0001). At 145 days, total eye size was significantly reduced compared with control (p = 0.03), and retinal measures in the ventral periphery (p = 0.0001), but not the area centralis (p = 0.19), remained significantly different from control.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Betamethasone', 'Drug Administration Schedule', 'Embryonic and Fetal Development', 'Eye', 'Female', 'Glucocorticoids', 'Maternal-Fetal Exchange', 'Pregnancy', 'Prenatal Exposure Delayed Effects', 'Retina', 'Sheep']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,734,528 | Does ethnomedical aspects of the commonly used toothbrush stick in Ethiopia? | {
"contexts": [
"To determine the botanical identity, cytotoxicity, and antibacterial property of the commonly used toothbrush sticks in Ethiopia.",
"Research laboratories of the departments of Biology and Chemistry, Addis Ababa University between December 1993 and May 1995.",
"The study was performed by purchasing the commonly used toothbrush sticks from street markets in various towns of Ethiopia. Voucher specimens were collected and their botanical identity was determined following floral keys. The toothbrush sticks were ground in a mill and soaked in absolute methanol for 24 hours and filtered. The filtrates were dried in a rotary evaporator and the crude extracts were stored at 4 degrees C. The crude methanol extracts were used to test their antibacterial activity by impregnating into filter paper discs and placing on test plates of Staphylococcus aureus and Bacillus cerues. Their lethality to brine shrimp (Artemia salina) was performed following standard procedures.",
"Twenty different species of plant used as toothbrush were collected and their botanical identity determined. Crude methanol extracts of only Agave sisalana, Birbira and Hypericum revolutum test concentrations up to 500 micrograms/ml showed weak toxicity to brine shrimp. All the extracts showed antibacterial activity against Staphylococcus aureus and Bacillus cereus by agar diffusion method."
],
"labels": [
"OBJECTIVE",
"METHODS",
"METHODS",
"RESULTS"
],
"meshes": [
"Attitude to Health",
"Bacteria",
"Drug Evaluation, Preclinical",
"Ethiopia",
"Ethnobotany",
"Health Knowledge, Attitudes, Practice",
"Humans",
"Medicine, African Traditional",
"Plant Extracts",
"Plants, Medicinal",
"Toothbrushing"
]
} | Toothbrush sticks can be used by the vast majority of people who cannot afford buying the commercial toothbrush and toothpaste. The toothbrush sticks may be important for the oral and dental hygiene of the users and hence may be useful in decreasing dental caries. Further studies should focus on the effect of the toothbrush sticks against other common bacteria that are associated with dental diseases. | yes | [
{
"from": "human",
"value": "Question: Does ethnomedical aspects of the commonly used toothbrush stick in Ethiopia?\nContext: {'contexts': ['To determine the botanical identity, cytotoxicity, and antibacterial property of the commonly used toothbrush sticks in Ethiopia.', 'Research laboratories of the departments of Biology and Chemistry, Addis Ababa University between December 1993 and May 1995.', 'The study was performed by purchasing the commonly used toothbrush sticks from street markets in various towns of Ethiopia. Voucher specimens were collected and their botanical identity was determined following floral keys. The toothbrush sticks were ground in a mill and soaked in absolute methanol for 24 hours and filtered. The filtrates were dried in a rotary evaporator and the crude extracts were stored at 4 degrees C. The crude methanol extracts were used to test their antibacterial activity by impregnating into filter paper discs and placing on test plates of Staphylococcus aureus and Bacillus cerues. Their lethality to brine shrimp (Artemia salina) was performed following standard procedures.', 'Twenty different species of plant used as toothbrush were collected and their botanical identity determined. Crude methanol extracts of only Agave sisalana, Birbira and Hypericum revolutum test concentrations up to 500 micrograms/ml showed weak toxicity to brine shrimp. All the extracts showed antibacterial activity against Staphylococcus aureus and Bacillus cereus by agar diffusion method.'], 'labels': ['OBJECTIVE', 'METHODS', 'METHODS', 'RESULTS'], 'meshes': ['Attitude to Health', 'Bacteria', 'Drug Evaluation, Preclinical', 'Ethiopia', 'Ethnobotany', 'Health Knowledge, Attitudes, Practice', 'Humans', 'Medicine, African Traditional', 'Plant Extracts', 'Plants, Medicinal', 'Toothbrushing']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,727,493 | Does modulation of single motor unit discharge using magnetic stimulation of the motor cortex in incomplete spinal cord injury? | {
"contexts": [
"Motor evoked potentials (MEPs) and inhibition of voluntary contraction to transcranial magnetic stimulation (TMS) of the motor cortex have longer latencies than normal in patients with incomplete spinal cord injury (iSCI) when assessed using surface EMG. This study now examines the modulation of single motor unit discharges to TMS with the aim of improving resolution of the excitatory and inhibitory responses seen previously in surface EMG recordings.",
"A group of five patients with iSCI (motor level C4-C7) was compared with a group of five healthy control subjects. Single motor unit discharges were recorded with concentric needle electrodes from the first dorsal interosseus muscle during weak voluntary contraction (2%-5% maximum). TMS was applied with a 9 cm circular stimulating coil centred over the vertex. Modulation of single motor unit discharges was assessed using peristimulus time histograms (PSTHs).",
"Mean (SEM) threshold (expressed as percentage of maximum stimulator output (%MSO)) for the excitatory peak (excitation) or inhibitory trough (inhibition) in the PSTHs was higher (p<0.05) in the patients (excitation = 47.1 (5.9) %MSO; inhibition = 44.3 (3.2) %MSO) than in controls (excitation=31.6 (1.2) %MSO; inhibition = 27.4 (1.0) %MSO). Mean latencies of excitation and inhibition were longer (p<0.05) in the patients (excitation=35 (1.8) ms; inhibition = 47.1 (1.8) ms) than in the controls (excitation = 21.1 (1.6) ms; inhibition = 27 (0.4) ms). Furthermore, the latency difference (inhibition-excitation) was longer (p<0.05) in the patients (10.4 (2.1) ms) than in the controls (6.2 (0.6) ms)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Female",
"Humans",
"Magnetics",
"Male",
"Middle Aged",
"Motor Cortex",
"Motor Neurons",
"Reaction Time",
"Spinal Cord Injuries"
]
} | Increased thresholds and latencies of excitation and inhibition may reflect degraded corticospinal transmission in the spinal cord. However, the relatively greater increase in the latency of inhibition compared with excitation in the patients with iSCI may reflect a weak or absent early component of cortical inhibition. Such a change in cortical inhibition may relate to the restoration of useful motor function after iSCI. | yes | [
{
"from": "human",
"value": "Question: Does modulation of single motor unit discharge using magnetic stimulation of the motor cortex in incomplete spinal cord injury?\nContext: {'contexts': ['Motor evoked potentials (MEPs) and inhibition of voluntary contraction to transcranial magnetic stimulation (TMS) of the motor cortex have longer latencies than normal in patients with incomplete spinal cord injury (iSCI) when assessed using surface EMG. This study now examines the modulation of single motor unit discharges to TMS with the aim of improving resolution of the excitatory and inhibitory responses seen previously in surface EMG recordings.', 'A group of five patients with iSCI (motor level C4-C7) was compared with a group of five healthy control subjects. Single motor unit discharges were recorded with concentric needle electrodes from the first dorsal interosseus muscle during weak voluntary contraction (2%-5% maximum). TMS was applied with a 9 cm circular stimulating coil centred over the vertex. Modulation of single motor unit discharges was assessed using peristimulus time histograms (PSTHs).', 'Mean (SEM) threshold (expressed as percentage of maximum stimulator output (%MSO)) for the excitatory peak (excitation) or inhibitory trough (inhibition) in the PSTHs was higher (p<0.05) in the patients (excitation = 47.1 (5.9) %MSO; inhibition = 44.3 (3.2) %MSO) than in controls (excitation=31.6 (1.2) %MSO; inhibition = 27.4 (1.0) %MSO). Mean latencies of excitation and inhibition were longer (p<0.05) in the patients (excitation=35 (1.8) ms; inhibition = 47.1 (1.8) ms) than in the controls (excitation = 21.1 (1.6) ms; inhibition = 27 (0.4) ms). Furthermore, the latency difference (inhibition-excitation) was longer (p<0.05) in the patients (10.4 (2.1) ms) than in the controls (6.2 (0.6) ms).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Female', 'Humans', 'Magnetics', 'Male', 'Middle Aged', 'Motor Cortex', 'Motor Neurons', 'Reaction Time', 'Spinal Cord Injuries']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,736,119 | Is resistive heating more effective than metallic-foil insulation in an experimental model of accidental hypothermia : A randomized controlled trial? | {
"contexts": [
"We study a resistive-heating blanket in a volunteer model of severe accidental hypothermia to evaluate differences in rates of rewarming, core temperature afterdrop, and body heat content and distribution during active and passive rewarming.",
"Eight volunteers participated in a crossover design on 2 days. The volunteers were anesthetized and cooled to 33 degrees C (91.4 degrees F); anesthesia was subsequently discontinued, and shivering was prevented with meperidine. On one randomly assigned day, the volunteers were rewarmed passively with reflective foil (passive insulation), whereas on the other they were covered with a carbon fiber-resistive heating blanket set to 42 degrees C (107.6 degrees F; active rewarming). Trunk and head temperature and heat content were calculated from core (tympanic membrane) temperature. Peripheral (arm and leg) tissue temperature and heat content were estimated by using fourth-order regressions and integration over volume from 30 tissue and skin temperatures.",
"Core heat content increased 73+/-14 kcal (mean+/-SD) during 3 hours of active warming, but only 31+/-24 kcal with passive insulation, a difference of 41+/-20 kcal (95% confidence interval [CI] 27 to 55 kcal; P <. 001). Peripheral tissue heat content increased linearly by 111+/-16 kcal during active warming but only by 38+/-31 kcal during passive warming, a difference of 74+/-34 kcal (95% CI 50 to 97; P <.001). Consequently, total body heat increased 183+/-22 kcal during active warming but only 68+/-54 kcal with passive insulation, a difference of 115+/-42 kcal (95% CI 86 to 144 kcal; P <.001). Core temperature increased from 32.9 degrees C+/-0.2 degrees C to 35.2 degrees C+/-0. 4 degrees C during 3 hours of active warming, a difference of 2.3 degrees C+/-0.4 degrees C. In contrast, core temperature with foil insulation only increased from 32.9 degrees C+/-0.2 degrees C to 33. 8 degrees C+/-0.5 degrees C, a difference of only 0.8 degrees C+/-0. 4 degrees C. The difference in the core temperature increase between the two treatments was thus 1.5 degrees C+/-0.4 degrees C (95% CI 1. 2 degrees C to 1.7 degrees C; P <.001 between treatments). Active warming was not associated with an afterdrop, whereas the afterdrop was 0.2 degrees C+/-0.2 degrees C and lasted a median of 45 minutes (interquartile range, 41 to 64 minutes) with passive insulation."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Bedding and Linens",
"Body Temperature",
"Carbon",
"Cross-Over Studies",
"Energy Metabolism",
"Equipment Design",
"Heart Rate",
"Humans",
"Hypothermia",
"Male",
"Metals",
"Rewarming",
"Skin Temperature"
]
} | Resistive heating more than doubles the rewarming rate compared with that produced by reflective metal foil and does so without producing an afterdrop. It is therefore likely to be useful in the prehospital setting. | yes | [
{
"from": "human",
"value": "Question: Is resistive heating more effective than metallic-foil insulation in an experimental model of accidental hypothermia : A randomized controlled trial?\nContext: {'contexts': ['We study a resistive-heating blanket in a volunteer model of severe accidental hypothermia to evaluate differences in rates of rewarming, core temperature afterdrop, and body heat content and distribution during active and passive rewarming.', 'Eight volunteers participated in a crossover design on 2 days. The volunteers were anesthetized and cooled to 33 degrees C (91.4 degrees F); anesthesia was subsequently discontinued, and shivering was prevented with meperidine. On one randomly assigned day, the volunteers were rewarmed passively with reflective foil (passive insulation), whereas on the other they were covered with a carbon fiber-resistive heating blanket set to 42 degrees C (107.6 degrees F; active rewarming). Trunk and head temperature and heat content were calculated from core (tympanic membrane) temperature. Peripheral (arm and leg) tissue temperature and heat content were estimated by using fourth-order regressions and integration over volume from 30 tissue and skin temperatures.', 'Core heat content increased 73+/-14 kcal (mean+/-SD) during 3 hours of active warming, but only 31+/-24 kcal with passive insulation, a difference of 41+/-20 kcal (95% confidence interval [CI] 27 to 55 kcal; P <. 001). Peripheral tissue heat content increased linearly by 111+/-16 kcal during active warming but only by 38+/-31 kcal during passive warming, a difference of 74+/-34 kcal (95% CI 50 to 97; P <.001). Consequently, total body heat increased 183+/-22 kcal during active warming but only 68+/-54 kcal with passive insulation, a difference of 115+/-42 kcal (95% CI 86 to 144 kcal; P <.001). Core temperature increased from 32.9 degrees C+/-0.2 degrees C to 35.2 degrees C+/-0. 4 degrees C during 3 hours of active warming, a difference of 2.3 degrees C+/-0.4 degrees C. In contrast, core temperature with foil insulation only increased from 32.9 degrees C+/-0.2 degrees C to 33. 8 degrees C+/-0.5 degrees C, a difference of only 0.8 degrees C+/-0. 4 degrees C. The difference in the core temperature increase between the two treatments was thus 1.5 degrees C+/-0.4 degrees C (95% CI 1. 2 degrees C to 1.7 degrees C; P <.001 between treatments). Active warming was not associated with an afterdrop, whereas the afterdrop was 0.2 degrees C+/-0.2 degrees C and lasted a median of 45 minutes (interquartile range, 41 to 64 minutes) with passive insulation.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Bedding and Linens', 'Body Temperature', 'Carbon', 'Cross-Over Studies', 'Energy Metabolism', 'Equipment Design', 'Heart Rate', 'Humans', 'Hypothermia', 'Male', 'Metals', 'Rewarming', 'Skin Temperature']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,747,568 | Do the cost of burn care and implications for efficient care? | {
"contexts": [
"To clarify the social issues and problems associated with burn care in Japan, based on a cost analysis of acute burn care.",
"A retrospective review was undertaken of 71 patients admitted with burns at Nippon Medical School between January 1 and December 31, 1997. A cost analysis was performed for three major burn patients with a burn surface area (BSA) of 70% to 80% and three minor burn patients with a BSA of 20% to 30%. A questionnaire was administered to both burn patients and medical providers in all 127 emergency centers to help improve long-term quality of life (QOL).",
"80% of burn patients were under age 70. In the major burn cases, the amount of reimbursement according to the government-regulated fee schedule was much less than the cost of treatment. The ratio of the cost of both medication and materials to total cost of treatment was higher for patients with major burns. Patients responding to the survey acknowledged being generally happy despite suffering from psychological and financial problems. A total of 413 medical providers from 63 institutions responded to the survey regarding improving long-term QOL."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Aged",
"Burns",
"Child",
"Costs and Cost Analysis",
"Hospital Charges",
"Humans",
"Japan",
"Length of Stay",
"Middle Aged",
"Quality-Adjusted Life Years",
"Retrospective Studies",
"Severity of Illness Index",
"Surveys and Questionnaires"
]
} | Acute burn care is a costly service. The goal of burn care should shift from saving lives to allowing for a productive return to society. Quality improvement, outcome measurement, and technology assessment combined with health economics research for burn care should be carried out in Japan. | yes | [
{
"from": "human",
"value": "Question: Do the cost of burn care and implications for efficient care?\nContext: {'contexts': ['To clarify the social issues and problems associated with burn care in Japan, based on a cost analysis of acute burn care.', 'A retrospective review was undertaken of 71 patients admitted with burns at Nippon Medical School between January 1 and December 31, 1997. A cost analysis was performed for three major burn patients with a burn surface area (BSA) of 70% to 80% and three minor burn patients with a BSA of 20% to 30%. A questionnaire was administered to both burn patients and medical providers in all 127 emergency centers to help improve long-term quality of life (QOL).', '80% of burn patients were under age 70. In the major burn cases, the amount of reimbursement according to the government-regulated fee schedule was much less than the cost of treatment. The ratio of the cost of both medication and materials to total cost of treatment was higher for patients with major burns. Patients responding to the survey acknowledged being generally happy despite suffering from psychological and financial problems. A total of 413 medical providers from 63 institutions responded to the survey regarding improving long-term QOL.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Aged', 'Burns', 'Child', 'Costs and Cost Analysis', 'Hospital Charges', 'Humans', 'Japan', 'Length of Stay', 'Middle Aged', 'Quality-Adjusted Life Years', 'Retrospective Studies', 'Severity of Illness Index', 'Surveys and Questionnaires']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,727,654 | Does angiotensin II receptor blockade attenuate the deleterious effects of exercise training on post-MI ventricular remodelling in rats? | {
"contexts": [
"The effects of exercise training on LV remodelling following large anterior myocardial infarction (MI) remains controversial. Blockade of the renin-angiotensin system has been shown to prevent ventricular dilation and deleterious remodeling. We therefore tested, in a rat model of chronic MI, whether any potentially deleterious effects of exercise on post-MI remodelling could be ameliorated by angiotensin II receptor blockade.",
"Male Wistar rats underwent coronary ligation or sham operation. Treatment with losartan (10 mg/kg/day) began 1 week post-MI and moderate treadmill exercise (25 m/min, 60 min/day, 5 days/week) was initiated 2 weeks post-MI. Systolic and diastolic pressure-volume relationships were measured in isolated, red-cell perfused, isovolumically beating hearts 8 weeks post-MI. Morphometric measurements were performed in trichrome stained cross sections of the heart. Five groups of animals were compared: sham (n=13), control MI (MI; n=11), MI plus losartan (MI-Los; n=13), MI plus exercise (MI-Ex; n=10) and MI plus exercise and losartan (MI-Ex-Los; n=12).",
"Infarct size (% of left ventricle, LV) was similar among the infarcted groups [MI=43+/-4%, MI-Los=49+/-2%, MI-Ex=45+/-1%, MI-Ex-Los=48+/-2% (NS)]. Exercise, losartan and exercise+losartan treatments all attenuated LV dilation post-MI to a similar degree. Exercise training increased LV developed pressure in both untreated and losartan treated hearts (P<0.05 vs. other MI groups). In addition, exercise resulted in additional scar thinning in untreated hearts, while no additional scar thinning was seen in post-infarct hearts receiving both losartan and exercise."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Analysis of Variance",
"Angiotensin Receptor Antagonists",
"Animals",
"Anti-Arrhythmia Agents",
"Losartan",
"Male",
"Myocardial Infarction",
"Myocardium",
"Perfusion",
"Physical Conditioning, Animal",
"Rats",
"Rats, Wistar",
"Receptor, Angiotensin, Type 1",
"Receptor, Angiotensin, Type 2",
"Ventricular Remodeling"
]
} | Following large anterior MI, losartan attenuated LV dilation and scar thinning. In untreated animals, exercise decreased dilation, but also contributed to scar thinning. Therefore, exercise concurrent with blockade of the renin-angiotensin system may provide optimal therapeutic benefit following large anterior MI. | yes | [
{
"from": "human",
"value": "Question: Does angiotensin II receptor blockade attenuate the deleterious effects of exercise training on post-MI ventricular remodelling in rats?\nContext: {'contexts': ['The effects of exercise training on LV remodelling following large anterior myocardial infarction (MI) remains controversial. Blockade of the renin-angiotensin system has been shown to prevent ventricular dilation and deleterious remodeling. We therefore tested, in a rat model of chronic MI, whether any potentially deleterious effects of exercise on post-MI remodelling could be ameliorated by angiotensin II receptor blockade.', 'Male Wistar rats underwent coronary ligation or sham operation. Treatment with losartan (10 mg/kg/day) began 1 week post-MI and moderate treadmill exercise (25 m/min, 60 min/day, 5 days/week) was initiated 2 weeks post-MI. Systolic and diastolic pressure-volume relationships were measured in isolated, red-cell perfused, isovolumically beating hearts 8 weeks post-MI. Morphometric measurements were performed in trichrome stained cross sections of the heart. Five groups of animals were compared: sham (n=13), control MI (MI; n=11), MI plus losartan (MI-Los; n=13), MI plus exercise (MI-Ex; n=10) and MI plus exercise and losartan (MI-Ex-Los; n=12).', 'Infarct size (% of left ventricle, LV) was similar among the infarcted groups [MI=43+/-4%, MI-Los=49+/-2%, MI-Ex=45+/-1%, MI-Ex-Los=48+/-2% (NS)]. Exercise, losartan and exercise+losartan treatments all attenuated LV dilation post-MI to a similar degree. Exercise training increased LV developed pressure in both untreated and losartan treated hearts (P<0.05 vs. other MI groups). In addition, exercise resulted in additional scar thinning in untreated hearts, while no additional scar thinning was seen in post-infarct hearts receiving both losartan and exercise.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Analysis of Variance', 'Angiotensin Receptor Antagonists', 'Animals', 'Anti-Arrhythmia Agents', 'Losartan', 'Male', 'Myocardial Infarction', 'Myocardium', 'Perfusion', 'Physical Conditioning, Animal', 'Rats', 'Rats, Wistar', 'Receptor, Angiotensin, Type 1', 'Receptor, Angiotensin, Type 2', 'Ventricular Remodeling']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,727,655 | Is type 2 angiotensin II receptor downregulated in cardiomyocytes of patients with heart failure? | {
"contexts": [
"The human heart expresses type 2 angiotensin (AT(2)) receptor, but the function is poorly defined.",
"In the present study, we investigated (1) the cellular localization of the AT(2) receptor and (2) the relationship between the AT(2) receptor protein expression and the cardiac function of patients with ischemic heart disease. The receptor localization was assessed by immunohistochemistry and the protein expression was quantified by Western blotting in atrial tissues freshly obtained from 22 patients undergoing coronary artery bypass graft surgery (63.0+/-11.0 years old; male ratio, 85%). Prior to the surgery, blood was drawn for determination of atrial-natriuretic hormone level and the left ventricular function was assessed by ultrasound cardiography.",
"The results of immunohistochemistry showed that the AT(2) receptor was localized to cardiomyocytes and was not present in fibroblasts, vascular smooth muscles, or vascular endothelium. Atrial tissues showed various degrees of structural remodeling, but the localization of the AT(2) receptor was not altered in any tissue sections. The amount of the AT(2) receptor was negatively correlated with end-diastolic left ventricular diastolic dimension (r=-0.56, P<0.01), calculated left ventricular mass index (r=-0.51, P<0.02) and the plasma atrial natriuretic peptide (ANP) concentration (r=-0. 62, P<0.01) and positively correlated with left ventricular ejection fraction (r=0.48, P<0.05)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Aged, 80 and over",
"Blotting, Western",
"Coronary Artery Bypass",
"Echocardiography",
"Female",
"Heart Failure",
"Humans",
"Immunohistochemistry",
"Male",
"Middle Aged",
"Myocardium",
"Receptor, Angiotensin, Type 1",
"Receptor, Angiotensin, Type 2",
"Receptors, Angiotensin",
"Ventricular Dysfunction, Left"
]
} | (1) The AT(2) receptor is localized to cardiomyocytes independently of the cardiac function. (2) Left ventricular dysfunction is associated with decreased expression of myocardial AT(2) receptor protein. | yes | [
{
"from": "human",
"value": "Question: Is type 2 angiotensin II receptor downregulated in cardiomyocytes of patients with heart failure?\nContext: {'contexts': ['The human heart expresses type 2 angiotensin (AT(2)) receptor, but the function is poorly defined.', 'In the present study, we investigated (1) the cellular localization of the AT(2) receptor and (2) the relationship between the AT(2) receptor protein expression and the cardiac function of patients with ischemic heart disease. The receptor localization was assessed by immunohistochemistry and the protein expression was quantified by Western blotting in atrial tissues freshly obtained from 22 patients undergoing coronary artery bypass graft surgery (63.0+/-11.0 years old; male ratio, 85%). Prior to the surgery, blood was drawn for determination of atrial-natriuretic hormone level and the left ventricular function was assessed by ultrasound cardiography.', 'The results of immunohistochemistry showed that the AT(2) receptor was localized to cardiomyocytes and was not present in fibroblasts, vascular smooth muscles, or vascular endothelium. Atrial tissues showed various degrees of structural remodeling, but the localization of the AT(2) receptor was not altered in any tissue sections. The amount of the AT(2) receptor was negatively correlated with end-diastolic left ventricular diastolic dimension (r=-0.56, P<0.01), calculated left ventricular mass index (r=-0.51, P<0.02) and the plasma atrial natriuretic peptide (ANP) concentration (r=-0. 62, P<0.01) and positively correlated with left ventricular ejection fraction (r=0.48, P<0.05).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Aged, 80 and over', 'Blotting, Western', 'Coronary Artery Bypass', 'Echocardiography', 'Female', 'Heart Failure', 'Humans', 'Immunohistochemistry', 'Male', 'Middle Aged', 'Myocardium', 'Receptor, Angiotensin, Type 1', 'Receptor, Angiotensin, Type 2', 'Receptors, Angiotensin', 'Ventricular Dysfunction, Left']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,750,746 | Does hypothermic circulatory arrest cause multisystem vascular endothelial dysfunction and apoptosis? | {
"contexts": [
"Multiple organ failure after deep hypothermic circulatory arrest (DHCA) may occur secondary to endothelial dysfunction and apoptosis. We sought to determine if DHCA causes endothelial dysfunction and apoptosis in brain, kidney, lungs, and other tissues.",
"Anesthetized pigs on cardiopulmonary bypass were: (1) cooled to 18 degrees C, and had their circulation arrested (60 minutes) and reperfused at 37 degrees C for 90 minutes (DHCA, n = 8); or (2) time-matched normothermic controls on bypass (CPB, n = 6). Endothelial function in cerebral, pulmonary, and renal vessels was assessed by vasorelaxation responses to endothelial-specific bradykinin (BK) or acetylcholine (ACh), and smooth muscle-specific nitroprusside.",
"In vivo transcranial vasorelaxation responses to ACh were similar between the two groups. In small-caliber cerebral arteries, endothelial relaxation (BK) was impaired in CPB vs DHCA (maximal 55% +/- 2% [p < 0.05] vs 100% +/- 6%). Pulmonary artery ACh responses were comparable between CPB (110% +/- 10%) and DHCA (83% +/- 6%), but responses in pulmonary vein were impaired in DHCA (109% +/- 3%, p < 0.05) relative to CPB (137% +/- 6%). In renal arteries, endothelial (ACh) responses were impaired in DHCA (71% +/- 13%) relative to CPB (129% +/- 14%). Apoptosis (DNA laddering) occurred primarily in duodenal tissue, with a greater frequency in DHCA (56%, p < 0.05) compared with normothermic CPB (17%) and nonbypass controls (0%)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Apoptosis",
"Brain",
"Cardiopulmonary Bypass",
"Endothelium, Vascular",
"Heart Arrest, Induced",
"Hypothermia, Induced",
"Kidney",
"Lung",
"Swine",
"Vascular Diseases"
]
} | DHCA is associated with endothelial dysfunction in cerebral microvessels but not in the in vivo transcranial vasculature; in addition, endothelial dysfunction was noted in large-caliber renal arteries and pulmonary veins. DHCA is also associated with duodenal apoptosis. Vascular endothelial dysfunction and apoptosis may be involved in the pathophysiology of multisystem organ failure after DHCA. | yes | [
{
"from": "human",
"value": "Question: Does hypothermic circulatory arrest cause multisystem vascular endothelial dysfunction and apoptosis?\nContext: {'contexts': ['Multiple organ failure after deep hypothermic circulatory arrest (DHCA) may occur secondary to endothelial dysfunction and apoptosis. We sought to determine if DHCA causes endothelial dysfunction and apoptosis in brain, kidney, lungs, and other tissues.', 'Anesthetized pigs on cardiopulmonary bypass were: (1) cooled to 18 degrees C, and had their circulation arrested (60 minutes) and reperfused at 37 degrees C for 90 minutes (DHCA, n = 8); or (2) time-matched normothermic controls on bypass (CPB, n = 6). Endothelial function in cerebral, pulmonary, and renal vessels was assessed by vasorelaxation responses to endothelial-specific bradykinin (BK) or acetylcholine (ACh), and smooth muscle-specific nitroprusside.', 'In vivo transcranial vasorelaxation responses to ACh were similar between the two groups. In small-caliber cerebral arteries, endothelial relaxation (BK) was impaired in CPB vs DHCA (maximal 55% +/- 2% [p < 0.05] vs 100% +/- 6%). Pulmonary artery ACh responses were comparable between CPB (110% +/- 10%) and DHCA (83% +/- 6%), but responses in pulmonary vein were impaired in DHCA (109% +/- 3%, p < 0.05) relative to CPB (137% +/- 6%). In renal arteries, endothelial (ACh) responses were impaired in DHCA (71% +/- 13%) relative to CPB (129% +/- 14%). Apoptosis (DNA laddering) occurred primarily in duodenal tissue, with a greater frequency in DHCA (56%, p < 0.05) compared with normothermic CPB (17%) and nonbypass controls (0%).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Apoptosis', 'Brain', 'Cardiopulmonary Bypass', 'Endothelium, Vascular', 'Heart Arrest, Induced', 'Hypothermia, Induced', 'Kidney', 'Lung', 'Swine', 'Vascular Diseases']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,739,524 | Is adrenomedullin increased in the fetoplacental circulation in intrauterine growth restriction with abnormal umbilical artery waveforms? | {
"contexts": [
"To examine whether adrenomedullin, a novel vasoactive peptide produced by the placenta, participates in the uteroplacental hemodynamic alterations in intrauterine growth restriction, we studied the correlation between adrenomedullin levels and fetoplacental blood flow.",
"Maternal and umbilical blood samples were collected in pregnancies complicated by intrauterine growth restriction with abnormal umbilical artery Doppler findings and in control pregnancies. Adrenomedullin levels were measured by means of a specific radioimmunoassay, and flow velocimetry waveforms were recorded from uterine, umbilical, and fetal middle cerebral arteries.",
"Mean adrenomedullin values in umbilical plasma were higher (P <.05) in patients with intrauterine growth restriction (63.7 +/- 34.2 pg/mL; n = 16) than in control subjects (38.1 +/- 14.8 pg/mL; n = 16). A significant correlation was found between maternal adrenomedullin levels and umbilical artery pulsatility index. Moreover, fetal adrenomedullin concentrations correlated negatively with middle cerebral artery pulsatility index and positively with umbilical artery pulsatility index/middle cerebral artery pulsatility index ratio."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adrenomedullin",
"Adult",
"Birth Weight",
"Blood Flow Velocity",
"Female",
"Fetal Growth Retardation",
"Gestational Age",
"Humans",
"Peptides",
"Placental Insufficiency",
"Pregnancy",
"Ultrasonography, Prenatal"
]
} | This study provides evidence that adrenomedullin is increased in fetuses with intrauterine growth restriction in response to reduced uteroplacental blood flow and suggests that it may participate in the fetal hemodynamic modifications. | yes | [
{
"from": "human",
"value": "Question: Is adrenomedullin increased in the fetoplacental circulation in intrauterine growth restriction with abnormal umbilical artery waveforms?\nContext: {'contexts': ['To examine whether adrenomedullin, a novel vasoactive peptide produced by the placenta, participates in the uteroplacental hemodynamic alterations in intrauterine growth restriction, we studied the correlation between adrenomedullin levels and fetoplacental blood flow.', 'Maternal and umbilical blood samples were collected in pregnancies complicated by intrauterine growth restriction with abnormal umbilical artery Doppler findings and in control pregnancies. Adrenomedullin levels were measured by means of a specific radioimmunoassay, and flow velocimetry waveforms were recorded from uterine, umbilical, and fetal middle cerebral arteries.', 'Mean adrenomedullin values in umbilical plasma were higher (P <.05) in patients with intrauterine growth restriction (63.7 +/- 34.2 pg/mL; n = 16) than in control subjects (38.1 +/- 14.8 pg/mL; n = 16). A significant correlation was found between maternal adrenomedullin levels and umbilical artery pulsatility index. Moreover, fetal adrenomedullin concentrations correlated negatively with middle cerebral artery pulsatility index and positively with umbilical artery pulsatility index/middle cerebral artery pulsatility index ratio.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adrenomedullin', 'Adult', 'Birth Weight', 'Blood Flow Velocity', 'Female', 'Fetal Growth Retardation', 'Gestational Age', 'Humans', 'Peptides', 'Placental Insufficiency', 'Pregnancy', 'Ultrasonography, Prenatal']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,728,212 | Is loss of CO2 reactivity of cerebral blood flow associated with severe brain damage in mechanically ventilated very low birth weight infants? | {
"contexts": [
"Early detection of pathophysiological factors associated with permanent and severe brain damage in preterm infants requiring intensive care is a major issue in neonatal neurology. The aim of this study was to investigate if an abnormal CO2 reactivity of cerebral blood flow in high risk very low birth weight infants is associated with severe brain injury demonstrated at autopsy or by neurodevelopment examination at 18 months.",
"The CO2 reactivity of cerebral blood flow (xenon-133) was measured in 18 mechanically ventilated, severely ill, very low birthweight infants (gestational age 26-32 weeks, birthweight: 630-1360 g) during the first 36 hours of life. Cerebral outcome was assessed on autopsy findings (n = 8) or at the age of 18 months using Bayley developmental scales (n = 10).",
"Eight infants with normal development at 18 months (within mean +/- 2.5 SD of reference group) and two infants with normal cerebral autopsy findings had a median CO2 reactivity of 24.4%/kPa CO2 (interquartile range 14.7-41.2). Two infants with abnormal development (> 2.5 SD below mean) and six infants with hypoxic-ischaemic encephalopathy at autopsy has a median CO2 reactivity of 3.4%/kPa CO2 (interquartile range 8.0-11.7)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Brain",
"Brain Damage, Chronic",
"Carbon Dioxide",
"Female",
"Follow-Up Studies",
"Humans",
"Hypoxia-Ischemia, Brain",
"Infant",
"Infant, Newborn",
"Infant, Premature, Diseases",
"Infant, Very Low Birth Weight",
"Male",
"Regional Blood Flow",
"Respiration, Artificial",
"Vascular Resistance"
]
} | In mechanically ventilated very low birthweight infants low CO2 reactivity of cerebral blood flow (below 10%/kPa CO2) during the first 36 hours of life was associated with poor neurodevelopmental outcome or hypoxic-ischaemic encephalopathy at autopsy. Loss of CO2 reactivity may play a role in the pathogenesis of hypoxic ischaemic encephalopathy. It is a candidate for predicting early severe brain damage in preterm infants requiring intensive care and for controlling the effect of early interventions. | yes | [
{
"from": "human",
"value": "Question: Is loss of CO2 reactivity of cerebral blood flow associated with severe brain damage in mechanically ventilated very low birth weight infants?\nContext: {'contexts': ['Early detection of pathophysiological factors associated with permanent and severe brain damage in preterm infants requiring intensive care is a major issue in neonatal neurology. The aim of this study was to investigate if an abnormal CO2 reactivity of cerebral blood flow in high risk very low birth weight infants is associated with severe brain injury demonstrated at autopsy or by neurodevelopment examination at 18 months.', 'The CO2 reactivity of cerebral blood flow (xenon-133) was measured in 18 mechanically ventilated, severely ill, very low birthweight infants (gestational age 26-32 weeks, birthweight: 630-1360 g) during the first 36 hours of life. Cerebral outcome was assessed on autopsy findings (n = 8) or at the age of 18 months using Bayley developmental scales (n = 10).', 'Eight infants with normal development at 18 months (within mean +/- 2.5 SD of reference group) and two infants with normal cerebral autopsy findings had a median CO2 reactivity of 24.4%/kPa CO2 (interquartile range 14.7-41.2). Two infants with abnormal development (> 2.5 SD below mean) and six infants with hypoxic-ischaemic encephalopathy at autopsy has a median CO2 reactivity of 3.4%/kPa CO2 (interquartile range 8.0-11.7).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Brain', 'Brain Damage, Chronic', 'Carbon Dioxide', 'Female', 'Follow-Up Studies', 'Humans', 'Hypoxia-Ischemia, Brain', 'Infant', 'Infant, Newborn', 'Infant, Premature, Diseases', 'Infant, Very Low Birth Weight', 'Male', 'Regional Blood Flow', 'Respiration, Artificial', 'Vascular Resistance']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,732,289 | Are presence and extent of extrapancreatic fluid collections indicators of severe acute pancreatitis? | {
"contexts": [
"It has been suggested that early localization of both necrosis and extrapancreatic fluid collections by contrast-enhanced computed tomography (CT) can predict the outcome in severe acute pancreatitis. These two assumptions were evaluated.",
"This study comprises 228 patients with a first attack of acute pancreatitis admitted to our clinic from 1987 to 1995 and for whom the prognostic value of a contrast-enhanced CT obtained within 72 h of admission was prospectively evaluated. These CTs were retrospectively re-evaluated for the localization of pancreatic necrosis and extrapancreatic fluid collections. The indication for dialysis and artificial ventilation, the development of pancreatic pseudocysts, the necessity for surgery (necrosectomy), and mortality were used as clinical parameters.",
"There was a significant correlation between the presence of pancreatic necrosis and extrapancreatic fluid collections versus the clinical parameters. The localization of pancreatic necrosis was of no importance for the outcome of the disease, whereas the increasing amount of extrapancreatic fluid collections paralleled the severity of acute pancreatitis."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Abdomen",
"Acute Disease",
"Adult",
"Body Fluids",
"Evaluation Studies as Topic",
"Humans",
"Middle Aged",
"Models, Biological",
"Necrosis",
"Pancreas",
"Pancreatitis",
"Radiography, Abdominal",
"Severity of Illness Index",
"Tomography, X-Ray Computed"
]
} | Pancreatic necrosis and extrapancreatic fluid collections are indicators for severe acute pancreatitis. Whereas the localization of pancreatic necrosis is not important for the outcome of the disease, the extent of extrapancreatic fluid collections is significantly correlated with a severe course. | yes | [
{
"from": "human",
"value": "Question: Are presence and extent of extrapancreatic fluid collections indicators of severe acute pancreatitis?\nContext: {'contexts': ['It has been suggested that early localization of both necrosis and extrapancreatic fluid collections by contrast-enhanced computed tomography (CT) can predict the outcome in severe acute pancreatitis. These two assumptions were evaluated.', 'This study comprises 228 patients with a first attack of acute pancreatitis admitted to our clinic from 1987 to 1995 and for whom the prognostic value of a contrast-enhanced CT obtained within 72 h of admission was prospectively evaluated. These CTs were retrospectively re-evaluated for the localization of pancreatic necrosis and extrapancreatic fluid collections. The indication for dialysis and artificial ventilation, the development of pancreatic pseudocysts, the necessity for surgery (necrosectomy), and mortality were used as clinical parameters.', 'There was a significant correlation between the presence of pancreatic necrosis and extrapancreatic fluid collections versus the clinical parameters. The localization of pancreatic necrosis was of no importance for the outcome of the disease, whereas the increasing amount of extrapancreatic fluid collections paralleled the severity of acute pancreatitis.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Abdomen', 'Acute Disease', 'Adult', 'Body Fluids', 'Evaluation Studies as Topic', 'Humans', 'Middle Aged', 'Models, Biological', 'Necrosis', 'Pancreas', 'Pancreatitis', 'Radiography, Abdominal', 'Severity of Illness Index', 'Tomography, X-Ray Computed']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,738,224 | Is human tumor growth inhibited by a vaccinia virus carrying the E2 gene of bovine papillomavirus? | {
"contexts": [
"Papillomavirus is the etiologic agent associated with cervical carcinoma. The papilloma E2 protein is able to regulate negatively the expression of E6 and E7 papilloma oncoproteins. Therefore, a new, highly attenuated vaccinia virus known as modified vaccinia virus Ankara (MVA), which carries the papillomavirus E2 gene, was used for the treatment of tumors associated with human papillomavirus.",
"Analysis of expression of the E2 gene from the recombinant vaccinia virus was performed by reverse transcription-polymerase chain reaction of RNA isolated from infected cells. Detection of the E2 protein was done by immunoprecipitation from proteins labeled with [(35)S]-methionine, isolated from infected cells. The therapeutic effect of the MVA E2 recombinant virus over human tumors was tested in nude mice bearing tumors generated by inoculation of HeLa cells. Series of 10 nude mice with tumors of different sizes were injected with MVA, MVA E2, or phosphate-buffered saline. Tumor size was monitored every week to assess growth.",
"The MVA E2 recombinant virus efficiently expressed the E2 protein in BS-C-1 cells. This protein was able to repress, in vivo, the papillomavirus P105 promoter, which controls the expression of the E6 and E7 oncoproteins. In nude mice the MVA E2 virus reduced tumor growth very efficiently. In contrast, tumors continued to grow in mice treated with MVA or PBS. The life expectancy of MVA E2-treated mice was also increased three- to fourfold compared with that of animals that received MVA or PBS."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"3T3 Cells",
"Animals",
"Apoptosis",
"Cell Line",
"Chick Embryo",
"DNA-Binding Proteins",
"Disease-Free Survival",
"Genetic Therapy",
"HeLa Cells",
"Humans",
"Male",
"Mice",
"Mice, Nude",
"Models, Genetic",
"Neoplasm Transplantation",
"Plasmids",
"Promoter Regions, Genetic",
"Recombinant Proteins",
"Reverse Transcriptase Polymerase Chain Reaction",
"Time Factors",
"Vaccinia virus",
"Viral Proteins",
"beta-Galactosidase"
]
} | The growth of human tumors was efficiently inhibited by the MVA E2 recombinant vaccinia virus. The absence of side effects in treated animals suggested that the MVA E2 virus is a safe biologic agent that could in the future be used in humans for the treatment of cervical carcinoma. | yes | [
{
"from": "human",
"value": "Question: Is human tumor growth inhibited by a vaccinia virus carrying the E2 gene of bovine papillomavirus?\nContext: {'contexts': ['Papillomavirus is the etiologic agent associated with cervical carcinoma. The papilloma E2 protein is able to regulate negatively the expression of E6 and E7 papilloma oncoproteins. Therefore, a new, highly attenuated vaccinia virus known as modified vaccinia virus Ankara (MVA), which carries the papillomavirus E2 gene, was used for the treatment of tumors associated with human papillomavirus.', 'Analysis of expression of the E2 gene from the recombinant vaccinia virus was performed by reverse transcription-polymerase chain reaction of RNA isolated from infected cells. Detection of the E2 protein was done by immunoprecipitation from proteins labeled with [(35)S]-methionine, isolated from infected cells. The therapeutic effect of the MVA E2 recombinant virus over human tumors was tested in nude mice bearing tumors generated by inoculation of HeLa cells. Series of 10 nude mice with tumors of different sizes were injected with MVA, MVA E2, or phosphate-buffered saline. Tumor size was monitored every week to assess growth.', 'The MVA E2 recombinant virus efficiently expressed the E2 protein in BS-C-1 cells. This protein was able to repress, in vivo, the papillomavirus P105 promoter, which controls the expression of the E6 and E7 oncoproteins. In nude mice the MVA E2 virus reduced tumor growth very efficiently. In contrast, tumors continued to grow in mice treated with MVA or PBS. The life expectancy of MVA E2-treated mice was also increased three- to fourfold compared with that of animals that received MVA or PBS.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['3T3 Cells', 'Animals', 'Apoptosis', 'Cell Line', 'Chick Embryo', 'DNA-Binding Proteins', 'Disease-Free Survival', 'Genetic Therapy', 'HeLa Cells', 'Humans', 'Male', 'Mice', 'Mice, Nude', 'Models, Genetic', 'Neoplasm Transplantation', 'Plasmids', 'Promoter Regions, Genetic', 'Recombinant Proteins', 'Reverse Transcriptase Polymerase Chain Reaction', 'Time Factors', 'Vaccinia virus', 'Viral Proteins', 'beta-Galactosidase']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,738,227 | Is squamous papilloma of the urinary tract unrelated to condyloma acuminata? | {
"contexts": [
"To the authors' knowledge, there is no previous report of squamous papilloma of the urinary tract. It is uncertain whether there is a correlation between squamous papilloma, condyloma acuminatum, and verrucous carcinoma.",
"The authors evaluated the clinical and pathologic features of squamous papilloma (5 of the bladder, 2 of the urethra), condyloma acuminatum (3 cases), and verrucous carcinoma (3 cases) of the urinary bladder and performed human papillomavirus (HPV) DNA in situ hybridization studies to determine whether HPV was a common feature shared by these lesions. In addition, DNA ploidy evaluation by image cytometry and p53 immunohistochemical staining were performed.",
"Squamous papilloma of the urinary tract occurred in elderly women and followed a benign clinical course with infrequent recurrence. All squamous papillomas were HPV DNA negative and DNA diploid with no or minimal p53 nuclear accumulation. Condyloma acuminata of the bladder contained HPV DNA, increased p53 protein expression, and aneuploid DNA content. All three cases of condyloma acuminata were associated with coexistent condylomata of the external genitalia, and two required pelvic exenteration for uncontrolled expansile growth. Verrucous carcinoma of the bladder occurred in elderly patients. All three cases of verrucous carcinoma were negative for HPV DNA and DNA aneuploid, and they exhibited consistent p53 expression."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Carcinoma, Verrucous",
"Condylomata Acuminata",
"Diagnosis, Differential",
"Female",
"Humans",
"Immunohistochemistry",
"In Situ Hybridization",
"Male",
"Middle Aged",
"Papilloma",
"Papillomaviridae",
"Ploidies",
"Tumor Suppressor Protein p53",
"Urologic Neoplasms"
]
} | These data indicate that squamous papilloma is a distinct entity not related to condyloma or verrucous carcinoma. These lesions are benign, HPV DNA negative, DNA diploid, and they lack p53 overaccumulation. | yes | [
{
"from": "human",
"value": "Question: Is squamous papilloma of the urinary tract unrelated to condyloma acuminata?\nContext: {'contexts': [\"To the authors' knowledge, there is no previous report of squamous papilloma of the urinary tract. It is uncertain whether there is a correlation between squamous papilloma, condyloma acuminatum, and verrucous carcinoma.\", 'The authors evaluated the clinical and pathologic features of squamous papilloma (5 of the bladder, 2 of the urethra), condyloma acuminatum (3 cases), and verrucous carcinoma (3 cases) of the urinary bladder and performed human papillomavirus (HPV) DNA in situ hybridization studies to determine whether HPV was a common feature shared by these lesions. In addition, DNA ploidy evaluation by image cytometry and p53 immunohistochemical staining were performed.', 'Squamous papilloma of the urinary tract occurred in elderly women and followed a benign clinical course with infrequent recurrence. All squamous papillomas were HPV DNA negative and DNA diploid with no or minimal p53 nuclear accumulation. Condyloma acuminata of the bladder contained HPV DNA, increased p53 protein expression, and aneuploid DNA content. All three cases of condyloma acuminata were associated with coexistent condylomata of the external genitalia, and two required pelvic exenteration for uncontrolled expansile growth. Verrucous carcinoma of the bladder occurred in elderly patients. All three cases of verrucous carcinoma were negative for HPV DNA and DNA aneuploid, and they exhibited consistent p53 expression.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Carcinoma, Verrucous', 'Condylomata Acuminata', 'Diagnosis, Differential', 'Female', 'Humans', 'Immunohistochemistry', 'In Situ Hybridization', 'Male', 'Middle Aged', 'Papilloma', 'Papillomaviridae', 'Ploidies', 'Tumor Suppressor Protein p53', 'Urologic Neoplasms']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,740,142 | Does endothelial cell dysfunction correlate differentially with survival in primary and secondary pulmonary hypertension? | {
"contexts": [
"Plasma von Willebrand factor antigen (vWF:Ag) has been used as a marker of endothelial perturbation in a number of vascular disorders. In this study, vWF:Ag was determined as an attempt to evaluate the severity of endothelial cell dysfunction in primary pulmonary hypertension (PPH) and congenital heart disease-associated pulmonary hypertension (CHD-PH) comparatively and to determine its impact on short-term survival.",
"Clinical, hemodynamic, and biochemical data were obtained from 11 patients with PPH and 24 with CHD-PH. Patient groups were similar in terms of age and pulmonary artery pressure. vWF:Ag was measured by electroimmunodiffusion. Patients were followed up for 1 year and at that time, data collected at the beginning of the study were subjected to univariate and multivariate analyses. vWF:Ag was increased in patients (normal reference value 87% +/- 23% activity, mean +/- SD), with higher levels in the PPH group (231% +/- 89%) in comparison with the CHD-PH group (127% +/- 68%) (P <.001). Multivariate analysis showed that survival was influenced by the underlying cause of pulmonary hypertension and vWF:Ag levels but not by patient age, sex, or pulmonary artery pressure. Seven of 10 nonsurvivors but only 4 of 25 survivors had PPH (P =.007). vWF:Ag was 255% +/- 90% in the nonsurvivor group and 121% +/- 54% in the survivors (P <.001)."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Child",
"Child, Preschool",
"Endothelium, Vascular",
"Female",
"Follow-Up Studies",
"Heart Defects, Congenital",
"Hemodynamics",
"Humans",
"Hypertension, Pulmonary",
"Infant",
"Male",
"Middle Aged",
"Pulmonary Wedge Pressure",
"Survival Rate",
"von Willebrand Factor"
]
} | Our findings suggest that short-term survival is related to the severity of endothelial cell dysfunction in pulmonary hypertension. In addition, exceedingly high vWF:Ag levels in PPH might reflect a particular pattern of endothelial cell dysfunction that could be associated with decreased short-term life expectancy in this disorder compared with secondary forms of pulmonary hypertension. | yes | [
{
"from": "human",
"value": "Question: Does endothelial cell dysfunction correlate differentially with survival in primary and secondary pulmonary hypertension?\nContext: {'contexts': ['Plasma von Willebrand factor antigen (vWF:Ag) has been used as a marker of endothelial perturbation in a number of vascular disorders. In this study, vWF:Ag was determined as an attempt to evaluate the severity of endothelial cell dysfunction in primary pulmonary hypertension (PPH) and congenital heart disease-associated pulmonary hypertension (CHD-PH) comparatively and to determine its impact on short-term survival.', 'Clinical, hemodynamic, and biochemical data were obtained from 11 patients with PPH and 24 with CHD-PH. Patient groups were similar in terms of age and pulmonary artery pressure. vWF:Ag was measured by electroimmunodiffusion. Patients were followed up for 1 year and at that time, data collected at the beginning of the study were subjected to univariate and multivariate analyses. vWF:Ag was increased in patients (normal reference value 87% +/- 23% activity, mean +/- SD), with higher levels in the PPH group (231% +/- 89%) in comparison with the CHD-PH group (127% +/- 68%) (P <.001). Multivariate analysis showed that survival was influenced by the underlying cause of pulmonary hypertension and vWF:Ag levels but not by patient age, sex, or pulmonary artery pressure. Seven of 10 nonsurvivors but only 4 of 25 survivors had PPH (P =.007). vWF:Ag was 255% +/- 90% in the nonsurvivor group and 121% +/- 54% in the survivors (P <.001).'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Child', 'Child, Preschool', 'Endothelium, Vascular', 'Female', 'Follow-Up Studies', 'Heart Defects, Congenital', 'Hemodynamics', 'Humans', 'Hypertension, Pulmonary', 'Infant', 'Male', 'Middle Aged', 'Pulmonary Wedge Pressure', 'Survival Rate', 'von Willebrand Factor']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,735,925 | Does cure of Helicobacter pylori infection improve symptoms in non-ulcer dyspepsia patients-a double-blind placebo-controlled study? | {
"contexts": [
"It remains controversial whether the cure of H. pylori infection improves NUD symptoms.",
"To conduct a double-blind placebo-controlled single centre study with concealed allocation to investigate this question.",
"Ninety NUD patients with H. pylori infection were randomly assigned to either the treatment group (50 patients) or placebo group (40 patients). The treatment group received omeprazole, amoxycillin, clarithromycin and the placebo group received omeprazole and placebos for 7 days. Symptoms were assessed every week for up to 12 weeks after completion of medication by a symptom questionnaire. Alteration of histological parameters for gastritis was also evaluated.",
"The infection was cured in 41 out of 48 patients in the treatment group and none in the placebo group. There was no significant difference in the mean symptom scores at any assessment point up to 12 weeks between the treatment and placebo groups. Regarding histological parameters, activity and inflammation, not atrophy or intestinal metaplasia, were significantly improved in the treatment group."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Amoxicillin",
"Anti-Bacterial Agents",
"Anti-Ulcer Agents",
"Clarithromycin",
"Double-Blind Method",
"Dyspepsia",
"Female",
"Helicobacter Infections",
"Helicobacter pylori",
"Humans",
"Male",
"Middle Aged",
"Omeprazole",
"Patient Compliance",
"Penicillins",
"Time Factors",
"Treatment Outcome"
]
} | Although histological parameters were significantly improved in the treatment group, there was no significant improvement in symptoms of NUD in the treatment group compared to placebo. | no | [
{
"from": "human",
"value": "Question: Does cure of Helicobacter pylori infection improve symptoms in non-ulcer dyspepsia patients-a double-blind placebo-controlled study?\nContext: {'contexts': ['It remains controversial whether the cure of H. pylori infection improves NUD symptoms.', 'To conduct a double-blind placebo-controlled single centre study with concealed allocation to investigate this question.', 'Ninety NUD patients with H. pylori infection were randomly assigned to either the treatment group (50 patients) or placebo group (40 patients). The treatment group received omeprazole, amoxycillin, clarithromycin and the placebo group received omeprazole and placebos for 7 days. Symptoms were assessed every week for up to 12 weeks after completion of medication by a symptom questionnaire. Alteration of histological parameters for gastritis was also evaluated.', 'The infection was cured in 41 out of 48 patients in the treatment group and none in the placebo group. There was no significant difference in the mean symptom scores at any assessment point up to 12 weeks between the treatment and placebo groups. Regarding histological parameters, activity and inflammation, not atrophy or intestinal metaplasia, were significantly improved in the treatment group.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Amoxicillin', 'Anti-Bacterial Agents', 'Anti-Ulcer Agents', 'Clarithromycin', 'Double-Blind Method', 'Dyspepsia', 'Female', 'Helicobacter Infections', 'Helicobacter pylori', 'Humans', 'Male', 'Middle Aged', 'Omeprazole', 'Patient Compliance', 'Penicillins', 'Time Factors', 'Treatment Outcome']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
10,744,792 | Does the distinct HERG missense mutation L564P cause long QT syndrome in one French Canadian family? | {
"contexts": [
"Long QT syndrome is a congenital abnormality of cardiac repolarization causing syncope and sudden death from ventricular tachyarrhythmias known as torsades de pointes. This hereditary cardiac disorder often shows an increase of the value of the QT interval corrected for heart rate over 0.45 s in a 12-lead electrocardiogram.",
"To find and identify pertinent mutations occurring in French Canadians by extracting genomic DNA from blood samples and performing a combination of polymerase chain reaction (PCR), single-strand conformational polymorphism and DNA sequencing.",
"A novel mutation was identified in the S5 region of the HERG potassium channel. In codon 564 CTA, T was replaced by C, resulting in a leucine to proline substitution. Two family members had the mutation in two distinct generations. A new restriction site was created at this position and therefore enabled the development of a rapid diagnostic test using PCR. HERG wild type and mutant potassium channel mRNAs were then expressed in Xenopus laevis oocytes."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Adult",
"Canada",
"Cation Transport Proteins",
"Child",
"DNA-Binding Proteins",
"ERG1 Potassium Channel",
"Electrophysiology",
"Ether-A-Go-Go Potassium Channels",
"Female",
"Humans",
"Long QT Syndrome",
"Male",
"Mutation, Missense",
"Polymerase Chain Reaction",
"Polymorphism, Single-Stranded Conformational",
"Potassium Channels",
"Potassium Channels, Voltage-Gated",
"Trans-Activators",
"Transcriptional Regulator ERG"
]
} | This electrophysiological study suggests that coexpression of HERG wild type and mutant L564P results in a dominant negative effect of the mutation. | yes | [
{
"from": "human",
"value": "Question: Does the distinct HERG missense mutation L564P cause long QT syndrome in one French Canadian family?\nContext: {'contexts': ['Long QT syndrome is a congenital abnormality of cardiac repolarization causing syncope and sudden death from ventricular tachyarrhythmias known as torsades de pointes. This hereditary cardiac disorder often shows an increase of the value of the QT interval corrected for heart rate over 0.45 s in a 12-lead electrocardiogram.', 'To find and identify pertinent mutations occurring in French Canadians by extracting genomic DNA from blood samples and performing a combination of polymerase chain reaction (PCR), single-strand conformational polymorphism and DNA sequencing.', 'A novel mutation was identified in the S5 region of the HERG potassium channel. In codon 564 CTA, T was replaced by C, resulting in a leucine to proline substitution. Two family members had the mutation in two distinct generations. A new restriction site was created at this position and therefore enabled the development of a rapid diagnostic test using PCR. HERG wild type and mutant potassium channel mRNAs were then expressed in Xenopus laevis oocytes.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'RESULTS'], 'meshes': ['Adult', 'Canada', 'Cation Transport Proteins', 'Child', 'DNA-Binding Proteins', 'ERG1 Potassium Channel', 'Electrophysiology', 'Ether-A-Go-Go Potassium Channels', 'Female', 'Humans', 'Long QT Syndrome', 'Male', 'Mutation, Missense', 'Polymerase Chain Reaction', 'Polymorphism, Single-Stranded Conformational', 'Potassium Channels', 'Potassium Channels, Voltage-Gated', 'Trans-Activators', 'Transcriptional Regulator ERG']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,731,552 | Does human ovarian follicular fluid have functional systems for the generation and modulation of thrombin? | {
"contexts": [
"To determine whether prothrombin is present in follicular fluid and whether the enzymatic pathways for prothrombin activation are similar to those in plasma.",
"Follicular fluid samples collected at the time of oocyte harvest for an assisted reproductive technology procedure (ART) were analyzed for a panel of hemostatic proteins with use of a combination of functional, chromogenic, and Western ligand blot analysis.",
"An ART clinic and an academic research laboratory.",
"Women undergoing ART.",
"None.",
"Determination of components of thrombin generation and thrombin modulatory systems using functional and antigenic assay procedures.",
"Both prothrombin and components of the prothrombinase enzyme complex, which includes factors V, VII, and X, are present in follicular fluid. Other hemostatic proteins, including factors VIII and IX and vonWillebrand factor, are absent. The direct activation of prothrombin to thrombin is similar in follicular fluid and plasma. Like plasma, inhibitors of both thrombin and thrombin generation, including antithrombin, protein C, and alpha2-macroglobulin, are present in follicular fluid."
],
"labels": [
"OBJECTIVE",
"METHODS",
"METHODS",
"METHODS",
"METHODS",
"METHODS",
"RESULTS"
],
"meshes": [
"Blood Proteins",
"Ceruloplasmin",
"Factor IX",
"Factor VII",
"Factor X",
"Female",
"Follicular Fluid",
"Humans",
"Protein C",
"Proteins",
"Prothrombin",
"Thrombin",
"von Willebrand Factor"
]
} | Only a select group of hemostatic plasma proteins are present in follicular fluid. There is no direct correlation between molecular size and concentration of individual proteins in follicular fluid. These results indicate that the proteins involved in the thrombin-generating and thrombin modulatory pathways may be derived from ovarian cells, suggesting that thrombin may have a role in folliculogenesis. | yes | [
{
"from": "human",
"value": "Question: Does human ovarian follicular fluid have functional systems for the generation and modulation of thrombin?\nContext: {'contexts': ['To determine whether prothrombin is present in follicular fluid and whether the enzymatic pathways for prothrombin activation are similar to those in plasma.', 'Follicular fluid samples collected at the time of oocyte harvest for an assisted reproductive technology procedure (ART) were analyzed for a panel of hemostatic proteins with use of a combination of functional, chromogenic, and Western ligand blot analysis.', 'An ART clinic and an academic research laboratory.', 'Women undergoing ART.', 'None.', 'Determination of components of thrombin generation and thrombin modulatory systems using functional and antigenic assay procedures.', 'Both prothrombin and components of the prothrombinase enzyme complex, which includes factors V, VII, and X, are present in follicular fluid. Other hemostatic proteins, including factors VIII and IX and vonWillebrand factor, are absent. The direct activation of prothrombin to thrombin is similar in follicular fluid and plasma. Like plasma, inhibitors of both thrombin and thrombin generation, including antithrombin, protein C, and alpha2-macroglobulin, are present in follicular fluid.'], 'labels': ['OBJECTIVE', 'METHODS', 'METHODS', 'METHODS', 'METHODS', 'METHODS', 'RESULTS'], 'meshes': ['Blood Proteins', 'Ceruloplasmin', 'Factor IX', 'Factor VII', 'Factor X', 'Female', 'Follicular Fluid', 'Humans', 'Protein C', 'Proteins', 'Prothrombin', 'Thrombin', 'von Willebrand Factor']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,735,415 | Does coronary oxygen persufflation combined with HTK cardioplegia prolong the preservation time in heart transplantation? | {
"contexts": [
"One of the most restricting factors remaining in heart transplantation is the limited myocardial ischemia time. A new approach towards the prolongation of this time is the combination of primary cardioplegic arrest followed by continuous coronary oxygen persufflation (COP) with gaseous oxygen.",
"This technique was applied in pig hearts, which we transplanted orthotopically after cardioplegic arrest by original (n = 5) and modified (addition of hyaluronidase: n = 11) Bretschneider HTK solution and 14 h of hypothermic preservation. Depending on the different preservation techniques, we created four groups: (1), original HTK (HTK), n = 5; (2), modified HTK (mHTK), n = 5; (3), modified HTK solution plus COP (mHTK + COP), n = 6; and (4), as a control five hearts were transplanted after cardioplegic arrest by the original HTK solution and a cold ischemia time of 3 h comparable to clinical routine procedure.",
"After 14 h of preservation and orthotopic transplantation, cardiac functional recovery in mHTK + COP hearts was similar to control hearts, and improved compared to hearts of both other groups. Hemodynamics were significantly better in hearts preserved by mHTK + COP and in the control group compared to the HTK-hearts (P < 0.05), not significant compared to mHTK hearts (dp/dt(max) in % of preoperative +/- standard error of mean (SEM): mHTK + COP, 85 +/- 9; control, 85 +/- 10.5; mHTK, 59 +/- 14; HTK, 50 +/- 4). The cardiac output (CO) in % of preoperative was: mHTK + COP, 68 +/- 5.4; control, 64 +/- 4; mHTK, 44 +/- 2.7; HTK, 25 +/- 11. The ATP of left ventricular myocardium in mHTK + COP hearts at 14.7 +/- 1 micromol/g dry weight (DW) and in the control at 14.59 +/- 1.8 was higher compared to that in mHTK at 12.2 +/- 2.8 (P is non-significant (n.s.) versus mHTK + COP and control) and in HTK-hearts at 7.0 +/- 0.5 (P < 0.05 versus mHTK + COP and control). CK-MB in percent of CK showed no increase in either group."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Cardioplegic Solutions",
"Creatine Kinase",
"Glucose",
"Heart",
"Heart Arrest, Induced",
"Heart Transplantation",
"Hemodynamics",
"Isoenzymes",
"Mannitol",
"Myocardium",
"Organ Preservation",
"Oxygen",
"Oxygen Consumption",
"Potassium Chloride",
"Procaine",
"Swine"
]
} | These data show that COP combined with a mHTK solution represents a potential alternative to complement currently used cold storage techniques for prolonged preservation periods. | yes | [
{
"from": "human",
"value": "Question: Does coronary oxygen persufflation combined with HTK cardioplegia prolong the preservation time in heart transplantation?\nContext: {'contexts': ['One of the most restricting factors remaining in heart transplantation is the limited myocardial ischemia time. A new approach towards the prolongation of this time is the combination of primary cardioplegic arrest followed by continuous coronary oxygen persufflation (COP) with gaseous oxygen.', 'This technique was applied in pig hearts, which we transplanted orthotopically after cardioplegic arrest by original (n = 5) and modified (addition of hyaluronidase: n = 11) Bretschneider HTK solution and 14 h of hypothermic preservation. Depending on the different preservation techniques, we created four groups: (1), original HTK (HTK), n = 5; (2), modified HTK (mHTK), n = 5; (3), modified HTK solution plus COP (mHTK + COP), n = 6; and (4), as a control five hearts were transplanted after cardioplegic arrest by the original HTK solution and a cold ischemia time of 3 h comparable to clinical routine procedure.', 'After 14 h of preservation and orthotopic transplantation, cardiac functional recovery in mHTK + COP hearts was similar to control hearts, and improved compared to hearts of both other groups. Hemodynamics were significantly better in hearts preserved by mHTK + COP and in the control group compared to the HTK-hearts (P < 0.05), not significant compared to mHTK hearts (dp/dt(max) in % of preoperative +/- standard error of mean (SEM): mHTK + COP, 85 +/- 9; control, 85 +/- 10.5; mHTK, 59 +/- 14; HTK, 50 +/- 4). The cardiac output (CO) in % of preoperative was: mHTK + COP, 68 +/- 5.4; control, 64 +/- 4; mHTK, 44 +/- 2.7; HTK, 25 +/- 11. The ATP of left ventricular myocardium in mHTK + COP hearts at 14.7 +/- 1 micromol/g dry weight (DW) and in the control at 14.59 +/- 1.8 was higher compared to that in mHTK at 12.2 +/- 2.8 (P is non-significant (n.s.) versus mHTK + COP and control) and in HTK-hearts at 7.0 +/- 0.5 (P < 0.05 versus mHTK + COP and control). CK-MB in percent of CK showed no increase in either group.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Cardioplegic Solutions', 'Creatine Kinase', 'Glucose', 'Heart', 'Heart Arrest, Induced', 'Heart Transplantation', 'Hemodynamics', 'Isoenzymes', 'Mannitol', 'Myocardium', 'Organ Preservation', 'Oxygen', 'Oxygen Consumption', 'Potassium Chloride', 'Procaine', 'Swine']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,735,591 | Does interleukin-1 stimulate human uterine prostaglandin production through induction of cyclooxygenase-2 expression? | {
"contexts": [
"Uterine infection occurs in as much as 20% of preterm labor and results in increased decidual cytokines. The objective of this study was to examine the effect of interleukin-1 (IL-1) and the cyclooxygenase-2 (COX-2) inhibitor, NS-398, on myometrial prostaglandin (PG) production and COX-2 expression.",
"Human uterine myocytes were stimulated with IL-1 (0-50 ng/mL) over 24 hr. PGE2, PGF2alpha, and 6-keto F1alpha were measured by enzyme-linked immunosorbent assay. Both COX-1 and COX-2 proteins and mRNA were measured by western and northern blot, respectively.",
"IL-1 increased PG production beginning at 6 hr, COX-2 protein increased beginning at 4 hr and continued to increase at 24 hr. COX-2 mRNA increased at 2 hr and peaked at 4 hr. NS-398 blocked PG production but had no effect on COX-2 protein or mRNA."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Cells, Cultured",
"Cyclooxygenase 2",
"Dinoprost",
"Dinoprostone",
"Enzyme Induction",
"Epoprostenol",
"Female",
"Humans",
"Interleukin-1",
"Isoenzymes",
"Membrane Proteins",
"Myometrium",
"Pregnancy",
"Prostaglandin-Endoperoxide Synthases",
"Prostaglandins",
"RNA, Messenger"
]
} | IL-1 increases PG production by myometrium by increased COX-2 expression. NS-398 completely blocks IL-1-induced PG production. With intrauterine infection, IL-1 may induce labor through the autocrine production of uterotonic PGs. | yes | [
{
"from": "human",
"value": "Question: Does interleukin-1 stimulate human uterine prostaglandin production through induction of cyclooxygenase-2 expression?\nContext: {'contexts': ['Uterine infection occurs in as much as 20% of preterm labor and results in increased decidual cytokines. The objective of this study was to examine the effect of interleukin-1 (IL-1) and the cyclooxygenase-2 (COX-2) inhibitor, NS-398, on myometrial prostaglandin (PG) production and COX-2 expression.', 'Human uterine myocytes were stimulated with IL-1 (0-50 ng/mL) over 24 hr. PGE2, PGF2alpha, and 6-keto F1alpha were measured by enzyme-linked immunosorbent assay. Both COX-1 and COX-2 proteins and mRNA were measured by western and northern blot, respectively.', 'IL-1 increased PG production beginning at 6 hr, COX-2 protein increased beginning at 4 hr and continued to increase at 24 hr. COX-2 mRNA increased at 2 hr and peaked at 4 hr. NS-398 blocked PG production but had no effect on COX-2 protein or mRNA.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Cells, Cultured', 'Cyclooxygenase 2', 'Dinoprost', 'Dinoprostone', 'Enzyme Induction', 'Epoprostenol', 'Female', 'Humans', 'Interleukin-1', 'Isoenzymes', 'Membrane Proteins', 'Myometrium', 'Pregnancy', 'Prostaglandin-Endoperoxide Synthases', 'Prostaglandins', 'RNA, Messenger']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,737,573 | Is video-assisted evacuation of empyema the preferred procedure for management of pleural space infections? | {
"contexts": [
"Empyema remains a cause of morbidity and mortality. Thoracoscopy has proved its versatility in the management of pleural space disorders. The suitability of video-assisted thoracic surgery (VATS) for decortication in the management of the fibrotic stage of empyema is unclear.",
"VATS evacuation of empyema and decortication was performed on seventeen patients presenting with pleural space infections. A retrospective review was performed and constitutes the basis of this report.",
"VATS evacuation of empyema and decortication was successfully performed in 13 of 17 patients. Blood loss was 325 +/- 331 cc. Mean hospital stay was 18 +/- 10 days. Postoperative hospitalization was 11 +/- 7 days. Chest tubes remained in place for 7 +/- 3 days. There were no operative mortalities."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Blood Loss, Surgical",
"Chest Tubes",
"Empyema, Pleural",
"Female",
"Humans",
"Length of Stay",
"Male",
"Middle Aged",
"Retrospective Studies",
"Thoracic Surgery, Video-Assisted",
"Tomography, X-Ray Computed"
]
} | Video-assisted evacuation of empyema and decortication is an effective modality in the management of the exudative and fibrinopurulent stages of empyema. An organized empyema should be approached thoracoscopically, but may require open decortication. | yes | [
{
"from": "human",
"value": "Question: Is video-assisted evacuation of empyema the preferred procedure for management of pleural space infections?\nContext: {'contexts': ['Empyema remains a cause of morbidity and mortality. Thoracoscopy has proved its versatility in the management of pleural space disorders. The suitability of video-assisted thoracic surgery (VATS) for decortication in the management of the fibrotic stage of empyema is unclear.', 'VATS evacuation of empyema and decortication was performed on seventeen patients presenting with pleural space infections. A retrospective review was performed and constitutes the basis of this report.', 'VATS evacuation of empyema and decortication was successfully performed in 13 of 17 patients. Blood loss was 325 +/- 331 cc. Mean hospital stay was 18 +/- 10 days. Postoperative hospitalization was 11 +/- 7 days. Chest tubes remained in place for 7 +/- 3 days. There were no operative mortalities.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Blood Loss, Surgical', 'Chest Tubes', 'Empyema, Pleural', 'Female', 'Humans', 'Length of Stay', 'Male', 'Middle Aged', 'Retrospective Studies', 'Thoracic Surgery, Video-Assisted', 'Tomography, X-Ray Computed']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,738,946 | Is the expression of three types of CINCs by lipopolysaccharide-stimulated rat macrophages inhibited similarly by anti-inflammatory steroids? | {
"contexts": [
"Expression of CINCs was regulated differentially in lipopolysaccharide-stimulated rat macrophages. We examined whether the expression of CINCs in lipopolysaccharide-stimulated rat macrophages is similarly inhibited by anti-inflammatory drugs.",
"Rat peritoneal macrophages were stimulated by lipopolysaccharide in the presence of anti-inflammatory steroids (dexamethasone, prednisolone and hydrocortisone) or non-steroidal anti-inflammatory drugs (indomethacin and piroxicam). The production and mRNA expression of three types of CINCs were measured using enzyme-linked immunosorbent assay and northern hybridization.",
"Anti-inflammatory steroids; dexamethasone, prednisolone and hydrocortisone, dose-dependently inhibited the production of CINC-1, -2 and -3, whose inhibitory patterns were similar to each other. Furthermore mRNA expression of each CINC was inhibited by dexamethasone in a dose-dependent manner. In contrast, non-steroidal anti-inflammatory drugs, indomethacin and piroxicam were without effect. Expression of each CINC was regulated differently; the production of CINC-1 reached a maximum at 12 h and then slightly decreased after lipopolysaccharide stimulation, whereas that of CINC-2 and CINC-3 increased up to 24 h. Dexamethasone inhibited the CINCs production and mRNA expression at 9 h after lipopolysaccharide stimulation."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Anti-Inflammatory Agents",
"Anti-Inflammatory Agents, Non-Steroidal",
"Cells, Cultured",
"Chemokine CXCL1",
"Chemokines, CXC",
"Chemotactic Factors",
"Dexamethasone",
"Gene Expression",
"Growth Substances",
"Hydrocortisone",
"Intercellular Signaling Peptides and Proteins",
"Kinetics",
"Lipopolysaccharides",
"Macrophages, Peritoneal",
"Male",
"Prednisolone",
"RNA, Messenger",
"Rats",
"Rats, Wistar"
]
} | These results indicate no difference among CINC-1, -2 and -3 in the inhibition of production and mRNA expression of CINCs by anti-inflammatory steroids, although lipopolysaccharide differentially induces expression of each CINC expression in culture of rat macrophages. | yes | [
{
"from": "human",
"value": "Question: Is the expression of three types of CINCs by lipopolysaccharide-stimulated rat macrophages inhibited similarly by anti-inflammatory steroids?\nContext: {'contexts': ['Expression of CINCs was regulated differentially in lipopolysaccharide-stimulated rat macrophages. We examined whether the expression of CINCs in lipopolysaccharide-stimulated rat macrophages is similarly inhibited by anti-inflammatory drugs.', 'Rat peritoneal macrophages were stimulated by lipopolysaccharide in the presence of anti-inflammatory steroids (dexamethasone, prednisolone and hydrocortisone) or non-steroidal anti-inflammatory drugs (indomethacin and piroxicam). The production and mRNA expression of three types of CINCs were measured using enzyme-linked immunosorbent assay and northern hybridization.', 'Anti-inflammatory steroids; dexamethasone, prednisolone and hydrocortisone, dose-dependently inhibited the production of CINC-1, -2 and -3, whose inhibitory patterns were similar to each other. Furthermore mRNA expression of each CINC was inhibited by dexamethasone in a dose-dependent manner. In contrast, non-steroidal anti-inflammatory drugs, indomethacin and piroxicam were without effect. Expression of each CINC was regulated differently; the production of CINC-1 reached a maximum at 12 h and then slightly decreased after lipopolysaccharide stimulation, whereas that of CINC-2 and CINC-3 increased up to 24 h. Dexamethasone inhibited the CINCs production and mRNA expression at 9 h after lipopolysaccharide stimulation.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Anti-Inflammatory Agents', 'Anti-Inflammatory Agents, Non-Steroidal', 'Cells, Cultured', 'Chemokine CXCL1', 'Chemokines, CXC', 'Chemotactic Factors', 'Dexamethasone', 'Gene Expression', 'Growth Substances', 'Hydrocortisone', 'Intercellular Signaling Peptides and Proteins', 'Kinetics', 'Lipopolysaccharides', 'Macrophages, Peritoneal', 'Male', 'Prednisolone', 'RNA, Messenger', 'Rats', 'Rats, Wistar']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,735,706 | Does continuous pulmonary perfusion during cardiopulmonary bypass prevent lung injury in infants? | {
"contexts": [
"Lung injury after cardiopulmonary bypass is a serious complication for infants with congenital heart disease and pulmonary hypertension. Excessive neutrophil sequestration in the lung occurring after reestablishment of pulmonary circulation implies that interaction between neutrophils and pulmonary endothelium is the major cause of lung injury.",
"Thirty infants with either ventricular septal defect or atrioventricular septal defect and with pulmonary hypertension were enrolled in this study. We performed continuous pulmonary perfusion during total cardiopulmonary bypass on 16 patients (perfused group) and conventional cardiopulmonary bypass on 14 patients (control group). PaO2/FiO2 and neutrophil counts were assessed from immediately before surgery to 24 hours after termination of cardiopulmonary bypass.",
"PaO2/FiO2 was higher in the perfused group than in the control group, and the difference was significant throughout the study period. Neutrophil counts decreased below prebypass values in both groups at 30 minutes after aortic unclamping, and the difference was significant in the control group but was not in the perfused group. Duration of postoperative ventilatory support was significantly less in the perfused group."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Cardiopulmonary Bypass",
"Heart Septal Defects, Atrial",
"Heart Septal Defects, Ventricular",
"Humans",
"Infant",
"Perfusion",
"Reperfusion Injury",
"Respiratory Insufficiency"
]
} | Our study demonstrates that arrested pulmonary circulation during cardiopulmonary bypass is the major risk factor of lung injury and that continuous pulmonary perfusion is effective in preventing lung injury. | yes | [
{
"from": "human",
"value": "Question: Does continuous pulmonary perfusion during cardiopulmonary bypass prevent lung injury in infants?\nContext: {'contexts': ['Lung injury after cardiopulmonary bypass is a serious complication for infants with congenital heart disease and pulmonary hypertension. Excessive neutrophil sequestration in the lung occurring after reestablishment of pulmonary circulation implies that interaction between neutrophils and pulmonary endothelium is the major cause of lung injury.', 'Thirty infants with either ventricular septal defect or atrioventricular septal defect and with pulmonary hypertension were enrolled in this study. We performed continuous pulmonary perfusion during total cardiopulmonary bypass on 16 patients (perfused group) and conventional cardiopulmonary bypass on 14 patients (control group). PaO2/FiO2 and neutrophil counts were assessed from immediately before surgery to 24 hours after termination of cardiopulmonary bypass.', 'PaO2/FiO2 was higher in the perfused group than in the control group, and the difference was significant throughout the study period. Neutrophil counts decreased below prebypass values in both groups at 30 minutes after aortic unclamping, and the difference was significant in the control group but was not in the perfused group. Duration of postoperative ventilatory support was significantly less in the perfused group.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Cardiopulmonary Bypass', 'Heart Septal Defects, Atrial', 'Heart Septal Defects, Ventricular', 'Humans', 'Infant', 'Perfusion', 'Reperfusion Injury', 'Respiratory Insufficiency']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,726,718 | Does doxazosin modify Bcl-2 and Bax protein expression in the left ventricle of spontaneously hypertensive rats? | {
"contexts": [
"Increased apoptosis has recently been reported in the heart of spontaneously hypertensive rats (SHRs).",
"To investigate the molecular basis of apoptosis in the left ventricle of SHRs in terms of the expression of Bcl-2 protein (which protects from apoptosis) and Bax protein (which acts as an apoptotic promoter). In addition, we analysed the involvement of alpha -adrenergic receptors in the left ventricular apoptosis of SHRs.",
"The study was performed in untreated SHRs (n=16) and SHRs that were orally treated with doxazosin (10 mg/kg body weight per day, for 15 days), a selective alpha1-receptor blocker (n=16). A group of Wistar-Kyoto (WKY) rats (n=16) was used as the control.",
"The left ventricles of untreated SHRs showed a significant increase in Bcl-2 protein expression and a reduced presence of Bax protein. The ratio of Bcl-2:Bax in SHRs was higher than in WKY rats, suggesting an anti-apoptotic state. Paradoxically, both the number of apoptotic cardiac cells and the cleavage of an 85-kDa fragment of the poly (ADP-ribose) polymerase (PARP), a marker of caspase-3 activity, were higher in the left ventricle of SHRs than in WKY rats, suggesting an apoptotic situation. Bax promotes cell apoptosis when it is bound to Bcl-2. We then determined the abundance of Bax-Bcl-2 complexes in the left ventricle of the two groups of animals. Bax-Bcl-2 complexes were more abundant in SHRs than WKY rats. In a second set of experiments, we analysed the role of alpha1-adrenergic blockade by doxazosin in the above-described mechanisms. Doxazosin treatment reduced the formation of Bax-Bcl-2 complexes in the left ventricle of SHRs, and this was accompanied by a decrease in the levels of 85kDa PARP and a reduction in apoptotic left ventricular cells."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Apoptosis",
"Blood Pressure",
"Caspase 3",
"Caspases",
"Doxazosin",
"Heart Ventricles",
"Hypertension",
"Hypertrophy, Left Ventricular",
"Male",
"Myocardium",
"Proto-Oncogene Proteins",
"Proto-Oncogene Proteins c-bcl-2",
"Rats",
"Rats, Inbred SHR",
"Rats, Inbred WKY",
"Reference Values",
"bcl-2-Associated X Protein"
]
} | The present work suggests that the presence of Bax-Bcl-2 complexes in the left ventricle could be a more reliable marker of the apoptotic state than the determination of the absolute expression of Bcl-2 and Bax proteins. Moreover, the inhibition of alpha1 -adrenergic receptors by doxazosin decreased the abundance of BaxBcl-2 complexes and promoted a reduction of apoptosis in the left ventricle of SHRs. | yes | [
{
"from": "human",
"value": "Question: Does doxazosin modify Bcl-2 and Bax protein expression in the left ventricle of spontaneously hypertensive rats?\nContext: {'contexts': ['Increased apoptosis has recently been reported in the heart of spontaneously hypertensive rats (SHRs).', 'To investigate the molecular basis of apoptosis in the left ventricle of SHRs in terms of the expression of Bcl-2 protein (which protects from apoptosis) and Bax protein (which acts as an apoptotic promoter). In addition, we analysed the involvement of alpha -adrenergic receptors in the left ventricular apoptosis of SHRs.', 'The study was performed in untreated SHRs (n=16) and SHRs that were orally treated with doxazosin (10 mg/kg body weight per day, for 15 days), a selective alpha1-receptor blocker (n=16). A group of Wistar-Kyoto (WKY) rats (n=16) was used as the control.', 'The left ventricles of untreated SHRs showed a significant increase in Bcl-2 protein expression and a reduced presence of Bax protein. The ratio of Bcl-2:Bax in SHRs was higher than in WKY rats, suggesting an anti-apoptotic state. Paradoxically, both the number of apoptotic cardiac cells and the cleavage of an 85-kDa fragment of the poly (ADP-ribose) polymerase (PARP), a marker of caspase-3 activity, were higher in the left ventricle of SHRs than in WKY rats, suggesting an apoptotic situation. Bax promotes cell apoptosis when it is bound to Bcl-2. We then determined the abundance of Bax-Bcl-2 complexes in the left ventricle of the two groups of animals. Bax-Bcl-2 complexes were more abundant in SHRs than WKY rats. In a second set of experiments, we analysed the role of alpha1-adrenergic blockade by doxazosin in the above-described mechanisms. Doxazosin treatment reduced the formation of Bax-Bcl-2 complexes in the left ventricle of SHRs, and this was accompanied by a decrease in the levels of 85kDa PARP and a reduction in apoptotic left ventricular cells.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Apoptosis', 'Blood Pressure', 'Caspase 3', 'Caspases', 'Doxazosin', 'Heart Ventricles', 'Hypertension', 'Hypertrophy, Left Ventricular', 'Male', 'Myocardium', 'Proto-Oncogene Proteins', 'Proto-Oncogene Proteins c-bcl-2', 'Rats', 'Rats, Inbred SHR', 'Rats, Inbred WKY', 'Reference Values', 'bcl-2-Associated X Protein']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,735,671 | Does superoxide possibly produced in endothelial cells mediate the neutrophil-induced lung injury? | {
"contexts": [
"The mechanism by which stimulated neutrophils (polymorphonuclear leukocytes [PMNs]) damage pulmonary vascular endothelium was investigated.",
"The ability of unstimulated and mechanically stimulated PMNs to adhere to pulmonary endothelial cells and, thereby, alter pulmonary vascular permeability was tested. Each series was conducted on 6 rats. To stimulate PMNs, they were agitated gently in a glass vial for 10 seconds.",
"Perfusing lungs with the stimulated PMNs elicited a fivefold increase in permeability compared with lungs perfused with the unstimulated cells. This increase in permeability was blocked completely by preincubation of stimulated PMNs with CD18 monoclonal antibody. This increase in permeability was also blocked completely by superoxide dismutase (SOD) or the xanthine oxidase (XO) inhibitor allopurinol. Pulmonary vascular hemodynamics were unaffected by any treatment protocol. The accumulation of stimulated PMNs within the lungs was not inhibited by SOD but was partially blocked by allopurinol."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Capillary Permeability",
"Endothelium, Vascular",
"Fluorescent Antibody Technique",
"In Vitro Techniques",
"Lung",
"Male",
"Neutrophils",
"Peroxidase",
"Rats",
"Rats, Sprague-Dawley",
"Superoxides"
]
} | These findings suggest that stimulated PMN-induced increases in pulmonary vascular filtration resulted from endothelial cell injury caused by superoxide anion possibly generated by XO, exclusively present in the endothelial cells. | yes | [
{
"from": "human",
"value": "Question: Does superoxide possibly produced in endothelial cells mediate the neutrophil-induced lung injury?\nContext: {'contexts': ['The mechanism by which stimulated neutrophils (polymorphonuclear leukocytes [PMNs]) damage pulmonary vascular endothelium was investigated.', 'The ability of unstimulated and mechanically stimulated PMNs to adhere to pulmonary endothelial cells and, thereby, alter pulmonary vascular permeability was tested. Each series was conducted on 6 rats. To stimulate PMNs, they were agitated gently in a glass vial for 10 seconds.', 'Perfusing lungs with the stimulated PMNs elicited a fivefold increase in permeability compared with lungs perfused with the unstimulated cells. This increase in permeability was blocked completely by preincubation of stimulated PMNs with CD18 monoclonal antibody. This increase in permeability was also blocked completely by superoxide dismutase (SOD) or the xanthine oxidase (XO) inhibitor allopurinol. Pulmonary vascular hemodynamics were unaffected by any treatment protocol. The accumulation of stimulated PMNs within the lungs was not inhibited by SOD but was partially blocked by allopurinol.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Capillary Permeability', 'Endothelium, Vascular', 'Fluorescent Antibody Technique', 'In Vitro Techniques', 'Lung', 'Male', 'Neutrophils', 'Peroxidase', 'Rats', 'Rats, Sprague-Dawley', 'Superoxides']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,728,420 | Are human connexin40 gap junction channels modulated by cAMP? | {
"contexts": [
"Gap junction channels provide for direct electrical coupling between cells, and play an important role in homeostasis and electrical coupling. One of the proteins that form gap junctions, Connexin40 (Cx40), shows restricted expression in the body, and is found in blood vessels and in the atrium and conduction system of the heart. We have investigated whether gap junction channels formed of Cx40 are modulated by protein-kinase-A-mediated phosphorylation.",
"A communication-deficient human hepatoma cell line (SKHep1) was stably transfected with human Cx40 cDNA and the properties of Cx40 gap junctions channels and their modulation by cAMP were analyzed using immunocytochemistry, Western blotting, dual patch clamp, and dye coupling.",
"Administration of 1 mM 8-Br-cAMP resulted in a mobility shift of Cx40 protein on western blot and increased macroscopic gap junctional conductance between cell pairs by 46.2 +/- 12.0% (mean +/- S.E.M., n = 8). Under control conditions, single channel experiments revealed three single channel conductances around 30, 80 and 120 pS. When cAMP was added, channel conductances of 46 and 120 pS were observed. In monolayers, cAMP also increased the permeability of Cx40 gap junction channels for Lucifer Yellow by 58%."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"8-Bromo Cyclic Adenosine Monophosphate",
"Blotting, Western",
"Connexins",
"Cyclic AMP",
"Electric Conductivity",
"Gap Junctions",
"Humans",
"Immunohistochemistry",
"Isoquinolines",
"Patch-Clamp Techniques",
"Transfection",
"Tumor Cells, Cultured"
]
} | Macroscopic conductance and permeability of Cx40 gap junctions is strongly increased by cAMP and may play a role in the regulation of intercellular communication in the heart and vasculature. | yes | [
{
"from": "human",
"value": "Question: Are human connexin40 gap junction channels modulated by cAMP?\nContext: {'contexts': ['Gap junction channels provide for direct electrical coupling between cells, and play an important role in homeostasis and electrical coupling. One of the proteins that form gap junctions, Connexin40 (Cx40), shows restricted expression in the body, and is found in blood vessels and in the atrium and conduction system of the heart. We have investigated whether gap junction channels formed of Cx40 are modulated by protein-kinase-A-mediated phosphorylation.', 'A communication-deficient human hepatoma cell line (SKHep1) was stably transfected with human Cx40 cDNA and the properties of Cx40 gap junctions channels and their modulation by cAMP were analyzed using immunocytochemistry, Western blotting, dual patch clamp, and dye coupling.', 'Administration of 1 mM 8-Br-cAMP resulted in a mobility shift of Cx40 protein on western blot and increased macroscopic gap junctional conductance between cell pairs by 46.2 +/- 12.0% (mean +/- S.E.M., n = 8). Under control conditions, single channel experiments revealed three single channel conductances around 30, 80 and 120 pS. When cAMP was added, channel conductances of 46 and 120 pS were observed. In monolayers, cAMP also increased the permeability of Cx40 gap junction channels for Lucifer Yellow by 58%.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['8-Bromo Cyclic Adenosine Monophosphate', 'Blotting, Western', 'Connexins', 'Cyclic AMP', 'Electric Conductivity', 'Gap Junctions', 'Humans', 'Immunohistochemistry', 'Isoquinolines', 'Patch-Clamp Techniques', 'Transfection', 'Tumor Cells, Cultured']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,743,075 | Does [ Genistein suppress growth stimulatory effect of growth factors in HCE 16/3 cells ]? | {
"contexts": [
"The role of genistein in the effect of growth factors (KGF and EGF) on the growth of HPV 16 DNA-immortalized human cervical epithelial cells (HCE 16/3 cells) was studied.",
"Genistein affected the modulation effect of the growth factors on the growth of HCE 16/3 cells using [3H]-thymidine incorporation, immunocapture assay of uPA and tyrosine kinase assay.",
"The growth factors stimulated growth of HCE 16/3 cells in serum-free medium. However, genistein suppressed the growth stimulatory effect of growth factors on HCE 16/3 cells and also reduced KGF-enhanced uPA secretion in this cell line. The inhibitory effects might be associated with its attenuation of activity of tyrosine kinases of growth factors."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Antineoplastic Agents",
"Cell Division",
"Cells, Cultured",
"Cells, Immobilized",
"Cervix Uteri",
"Epidermal Growth Factor",
"Epithelial Cells",
"Female",
"Fibroblast Growth Factor 10",
"Fibroblast Growth Factor 7",
"Fibroblast Growth Factors",
"Genistein",
"Growth Substances",
"Humans",
"Urokinase-Type Plasminogen Activator"
]
} | The results suggest that genistein have potential value in the prevention and treatment of some tumors in vivo. | yes | [
{
"from": "human",
"value": "Question: Does [ Genistein suppress growth stimulatory effect of growth factors in HCE 16/3 cells ]?\nContext: {'contexts': ['The role of genistein in the effect of growth factors (KGF and EGF) on the growth of HPV 16 DNA-immortalized human cervical epithelial cells (HCE 16/3 cells) was studied.', 'Genistein affected the modulation effect of the growth factors on the growth of HCE 16/3 cells using [3H]-thymidine incorporation, immunocapture assay of uPA and tyrosine kinase assay.', 'The growth factors stimulated growth of HCE 16/3 cells in serum-free medium. However, genistein suppressed the growth stimulatory effect of growth factors on HCE 16/3 cells and also reduced KGF-enhanced uPA secretion in this cell line. The inhibitory effects might be associated with its attenuation of activity of tyrosine kinases of growth factors.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Antineoplastic Agents', 'Cell Division', 'Cells, Cultured', 'Cells, Immobilized', 'Cervix Uteri', 'Epidermal Growth Factor', 'Epithelial Cells', 'Female', 'Fibroblast Growth Factor 10', 'Fibroblast Growth Factor 7', 'Fibroblast Growth Factors', 'Genistein', 'Growth Substances', 'Humans', 'Urokinase-Type Plasminogen Activator']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,731,888 | Does rapid intermittent compression increase skin circulation in chronically ischemic legs with infra-popliteal arterial obstruction? | {
"contexts": [
"Intermittent pneumatic compression (IPC) has been shown, by duplex, to increase popliteal artery flow in normal legs and in legs with superficial femoral artery occlusion. The objective of this study was to see if IPC improves distal circulation in legs with severe infra-popliteal disease.",
"Sixteen chronically ischemic legs with arteriographically demonstrated crural or pedal disease were studied during compression with an ArtAssist compression-device. This device delivers rapid compression of the foot and calf. Cutaneous laser-Doppler flux was measured continuously at the dorsal aspect of the distal forefoot. The findings were compared to those in thirteen normal controls of similar age.",
"In ischemic legs, the spontaneous changes in skin-flux are minimal: mean resting flux in sitting position was 0.87 +/- 0.46 AU (Arbitrary Units). Upon activation of the compression device the maximum flux increased to 4.55 +/- 1.35 AU. The difference was statistically significant (p < 0.001). This response was similar to that in normal controls."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Aged, 80 and over",
"Bandages",
"Blood Flow Velocity",
"Female",
"Foot",
"Humans",
"Ischemia",
"Laser-Doppler Flowmetry",
"Leg",
"Male",
"Middle Aged",
"Skin",
"Treatment Outcome"
]
} | Arterial flow augmentation upon compression is associated with increased skin-flux. This response remains present in severe disease of the crural outflow-arteries. Further investigation to define the role of intermittent compression for management of chronic arterial disease is warranted. | yes | [
{
"from": "human",
"value": "Question: Does rapid intermittent compression increase skin circulation in chronically ischemic legs with infra-popliteal arterial obstruction?\nContext: {'contexts': ['Intermittent pneumatic compression (IPC) has been shown, by duplex, to increase popliteal artery flow in normal legs and in legs with superficial femoral artery occlusion. The objective of this study was to see if IPC improves distal circulation in legs with severe infra-popliteal disease.', 'Sixteen chronically ischemic legs with arteriographically demonstrated crural or pedal disease were studied during compression with an ArtAssist compression-device. This device delivers rapid compression of the foot and calf. Cutaneous laser-Doppler flux was measured continuously at the dorsal aspect of the distal forefoot. The findings were compared to those in thirteen normal controls of similar age.', 'In ischemic legs, the spontaneous changes in skin-flux are minimal: mean resting flux in sitting position was 0.87 +/- 0.46 AU (Arbitrary Units). Upon activation of the compression device the maximum flux increased to 4.55 +/- 1.35 AU. The difference was statistically significant (p < 0.001). This response was similar to that in normal controls.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Aged, 80 and over', 'Bandages', 'Blood Flow Velocity', 'Female', 'Foot', 'Humans', 'Ischemia', 'Laser-Doppler Flowmetry', 'Leg', 'Male', 'Middle Aged', 'Skin', 'Treatment Outcome']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,746,487 | Does insulin resistance alone explain the clustering of cardiovascular risk factors in southern India? | {
"contexts": [
"To determine whether insulin resistance (IR calculated using the HOMA model) has a dominant role in the clustering of cardiovascular risk factors in the Asian Indian population.",
"A total of 654 non-diabetic subjects aged > or =40 years (male 396: female 258) were selected from a population survey. They had estimates of fasting and 2 h plasma glucose, insulin levels, body mass index (BMI), waist-to-hip ratio (WHR) and blood pressure. Factor analysis was carried out using the principle components analysis (PCA) with varimax orthogonal rotation of continuously distributed variables, considered to represent the components of insulin resistance syndrome including the calculated IR.",
"There were three major clusters of cardiovascular disease (CVD) risk variables in men and four clusters in women. Insulin resistance, 2 h plasma glucose, insulin and obesity aggregated as the major domain. Insulin resistance was not linked with hypertension. BMI was a common link for all the three factors in men, and for three of the four in women."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Blood Glucose",
"Blood Pressure",
"Body Constitution",
"Body Mass Index",
"Cardiovascular Diseases",
"Cluster Analysis",
"Female",
"Humans",
"Hypertension",
"India",
"Insulin",
"Insulin Resistance",
"Male",
"Middle Aged",
"Obesity",
"Risk Factors"
]
} | Insulin resistance is not the only underlying factor for the clustering of CVD risk factors in south Indians. These findings are consistent with the presence of several distinct physiological domains, as shown in other ethnic groups. | no | [
{
"from": "human",
"value": "Question: Does insulin resistance alone explain the clustering of cardiovascular risk factors in southern India?\nContext: {'contexts': ['To determine whether insulin resistance (IR calculated using the HOMA model) has a dominant role in the clustering of cardiovascular risk factors in the Asian Indian population.', 'A total of 654 non-diabetic subjects aged > or =40 years (male 396: female 258) were selected from a population survey. They had estimates of fasting and 2 h plasma glucose, insulin levels, body mass index (BMI), waist-to-hip ratio (WHR) and blood pressure. Factor analysis was carried out using the principle components analysis (PCA) with varimax orthogonal rotation of continuously distributed variables, considered to represent the components of insulin resistance syndrome including the calculated IR.', 'There were three major clusters of cardiovascular disease (CVD) risk variables in men and four clusters in women. Insulin resistance, 2 h plasma glucose, insulin and obesity aggregated as the major domain. Insulin resistance was not linked with hypertension. BMI was a common link for all the three factors in men, and for three of the four in women.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Blood Glucose', 'Blood Pressure', 'Body Constitution', 'Body Mass Index', 'Cardiovascular Diseases', 'Cluster Analysis', 'Female', 'Humans', 'Hypertension', 'India', 'Insulin', 'Insulin Resistance', 'Male', 'Middle Aged', 'Obesity', 'Risk Factors']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
10,732,902 | Do early and intermediate-term complications of self-expanding stents limit its potential application in children with congenital heart disease? | {
"contexts": [
"We report on the early and intermediate-term follow-up results of self-expanding Wallstent (Schneider, Switzerland) implanted in children with congenital heart disease.",
"The inherent shortcomings of balloon-expandable stents prompted the trial of an alternative stent.",
"Twenty patients underwent 22 implantations of 25 self-expanding Wallstents between December 1993 and June 1997 in two institutions. The mean age and weight were 10.8+/-4.5 years and 30.5+/-14.2 kg, respectively. The patients were divided into two groups: 1) Group I comprised 17 patients with pulmonary arterial stenoses, 2) Group II comprised four patients with venous stenoses (one belonged to both groups). Sixteen patients underwent recatheterization at a median of 5.8 months (range 0.5 to 31, mean 8.1 months) after stenting. Hemodynamic and angiographic changes after the interventional procedures and complications were documented.",
"All the stents were successfully deployed in the intended position. In Group I, the narrowest diameter of the stented vessel increased from 4.1+/-1.5 to 8+/-2 mm (95% increase, p < 0.0001) while the systolic pressure gradient across decreased from 24.6+/-15.8 to 12.1+/-11.4 mm Hg (51% decrease, p = 0.001). In Group II, the dimensional changes of the narrowest segment increased from 4.3+/-0.5 to 7.5+/-0.4 mm (75% increase, p = 0.003), and the pressure gradient reduced from 5.0+/-2.9 to 0.9+/-1.0 mm Hg (82% decrease, p = 0.04) across the stented venous channel. Distal migration of two optimally positioned stents occurred within 24 h of implantation. At recatheterization, significant neointimal ingrowth (>30% of the expanded diameter) was noted in 7 (28%) of the 25 implanted stents. This responded poorly to balloon dilation. Predisposing factors for the neointimal ingrowth included stents of smaller diameter (<9 mm) and longer period after implantation."
],
"labels": [
"OBJECTIVE",
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Angiography",
"Angioplasty, Balloon",
"Child",
"Child, Preschool",
"Constriction, Pathologic",
"Equipment Failure Analysis",
"Female",
"Follow-Up Studies",
"Heart Defects, Congenital",
"Hemodynamics",
"Humans",
"Male",
"Prosthesis Design",
"Pulmonary Artery",
"Pulmonary Veno-Occlusive Disease",
"Retreatment",
"Stents",
"Treatment Outcome"
]
} | Self-expanding Wallstent could be deployed easily and safely to relieve vascular stenoses in children. The complications of distal migration, significant neointimal ingrowth and its unyielding design to overdilation limit its application to this patient group. | yes | [
{
"from": "human",
"value": "Question: Do early and intermediate-term complications of self-expanding stents limit its potential application in children with congenital heart disease?\nContext: {'contexts': ['We report on the early and intermediate-term follow-up results of self-expanding Wallstent (Schneider, Switzerland) implanted in children with congenital heart disease.', 'The inherent shortcomings of balloon-expandable stents prompted the trial of an alternative stent.', 'Twenty patients underwent 22 implantations of 25 self-expanding Wallstents between December 1993 and June 1997 in two institutions. The mean age and weight were 10.8+/-4.5 years and 30.5+/-14.2 kg, respectively. The patients were divided into two groups: 1) Group I comprised 17 patients with pulmonary arterial stenoses, 2) Group II comprised four patients with venous stenoses (one belonged to both groups). Sixteen patients underwent recatheterization at a median of 5.8 months (range 0.5 to 31, mean 8.1 months) after stenting. Hemodynamic and angiographic changes after the interventional procedures and complications were documented.', 'All the stents were successfully deployed in the intended position. In Group I, the narrowest diameter of the stented vessel increased from 4.1+/-1.5 to 8+/-2 mm (95% increase, p < 0.0001) while the systolic pressure gradient across decreased from 24.6+/-15.8 to 12.1+/-11.4 mm Hg (51% decrease, p = 0.001). In Group II, the dimensional changes of the narrowest segment increased from 4.3+/-0.5 to 7.5+/-0.4 mm (75% increase, p = 0.003), and the pressure gradient reduced from 5.0+/-2.9 to 0.9+/-1.0 mm Hg (82% decrease, p = 0.04) across the stented venous channel. Distal migration of two optimally positioned stents occurred within 24 h of implantation. At recatheterization, significant neointimal ingrowth (>30% of the expanded diameter) was noted in 7 (28%) of the 25 implanted stents. This responded poorly to balloon dilation. Predisposing factors for the neointimal ingrowth included stents of smaller diameter (<9 mm) and longer period after implantation.'], 'labels': ['OBJECTIVE', 'BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Angiography', 'Angioplasty, Balloon', 'Child', 'Child, Preschool', 'Constriction, Pathologic', 'Equipment Failure Analysis', 'Female', 'Follow-Up Studies', 'Heart Defects, Congenital', 'Hemodynamics', 'Humans', 'Male', 'Prosthesis Design', 'Pulmonary Artery', 'Pulmonary Veno-Occlusive Disease', 'Retreatment', 'Stents', 'Treatment Outcome']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,732,906 | Does local adenovirus-mediated transfer of C-type natriuretic peptide suppress vascular remodeling in porcine coronary arteries in vivo? | {
"contexts": [
"This study was designed to examine whether or not adenovirus-mediated gene transfer of C-type natriuretic peptide (CNP) can prevent coronary restenotic changes after balloon injury in pigs in vivo.",
"Gene therapy to prevent restenosis after percutaneous transluminal coronary angioplasty (PTCA) might be useful but requires a method applicable for in vivo gene delivery into the coronary artery as well as the efficient vector encoding a potent antiproliferative substance. We tested whether the adenovirus-mediated gene transfer of CNP by use of an infiltrator angioplasty balloon catheter (IABC) might prevent the coronary restenotic changes after balloon injury.",
"Balloon angioplasty was performed in the left anterior descending and the left circumflex coronary artery in pigs. Immediately after the balloon injury, adenovirus solution encoding either CNP (AdCACNP) or beta-galactosidase (AdCALacZ) gene was injected with IABC into the balloon-injured coronary segments. Expression of CNP was assessed by immunohistochemical staining and cyclic guanosine 3',5'-monophosphate (cGMP) measurement. Coronary restenotic changes were evaluated by both angiographic and histological examinations.",
"CNP was highly expressed in the media and the adventitia of the coronary artery at the AdCACNP-transfected but not at the AdCALacZ-transfected segment. In the AdCALacZ-transfected segment, vascular cGMP levels tended to be reduced as compared with the untreated segment, whereas in the AdCACNP-transfected segment, vascular cGMP levels were restored. Angiographic coronary stenosis was significantly less at the AdCACNP-transfected than at the AdCALacZ-transfected segment. Histological examination revealed that this was achieved primarily by the marked inhibition of the geometric remodeling of the coronary artery by the CNP gene transfer."
],
"labels": [
"OBJECTIVE",
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adenoviridae",
"Angioplasty, Balloon, Coronary",
"Animals",
"Coronary Angiography",
"Coronary Circulation",
"Coronary Disease",
"Coronary Vessels",
"Gene Expression Regulation",
"Gene Transfer Techniques",
"Genetic Therapy",
"Natriuretic Peptide, C-Type",
"Recurrence",
"Swine"
]
} | Adenovirus-mediated CNP gene transfer with the IABC system may be a useful gene therapy to prevent restenosis after PTCA in vivo. | yes | [
{
"from": "human",
"value": "Question: Does local adenovirus-mediated transfer of C-type natriuretic peptide suppress vascular remodeling in porcine coronary arteries in vivo?\nContext: {'contexts': ['This study was designed to examine whether or not adenovirus-mediated gene transfer of C-type natriuretic peptide (CNP) can prevent coronary restenotic changes after balloon injury in pigs in vivo.', 'Gene therapy to prevent restenosis after percutaneous transluminal coronary angioplasty (PTCA) might be useful but requires a method applicable for in vivo gene delivery into the coronary artery as well as the efficient vector encoding a potent antiproliferative substance. We tested whether the adenovirus-mediated gene transfer of CNP by use of an infiltrator angioplasty balloon catheter (IABC) might prevent the coronary restenotic changes after balloon injury.', \"Balloon angioplasty was performed in the left anterior descending and the left circumflex coronary artery in pigs. Immediately after the balloon injury, adenovirus solution encoding either CNP (AdCACNP) or beta-galactosidase (AdCALacZ) gene was injected with IABC into the balloon-injured coronary segments. Expression of CNP was assessed by immunohistochemical staining and cyclic guanosine 3',5'-monophosphate (cGMP) measurement. Coronary restenotic changes were evaluated by both angiographic and histological examinations.\", 'CNP was highly expressed in the media and the adventitia of the coronary artery at the AdCACNP-transfected but not at the AdCALacZ-transfected segment. In the AdCALacZ-transfected segment, vascular cGMP levels tended to be reduced as compared with the untreated segment, whereas in the AdCACNP-transfected segment, vascular cGMP levels were restored. Angiographic coronary stenosis was significantly less at the AdCACNP-transfected than at the AdCALacZ-transfected segment. Histological examination revealed that this was achieved primarily by the marked inhibition of the geometric remodeling of the coronary artery by the CNP gene transfer.'], 'labels': ['OBJECTIVE', 'BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adenoviridae', 'Angioplasty, Balloon, Coronary', 'Animals', 'Coronary Angiography', 'Coronary Circulation', 'Coronary Disease', 'Coronary Vessels', 'Gene Expression Regulation', 'Gene Transfer Techniques', 'Genetic Therapy', 'Natriuretic Peptide, C-Type', 'Recurrence', 'Swine']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,749,621 | Does neutrophil adhesion to vascular prosthetic surfaces trigger nonapoptotic cell death? | {
"contexts": [
"To test the hypothesis that neutrophil adhesion to expanded polytetrafluoroethylene (ePTFE) and Dacron triggers cell death.",
"Vascular prosthetic infections are intransigent clinical dilemmas associated with excessive rates of death and complications. Impaired neutrophil function has been implicated in the infection of implanted cardiovascular devices. ePTFE and Dacron are potent neutrophil stimuli able to elicit activation responses such as reactive oxygen species production independent of exogenous/soluble agonists. Reactive oxygen species that are released into the medium when neutrophils are challenged by soluble agonists are known to cause self-destruction. The authors therefore sought to examine whether neutrophil adhesion to prosthetic graft materials decreases neutrophil viability by means of reactive oxygen species production.",
"Neutrophils were adhered to surfaces for up to 6 hours. Cell viability was monitored with propidium iodide staining and lactate dehydrogenase release.",
"Within 6 hours of adhesion to ePTFE and Dacron, respectively, 59% +/- 11% and 44% +/- 5% (n = 7) of the neutrophils were stained by propidium iodide. Indistinguishable results were obtained with plasma-coated ePTFE and Dacron. In contrast, less than 2% of the neutrophils adherent to fibrinogen-, immunoglobin-, or fetal bovine serum-coated polystyrene surfaces for 6 hours were positive for propidium iodide. The increase in membrane permeability to propidium iodide was accompanied by a two- to threefold increase in lactate dehydrogenase release. Pretreatment of neutrophils with N-acetyl-L-cysteine, cytochalasin D, or cyclosporin A significantly reduced the number of propidium iodide-positive ePTFE and Dacron adherent neutrophils."
],
"labels": [
"OBJECTIVE",
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Blood Vessel Prosthesis",
"Cell Adhesion",
"Cell Death",
"Cell Survival",
"Cytochalasin D",
"Humans",
"Neutrophils",
"Nucleic Acid Synthesis Inhibitors",
"Polyethylene Terephthalates",
"Polytetrafluoroethylene",
"Reactive Oxygen Species"
]
} | Neutrophil adhesion to ePTFE and Dacron triggers a rapid nonapoptotic cell death. The effect of ePTFE and Dacron on neutrophil viability appears to be caused by reactive oxygen species production. The premature death of graft-adherent neutrophils provides a novel explanation of the defect in neutrophil bacterial killing associated with vascular prosthetic grafts. | yes | [
{
"from": "human",
"value": "Question: Does neutrophil adhesion to vascular prosthetic surfaces trigger nonapoptotic cell death?\nContext: {'contexts': ['To test the hypothesis that neutrophil adhesion to expanded polytetrafluoroethylene (ePTFE) and Dacron triggers cell death.', 'Vascular prosthetic infections are intransigent clinical dilemmas associated with excessive rates of death and complications. Impaired neutrophil function has been implicated in the infection of implanted cardiovascular devices. ePTFE and Dacron are potent neutrophil stimuli able to elicit activation responses such as reactive oxygen species production independent of exogenous/soluble agonists. Reactive oxygen species that are released into the medium when neutrophils are challenged by soluble agonists are known to cause self-destruction. The authors therefore sought to examine whether neutrophil adhesion to prosthetic graft materials decreases neutrophil viability by means of reactive oxygen species production.', 'Neutrophils were adhered to surfaces for up to 6 hours. Cell viability was monitored with propidium iodide staining and lactate dehydrogenase release.', 'Within 6 hours of adhesion to ePTFE and Dacron, respectively, 59% +/- 11% and 44% +/- 5% (n = 7) of the neutrophils were stained by propidium iodide. Indistinguishable results were obtained with plasma-coated ePTFE and Dacron. In contrast, less than 2% of the neutrophils adherent to fibrinogen-, immunoglobin-, or fetal bovine serum-coated polystyrene surfaces for 6 hours were positive for propidium iodide. The increase in membrane permeability to propidium iodide was accompanied by a two- to threefold increase in lactate dehydrogenase release. Pretreatment of neutrophils with N-acetyl-L-cysteine, cytochalasin D, or cyclosporin A significantly reduced the number of propidium iodide-positive ePTFE and Dacron adherent neutrophils.'], 'labels': ['OBJECTIVE', 'BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Blood Vessel Prosthesis', 'Cell Adhesion', 'Cell Death', 'Cell Survival', 'Cytochalasin D', 'Humans', 'Neutrophils', 'Nucleic Acid Synthesis Inhibitors', 'Polyethylene Terephthalates', 'Polytetrafluoroethylene', 'Reactive Oxygen Species']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,749,628 | Does injury to dorsal root ganglia alter innervation of spinal cord dorsal horn lamina involved in nociception? | {
"contexts": [
"A study of the relation between the development of mechanical allodynia and the reorganization of primary afferent terminals in the sensory lamina of the rat spinal cord dorsal horn after partial dorsal root ganglion injury in rats.",
"To investigate the pathologic mechanisms of mechanical allodynia after partial dorsal root ganglion injury.",
"After experimental peripheral nerve injury causing neuropathic pain, myelinated afferent fibers sprout into lamina II of the dorsal horn. This lamina is associated with nociceptive-specific neurons that generally are not stimulated by myelinated fiber input from mechanical receptors. These morphologic changes are suggested to have significance in the pathogenesis of chronic mechanical allodynia, although it is not known whether this kind of morphologic change occurs after dorsal root ganglion injury.",
"After partial dorsal root ganglion crush injury, the mechanical force causing footpad withdrawal was measured with von Frey hairs, and myelinated primary afferents were labeled with cholera toxin B subunit horseradish peroxidase, a selective myelinated fiber tracer that identifies transganglionic synapses.",
"After partial dorsal root ganglion injury, mechanical allodynia developed in the corresponding footpad within 3 days and persisted throughout the experimental period. At 2 and 4 weeks after the injury, B subunit horseradish peroxidase-positive fibers, presumably myelinated afferents, were observed to be sprouting into lamina II of the dorsal horn on the injured side, but not on the contralateral control side."
],
"labels": [
"METHODS",
"OBJECTIVE",
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Afferent Pathways",
"Animals",
"Behavior, Animal",
"Cell Count",
"Cholera Toxin",
"Ganglia, Spinal",
"Horseradish Peroxidase",
"Nerve Crush",
"Nerve Fibers",
"Neuronal Plasticity",
"Nociceptors",
"Pain",
"Posterior Horn Cells",
"Rats",
"Rats, Sprague-Dawley",
"Touch"
]
} | Morphologic change in spinal cord dorsal horn lamina II occurs after partial dorsal root ganglion injury. This change may have significance in the pathogenesis of chronic mechanical allodynia after partial dorsal root ganglion injury. | yes | [
{
"from": "human",
"value": "Question: Does injury to dorsal root ganglia alter innervation of spinal cord dorsal horn lamina involved in nociception?\nContext: {'contexts': ['A study of the relation between the development of mechanical allodynia and the reorganization of primary afferent terminals in the sensory lamina of the rat spinal cord dorsal horn after partial dorsal root ganglion injury in rats.', 'To investigate the pathologic mechanisms of mechanical allodynia after partial dorsal root ganglion injury.', 'After experimental peripheral nerve injury causing neuropathic pain, myelinated afferent fibers sprout into lamina II of the dorsal horn. This lamina is associated with nociceptive-specific neurons that generally are not stimulated by myelinated fiber input from mechanical receptors. These morphologic changes are suggested to have significance in the pathogenesis of chronic mechanical allodynia, although it is not known whether this kind of morphologic change occurs after dorsal root ganglion injury.', 'After partial dorsal root ganglion crush injury, the mechanical force causing footpad withdrawal was measured with von Frey hairs, and myelinated primary afferents were labeled with cholera toxin B subunit horseradish peroxidase, a selective myelinated fiber tracer that identifies transganglionic synapses.', 'After partial dorsal root ganglion injury, mechanical allodynia developed in the corresponding footpad within 3 days and persisted throughout the experimental period. At 2 and 4 weeks after the injury, B subunit horseradish peroxidase-positive fibers, presumably myelinated afferents, were observed to be sprouting into lamina II of the dorsal horn on the injured side, but not on the contralateral control side.'], 'labels': ['METHODS', 'OBJECTIVE', 'BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Afferent Pathways', 'Animals', 'Behavior, Animal', 'Cell Count', 'Cholera Toxin', 'Ganglia, Spinal', 'Horseradish Peroxidase', 'Nerve Crush', 'Nerve Fibers', 'Neuronal Plasticity', 'Nociceptors', 'Pain', 'Posterior Horn Cells', 'Rats', 'Rats, Sprague-Dawley', 'Touch']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,739,535 | Does nitric oxide modulate angiotensin II-induced drinking behavior in the near-term ovine fetus? | {
"contexts": [
"Human and ovine fetuses demonstrate an enhanced rate of spontaneous and angiotensin II-stimulated swallowing. Angiotensin II and nitric oxide synthase have been localized to thirst centers in the brain. This study was performed to determine whether central nitric oxide contributes to the regulation of angiotensin II-induced fetal swallowing.",
"Six pregnant ewes with near-term singleton fetuses were chronically prepared with fetal vascular and lateral ventricle catheters and electrocorticogram and esophageal electromyogram electrodes. After a 2-hour control period, fetuses were administered serial lateral ventricle injections (1 mL) of angiotensin II (3.2 microg; time, 2 hours) and N omega-nitro-L -arginine methyl ester (3 mg; time, 3 hours) and a repeat angiotensin II injection (3.2 microg; time, 5 hours). All fetuses received an additional control study of lateral ventricle injections of artificial cerebrospinal fluid on a previous day.",
"Angiotensin II injection significantly increased mean +/- SEM fetal swallowing (0.9 +/- 0.1 to 2.7 +/- 0.4 swallows/min). N omega-nitro-L -arginine methyl ester significantly decreased fetal swallowing to below the basal rate (0.4 +/- 0.1 swallows/min), and swallowing did not increase with the second angiotensin II dose (in the presence of nitric oxide blockade)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Angiotensin II",
"Animals",
"Behavior, Animal",
"Deglutition",
"Drinking Behavior",
"Enzyme Inhibitors",
"Female",
"Fetus",
"Gestational Age",
"Hemodynamics",
"Injections, Intraventricular",
"NG-Nitroarginine Methyl Ester",
"Nitric Oxide",
"Pregnancy",
"Sheep"
]
} | These results demonstrate that inhibition of central nitric oxide suppresses fetal swallowing behavior in response to central angiotensin II. We speculate that tonic nitric oxide facilitates angiotensin II swallowing stimulation by maintenance of glutamate activation of hypothalamic N -methyl-D -aspartate receptors. | yes | [
{
"from": "human",
"value": "Question: Does nitric oxide modulate angiotensin II-induced drinking behavior in the near-term ovine fetus?\nContext: {'contexts': ['Human and ovine fetuses demonstrate an enhanced rate of spontaneous and angiotensin II-stimulated swallowing. Angiotensin II and nitric oxide synthase have been localized to thirst centers in the brain. This study was performed to determine whether central nitric oxide contributes to the regulation of angiotensin II-induced fetal swallowing.', 'Six pregnant ewes with near-term singleton fetuses were chronically prepared with fetal vascular and lateral ventricle catheters and electrocorticogram and esophageal electromyogram electrodes. After a 2-hour control period, fetuses were administered serial lateral ventricle injections (1 mL) of angiotensin II (3.2 microg; time, 2 hours) and N omega-nitro-L -arginine methyl ester (3 mg; time, 3 hours) and a repeat angiotensin II injection (3.2 microg; time, 5 hours). All fetuses received an additional control study of lateral ventricle injections of artificial cerebrospinal fluid on a previous day.', 'Angiotensin II injection significantly increased mean +/- SEM fetal swallowing (0.9 +/- 0.1 to 2.7 +/- 0.4 swallows/min). N omega-nitro-L -arginine methyl ester significantly decreased fetal swallowing to below the basal rate (0.4 +/- 0.1 swallows/min), and swallowing did not increase with the second angiotensin II dose (in the presence of nitric oxide blockade).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Angiotensin II', 'Animals', 'Behavior, Animal', 'Deglutition', 'Drinking Behavior', 'Enzyme Inhibitors', 'Female', 'Fetus', 'Gestational Age', 'Hemodynamics', 'Injections, Intraventricular', 'NG-Nitroarginine Methyl Ester', 'Nitric Oxide', 'Pregnancy', 'Sheep']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,748,446 | Is cyclin D1 expression predictive of occult metastases in head and neck cancer patients with clinically negative cervical lymph nodes? | {
"contexts": [
"The aim of this study was to investigate the value of p53 and cyclin D1 gene expression in predicting the risk of occult lymph node metastases in patients with head and neck squamous cell carcinoma (HNSCC).",
"The expression of cyclin D1 and p53 was evaluated by means of immunohistochemical analysis in 32 HNSCC patients with clinically and radiologically negative lymph nodes in whom metastatic involvement was subsequently demonstrated at histologic examination (pN+). A group of 64 head and neck cancer patients with histologically negative laterocervical lymph nodes (pN0) was used as a control.",
"Cyclin D1 and p53 expression were observed respectively in 42 (43.7%) and 48 cases (50%). Cyclin D1 expression significantly correlated with tumor extension and advanced clinical stage (p =.002 and p =.001, respectively). At univariate regression analysis, cyclin D1 expression significantly correlated with the presence of occult lymph node metastases (p =. 0007), and it remained an independent predictor at multivariate regression analysis (p =.0059)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Analysis of Variance",
"Biomarkers, Tumor",
"Biopsy, Needle",
"Carcinoma, Squamous Cell",
"Cyclin D1",
"Female",
"Head and Neck Neoplasms",
"Humans",
"Immunohistochemistry",
"Logistic Models",
"Lymph Node Excision",
"Lymph Nodes",
"Lymphatic Metastasis",
"Male",
"Middle Aged",
"Multivariate Analysis",
"Neoplasm Staging",
"Predictive Value of Tests",
"Sensitivity and Specificity",
"Survival Rate",
"Tumor Suppressor Protein p53"
]
} | Our study indicates that the expression of cyclin D1 correlates with the presence of occult cervical metastases in head and neck carcinoma patients, thus suggesting that its immunohistochemical evaluation in biopsy samples may be used as an additional tool for identifying patients to be treated with elective neck dissection. | yes | [
{
"from": "human",
"value": "Question: Is cyclin D1 expression predictive of occult metastases in head and neck cancer patients with clinically negative cervical lymph nodes?\nContext: {'contexts': ['The aim of this study was to investigate the value of p53 and cyclin D1 gene expression in predicting the risk of occult lymph node metastases in patients with head and neck squamous cell carcinoma (HNSCC).', 'The expression of cyclin D1 and p53 was evaluated by means of immunohistochemical analysis in 32 HNSCC patients with clinically and radiologically negative lymph nodes in whom metastatic involvement was subsequently demonstrated at histologic examination (pN+). A group of 64 head and neck cancer patients with histologically negative laterocervical lymph nodes (pN0) was used as a control.', 'Cyclin D1 and p53 expression were observed respectively in 42 (43.7%) and 48 cases (50%). Cyclin D1 expression significantly correlated with tumor extension and advanced clinical stage (p =.002 and p =.001, respectively). At univariate regression analysis, cyclin D1 expression significantly correlated with the presence of occult lymph node metastases (p =. 0007), and it remained an independent predictor at multivariate regression analysis (p =.0059).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Analysis of Variance', 'Biomarkers, Tumor', 'Biopsy, Needle', 'Carcinoma, Squamous Cell', 'Cyclin D1', 'Female', 'Head and Neck Neoplasms', 'Humans', 'Immunohistochemistry', 'Logistic Models', 'Lymph Node Excision', 'Lymph Nodes', 'Lymphatic Metastasis', 'Male', 'Middle Aged', 'Multivariate Analysis', 'Neoplasm Staging', 'Predictive Value of Tests', 'Sensitivity and Specificity', 'Survival Rate', 'Tumor Suppressor Protein p53']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,729,244 | Does gene therapy enhance the antiproliferative effect of radiation in intimal hyperplasia? | {
"contexts": [
"Although ionizing radiation (IR) has been demonstrated to attenuate vessel wall restenosis and intimal hyperplasia (IH), dose-related mural injury and atrophy are possible deleterious side effects. We tested the hypothesis that a radiosensitizing strategy may improve IR-induced inhibition of in vivo vascular smooth muscle cells (VSMCs) without influencing apoptotic cell death.",
"In 28 New Zealand White rabbits, the right common carotid artery (CCA) was injured and subjected to low-flow conditions to promote IH. The CCA was transfected with an adenoviral vector incorporating the cytosine deaminase (CD) gene (1 x 10(9) PFU/ml). 5-Fluorocytosine (5-FC), a prodrug that is converted to the radiosensitizing agent 5-fluorouracil (5-FU) by CD, was thereafter administered intravenously. The CCA was exposed to 5 Gy IR at 24 h. Intimal/medial (I/M) area and thickness ratios were determined in the harvested CCAs at 14 days. VSMC proliferative and apoptotic indices were assessed with immunohistochemistry.",
"A 50% reduction in I/M area was found in rabbits treated with IR and IR + CD/5-FC (0.19 +/- 0.03 and 0.18 +/- 0.02) when compared with untreated controls (UC) (0.37 +/- 0.06) (P = 0.005). This finding was substantiated by attenuation of I/M thickness in the IR groups [0.47 +/- 0.13 (IR), 0.41 +/- 0.11 (IR + CD/5-FC), 0.61 +/- 0.17 (UC)] (P = 0.007). The number of proliferating VSMCs was notably smaller when IR was combined with CD/5-FC (4.17 +/- 1.16 vs 2.97 +/- 1.09 log transformed cells/mm(2), P < 0.07). Apoptosis was similar in all groups."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Apoptosis",
"Carotid Artery, Common",
"Cell Division",
"Cytosine Deaminase",
"Flucytosine",
"Genetic Therapy",
"Hemodynamics",
"Hyperplasia",
"Male",
"Muscle, Smooth, Vascular",
"Nucleoside Deaminases",
"Prodrugs",
"Rabbits",
"Tunica Intima"
]
} | Both IR alone and IR combined with a radiosensitizing agent are effective in attenuating experimental IH. However, combination therapy is synergistic and achieves greater inhibition of VSMC proliferation and may involve selective killing of radioresistant S-phase VSMCs. IR + CD/5-FC represents a novel therapeutic strategy that offers potential for long-term control of IH. | yes | [
{
"from": "human",
"value": "Question: Does gene therapy enhance the antiproliferative effect of radiation in intimal hyperplasia?\nContext: {'contexts': ['Although ionizing radiation (IR) has been demonstrated to attenuate vessel wall restenosis and intimal hyperplasia (IH), dose-related mural injury and atrophy are possible deleterious side effects. We tested the hypothesis that a radiosensitizing strategy may improve IR-induced inhibition of in vivo vascular smooth muscle cells (VSMCs) without influencing apoptotic cell death.', 'In 28 New Zealand White rabbits, the right common carotid artery (CCA) was injured and subjected to low-flow conditions to promote IH. The CCA was transfected with an adenoviral vector incorporating the cytosine deaminase (CD) gene (1 x 10(9) PFU/ml). 5-Fluorocytosine (5-FC), a prodrug that is converted to the radiosensitizing agent 5-fluorouracil (5-FU) by CD, was thereafter administered intravenously. The CCA was exposed to 5 Gy IR at 24 h. Intimal/medial (I/M) area and thickness ratios were determined in the harvested CCAs at 14 days. VSMC proliferative and apoptotic indices were assessed with immunohistochemistry.', 'A 50% reduction in I/M area was found in rabbits treated with IR and IR + CD/5-FC (0.19 +/- 0.03 and 0.18 +/- 0.02) when compared with untreated controls (UC) (0.37 +/- 0.06) (P = 0.005). This finding was substantiated by attenuation of I/M thickness in the IR groups [0.47 +/- 0.13 (IR), 0.41 +/- 0.11 (IR + CD/5-FC), 0.61 +/- 0.17 (UC)] (P = 0.007). The number of proliferating VSMCs was notably smaller when IR was combined with CD/5-FC (4.17 +/- 1.16 vs 2.97 +/- 1.09 log transformed cells/mm(2), P < 0.07). Apoptosis was similar in all groups.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Apoptosis', 'Carotid Artery, Common', 'Cell Division', 'Cytosine Deaminase', 'Flucytosine', 'Genetic Therapy', 'Hemodynamics', 'Hyperplasia', 'Male', 'Muscle, Smooth, Vascular', 'Nucleoside Deaminases', 'Prodrugs', 'Rabbits', 'Tunica Intima']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,729,246 | Is inhibition of intestinal tumors by curcumin associated with changes in the intestinal immune cell profile? | {
"contexts": [
"The C57BL/6J-Min/+ (Min/+) mouse bears a germline mutation in Apc and is therefore a model for familial adenomatous polyposis and sporadic colorectal cancer. Min/+ intestinal mucosa exhibits a marked tendency for spontaneous adenoma formation. Curcumin is a phenolic antioxidant known for its antitumor and immune modulatory functions in vitro. Curcumin prevents adenoma formation in Min/+ mice, through a mechanism that may be related to its immunomodulatory properties.",
"To study the relationship between intestinal immunity and curcumin-induced antitumor response, we used immunohistochemistry to characterize the effect of curcumin treatment on resident intestinal immune effector cells in Min/+ mice."
],
"labels": [
"BACKGROUND",
"METHODS"
],
"meshes": [
"Adenomatous Polyposis Coli Protein",
"Animals",
"Antineoplastic Agents",
"B-Lymphocytes",
"CD4 Lymphocyte Count",
"CD4-Positive T-Lymphocytes",
"Curcumin",
"Cytoskeletal Proteins",
"Germ-Line Mutation",
"Immune System",
"Immunohistochemistry",
"Intestinal Mucosa",
"Intestinal Neoplasms",
"Intestines",
"Lymphocyte Count",
"Mice",
"Mice, Inbred C57BL",
"Mice, Mutant Strains"
]
} | These results show that mucosal CD4(+) T cells and B cells increase in animals treated with curcumin, suggesting that curcumin modulates lymphocyte-mediated immune functions. | yes | [
{
"from": "human",
"value": "Question: Is inhibition of intestinal tumors by curcumin associated with changes in the intestinal immune cell profile?\nContext: {'contexts': ['The C57BL/6J-Min/+ (Min/+) mouse bears a germline mutation in Apc and is therefore a model for familial adenomatous polyposis and sporadic colorectal cancer. Min/+ intestinal mucosa exhibits a marked tendency for spontaneous adenoma formation. Curcumin is a phenolic antioxidant known for its antitumor and immune modulatory functions in vitro. Curcumin prevents adenoma formation in Min/+ mice, through a mechanism that may be related to its immunomodulatory properties.', 'To study the relationship between intestinal immunity and curcumin-induced antitumor response, we used immunohistochemistry to characterize the effect of curcumin treatment on resident intestinal immune effector cells in Min/+ mice.'], 'labels': ['BACKGROUND', 'METHODS'], 'meshes': ['Adenomatous Polyposis Coli Protein', 'Animals', 'Antineoplastic Agents', 'B-Lymphocytes', 'CD4 Lymphocyte Count', 'CD4-Positive T-Lymphocytes', 'Curcumin', 'Cytoskeletal Proteins', 'Germ-Line Mutation', 'Immune System', 'Immunohistochemistry', 'Intestinal Mucosa', 'Intestinal Neoplasms', 'Intestines', 'Lymphocyte Count', 'Mice', 'Mice, Inbred C57BL', 'Mice, Mutant Strains']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,729,241 | Does aggregation substance promote colonic mucosal invasion of Enterococcus faecalis in an ex vivo model? | {
"contexts": [
"Bacterial translocation through the gastrointestinal tract is the crucial step in the pathogenesis of intraabdominal infections. We assessed whether aggregation substance (AS), a bacterial adhesin and virulence factor of Enterococcus faecalis, promotes bacterial translocation and colonic mucosal invasion in an ex vivo experiment.",
"Colonic mucosa of male Wistar rats was placed in a modified Ussing system. The mucosal side of the chamber was filled with a suspension of E. faecalis OG1X:pAM721 (AS-positive) or E. faecalis OG1X (AS-negative). The serosal side was filled with sterile Dulbecco's modified Eagle's medium. For assessment of colonic mucosal invasion the mucosal side was incubated for 2.5 h with a suspension of AS-positive or AS-negative enterococci. After being washed, a solution of gentamicin and penicillin G in tissue culture medium was added on both sides in order to kill extracellular bacteria. Subsequently, the mucosa was removed from the system, washed, lysed with Triton X-100, and homogenized. Viable intramural bacteria were quantified by plating serial dilutions of the homogenate on Todd-Hewitt broth agar plates. To quantify bacterial translocation samples which were taken at various time points from the serosal side were plated on Todd-Hewitt broth agar plates and colony forming units (CFU) were determined.",
"Invasion of the AS-positive E. faecalis strain OG1X:pAM721 into the colonic mucosa was significantly higher than invasion rates of the AS-negative strain OG1X (2.88 log(10) CFU/ml vs 1.73 log(10) CFU/ml; P = 0.02). However, none of the tested strains was found to translocate from the mucosal to the serosal side within the incubation time of 4 h."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Bacterial Proteins",
"Bacterial Translocation",
"Colon",
"Enterococcus faecalis",
"Intestinal Mucosa",
"Male",
"Rats",
"Rats, Wistar",
"Salmonella typhimurium",
"Sex Attractants"
]
} | The aggregation substance promotes invasion of E. faecalis into colonic mucosa. | yes | [
{
"from": "human",
"value": "Question: Does aggregation substance promote colonic mucosal invasion of Enterococcus faecalis in an ex vivo model?\nContext: {'contexts': ['Bacterial translocation through the gastrointestinal tract is the crucial step in the pathogenesis of intraabdominal infections. We assessed whether aggregation substance (AS), a bacterial adhesin and virulence factor of Enterococcus faecalis, promotes bacterial translocation and colonic mucosal invasion in an ex vivo experiment.', \"Colonic mucosa of male Wistar rats was placed in a modified Ussing system. The mucosal side of the chamber was filled with a suspension of E. faecalis OG1X:pAM721 (AS-positive) or E. faecalis OG1X (AS-negative). The serosal side was filled with sterile Dulbecco's modified Eagle's medium. For assessment of colonic mucosal invasion the mucosal side was incubated for 2.5 h with a suspension of AS-positive or AS-negative enterococci. After being washed, a solution of gentamicin and penicillin G in tissue culture medium was added on both sides in order to kill extracellular bacteria. Subsequently, the mucosa was removed from the system, washed, lysed with Triton X-100, and homogenized. Viable intramural bacteria were quantified by plating serial dilutions of the homogenate on Todd-Hewitt broth agar plates. To quantify bacterial translocation samples which were taken at various time points from the serosal side were plated on Todd-Hewitt broth agar plates and colony forming units (CFU) were determined.\", 'Invasion of the AS-positive E. faecalis strain OG1X:pAM721 into the colonic mucosa was significantly higher than invasion rates of the AS-negative strain OG1X (2.88 log(10) CFU/ml vs 1.73 log(10) CFU/ml; P = 0.02). However, none of the tested strains was found to translocate from the mucosal to the serosal side within the incubation time of 4 h.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Bacterial Proteins', 'Bacterial Translocation', 'Colon', 'Enterococcus faecalis', 'Intestinal Mucosa', 'Male', 'Rats', 'Rats, Wistar', 'Salmonella typhimurium', 'Sex Attractants']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,728,118 | Does physician disclosure of healthy personal behaviors improve credibility and ability to motivate? | {
"contexts": [
"While some studies have shown that physicians with healthy personal habits are especially likely to discuss prevention with their patients, to our knowledge no one has published information testing whether physician credibility and patient motivation to adopt healthier habits are enhanced by physician's disclosures of their own healthy behaviors.",
"Two brief health education videos about improving diet and exercise were produced and shown to subjects (n1 = 66, n2 = 65) in an Emory University general medical clinic waiting room in Atlanta, Ga. In one video, the physician revealed an additional half minute of information about her personal healthy dietary and exercise practices and had a bike helmet and an apple visible on her desk (physician-disclosure video). In the other video, discussion of personal practices and the apple and bike helmet were not included (control video).",
"Viewers of the physician-disclosure video considered the physician to be generally healthier, some-what more believable, and more motivating than did viewers of the control video. They also rated this physician to be specifically more believable and motivating regarding exercise and diet (P < or = .001)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Aged, 80 and over",
"Case-Control Studies",
"Female",
"Health Behavior",
"Humans",
"Life Style",
"Male",
"Middle Aged",
"Motivation",
"Patients",
"Physicians",
"Surveys and Questionnaires",
"Videotape Recording"
]
} | Physicians' abilities to motivate patients to adopt healthy habits can be enhanced by conveying their own healthy habits. Educational institutions should consider encouraging health professionals-in-training to practice and demonstrate healthy personal lifestyles. | yes | [
{
"from": "human",
"value": "Question: Does physician disclosure of healthy personal behaviors improve credibility and ability to motivate?\nContext: {'contexts': [\"While some studies have shown that physicians with healthy personal habits are especially likely to discuss prevention with their patients, to our knowledge no one has published information testing whether physician credibility and patient motivation to adopt healthier habits are enhanced by physician's disclosures of their own healthy behaviors.\", 'Two brief health education videos about improving diet and exercise were produced and shown to subjects (n1 = 66, n2 = 65) in an Emory University general medical clinic waiting room in Atlanta, Ga. In one video, the physician revealed an additional half minute of information about her personal healthy dietary and exercise practices and had a bike helmet and an apple visible on her desk (physician-disclosure video). In the other video, discussion of personal practices and the apple and bike helmet were not included (control video).', 'Viewers of the physician-disclosure video considered the physician to be generally healthier, some-what more believable, and more motivating than did viewers of the control video. They also rated this physician to be specifically more believable and motivating regarding exercise and diet (P < or = .001).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Aged, 80 and over', 'Case-Control Studies', 'Female', 'Health Behavior', 'Humans', 'Life Style', 'Male', 'Middle Aged', 'Motivation', 'Patients', 'Physicians', 'Surveys and Questionnaires', 'Videotape Recording']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,741,440 | Does pneumoperitoneum with carbon dioxide enhance liver metastases of cancer cells implanted into the portal vein in rabbits? | {
"contexts": [
"Little is known about the role of the CO2 pneumoperitoneum on tumor cells that spread from the portal system into the liver during laparoscopic surgery for gastrointestinal malignancies. Therefore, we designed a study to investigate the effect of CO2 pneumoperitoneum on cancer cells implanted in the portal vein in a rabbit model.",
"Immediately after intraportal inoculation of 2.5x10(5) cells of VX2 cancer, the rabbits received either CO2 pneumoperitoneum at a pressure of 10 mm Hg for 30 min (pneumoperitoneum group, n = 14) or laparotomy alone for 30 min (laparotomy group, n = 14).",
"The number (p<0.01) and area of cancer nodules (p = 0.045) on the liver surface on day 17 were greater in the pneumoperitoneum group than in the laparotomy group. The frequency of cancer nodules >3.0 mm in diameter was higher in the pneumoperitoneum group than in the laparotomy group (p<0.001)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Carbon Dioxide",
"Disease Progression",
"Gastrointestinal Neoplasms",
"Laparoscopy",
"Liver Neoplasms, Experimental",
"Male",
"Neoplasm Seeding",
"Neoplasm Transplantation",
"Pneumoperitoneum, Artificial",
"Portal Vein",
"Rabbits"
]
} | Compared with laparotomy, CO2 pneumoperitoneum enhanced the development of liver metastases in this experimental model. | yes | [
{
"from": "human",
"value": "Question: Does pneumoperitoneum with carbon dioxide enhance liver metastases of cancer cells implanted into the portal vein in rabbits?\nContext: {'contexts': ['Little is known about the role of the CO2 pneumoperitoneum on tumor cells that spread from the portal system into the liver during laparoscopic surgery for gastrointestinal malignancies. Therefore, we designed a study to investigate the effect of CO2 pneumoperitoneum on cancer cells implanted in the portal vein in a rabbit model.', 'Immediately after intraportal inoculation of 2.5x10(5) cells of VX2 cancer, the rabbits received either CO2 pneumoperitoneum at a pressure of 10 mm Hg for 30 min (pneumoperitoneum group, n = 14) or laparotomy alone for 30 min (laparotomy group, n = 14).', 'The number (p<0.01) and area of cancer nodules (p = 0.045) on the liver surface on day 17 were greater in the pneumoperitoneum group than in the laparotomy group. The frequency of cancer nodules >3.0 mm in diameter was higher in the pneumoperitoneum group than in the laparotomy group (p<0.001).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Carbon Dioxide', 'Disease Progression', 'Gastrointestinal Neoplasms', 'Laparoscopy', 'Liver Neoplasms, Experimental', 'Male', 'Neoplasm Seeding', 'Neoplasm Transplantation', 'Pneumoperitoneum, Artificial', 'Portal Vein', 'Rabbits']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,735,931 | Does fasting induce impairment of gastric mucosal integrity in non-insulin-dependent diabetic ( db/db ) mice? | {
"contexts": [
"Although diabetic patients often have gastrointestinal complications, the gastric mucosal function in diabetes has not been well documented.",
"To investigate the effect of fasting on the gastric mucosa in C57BL/KsJ-db +/+ db (db/db) mice, genetically non-insulin-dependent diabetic animals.",
"Blood glucose levels, gastric mucosal morphology, and the amount of gastric mucin were examined before and after 18 h of fasting with free access to water in db/db mice and their non-diabetic littermates (db/m).",
"Although 18 h of fasting reduced the blood glucose levels of both db/db and db/m mice, fasting decreased the amount of gastric adherent mucin and caused haemorrhagic gastric lesions only in db/db mice. After fasting, oral administration of ethanol induced much more severe gastric damage in db/db than in db/m mice. The above fasting-induced gastric damage such as haemorrhagic lesions, loss of the mucin, and the increased sensitivity to ethanol worsened as the duration of diabetes became longer. Glucose ingestion in drinking water during the fasting counteracted the fall in blood glucose and prevented the decrease in the amount of gastric mucin and the formation of gastric mucosal lesions in db/db mice."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aging",
"Animals",
"Blood Glucose",
"Body Temperature",
"Diabetes Mellitus, Experimental",
"Diabetes Mellitus, Type 2",
"Fasting",
"Female",
"Gastric Mucosa",
"Male",
"Mice",
"Mice, Inbred C57BL",
"Mucins",
"Time Factors"
]
} | These findings indicate that fasting-induced glucose deficit causes gastric mucosal lesions and increases the susceptibility of gastric mucosa to noxious agents owing to the loss of mucus glycoprotein in db/db mice. Prolonged diabetes is likely to augment the severity of fasting-induced impairment of the gastric mucosal function. | yes | [
{
"from": "human",
"value": "Question: Does fasting induce impairment of gastric mucosal integrity in non-insulin-dependent diabetic ( db/db ) mice?\nContext: {'contexts': ['Although diabetic patients often have gastrointestinal complications, the gastric mucosal function in diabetes has not been well documented.', 'To investigate the effect of fasting on the gastric mucosa in C57BL/KsJ-db +/+ db (db/db) mice, genetically non-insulin-dependent diabetic animals.', 'Blood glucose levels, gastric mucosal morphology, and the amount of gastric mucin were examined before and after 18 h of fasting with free access to water in db/db mice and their non-diabetic littermates (db/m).', 'Although 18 h of fasting reduced the blood glucose levels of both db/db and db/m mice, fasting decreased the amount of gastric adherent mucin and caused haemorrhagic gastric lesions only in db/db mice. After fasting, oral administration of ethanol induced much more severe gastric damage in db/db than in db/m mice. The above fasting-induced gastric damage such as haemorrhagic lesions, loss of the mucin, and the increased sensitivity to ethanol worsened as the duration of diabetes became longer. Glucose ingestion in drinking water during the fasting counteracted the fall in blood glucose and prevented the decrease in the amount of gastric mucin and the formation of gastric mucosal lesions in db/db mice.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aging', 'Animals', 'Blood Glucose', 'Body Temperature', 'Diabetes Mellitus, Experimental', 'Diabetes Mellitus, Type 2', 'Fasting', 'Female', 'Gastric Mucosa', 'Male', 'Mice', 'Mice, Inbred C57BL', 'Mucins', 'Time Factors']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,728,019 | Are circulating levels of IL-1beta , a prothrombotic cytokine , elevated in unstable angina versus stable angina? | {
"contexts": [
"Multiple studies support a role for inflammation in the pathogenesis of coronary atherosclerosis and unstable cardiac syndromes. However, of the known proinflammatory cytokines, only elevated plasma levels of interleukin-6 have been linked to unstable angina. We sought to examine the plasma levels of other major proinflammatory cytokines in similar clinical settings and to determine the extent of the relationship between inflammation and unstable coronary syndromes by measuring the levels of various proinflammatory cytokines in patients with stable and unstable angina.",
"We measured plasma levels of interleukin-1 beta (IL-1beta), tumor necrosis factor alpha (TNF-alpha), and interleukin 6 (IL-6) in 97 patients: 67 with stable angina, 24 with unstable angina, and 15 healthy controls.",
"Mean levels of IL-1beta were significantly higher in patients with unstable angina as compared to patients with stable angina (p =.009). Levels of IL-6 were significantly higher than control patients for both stable angina and unstable angina patients (p =.031 and.006, respectively). No significant differences were found in the levels of TNF-alpha."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Angina Pectoris",
"Angina, Unstable",
"Enzyme-Linked Immunosorbent Assay",
"Female",
"Humans",
"Interleukin-1",
"Interleukin-6",
"Male",
"Middle Aged",
"Statistics, Nonparametric",
"Tumor Necrosis Factor-alpha"
]
} | Our results suggest that both IL-1beta and IL-6 contribute to the pathogenesis of unstable angina, and that the profile of circulating plasma levels of proinflammatory cytokines differs in unstable angina from that in stable angina. Abbreviated Abstract. Multiple studies support a role for inflammation in the pathogenesis of coronary atherosclerosis and unstable cardiac syndromes. We measured plasma levels of interleukin-1 beta (IL-1beta), tumor necrosis factor alpha (TNF-alpha), and interleukin 6 (IL-6) in patients with stable and unstable coronary syndromes. Levels of IL-1beta and IL-6 were found to be elevated in patients with unstable coronary syndromes. No significant differences were found in the levels of TNF-alpha. Our results suggest that both IL-1beta and IL-6 contribute to the pathogenesis of unstable angina. | yes | [
{
"from": "human",
"value": "Question: Are circulating levels of IL-1beta , a prothrombotic cytokine , elevated in unstable angina versus stable angina?\nContext: {'contexts': ['Multiple studies support a role for inflammation in the pathogenesis of coronary atherosclerosis and unstable cardiac syndromes. However, of the known proinflammatory cytokines, only elevated plasma levels of interleukin-6 have been linked to unstable angina. We sought to examine the plasma levels of other major proinflammatory cytokines in similar clinical settings and to determine the extent of the relationship between inflammation and unstable coronary syndromes by measuring the levels of various proinflammatory cytokines in patients with stable and unstable angina.', 'We measured plasma levels of interleukin-1 beta (IL-1beta), tumor necrosis factor alpha (TNF-alpha), and interleukin 6 (IL-6) in 97 patients: 67 with stable angina, 24 with unstable angina, and 15 healthy controls.', 'Mean levels of IL-1beta were significantly higher in patients with unstable angina as compared to patients with stable angina (p =.009). Levels of IL-6 were significantly higher than control patients for both stable angina and unstable angina patients (p =.031 and.006, respectively). No significant differences were found in the levels of TNF-alpha.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Angina Pectoris', 'Angina, Unstable', 'Enzyme-Linked Immunosorbent Assay', 'Female', 'Humans', 'Interleukin-1', 'Interleukin-6', 'Male', 'Middle Aged', 'Statistics, Nonparametric', 'Tumor Necrosis Factor-alpha']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,753,065 | Does dendritic cell-based genetic immunization in mice with a recombinant adenovirus encoding murine TRP2 induce effective anti-melanoma immunity? | {
"contexts": [
"The induction of cellular immune responses to melanocyte-specific enzymes such as the tyrosinase family of proteins is the goal of various clinical studies for the immunotherapy of melanoma. Tyrosinase-related protein-2 (TRP2) is an attractive model antigen for preclinical studies in C57BL/6 mice because it is naturally expressed by the murine B16 melanoma and can be recognized by self-reactive cytolytic T lymphocytes (CTL). Here we describe efforts to develop genetic immunization with dendritic cells (DC) for the immunotherapy of melanoma in this clinically relevant system.",
"Recombinant adenoviruses encoding green fluorescent protein (Ad-EGFP) and murine TRP2 (Ad-mTRP2) were constructed using Cre-loxP-mediated recombination. DC were generated in vitro from precursors in bone marrow and transduced with Ad-EGFP or Ad-mTRP2. Mice were immunized by direct injection of adenovirus or by injection of Ad-transduced DC. Induction of tumor immunity was assessed by intravenous challenge with B16 melanoma cells and enumeration of experimentally induced lung metastases.",
"Flowcytometric analysis of DC transduced with Ad-EGFP demonstrated endogenous fluorescence due to cytoplasmatic expression of EGFP in 30-60% of cells. Ad-EGFP-transduced DC simultaneously displayed the DC-specific marker NLDC145 and high levels of MHC and costimulatory molecules on their cell surface. Transduction of DC with Ad-mTRP2 resulted in strong intracellular expression of TRP2 which could be readily detected by immunostaining. Importantly, immunization of mice with cultured Ad-mTRP2-transduced DC completely prevented the development of lung metastases following an intravenous challenge with B16 melanoma cells. This striking protective effect was observed with both the intravenous and the subcutaneous route of DC immunization. In vivo depletion of T-cell subsets suggested that the protective effect of an immunization with Ad-mTRP2-transduced DC involved both CD8+ and CD4+ T-cells."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adenoviridae",
"Animals",
"Antigens, Neoplasm",
"Cancer Vaccines",
"Cells, Cultured",
"Dendritic Cells",
"Female",
"Flow Cytometry",
"Genes, Reporter",
"Genetic Vectors",
"Graft Rejection",
"Immune Tolerance",
"Immunization",
"Immunotherapy, Active",
"Intramolecular Oxidoreductases",
"Melanoma, Experimental",
"Mice",
"Mice, Inbred C57BL",
"Neoplasm Transplantation"
]
} | Our results demonstrate that DC-based genetic immunization of mice with TRP2, a clinically relevant melanocyte-specific self-antigen, induces effective cellular immunity and prevents metastatic growth of B16 melanoma cells in vivo. | yes | [
{
"from": "human",
"value": "Question: Does dendritic cell-based genetic immunization in mice with a recombinant adenovirus encoding murine TRP2 induce effective anti-melanoma immunity?\nContext: {'contexts': ['The induction of cellular immune responses to melanocyte-specific enzymes such as the tyrosinase family of proteins is the goal of various clinical studies for the immunotherapy of melanoma. Tyrosinase-related protein-2 (TRP2) is an attractive model antigen for preclinical studies in C57BL/6 mice because it is naturally expressed by the murine B16 melanoma and can be recognized by self-reactive cytolytic T lymphocytes (CTL). Here we describe efforts to develop genetic immunization with dendritic cells (DC) for the immunotherapy of melanoma in this clinically relevant system.', 'Recombinant adenoviruses encoding green fluorescent protein (Ad-EGFP) and murine TRP2 (Ad-mTRP2) were constructed using Cre-loxP-mediated recombination. DC were generated in vitro from precursors in bone marrow and transduced with Ad-EGFP or Ad-mTRP2. Mice were immunized by direct injection of adenovirus or by injection of Ad-transduced DC. Induction of tumor immunity was assessed by intravenous challenge with B16 melanoma cells and enumeration of experimentally induced lung metastases.', 'Flowcytometric analysis of DC transduced with Ad-EGFP demonstrated endogenous fluorescence due to cytoplasmatic expression of EGFP in 30-60% of cells. Ad-EGFP-transduced DC simultaneously displayed the DC-specific marker NLDC145 and high levels of MHC and costimulatory molecules on their cell surface. Transduction of DC with Ad-mTRP2 resulted in strong intracellular expression of TRP2 which could be readily detected by immunostaining. Importantly, immunization of mice with cultured Ad-mTRP2-transduced DC completely prevented the development of lung metastases following an intravenous challenge with B16 melanoma cells. This striking protective effect was observed with both the intravenous and the subcutaneous route of DC immunization. In vivo depletion of T-cell subsets suggested that the protective effect of an immunization with Ad-mTRP2-transduced DC involved both CD8+ and CD4+ T-cells.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adenoviridae', 'Animals', 'Antigens, Neoplasm', 'Cancer Vaccines', 'Cells, Cultured', 'Dendritic Cells', 'Female', 'Flow Cytometry', 'Genes, Reporter', 'Genetic Vectors', 'Graft Rejection', 'Immune Tolerance', 'Immunization', 'Immunotherapy, Active', 'Intramolecular Oxidoreductases', 'Melanoma, Experimental', 'Mice', 'Mice, Inbred C57BL', 'Neoplasm Transplantation']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,731,402 | Do new Q waves on the presenting electrocardiogram independently predict increased cardiac mortality following a first ST-elevation myocardial infarction? | {
"contexts": [
"The prognostic significance of pathological Q waves appearing in the acute phase of myocardial infarction has not been determined. We investigated whether new Q waves on the presenting electrocardiogram of patients with acute ST-segment elevation were independently associated with a worse outcome after a first myocardial infarction.",
"The presence or absence of new Q waves on the presenting electrocardiogram was assessed in 481 patients who presented within 4 h of symptom onset and were randomized to receive either captopril or placebo within 2 h of streptokinase therapy for myocardial infarction. Ventriculography was performed at 22+/-6 days and mortality status was obtained at a median follow-up of 5.6 years. New Q waves were associated with a lower ejection fraction (51+/-13% vs 61+/-12%, P<0.0001), a larger end-systolic volume index (37 ml vs 28 ml, P<0.001), and increased cardiac mortality at 30 days (7% vs 2%, P=0.01) and at follow-up (17% vs 7%, P=0.002). On multivariate analysis, age (P<0.01), new Q waves at presentation (P<0.01) and a history of angina (P=0.046) were independent predictors of cardiac mortality, whereas randomization to captopril and the time from symptom onset to streptokinase administration were not."
],
"labels": [
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Aged",
"Angiotensin-Converting Enzyme Inhibitors",
"Captopril",
"Electrocardiography",
"Female",
"Fibrinolytic Agents",
"Heart Conduction System",
"Humans",
"Male",
"Middle Aged",
"Myocardial Infarction",
"New Zealand",
"Predictive Value of Tests",
"Streptokinase",
"Survival Analysis"
]
} | New Q waves at presentation are independently associated with a worse outcome after a first myocardial infarction. The presence of new Q waves on the presenting electrocardiogram allows very early identification of patients at risk of increased cardiac mortality. | yes | [
{
"from": "human",
"value": "Question: Do new Q waves on the presenting electrocardiogram independently predict increased cardiac mortality following a first ST-elevation myocardial infarction?\nContext: {'contexts': ['The prognostic significance of pathological Q waves appearing in the acute phase of myocardial infarction has not been determined. We investigated whether new Q waves on the presenting electrocardiogram of patients with acute ST-segment elevation were independently associated with a worse outcome after a first myocardial infarction.', 'The presence or absence of new Q waves on the presenting electrocardiogram was assessed in 481 patients who presented within 4 h of symptom onset and were randomized to receive either captopril or placebo within 2 h of streptokinase therapy for myocardial infarction. Ventriculography was performed at 22+/-6 days and mortality status was obtained at a median follow-up of 5.6 years. New Q waves were associated with a lower ejection fraction (51+/-13% vs 61+/-12%, P<0.0001), a larger end-systolic volume index (37 ml vs 28 ml, P<0.001), and increased cardiac mortality at 30 days (7% vs 2%, P=0.01) and at follow-up (17% vs 7%, P=0.002). On multivariate analysis, age (P<0.01), new Q waves at presentation (P<0.01) and a history of angina (P=0.046) were independent predictors of cardiac mortality, whereas randomization to captopril and the time from symptom onset to streptokinase administration were not.'], 'labels': ['OBJECTIVE', 'RESULTS'], 'meshes': ['Aged', 'Angiotensin-Converting Enzyme Inhibitors', 'Captopril', 'Electrocardiography', 'Female', 'Fibrinolytic Agents', 'Heart Conduction System', 'Humans', 'Male', 'Middle Aged', 'Myocardial Infarction', 'New Zealand', 'Predictive Value of Tests', 'Streptokinase', 'Survival Analysis']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,744,093 | Does subgroup analysis and other ( mis ) used of baseline data in clinical trials? | {
"contexts": [
"Baseline data collected on each patient at randomisation in controlled clinical trials can be used to describe the population of patients, to assess comparability of treatment groups, to achieve balanced randomisation, to adjust treatment comparisons for prognostic factors, and to undertake subgroup analyses. We assessed the extent and quality of such practices in major clinical trial reports.",
"A sample of 50 consecutive clinical-trial reports was obtained from four major medical journals during July to September, 1997. We tabulated the detailed information on uses of baseline data by use of a standard form.",
"Most trials presented baseline comparability in a table. These tables were often unduly large, and about half the trials inappropriately used significance tests for baseline comparison. Methods of randomisation, including possible stratification, were often poorly described. There was little consistency over whether to use covariate adjustment and the criteria for selecting baseline factors for which to adjust were often unclear. Most trials emphasised the simple unadjusted results and covariate adjustment usually made negligible difference. Two-thirds of the reports presented subgroup findings, but mostly without appropriate statistical tests for interaction. Many reports put too much emphasis on subgroup analyses that commonly lacked statistical power."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Bias",
"Data Collection",
"Data Interpretation, Statistical",
"Humans",
"Randomized Controlled Trials as Topic"
]
} | Clinical trials need a predefined statistical analysis plan for uses of baseline data, especially covariate-adjusted analyses and subgroup analyses. Investigators and journals need to adopt improved standards of statistical reporting, and exercise caution when drawing conclusions from subgroup findings. | yes | [
{
"from": "human",
"value": "Question: Does subgroup analysis and other ( mis ) used of baseline data in clinical trials?\nContext: {'contexts': ['Baseline data collected on each patient at randomisation in controlled clinical trials can be used to describe the population of patients, to assess comparability of treatment groups, to achieve balanced randomisation, to adjust treatment comparisons for prognostic factors, and to undertake subgroup analyses. We assessed the extent and quality of such practices in major clinical trial reports.', 'A sample of 50 consecutive clinical-trial reports was obtained from four major medical journals during July to September, 1997. We tabulated the detailed information on uses of baseline data by use of a standard form.', 'Most trials presented baseline comparability in a table. These tables were often unduly large, and about half the trials inappropriately used significance tests for baseline comparison. Methods of randomisation, including possible stratification, were often poorly described. There was little consistency over whether to use covariate adjustment and the criteria for selecting baseline factors for which to adjust were often unclear. Most trials emphasised the simple unadjusted results and covariate adjustment usually made negligible difference. Two-thirds of the reports presented subgroup findings, but mostly without appropriate statistical tests for interaction. Many reports put too much emphasis on subgroup analyses that commonly lacked statistical power.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Bias', 'Data Collection', 'Data Interpretation, Statistical', 'Humans', 'Randomized Controlled Trials as Topic']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,753,745 | Does mAP kinase signaling induce nuclear reorganization in budding yeast? | {
"contexts": [
"During the mating pheromone response in budding yeast, activation of a mitogen-activated protein kinase (MAP kinase) cascade results in well-characterized changes in cytoskeletal organization and gene expression. Spatial reorganization of genes within the nucleus has been documented during cell-type differentiation in mammalian cells, but no information was previously available on the morphology of the yeast nucleus during the major transcriptional reprogramming that accompanies zygote formation.",
"We find that in response to mating pheromone, budding yeast nuclei assume an unusual dumbbell shape, reflecting a spatial separation of chromosomal and nucleolar domains. Within the chromosomal domain, telomeric foci persist and maintain their associated complement of Sir proteins. The nucleolus, on the other hand, assumes a novel cup-shaped morphology and a position distal to the mating projection tip. Although microtubules are required for this orientation with respect to the projection tip, neither microtubules nor actin polymerization are necessary for the observed changes in nuclear shape. We find that activation of the pheromone-response MAP kinase pathway by ectopic expression of STE4 or STE11 leads to identical nuclear and nucleolar reorganization in the absence of pheromone. Mutation of downstream effector MAP kinases Fus3p and Kss1p, or of the transcriptional regulator Ste12p, blocks nuclear shape changes, whereas overexpression of Ste12p promotes dumbbell-shaped nuclei in the absence of pheromone."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Actins",
"Cell Nucleolus",
"Cell Nucleus",
"Fungal Proteins",
"MAP Kinase Kinase Kinases",
"MAP Kinase Signaling System",
"Pheromones",
"Saccharomyces cerevisiae",
"Saccharomyces cerevisiae Proteins",
"Schizosaccharomyces pombe Proteins",
"Telomere",
"Transcription Factors",
"Zygote"
]
} | Nuclear remodeling occurs when the MAP kinase cascade is activated by yeast pheromone, but it is independent of the cytoskeletal reorganization regulated by the same signaling pathway. Activation of the Ste12p transcription factor is necessary, and may be sufficient, for the changes in nuclear structure that coincide with developmentally significant changes in gene expression. | yes | [
{
"from": "human",
"value": "Question: Does mAP kinase signaling induce nuclear reorganization in budding yeast?\nContext: {'contexts': ['During the mating pheromone response in budding yeast, activation of a mitogen-activated protein kinase (MAP kinase) cascade results in well-characterized changes in cytoskeletal organization and gene expression. Spatial reorganization of genes within the nucleus has been documented during cell-type differentiation in mammalian cells, but no information was previously available on the morphology of the yeast nucleus during the major transcriptional reprogramming that accompanies zygote formation.', 'We find that in response to mating pheromone, budding yeast nuclei assume an unusual dumbbell shape, reflecting a spatial separation of chromosomal and nucleolar domains. Within the chromosomal domain, telomeric foci persist and maintain their associated complement of Sir proteins. The nucleolus, on the other hand, assumes a novel cup-shaped morphology and a position distal to the mating projection tip. Although microtubules are required for this orientation with respect to the projection tip, neither microtubules nor actin polymerization are necessary for the observed changes in nuclear shape. We find that activation of the pheromone-response MAP kinase pathway by ectopic expression of STE4 or STE11 leads to identical nuclear and nucleolar reorganization in the absence of pheromone. Mutation of downstream effector MAP kinases Fus3p and Kss1p, or of the transcriptional regulator Ste12p, blocks nuclear shape changes, whereas overexpression of Ste12p promotes dumbbell-shaped nuclei in the absence of pheromone.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Actins', 'Cell Nucleolus', 'Cell Nucleus', 'Fungal Proteins', 'MAP Kinase Kinase Kinases', 'MAP Kinase Signaling System', 'Pheromones', 'Saccharomyces cerevisiae', 'Saccharomyces cerevisiae Proteins', 'Schizosaccharomyces pombe Proteins', 'Telomere', 'Transcription Factors', 'Zygote']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,753,746 | Does a protein complex containing Inscuteable and the Galpha-binding protein Pins orient asymmetric cell divisions in Drosophila? | {
"contexts": [
"In the fruit fly Drosophila, the Inscuteable protein localises to the apical cell cortex in neuroblasts and directs both the apical-basal orientation of the mitotic spindle and the basal localisation of the protein determinants Numb and Prospero during mitosis. Asymmetric localisation of Inscuteable is initiated during neuroblast delamination by direct binding to Bazooka, an apically localised protein that contains protein-interaction motifs known as PDZ domains. How apically localised Inscuteable directs asymmetric cell divisions is unclear.",
"A novel 70 kDa protein called Partner of Inscuteable (Pins) and a heterotrimeric G-protein alpha subunit were found to bind specifically to the functional domain of Inscuteable in vivo. The predicted sequence of Pins contained tetratrico-peptide repeats (TPRs) and motifs implicated in binding Galpha proteins. Pins colocalised with Inscuteable at the apical cell cortex in interphase and mitotic neuroblasts. Asymmetric localisation of Pins required both Inscuteable and Bazooka. In epithelial cells, which do not express inscuteable, Pins was not apically localised but could be recruited to the apical cortex by ectopic expression of Inscuteable. In pins mutants, these epithelial cells were not affected, but neuroblasts showed defects in the orientation of their mitotic spindle and the basal asymmetric localisation of Numb and Miranda during metaphase. Although localisation of Inscuteable in pins mutants was initiated correctly during neuroblast delamination, Inscuteable became homogeneously distributed in the cytoplasm during mitosis."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Amino Acid Sequence",
"Animals",
"Biological Transport",
"Carrier Proteins",
"Cell Cycle Proteins",
"Cell Division",
"Cell Polarity",
"Cytoskeletal Proteins",
"Drosophila",
"Drosophila Proteins",
"Epithelial Cells",
"Heterotrimeric GTP-Binding Proteins",
"Insect Proteins",
"Intracellular Signaling Peptides and Proteins",
"Models, Biological",
"Molecular Sequence Data",
"Nerve Tissue",
"Neuropeptides",
"Signal Transduction",
"Stem Cells"
]
} | Pins and Inscuteable are dependent on each other for asymmetric localisation in delaminated neuroblasts. The binding of Pins to Galpha protein offers the intriguing possibility that Inscuteable and Pins might orient asymmetric cell divisions by localising or locally modulating a heterotrimeric G-protein signalling cascade at the apical cell cortex. | yes | [
{
"from": "human",
"value": "Question: Does a protein complex containing Inscuteable and the Galpha-binding protein Pins orient asymmetric cell divisions in Drosophila?\nContext: {'contexts': ['In the fruit fly Drosophila, the Inscuteable protein localises to the apical cell cortex in neuroblasts and directs both the apical-basal orientation of the mitotic spindle and the basal localisation of the protein determinants Numb and Prospero during mitosis. Asymmetric localisation of Inscuteable is initiated during neuroblast delamination by direct binding to Bazooka, an apically localised protein that contains protein-interaction motifs known as PDZ domains. How apically localised Inscuteable directs asymmetric cell divisions is unclear.', 'A novel 70 kDa protein called Partner of Inscuteable (Pins) and a heterotrimeric G-protein alpha subunit were found to bind specifically to the functional domain of Inscuteable in vivo. The predicted sequence of Pins contained tetratrico-peptide repeats (TPRs) and motifs implicated in binding Galpha proteins. Pins colocalised with Inscuteable at the apical cell cortex in interphase and mitotic neuroblasts. Asymmetric localisation of Pins required both Inscuteable and Bazooka. In epithelial cells, which do not express inscuteable, Pins was not apically localised but could be recruited to the apical cortex by ectopic expression of Inscuteable. In pins mutants, these epithelial cells were not affected, but neuroblasts showed defects in the orientation of their mitotic spindle and the basal asymmetric localisation of Numb and Miranda during metaphase. Although localisation of Inscuteable in pins mutants was initiated correctly during neuroblast delamination, Inscuteable became homogeneously distributed in the cytoplasm during mitosis.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Amino Acid Sequence', 'Animals', 'Biological Transport', 'Carrier Proteins', 'Cell Cycle Proteins', 'Cell Division', 'Cell Polarity', 'Cytoskeletal Proteins', 'Drosophila', 'Drosophila Proteins', 'Epithelial Cells', 'Heterotrimeric GTP-Binding Proteins', 'Insect Proteins', 'Intracellular Signaling Peptides and Proteins', 'Models, Biological', 'Molecular Sequence Data', 'Nerve Tissue', 'Neuropeptides', 'Signal Transduction', 'Stem Cells']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,735,809 | Does pentobarbital have curare-like effects on adult-type nicotinic acetylcholine receptor channel currents? | {
"contexts": [
"Pentobarbital (PB) is widely used as a short-term sedative and anticonvulsive drug with a side-effect of relaxing muscle tone. We investigated block of nicotinic acetylcholine receptor (nAChR) channel currents by PB using the patch-clamp technique in combination with an ultrafast system for solution exchange. As a preparation, recombinant rat adult-type nAChR channels transiently expressed in HEK293 cells were used. Appli-cation of 1 mM acetylcholine to small cells or outside-out patches showed a transient current with fast activation and desensitization kinetics. Adding PB to the acetylcholine-containing solution resulted in a decrease of the time constant of current decay and of the peak current amplitude starting at concentrations >0.01 mM PB. Preincubation of nAChR channels with PB led to a decrease of the peak current amplitude without alteration of activation and desensitization kinetics caused by competitive block of nAChR channels. In conclusion, similar to the effect of d-Tubocurarine, block of nAChR channel currents by PB can be explained by a combination of open-channel and competitive block."
],
"labels": [
"UNLABELLED"
],
"meshes": [
"Acetylcholine",
"Animals",
"Dose-Response Relationship, Drug",
"Humans",
"Ion Channels",
"Mice",
"Neuromuscular Nondepolarizing Agents",
"Pentobarbital",
"Rats",
"Receptors, Nicotinic"
]
} | The interaction between adult-type nicotinic acetylcholine receptors, acetylcholine, and pentobarbital was biophysically investigated by using the patch-clamp technique in combination with tools for ultrafast solution exchange. PB elicited open-channel block and competitive block of nicotinic acetylcholine receptor channel currents, whereas the latter seems to be effective in clinically relevant concentrations. | yes | [
{
"from": "human",
"value": "Question: Does pentobarbital have curare-like effects on adult-type nicotinic acetylcholine receptor channel currents?\nContext: {'contexts': ['Pentobarbital (PB) is widely used as a short-term sedative and anticonvulsive drug with a side-effect of relaxing muscle tone. We investigated block of nicotinic acetylcholine receptor (nAChR) channel currents by PB using the patch-clamp technique in combination with an ultrafast system for solution exchange. As a preparation, recombinant rat adult-type nAChR channels transiently expressed in HEK293 cells were used. Appli-cation of 1 mM acetylcholine to small cells or outside-out patches showed a transient current with fast activation and desensitization kinetics. Adding PB to the acetylcholine-containing solution resulted in a decrease of the time constant of current decay and of the peak current amplitude starting at concentrations >0.01 mM PB. Preincubation of nAChR channels with PB led to a decrease of the peak current amplitude without alteration of activation and desensitization kinetics caused by competitive block of nAChR channels. In conclusion, similar to the effect of d-Tubocurarine, block of nAChR channel currents by PB can be explained by a combination of open-channel and competitive block.'], 'labels': ['UNLABELLED'], 'meshes': ['Acetylcholine', 'Animals', 'Dose-Response Relationship, Drug', 'Humans', 'Ion Channels', 'Mice', 'Neuromuscular Nondepolarizing Agents', 'Pentobarbital', 'Rats', 'Receptors, Nicotinic']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,735,801 | Is n-methyl-D-aspartate receptor channel block by meperidine dependent on extracellular pH? | {
"contexts": [
"Large concentrations of meperidine inhibit N-methyl-D-aspartate-(NMDA) receptor channels by channel block mechanisms. Extracellular pH regulates the activity and drug sensitivity of NMDA-receptor channels. We examined the influence of extracellular pH on sensitivity to meperidine of epsilon/zeta heteromeric NMDA-receptor channels expressed in Xenopus oocytes. Inhibition of epsilon1/zeta1, epsilon2/zeta1, epsilon3/zeta1, and epsilon4/zeta1 channels by meperidine was dependent on pH, with more inhibition at acidic pH and less inhibition at alkaline pH. The degree of voltage-dependence of meperidine block was only slightly affected by changes in pH, whereas affinity for meperidine was greatly reduced at alkaline pH. Furthermore, interaction of meperidine with Mg(2+) block was reduced at alkaline pH. Because the percentage of the protonated form of meperidine is only slightly affected by pH, changes in properties of the meperidine binding site may be involved in mechanisms of alteration of meperidine potency by pH."
],
"labels": [
"UNLABELLED"
],
"meshes": [
"Analgesics, Opioid",
"Animals",
"Female",
"Hydrogen-Ion Concentration",
"Ion Channels",
"Magnesium",
"Meperidine",
"Pregnancy",
"Receptors, N-Methyl-D-Aspartate",
"Xenopus laevis"
]
} | At acidic pH the potency of meperidine for N-methyl-D-aspartate-receptor channels was increased. Any antinociceptive and neuroprotective benefit from the N-methyl-D-aspartate-receptor antagonist property of meperidine may be pH dependent. | yes | [
{
"from": "human",
"value": "Question: Is n-methyl-D-aspartate receptor channel block by meperidine dependent on extracellular pH?\nContext: {'contexts': ['Large concentrations of meperidine inhibit N-methyl-D-aspartate-(NMDA) receptor channels by channel block mechanisms. Extracellular pH regulates the activity and drug sensitivity of NMDA-receptor channels. We examined the influence of extracellular pH on sensitivity to meperidine of epsilon/zeta heteromeric NMDA-receptor channels expressed in Xenopus oocytes. Inhibition of epsilon1/zeta1, epsilon2/zeta1, epsilon3/zeta1, and epsilon4/zeta1 channels by meperidine was dependent on pH, with more inhibition at acidic pH and less inhibition at alkaline pH. The degree of voltage-dependence of meperidine block was only slightly affected by changes in pH, whereas affinity for meperidine was greatly reduced at alkaline pH. Furthermore, interaction of meperidine with Mg(2+) block was reduced at alkaline pH. Because the percentage of the protonated form of meperidine is only slightly affected by pH, changes in properties of the meperidine binding site may be involved in mechanisms of alteration of meperidine potency by pH.'], 'labels': ['UNLABELLED'], 'meshes': ['Analgesics, Opioid', 'Animals', 'Female', 'Hydrogen-Ion Concentration', 'Ion Channels', 'Magnesium', 'Meperidine', 'Pregnancy', 'Receptors, N-Methyl-D-Aspartate', 'Xenopus laevis']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,741,439 | Is lymphocyte proliferation in mice after a full laparotomy the same whether performed in a sealed carbon dioxide chamber or in room air? | {
"contexts": [
"Our laboratory has demonstrated that significantly more cell-mediated immunosuppression occurs after full laparotomy than after either anesthesia control or carbon dioxide (CO2) pneumoperitoneum. We further demonstrated that the postoperative immunosuppression is related to the length of the incision. Other investigators believe that the immunosuppression observed after laparotomy is caused by peritoneal exposure to small amounts of lipopolysaccharide found in circulating air. They believe that the better-preserved immune function associated with laparoscopic surgery results from the avoidance of air contamination of the peritoneal cavity. To investigate this hypothesis, we determined and compared postoperative lymphocyte proliferation rates after (a) laparotomy in room air, (b) laparotomy in a CO2 chamber, (c) CO2 insufflation in a murine model, and (d) anesthesia alone.",
"Female C3H/He mice (n = 21) were divided randomly into four groups: (a) anesthesia control, (b) air laparotomy, (c) CO2 laparotomy, and (d) CO2 insufflation. The control mice underwent no procedure. The group 2 animals underwent a full midline incision (xiphoid to pubis) and exposure to room air for 20 min and then were clipped closed. The group 3 mice underwent a full midline incision in a sealed CO2 chamber for 20 min, and the group 4 mice insufflation with CO2 gas at 4 to 6 mm Hg for 20 min. Splenocytes were harvested from all the animals on day 2 after the interventions. Lymphocyte proliferation then was assessed using the nonradioactive colorimetric MTS/PMS system 72 h after concanavalin-A stimulation.",
"There was no significant difference in lymphocyte proliferation between the air and CO2 laparotomy groups. Lymphocyte proliferation in the anesthesia control and CO2 insufflation groups was significantly higher than in both the air laparotomy (p<0.05) and CO2 laparotomy (p<0.05) groups (p values by Tukey-Kramer test). There was no significant difference between the anesthesia control and CO2 pneumoperitoneum groups."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Air",
"Animals",
"Carbon Dioxide",
"Cell Division",
"Female",
"Immune Tolerance",
"Immunity, Cellular",
"Laparotomy",
"Lymphocyte Activation",
"Lymphocytes",
"Mice",
"Mice, Inbred C3H",
"Pneumoperitoneum, Artificial"
]
} | Our results suggest that full laparotomy performed in a sealed CO2 chamber compared to room air laparotomy resulted in similar suppression of lymphocyte proliferation. Furthermore, no significant suppression of lymphocyte proliferation was observed in the CO2 pneumoperitoneum group. These results, with regard to lymphocyte proliferation rates, refute the hypothesis that postoperative immunosuppression is related to air exposure and support the alternative hypothesis that immunosuppression is related to incision length. | yes | [
{
"from": "human",
"value": "Question: Is lymphocyte proliferation in mice after a full laparotomy the same whether performed in a sealed carbon dioxide chamber or in room air?\nContext: {'contexts': ['Our laboratory has demonstrated that significantly more cell-mediated immunosuppression occurs after full laparotomy than after either anesthesia control or carbon dioxide (CO2) pneumoperitoneum. We further demonstrated that the postoperative immunosuppression is related to the length of the incision. Other investigators believe that the immunosuppression observed after laparotomy is caused by peritoneal exposure to small amounts of lipopolysaccharide found in circulating air. They believe that the better-preserved immune function associated with laparoscopic surgery results from the avoidance of air contamination of the peritoneal cavity. To investigate this hypothesis, we determined and compared postoperative lymphocyte proliferation rates after (a) laparotomy in room air, (b) laparotomy in a CO2 chamber, (c) CO2 insufflation in a murine model, and (d) anesthesia alone.', 'Female C3H/He mice (n = 21) were divided randomly into four groups: (a) anesthesia control, (b) air laparotomy, (c) CO2 laparotomy, and (d) CO2 insufflation. The control mice underwent no procedure. The group 2 animals underwent a full midline incision (xiphoid to pubis) and exposure to room air for 20 min and then were clipped closed. The group 3 mice underwent a full midline incision in a sealed CO2 chamber for 20 min, and the group 4 mice insufflation with CO2 gas at 4 to 6 mm Hg for 20 min. Splenocytes were harvested from all the animals on day 2 after the interventions. Lymphocyte proliferation then was assessed using the nonradioactive colorimetric MTS/PMS system 72 h after concanavalin-A stimulation.', 'There was no significant difference in lymphocyte proliferation between the air and CO2 laparotomy groups. Lymphocyte proliferation in the anesthesia control and CO2 insufflation groups was significantly higher than in both the air laparotomy (p<0.05) and CO2 laparotomy (p<0.05) groups (p values by Tukey-Kramer test). There was no significant difference between the anesthesia control and CO2 pneumoperitoneum groups.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Air', 'Animals', 'Carbon Dioxide', 'Cell Division', 'Female', 'Immune Tolerance', 'Immunity, Cellular', 'Laparotomy', 'Lymphocyte Activation', 'Lymphocytes', 'Mice', 'Mice, Inbred C3H', 'Pneumoperitoneum, Artificial']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,754,477 | Is the GH response to low-dose bolus growth hormone-releasing hormone ( GHRH ( 1-29 ) NH2 ) attenuated in patients with longstanding post-irradiation GH insufficiency? | {
"contexts": [
"Previous studies have suggested that post-irradiation GH insufficiency results from a loss of GHRH secretion, since many patients were able to release GH following exogenous GHRH stimulation. However, supramaximal doses of GHRH were used and the response may decline with time after radiotherapy. We re-evaluated the GHRH dose-response curve in patients post cranial irradiation and in controls.",
"Randomized controlled study.",
"Five adult male long-term survivors of childhood brain tumours (median age 21.8 years (18.4-26.7); 13.7 years (11.4-15.7) post-radiotherapy, >30Gy) and five matched controls were studied. An intravenous bolus of GHRH(1-29)NH(2) was administered in doses at the lower (0.05 microg/kg) and upper (0.15 microg/kg) range of the dose-response curves for young males, as well as the standard supramaximal dose (1. 0 microg/kg). GH was measured before stimulation, every 2min for the first hour and every 5min for the second hour. All studies were conducted in a random fashion.",
"Significantly lower peak and area under the curve (AUC) GH concentrations occurred in the irradiated group using 0.15 microg/kg (median peak Irradiated, 4. 5mU/l vs median Controls, 37.4mU/l; P<0.01) and 1.0 microg/kg (median peak Irradiated, 4.8mU/l vs median Controls, 15.2mU/l; P<0. 05) GHRH(1-29)NH(2). In irradiated subjects there was an incremental rise in GH output with increasing doses of GHRH(1-29)NH(2 )(median AUC: 122mU/l.min vs 179mU/l.min vs 268mU/l.min; P=0.007) reflecting altered pituitary sensitivity and reduced responsiveness."
],
"labels": [
"OBJECTIVE",
"METHODS",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Brain Neoplasms",
"Human Growth Hormone",
"Humans",
"Male",
"Radiation Injuries",
"Reference Values",
"Sermorelin",
"Time Factors"
]
} | The GH response to bolus GHRH(1-29)NH(2) is attenuated in adult long-term survivors of childhood brain tumours. This may reflect direct pituitary damage and/or the loss of the tropic effects of chronic GHRH deficiency. | yes | [
{
"from": "human",
"value": "Question: Is the GH response to low-dose bolus growth hormone-releasing hormone ( GHRH ( 1-29 ) NH2 ) attenuated in patients with longstanding post-irradiation GH insufficiency?\nContext: {'contexts': ['Previous studies have suggested that post-irradiation GH insufficiency results from a loss of GHRH secretion, since many patients were able to release GH following exogenous GHRH stimulation. However, supramaximal doses of GHRH were used and the response may decline with time after radiotherapy. We re-evaluated the GHRH dose-response curve in patients post cranial irradiation and in controls.', 'Randomized controlled study.', 'Five adult male long-term survivors of childhood brain tumours (median age 21.8 years (18.4-26.7); 13.7 years (11.4-15.7) post-radiotherapy, >30Gy) and five matched controls were studied. An intravenous bolus of GHRH(1-29)NH(2) was administered in doses at the lower (0.05 microg/kg) and upper (0.15 microg/kg) range of the dose-response curves for young males, as well as the standard supramaximal dose (1. 0 microg/kg). GH was measured before stimulation, every 2min for the first hour and every 5min for the second hour. All studies were conducted in a random fashion.', 'Significantly lower peak and area under the curve (AUC) GH concentrations occurred in the irradiated group using 0.15 microg/kg (median peak Irradiated, 4. 5mU/l vs median Controls, 37.4mU/l; P<0.01) and 1.0 microg/kg (median peak Irradiated, 4.8mU/l vs median Controls, 15.2mU/l; P<0. 05) GHRH(1-29)NH(2). In irradiated subjects there was an incremental rise in GH output with increasing doses of GHRH(1-29)NH(2 )(median AUC: 122mU/l.min vs 179mU/l.min vs 268mU/l.min; P=0.007) reflecting altered pituitary sensitivity and reduced responsiveness.'], 'labels': ['OBJECTIVE', 'METHODS', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Brain Neoplasms', 'Human Growth Hormone', 'Humans', 'Male', 'Radiation Injuries', 'Reference Values', 'Sermorelin', 'Time Factors']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,737,575 | Is transthoracic ultrasonography an alternative to subxyphoid ultrasonography for the diagnosis of hemopericardium in penetrating precordial trauma? | {
"contexts": [
"Surgeon-performed ultrasonography is increasingly becoming part of the initial evaluation of patients after blunt or penetrating trauma. Currently, most institutions obtain a subxyphoid or subcostal view of the heart and pericardial space, and a three-view ultrasonogram of the abdomen to detect blood in the pericardial sac or in three dependent abdominal areas.",
"A left parastemal standard transverse transthoracic view is described in addition to the aforementioned views. This facilitates the visualization of the pericardial sac when a subxyphoid or subcostal view cannot be obtained because of anatomical reasons (narrow subxyphoid space) or local factors (pain, fractures, subcutaneous emphysema, or chest wall contusion).",
"The transthoracic view can be useful in patients where the subxyphoid view is difficult to obtain through the conventional approach. In most patients an excellent view of the pericardial sac and ventricles can be obtained and, therefore, expedites the diagnosis and treatment of patients with hemopericardium."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Abdominal Injuries",
"Cardiac Tamponade",
"Humans",
"Intraoperative Care",
"Pericardial Effusion",
"Thoracic Injuries",
"Ultrasonography",
"Wounds, Penetrating"
]
} | Surgeon-performed ultrasonography has become the diagnostic test of choice for patients suspected of having hemopericardium and cardiac tamponade. Transthoracic ultrasonography is an excellent alternative for those patients where a subxyphoid or subcostal view to visualize the pericardial sac and heart cannot be obtained owing to local or anatomical factors. | yes | [
{
"from": "human",
"value": "Question: Is transthoracic ultrasonography an alternative to subxyphoid ultrasonography for the diagnosis of hemopericardium in penetrating precordial trauma?\nContext: {'contexts': ['Surgeon-performed ultrasonography is increasingly becoming part of the initial evaluation of patients after blunt or penetrating trauma. Currently, most institutions obtain a subxyphoid or subcostal view of the heart and pericardial space, and a three-view ultrasonogram of the abdomen to detect blood in the pericardial sac or in three dependent abdominal areas.', 'A left parastemal standard transverse transthoracic view is described in addition to the aforementioned views. This facilitates the visualization of the pericardial sac when a subxyphoid or subcostal view cannot be obtained because of anatomical reasons (narrow subxyphoid space) or local factors (pain, fractures, subcutaneous emphysema, or chest wall contusion).', 'The transthoracic view can be useful in patients where the subxyphoid view is difficult to obtain through the conventional approach. In most patients an excellent view of the pericardial sac and ventricles can be obtained and, therefore, expedites the diagnosis and treatment of patients with hemopericardium.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Abdominal Injuries', 'Cardiac Tamponade', 'Humans', 'Intraoperative Care', 'Pericardial Effusion', 'Thoracic Injuries', 'Ultrasonography', 'Wounds, Penetrating']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,751,260 | Does eEG predict surgical outcome in lesional frontal lobe epilepsy? | {
"contexts": [
"Because of the relatively poor results of frontal lobe epilepsy (FLE) surgery, identification of prognostic factors for surgical outcome is of great importance.",
"To identify predictive factors for FLE surgery, we analyzed the data of 61 patients (mean age at surgery 19.2) who had undergone presurgical evaluation and resective surgery in the frontal lobe. Postoperative follow-up ranged from 0.5 to 5 years (mean 1.78). Fifty-nine patients had MRI-detectable lesions. Histopathologic examination showed dysplasia (57.4%), tumor (16.4%), or other lesions (26.2%). Thirty postoperatively seizure-free patients were compared with 31 non-seizure-free patients with respect to clinical history, seizure semiology, EEG and neuroimaging data, resected area, and postoperative data including histopathology.",
"Three preoperative and two postoperative variables were related to poor outcome: generalized epileptiform discharges, generalized slowing, use of intracranial electrodes, incomplete resection detected by MRI, and postoperative epileptiform discharges. The only preoperative factor associated with seizure-free outcome was the absence of generalized EEG signs. Multivariate analysis showed that only the absence of generalized EEG signs predicts the outcome independently. Moreover, the occurrence of a somatosensory aura, secondarily generalized seizures, and negative MRI was identified as additional independent risk factors for poor surgical results."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Brain Neoplasms",
"Child",
"Disease-Free Survival",
"Electroencephalography",
"Epilepsy, Frontal Lobe",
"Female",
"Frontal Lobe",
"Humans",
"Magnetic Resonance Imaging",
"Male",
"Multivariate Analysis",
"Postoperative Complications",
"Predictive Value of Tests",
"Prognosis",
"Seizures",
"Sex Distribution",
"Treatment Outcome"
]
} | The absence of generalized EEG signs is the most predictive variable for a seizure-free outcome in FLE surgery. Furthermore, nonlesional MRI, somatosensory aura, and secondarily generalized seizures are risk factors for poor surgical results. | yes | [
{
"from": "human",
"value": "Question: Does eEG predict surgical outcome in lesional frontal lobe epilepsy?\nContext: {'contexts': ['Because of the relatively poor results of frontal lobe epilepsy (FLE) surgery, identification of prognostic factors for surgical outcome is of great importance.', 'To identify predictive factors for FLE surgery, we analyzed the data of 61 patients (mean age at surgery 19.2) who had undergone presurgical evaluation and resective surgery in the frontal lobe. Postoperative follow-up ranged from 0.5 to 5 years (mean 1.78). Fifty-nine patients had MRI-detectable lesions. Histopathologic examination showed dysplasia (57.4%), tumor (16.4%), or other lesions (26.2%). Thirty postoperatively seizure-free patients were compared with 31 non-seizure-free patients with respect to clinical history, seizure semiology, EEG and neuroimaging data, resected area, and postoperative data including histopathology.', 'Three preoperative and two postoperative variables were related to poor outcome: generalized epileptiform discharges, generalized slowing, use of intracranial electrodes, incomplete resection detected by MRI, and postoperative epileptiform discharges. The only preoperative factor associated with seizure-free outcome was the absence of generalized EEG signs. Multivariate analysis showed that only the absence of generalized EEG signs predicts the outcome independently. Moreover, the occurrence of a somatosensory aura, secondarily generalized seizures, and negative MRI was identified as additional independent risk factors for poor surgical results.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Brain Neoplasms', 'Child', 'Disease-Free Survival', 'Electroencephalography', 'Epilepsy, Frontal Lobe', 'Female', 'Frontal Lobe', 'Humans', 'Magnetic Resonance Imaging', 'Male', 'Multivariate Analysis', 'Postoperative Complications', 'Predictive Value of Tests', 'Prognosis', 'Seizures', 'Sex Distribution', 'Treatment Outcome']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,753,285 | Does adenoviral-mediated expression of antisense RNA to basic fibroblast growth factor reduce tangential stress in arterialized vein grafts? | {
"contexts": [
"The purpose of this study was to test whether basic fibroblast growth factor (bFGF) participates in arterialized vein graft remodeling.",
"Rabbits underwent in vivo gene transfer and carotid interposition vein grafting. Segments of external jugular vein were infected with an adenovirus that expressed antisense bFGF RNA (Ad.ASbFGF) at 1 x 10(10) PFU/mL to inhibit new synthesis of bFGF by cells in the vein graft wall. Control rabbits were treated with either adenovirus that encoded beta-galactosidase (Ad.lacZ) at 1 x 10(10) PFU/mL or vehicle (phosphate-buffered saline solution [PBS]). At 3 days, 3 grafts per treatment group were harvested for the determination of gene expression of ASbFGF RNA by reverse transcriptase-polymerase chain reaction. Rabbits were killed, and perfusion was fixed 2 months after the grafting. Total wall thickness and lumen circumference of vein grafts and normal arteries were measured in cross sections. Calculated mean tangential stress (+/-SD) for the ASbFGF-treated group and controls was compared for significance. Grafts were immunohistochemically stained to assess bFGF protein production.",
"Only the grafts infected with the Ad.ASbFGF gene expressed ASbFGF RNA. Grafts that were treated with Ad.ASbFGF displayed lower tangential stress (10.9 +/- 2.3 dynes/cm(2)) than PBS alone (22 +/- 2.8 dynes/cm(2)) or Ad. lacZ-treated controls (20.6 +/- 5.4 dynes/cm(2); P <.001). Tangential stress in the Ad.ASbFGF group was comparable to a normal carotid artery (13.9 +/- 2.1 dynes/cm(2)). The difference in mean total wall thickness was significant among the 3 treatment groups: Ad.ASbFGF, 164 +/- 3.4 microm); Ad.lacZ, 100 +/- 3.3 microm; and PBS, 96 +/- 3.6 microm; P <.01). Luminal circumference was not different among the groups. The Ad.ASbFGF-treated vein graft wall was composed of thick layers of concentric smooth muscle cells and elastin fibers in contrast to the sponge-like appearance observed in control arterialized vein grafts. Reduction in bFGF protein was noted only in the Ad.ASbFGF-treated group."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adenoviridae",
"Analysis of Variance",
"Animals",
"Carotid Artery, Common",
"Elastin",
"Fibroblast Growth Factor 2",
"Gene Expression Regulation, Viral",
"Gene Transfer Techniques",
"Hemorheology",
"Immunohistochemistry",
"Jugular Veins",
"Male",
"Muscle, Smooth, Vascular",
"Polymerase Chain Reaction",
"RNA, Antisense",
"Rabbits",
"Stress, Mechanical",
"Up-Regulation"
]
} | Inhibition of bFGF synthesis in vivo with the use of adenoviral gene transfer of antisense RNA to bFGF promotes a vein graft with decreased tangential stress while maintaining the luminal area. The vein graft wall is remodeled and qualitatively resembles an artery so that wall tangential stress in Ad.ASbFGF and normal artery are not significantly different. The lack of significant difference in lumen circumference among groups suggests that wall thickening in the Ad. ASbFGF grafts is not at the expense of luminal narrowing. Our results suggest that ASbFGF RNA expression may represent an effective strategy in limiting the failure of arterialized venous conduits. | yes | [
{
"from": "human",
"value": "Question: Does adenoviral-mediated expression of antisense RNA to basic fibroblast growth factor reduce tangential stress in arterialized vein grafts?\nContext: {'contexts': ['The purpose of this study was to test whether basic fibroblast growth factor (bFGF) participates in arterialized vein graft remodeling.', 'Rabbits underwent in vivo gene transfer and carotid interposition vein grafting. Segments of external jugular vein were infected with an adenovirus that expressed antisense bFGF RNA (Ad.ASbFGF) at 1 x 10(10) PFU/mL to inhibit new synthesis of bFGF by cells in the vein graft wall. Control rabbits were treated with either adenovirus that encoded beta-galactosidase (Ad.lacZ) at 1 x 10(10) PFU/mL or vehicle (phosphate-buffered saline solution [PBS]). At 3 days, 3 grafts per treatment group were harvested for the determination of gene expression of ASbFGF RNA by reverse transcriptase-polymerase chain reaction. Rabbits were killed, and perfusion was fixed 2 months after the grafting. Total wall thickness and lumen circumference of vein grafts and normal arteries were measured in cross sections. Calculated mean tangential stress (+/-SD) for the ASbFGF-treated group and controls was compared for significance. Grafts were immunohistochemically stained to assess bFGF protein production.', 'Only the grafts infected with the Ad.ASbFGF gene expressed ASbFGF RNA. Grafts that were treated with Ad.ASbFGF displayed lower tangential stress (10.9 +/- 2.3 dynes/cm(2)) than PBS alone (22 +/- 2.8 dynes/cm(2)) or Ad. lacZ-treated controls (20.6 +/- 5.4 dynes/cm(2); P <.001). Tangential stress in the Ad.ASbFGF group was comparable to a normal carotid artery (13.9 +/- 2.1 dynes/cm(2)). The difference in mean total wall thickness was significant among the 3 treatment groups: Ad.ASbFGF, 164 +/- 3.4 microm); Ad.lacZ, 100 +/- 3.3 microm; and PBS, 96 +/- 3.6 microm; P <.01). Luminal circumference was not different among the groups. The Ad.ASbFGF-treated vein graft wall was composed of thick layers of concentric smooth muscle cells and elastin fibers in contrast to the sponge-like appearance observed in control arterialized vein grafts. Reduction in bFGF protein was noted only in the Ad.ASbFGF-treated group.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adenoviridae', 'Analysis of Variance', 'Animals', 'Carotid Artery, Common', 'Elastin', 'Fibroblast Growth Factor 2', 'Gene Expression Regulation, Viral', 'Gene Transfer Techniques', 'Hemorheology', 'Immunohistochemistry', 'Jugular Veins', 'Male', 'Muscle, Smooth, Vascular', 'Polymerase Chain Reaction', 'RNA, Antisense', 'Rabbits', 'Stress, Mechanical', 'Up-Regulation']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,733,756 | Do pulmonary hemodynamics contribute to indicate priority for lung transplantation in patients with cystic fibrosis? | {
"contexts": [
"Lung transplantation is a viable option for patients with cystic fibrosis. The current strategy of selection, based on spirometry and deterioration of quality of life, results in a high mortality on the waiting list. We reviewed the case histories of patients with cystic fibrosis accepted for lung transplantation to ascertain whether pulmonary hemodynamics could contribute to predict life expectancy.",
"Forty-five patients with cystic fibrosis were accepted: 11 died on the waiting list (group I), 24 underwent transplantation (group II), and 10 are still waiting (group III). During evaluation we recorded spirometry, oxygen requirement, ratio of arterial oxygen tension to inspired oxygen fraction (PaO (2)/FIO (2)), arterial carbon dioxide tension (PaCO (2)), 6-minute walk test results, right ventricular ejection fraction, echocardiography, and pulmonary hemodynamics. We compared data from group I, II, and III patients. A comparison was also made within group II between the data collected at the time of evaluation and at the time of transplantation to quantify the deterioration during the waiting time.",
"The waiting time, spirometry, 6-minute walk test results, and right ventricular ejection fraction did not differ among the three groups. A statistically significant difference was found for PaO (2)/FIO (2), PaCO (2), mean pulmonary artery pressure, cardiac index, pulmonary arterial wedge pressure, and intrapulmonary shunt between groups I and II. Groups I and III showed statistically significant differences for mean pulmonary artery pressure, PaO (2)/FIO (2), and systemic vascular resistance indexed. No differences were observed between groups II and III. The comparison within group II showed a significant deterioration of pulmonary hemodynamics during the waiting time."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Blood Pressure",
"Carbon Dioxide",
"Child",
"Cystic Fibrosis",
"Female",
"Hemodynamics",
"Humans",
"Lung Transplantation",
"Male",
"Oxygen",
"Patient Selection",
"Pulmonary Circulation",
"Pulmonary Gas Exchange",
"Spirometry",
"Stroke Volume",
"Vascular Resistance",
"Waiting Lists"
]
} | Pulmonary hemodynamics are worst in patients dying on the waiting list and deteriorate significantly during the waiting time. They may thus contribute to establish priority for lung transplantation in patients with cystic fibrosis. | yes | [
{
"from": "human",
"value": "Question: Do pulmonary hemodynamics contribute to indicate priority for lung transplantation in patients with cystic fibrosis?\nContext: {'contexts': ['Lung transplantation is a viable option for patients with cystic fibrosis. The current strategy of selection, based on spirometry and deterioration of quality of life, results in a high mortality on the waiting list. We reviewed the case histories of patients with cystic fibrosis accepted for lung transplantation to ascertain whether pulmonary hemodynamics could contribute to predict life expectancy.', 'Forty-five patients with cystic fibrosis were accepted: 11 died on the waiting list (group I), 24 underwent transplantation (group II), and 10 are still waiting (group III). During evaluation we recorded spirometry, oxygen requirement, ratio of arterial oxygen tension to inspired oxygen fraction (PaO (2)/FIO (2)), arterial carbon dioxide tension (PaCO (2)), 6-minute walk test results, right ventricular ejection fraction, echocardiography, and pulmonary hemodynamics. We compared data from group I, II, and III patients. A comparison was also made within group II between the data collected at the time of evaluation and at the time of transplantation to quantify the deterioration during the waiting time.', 'The waiting time, spirometry, 6-minute walk test results, and right ventricular ejection fraction did not differ among the three groups. A statistically significant difference was found for PaO (2)/FIO (2), PaCO (2), mean pulmonary artery pressure, cardiac index, pulmonary arterial wedge pressure, and intrapulmonary shunt between groups I and II. Groups I and III showed statistically significant differences for mean pulmonary artery pressure, PaO (2)/FIO (2), and systemic vascular resistance indexed. No differences were observed between groups II and III. The comparison within group II showed a significant deterioration of pulmonary hemodynamics during the waiting time.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Blood Pressure', 'Carbon Dioxide', 'Child', 'Cystic Fibrosis', 'Female', 'Hemodynamics', 'Humans', 'Lung Transplantation', 'Male', 'Oxygen', 'Patient Selection', 'Pulmonary Circulation', 'Pulmonary Gas Exchange', 'Spirometry', 'Stroke Volume', 'Vascular Resistance', 'Waiting Lists']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,733,757 | Are transgenic swine lungs expressing human CD59 protected from injury in a pig-to-human model of xenotransplantation? | {
"contexts": [
"Pulmonary xenotransplantation is currently limited by hyperacute rejection mediated in part by xenoreactive natural antibody and complement. Transgenic swine organs that express the human complement regulatory protein CD59 have demonstrated improved survival in models of pig-to-primate xenotransplantation.",
"The purpose of this study was to evaluate transgenic swine lungs that express the human complement regulatory protein CD59 in a model of pig-to-human xenotransplantation.",
"Transgenic swine lungs (n = 5, experimental group) and outbred swine lungs (n = 6, control group) were perfused with fresh, whole human blood through a centrifugal pump on an ex vivo circuit. Functional data were collected throughout perfusion. Immunoglobulin and complement studies were performed on perfusate samples, and both histologic and immunofluorescent analyses were performed on tissue sections.",
"Mean lung survival for the experimental group was increased when compared with controls, 240 +/- 0 minutes versus 35.3 +/- 14.5 minutes, respectively, with a P value of less than.01. A decreased rise in pulmonary vascular resistance at 15 minutes was observed in the experimental group (343 +/- 87 mm Hg. L(-1). min(-1), in contrast to the control group (1579 +/- 722 mm Hg. L(-1). min(-1); P <.01). Pulmonary compliance at 15 minutes was improved for the experimental group versus control group (9.31 +/- 1.41 mL. cm(-2) H(2)O and 4.11 +/- 2.84 mL. cm(-2) H(2)O, respectively; P <.01). SC5b-9 generation in the plasma perfusate was delayed for the experimental group versus the control group. Immunofluorescent examination of tissue sections demonstrated equivalent deposition of immunoglobulin G, immunoglobulin M, C1q, and C3 in both groups, with reduced deposition of C9 in the experimental group."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"CD59 Antigens",
"Complement C3a",
"Complement Hemolytic Activity Assay",
"Fluorescent Antibody Technique",
"Graft Survival",
"Humans",
"Immunoglobulin G",
"Immunoglobulin M",
"In Vitro Techniques",
"Lung",
"Lung Compliance",
"Lung Transplantation",
"Pulmonary Circulation",
"Swine",
"Transplantation, Heterologous",
"Vascular Resistance"
]
} | Transgenic swine pulmonary xenografts that express the human complement regulatory protein CD59 demonstrated improved function and survival in an ex vivo model of pig-to-human xenotransplantation. | yes | [
{
"from": "human",
"value": "Question: Are transgenic swine lungs expressing human CD59 protected from injury in a pig-to-human model of xenotransplantation?\nContext: {'contexts': ['Pulmonary xenotransplantation is currently limited by hyperacute rejection mediated in part by xenoreactive natural antibody and complement. Transgenic swine organs that express the human complement regulatory protein CD59 have demonstrated improved survival in models of pig-to-primate xenotransplantation.', 'The purpose of this study was to evaluate transgenic swine lungs that express the human complement regulatory protein CD59 in a model of pig-to-human xenotransplantation.', 'Transgenic swine lungs (n = 5, experimental group) and outbred swine lungs (n = 6, control group) were perfused with fresh, whole human blood through a centrifugal pump on an ex vivo circuit. Functional data were collected throughout perfusion. Immunoglobulin and complement studies were performed on perfusate samples, and both histologic and immunofluorescent analyses were performed on tissue sections.', 'Mean lung survival for the experimental group was increased when compared with controls, 240 +/- 0 minutes versus 35.3 +/- 14.5 minutes, respectively, with a P value of less than.01. A decreased rise in pulmonary vascular resistance at 15 minutes was observed in the experimental group (343 +/- 87 mm Hg. L(-1). min(-1), in contrast to the control group (1579 +/- 722 mm Hg. L(-1). min(-1); P <.01). Pulmonary compliance at 15 minutes was improved for the experimental group versus control group (9.31 +/- 1.41 mL. cm(-2) H(2)O and 4.11 +/- 2.84 mL. cm(-2) H(2)O, respectively; P <.01). SC5b-9 generation in the plasma perfusate was delayed for the experimental group versus the control group. Immunofluorescent examination of tissue sections demonstrated equivalent deposition of immunoglobulin G, immunoglobulin M, C1q, and C3 in both groups, with reduced deposition of C9 in the experimental group.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'CD59 Antigens', 'Complement C3a', 'Complement Hemolytic Activity Assay', 'Fluorescent Antibody Technique', 'Graft Survival', 'Humans', 'Immunoglobulin G', 'Immunoglobulin M', 'In Vitro Techniques', 'Lung', 'Lung Compliance', 'Lung Transplantation', 'Pulmonary Circulation', 'Swine', 'Transplantation, Heterologous', 'Vascular Resistance']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,746,589 | Does comparison of immunoglobulin G heavy-chain sequences in MS and SSPE brains reveal an antigen-driven response? | {
"contexts": [
"To better understand B-cell activation in MS by analyzing the immunoglobulin (Ig)G heavy chain variable region (VH) repertoire found in MS brains and comparing it with brain VH sequences in individuals with subacute sclerosing panencephalitis (SSPE)--a chronic encephalitis produced by measles virus (MV)-and characterized by an antigen-driven oligoclonal IgG response to MV antigens.",
"The specificity of oligoclonal IgG in MS CSF and plaques, and their relevance to the pathogenesis of MS is unknown.",
"Nested PCR was used to amplify and sequence the rearranged IgG heavy-chain VH repertoire in plaques of three acute MS brains and in three SSPE brains. A representative population of VH sequences from each tissue was aligned to the known 51 functional VH germline segments. From this the authors determined the closest VH family germline segment, and the degree and location of somatic mutations for each unique IgG.",
"As expected for an antigen-driven response against MV antigens, most VH sequences from the SSPE brains were mutated extensively compared with their closest germline segments. Furthermore, SSPE VH sequences accumulated replacement mutations preferentially in the complementary-determining regions (CDRs) relative to framework regions-features normally observed during antigen-driven selection. A comparison of VH family and germline usage also demonstrated that each SSPE brain had its own unique IgG response. When the authors compared the VH response in MS plaques with SSPE, MS VH sequences were also mutated extensively, displayed a preferential accumulation of replacement mutations in CDRs, and were unique in each MS brain."
],
"labels": [
"OBJECTIVE",
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Blotting, Northern",
"Brain",
"Female",
"Gene Library",
"Humans",
"Immunoglobulin G",
"Male",
"Multiple Sclerosis",
"RNA Probes",
"Subacute Sclerosing Panencephalitis"
]
} | The presence of an antigen-driven response in MS, rather than a nonconventional mechanism of B-cell activation, warrants additional analysis of the specificity of IgG in MS brain and CSF. | yes | [
{
"from": "human",
"value": "Question: Does comparison of immunoglobulin G heavy-chain sequences in MS and SSPE brains reveal an antigen-driven response?\nContext: {'contexts': ['To better understand B-cell activation in MS by analyzing the immunoglobulin (Ig)G heavy chain variable region (VH) repertoire found in MS brains and comparing it with brain VH sequences in individuals with subacute sclerosing panencephalitis (SSPE)--a chronic encephalitis produced by measles virus (MV)-and characterized by an antigen-driven oligoclonal IgG response to MV antigens.', 'The specificity of oligoclonal IgG in MS CSF and plaques, and their relevance to the pathogenesis of MS is unknown.', 'Nested PCR was used to amplify and sequence the rearranged IgG heavy-chain VH repertoire in plaques of three acute MS brains and in three SSPE brains. A representative population of VH sequences from each tissue was aligned to the known 51 functional VH germline segments. From this the authors determined the closest VH family germline segment, and the degree and location of somatic mutations for each unique IgG.', 'As expected for an antigen-driven response against MV antigens, most VH sequences from the SSPE brains were mutated extensively compared with their closest germline segments. Furthermore, SSPE VH sequences accumulated replacement mutations preferentially in the complementary-determining regions (CDRs) relative to framework regions-features normally observed during antigen-driven selection. A comparison of VH family and germline usage also demonstrated that each SSPE brain had its own unique IgG response. When the authors compared the VH response in MS plaques with SSPE, MS VH sequences were also mutated extensively, displayed a preferential accumulation of replacement mutations in CDRs, and were unique in each MS brain.'], 'labels': ['OBJECTIVE', 'BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Blotting, Northern', 'Brain', 'Female', 'Gene Library', 'Humans', 'Immunoglobulin G', 'Male', 'Multiple Sclerosis', 'RNA Probes', 'Subacute Sclerosing Panencephalitis']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,728,418 | Are biphasic redistribution of muscarinic receptor and the altered receptor phosphorylation and gene transcription underlying mechanisms in the rat heart during sepsis? | {
"contexts": [
"The purpose of this study was to investigate intracellular redistribution of muscarinic cholinergic receptor (m2AChR) and the roles of receptor phosphorylation and gene transcription as underlying mechanisms in the rat heart during different phases of sepsis.",
"Sepsis was induced by cecal ligation and puncture (CLP). The density of m2AChR in the sarcolemmal and light vesicle fractions was studied using [3H]-quinuclidinyl benzilate ([3H]-QNB). Phosphorylation of m2AChR was studied by labeling of the myocardial ATP pool by perfusing isolated hearts with [32P]H3PO4 followed by identification of the phosphorylated m2AChR with SDS-PAGE. The steady-state level of m2AChR mRNA was determined by RT-PCR and Southern blot analysis.",
"Septic rat hearts exhibit an initial hypercardiodynamic (9 h after CLP, early sepsis) and a subsequent hypocardiodynamic (18 h after CLP, late sepsis) state. During early sepsis, the Bmax for [3H]-QNB binding was increased in sarcolemma (+69%) but decreased in light vesicles (-22%), whereas during late sepsis, the Bmax was decreased in sarcolemma (-20%) but increased in light vesicles (+32%). The sum of Bmax for sarcolemmal and light vesicle fractions was increased during early sepsis (+43%) but decreased during late sepsis (-14%). The phosphorylation of m2AChR was decreased during early sepsis (-73%) but increased during late sepsis (+36% to +90%). The m2AChR mRNA abundance was increased during early sepsis (+52%) but decreased during late sepsis (-28%)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Analysis of Variance",
"Animals",
"Blotting, Southern",
"Cell Membrane",
"Disease Progression",
"Intracellular Fluid",
"Male",
"Myocardium",
"Phosphorylation",
"RNA, Messenger",
"Rats",
"Rats, Sprague-Dawley",
"Receptor, Muscarinic M2",
"Receptors, Muscarinic",
"Reverse Transcriptase Polymerase Chain Reaction",
"Sarcolemma",
"Sepsis",
"Transcription, Genetic"
]
} | The m2AChR in the rat heart was externalized from light vesicles to sarcolemma (overexpression) during early sepsis but internalized from surface membranes to intracellular sites (underexpression) during late sepsis. Furthermore, changes in the receptor phosphorylation and gene transcription are responsible for the biphasic redistribution and the altered expression of m2AChR in the rat heart during the progression of sepsis. | yes | [
{
"from": "human",
"value": "Question: Are biphasic redistribution of muscarinic receptor and the altered receptor phosphorylation and gene transcription underlying mechanisms in the rat heart during sepsis?\nContext: {'contexts': ['The purpose of this study was to investigate intracellular redistribution of muscarinic cholinergic receptor (m2AChR) and the roles of receptor phosphorylation and gene transcription as underlying mechanisms in the rat heart during different phases of sepsis.', 'Sepsis was induced by cecal ligation and puncture (CLP). The density of m2AChR in the sarcolemmal and light vesicle fractions was studied using [3H]-quinuclidinyl benzilate ([3H]-QNB). Phosphorylation of m2AChR was studied by labeling of the myocardial ATP pool by perfusing isolated hearts with [32P]H3PO4 followed by identification of the phosphorylated m2AChR with SDS-PAGE. The steady-state level of m2AChR mRNA was determined by RT-PCR and Southern blot analysis.', 'Septic rat hearts exhibit an initial hypercardiodynamic (9 h after CLP, early sepsis) and a subsequent hypocardiodynamic (18 h after CLP, late sepsis) state. During early sepsis, the Bmax for [3H]-QNB binding was increased in sarcolemma (+69%) but decreased in light vesicles (-22%), whereas during late sepsis, the Bmax was decreased in sarcolemma (-20%) but increased in light vesicles (+32%). The sum of Bmax for sarcolemmal and light vesicle fractions was increased during early sepsis (+43%) but decreased during late sepsis (-14%). The phosphorylation of m2AChR was decreased during early sepsis (-73%) but increased during late sepsis (+36% to +90%). The m2AChR mRNA abundance was increased during early sepsis (+52%) but decreased during late sepsis (-28%).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Analysis of Variance', 'Animals', 'Blotting, Southern', 'Cell Membrane', 'Disease Progression', 'Intracellular Fluid', 'Male', 'Myocardium', 'Phosphorylation', 'RNA, Messenger', 'Rats', 'Rats, Sprague-Dawley', 'Receptor, Muscarinic M2', 'Receptors, Muscarinic', 'Reverse Transcriptase Polymerase Chain Reaction', 'Sarcolemma', 'Sepsis', 'Transcription, Genetic']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,728,416 | Does the bradycardic agent zatebradine enhance baroreflex sensitivity and heart rate variability in rats early after myocardial infarction? | {
"contexts": [
"The bradycardic agent zatebradine (UL-FS 49) reduces heart rate without negative inotropic or proarrhythmic effects. The aim was to experimentally characterize the influence of zatebradine on arterial baroreflex sensitivity (BRS) and heart rate variability (HRV) which are generally considered as estimates of vagal activity and have prognostic value in patients after myocardial infarction (MI).",
"Conscious rats were studied 3 days after left coronary artery ligation or sham-operation (SH). BRS was determined by linear regression analysis of RR-interval and mean arterial pressure changes evoked by intravenous (i.v.) injections of methoxamine and nitroprusside. HRV at rest was calculated from high-resolution electrocardiogram-recordings.",
"In MI-rats heart rate was similar to SH-rats, mean arterial pressure was lower and both BRS and HRV were markedly reduced. Zatebradine (0.5 mg/kg i.v.) reduced heart rate in MI-rats from 400 +/- 15 to 350 +/- 19 and in SH-rats from 390 +/- 19 to 324 +/- 6 beats/min without changing mean arterial pressure. Both BRS and HRV were restored in MI- and further increased in SH-rats by the drug. Effects of 0.05, 0.5 and 5 mg/kg zatebradine revealed a dose-dependency of heart rate reduction. The lowest dose enhanced reflex bradycardia despite little effect on heart rate and lack of effect on both reflex tachycardia and HRV."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Analysis of Variance",
"Animals",
"Baroreflex",
"Benzazepines",
"Cardiotonic Agents",
"Heart",
"Heart Rate",
"Linear Models",
"Male",
"Myocardial Infarction",
"Rats",
"Rats, Sprague-Dawley",
"Statistics, Nonparametric"
]
} | Both BRS and HRV are reduced in rats early after MI, indicating a depressed reflex and tonic vagal activity. Treatment with zatebradine enhances both BRS and HRV. These data suggest that the drug has both peripheral and central effects, leading to an increase of vagal control of heart rate. | yes | [
{
"from": "human",
"value": "Question: Does the bradycardic agent zatebradine enhance baroreflex sensitivity and heart rate variability in rats early after myocardial infarction?\nContext: {'contexts': ['The bradycardic agent zatebradine (UL-FS 49) reduces heart rate without negative inotropic or proarrhythmic effects. The aim was to experimentally characterize the influence of zatebradine on arterial baroreflex sensitivity (BRS) and heart rate variability (HRV) which are generally considered as estimates of vagal activity and have prognostic value in patients after myocardial infarction (MI).', 'Conscious rats were studied 3 days after left coronary artery ligation or sham-operation (SH). BRS was determined by linear regression analysis of RR-interval and mean arterial pressure changes evoked by intravenous (i.v.) injections of methoxamine and nitroprusside. HRV at rest was calculated from high-resolution electrocardiogram-recordings.', 'In MI-rats heart rate was similar to SH-rats, mean arterial pressure was lower and both BRS and HRV were markedly reduced. Zatebradine (0.5 mg/kg i.v.) reduced heart rate in MI-rats from 400 +/- 15 to 350 +/- 19 and in SH-rats from 390 +/- 19 to 324 +/- 6 beats/min without changing mean arterial pressure. Both BRS and HRV were restored in MI- and further increased in SH-rats by the drug. Effects of 0.05, 0.5 and 5 mg/kg zatebradine revealed a dose-dependency of heart rate reduction. The lowest dose enhanced reflex bradycardia despite little effect on heart rate and lack of effect on both reflex tachycardia and HRV.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Analysis of Variance', 'Animals', 'Baroreflex', 'Benzazepines', 'Cardiotonic Agents', 'Heart', 'Heart Rate', 'Linear Models', 'Male', 'Myocardial Infarction', 'Rats', 'Rats, Sprague-Dawley', 'Statistics, Nonparametric']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,728,413 | Does accumulation of oxidized LDL in human semilunar valves correlate with coronary atherosclerosis? | {
"contexts": [
"Recent data indicate that oxidized low-density lipoprotein (ox-LDL) has several proatherogenic effects, e.g. induction of macrophage chemoattractants, adhesion molecules, cytokines, type-1 plasminogen activator inhibitor and platelet-derived growth factor A-chain by smooth muscle cells. Therefore, ox-LDL has been utilized as a marker of oxidative modification of proteins in atherosclerosis. Because heart valves consist of smooth muscle cells, fibroblasts and endothelial cells, and because valvular disease and coronary atherosclerosis could result from similar biological processes, we investigated ox-LDL accumulation in isolated aortic and pulmonary valves and coronary arteries from patients with angiographically proven coronary heart disease (CHD, n = 19), patients with idiopathic congestive heart failure (IDCM = idiopathic dilated cardiomyopathy, n = 20), and transplant donors.",
"Masson-Goldner staining and immunohistochemistry utilizing anti ox-LDL and CD68 were performed on paraffin sections of freshly isolated semilunar valves. Data were analyzed by digital image planimetry and by visual scoring of staining intensity.",
"Ox-LDL immunoreactivity was identified in the vascular aspect of the attachment line, in the deep valve stroma, and in the ventricular and vascular endothelium of the semilunar valves, colocalizing with macrophages. Valvular ox-LDL area was significantly increased in CHD-patients (P < 0.03) and IDCM-patients (P < 0.04) compared with controls. More ox-LDL was accumulating in the pulmonary valves than in the aortic valves (P = 0.04) as assessed by area and staining intensity. Valvular ox-LDL area in pulmonary valve and aortic valve was significantly correlated with ox-LDL accumulation in the intimal layer (P < 0.001) and medial layer (P < 0.001) of coronary arteries from the same patients."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Analysis of Variance",
"Antigens, CD",
"Antigens, Differentiation, Myelomonocytic",
"Aortic Valve",
"Biomarkers",
"Coronary Artery Disease",
"Coronary Vessels",
"Female",
"Heart Failure",
"Heart Transplantation",
"Heart Valves",
"Humans",
"Image Processing, Computer-Assisted",
"Immunohistochemistry",
"Lipoproteins, LDL",
"Male",
"Middle Aged",
"Oxidation-Reduction",
"Pulmonary Valve"
]
} | The data suggest that the biological process leading to ox-LDL accumulation in coronary atherosclerosis also involves heart valves. Therefore, accumulation of the oxidative stress marker ox-LDL in heart valves illustrates atherosclerosis as an additional mechanisms accelerating valvular degeneration in these patients. | yes | [
{
"from": "human",
"value": "Question: Does accumulation of oxidized LDL in human semilunar valves correlate with coronary atherosclerosis?\nContext: {'contexts': ['Recent data indicate that oxidized low-density lipoprotein (ox-LDL) has several proatherogenic effects, e.g. induction of macrophage chemoattractants, adhesion molecules, cytokines, type-1 plasminogen activator inhibitor and platelet-derived growth factor A-chain by smooth muscle cells. Therefore, ox-LDL has been utilized as a marker of oxidative modification of proteins in atherosclerosis. Because heart valves consist of smooth muscle cells, fibroblasts and endothelial cells, and because valvular disease and coronary atherosclerosis could result from similar biological processes, we investigated ox-LDL accumulation in isolated aortic and pulmonary valves and coronary arteries from patients with angiographically proven coronary heart disease (CHD, n = 19), patients with idiopathic congestive heart failure (IDCM = idiopathic dilated cardiomyopathy, n = 20), and transplant donors.', 'Masson-Goldner staining and immunohistochemistry utilizing anti ox-LDL and CD68 were performed on paraffin sections of freshly isolated semilunar valves. Data were analyzed by digital image planimetry and by visual scoring of staining intensity.', 'Ox-LDL immunoreactivity was identified in the vascular aspect of the attachment line, in the deep valve stroma, and in the ventricular and vascular endothelium of the semilunar valves, colocalizing with macrophages. Valvular ox-LDL area was significantly increased in CHD-patients (P < 0.03) and IDCM-patients (P < 0.04) compared with controls. More ox-LDL was accumulating in the pulmonary valves than in the aortic valves (P = 0.04) as assessed by area and staining intensity. Valvular ox-LDL area in pulmonary valve and aortic valve was significantly correlated with ox-LDL accumulation in the intimal layer (P < 0.001) and medial layer (P < 0.001) of coronary arteries from the same patients.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Analysis of Variance', 'Antigens, CD', 'Antigens, Differentiation, Myelomonocytic', 'Aortic Valve', 'Biomarkers', 'Coronary Artery Disease', 'Coronary Vessels', 'Female', 'Heart Failure', 'Heart Transplantation', 'Heart Valves', 'Humans', 'Image Processing, Computer-Assisted', 'Immunohistochemistry', 'Lipoproteins, LDL', 'Male', 'Middle Aged', 'Oxidation-Reduction', 'Pulmonary Valve']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,746,455 | Does recombinant kringle 1-3 of plasminogen inhibit rabbit corneal angiogenesis induced by angiogenin? | {
"contexts": [
"Angiostatin is a potent angiogenesis inhibitor that has been identified as a cryptic fragment of plasminogen molecule containing the first four kringle domain. Angiogenin, a 14-kDa monomeric protein, a potent blood vessel inducer, is expressed in tumors and present in mammalian plasma. The purpose of this study was to determine whether recombinant kringle 1-3 (rKI-3) of human plasminogen could interfere with angiogenesis induced by angiogenin and to evaluate the role of angiogenin in corneal angiogenesis in rabbit.",
"A Hydron polymer pellet containing 2.0 microg of angiogenin was implanted intrastromally into the superior cornea of each of 44 rabbit eyes. All eyes received an intrastromal pellet and were randomized into either one group treated with 12.5 microg of rKI-3 (n = 25) or the other group treated with phosphate-buffered saline (PBS; n = 19). Both pellets were positioned in parallel at the site 1.2 mm from the superior limbus. Two masked observers kept the angiogenesis score daily, based on the number and the length of new vessels. The corneas with induced angiogenesis also were examined histologically.",
"On the third day of the angiogenin pellets implantation, the eye treated with rKI-3 had less angiogenesis (mean score, 4.2 +/- 6.6) than eye treated with PBS (mean score, 16.1 +/- 17.1; p < 0.05, Mann-Whitney U test). The cornea treated with PBS also showed much more leukocyte adhesion than the cornea treated with rKI-3."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Angiogenesis Inducing Agents",
"Animals",
"Antineoplastic Agents",
"Cell Adhesion",
"Cornea",
"Corneal Neovascularization",
"Disease Models, Animal",
"Drug Implants",
"Leukocytes",
"Male",
"Peptide Fragments",
"Plasminogen",
"Rabbits",
"Random Allocation",
"Recombinant Proteins",
"Ribonuclease, Pancreatic"
]
} | Recombinant kringle 1-3 appears to inhibit angiogenin-induced angiogenesis in a rabbit corneal pocket assay. Recombinant kringle 1-3 may have therapeutic potential as an antiangiogenic agent. | yes | [
{
"from": "human",
"value": "Question: Does recombinant kringle 1-3 of plasminogen inhibit rabbit corneal angiogenesis induced by angiogenin?\nContext: {'contexts': ['Angiostatin is a potent angiogenesis inhibitor that has been identified as a cryptic fragment of plasminogen molecule containing the first four kringle domain. Angiogenin, a 14-kDa monomeric protein, a potent blood vessel inducer, is expressed in tumors and present in mammalian plasma. The purpose of this study was to determine whether recombinant kringle 1-3 (rKI-3) of human plasminogen could interfere with angiogenesis induced by angiogenin and to evaluate the role of angiogenin in corneal angiogenesis in rabbit.', 'A Hydron polymer pellet containing 2.0 microg of angiogenin was implanted intrastromally into the superior cornea of each of 44 rabbit eyes. All eyes received an intrastromal pellet and were randomized into either one group treated with 12.5 microg of rKI-3 (n = 25) or the other group treated with phosphate-buffered saline (PBS; n = 19). Both pellets were positioned in parallel at the site 1.2 mm from the superior limbus. Two masked observers kept the angiogenesis score daily, based on the number and the length of new vessels. The corneas with induced angiogenesis also were examined histologically.', 'On the third day of the angiogenin pellets implantation, the eye treated with rKI-3 had less angiogenesis (mean score, 4.2 +/- 6.6) than eye treated with PBS (mean score, 16.1 +/- 17.1; p < 0.05, Mann-Whitney U test). The cornea treated with PBS also showed much more leukocyte adhesion than the cornea treated with rKI-3.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Angiogenesis Inducing Agents', 'Animals', 'Antineoplastic Agents', 'Cell Adhesion', 'Cornea', 'Corneal Neovascularization', 'Disease Models, Animal', 'Drug Implants', 'Leukocytes', 'Male', 'Peptide Fragments', 'Plasminogen', 'Rabbits', 'Random Allocation', 'Recombinant Proteins', 'Ribonuclease, Pancreatic']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,751,524 | Is [ The common C677T polymorphism in the methylenetetrahydrofolate reductase gene associated with neural tube defects and preeclampsia ]? | {
"contexts": [
"To assess whether methylenetetrahydrofolate reductase(MTHFR) gene C677T polymorphism is associated with neural tube defects and preeclampsia.",
"Twenty- four mothers who had given birth to normal children, 27 mothers who had given birth to NTDs children, 120 normal women, and 57 women who had suffered from preeclampsia were genotyped for C677T polymorphism by using PCR/RFLP method.",
"(1) VV genotype frequency in the normal mothers group it was 0.13, while in the NTDs mothers group it was 0.33; mothers with VV genotype were at 3 times increased risk to have a NTDs child, compared with the normal mothers. (2) In the normal women group VV genotype frequency was 0.15, while in the preeclampsia women group it was 0.31; women with VV genotype were at 2.5 times increased risk to have preeclampsia, compared with the normal women."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Female",
"Genotype",
"Humans",
"Methylenetetrahydrofolate Reductase (NADPH2)",
"Neural Tube Defects",
"Oxidoreductases Acting on CH-NH Group Donors",
"Polymerase Chain Reaction",
"Polymorphism, Genetic",
"Pre-Eclampsia",
"Pregnancy"
]
} | The authors believe that MTHFR VV genotype is associated with the development of NTDs and preeclampsia. | yes | [
{
"from": "human",
"value": "Question: Is [ The common C677T polymorphism in the methylenetetrahydrofolate reductase gene associated with neural tube defects and preeclampsia ]?\nContext: {'contexts': ['To assess whether methylenetetrahydrofolate reductase(MTHFR) gene C677T polymorphism is associated with neural tube defects and preeclampsia.', 'Twenty- four mothers who had given birth to normal children, 27 mothers who had given birth to NTDs children, 120 normal women, and 57 women who had suffered from preeclampsia were genotyped for C677T polymorphism by using PCR/RFLP method.', '(1) VV genotype frequency in the normal mothers group it was 0.13, while in the NTDs mothers group it was 0.33; mothers with VV genotype were at 3 times increased risk to have a NTDs child, compared with the normal mothers. (2) In the normal women group VV genotype frequency was 0.15, while in the preeclampsia women group it was 0.31; women with VV genotype were at 2.5 times increased risk to have preeclampsia, compared with the normal women.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Female', 'Genotype', 'Humans', 'Methylenetetrahydrofolate Reductase (NADPH2)', 'Neural Tube Defects', 'Oxidoreductases Acting on CH-NH Group Donors', 'Polymerase Chain Reaction', 'Polymorphism, Genetic', 'Pre-Eclampsia', 'Pregnancy']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,746,533 | Does ropivacaine attenuate pulmonary vasoconstriction induced by thromboxane A2 analogue in the isolated perfused rat lung? | {
"contexts": [
"Thromboxane A2 (TXA2) activation is involved in several pathophysiological states in producing pulmonary hypertension. Local anesthetics (LA) inhibit signaling of TXA2 receptors expressed in cell models. Therefore, we hypothesized that LA may inhibit pulmonary vasoconstriction induced by the TXA2 analogue U 46619 in an isolated lung model.",
"Isolated rat lungs were perfused with physiological saline solution and autologous blood with or without the LA lidocaine, bupivacaine, ropivacaine, or the permanently charged lidocaine analogue QX 314 (all 1 microg/mL) as a pretreatment. Subsequently, pulmonary vasoconstriction was induced by 3 concentrations of U 46619 (25, 50, and 100 ng/mL) and the change in pulmonary artery pressure (Pa) was compared with each LA. In a second experiment, Pa responses to angiotensin II (0.1 microg), hypoxic pulmonary vasoconstriction (HPV, 3% O2 for 10 minutes), or phenylephrine (0.1 microg) were assessed to determine the specificity of ropivacaine effects on TXA2 receptors. Finally, reversibility of pulmonary vasoconstriction was determined by adding ropivacaine to the perfusate after pulmonary vasoconstriction was established with U 46619.",
"Ropivacaine, but not bupivacaine, lidocaine, or QX 314 significantly attenuated pulmonary vasoconstriction induced by 50 ng/mL U 46619 (35.9%, P<.003) or 100 ng/mL U 46619 (45.2%, P<.001). This effect of ropivacaine was likely to be specific for the thromboxane receptor because pulmonary vasoconstriction induced by angiotensin II, HPV, or phenylephrine was not altered. Ropivacaine did not reverse vasoconstriction when it was administered after U 46619."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid",
"Amides",
"Anesthetics, Local",
"Angiotensin II",
"Animals",
"Blood Pressure",
"Bupivacaine",
"Disease Models, Animal",
"Hypoxia",
"Lidocaine",
"Lung",
"Perfusion",
"Phenylephrine",
"Pulmonary Artery",
"Rats",
"Receptors, Thromboxane",
"Ropivacaine",
"Signal Transduction",
"Vasoconstriction",
"Vasoconstrictor Agents"
]
} | Ropivacaine, but not lidocaine, bupivacaine, or QX 314 at 1 microg/mL, attenuates U 46619-induced pulmonary vasoconstriction in an isolated perfused rat lung model. These results support evidence that the clinically used enantiomer S(-)-ropivacaine may inhibit TXA2 signaling. | yes | [
{
"from": "human",
"value": "Question: Does ropivacaine attenuate pulmonary vasoconstriction induced by thromboxane A2 analogue in the isolated perfused rat lung?\nContext: {'contexts': ['Thromboxane A2 (TXA2) activation is involved in several pathophysiological states in producing pulmonary hypertension. Local anesthetics (LA) inhibit signaling of TXA2 receptors expressed in cell models. Therefore, we hypothesized that LA may inhibit pulmonary vasoconstriction induced by the TXA2 analogue U 46619 in an isolated lung model.', 'Isolated rat lungs were perfused with physiological saline solution and autologous blood with or without the LA lidocaine, bupivacaine, ropivacaine, or the permanently charged lidocaine analogue QX 314 (all 1 microg/mL) as a pretreatment. Subsequently, pulmonary vasoconstriction was induced by 3 concentrations of U 46619 (25, 50, and 100 ng/mL) and the change in pulmonary artery pressure (Pa) was compared with each LA. In a second experiment, Pa responses to angiotensin II (0.1 microg), hypoxic pulmonary vasoconstriction (HPV, 3% O2 for 10 minutes), or phenylephrine (0.1 microg) were assessed to determine the specificity of ropivacaine effects on TXA2 receptors. Finally, reversibility of pulmonary vasoconstriction was determined by adding ropivacaine to the perfusate after pulmonary vasoconstriction was established with U 46619.', 'Ropivacaine, but not bupivacaine, lidocaine, or QX 314 significantly attenuated pulmonary vasoconstriction induced by 50 ng/mL U 46619 (35.9%, P<.003) or 100 ng/mL U 46619 (45.2%, P<.001). This effect of ropivacaine was likely to be specific for the thromboxane receptor because pulmonary vasoconstriction induced by angiotensin II, HPV, or phenylephrine was not altered. Ropivacaine did not reverse vasoconstriction when it was administered after U 46619.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid', 'Amides', 'Anesthetics, Local', 'Angiotensin II', 'Animals', 'Blood Pressure', 'Bupivacaine', 'Disease Models, Animal', 'Hypoxia', 'Lidocaine', 'Lung', 'Perfusion', 'Phenylephrine', 'Pulmonary Artery', 'Rats', 'Receptors, Thromboxane', 'Ropivacaine', 'Signal Transduction', 'Vasoconstriction', 'Vasoconstrictor Agents']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,729,807 | Does leukocyte depletion of red cell components prevent exposure of transfusion recipients to neutrophil elastase? | {
"contexts": [
"Polymorphonuclear leukocytes contain a large number of enzymes and bactericidal proteins stored in granules. Neutrophil activation induces degranulation and immediate release of these bioactive substances, including human neutrophil elastase (HNE) also known as elastase-2 (ELA2), which may contaminate whole blood units and blood components.",
"The HNE concentration was determined in the supernatants of blood components with a commercial enzyme-linked immunosorbent assay (ELISA). The effect of leukocyte depletion and storage was evaluated by testing whole blood, buffy-coat-reduced, and leukocyte-depleted red cell units. Buffy-coat-derived platelets and plasma were also tested.",
"HNE concentrations at day 1 were about 50 microg/l in all types of red cell components with the exception of leukocyte-depleted red cells (<0.26 microg/l). In leukocyte-depleted red cells, platelets and plasma, no significant increase was observed during storage. In whole-blood units and buffy-coat-reduced red cells, the HNE concentrations increased steadily and often exceeded 1,000 microg/l when the units expired."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Biological Assay",
"Blood",
"Blood Cell Count",
"Blood Platelets",
"Blood Preservation",
"Cell Separation",
"Cytochalasin B",
"Erythrocytes",
"Humans",
"Leukocyte Elastase",
"Lymphocyte Depletion",
"N-Formylmethionine Leucyl-Phenylalanine",
"Neutrophil Activation",
"Neutrophils",
"Plasma"
]
} | Leukocyte depletion may limit the inadvertent infusion of bioactive substances derived from polymorphonuclear leukocytes, of which HNE is but one example. The accumulation of HNE in buffy-coat-reduced red cells may be greater than that of whole blood units. HNE accumulates during storage and its quantity may have pathophysiologic significance. Platelets and plasma derived from buffy coats contain some HNE, but leukocyte-depleted red cells virtually none. However, we consider the accumulation of HNE in these components not to be clinically important. The quantities, kinetics, and occurrence in various blood components of HNE contamination differ from those observed with cytokines. | yes | [
{
"from": "human",
"value": "Question: Does leukocyte depletion of red cell components prevent exposure of transfusion recipients to neutrophil elastase?\nContext: {'contexts': ['Polymorphonuclear leukocytes contain a large number of enzymes and bactericidal proteins stored in granules. Neutrophil activation induces degranulation and immediate release of these bioactive substances, including human neutrophil elastase (HNE) also known as elastase-2 (ELA2), which may contaminate whole blood units and blood components.', 'The HNE concentration was determined in the supernatants of blood components with a commercial enzyme-linked immunosorbent assay (ELISA). The effect of leukocyte depletion and storage was evaluated by testing whole blood, buffy-coat-reduced, and leukocyte-depleted red cell units. Buffy-coat-derived platelets and plasma were also tested.', 'HNE concentrations at day 1 were about 50 microg/l in all types of red cell components with the exception of leukocyte-depleted red cells (<0.26 microg/l). In leukocyte-depleted red cells, platelets and plasma, no significant increase was observed during storage. In whole-blood units and buffy-coat-reduced red cells, the HNE concentrations increased steadily and often exceeded 1,000 microg/l when the units expired.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Biological Assay', 'Blood', 'Blood Cell Count', 'Blood Platelets', 'Blood Preservation', 'Cell Separation', 'Cytochalasin B', 'Erythrocytes', 'Humans', 'Leukocyte Elastase', 'Lymphocyte Depletion', 'N-Formylmethionine Leucyl-Phenylalanine', 'Neutrophil Activation', 'Neutrophils', 'Plasma']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,729,806 | Is allogeneic red blood cell transfusion an independent risk factor for the development of postoperative bacterial infection? | {
"contexts": [
"Allogeneic red blood cell transfusions may exert immunomodulatory effects in recipients including an increased rate of postoperative bacterial infection. It is controversial whether allogeneic transfusion is an independent predictor for the development of postoperative bacterial infection.",
"We analysed a prospectively collected database of 1,349 patients undergoing colorectal surgery in 11 centres across Canada. The primary outcome was the development of either a postoperative wound infection or intra-abdominal sepsis in transfused and nontransfused patients. The effect of allogeneic transfusion on postoperative infection was evaluated with adjustment for all the confounding factors in a multiple regression analysis.",
"The 282 patients who received a total of 832 allogeneic units had a significantly higher frequency of wound infections and intra-abdominal sepsis than the patients who were not transfused (25. 9 vs. 14.2%, p = 0.001). A significant dose-response relationship between transfusion and infection rate was demonstrated. Multiple regression analysis identified allogeneic transfusion as a statistically significant independent predictor for postoperative bacterial infection (OR 1.18, 95% CI 1.05-1.33, p = 0.007). Other independent predictors were anastomotic leak, repeat operation, patient age and preoperative haemoglobin level. The mortality rate was also significantly higher in the transfused group."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Abdomen",
"Analysis of Variance",
"Bacterial Infections",
"Cohort Studies",
"Colorectal Surgery",
"Erythrocyte Transfusion",
"Female",
"Humans",
"Male",
"Middle Aged",
"Multivariate Analysis",
"Prospective Studies",
"Risk Factors",
"Sepsis",
"Survival Rate",
"Wound Infection"
]
} | These data support the hypothesis that allogeneic red cell transfusion is an independent risk factor for the development of postoperative bacterial infection in patients undergoing colorectal surgery. This association provides further reason to minimise exposure to allogeneic transfusions in the perioperative setting. | yes | [
{
"from": "human",
"value": "Question: Is allogeneic red blood cell transfusion an independent risk factor for the development of postoperative bacterial infection?\nContext: {'contexts': ['Allogeneic red blood cell transfusions may exert immunomodulatory effects in recipients including an increased rate of postoperative bacterial infection. It is controversial whether allogeneic transfusion is an independent predictor for the development of postoperative bacterial infection.', 'We analysed a prospectively collected database of 1,349 patients undergoing colorectal surgery in 11 centres across Canada. The primary outcome was the development of either a postoperative wound infection or intra-abdominal sepsis in transfused and nontransfused patients. The effect of allogeneic transfusion on postoperative infection was evaluated with adjustment for all the confounding factors in a multiple regression analysis.', 'The 282 patients who received a total of 832 allogeneic units had a significantly higher frequency of wound infections and intra-abdominal sepsis than the patients who were not transfused (25. 9 vs. 14.2%, p = 0.001). A significant dose-response relationship between transfusion and infection rate was demonstrated. Multiple regression analysis identified allogeneic transfusion as a statistically significant independent predictor for postoperative bacterial infection (OR 1.18, 95% CI 1.05-1.33, p = 0.007). Other independent predictors were anastomotic leak, repeat operation, patient age and preoperative haemoglobin level. The mortality rate was also significantly higher in the transfused group.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Abdomen', 'Analysis of Variance', 'Bacterial Infections', 'Cohort Studies', 'Colorectal Surgery', 'Erythrocyte Transfusion', 'Female', 'Humans', 'Male', 'Middle Aged', 'Multivariate Analysis', 'Prospective Studies', 'Risk Factors', 'Sepsis', 'Survival Rate', 'Wound Infection']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,744,793 | Are increased levels of basic fibroblast growth factor found in the cross-clamped heart during cardiopulmonary bypass? | {
"contexts": [
"High concentrations of fibroblast growth factors (FGFs) are found in the heart. Even higher levels are measured during ischemia. Exogenous administration of FGF to ischemic myocardium promotes synthesis of collateral coronary circulation and induces local myocardial hypertrophy. The kinetics and the contribution of the heart and lungs to circulating basic FGF (bFGF) levels during cardiac surgery were characterized.",
"Plasma bFGF levels were measured in seven adults undergoing coronary artery bypass operations and 11 neonates undergoing congenital cardiac anomaly repair during cardiopulmonary bypass.",
"In both the adult and the neonatal groups, bFGF plasma levels increased significantly immediately after removal of the aortic cross-clamp (adult group 15.43+/-6.3 aorta cross-clamped versus 29+/-4.1 after release, P=0.011; neonatal group 17.09+/-9.43 aorta cross-clamped versus 43.55+/-14.25 after release, P=0.004) and declined thereafter. In the adult group, higher levels of bFGF were recorded in blood recovered from the coronary sinus than in the aortic root during aortic cross-clamping (63.14+/-14.42 versus 43.86+/-12.05, P=0.011), and in both, levels were significantly higher than the peripheral measurements."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Cardiopulmonary Bypass",
"Constriction",
"Coronary Artery Bypass",
"Coronary Disease",
"Female",
"Fibroblast Growth Factor 2",
"Heart Defects, Congenital",
"Humans",
"Infant",
"Infant, Newborn",
"Male",
"Middle Aged",
"Myocardial Reperfusion Injury",
"Myocardium"
]
} | Plasma bFGF levels increase during cardiopulmonary bypass. The source of this elevation is the lungs and heart. | yes | [
{
"from": "human",
"value": "Question: Are increased levels of basic fibroblast growth factor found in the cross-clamped heart during cardiopulmonary bypass?\nContext: {'contexts': ['High concentrations of fibroblast growth factors (FGFs) are found in the heart. Even higher levels are measured during ischemia. Exogenous administration of FGF to ischemic myocardium promotes synthesis of collateral coronary circulation and induces local myocardial hypertrophy. The kinetics and the contribution of the heart and lungs to circulating basic FGF (bFGF) levels during cardiac surgery were characterized.', 'Plasma bFGF levels were measured in seven adults undergoing coronary artery bypass operations and 11 neonates undergoing congenital cardiac anomaly repair during cardiopulmonary bypass.', 'In both the adult and the neonatal groups, bFGF plasma levels increased significantly immediately after removal of the aortic cross-clamp (adult group 15.43+/-6.3 aorta cross-clamped versus 29+/-4.1 after release, P=0.011; neonatal group 17.09+/-9.43 aorta cross-clamped versus 43.55+/-14.25 after release, P=0.004) and declined thereafter. In the adult group, higher levels of bFGF were recorded in blood recovered from the coronary sinus than in the aortic root during aortic cross-clamping (63.14+/-14.42 versus 43.86+/-12.05, P=0.011), and in both, levels were significantly higher than the peripheral measurements.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Cardiopulmonary Bypass', 'Constriction', 'Coronary Artery Bypass', 'Coronary Disease', 'Female', 'Fibroblast Growth Factor 2', 'Heart Defects, Congenital', 'Humans', 'Infant', 'Infant, Newborn', 'Male', 'Middle Aged', 'Myocardial Reperfusion Injury', 'Myocardium']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
10,735,777 | Does milrinone attenuate serotonin-induced pulmonary hypertension and bronchoconstriction in dogs? | {
"contexts": [
"We determined whether milrinone, a phosphodiesterase III inhibitor, attenuates serotonin-induced (5-hydroxytryptamine [5HT]) pulmonary hypertension (PH) and bronchoconstriction. Dogs were anesthetized with pentobarbital (30 mg/kg + 2 mg. kg(-1). h(-1)). Bronchoconstriction and PH were elicited by 5HT (10 microg/kg + 1.0 mg. kg(-1). h(-1)). Pulmonary vascular resistance was used to assess PH. Bronchoconstriction was also assessed by changes in bronchial cross-sectional area obtained from our bronchoscopic method. At 30 min after 5HT infusion started, seven dogs were given milrinone: 0 (saline), 5, 50, 500, and 5000 microg/kg at 10-min intervals. The other 12 dogs were given milrinone 5000 microg/kg 30 min after 5HT infusion, and 5 min later were given propranolol 0.2 mg/kg (n = 6) or saline (n = 6) IV. The 5HT significantly increased percentage of pulmonary vascular resistance to 208% +/- 27% and decreased percentage of bronchial cross-sectional area to 52% +/- 5% of the basal. Milrinone significantly attenuated both PH and bronchoconstriction in a dose-dependent manner. However, -log 50% effective concentration (mean ED(50) in microg/kg) of milrinone for bronchoconstriction: 4.32 +/- 0.13 (47.6) was significantly smaller than that for PH: 3.84 +/- 0.29 (144.9) (P < 0.01). In addition, the spasmolytic effects of milrinone (5000 microg/kg) were not antagonized by propranolol, although this dose significantly increased plasma catecholamines. In conclusion, milrinone attenuates 5HT-induced PH and bronchoconstriction; however, this drug may be more sensitive to phosphodiesterase III in the airway smooth muscle than in pulmonary vascular smooth muscle. In addition, the relaxant effects could not be caused by beta-adrenoceptor activation because beta-blocker did not antagonize."
],
"labels": [
"UNLABELLED"
],
"meshes": [
"Animals",
"Bronchoconstriction",
"Catecholamines",
"Dogs",
"Hypertension, Pulmonary",
"Milrinone",
"Phosphodiesterase Inhibitors",
"Propranolol",
"Serotonin"
]
} | We studied the effects of milrinone on serotonin-induced pulmonary hypertension and bronchoconstriction in dogs. Milrinone produces pulmonary vasodilation and bronchodilation, whose effects may not be caused by beta-adrenoceptor activation. In addition, this drug may be more sensitive to phosphodiesterase III in the airway smooth muscle than that in pulmonary vascular smooth muscle. | yes | [
{
"from": "human",
"value": "Question: Does milrinone attenuate serotonin-induced pulmonary hypertension and bronchoconstriction in dogs?\nContext: {'contexts': ['We determined whether milrinone, a phosphodiesterase III inhibitor, attenuates serotonin-induced (5-hydroxytryptamine [5HT]) pulmonary hypertension (PH) and bronchoconstriction. Dogs were anesthetized with pentobarbital (30 mg/kg + 2 mg. kg(-1). h(-1)). Bronchoconstriction and PH were elicited by 5HT (10 microg/kg + 1.0 mg. kg(-1). h(-1)). Pulmonary vascular resistance was used to assess PH. Bronchoconstriction was also assessed by changes in bronchial cross-sectional area obtained from our bronchoscopic method. At 30 min after 5HT infusion started, seven dogs were given milrinone: 0 (saline), 5, 50, 500, and 5000 microg/kg at 10-min intervals. The other 12 dogs were given milrinone 5000 microg/kg 30 min after 5HT infusion, and 5 min later were given propranolol 0.2 mg/kg (n = 6) or saline (n = 6) IV. The 5HT significantly increased percentage of pulmonary vascular resistance to 208% +/- 27% and decreased percentage of bronchial cross-sectional area to 52% +/- 5% of the basal. Milrinone significantly attenuated both PH and bronchoconstriction in a dose-dependent manner. However, -log 50% effective concentration (mean ED(50) in microg/kg) of milrinone for bronchoconstriction: 4.32 +/- 0.13 (47.6) was significantly smaller than that for PH: 3.84 +/- 0.29 (144.9) (P < 0.01). In addition, the spasmolytic effects of milrinone (5000 microg/kg) were not antagonized by propranolol, although this dose significantly increased plasma catecholamines. In conclusion, milrinone attenuates 5HT-induced PH and bronchoconstriction; however, this drug may be more sensitive to phosphodiesterase III in the airway smooth muscle than in pulmonary vascular smooth muscle. In addition, the relaxant effects could not be caused by beta-adrenoceptor activation because beta-blocker did not antagonize.'], 'labels': ['UNLABELLED'], 'meshes': ['Animals', 'Bronchoconstriction', 'Catecholamines', 'Dogs', 'Hypertension, Pulmonary', 'Milrinone', 'Phosphodiesterase Inhibitors', 'Propranolol', 'Serotonin']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,767,615 | Is nonadherence with ambulatory saliva sampling associated with biased salivary testosterone estimates? | {
"contexts": [
"Nonadherence with scheduled saliva sampling, as encountered in ambulatory settings, can bias the estimation of salivary cortisol concentrations. This study is the first to estimate if such nonadherence is also associated with biased salivary testosterone concentration estimates.",
"Using a standard ambulatory saliva-sampling protocol, we instructed pregnant women to collect saliva samples on two consecutive days at awakening, 1100h, 1500h, 2000h, and 2200h. We estimated testosterone concentrations in the saliva samples and participants' actual sampling times with an electronic medication event-monitoring system. We classified a saliva sample as adherent if it was sampled within a specific time window relative to its scheduled sampling time. We used a mixed-model analysis to distinguish between trait (number of adherent saliva samples per participant) and state (adherence status of a specific sample) adherence.",
"We included 60 pregnant women in this study. Seventy-five percent (448 of 600) of the scheduled samples indicated adherence with the sampling schedule. Participants' trait adherence was associated with their diurnal profiles of salivary testosterone estimates; that is, adherent participants had higher salivary testosterone estimates compared with nonadherent participants, F(1,58)=5.41, p=0.023, Cohen's d=0.67. The state adherence of a sample was associated with the salivary testosterone estimate of the related sample, F(1,469)=4.48, p=0.035, Cohen's d=0.20, with delayed sampling associated with lower salivary testosterone estimates."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Circadian Rhythm",
"Female",
"Humans",
"Patient Compliance",
"Pregnancy",
"Saliva",
"Specimen Handling",
"Testosterone"
]
} | The results suggest that common ambulatory nonadherence with scheduled saliva sampling is associated with biased salivary testosterone estimates. They will inform further studies estimating salivary testosterone with ambulatory saliva-sampling designs and highlight the relevance of strategies to improve or confirm adherence, beyond routinely used instructions. | yes | [
{
"from": "human",
"value": "Question: Is nonadherence with ambulatory saliva sampling associated with biased salivary testosterone estimates?\nContext: {'contexts': ['Nonadherence with scheduled saliva sampling, as encountered in ambulatory settings, can bias the estimation of salivary cortisol concentrations. This study is the first to estimate if such nonadherence is also associated with biased salivary testosterone concentration estimates.', \"Using a standard ambulatory saliva-sampling protocol, we instructed pregnant women to collect saliva samples on two consecutive days at awakening, 1100h, 1500h, 2000h, and 2200h. We estimated testosterone concentrations in the saliva samples and participants' actual sampling times with an electronic medication event-monitoring system. We classified a saliva sample as adherent if it was sampled within a specific time window relative to its scheduled sampling time. We used a mixed-model analysis to distinguish between trait (number of adherent saliva samples per participant) and state (adherence status of a specific sample) adherence.\", \"We included 60 pregnant women in this study. Seventy-five percent (448 of 600) of the scheduled samples indicated adherence with the sampling schedule. Participants' trait adherence was associated with their diurnal profiles of salivary testosterone estimates; that is, adherent participants had higher salivary testosterone estimates compared with nonadherent participants, F(1,58)=5.41, p=0.023, Cohen's d=0.67. The state adherence of a sample was associated with the salivary testosterone estimate of the related sample, F(1,469)=4.48, p=0.035, Cohen's d=0.20, with delayed sampling associated with lower salivary testosterone estimates.\"], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Circadian Rhythm', 'Female', 'Humans', 'Patient Compliance', 'Pregnancy', 'Saliva', 'Specimen Handling', 'Testosterone']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,774,513 | Does differential proteomic analysis of grapevine leave by iTRAQ reveals responses to heat stress and subsequent recovery? | {
"contexts": [
"High temperature is a major environmental factor limiting grape yield and affecting berry quality. Thermotolerance includes the direct response to heat stress and the ability to recover from heat stress. To better understand the mechanism of the thermotolerance of Vitis, we combined a physiological analysis with iTRAQ-based proteomics of Vitis vinifera cv Cabernet Sauvignon, subjected to 43°C for 6 h, and then followed by recovery at 25/18°C.",
"High temperature increased the concentrations of TBARS and inhibited electronic transport in photosynthesis apparatus, indicating that grape leaves were damaged by heat stress. However, these physiological changes rapidly returned to control levels during the subsequent recovery phase from heat stress. One hundred and seventy-four proteins were differentially expressed under heat stress and/or during the recovery phase, in comparison to unstressed controls, respectively. Stress and recovery conditions shared 42 proteins, while 113 and 103 proteins were respectively identified under heat stress and recovery conditions alone. Based on MapMan ontology, functional categories for these dysregulated proteins included mainly photosynthesis (about 20%), proteins (13%), and stress (8%). The subcellular localization using TargetP showed most proteins were located in the chloroplasts (34%), secretory pathways (8%) and mitochondrion (3%)."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Cell Membrane",
"Electron Transport",
"Gene Ontology",
"Heat-Shock Response",
"Isotope Labeling",
"Photosynthesis",
"Photosystem II Protein Complex",
"Plant Leaves",
"Plant Proteins",
"Protein Transport",
"Proteomics",
"Sequence Homology, Amino Acid",
"Stress, Physiological",
"Subcellular Fractions",
"Temperature",
"Thiobarbituric Acid Reactive Substances",
"Vitis"
]
} | On the basis of these findings, we proposed that some proteins related to electron transport chain of photosynthesis, antioxidant enzymes, HSPs and other stress response proteins, and glycolysis may play key roles in enhancing grapevine adaptation to and recovery capacity from heat stress. These results provide a better understanding of the proteins involved in, and mechanisms of thermotolerance in grapevines. | yes | [
{
"from": "human",
"value": "Question: Does differential proteomic analysis of grapevine leave by iTRAQ reveals responses to heat stress and subsequent recovery?\nContext: {'contexts': ['High temperature is a major environmental factor limiting grape yield and affecting berry quality. Thermotolerance includes the direct response to heat stress and the ability to recover from heat stress. To better understand the mechanism of the thermotolerance of Vitis, we combined a physiological analysis with iTRAQ-based proteomics of Vitis vinifera cv Cabernet Sauvignon, subjected to 43°C for 6 h, and then followed by recovery at 25/18°C.', 'High temperature increased the concentrations of TBARS and inhibited electronic transport in photosynthesis apparatus, indicating that grape leaves were damaged by heat stress. However, these physiological changes rapidly returned to control levels during the subsequent recovery phase from heat stress. One hundred and seventy-four proteins were differentially expressed under heat stress and/or during the recovery phase, in comparison to unstressed controls, respectively. Stress and recovery conditions shared 42 proteins, while 113 and 103 proteins were respectively identified under heat stress and recovery conditions alone. Based on MapMan ontology, functional categories for these dysregulated proteins included mainly photosynthesis (about 20%), proteins (13%), and stress (8%). The subcellular localization using TargetP showed most proteins were located in the chloroplasts (34%), secretory pathways (8%) and mitochondrion (3%).'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Cell Membrane', 'Electron Transport', 'Gene Ontology', 'Heat-Shock Response', 'Isotope Labeling', 'Photosynthesis', 'Photosystem II Protein Complex', 'Plant Leaves', 'Plant Proteins', 'Protein Transport', 'Proteomics', 'Sequence Homology, Amino Acid', 'Stress, Physiological', 'Subcellular Fractions', 'Temperature', 'Thiobarbituric Acid Reactive Substances', 'Vitis']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,753,506 | Is subcutaneous adipose tissue zinc-α2-glycoprotein associated with adipose tissue and whole-body insulin sensitivity? | {
"contexts": [
"To examine the regulatory aspects of zinc-α2-glycoprotein (ZAG) association with obesity-related insulin resistance.",
"ZAG mRNA and protein were analyzed in subcutaneous adipose tissue (AT) and circulation of lean, obese, prediabetic, and type 2 diabetic men; both subcutaneous and visceral AT were explored in lean and extremely obese. Clinical and ex vivo findings were corroborated by results of in vitro ZAG silencing experiment.",
"Subcutaneous AT ZAG was reduced in obesity, with a trend to further decrease with prediabetes and type 2 diabetes. ZAG was 3.3-fold higher in subcutaneous than in visceral AT of lean individuals. All differences were lost in extreme obesity. Obesity-associated changes in AT were not paralleled by alterations of circulating ZAG. Subcutaneous AT ZAG correlated with adiposity, adipocyte hypertrophy, whole-body and AT insulin sensitivity, mitochondrial content, expression of GLUT4, PGC1α, and adiponectin. Subcutaneous AT ZAG and adipocyte size were the only predictors of insulin sensitivity, independent on age and BMI. Silencing ZAG resulted in reduced adiponectin, IRS1, GLUT4, and PGC1α gene expression in primary human adipocytes."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adipocytes",
"Adiponectin",
"Adiposity",
"Adult",
"Diabetes Mellitus, Type 2",
"Female",
"Gene Expression",
"Gene Silencing",
"Glucose Transporter Type 4",
"Humans",
"Insulin Receptor Substrate Proteins",
"Insulin Resistance",
"Intra-Abdominal Fat",
"Male",
"Middle Aged",
"Obesity",
"Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha",
"Prediabetic State",
"RNA, Messenger",
"Seminal Plasma Proteins",
"Subcutaneous Fat",
"Transcription Factors"
]
} | ZAG in subcutaneous, but not in visceral AT, was markedly reduced in obesity. Clinical, cellular, and molecular evidence indicate that ZAG plays an important role in modulating whole-body and AT insulin sensitivity. | yes | [
{
"from": "human",
"value": "Question: Is subcutaneous adipose tissue zinc-α2-glycoprotein associated with adipose tissue and whole-body insulin sensitivity?\nContext: {'contexts': ['To examine the regulatory aspects of zinc-α2-glycoprotein (ZAG) association with obesity-related insulin resistance.', 'ZAG mRNA and protein were analyzed in subcutaneous adipose tissue (AT) and circulation of lean, obese, prediabetic, and type 2 diabetic men; both subcutaneous and visceral AT were explored in lean and extremely obese. Clinical and ex vivo findings were corroborated by results of in vitro ZAG silencing experiment.', 'Subcutaneous AT ZAG was reduced in obesity, with a trend to further decrease with prediabetes and type 2 diabetes. ZAG was 3.3-fold higher in subcutaneous than in visceral AT of lean individuals. All differences were lost in extreme obesity. Obesity-associated changes in AT were not paralleled by alterations of circulating ZAG. Subcutaneous AT ZAG correlated with adiposity, adipocyte hypertrophy, whole-body and AT insulin sensitivity, mitochondrial content, expression of GLUT4, PGC1α, and adiponectin. Subcutaneous AT ZAG and adipocyte size were the only predictors of insulin sensitivity, independent on age and BMI. Silencing ZAG resulted in reduced adiponectin, IRS1, GLUT4, and PGC1α gene expression in primary human adipocytes.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adipocytes', 'Adiponectin', 'Adiposity', 'Adult', 'Diabetes Mellitus, Type 2', 'Female', 'Gene Expression', 'Gene Silencing', 'Glucose Transporter Type 4', 'Humans', 'Insulin Receptor Substrate Proteins', 'Insulin Resistance', 'Intra-Abdominal Fat', 'Male', 'Middle Aged', 'Obesity', 'Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha', 'Prediabetic State', 'RNA, Messenger', 'Seminal Plasma Proteins', 'Subcutaneous Fat', 'Transcription Factors']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,753,502 | Is excess weight in preschool children with a history of severe bronchiolitis associated with asthma? | {
"contexts": [
"The relationship between excess weight gain and asthma in childhood remains inadequately defined. The aim of this study was to evaluate, as part of a prospective post-bronchiolitis follow-up, whether there is a link between earlier or current overweight or obesity and asthma or asthma symptoms at 5-7 years of age.",
"In all, 151 former bronchiolitis patients were followed-up until the mean age of 6.45 years. At the control visit, the weights and heights were measured, and the asthma symptoms and medications for asthma were recorded. The weight status was expressed as body mass index (BMI) z-scores (zBMI).",
"There were 10 obese and 31 overweight (zBMI over national references) children. In adjusted analyses, presence of current asthma at 6-7 years of age (aOR 3.05, 95% CI 1.02-9.93) differed between overweight and normal weight children. Further, asthma ever, asthma at age 4-5 years, asthma at age 5-6 years, use of bronchodilators ever and use of ICSs during the last 12 months were more common in currently overweight than in normal weight children. Obesity was associated only with current asthma and asthma ever. Instead, there were no significant associations between birth weight, excess weight gain in infancy, or overweight at age 1.5 years, and later asthma, asthma symptoms or use of asthma medication."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Asthma",
"Birth Weight",
"Body Mass Index",
"Body Weight",
"Bronchiolitis",
"Child",
"Child, Preschool",
"Female",
"Follow-Up Studies",
"Humans",
"Male",
"Obesity",
"Overweight",
"Prospective Studies",
"Risk Factors",
"Weight Gain"
]
} | Asthma was more common in currently overweight than in normal weight former bronchiolitis patients at preschool age and early school age. | yes | [
{
"from": "human",
"value": "Question: Is excess weight in preschool children with a history of severe bronchiolitis associated with asthma?\nContext: {'contexts': ['The relationship between excess weight gain and asthma in childhood remains inadequately defined. The aim of this study was to evaluate, as part of a prospective post-bronchiolitis follow-up, whether there is a link between earlier or current overweight or obesity and asthma or asthma symptoms at 5-7 years of age.', 'In all, 151 former bronchiolitis patients were followed-up until the mean age of 6.45 years. At the control visit, the weights and heights were measured, and the asthma symptoms and medications for asthma were recorded. The weight status was expressed as body mass index (BMI) z-scores (zBMI).', 'There were 10 obese and 31 overweight (zBMI over national references) children. In adjusted analyses, presence of current asthma at 6-7 years of age (aOR 3.05, 95% CI 1.02-9.93) differed between overweight and normal weight children. Further, asthma ever, asthma at age 4-5 years, asthma at age 5-6 years, use of bronchodilators ever and use of ICSs during the last 12 months were more common in currently overweight than in normal weight children. Obesity was associated only with current asthma and asthma ever. Instead, there were no significant associations between birth weight, excess weight gain in infancy, or overweight at age 1.5 years, and later asthma, asthma symptoms or use of asthma medication.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Asthma', 'Birth Weight', 'Body Mass Index', 'Body Weight', 'Bronchiolitis', 'Child', 'Child, Preschool', 'Female', 'Follow-Up Studies', 'Humans', 'Male', 'Obesity', 'Overweight', 'Prospective Studies', 'Risk Factors', 'Weight Gain']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,754,896 | Does sentinel lymph node biopsy before mastectomy and immediate breast reconstruction significantly delay surgery in early breast cancer? | {
"contexts": [
"Sentinel lymph node biopsy (SLNB) before mastectomy and immediate breast reconstruction (IBR) may help to avoid the negative cosmetic effects of radiotherapy on reconstructed breasts in lymph node-positive patients. Concerns have been raised regarding possible delays whilst awaiting the SLNB result prior to definitive surgery, which needs to be performed within 31 days of cancer diagnosis. The aim was to investigate whether initial SLNB delays mastectomy and IBR.",
"All patients who had IBR between January 2005 and 2007 were reviewed retrospectively. Before October 2005 axillary staging was performed simultaneously with mastectomy and IBR (Group I). After October 2005, SLNB was performed as an initial procedure and patients with positive SLNB were only offered a temporary tissue expander to be replaced by autogenous reconstruction after completing the cancer treatment (Group II). Date of diagnosis and waiting times were recorded and the two groups were compared. Different reasons for delays in treatment were studied.",
"One hundred and thirty-nine IBR (123 patients) were included in the statistical analysis (67 IBR in Group I and 72 IBR in Group II). Seventy-one patients (57.7%) had no delay (mean waiting time of 23 days). Fifty-two patients (42.3%) had delay longer than 31 days (mean waiting time of 66 days). Group I patients had a mean waiting time (standard deviation) of 38.8 (38) days and Group II patients 42.7 (24) days (p = 0.51)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Breast Neoplasms",
"Carcinoma, Ductal, Breast",
"Carcinoma, Intraductal, Noninfiltrating",
"Female",
"Humans",
"Mammaplasty",
"Mastectomy",
"Middle Aged",
"Preoperative Care",
"Retrospective Studies",
"Sentinel Lymph Node Biopsy",
"Time Factors"
]
} | In this group of patients, SLNB before mastectomy and IBR does not significantly delay definitive breast cancer surgery. | no | [
{
"from": "human",
"value": "Question: Does sentinel lymph node biopsy before mastectomy and immediate breast reconstruction significantly delay surgery in early breast cancer?\nContext: {'contexts': ['Sentinel lymph node biopsy (SLNB) before mastectomy and immediate breast reconstruction (IBR) may help to avoid the negative cosmetic effects of radiotherapy on reconstructed breasts in lymph node-positive patients. Concerns have been raised regarding possible delays whilst awaiting the SLNB result prior to definitive surgery, which needs to be performed within 31 days of cancer diagnosis. The aim was to investigate whether initial SLNB delays mastectomy and IBR.', 'All patients who had IBR between January 2005 and 2007 were reviewed retrospectively. Before October 2005 axillary staging was performed simultaneously with mastectomy and IBR (Group I). After October 2005, SLNB was performed as an initial procedure and patients with positive SLNB were only offered a temporary tissue expander to be replaced by autogenous reconstruction after completing the cancer treatment (Group II). Date of diagnosis and waiting times were recorded and the two groups were compared. Different reasons for delays in treatment were studied.', 'One hundred and thirty-nine IBR (123 patients) were included in the statistical analysis (67 IBR in Group I and 72 IBR in Group II). Seventy-one patients (57.7%) had no delay (mean waiting time of 23 days). Fifty-two patients (42.3%) had delay longer than 31 days (mean waiting time of 66 days). Group I patients had a mean waiting time (standard deviation) of 38.8 (38) days and Group II patients 42.7 (24) days (p = 0.51).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Breast Neoplasms', 'Carcinoma, Ductal, Breast', 'Carcinoma, Intraductal, Noninfiltrating', 'Female', 'Humans', 'Mammaplasty', 'Mastectomy', 'Middle Aged', 'Preoperative Care', 'Retrospective Studies', 'Sentinel Lymph Node Biopsy', 'Time Factors']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
24,759,911 | Is the Exercise Medicine Global Health Initiative : a 2014 update? | {
"contexts": [
"A third of the world's population does not engage in recommended levels of physical activity (PA), leading to substantial health and economic burdens. The healthcare sector offers a variety of resources that can help counsel, refer and deliver PA promotion programmes for purposes of primordial, primary, secondary and tertiary prevention. Substantial evidence already exists in support of multipronged PA counselling, prescription and referral strategies, in particular those linking healthcare and community-based resources.",
"The Exercise is Medicine (EIM) initiative was introduced in 2007 to advance the implementation of evidence-based strategies to elevate the status of PA in healthcare. In this article, we describe the evolution and global expansion of the EIM initiative, its components, their implementation, an evaluation framework and future initiative activities.",
"Until now, EIM has a presence in 39 countries with EIM Regional Centers established in North America, Latin America, Europe, Africa, Southeast Asia, China and Australasia. The EIM Global Health Initiative is transitioning from its initial phase of infrastructure and awareness building to a phase of programme implementation, with an emphasis in low-to-middle income countries, where 80% of deaths due to non-communicable diseases already occur, but where a large gap in research and implementation of PA strategies exists."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Biomedical Technology",
"Community Health Services",
"Counseling",
"Exercise Therapy",
"Forecasting",
"Global Health",
"Health Behavior",
"Health Personnel",
"Health Plan Implementation",
"Health Promotion",
"Health Status Indicators",
"Humans",
"International Cooperation",
"Referral and Consultation"
]
} | Broad implementation of PA counselling and referral systems, as clinical practice standard of care, has the potential to improve PA at the population level by complementing and leveraging other efforts and to contribute to achieving global targets for the reduction of inactivity and related morbidity and mortality. | yes | [
{
"from": "human",
"value": "Question: Is the Exercise Medicine Global Health Initiative : a 2014 update?\nContext: {'contexts': [\"A third of the world's population does not engage in recommended levels of physical activity (PA), leading to substantial health and economic burdens. The healthcare sector offers a variety of resources that can help counsel, refer and deliver PA promotion programmes for purposes of primordial, primary, secondary and tertiary prevention. Substantial evidence already exists in support of multipronged PA counselling, prescription and referral strategies, in particular those linking healthcare and community-based resources.\", 'The Exercise is Medicine (EIM) initiative was introduced in 2007 to advance the implementation of evidence-based strategies to elevate the status of PA in healthcare. In this article, we describe the evolution and global expansion of the EIM initiative, its components, their implementation, an evaluation framework and future initiative activities.', 'Until now, EIM has a presence in 39 countries with EIM Regional Centers established in North America, Latin America, Europe, Africa, Southeast Asia, China and Australasia. The EIM Global Health Initiative is transitioning from its initial phase of infrastructure and awareness building to a phase of programme implementation, with an emphasis in low-to-middle income countries, where 80% of deaths due to non-communicable diseases already occur, but where a large gap in research and implementation of PA strategies exists.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Biomedical Technology', 'Community Health Services', 'Counseling', 'Exercise Therapy', 'Forecasting', 'Global Health', 'Health Behavior', 'Health Personnel', 'Health Plan Implementation', 'Health Promotion', 'Health Status Indicators', 'Humans', 'International Cooperation', 'Referral and Consultation']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,748,218 | Is chronic inflammation in benign prostate tissue associated with high-grade prostate cancer in the placebo arm of the prostate cancer prevention trial? | {
"contexts": [
"Chronic inflammation is hypothesized to influence prostate cancer development, although a definitive link has not been established.",
"Prostate cancer cases (N = 191) detected on a for-cause (clinically indicated) or end-of-study (protocol directed) biopsy, and frequency-matched controls (N = 209), defined as negative for cancer on an end-of-study biopsy, were sampled from the placebo arm of the Prostate Cancer Prevention Trial. Inflammation prevalence and extent in benign areas of biopsy cores were visually assessed using digital images of hematoxylin and eosin-stained sections. Logistic regression was used to estimate associations.",
"Of note, 86.2% of cases and 78.2% of controls had at least one biopsy core (of three assessed) with inflammation in benign areas, most of which was chronic. Men who had at least one biopsy core with inflammation had 1.78 [95% confidence interval (CI), 1.04-3.06] times the odds of prostate cancer compared with men who had zero cores with inflammation. The association was stronger for high-grade disease (Gleason sum 7-10, N = 94; OR, 2.24; 95% CI, 1.06-4.71). These patterns were present when restricting to cases and controls in whom intraprostatic inflammation was the least likely to have influenced biopsy recommendation because their prostate-specific antigen (PSA) was low (<2 ng/mL at biopsy)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Case-Control Studies",
"Chronic Disease",
"Follow-Up Studies",
"Humans",
"Inflammation",
"Male",
"Middle Aged",
"Neoplasm Grading",
"Neoplasm Staging",
"Prognosis",
"Prostate",
"Prostate-Specific Antigen",
"Prostatic Neoplasms",
"Survival Rate"
]
} | Inflammation, most of which was chronic, was common in benign prostate tissue, and was positively associated with prostate cancer, especially high grade. The association did not seem to be due to detection bias. | yes | [
{
"from": "human",
"value": "Question: Is chronic inflammation in benign prostate tissue associated with high-grade prostate cancer in the placebo arm of the prostate cancer prevention trial?\nContext: {'contexts': ['Chronic inflammation is hypothesized to influence prostate cancer development, although a definitive link has not been established.', 'Prostate cancer cases (N = 191) detected on a for-cause (clinically indicated) or end-of-study (protocol directed) biopsy, and frequency-matched controls (N = 209), defined as negative for cancer on an end-of-study biopsy, were sampled from the placebo arm of the Prostate Cancer Prevention Trial. Inflammation prevalence and extent in benign areas of biopsy cores were visually assessed using digital images of hematoxylin and eosin-stained sections. Logistic regression was used to estimate associations.', 'Of note, 86.2% of cases and 78.2% of controls had at least one biopsy core (of three assessed) with inflammation in benign areas, most of which was chronic. Men who had at least one biopsy core with inflammation had 1.78 [95% confidence interval (CI), 1.04-3.06] times the odds of prostate cancer compared with men who had zero cores with inflammation. The association was stronger for high-grade disease (Gleason sum 7-10, N = 94; OR, 2.24; 95% CI, 1.06-4.71). These patterns were present when restricting to cases and controls in whom intraprostatic inflammation was the least likely to have influenced biopsy recommendation because their prostate-specific antigen (PSA) was low (<2 ng/mL at biopsy).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Case-Control Studies', 'Chronic Disease', 'Follow-Up Studies', 'Humans', 'Inflammation', 'Male', 'Middle Aged', 'Neoplasm Grading', 'Neoplasm Staging', 'Prognosis', 'Prostate', 'Prostate-Specific Antigen', 'Prostatic Neoplasms', 'Survival Rate']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,768,239 | Does neutralization of vascular endothelial growth factor slow progression of retinal nonperfusion in patients with diabetic macular edema? | {
"contexts": [
"To determine the effect of suppression of vascular endothelial growth factor (VEGF) by monthly injection of ranibizumab on posterior retinal nonperfusion (RNP) in patients with diabetic macular edema (DME).",
"Unplanned retrospective analysis of prospectively collected data from 2 randomized, sham injection-controlled, double-masked, multicenter clinical trials.",
"Six hundred sixty-six patients with DME.",
"An independent reading center measured the area of RNP on fluorescein angiograms obtained in the phase 3 RISE and RIDE trials.",
"The percentage of patients with no posterior RNP.",
"The percentage of patients with no posterior RNP decreased in the sham group between baseline and month 24, but remained relatively stable in the 2 ranibizumab groups. After month 24, the sham group crossed over to receive monthly injections of ranibizumab 0.5 mg, and the differences between the sham and ranibizumab groups were reduced. The percentage of patients who showed an increase in posterior RNP from baseline increased over time in all 3 groups, but at a faster rate in the sham group, resulting in statistically significant differences at every time point between months 3 (9.6% vs. 18.5%; P = 0.016) and 24 (16.1% vs. 37.6%; P<0.0001) for ranibizumab 0.5 mg versus sham and from months 6 (12.3% vs. 23.0%; P = 0.013) through 24 (15.0% vs. 37.6%; P<0.0001) for ranibizumab 0.3 mg. Initiation of ranibizumab in the sham group at month 24 was followed by reduction in the percentage of patients with an increase in posterior RNP from baseline at months 30 and 36, whereas the 2 ranibizumab groups continued their gradual rise."
],
"labels": [
"OBJECTIVE",
"METHODS",
"METHODS",
"METHODS",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Angiogenesis Inhibitors",
"Antibodies, Monoclonal, Humanized",
"Diabetic Retinopathy",
"Disease Progression",
"Double-Blind Method",
"Female",
"Humans",
"Macular Edema",
"Male",
"Middle Aged",
"Ranibizumab",
"Regional Blood Flow",
"Retinal Vein Occlusion",
"Retrospective Studies",
"Vascular Endothelial Growth Factor A"
]
} | Just as high VEGF levels contribute to progression of retinal nonperfusion in retinal vein occlusion, the same is true in patients with DME, suggesting that regardless of the underlying disease process, high levels of VEGF can cause closure of retinal vessels. However, our data also suggest that VEGF-induced worsening of retinal perfusion in DME is superimposed on another cause of more gradually worsening perfusion, possibly glucotoxicity. Thus, monthly injections of ranibizumab can slow, but not completely prevent, retinal capillary closure in patients with DME. | yes | [
{
"from": "human",
"value": "Question: Does neutralization of vascular endothelial growth factor slow progression of retinal nonperfusion in patients with diabetic macular edema?\nContext: {'contexts': ['To determine the effect of suppression of vascular endothelial growth factor (VEGF) by monthly injection of ranibizumab on posterior retinal nonperfusion (RNP) in patients with diabetic macular edema (DME).', 'Unplanned retrospective analysis of prospectively collected data from 2 randomized, sham injection-controlled, double-masked, multicenter clinical trials.', 'Six hundred sixty-six patients with DME.', 'An independent reading center measured the area of RNP on fluorescein angiograms obtained in the phase 3 RISE and RIDE trials.', 'The percentage of patients with no posterior RNP.', 'The percentage of patients with no posterior RNP decreased in the sham group between baseline and month 24, but remained relatively stable in the 2 ranibizumab groups. After month 24, the sham group crossed over to receive monthly injections of ranibizumab 0.5 mg, and the differences between the sham and ranibizumab groups were reduced. The percentage of patients who showed an increase in posterior RNP from baseline increased over time in all 3 groups, but at a faster rate in the sham group, resulting in statistically significant differences at every time point between months 3 (9.6% vs. 18.5%; P = 0.016) and 24 (16.1% vs. 37.6%; P<0.0001) for ranibizumab 0.5 mg versus sham and from months 6 (12.3% vs. 23.0%; P = 0.013) through 24 (15.0% vs. 37.6%; P<0.0001) for ranibizumab 0.3 mg. Initiation of ranibizumab in the sham group at month 24 was followed by reduction in the percentage of patients with an increase in posterior RNP from baseline at months 30 and 36, whereas the 2 ranibizumab groups continued their gradual rise.'], 'labels': ['OBJECTIVE', 'METHODS', 'METHODS', 'METHODS', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Angiogenesis Inhibitors', 'Antibodies, Monoclonal, Humanized', 'Diabetic Retinopathy', 'Disease Progression', 'Double-Blind Method', 'Female', 'Humans', 'Macular Edema', 'Male', 'Middle Aged', 'Ranibizumab', 'Regional Blood Flow', 'Retinal Vein Occlusion', 'Retrospective Studies', 'Vascular Endothelial Growth Factor A']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,775,300 | Does inhibition of fructan-fermenting equine faecal bacteria and Streptococcus bovis by hop ( Humulus lupulus L. ) β-acid? | {
"contexts": [
"The goals of this study were to determine if β-acid from hops (Humulus lupulus L.) could be used to control fructan fermentation by equine hindgut micro-organisms, and to verify the antimicrobial mode of action on Streptococcus bovis, which has been implicated in fructan fermentation, hindgut acidosis and pasture-associated laminitis (PAL) in the horse.",
"Suspensions of uncultivated equine faecal micro-organisms produced fermentation acids when inulin (model fructan) was the substrate, but β-acid (i.e. lupulone) concentrations ≥9 ppm inhibited lactate production and mitigated the decrease in pH. Inulin-fermenting Strep. bovis was isolated from the β-acid-free suspensions after enrichment with inulin. The isolates were sensitive to β-acid, which decreased the viable number of streptococci in faecal suspensions, as well as growth, lactate production and the intracellular potassium of Strep. bovis in pure culture."
],
"labels": [
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Animals",
"Anti-Bacterial Agents",
"Bacteria",
"Feces",
"Fermentation",
"Horses",
"Humulus",
"Hydrogen-Ion Concentration",
"Inulin",
"Streptococcus bovis",
"Terpenes"
]
} | These results are consistent with the hypothesis that hops β-acid prevented the growth of fructan-fermenting equine faecal bacteria, and that the mechanism of action was dissipation of the intracellular potassium of Strep. bovis. | yes | [
{
"from": "human",
"value": "Question: Does inhibition of fructan-fermenting equine faecal bacteria and Streptococcus bovis by hop ( Humulus lupulus L. ) β-acid?\nContext: {'contexts': ['The goals of this study were to determine if β-acid from hops (Humulus lupulus L.) could be used to control fructan fermentation by equine hindgut micro-organisms, and to verify the antimicrobial mode of action on Streptococcus bovis, which has been implicated in fructan fermentation, hindgut acidosis and pasture-associated laminitis (PAL) in the horse.', 'Suspensions of uncultivated equine faecal micro-organisms produced fermentation acids when inulin (model fructan) was the substrate, but β-acid (i.e. lupulone) concentrations ≥9\\xa0ppm inhibited lactate production and mitigated the decrease in pH. Inulin-fermenting Strep.\\xa0bovis was isolated from the β-acid-free suspensions after enrichment with inulin. The isolates were sensitive to β-acid, which decreased the viable number of streptococci in faecal suspensions, as well as growth, lactate production and the intracellular potassium of Strep.\\xa0bovis in pure culture.'], 'labels': ['OBJECTIVE', 'RESULTS'], 'meshes': ['Animals', 'Anti-Bacterial Agents', 'Bacteria', 'Feces', 'Fermentation', 'Horses', 'Humulus', 'Hydrogen-Ion Concentration', 'Inulin', 'Streptococcus bovis', 'Terpenes']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,749,095 | Does addition of clonidine in caudal anesthesia in children increase duration of post-operative analgesia? | {
"contexts": [
"Pain in infancy is a developmental process. Due to the underdeveloped pain pathways in the spinal cord, the threshold of stimulation and sensation of pain is low at birth and has potential impacts on increasing the central effects of pain. Primary trauma during infancy can cause long term changes in structure and function of pain pathways that continue until adulthood. Lack of pain management in children can result in morbidity and mortality.",
"In this study we examined the duration of post-operative analgesia in children when clonidine is added to bupivacaine in caudal anesthesia.",
"In this clinical trial, 40 children aged 1-8 years who were candidates for elective inguinal hernia repair were studied. Induction and maintenance of anesthesia were achieved using sodium thiopenthal, halothane and nitrous oxide. Children were randomly divided into 2 groups in a double-blind fashion, and were given caudal anesthesia with 0.125% bupivacaine (1ml/kg) alone or b bupivacaine plus 2 μg/kg clonidine. Blood pressure and heart rate were recorded peri-operatively. Analgesia was evaluated using objective pain scale (OPS) and sedation was assessed using Ramsay sedation scale (RSS). Acetaminophen was administered rectally for cases with OPS score greater than five.",
"Duration of analgesia was found to be significantly longer in the group given bupivacaine plus clonidine (mean 417.50 min vs. 162.00 min). Peri-operative hypotension or bradycardia, post-operative respiratory depression, nausea or vomiting were not recorded in any patient."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": []
} | We concluded that addition of clonidine to bupivacaine prolongs the duration of post-operative analgesia without any respiratory or hemodynamic side-effects. | yes | [
{
"from": "human",
"value": "Question: Does addition of clonidine in caudal anesthesia in children increase duration of post-operative analgesia?\nContext: {'contexts': ['Pain in infancy is a developmental process. Due to the underdeveloped pain pathways in the spinal cord, the threshold of stimulation and sensation of pain is low at birth and has potential impacts on increasing the central effects of pain. Primary trauma during infancy can cause long term changes in structure and function of pain pathways that continue until adulthood. Lack of pain management in children can result in morbidity and mortality.', 'In this study we examined the duration of post-operative analgesia in children when clonidine is added to bupivacaine in caudal anesthesia.', 'In this clinical trial, 40 children aged 1-8 years who were candidates for elective inguinal hernia repair were studied. Induction and maintenance of anesthesia were achieved using sodium thiopenthal, halothane and nitrous oxide. Children were randomly divided into 2 groups in a double-blind fashion, and were given caudal anesthesia with 0.125% bupivacaine (1ml/kg) alone or b bupivacaine plus 2 μg/kg clonidine. Blood pressure and heart rate were recorded peri-operatively. Analgesia was evaluated using objective pain scale (OPS) and sedation was assessed using Ramsay sedation scale (RSS). Acetaminophen was administered rectally for cases with OPS score greater than five.', 'Duration of analgesia was found to be significantly longer in the group given bupivacaine plus clonidine (mean 417.50 min vs. 162.00 min). Peri-operative hypotension or bradycardia, post-operative respiratory depression, nausea or vomiting were not recorded in any patient.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,766,056 | Does alcohol withdrawal alleviate adipose tissue inflammation in patients with alcoholic liver disease? | {
"contexts": [
"Patients with alcoholic liver disease (ALD) display inflammation of the subcutaneous adipose tissue (SAT) which correlates with liver lesions. We examined macrophage markers and polarization in the SAT of alcoholic patients and adipokine expression according to liver inflammation; we studied the consequences of alcohol withdrawal.",
"Forty-seven patients with ALD were prospectively included. SAT and blood samples were collected at inclusion and after 1 week of alcohol withdrawal. Pro-inflammatory cytokines/chemokines, inflammasome components and products, adipokine expression levels, macrophage markers and polarization in liver and SAT samples were assessed by RT-PCR arrays.",
"mRNA expression level of chemokines (IL8, semaphorin 7A) correlated with hepatic steatosis in both liver and SAT. Liver expression of inflammasome components (IL1β, IL18, caspase-1) and SAT IL6 and CCL2 correlated with liver damage. In patients with mild ALD, 1 week of alcohol withdrawal was sufficient to decrease expression level of total macrophage markers in the adipose tissue, to orient adipose tissue macrophages (ATM) towards an anti-inflammatory M2 phenotype and to decrease the mRNA expression of cytokines/chemokines (IL18, CCL2, osteopontin, semaphorin 7A). In patients with severe ALD, 1 week of abstinence was also associated with an increase in CCL18 expression."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adipokines",
"Adipose Tissue",
"Adult",
"Alcohol Abstinence",
"Biomarkers",
"Cytokines",
"Female",
"Humans",
"Liver",
"Liver Diseases, Alcoholic",
"Macrophages",
"Male",
"Middle Aged",
"Panniculitis",
"Prospective Studies"
]
} | In alcoholic patients, upregulation of chemotactic factors in the liver and SAT is an early event that begins as early as the steatosis stage. The inflammasome pathway is upregulated in the liver of patients with ALD. One week of alcohol withdrawal alleviates macrophage infiltration in SAT and orients ATM towards a M2 anti-inflammatory phenotype; this implicates alcohol in adipose tissue inflammation (ClinicalTrials.gov NCT00388323). | yes | [
{
"from": "human",
"value": "Question: Does alcohol withdrawal alleviate adipose tissue inflammation in patients with alcoholic liver disease?\nContext: {'contexts': ['Patients with alcoholic liver disease (ALD) display inflammation of the subcutaneous adipose tissue (SAT) which correlates with liver lesions. We examined macrophage markers and polarization in the SAT of alcoholic patients and adipokine expression according to liver inflammation; we studied the consequences of alcohol withdrawal.', 'Forty-seven patients with ALD were prospectively included. SAT and blood samples were collected at inclusion and after 1\\xa0week of alcohol withdrawal. Pro-inflammatory cytokines/chemokines, inflammasome components and products, adipokine expression levels, macrophage markers and polarization in liver and SAT samples were assessed by RT-PCR arrays.', 'mRNA expression level of chemokines (IL8, semaphorin 7A) correlated with hepatic steatosis in both liver and SAT. Liver expression of inflammasome components (IL1β, IL18, caspase-1) and SAT IL6 and CCL2 correlated with liver damage. In patients with mild ALD, 1\\xa0week of alcohol withdrawal was sufficient to decrease expression level of total macrophage markers in the adipose tissue, to orient adipose tissue macrophages (ATM) towards an anti-inflammatory M2 phenotype and to decrease the mRNA expression of cytokines/chemokines (IL18, CCL2, osteopontin, semaphorin 7A). In patients with severe ALD, 1\\xa0week of abstinence was also associated with an increase in CCL18 expression.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adipokines', 'Adipose Tissue', 'Adult', 'Alcohol Abstinence', 'Biomarkers', 'Cytokines', 'Female', 'Humans', 'Liver', 'Liver Diseases, Alcoholic', 'Macrophages', 'Male', 'Middle Aged', 'Panniculitis', 'Prospective Studies']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,766,977 | Is galectin-3 independently associated with cardiovascular mortality in community-dwelling older adults without known cardiovascular disease : The Rancho Bernardo Study? | {
"contexts": [
"Galectin-3 is a marker of myocardial fibrosis that has been implicated in the pathophysiologic pathway of fibrosis; its association with all-cause and cardiovascular disease (CVD) mortality in a community-based cohort free of baseline CVD has not been reported. Our aim was to determine the association between galectin-3 levels and all-cause and CVD mortality in community-dwelling older adults without known CVD.",
"We measured plasma galectin-3 levels in 1,393 Rancho Bernardo Study participants without CVD with a mean age of 70 years. Participants were followed up for a mean of 11 years for coronary heart disease, CVD mortality, and all-cause mortality.",
"During follow-up, 436 participants died (169 from CVD). In models adjusted for traditional CVD risk factors and renal function, galectin-3 was a significant predictor of CVD mortality (hazard ratio [HR] per SD log increase 1.30, 95% CI 1.10-1.53) and all-cause mortality (HR 1.12, 1.01-1.24), but not coronary heart disease (HR 1.09, 0.92-1.30). After further adjusting for N-terminal pro B-type natriuretic peptide, galectin-3 remained an independent predictor (HR 1.24, 1.05-1.47) of CVD mortality. Galectin-3 improved the c statistic (0.847-0.851, P = .003) for prediction of CVD death. Net reclassification improvement (>0) with the addition of galectin-3 was 35% (P < .0001); the integrated discrimination index was also significant (P = .03). Participants with both galectin-3 and N-terminal pro B-type natriuretic peptide above the median had increased risk of CVD death vs those with higher levels of only 1 of these markers (HR 1.74, 1.24-2.43)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Age Factors",
"Aged",
"Aged, 80 and over",
"Biomarkers",
"California",
"Cardiovascular Diseases",
"Cause of Death",
"Female",
"Follow-Up Studies",
"Galectin 3",
"Humans",
"Informed Consent",
"Male",
"Middle Aged",
"Predictive Value of Tests",
"Prognosis",
"Prospective Studies",
"Risk Assessment",
"Risk Factors",
"Survival Rate",
"Time Factors"
]
} | Higher levels of galectin-3 are independently associated with all-cause and CVD mortality among community-dwelling older adults with no known CVD at baseline. | yes | [
{
"from": "human",
"value": "Question: Is galectin-3 independently associated with cardiovascular mortality in community-dwelling older adults without known cardiovascular disease : The Rancho Bernardo Study?\nContext: {'contexts': ['Galectin-3 is a marker of myocardial fibrosis that has been implicated in the pathophysiologic pathway of fibrosis; its association with all-cause and cardiovascular disease (CVD) mortality in a community-based cohort free of baseline CVD has not been reported. Our aim was to determine the association between galectin-3 levels and all-cause and CVD mortality in community-dwelling older adults without known CVD.', 'We measured plasma galectin-3 levels in 1,393 Rancho Bernardo Study participants without CVD with a mean age of 70 years. Participants were followed up for a mean of 11 years for coronary heart disease, CVD mortality, and all-cause mortality.', 'During follow-up, 436 participants died (169 from CVD). In models adjusted for traditional CVD risk factors and renal function, galectin-3 was a significant predictor of CVD mortality (hazard ratio [HR] per SD log increase 1.30, 95% CI 1.10-1.53) and all-cause mortality (HR 1.12, 1.01-1.24), but not coronary heart disease (HR 1.09, 0.92-1.30). After further adjusting for N-terminal pro B-type natriuretic peptide, galectin-3 remained an independent predictor (HR 1.24, 1.05-1.47) of CVD mortality. Galectin-3 improved the c statistic (0.847-0.851, P = .003) for prediction of CVD death. Net reclassification improvement (>0) with the addition of galectin-3 was 35% (P < .0001); the integrated discrimination index was also significant (P = .03). Participants with both galectin-3 and N-terminal pro B-type natriuretic peptide above the median had increased risk of CVD death vs those with higher levels of only 1 of these markers (HR 1.74, 1.24-2.43).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Age Factors', 'Aged', 'Aged, 80 and over', 'Biomarkers', 'California', 'Cardiovascular Diseases', 'Cause of Death', 'Female', 'Follow-Up Studies', 'Galectin 3', 'Humans', 'Informed Consent', 'Male', 'Middle Aged', 'Predictive Value of Tests', 'Prognosis', 'Prospective Studies', 'Risk Assessment', 'Risk Factors', 'Survival Rate', 'Time Factors']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,766,915 | Is round block technique a useful oncoplastic procedure for multicentric fibroadenomas? | {
"contexts": [
"Multicentric fibroadenomas, defined as multiple fibroadenomas located at different quadrants of the breast, occur in 10-20% of women with fibroadenoma. The surgical management of multicentric fibroadenomas may be troublesome for surgeons and patients. In this study, we report our preliminary experience using the \"round block technique\" in the management of women with multicentric fibroadenomas of the breast.",
"Records of patients with breast diseases managed with the round block technique were searched for in the Changhua Christian Hospital oncoplastic breast surgery database. The patients' clinicopathologic characteristics, type of surgery, operation time, blood loss, and complications were recorded. The cosmetic outcome was evaluated by the patient and operating surgeon two months after the surgery.",
"Twenty patients with multicentric fibroadenomas managed by the round block technique comprised the current study cohort. The mean age of the subjects was 36.5 ± 10.4 years. Twelve (60%) patients had tumors on one side of the breast, and eight (40%) had bilateral breast lesions. The average number of tumors removed was 3.3 ± 1.2 (range 2-6) per breast, and mean tumor size was 2.2 ± 0.5 cm. Three (15%) patients developed mild ecchymosis of the breast undergoing operation, which resolved spontaneously. One (5%) patient had partial nipple ischemia/necrosis due to 2 tumors excised near the nipple-areolar complex. The aesthetic results were evaluated as good in 19 (95%) patients and fair in 1 (5%)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Breast Neoplasms",
"Female",
"Fibroadenoma",
"Humans",
"Mastectomy, Segmental",
"Middle Aged",
"Neoplasm Staging",
"Nipples",
"Operative Time",
"Retrospective Studies",
"Young Adult"
]
} | The round block technique is a useful oncoplastic procedure for the management of multicentric fibroadenomas excised at the same time. | yes | [
{
"from": "human",
"value": "Question: Is round block technique a useful oncoplastic procedure for multicentric fibroadenomas?\nContext: {'contexts': ['Multicentric fibroadenomas, defined as multiple fibroadenomas located at different quadrants of the breast, occur in 10-20% of women with fibroadenoma. The surgical management of multicentric fibroadenomas may be troublesome for surgeons and patients. In this study, we report our preliminary experience using the \"round block technique\" in the management of women with multicentric fibroadenomas of the breast.', \"Records of patients with breast diseases managed with the round block technique were searched for in the Changhua Christian Hospital oncoplastic breast surgery database. The patients' clinicopathologic characteristics, type of surgery, operation time, blood loss, and complications were recorded. The cosmetic outcome was evaluated by the patient and operating surgeon two months after the surgery.\", 'Twenty patients with multicentric fibroadenomas managed by the round block technique comprised the current study cohort. The mean age of the subjects was 36.5\\xa0±\\xa010.4 years. Twelve (60%) patients had tumors on one side of the breast, and eight (40%) had bilateral breast lesions. The average number of tumors removed was 3.3\\xa0±\\xa01.2 (range 2-6) per breast, and mean tumor size was 2.2\\xa0±\\xa00.5\\xa0cm. Three (15%) patients developed mild ecchymosis of the breast undergoing operation, which resolved spontaneously. One (5%) patient had partial nipple ischemia/necrosis due to 2 tumors excised near the nipple-areolar complex. The aesthetic results were evaluated as good in 19 (95%) patients and fair in 1 (5%).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Breast Neoplasms', 'Female', 'Fibroadenoma', 'Humans', 'Mastectomy, Segmental', 'Middle Aged', 'Neoplasm Staging', 'Nipples', 'Operative Time', 'Retrospective Studies', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,768,021 | Does anterior fascial fixation reduce the parastomal hernia rate after radical cystectomy and ileal conduit? | {
"contexts": [
"To compare the rate of parastomal hernia in patients undergoing anterior fascial fixation of the ileal conduit with that in patients without fascial fixation. Limited data exist on whether anterior fascial fixation of the ileal conduit impacts the rate of parastomal hernia.",
"A total of 496 consecutive patients undergoing radical cystectomy and ileal conduit reconstruction from 1995 to 2012 were retrospectively evaluated for parastomal hernia. All patients had a 2-fingerbreadth aperture and the ileal conduit brought through the rectus muscle and sheath. Patients were divided into 1 of 3 groups based on stoma fixation and/or reinforcement: anterior fascial fixation, posterior reinforcement, or no fascial fixation. A parastomal hernia was defined as a palpable bulge at the stoma site. Multivariate logistic regression was conducted for the primary end point of parastomal hernia, controlling for other patient- and treatment-related factors that might affect the rate of parastomal hernia.",
"Median follow-up was 16 months (range, 1-189 months). The parastomal hernia rate was significantly greater in the anterior fascial suture group (43 of 281; 15.3%) than the no fascial suture group (12 of 164; 7.3%; P=.02). Multivariate logistic regression analysis modeled for the occurrence of a parastomal hernia demonstrated that anterior fascial fixation was an independent predictor of the development of parastomal hernia (odds ratio, 2.3; 95% confidence interval, 1.03-5.14; P=.04)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Cohort Studies",
"Cystectomy",
"Fasciotomy",
"Female",
"Follow-Up Studies",
"Hernia, Ventral",
"Humans",
"Incidence",
"Logistic Models",
"Male",
"Middle Aged",
"Multivariate Analysis",
"Predictive Value of Tests",
"Reconstructive Surgical Procedures",
"Retrospective Studies",
"Risk Assessment",
"Surgical Stomas",
"Suture Techniques",
"Tensile Strength",
"Time Factors",
"Treatment Outcome",
"Urinary Bladder Neoplasms",
"Urinary Diversion"
]
} | Anterior fascial fixation of the ileal conduit does not reduce the risk of parastomal hernia formation compared with the patients treated without fascial fixation. Surgeons should consider avoiding anterior suture fixation during ileal conduit creation. | no | [
{
"from": "human",
"value": "Question: Does anterior fascial fixation reduce the parastomal hernia rate after radical cystectomy and ileal conduit?\nContext: {'contexts': ['To compare the rate of parastomal hernia in patients undergoing anterior fascial fixation of the ileal conduit with that in patients without fascial fixation. Limited data exist on whether anterior fascial fixation of the ileal conduit impacts the rate of parastomal hernia.', 'A total of 496 consecutive patients undergoing radical cystectomy and ileal conduit reconstruction from 1995 to 2012 were retrospectively evaluated for parastomal hernia. All patients had a 2-fingerbreadth aperture and the ileal conduit brought through the rectus muscle and sheath. Patients were divided into 1 of 3 groups based on stoma fixation and/or reinforcement: anterior fascial fixation, posterior reinforcement, or no fascial fixation. A parastomal hernia was defined as a palpable bulge at the stoma site. Multivariate logistic regression was conducted for the primary end point of parastomal hernia, controlling for other patient- and treatment-related factors that might affect the rate of parastomal hernia.', 'Median follow-up was 16 months (range, 1-189 months). The parastomal hernia rate was significantly greater in the anterior fascial suture group (43 of 281; 15.3%) than the no fascial suture group (12 of 164; 7.3%; P=.02). Multivariate logistic regression analysis modeled for the occurrence of a parastomal hernia demonstrated that anterior fascial fixation was an independent predictor of the development of parastomal hernia (odds ratio, 2.3; 95% confidence interval, 1.03-5.14; P=.04).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Cohort Studies', 'Cystectomy', 'Fasciotomy', 'Female', 'Follow-Up Studies', 'Hernia, Ventral', 'Humans', 'Incidence', 'Logistic Models', 'Male', 'Middle Aged', 'Multivariate Analysis', 'Predictive Value of Tests', 'Reconstructive Surgical Procedures', 'Retrospective Studies', 'Risk Assessment', 'Surgical Stomas', 'Suture Techniques', 'Tensile Strength', 'Time Factors', 'Treatment Outcome', 'Urinary Bladder Neoplasms', 'Urinary Diversion']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
24,760,237 | Does use of prototype two-channel endoscope with elevator enable larger lift-and-snare endoscopic mucosal resection in a porcine model? | {
"contexts": [
"Flat and depressed lesions are becoming increasingly recognized in the esophagus, stomach, and colon. Various techniques have been described for endoscopic mucosal resection (EMR) of these lesions.",
"To evaluate the efficacy of lift-grasp-cut EMR using a prototype dual-channel forward-viewing endoscope with an instrument elevator in one accessory channel (dual-channel elevator scope) as compared to standard dual-channel endoscopes.",
"EMR was performed using a lift-grasp-cut technique on normal flat rectosigmoid or gastric mucosa in live porcine models after submucosal injection of 4 mL of saline using a dual-channel elevator scope or a standard dual-channel endoscope. With the dual-channel elevator scope, the elevator was used to attain further lifting of the mucosa. The primary endpoint was size of the EMR specimen and the secondary endpoint was number of complications.",
"Twelve experiments were performed (six gastric and six colonic). Mean specimen diameter was 2.27 cm with the dual-channel elevator scope and 1.34 cm with the dual-channel endoscope (P = 0.018). Two colonic perforations occurred with the dual-channel endoscope, vs no complications with the dual-channel elevator scope."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": []
} | The increased lift of the mucosal epithelium, through use of the dual-channel elevator scope, allows for larger EMR when using a lift-grasp-cut technique. Noting the thin nature of the porcine colonic wall, use of the elevator may also make this technique safer. | yes | [
{
"from": "human",
"value": "Question: Does use of prototype two-channel endoscope with elevator enable larger lift-and-snare endoscopic mucosal resection in a porcine model?\nContext: {'contexts': ['Flat and depressed lesions are becoming increasingly recognized in the esophagus, stomach, and colon. Various techniques have been described for endoscopic mucosal resection (EMR) of these lesions.', 'To evaluate the efficacy of lift-grasp-cut EMR using a prototype dual-channel forward-viewing endoscope with an instrument elevator in one accessory channel (dual-channel elevator scope) as compared to standard dual-channel endoscopes.', 'EMR was performed using a lift-grasp-cut technique on normal flat rectosigmoid or gastric mucosa in live porcine models after submucosal injection of 4 mL of saline using a dual-channel elevator scope or a standard dual-channel endoscope. With the dual-channel elevator scope, the elevator was used to attain further lifting of the mucosa. The primary endpoint was size of the EMR specimen and the secondary endpoint was number of complications.', 'Twelve experiments were performed (six gastric and six colonic). Mean specimen diameter was 2.27 cm with the dual-channel elevator scope and 1.34 cm with the dual-channel endoscope (P = 0.018). Two colonic perforations occurred with the dual-channel endoscope, vs no complications with the dual-channel elevator scope.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,769,273 | Is serum paraoxonase-1 activity more closely related to HDL particle concentration and large HDL particles than to HDL cholesterol in Type 2 diabetic and non-diabetic subjects? | {
"contexts": [
"We determined relationships of the anti-oxidative enzyme, paraoxonase-1 (PON-1), with high density lipoprotein (HDL) subfractions, and tested whether these relationships are stronger than those with HDL cholesterol and apolipoprotein A-I (apoA-I) in subjects with and without type 2 diabetes mellitus (T2DM).",
"Serum PON-1 (arylesterase activity) and HDL subfractions (nuclear magnetic resonance spectroscopy) were determined in 67 T2DM patients and in 56 non-diabetic subjects.",
"PON-1 activity, HDL cholesterol and apoA-I were decreased in T2DM (all p<0.05). The HDL particle concentration was unaltered, but large HDL particles, medium HDL particles and HDL particle size were decreased, whereas small HDL particles were increased in T2DM (all p<0.05). PON-1 was more closely related to HDL cholesterol than to apoA-I (p=0.001). In turn, the positive relationship of PON-1 with the HDL particle concentration and with large HDL particles was stronger than that with HDL cholesterol (both p<0.01). The inverse relationship of PON-1 with T2DM was only modestly attenuated by HDL cholesterol or HDL particle characteristics."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Aryldialkylphosphatase",
"Case-Control Studies",
"Diabetes Mellitus, Type 2",
"Female",
"Humans",
"Lipoproteins, HDL",
"Magnetic Resonance Spectroscopy",
"Male",
"Middle Aged"
]
} | PON-1 activity is more closely related to the HDL particle concentration or large HDL particles than to HDL cholesterol. Impaired PON-1 activity in T2DM is not to a considerable extent explained by altered HDL subfraction levels. | yes | [
{
"from": "human",
"value": "Question: Is serum paraoxonase-1 activity more closely related to HDL particle concentration and large HDL particles than to HDL cholesterol in Type 2 diabetic and non-diabetic subjects?\nContext: {'contexts': ['We determined relationships of the anti-oxidative enzyme, paraoxonase-1 (PON-1), with high density lipoprotein (HDL) subfractions, and tested whether these relationships are stronger than those with HDL cholesterol and apolipoprotein A-I (apoA-I) in subjects with and without type 2 diabetes mellitus (T2DM).', 'Serum PON-1 (arylesterase activity) and HDL subfractions (nuclear magnetic resonance spectroscopy) were determined in 67 T2DM patients and in 56 non-diabetic subjects.', 'PON-1 activity, HDL cholesterol and apoA-I were decreased in T2DM (all p<0.05). The HDL particle concentration was unaltered, but large HDL particles, medium HDL particles and HDL particle size were decreased, whereas small HDL particles were increased in T2DM (all p<0.05). PON-1 was more closely related to HDL cholesterol than to apoA-I (p=0.001). In turn, the positive relationship of PON-1 with the HDL particle concentration and with large HDL particles was stronger than that with HDL cholesterol (both p<0.01). The inverse relationship of PON-1 with T2DM was only modestly attenuated by HDL cholesterol or HDL particle characteristics.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Aryldialkylphosphatase', 'Case-Control Studies', 'Diabetes Mellitus, Type 2', 'Female', 'Humans', 'Lipoproteins, HDL', 'Magnetic Resonance Spectroscopy', 'Male', 'Middle Aged']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,776,597 | Does quantitative proteomics analysis reveal similar release profiles following specific PAR-1 or PAR-4 stimulation of platelets? | {
"contexts": [
"Platelets are a natural source of growth factors, cytokines and chemokines, that regulate angiogenesis and inflammation. It has been suggested that differential release of pro- and anti-angiogenic growth factors from platelet α-granules by protease-activated receptors (PAR) 1 and 4 may be important for the regulation of angiogenesis. We aimed to compare the releasates of unstimulated platelets with PAR-1- and PAR-4-stimulated platelets.",
"The release of β-thromboglobulin, platelet factor (PF)-4, thrombospondin, platelet-derived growth factor (PDGF)-A/B, regulated and normal T-cell expressed and secreted (RANTES/CCL5), endostatin, CXCL12, and vascular endothelial growth factor (VEGF) was measured with enzyme-linked immunosorbent assay (ELISA). Mass spectrometry (MS)-based quantitative proteomics identified 93 proteins from platelets stimulated with PAR-1 and PAR-4. A strong correlation between the factors released after either stimulus was observed (Spearman's r 0.94, P < 0.001). Analysis with ELISA showed that stimulation with PAR-1 or PAR-4 lead to non-differential release of β-thromboglobulin, PF-4, thrombospondin, PDGF-A/B, RANTES/CCL5, endostatin, CXCL12, and VEGF. Release of thrombospondin was slightly lower after PAR-1 stimulation (7.2 μg/mL), compared with PAR-4 induced release (9.8 μg/mL; P < 0.05)."
],
"labels": [
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Apoptosis Regulatory Proteins",
"Blood Platelets",
"Chemokine CXCL12",
"Enzyme-Linked Immunosorbent Assay",
"Fibrinogen",
"Humans",
"Mass Spectrometry",
"Neovascularization, Physiologic",
"P-Selectin",
"Platelet Activation",
"Platelet Glycoprotein GPIIb-IIIa Complex",
"Proteomics",
"Receptor, PAR-1",
"Secretory Vesicles",
"Vascular Endothelial Growth Factor A",
"beta-Thromboglobulin"
]
} | Both ELISA on established α-granule proteins and MS-based quantitative proteomics showed that the most abundant α-granule proteins are released in similar quantities from platelets after stimulation with either PAR-1 or PAR-4. Our findings provide evidence against the hypothesis that PAR-1 and PAR-4 stimulation of platelets trigger differential release of alpha-granule, but further studies are needed to draw conclusions for physiological conditions. | yes | [
{
"from": "human",
"value": "Question: Does quantitative proteomics analysis reveal similar release profiles following specific PAR-1 or PAR-4 stimulation of platelets?\nContext: {'contexts': ['Platelets are a natural source of growth factors, cytokines and chemokines, that regulate angiogenesis and inflammation. It has been suggested that differential release of pro- and anti-angiogenic growth factors from platelet α-granules by protease-activated receptors (PAR) 1 and 4 may be important for the regulation of angiogenesis. We aimed to compare the releasates of unstimulated platelets with PAR-1- and PAR-4-stimulated platelets.', \"The release of β-thromboglobulin, platelet factor (PF)-4, thrombospondin, platelet-derived growth factor (PDGF)-A/B, regulated and normal T-cell expressed and secreted (RANTES/CCL5), endostatin, CXCL12, and vascular endothelial growth factor (VEGF) was measured with enzyme-linked immunosorbent assay (ELISA). Mass spectrometry (MS)-based quantitative proteomics identified 93 proteins from platelets stimulated with PAR-1 and PAR-4. A strong correlation between the factors released after either stimulus was observed (Spearman's r 0.94, P < 0.001). Analysis with ELISA showed that stimulation with PAR-1 or PAR-4 lead to non-differential release of β-thromboglobulin, PF-4, thrombospondin, PDGF-A/B, RANTES/CCL5, endostatin, CXCL12, and VEGF. Release of thrombospondin was slightly lower after PAR-1 stimulation (7.2 μg/mL), compared with PAR-4 induced release (9.8 μg/mL; P < 0.05).\"], 'labels': ['OBJECTIVE', 'RESULTS'], 'meshes': ['Apoptosis Regulatory Proteins', 'Blood Platelets', 'Chemokine CXCL12', 'Enzyme-Linked Immunosorbent Assay', 'Fibrinogen', 'Humans', 'Mass Spectrometry', 'Neovascularization, Physiologic', 'P-Selectin', 'Platelet Activation', 'Platelet Glycoprotein GPIIb-IIIa Complex', 'Proteomics', 'Receptor, PAR-1', 'Secretory Vesicles', 'Vascular Endothelial Growth Factor A', 'beta-Thromboglobulin']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,776,599 | Does the tumour suppressor Ras-association domain family protein 1A ( RASSF1A ) regulate TNF-α signalling in cardiomyocytes? | {
"contexts": [
"Tumour necrosis factor-α (TNF-α) plays a key role in the regulation of cardiac contractility. Although cardiomyocytes are known to express the TNF-α receptors (TNFRs), the mechanism of TNF-α signal transmission is incompletely understood. The aim of this study was to investigate whether the tumour suppressor Ras-association domain family protein 1 isoform A (RASSF1A) modulates TNF-α signalling in cardiomyocytes.",
"We used RASSF1A knockout (RASSF1A(-/-)) mice and wild-type (WT) littermates in this study. Acute stimulation with a low dose of TNF-α (10 µg/kg iv) increased cardiac contractility and intracellular calcium transients' amplitude in WT mice. In contrast, RASSF1A(-/-) mice showed a blunted contractile response. Mechanistically, RASSF1A was essential in the formation of the TNFR complex (TNFRC), where it functions as an adaptor molecule to facilitate the recruitment of TNFR type 1-associated death domain protein and TNFR-associated factor 2 to form the TNF-α receptor complex. In the absence of RASSF1A, signal transmission from the TNF-α receptor complex to the downstream effectors, such as cytoplasmic phospholipase A2 and protein kinase A, was attenuated leading to the reduction in the activation of calcium handling molecules, such as L-type Ca(2+) channel and ryanodine receptors."
],
"labels": [
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Animals",
"Calcium Signaling",
"Mice",
"Mice, Knockout",
"Myocardial Contraction",
"Myocytes, Cardiac",
"NF-kappa B",
"Peptide Fragments",
"Rats",
"Rats, Sprague-Dawley",
"Receptors, Tumor Necrosis Factor",
"Sequence Deletion",
"Signal Transduction",
"TNF Receptor-Associated Death Domain Protein",
"TNF Receptor-Associated Factor 2",
"Tumor Necrosis Factor-alpha",
"Tumor Suppressor Proteins"
]
} | Our data indicate an essential role of RASSF1A in regulating TNF-α signalling in cardiomyocytes, with RASSF1A being key in the formation of the TNFRC and in signal transmission to the downstream targets. | yes | [
{
"from": "human",
"value": "Question: Does the tumour suppressor Ras-association domain family protein 1A ( RASSF1A ) regulate TNF-α signalling in cardiomyocytes?\nContext: {'contexts': ['Tumour necrosis factor-α (TNF-α) plays a key role in the regulation of cardiac contractility. Although cardiomyocytes are known to express the TNF-α receptors (TNFRs), the mechanism of TNF-α signal transmission is incompletely understood. The aim of this study was to investigate whether the tumour suppressor Ras-association domain family protein 1 isoform A (RASSF1A) modulates TNF-α signalling in cardiomyocytes.', \"We used RASSF1A knockout (RASSF1A(-/-)) mice and wild-type (WT) littermates in this study. Acute stimulation with a low dose of TNF-α (10 µg/kg iv) increased cardiac contractility and intracellular calcium transients' amplitude in WT mice. In contrast, RASSF1A(-/-) mice showed a blunted contractile response. Mechanistically, RASSF1A was essential in the formation of the TNFR complex (TNFRC), where it functions as an adaptor molecule to facilitate the recruitment of TNFR type 1-associated death domain protein and TNFR-associated factor 2 to form the TNF-α receptor complex. In the absence of RASSF1A, signal transmission from the TNF-α receptor complex to the downstream effectors, such as cytoplasmic phospholipase A2 and protein kinase A, was attenuated leading to the reduction in the activation of calcium handling molecules, such as L-type Ca(2+) channel and ryanodine receptors.\"], 'labels': ['OBJECTIVE', 'RESULTS'], 'meshes': ['Animals', 'Calcium Signaling', 'Mice', 'Mice, Knockout', 'Myocardial Contraction', 'Myocytes, Cardiac', 'NF-kappa B', 'Peptide Fragments', 'Rats', 'Rats, Sprague-Dawley', 'Receptors, Tumor Necrosis Factor', 'Sequence Deletion', 'Signal Transduction', 'TNF Receptor-Associated Death Domain Protein', 'TNF Receptor-Associated Factor 2', 'Tumor Necrosis Factor-alpha', 'Tumor Suppressor Proteins']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,764,455 | Does the H2.0-like homeobox transcription factor modulate yolk sac vascular remodeling in mouse embryos? | {
"contexts": [
"The H2.0-like homeobox transcription factor (HLX) plays an essential role in visceral organogenesis in mice and has been shown to regulate angiogenic sprouting in vitro and in zebrafish embryos. We therefore examined the role of HLX in vascular development in mouse and avian embryos.",
"In situ hybridization showed that Hlx is expressed in a subset of sprouting blood vessels in postnatal mouse retinas and embryos. Hlx expression was conserved in quail embryos and upregulated in blood vessels at the onset of circulation. In vitro assays showed that Hlx is dynamically regulated by growth factors and shear stress alterations. Proangiogenic vascular endothelial growth factor induces Hlx expression in cultured endothelial cells, whereas signals that induce stalk cell identity lead to a reduction in Hlx expression. HLX was also downregulated in embryos in which flow was ablated, whereas injection of a starch solution, which increases blood viscosity and therefore shear stress, causes an upregulation in HLX. HLX knockdown in vitro resulted in a reduction in tip cell marker expression and in reduced angiogenic sprouting, but Hlx(-/-) embryos showed no defect in vascular sprouting at E8.5, E9.5, or E11.5 in vivo. Vascular remodeling of the capillary plexus was altered in Hlx(-/-) embryos, with a modestly enlarged venous plexus and reduction of the arterial plexus."
],
"labels": [
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Animals",
"Blood Vessels",
"Blood Viscosity",
"Cells, Cultured",
"Embryo, Mammalian",
"Embryo, Nonmammalian",
"Gene Expression Regulation, Developmental",
"Gestational Age",
"Homeodomain Proteins",
"Humans",
"Mechanotransduction, Cellular",
"Mice",
"Mice, Knockout",
"Neovascularization, Physiologic",
"Quail",
"RNA Interference",
"Regional Blood Flow",
"Stress, Mechanical",
"Transcription Factors",
"Transfection",
"Yolk Sac"
]
} | Our findings indicate not only that Hlx regulates sprouting in vitro, but that its role in sprouting is nonessential in vivo. We find HLX is regulated by shear stress and a subtle defect in vascular remodeling is present in knockout embryos. | yes | [
{
"from": "human",
"value": "Question: Does the H2.0-like homeobox transcription factor modulate yolk sac vascular remodeling in mouse embryos?\nContext: {'contexts': ['The H2.0-like homeobox transcription factor (HLX) plays an essential role in visceral organogenesis in mice and has been shown to regulate angiogenic sprouting in vitro and in zebrafish embryos. We therefore examined the role of HLX in vascular development in mouse and avian embryos.', 'In situ hybridization showed that Hlx is expressed in a subset of sprouting blood vessels in postnatal mouse retinas and embryos. Hlx expression was conserved in quail embryos and upregulated in blood vessels at the onset of circulation. In vitro assays showed that Hlx is dynamically regulated by growth factors and shear stress alterations. Proangiogenic vascular endothelial growth factor induces Hlx expression in cultured endothelial cells, whereas signals that induce stalk cell identity lead to a reduction in Hlx expression. HLX was also downregulated in embryos in which flow was ablated, whereas injection of a starch solution, which increases blood viscosity and therefore shear stress, causes an upregulation in HLX. HLX knockdown in vitro resulted in a reduction in tip cell marker expression and in reduced angiogenic sprouting, but Hlx(-/-) embryos showed no defect in vascular sprouting at E8.5, E9.5, or E11.5 in vivo. Vascular remodeling of the capillary plexus was altered in Hlx(-/-) embryos, with a modestly enlarged venous plexus and reduction of the arterial plexus.'], 'labels': ['OBJECTIVE', 'RESULTS'], 'meshes': ['Animals', 'Blood Vessels', 'Blood Viscosity', 'Cells, Cultured', 'Embryo, Mammalian', 'Embryo, Nonmammalian', 'Gene Expression Regulation, Developmental', 'Gestational Age', 'Homeodomain Proteins', 'Humans', 'Mechanotransduction, Cellular', 'Mice', 'Mice, Knockout', 'Neovascularization, Physiologic', 'Quail', 'RNA Interference', 'Regional Blood Flow', 'Stress, Mechanical', 'Transcription Factors', 'Transfection', 'Yolk Sac']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,764,453 | Does tissue plasminogen activator promote postischemic neutrophil recruitment via its proteolytic and nonproteolytic properties? | {
"contexts": [
"Neutrophil infiltration of the postischemic tissue considerably contributes to organ dysfunction on ischemia/reperfusion injury. Beyond its established role in fibrinolysis, tissue-type plasminogen activator (tPA) has recently been implicated in nonfibrinolytic processes. The role of this serine protease in the recruitment process of neutrophils remains largely obscure.",
"Using in vivo microscopy on the postischemic cremaster muscle, neutrophil recruitment and microvascular leakage, but not fibrinogen deposition at the vessel wall, were significantly diminished in tPA(-/-) mice. Using cell transfer techniques, leukocyte and nonleukocyte tPA were found to mediate ischemia/reperfusion-elicited neutrophil responses. Intrascrotal but not intra-arterial application of recombinant tPA induced a dose-dependent increase in the recruitment of neutrophils, which was significantly higher compared with stimulation with a tPA mutant lacking catalytic activity. Whereas tPA-dependent transmigration of neutrophils was selectively reduced on the inhibition of plasmin or gelatinases, neutrophil intravascular adherence was significantly diminished on the blockade of mast cell activation or lipid mediator synthesis. Moreover, stimulation with tPA caused a significant elevation in the leakage of fluorescein isothiocyanate dextran to the perivascular tissue, which was completely abolished on neutrophil depletion. In vitro, tPA-elicited macromolecular leakage of endothelial cell layers was abrogated on the inhibition of its proteolytic activity."
],
"labels": [
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Animals",
"Capillary Permeability",
"Cells, Cultured",
"Chemotaxis, Leukocyte",
"Disease Models, Animal",
"Dose-Response Relationship, Drug",
"Endothelial Cells",
"Fibrinogen",
"Fibrinolysin",
"Gelatinases",
"Hemodynamics",
"Humans",
"Male",
"Mast Cells",
"Mice",
"Mice, Inbred C57BL",
"Mice, Knockout",
"Microcirculation",
"Microvessels",
"Muscles",
"Mutation",
"Neutrophil Infiltration",
"Neutrophils",
"Recombinant Proteins",
"Reperfusion Injury",
"Time Factors",
"Tissue Plasminogen Activator",
"Transendothelial and Transepithelial Migration"
]
} | Endogenously released tPA promotes neutrophil transmigration to reperfused tissue via proteolytic activation of plasmin and gelatinases. As a consequence, tPA on transmigrating neutrophils disrupts endothelial junctions allowing circulating tPA to extravasate to the perivascular tissue, which, in turn, amplifies neutrophil recruitment through the activation of mast cells and release of lipid mediators. | yes | [
{
"from": "human",
"value": "Question: Does tissue plasminogen activator promote postischemic neutrophil recruitment via its proteolytic and nonproteolytic properties?\nContext: {'contexts': ['Neutrophil infiltration of the postischemic tissue considerably contributes to organ dysfunction on ischemia/reperfusion injury. Beyond its established role in fibrinolysis, tissue-type plasminogen activator (tPA) has recently been implicated in nonfibrinolytic processes. The role of this serine protease in the recruitment process of neutrophils remains largely obscure.', 'Using in vivo microscopy on the postischemic cremaster muscle, neutrophil recruitment and microvascular leakage, but not fibrinogen deposition at the vessel wall, were significantly diminished in tPA(-/-) mice. Using cell transfer techniques, leukocyte and nonleukocyte tPA were found to mediate ischemia/reperfusion-elicited neutrophil responses. Intrascrotal but not intra-arterial application of recombinant tPA induced a dose-dependent increase in the recruitment of neutrophils, which was significantly higher compared with stimulation with a tPA mutant lacking catalytic activity. Whereas tPA-dependent transmigration of neutrophils was selectively reduced on the inhibition of plasmin or gelatinases, neutrophil intravascular adherence was significantly diminished on the blockade of mast cell activation or lipid mediator synthesis. Moreover, stimulation with tPA caused a significant elevation in the leakage of fluorescein isothiocyanate dextran to the perivascular tissue, which was completely abolished on neutrophil depletion. In vitro, tPA-elicited macromolecular leakage of endothelial cell layers was abrogated on the inhibition of its proteolytic activity.'], 'labels': ['OBJECTIVE', 'RESULTS'], 'meshes': ['Animals', 'Capillary Permeability', 'Cells, Cultured', 'Chemotaxis, Leukocyte', 'Disease Models, Animal', 'Dose-Response Relationship, Drug', 'Endothelial Cells', 'Fibrinogen', 'Fibrinolysin', 'Gelatinases', 'Hemodynamics', 'Humans', 'Male', 'Mast Cells', 'Mice', 'Mice, Inbred C57BL', 'Mice, Knockout', 'Microcirculation', 'Microvessels', 'Muscles', 'Mutation', 'Neutrophil Infiltration', 'Neutrophils', 'Recombinant Proteins', 'Reperfusion Injury', 'Time Factors', 'Tissue Plasminogen Activator', 'Transendothelial and Transepithelial Migration']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,764,451 | Does btk inhibition suppress agonist-induced human macrophage activation and inflammatory gene expression in RA synovial tissue explants? | {
"contexts": [
"Bruton's tyrosine kinase (Btk) is required for B lymphocyte and myeloid cell contributions to pathology in murine models of arthritis. Here, we examined the potential contributions of synovial Btk expression and activation to inflammation in rheumatoid arthritis (RA).",
"Btk was detected by immunohistochemistry and digital image analysis in synovial tissue from biologically naive RA (n=16) and psoriatic arthritis (PsA) (n=12) patients. Cell populations expressing Btk were identified by immunofluorescent double labelling confocal microscopy, quantitative (q-) PCR and immunoblotting. The effects of a Btk-specific inhibitor, RN486, on gene expression in human macrophages and RA synovial tissue explants (n=8) were assessed by qPCR, ELISA and single-plex assays.",
"Btk was expressed at equivalent levels in RA and PsA synovial tissue, restricted to B lymphocytes, monocytes, macrophages and mast cells. RN486 significantly inhibited macrophage IL-6 production induced by Fc receptor and CD40 ligation. RN486 also reduced mRNA expression of overlapping gene sets induced by IgG, CD40 ligand (CD40L) and RA synovial fluid, and significantly suppressed macrophage production of CD40L-induced IL-8, TNF, MMP-1 and MMP-10, LPS-induced MMP-1, MMP-7 and MMP-10 production, and spontaneous production of IL-6, PDGF, CXCL-9 and MMP-1 by RA synovial explants."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Agammaglobulinaemia Tyrosine Kinase",
"Aged",
"Arthritis, Rheumatoid",
"B-Lymphocytes",
"Female",
"Gene Expression",
"Humans",
"Immunohistochemistry",
"Interleukin-6",
"Isoquinolines",
"Macrophages",
"Male",
"Mast Cells",
"Microscopy, Confocal",
"Middle Aged",
"Protein-Tyrosine Kinases",
"Synovial Membrane"
]
} | Btk is expressed equivalently in RA and PsA synovial tissue, primarily in macrophages. Btk activity is needed to drive macrophage activation in response to multiple agonists relevant to inflammatory arthritis, and promotes RA synovial tissue cytokine and MMP production. Pharmacological targeting of Btk may be of therapeutic benefit in the treatment of RA and other inflammatory diseases. | yes | [
{
"from": "human",
"value": "Question: Does btk inhibition suppress agonist-induced human macrophage activation and inflammatory gene expression in RA synovial tissue explants?\nContext: {'contexts': [\"Bruton's tyrosine kinase (Btk) is required for B lymphocyte and myeloid cell contributions to pathology in murine models of arthritis. Here, we examined the potential contributions of synovial Btk expression and activation to inflammation in rheumatoid arthritis (RA).\", 'Btk was detected by immunohistochemistry and digital image analysis in synovial tissue from biologically naive RA (n=16) and psoriatic arthritis (PsA) (n=12) patients. Cell populations expressing Btk were identified by immunofluorescent double labelling confocal microscopy, quantitative (q-) PCR and immunoblotting. The effects of a Btk-specific inhibitor, RN486, on gene expression in human macrophages and RA synovial tissue explants (n=8) were assessed by qPCR, ELISA and single-plex assays.', 'Btk was expressed at equivalent levels in RA and PsA synovial tissue, restricted to B lymphocytes, monocytes, macrophages and mast cells. RN486 significantly inhibited macrophage IL-6 production induced by Fc receptor and CD40 ligation. RN486 also reduced mRNA expression of overlapping gene sets induced by IgG, CD40 ligand (CD40L) and RA synovial fluid, and significantly suppressed macrophage production of CD40L-induced IL-8, TNF, MMP-1 and MMP-10, LPS-induced MMP-1, MMP-7 and MMP-10 production, and spontaneous production of IL-6, PDGF, CXCL-9 and MMP-1 by RA synovial explants.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Agammaglobulinaemia Tyrosine Kinase', 'Aged', 'Arthritis, Rheumatoid', 'B-Lymphocytes', 'Female', 'Gene Expression', 'Humans', 'Immunohistochemistry', 'Interleukin-6', 'Isoquinolines', 'Macrophages', 'Male', 'Mast Cells', 'Microscopy, Confocal', 'Middle Aged', 'Protein-Tyrosine Kinases', 'Synovial Membrane']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,773,203 | Does modulation of fatty acid and bile acid metabolism by peroxisome proliferator-activated receptor α protect against alcoholic liver disease? | {
"contexts": [
"Chronic alcohol intake affects liver function and causes hepatic pathological changes. It has been shown that peroxisome proliferator-activated receptor α (PPARα)-null mice developed more pronounced hepatic changes than wild-type (WT) mice after chronic exposure to a diet containing 4% alcohol. The remarkable similarity between the histopathology of alcoholic liver disease (ALD) in Ppara-null model and in humans, and the fact that PPARα expression and activity in human liver are less than one-tenth of those in WT mouse liver make Ppara-null a good system to investigate ALD.",
"In this study, the Ppara-null model was used to elucidate the dynamic regulation of PPARα activity during chronic alcohol intake. Hepatic transcriptomic and metabolomic analyses were used to examine alterations of gene expression and metabolites associated with pathological changes. The changes triggered by alcohol consumption on gene expression and metabolites in Ppara-null mice were compared with those in WT mice.",
"The results showed that in the presence of PPARα, 3 major metabolic pathways in mitochondria, namely the fatty acid β-oxidation, the tricarboxylic acid cycle, and the electron transfer chain, were induced in response to a 2-month alcohol feeding, while these responses were greatly reduced in the absence of PPARα. In line with the transcriptional modulations of these metabolic pathways, a progressive accumulation of triglycerides, a robust increase in hepatic cholic acid and its derivatives, and a strong induction of fibrogenesis genes were observed exclusively in alcohol-fed Ppara-null mice."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Bile Acids and Salts",
"Ethanol",
"Fatty Acids",
"Fibrosis",
"Liver",
"Liver Diseases, Alcoholic",
"Male",
"Metabolomics",
"Mice",
"Mitochondria, Liver",
"Oligonucleotide Array Sequence Analysis",
"PPAR alpha"
]
} | These observations indicate that PPARα plays a protective role to enhance mitochondrial function in response to chronic alcohol consumption by adaptive transcriptional activation and suggest that activation of this nuclear receptor may be of therapeutic value in the treatment for ALD. | yes | [
{
"from": "human",
"value": "Question: Does modulation of fatty acid and bile acid metabolism by peroxisome proliferator-activated receptor α protect against alcoholic liver disease?\nContext: {'contexts': ['Chronic alcohol intake affects liver function and causes hepatic pathological changes. It has been shown that peroxisome proliferator-activated receptor α (PPARα)-null mice developed more pronounced hepatic changes than wild-type (WT) mice after chronic exposure to a diet containing 4% alcohol. The remarkable similarity between the histopathology of alcoholic liver disease (ALD) in Ppara-null model and in humans, and the fact that PPARα expression and activity in human liver are less than one-tenth of those in WT mouse liver make Ppara-null a good system to investigate ALD.', 'In this study, the Ppara-null model was used to elucidate the dynamic regulation of PPARα activity during chronic alcohol intake. Hepatic transcriptomic and metabolomic analyses were used to examine alterations of gene expression and metabolites associated with pathological changes. The changes triggered by alcohol consumption on gene expression and metabolites in Ppara-null mice were compared with those in WT mice.', 'The results showed that in the presence of PPARα, 3 major metabolic pathways in mitochondria, namely the fatty acid β-oxidation, the tricarboxylic acid cycle, and the electron transfer chain, were induced in response to a 2-month alcohol feeding, while these responses were greatly reduced in the absence of PPARα. In line with the transcriptional modulations of these metabolic pathways, a progressive accumulation of triglycerides, a robust increase in hepatic cholic acid and its derivatives, and a strong induction of fibrogenesis genes were observed exclusively in alcohol-fed Ppara-null mice.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Bile Acids and Salts', 'Ethanol', 'Fatty Acids', 'Fibrosis', 'Liver', 'Liver Diseases, Alcoholic', 'Male', 'Metabolomics', 'Mice', 'Mitochondria, Liver', 'Oligonucleotide Array Sequence Analysis', 'PPAR alpha']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,759,736 | Is brd4 essential for IL-1β-induced inflammation in human airway epithelial cells? | {
"contexts": [
"Chronic inflammation and oxidative stress are key features of chronic obstructive pulmonary disease (COPD). Oxidative stress enhances COPD inflammation under the control of the pro-inflammatory redox-sensitive transcription factor nuclear factor-kappaB (NF-κB). Histone acetylation plays a critical role in chronic inflammation and bromodomain and extra terminal (BET) proteins act as \"readers\" of acetylated histones. Therefore, we examined the role of BET proteins in particular Brd2 and Brd4 and their inhibitors (JQ1 and PFI-1) in oxidative stress- enhanced inflammation in human bronchial epithelial cells.",
"Human primary epithelial (NHBE) cells and BEAS-2B cell lines were stimulated with IL-1β (inflammatory stimulus) in the presence or absence of H2O2 (oxidative stress) and the effect of pre-treatment with bromodomain inhibitors (JQ1 and PFI-1) was investigated. Pro-inflammatory mediators (CXCL8 and IL-6) were measured by ELISA and transcripts by RT-PCR. H3 and H4 acetylation and recruitment of p65 and Brd4 to the native IL-8 and IL-6 promoters was investigated using chromatin immunoprecipitation (ChIP). The impact of Brd2 and Brd4 siRNA knockdown on inflammatory mediators was also investigated.",
"H2O2 enhanced IL1β-induced IL-6 and CXCL8 expression in NHBE and BEAS-2B cells whereas H2O2 alone did not have any affect. H3 acetylation at the IL-6 and IL-8 promoters was associated with recruitment of p65 and Brd4 proteins. Although p65 acetylation was increased this was not directly targeted by Brd4. The BET inhibitors JQ1 and PFI-1 significantly reduced IL-6 and CXCL8 expression whereas no effect was seen with the inactive enantiomer JQ1(-). Brd4, but not Brd2, knockdown markedly reduced IL-6 and CXCL8 release. JQ1 also inhibited p65 and Brd4 recruitment to the IL-6 and IL-8 promoters."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Azepines",
"Cell Line",
"Chromatin Immunoprecipitation",
"Enzyme-Linked Immunosorbent Assay",
"Epithelial Cells",
"Humans",
"Hydrogen Peroxide",
"Inflammation",
"Interleukin-1beta",
"Interleukin-6",
"Interleukin-8",
"Nuclear Proteins",
"Protein-Serine-Threonine Kinases",
"Transcription Factors",
"Triazoles"
]
} | Oxidative stress enhanced IL1β-induced IL-6 and CXCL8 expression was significantly reduced by Brd4 inhibition. Brd4 plays an important role in the regulation of inflammatory genes and provides a potential novel anti-inflammatory target. | yes | [
{
"from": "human",
"value": "Question: Is brd4 essential for IL-1β-induced inflammation in human airway epithelial cells?\nContext: {'contexts': ['Chronic inflammation and oxidative stress are key features of chronic obstructive pulmonary disease (COPD). Oxidative stress enhances COPD inflammation under the control of the pro-inflammatory redox-sensitive transcription factor nuclear factor-kappaB (NF-κB). Histone acetylation plays a critical role in chronic inflammation and bromodomain and extra terminal (BET) proteins act as \"readers\" of acetylated histones. Therefore, we examined the role of BET proteins in particular Brd2 and Brd4 and their inhibitors (JQ1 and PFI-1) in oxidative stress- enhanced inflammation in human bronchial epithelial cells.', 'Human primary epithelial (NHBE) cells and BEAS-2B cell lines were stimulated with IL-1β (inflammatory stimulus) in the presence or absence of H2O2 (oxidative stress) and the effect of pre-treatment with bromodomain inhibitors (JQ1 and PFI-1) was investigated. Pro-inflammatory mediators (CXCL8 and IL-6) were measured by ELISA and transcripts by RT-PCR. H3 and H4 acetylation and recruitment of p65 and Brd4 to the native IL-8 and IL-6 promoters was investigated using chromatin immunoprecipitation (ChIP). The impact of Brd2 and Brd4 siRNA knockdown on inflammatory mediators was also investigated.', 'H2O2 enhanced IL1β-induced IL-6 and CXCL8 expression in NHBE and BEAS-2B cells whereas H2O2 alone did not have any affect. H3 acetylation at the IL-6 and IL-8 promoters was associated with recruitment of p65 and Brd4 proteins. Although p65 acetylation was increased this was not directly targeted by Brd4. The BET inhibitors JQ1 and PFI-1 significantly reduced IL-6 and CXCL8 expression whereas no effect was seen with the inactive enantiomer JQ1(-). Brd4, but not Brd2, knockdown markedly reduced IL-6 and CXCL8 release. JQ1 also inhibited p65 and Brd4 recruitment to the IL-6 and IL-8 promoters.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Azepines', 'Cell Line', 'Chromatin Immunoprecipitation', 'Enzyme-Linked Immunosorbent Assay', 'Epithelial Cells', 'Humans', 'Hydrogen Peroxide', 'Inflammation', 'Interleukin-1beta', 'Interleukin-6', 'Interleukin-8', 'Nuclear Proteins', 'Protein-Serine-Threonine Kinases', 'Transcription Factors', 'Triazoles']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,755,659 | Is the aryl hydrocarbon receptor constitutively active in advanced prostate cancer cells? | {
"contexts": [
"Distant prostate cancers are commonly hormone refractory and exhibit increased growth no longer inhibited by androgen deprivation therapy. Understanding all molecular mechanisms contributing to uncontrolled growth is important to obtain effective treatment strategies for hormone refractory prostate cancers (HRPC). The aryl hydrocarbon receptor (AhR) affects a number of biological processes including cell growth and differentiation. Several studies have revealed that exogenous AhR ligands inhibit cellular proliferation but recent evidence suggests AhR may possess intrinsic functions that promote cellular proliferation in the absence of exogenous ligands.",
"qRT-PCR and western blot analysis was used to determine AhR mRNA and protein expression in hormone sensitive LNCaP cells as well as hormone refractory DU145, PC3 and PC3M prostate cancer cell lines. LNCaP cells express AhR mRNA and protein at a much lower level than the hormone refractory cell models. Cellular fractionation and immunocytochemistry revealed nuclear localization of AhR in the established hormone refractory cell lines while LNCaP cells are devoid of nuclear AhR protein. qRT-PCR analysis used to assess basal CYP1B1 levels and a xenobiotic responsive element binding assay confirmed ligand independent transcriptional activity of AhR in DU145, PC3 and PC3M cells. Basal CYP1B1 levels were decreased by treatment with specific AhR inhibitor, CH223191. An in vitro growth assay revealed that CH223191 inhibited growth of DU145, PC3 and PC3M cells in an androgen depleted environment. Immunohistochemical staining of prostate cancer tissues revealed increased nuclear localization of AhR in grade 2 and grade 3 cancers compared to the well differentiated grade 1 cancers."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Androgens",
"Basic Helix-Loop-Helix Transcription Factors",
"Cell Line, Tumor",
"Cell Nucleus",
"Cell Proliferation",
"Gene Expression Regulation, Neoplastic",
"Humans",
"Ligands",
"Male",
"Neoplasm Staging",
"Prostatic Neoplasms",
"Protein Transport",
"RNA, Messenger",
"Receptors, Aryl Hydrocarbon",
"Signal Transduction",
"Subcellular Fractions",
"Transcription, Genetic"
]
} | Together, these results show that AhR is constitutively active in advanced prostate cancer cell lines that model hormone refractory prostate cancer. Chemical ablation of AhR signaling can reduce the growth of advanced prostate cancer cells, an effect not achieved with androgen receptor inhibitors or growth in androgen depleted media. | yes | [
{
"from": "human",
"value": "Question: Is the aryl hydrocarbon receptor constitutively active in advanced prostate cancer cells?\nContext: {'contexts': ['Distant prostate cancers are commonly hormone refractory and exhibit increased growth no longer inhibited by androgen deprivation therapy. Understanding all molecular mechanisms contributing to uncontrolled growth is important to obtain effective treatment strategies for hormone refractory prostate cancers (HRPC). The aryl hydrocarbon receptor (AhR) affects a number of biological processes including cell growth and differentiation. Several studies have revealed that exogenous AhR ligands inhibit cellular proliferation but recent evidence suggests AhR may possess intrinsic functions that promote cellular proliferation in the absence of exogenous ligands.', 'qRT-PCR and western blot analysis was used to determine AhR mRNA and protein expression in hormone sensitive LNCaP cells as well as hormone refractory DU145, PC3 and PC3M prostate cancer cell lines. LNCaP cells express AhR mRNA and protein at a much lower level than the hormone refractory cell models. Cellular fractionation and immunocytochemistry revealed nuclear localization of AhR in the established hormone refractory cell lines while LNCaP cells are devoid of nuclear AhR protein. qRT-PCR analysis used to assess basal CYP1B1 levels and a xenobiotic responsive element binding assay confirmed ligand independent transcriptional activity of AhR in DU145, PC3 and PC3M cells. Basal CYP1B1 levels were decreased by treatment with specific AhR inhibitor, CH223191. An in vitro growth assay revealed that CH223191 inhibited growth of DU145, PC3 and PC3M cells in an androgen depleted environment. Immunohistochemical staining of prostate cancer tissues revealed increased nuclear localization of AhR in grade 2 and grade 3 cancers compared to the well differentiated grade 1 cancers.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Androgens', 'Basic Helix-Loop-Helix Transcription Factors', 'Cell Line, Tumor', 'Cell Nucleus', 'Cell Proliferation', 'Gene Expression Regulation, Neoplastic', 'Humans', 'Ligands', 'Male', 'Neoplasm Staging', 'Prostatic Neoplasms', 'Protein Transport', 'RNA, Messenger', 'Receptors, Aryl Hydrocarbon', 'Signal Transduction', 'Subcellular Fractions', 'Transcription, Genetic']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,758,774 | Does phosphodiesterase 2A localized in the spinal cord contribute to inflammatory pain processing? | {
"contexts": [
"Phosphodiesterase 2A (PDE2A) is an evolutionarily conserved enzyme that catalyzes the degradation of the cyclic nucleotides, cyclic adenosine monophosphate, and/or cyclic guanosine monophosphate. Recent studies reported the expression of PDE2A in the dorsal horn of the spinal cord, pointing to a potential contribution to the processing of pain. However, the functions of PDE2A in spinal pain processing in vivo remained elusive.",
"Immunohistochemistry, laser microdissection, and quantitative real-time reverse transcription polymerase chain reaction experiments were performed to characterize the localization and regulation of PDE2A protein and messenger RNA in the mouse spinal cord. Effects of the selective PDE2A inhibitor, BAY 60-7550 (Cayman Chemical, Ann Arbor, MI), in animal models of inflammatory pain (n = 6 to 10), neuropathic pain (n = 5 to 6), and after intrathecal injection of cyclic nucleotides (n = 6 to 8) were examined. Also, cyclic adenosine monophosphate and cyclic guanosine monophosphate levels in spinal cord tissues were measured by liquid chromatography tandem mass spectrometry.",
"The authors here demonstrate that PDE2A is distinctly expressed in neurons of the superficial dorsal horn of the spinal cord, and that its spinal expression is upregulated in response to hind paw inflammation. Administration of the selective PDE2A inhibitor, BAY 60-7550, increased the nociceptive behavior of mice in animal models of inflammatory pain. Moreover, BAY 60-7550 increased the pain hypersensitivity induced by intrathecal delivery of cyclic adenosine monophosphate, but not of cyclic guanosine monophosphate, and it increased the cyclic adenosine monophosphate levels in spinal cord tissues."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Behavior, Animal",
"Cyclic AMP",
"Cyclic GMP",
"Cyclic Nucleotide Phosphodiesterases, Type 2",
"Drug Hypersensitivity",
"Imidazoles",
"Immunohistochemistry",
"Inflammation",
"Injections, Spinal",
"Male",
"Mice",
"Mice, Inbred C57BL",
"Microdissection",
"Neuralgia",
"Pain",
"Pain Measurement",
"Phosphodiesterase Inhibitors",
"Posterior Horn Cells",
"Real-Time Polymerase Chain Reaction",
"Spinal Cord",
"Triazines",
"Up-Regulation",
"Zymosan"
]
} | Our findings indicate that PDE2A contributes to the processing of inflammatory pain in the spinal cord. | yes | [
{
"from": "human",
"value": "Question: Does phosphodiesterase 2A localized in the spinal cord contribute to inflammatory pain processing?\nContext: {'contexts': ['Phosphodiesterase 2A (PDE2A) is an evolutionarily conserved enzyme that catalyzes the degradation of the cyclic nucleotides, cyclic adenosine monophosphate, and/or cyclic guanosine monophosphate. Recent studies reported the expression of PDE2A in the dorsal horn of the spinal cord, pointing to a potential contribution to the processing of pain. However, the functions of PDE2A in spinal pain processing in vivo remained elusive.', 'Immunohistochemistry, laser microdissection, and quantitative real-time reverse transcription polymerase chain reaction experiments were performed to characterize the localization and regulation of PDE2A protein and messenger RNA in the mouse spinal cord. Effects of the selective PDE2A inhibitor, BAY 60-7550 (Cayman Chemical, Ann Arbor, MI), in animal models of inflammatory pain (n = 6 to 10), neuropathic pain (n = 5 to 6), and after intrathecal injection of cyclic nucleotides (n = 6 to 8) were examined. Also, cyclic adenosine monophosphate and cyclic guanosine monophosphate levels in spinal cord tissues were measured by liquid chromatography tandem mass spectrometry.', 'The authors here demonstrate that PDE2A is distinctly expressed in neurons of the superficial dorsal horn of the spinal cord, and that its spinal expression is upregulated in response to hind paw inflammation. Administration of the selective PDE2A inhibitor, BAY 60-7550, increased the nociceptive behavior of mice in animal models of inflammatory pain. Moreover, BAY 60-7550 increased the pain hypersensitivity induced by intrathecal delivery of cyclic adenosine monophosphate, but not of cyclic guanosine monophosphate, and it increased the cyclic adenosine monophosphate levels in spinal cord tissues.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Behavior, Animal', 'Cyclic AMP', 'Cyclic GMP', 'Cyclic Nucleotide Phosphodiesterases, Type 2', 'Drug Hypersensitivity', 'Imidazoles', 'Immunohistochemistry', 'Inflammation', 'Injections, Spinal', 'Male', 'Mice', 'Mice, Inbred C57BL', 'Microdissection', 'Neuralgia', 'Pain', 'Pain Measurement', 'Phosphodiesterase Inhibitors', 'Posterior Horn Cells', 'Real-Time Polymerase Chain Reaction', 'Spinal Cord', 'Triazines', 'Up-Regulation', 'Zymosan']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,758,773 | Does isoflurane impair learning and hippocampal long-term potentiation via the saturation of synaptic plasticity? | {
"contexts": [
"General anesthesia induces long-lasting cognitive and learning deficits. However, the underlying mechanism remains unknown. The GluA1 subunit of AMPAR is a key molecule for learning and synaptic plasticity, which requires trafficking of GluA1-containing AMPARs into the synapse.",
"Adult male rats were exposed to 1.8% isoflurane for 2 h and subjected to an inhibitory avoidance task, which is a hippocampus-dependent contextual fear learning paradigm (n = 16 to 39). The in vitro extracellular field potential of hippocampal synapses between the Schaffer collateral and the CA1 was evaluated using a multielectrode recorder (n = 6 per group). GluA1 expression in the synaptoneurosome was assessed using Western blotting (n = 5 to 8). The ubiquitination level of GluA1 was evaluated using immunoprecipitation and Western blotting (n = 7 per group).",
"Seven days after exposure to 1.8% isoflurane for 2 h (Iso1.8), the inhibitory avoidance learning (control vs. Iso1.8; 294 ± 34 vs. 138 ± 28, the mean ± SEM [%]; P = 0.002) and long-term potentiation (125.7 ± 6.1 vs. 105.7 ± 3.3; P < 0.001) were impaired. Iso1.8 also temporarily increased GluA1 in the synaptoneurosomes (100 ± 9.7 vs. 138.9 ± 8.9; P = 0.012) and reduced the GluA1 ubiquitination, a main degradation pathway of GluA1 (100 ± 8.7 vs. 71.1 ± 6.1; P = 0.014)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Anesthetics, Inhalation",
"Animals",
"Behavior, Animal",
"Blood Gas Analysis",
"Blotting, Western",
"Cognition",
"Hemodynamics",
"Hippocampus",
"Immunoprecipitation",
"Isoflurane",
"Learning",
"Long-Term Potentiation",
"Male",
"Microelectrodes",
"Neuronal Plasticity",
"Rats",
"Rats, Wistar",
"Real-Time Polymerase Chain Reaction",
"Receptors, AMPA",
"Synapses",
"Ubiquitination"
]
} | Isoflurane impairs hippocampal learning and modulates synaptic plasticity in the postanesthetic period. Increased GluA1 may reduce synaptic capacity for additional GluA1-containing AMPARs trafficking. | yes | [
{
"from": "human",
"value": "Question: Does isoflurane impair learning and hippocampal long-term potentiation via the saturation of synaptic plasticity?\nContext: {'contexts': ['General anesthesia induces long-lasting cognitive and learning deficits. However, the underlying mechanism remains unknown. The GluA1 subunit of AMPAR is a key molecule for learning and synaptic plasticity, which requires trafficking of GluA1-containing AMPARs into the synapse.', 'Adult male rats were exposed to 1.8% isoflurane for 2 h and subjected to an inhibitory avoidance task, which is a hippocampus-dependent contextual fear learning paradigm (n = 16 to 39). The in vitro extracellular field potential of hippocampal synapses between the Schaffer collateral and the CA1 was evaluated using a multielectrode recorder (n = 6 per group). GluA1 expression in the synaptoneurosome was assessed using Western blotting (n = 5 to 8). The ubiquitination level of GluA1 was evaluated using immunoprecipitation and Western blotting (n = 7 per group).', 'Seven days after exposure to 1.8% isoflurane for 2 h (Iso1.8), the inhibitory avoidance learning (control vs. Iso1.8; 294 ± 34 vs. 138 ± 28, the mean ± SEM [%]; P = 0.002) and long-term potentiation (125.7 ± 6.1 vs. 105.7 ± 3.3; P < 0.001) were impaired. Iso1.8 also temporarily increased GluA1 in the synaptoneurosomes (100 ± 9.7 vs. 138.9 ± 8.9; P = 0.012) and reduced the GluA1 ubiquitination, a main degradation pathway of GluA1 (100 ± 8.7 vs. 71.1 ± 6.1; P = 0.014).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Anesthetics, Inhalation', 'Animals', 'Behavior, Animal', 'Blood Gas Analysis', 'Blotting, Western', 'Cognition', 'Hemodynamics', 'Hippocampus', 'Immunoprecipitation', 'Isoflurane', 'Learning', 'Long-Term Potentiation', 'Male', 'Microelectrodes', 'Neuronal Plasticity', 'Rats', 'Rats, Wistar', 'Real-Time Polymerase Chain Reaction', 'Receptors, AMPA', 'Synapses', 'Ubiquitination']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,764,694 | Is a prior diagnosis of breast cancer a risk factor for breast cancer in BRCA1 and BRCA2 carriers? | {
"contexts": [
"The risk of breast cancer in carriers of BRCA1 and BRCA2 mutations is influenced by factors other than the genetic mutation itself. Modifying factors include a woman's reproductive history and family history of cancer. Risk factors are more likely to be present in women with breast cancer than in women without breast cancer, and therefore the risk of cancer in the two breasts should not be independent. It is not clear to what extent modifying factors influence the risk of a first primary or a contralateral breast cancer in BRCA carriers.",
"We conducted a matched case-control study of breast cancer among 3920 BRCA1 or BRCA2 mutation carriers. We asked whether a past history of breast cancer in the contralateral breast was a risk factor for breast cancer.",
"After adjustment for age, country of residence, and cancer treatment, a previous cancer of the right breast was found to be a significant risk factor for cancer of the left breast among BRCA1 or BRCA2 carriers (relative risk: 2.1; 95% confidence interval: 1.4 to 3.0; p < 0.0001)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": []
} | In a woman with a BRCA1 or BRCA2 mutation who is diagnosed with breast cancer, the risk of cancer in the contralateral breast depends on the first diagnosis. That observation supports the hypothesis that there are important genetic or non-genetic modifiers of cancer risk in BRCA carriers. Discovering risk modifiers might lead to greater personalization of risk assessment and management recommendations for BRCA-positive patients. | yes | [
{
"from": "human",
"value": "Question: Is a prior diagnosis of breast cancer a risk factor for breast cancer in BRCA1 and BRCA2 carriers?\nContext: {'contexts': [\"The risk of breast cancer in carriers of BRCA1 and BRCA2 mutations is influenced by factors other than the genetic mutation itself. Modifying factors include a woman's reproductive history and family history of cancer. Risk factors are more likely to be present in women with breast cancer than in women without breast cancer, and therefore the risk of cancer in the two breasts should not be independent. It is not clear to what extent modifying factors influence the risk of a first primary or a contralateral breast cancer in BRCA carriers.\", 'We conducted a matched case-control study of breast cancer among 3920 BRCA1 or BRCA2 mutation carriers. We asked whether a past history of breast cancer in the contralateral breast was a risk factor for breast cancer.', 'After adjustment for age, country of residence, and cancer treatment, a previous cancer of the right breast was found to be a significant risk factor for cancer of the left breast among BRCA1 or BRCA2 carriers (relative risk: 2.1; 95% confidence interval: 1.4 to 3.0; p < 0.0001).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,769,122 | Is handgrip strength but not appendicular lean mass an independent predictor of functional outcome in hip-fracture women : a short-term prospective study? | {
"contexts": [
"To investigate the contribution of muscle mass and handgrip strength in predicting the functional outcome after hip fracture in women.",
"Observational study.",
"Rehabilitation hospital.",
"White women (N=123 of 149) who were consecutively admitted to a rehabilitation hospital because of their first fracture of the hip.",
"Not applicable.",
"We measured appendicular lean mass (aLM) by dual-energy x-ray absorptiometry (DXA) 21.1 ± 8.7 (mean ± SD) days after hip fracture occurrence in the 123 women. On the same day, we assessed grip strength at the nondominant arm with a dynamometer. At the end of acute inpatient rehabilitation we measured the ability to function in activities of daily living by using the Barthel Index, and lower limb performance by using the Timed Up and Go (TUG) test.",
"We found significant correlations between handgrip strength measured before rehabilitation and Barthel Index scores after rehabilitation (ρ=.50; P<.001), Barthel Index effectiveness (ρ=.45; P<.001), and the TUG test (ρ=-.41; P<.001). Conversely, we found no significant correlations between aLM/height(2) and Barthel Index scores after rehabilitation (ρ=.075; P=.41), Barthel Index effectiveness (ρ=.06; P=.53), or the TUG test (ρ=.005; P=.96). Significant associations between grip strength and all the outcome measures persisted after adjustment for 8 potential confounders, including Barthel Index scores before rehabilitation, age, number of medications, number of comorbidities, pressure ulcers, concomitant infections, time between fracture occurrence and assessment, and aLM/height(2)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"METHODS",
"METHODS",
"METHODS",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Body Composition",
"Disability Evaluation",
"Female",
"Hand Strength",
"Hip Fractures",
"Humans",
"Muscle, Skeletal",
"Physical Therapy Modalities",
"Predictive Value of Tests",
"Prospective Studies",
"Recovery of Function",
"Treatment Outcome"
]
} | Grip strength, but not DXA-assessed aLM, significantly predicted short-term functional outcome in women after a hip fracture. | yes | [
{
"from": "human",
"value": "Question: Is handgrip strength but not appendicular lean mass an independent predictor of functional outcome in hip-fracture women : a short-term prospective study?\nContext: {'contexts': ['To investigate the contribution of muscle mass and handgrip strength in predicting the functional outcome after hip fracture in women.', 'Observational study.', 'Rehabilitation hospital.', 'White women (N=123 of 149) who were consecutively admitted to a rehabilitation hospital because of their first fracture of the hip.', 'Not applicable.', 'We measured appendicular lean mass (aLM) by dual-energy x-ray absorptiometry (DXA) 21.1 ± 8.7 (mean ± SD) days after hip fracture occurrence in the 123 women. On the same day, we assessed grip strength at the nondominant arm with a dynamometer. At the end of acute inpatient rehabilitation we measured the ability to function in activities of daily living by using the Barthel Index, and lower limb performance by using the Timed Up and Go (TUG) test.', 'We found significant correlations between handgrip strength measured before rehabilitation and Barthel Index scores after rehabilitation (ρ=.50; P<.001), Barthel Index effectiveness (ρ=.45; P<.001), and the TUG test (ρ=-.41; P<.001). Conversely, we found no significant correlations between aLM/height(2) and Barthel Index scores after rehabilitation (ρ=.075; P=.41), Barthel Index effectiveness (ρ=.06; P=.53), or the TUG test (ρ=.005; P=.96). Significant associations between grip strength and all the outcome measures persisted after adjustment for 8 potential confounders, including Barthel Index scores before rehabilitation, age, number of medications, number of comorbidities, pressure ulcers, concomitant infections, time between fracture occurrence and assessment, and aLM/height(2).'], 'labels': ['OBJECTIVE', 'METHODS', 'METHODS', 'METHODS', 'METHODS', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Body Composition', 'Disability Evaluation', 'Female', 'Hand Strength', 'Hip Fractures', 'Humans', 'Muscle, Skeletal', 'Physical Therapy Modalities', 'Predictive Value of Tests', 'Prospective Studies', 'Recovery of Function', 'Treatment Outcome']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
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