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[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nTo investigate the effects of moxibustion on the morphology and function of mast cells (MC) at Tianshu (ST25) in rats with trinitro-benzene-sulfonic acid (TNBS)-induced colitis. A total of 53 male Sprague-Dawley rats were randomly divided into a normal group and experimental group. In the experimental group, a rat model of TNBS-induced colitis was established, and the rats were then randomly divided into a model group, moxibustion group, moxibustion plus disodium cromoglycate (M + DC) group and moxibustion plus normal saline (M + NS) group. Rats in the moxibustion group received suspended moxibustion at bilateral ST25 for 10 min, once a day for 7 d. Rats in the M + DC and M + NS groups were pretreated with disodium cromoglycate and normal saline at bilateral ST25, respectively, and were then concurrently subjected to the same treatment as rats in the moxibustion group. The hematoxylin-eosin staining method was used to observe histology of the colon and the toluidine blue-improved method was used to observe mast cells at ST25 acupoint areas. An improvement in colonic injury in the moxibustion group was observed and the degranulation ratio of MC at ST25 acupoint was markedly higher in the moxibustion group than in the model group (45.91 ± 11.41 vs 32.58 ± 8.28, P < 0.05). After inhibition of degranulation of MC at ST25 by disodium cromoglycate, no improvement in colon tissue injury was observed.\n\nQuestion:\nDoes moxibustion activate mast cell degranulation at the ST25 in rats with colitis?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nTo investigate the effects of moxibustion on the morphology and function of mast cells (MC) at Tianshu (ST25) in rats with trinitro-benzene-sulfonic acid (TNBS)-induced colitis. A total of 53 male Sprague-Dawley rats were randomly divided into a normal group and experimental group. In the experimental group, a rat model of TNBS-induced colitis was established, and the rats were then randomly divided into a model group, moxibustion group, moxibustion plus disodium cromoglycate (M + DC) group and moxibustion plus normal saline (M + NS) group. Rats in the moxibustion group received suspended moxibustion at bilateral ST25 for 10 min, once a day for 7 d. Rats in the M + DC and M + NS groups were pretreated with disodium cromoglycate and normal saline at bilateral ST25, respectively, and were then concurrently subjected to the same treatment as rats in the moxibustion group. The hematoxylin-eosin staining method was used to observe histology of the colon and the toluidine blue-improved method was used to observe mast cells at ST25 acupoint areas. An improvement in colonic injury in the moxibustion group was observed and the degranulation ratio of MC at ST25 acupoint was markedly higher in the moxibustion group than in the model group (45.91 ± 11.41 vs 32.58 ± 8.28, P < 0.05). After inhibition of degranulation of MC at ST25 by disodium cromoglycate, no improvement in colon tissue injury was observed.\n\nQuestion:\nDoes moxibustion activate mast cell degranulation at the ST25 in rats with colitis?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nTo investigate the effects of moxibustion on the morphology and function of mast cells (MC) at Tianshu (ST25) in rats with trinitro-benzene-sulfonic acid (TNBS)-induced colitis. A total of 53 male Sprague-Dawley rats were randomly divided into a normal group and experimental group. In the experimental group, a rat model of TNBS-induced colitis was established, and the rats were then randomly divided into a model group, moxibustion group, moxibustion plus disodium cromoglycate (M + DC) group and moxibustion plus normal saline (M + NS) group. Rats in the moxibustion group received suspended moxibustion at bilateral ST25 for 10 min, once a day for 7 d. Rats in the M + DC and M + NS groups were pretreated with disodium cromoglycate and normal saline at bilateral ST25, respectively, and were then concurrently subjected to the same treatment as rats in the moxibustion group. The hematoxylin-eosin staining method was used to observe histology of the colon and the toluidine blue-improved method was used to observe mast cells at ST25 acupoint areas. An improvement in colonic injury in the moxibustion group was observed and the degranulation ratio of MC at ST25 acupoint was markedly higher in the moxibustion group than in the model group (45.91 ± 11.41 vs 32.58 ± 8.28, P < 0.05). After inhibition of degranulation of MC at ST25 by disodium cromoglycate, no improvement in colon tissue injury was observed.\n\nQuestion:\nDoes moxibustion activate mast cell degranulation at the ST25 in rats with colitis?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nThe purpose of this study was to evaluate optic nerve blood flow in primary open-angle glaucoma suspect eyes with normal automated visual fields, in an attempt to elucidate how early in the glaucomatous disease process changes in optic nerve blood flow become apparent. Twenty-one eyes (21 patients) suspected of having primary open-angle glaucoma were studied prospectively and compared with a previously reported cohort of 22 eyes (22 patients) with primary open-angle glaucoma and 15 eyes (15 subjects) of age-matched controls. Primary open-angle glaucoma suspect eyes had untreated intraocular pressure greater than 21 mm Hg and normal visual fields using Humphrey program 24-2 or 30-2 with a full threshold strategy. Laser Doppler flowmetry was used to measure optic nerve head blood velocity, volume, and flow at four quadrants in the optic nerve, in the cup, and in the foveola of one eye of each patient. The mean flow from the superotemporal rim, inferotemporal rim, and cup was calculated (Flow(3)) and identified as the main outcome measure. Measurements from primary open-angle glaucoma suspect eyes were compared with corresponding measurements from controls and eyes with primary open-angle glaucoma; a Student t test was employed with a Bonferroni corrected P value of.025 to account for comparisons of primary open-angle glaucoma suspects both to controls and to eyes with primary open-angle glaucoma. Compared with controls, Flow(3) was 24% lower in primary open-angle glaucoma suspect eyes (P <.0003). In primary open-angle glaucoma suspect eyes, flow was 16% lower in the superotemporal rim (P <.007), 35% lower in the cup (P <.007), and 22% lower in the inferotemporal neuroretinal rim (P <.029) compared with controls. No significant difference between primary open-angle glaucoma suspect and control eyes was seen in the inferonasal rim, superonasal rim, or foveola. No significant difference was detected at any location between primary open-angle glaucoma suspect eyes and eyes with primary open-angle glaucoma.\n\nQuestion:\nIs optic nerve blood flow diminished in eyes of primary open-angle glaucoma suspects?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nThe purpose of this study was to evaluate optic nerve blood flow in primary open-angle glaucoma suspect eyes with normal automated visual fields, in an attempt to elucidate how early in the glaucomatous disease process changes in optic nerve blood flow become apparent. Twenty-one eyes (21 patients) suspected of having primary open-angle glaucoma were studied prospectively and compared with a previously reported cohort of 22 eyes (22 patients) with primary open-angle glaucoma and 15 eyes (15 subjects) of age-matched controls. Primary open-angle glaucoma suspect eyes had untreated intraocular pressure greater than 21 mm Hg and normal visual fields using Humphrey program 24-2 or 30-2 with a full threshold strategy. Laser Doppler flowmetry was used to measure optic nerve head blood velocity, volume, and flow at four quadrants in the optic nerve, in the cup, and in the foveola of one eye of each patient. The mean flow from the superotemporal rim, inferotemporal rim, and cup was calculated (Flow(3)) and identified as the main outcome measure. Measurements from primary open-angle glaucoma suspect eyes were compared with corresponding measurements from controls and eyes with primary open-angle glaucoma; a Student t test was employed with a Bonferroni corrected P value of.025 to account for comparisons of primary open-angle glaucoma suspects both to controls and to eyes with primary open-angle glaucoma. Compared with controls, Flow(3) was 24% lower in primary open-angle glaucoma suspect eyes (P <.0003). In primary open-angle glaucoma suspect eyes, flow was 16% lower in the superotemporal rim (P <.007), 35% lower in the cup (P <.007), and 22% lower in the inferotemporal neuroretinal rim (P <.029) compared with controls. No significant difference between primary open-angle glaucoma suspect and control eyes was seen in the inferonasal rim, superonasal rim, or foveola. No significant difference was detected at any location between primary open-angle glaucoma suspect eyes and eyes with primary open-angle glaucoma.\n\nQuestion:\nIs optic nerve blood flow diminished in eyes of primary open-angle glaucoma suspects?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nThe purpose of this study was to evaluate optic nerve blood flow in primary open-angle glaucoma suspect eyes with normal automated visual fields, in an attempt to elucidate how early in the glaucomatous disease process changes in optic nerve blood flow become apparent. Twenty-one eyes (21 patients) suspected of having primary open-angle glaucoma were studied prospectively and compared with a previously reported cohort of 22 eyes (22 patients) with primary open-angle glaucoma and 15 eyes (15 subjects) of age-matched controls. Primary open-angle glaucoma suspect eyes had untreated intraocular pressure greater than 21 mm Hg and normal visual fields using Humphrey program 24-2 or 30-2 with a full threshold strategy. Laser Doppler flowmetry was used to measure optic nerve head blood velocity, volume, and flow at four quadrants in the optic nerve, in the cup, and in the foveola of one eye of each patient. The mean flow from the superotemporal rim, inferotemporal rim, and cup was calculated (Flow(3)) and identified as the main outcome measure. Measurements from primary open-angle glaucoma suspect eyes were compared with corresponding measurements from controls and eyes with primary open-angle glaucoma; a Student t test was employed with a Bonferroni corrected P value of.025 to account for comparisons of primary open-angle glaucoma suspects both to controls and to eyes with primary open-angle glaucoma. Compared with controls, Flow(3) was 24% lower in primary open-angle glaucoma suspect eyes (P <.0003). In primary open-angle glaucoma suspect eyes, flow was 16% lower in the superotemporal rim (P <.007), 35% lower in the cup (P <.007), and 22% lower in the inferotemporal neuroretinal rim (P <.029) compared with controls. No significant difference between primary open-angle glaucoma suspect and control eyes was seen in the inferonasal rim, superonasal rim, or foveola. No significant difference was detected at any location between primary open-angle glaucoma suspect eyes and eyes with primary open-angle glaucoma.\n\nQuestion:\nIs optic nerve blood flow diminished in eyes of primary open-angle glaucoma suspects?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nThe purpose of this study was to probe the pleiotrophic effects of Atorvastatin on intraplatelet-nitric oxide metabolism. Hyperlipidemic subjects (n = 19) were treated for 1 month (following a 3-week washout) with either Atorvastatin or placebo in a double-blinded randomized (n = 2, crossover), placebo-controlled study. Changes in the levels of intraplatelet nitric oxide synthase, nitrotyrosine were correlated with cholesterol, LDL-C, HDL-C and triglyceride levels. These studies indicate that with atrovastatin ecNOS levels increased on average by approximately approximately 1.7-fold (paired t-test p = 0.009). Interestingly, levels of nitrotyrosylated platelet proteins, an indication of peroxynitrite damage, decreased as ecNOS levels increased in presence of the drug (paired t-test p = 0.33). Atorvastatin, at 10 mg per day, lowered cholesterol and LDL-C levels in all patients with the average lowering of approximately 21% and approximately 17% respectively. The effect on HDL was not significant whilst triglyceride levels were lowered by an average of approximately 18%.\n\nQuestion:\nDoes atorvastatin increase ecNOS levels in human platelets of hyperlipidemic subjects?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nThe purpose of this study was to probe the pleiotrophic effects of Atorvastatin on intraplatelet-nitric oxide metabolism. Hyperlipidemic subjects (n = 19) were treated for 1 month (following a 3-week washout) with either Atorvastatin or placebo in a double-blinded randomized (n = 2, crossover), placebo-controlled study. Changes in the levels of intraplatelet nitric oxide synthase, nitrotyrosine were correlated with cholesterol, LDL-C, HDL-C and triglyceride levels. These studies indicate that with atrovastatin ecNOS levels increased on average by approximately approximately 1.7-fold (paired t-test p = 0.009). Interestingly, levels of nitrotyrosylated platelet proteins, an indication of peroxynitrite damage, decreased as ecNOS levels increased in presence of the drug (paired t-test p = 0.33). Atorvastatin, at 10 mg per day, lowered cholesterol and LDL-C levels in all patients with the average lowering of approximately 21% and approximately 17% respectively. The effect on HDL was not significant whilst triglyceride levels were lowered by an average of approximately 18%.\n\nQuestion:\nDoes atorvastatin increase ecNOS levels in human platelets of hyperlipidemic subjects?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nThe purpose of this study was to probe the pleiotrophic effects of Atorvastatin on intraplatelet-nitric oxide metabolism. Hyperlipidemic subjects (n = 19) were treated for 1 month (following a 3-week washout) with either Atorvastatin or placebo in a double-blinded randomized (n = 2, crossover), placebo-controlled study. Changes in the levels of intraplatelet nitric oxide synthase, nitrotyrosine were correlated with cholesterol, LDL-C, HDL-C and triglyceride levels. These studies indicate that with atrovastatin ecNOS levels increased on average by approximately approximately 1.7-fold (paired t-test p = 0.009). Interestingly, levels of nitrotyrosylated platelet proteins, an indication of peroxynitrite damage, decreased as ecNOS levels increased in presence of the drug (paired t-test p = 0.33). Atorvastatin, at 10 mg per day, lowered cholesterol and LDL-C levels in all patients with the average lowering of approximately 21% and approximately 17% respectively. The effect on HDL was not significant whilst triglyceride levels were lowered by an average of approximately 18%.\n\nQuestion:\nDoes atorvastatin increase ecNOS levels in human platelets of hyperlipidemic subjects?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nIschemia/reperfusion (I/R) injury is a major cause of primary graft dysfunction and renders an allograft more immunogenic in orthotopic liver transplantation (OLT). Panax notoginseng saponins (PNS) has been reported to exert protective effects against I/R injury to various organs. The objective of this study is to investigate whether PNS preconditioning protects rat liver grafts from I/R injury via an antiapoptotic pathway. Male Sprague-Dawley rats were used as donors and recipients of orthotopic liver transplantation (OLT) and were divided into PNS preconditioning group(group P) and normal saline control group (group N) randomly according to whether PNS (50 mg/kg) was injected intravenously 1 hour before liver grafts harvesting, and sham group (group S). The animals were separately killed 2, 6 and 24 hours after reperfusion. Plasma samples were collected for test of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Liver tissues were collected to detect histological changes, apoptosis and the expression of TNF-alpha, Bcl-2 and Caspase-3 mRNA. The serum levels of ALT and AST and the apoptosis index (AI) of liver tissue in group P were lower than in group N significantly 2, 6 and 24 hours after reperfusion. Compared with group N, the expression of TNF-alpha and Caspase-3 mRNA was reduced significantly in group P 2 and 6 hours after reperfusion and the expression of Bcl-2 mRNA was enhanced significantly in group P 6 and 24 hours after reperfusion.\n\nQuestion:\nDoes panax notoginseng saponins preconditioning protect rat liver grafts from ischemia/reperfusion injury via an antiapoptotic pathway?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nIschemia/reperfusion (I/R) injury is a major cause of primary graft dysfunction and renders an allograft more immunogenic in orthotopic liver transplantation (OLT). Panax notoginseng saponins (PNS) has been reported to exert protective effects against I/R injury to various organs. The objective of this study is to investigate whether PNS preconditioning protects rat liver grafts from I/R injury via an antiapoptotic pathway. Male Sprague-Dawley rats were used as donors and recipients of orthotopic liver transplantation (OLT) and were divided into PNS preconditioning group(group P) and normal saline control group (group N) randomly according to whether PNS (50 mg/kg) was injected intravenously 1 hour before liver grafts harvesting, and sham group (group S). The animals were separately killed 2, 6 and 24 hours after reperfusion. Plasma samples were collected for test of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Liver tissues were collected to detect histological changes, apoptosis and the expression of TNF-alpha, Bcl-2 and Caspase-3 mRNA. The serum levels of ALT and AST and the apoptosis index (AI) of liver tissue in group P were lower than in group N significantly 2, 6 and 24 hours after reperfusion. Compared with group N, the expression of TNF-alpha and Caspase-3 mRNA was reduced significantly in group P 2 and 6 hours after reperfusion and the expression of Bcl-2 mRNA was enhanced significantly in group P 6 and 24 hours after reperfusion.\n\nQuestion:\nDoes panax notoginseng saponins preconditioning protect rat liver grafts from ischemia/reperfusion injury via an antiapoptotic pathway?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nIschemia/reperfusion (I/R) injury is a major cause of primary graft dysfunction and renders an allograft more immunogenic in orthotopic liver transplantation (OLT). Panax notoginseng saponins (PNS) has been reported to exert protective effects against I/R injury to various organs. The objective of this study is to investigate whether PNS preconditioning protects rat liver grafts from I/R injury via an antiapoptotic pathway. Male Sprague-Dawley rats were used as donors and recipients of orthotopic liver transplantation (OLT) and were divided into PNS preconditioning group(group P) and normal saline control group (group N) randomly according to whether PNS (50 mg/kg) was injected intravenously 1 hour before liver grafts harvesting, and sham group (group S). The animals were separately killed 2, 6 and 24 hours after reperfusion. Plasma samples were collected for test of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Liver tissues were collected to detect histological changes, apoptosis and the expression of TNF-alpha, Bcl-2 and Caspase-3 mRNA. The serum levels of ALT and AST and the apoptosis index (AI) of liver tissue in group P were lower than in group N significantly 2, 6 and 24 hours after reperfusion. Compared with group N, the expression of TNF-alpha and Caspase-3 mRNA was reduced significantly in group P 2 and 6 hours after reperfusion and the expression of Bcl-2 mRNA was enhanced significantly in group P 6 and 24 hours after reperfusion.\n\nQuestion:\nDoes panax notoginseng saponins preconditioning protect rat liver grafts from ischemia/reperfusion injury via an antiapoptotic pathway?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nRecently rat vascular smooth-muscle cells (VSMC) have been shown to possess Epo receptor, and respond to various cytokines for producing nitric oxide (NO). In the present study we examined the effect of pharmacological dose of human recombinant erythropoietin (rHuEpo) on the IL-1beta-induced NO and cGMP production as well as inducible nitric oxide synthase (iNOS) in cultured rat VSMC. Nitrite, a stable metabolite of NO, and intracellular cGMP contents were assayed by Griess method and enzyme immunoassay. iNOS mRNA expression was analysed by Northern blotting. RHuEpo inhibited IL-1beta-induced nitrite production in a dose- and time-dependent manner with concomitant changes of intracellular cGMP contents. On the other hand, rHuEpo did not inhibit atrial natriuretic peptide- (ANP) or sodium nitroprusside (SNP)-induced nitrite and cGMP production at all. While rHuEpo inhibited IL-1beta-induced iNOS mRNA expression, rHuEpo vehicle did not affect IL-1beta-induced iNOS mRNA expression.\n\nQuestion:\nDoes human recombinant erythropoietin inhibit interleukin-1beta-stimulated nitric oxide and cyclic guanosine monophosphate production in cultured rat vascular smooth-muscle cells?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nRecently rat vascular smooth-muscle cells (VSMC) have been shown to possess Epo receptor, and respond to various cytokines for producing nitric oxide (NO). In the present study we examined the effect of pharmacological dose of human recombinant erythropoietin (rHuEpo) on the IL-1beta-induced NO and cGMP production as well as inducible nitric oxide synthase (iNOS) in cultured rat VSMC. Nitrite, a stable metabolite of NO, and intracellular cGMP contents were assayed by Griess method and enzyme immunoassay. iNOS mRNA expression was analysed by Northern blotting. RHuEpo inhibited IL-1beta-induced nitrite production in a dose- and time-dependent manner with concomitant changes of intracellular cGMP contents. On the other hand, rHuEpo did not inhibit atrial natriuretic peptide- (ANP) or sodium nitroprusside (SNP)-induced nitrite and cGMP production at all. While rHuEpo inhibited IL-1beta-induced iNOS mRNA expression, rHuEpo vehicle did not affect IL-1beta-induced iNOS mRNA expression.\n\nQuestion:\nDoes human recombinant erythropoietin inhibit interleukin-1beta-stimulated nitric oxide and cyclic guanosine monophosphate production in cultured rat vascular smooth-muscle cells?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nRecently rat vascular smooth-muscle cells (VSMC) have been shown to possess Epo receptor, and respond to various cytokines for producing nitric oxide (NO). In the present study we examined the effect of pharmacological dose of human recombinant erythropoietin (rHuEpo) on the IL-1beta-induced NO and cGMP production as well as inducible nitric oxide synthase (iNOS) in cultured rat VSMC. Nitrite, a stable metabolite of NO, and intracellular cGMP contents were assayed by Griess method and enzyme immunoassay. iNOS mRNA expression was analysed by Northern blotting. RHuEpo inhibited IL-1beta-induced nitrite production in a dose- and time-dependent manner with concomitant changes of intracellular cGMP contents. On the other hand, rHuEpo did not inhibit atrial natriuretic peptide- (ANP) or sodium nitroprusside (SNP)-induced nitrite and cGMP production at all. While rHuEpo inhibited IL-1beta-induced iNOS mRNA expression, rHuEpo vehicle did not affect IL-1beta-induced iNOS mRNA expression.\n\nQuestion:\nDoes human recombinant erythropoietin inhibit interleukin-1beta-stimulated nitric oxide and cyclic guanosine monophosphate production in cultured rat vascular smooth-muscle cells?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nKruppel-like factors (Klfs) are a family of transcription factors consisting of 17 members in mammals, Klf1-Klf17, which are involved in fundamental cellular physiological procedures, such as cell proliferation, differentiation, and apoptosis. However, their functions in embryonic development have been poorly understood. Our previous study has demonstrated that the pluripotency factor Klf4 participates in germ layer formation and axis patterning of Xenopus embryos by means of the regulation of key developmental signals. In the present study, we further investigated comprehensively the expression and functions of the klf family genes, klf2, klf5, klf6, klf7, klf8, klf11, klf15, and klf17, during the embryogenesis of Xenopus laevis. Spatio-temporal expression analyses demonstrate that these genes are transcribed both maternally and zygotically in Xenopus embryos, and during organogenesis and tissue differentiation, they are localized to a variety of placodes and tissues. Gain and loss of function studies manifest that Klf factors play different roles in germ layer formation and body axis patterning. Moreover, each Klf factor exhibits distinct regulatory effects on the expression of genes that are essential for germ layer formation and body axis patterning.\n\nQuestion:\nAre kruppel-like factor family genes expressed during Xenopus embryogenesis and involved in germ layer formation and body axis patterning?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nKruppel-like factors (Klfs) are a family of transcription factors consisting of 17 members in mammals, Klf1-Klf17, which are involved in fundamental cellular physiological procedures, such as cell proliferation, differentiation, and apoptosis. However, their functions in embryonic development have been poorly understood. Our previous study has demonstrated that the pluripotency factor Klf4 participates in germ layer formation and axis patterning of Xenopus embryos by means of the regulation of key developmental signals. In the present study, we further investigated comprehensively the expression and functions of the klf family genes, klf2, klf5, klf6, klf7, klf8, klf11, klf15, and klf17, during the embryogenesis of Xenopus laevis. Spatio-temporal expression analyses demonstrate that these genes are transcribed both maternally and zygotically in Xenopus embryos, and during organogenesis and tissue differentiation, they are localized to a variety of placodes and tissues. Gain and loss of function studies manifest that Klf factors play different roles in germ layer formation and body axis patterning. Moreover, each Klf factor exhibits distinct regulatory effects on the expression of genes that are essential for germ layer formation and body axis patterning.\n\nQuestion:\nAre kruppel-like factor family genes expressed during Xenopus embryogenesis and involved in germ layer formation and body axis patterning?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nKruppel-like factors (Klfs) are a family of transcription factors consisting of 17 members in mammals, Klf1-Klf17, which are involved in fundamental cellular physiological procedures, such as cell proliferation, differentiation, and apoptosis. However, their functions in embryonic development have been poorly understood. Our previous study has demonstrated that the pluripotency factor Klf4 participates in germ layer formation and axis patterning of Xenopus embryos by means of the regulation of key developmental signals. In the present study, we further investigated comprehensively the expression and functions of the klf family genes, klf2, klf5, klf6, klf7, klf8, klf11, klf15, and klf17, during the embryogenesis of Xenopus laevis. Spatio-temporal expression analyses demonstrate that these genes are transcribed both maternally and zygotically in Xenopus embryos, and during organogenesis and tissue differentiation, they are localized to a variety of placodes and tissues. Gain and loss of function studies manifest that Klf factors play different roles in germ layer formation and body axis patterning. Moreover, each Klf factor exhibits distinct regulatory effects on the expression of genes that are essential for germ layer formation and body axis patterning.\n\nQuestion:\nAre kruppel-like factor family genes expressed during Xenopus embryogenesis and involved in germ layer formation and body axis patterning?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nRecent efforts to increase CRT response by multiSPOT pacing (MSP) from multiple bipols on the same left ventricular lead are still inconclusive. The Left Ventricular (LV) MultiSPOTpacing for CRT (iSPOT) study compared the acute hemodynamic response of MSP pacing by using 3 electrodes on a quadripolar lead compared with conventional biventricular pacing (BiV). Patients with left bundle branch block (LBBB) underwent an acute hemodynamic study to determine the %change in LV+dP/dtmax from baseline atrial pacing compared to the following configurations: BiV pacing with the LV lead in a one of lateral veins, while pacing from the distal, mid, or proximal electrode and all 3 electrodes together (i.e. MSP). All measurements were repeated 4 times at 5 different atrioventricular delays. We also measured QRS-width and individual Q-LV durations. Protocol was completed in 24 patients, all with LBBB (QRS width 171±20 ms) and 58% ischemic aetiology. The percentage change in LV+dP/dtmax for MSP pacing was 31.0±3.3% (Mean±SE), which was not significantly superior to any BiV pacing configuration: 28.9±3.2% (LV-distal), 28.3±2.7% (LV-mid), and 29.5±3.0% (LV-prox), respectively. Correlation between LV+dP/dtmax and either QRS-width or Q-LV ratio was poor.\n\nQuestion:\nDoes in Heart Failure Patients with Left Bundle Branch Block Single Lead MultiSpot Left Ventricular Pacing Improve Acute Hemodynamic Response To Conventional Biventricular Pacing . A Multicenter Prospective , Interventional , Non-Randomized Study?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nRecent efforts to increase CRT response by multiSPOT pacing (MSP) from multiple bipols on the same left ventricular lead are still inconclusive. The Left Ventricular (LV) MultiSPOTpacing for CRT (iSPOT) study compared the acute hemodynamic response of MSP pacing by using 3 electrodes on a quadripolar lead compared with conventional biventricular pacing (BiV). Patients with left bundle branch block (LBBB) underwent an acute hemodynamic study to determine the %change in LV+dP/dtmax from baseline atrial pacing compared to the following configurations: BiV pacing with the LV lead in a one of lateral veins, while pacing from the distal, mid, or proximal electrode and all 3 electrodes together (i.e. MSP). All measurements were repeated 4 times at 5 different atrioventricular delays. We also measured QRS-width and individual Q-LV durations. Protocol was completed in 24 patients, all with LBBB (QRS width 171±20 ms) and 58% ischemic aetiology. The percentage change in LV+dP/dtmax for MSP pacing was 31.0±3.3% (Mean±SE), which was not significantly superior to any BiV pacing configuration: 28.9±3.2% (LV-distal), 28.3±2.7% (LV-mid), and 29.5±3.0% (LV-prox), respectively. Correlation between LV+dP/dtmax and either QRS-width or Q-LV ratio was poor.\n\nQuestion:\nDoes in Heart Failure Patients with Left Bundle Branch Block Single Lead MultiSpot Left Ventricular Pacing Improve Acute Hemodynamic Response To Conventional Biventricular Pacing . A Multicenter Prospective , Interventional , Non-Randomized Study?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nRecent efforts to increase CRT response by multiSPOT pacing (MSP) from multiple bipols on the same left ventricular lead are still inconclusive. The Left Ventricular (LV) MultiSPOTpacing for CRT (iSPOT) study compared the acute hemodynamic response of MSP pacing by using 3 electrodes on a quadripolar lead compared with conventional biventricular pacing (BiV). Patients with left bundle branch block (LBBB) underwent an acute hemodynamic study to determine the %change in LV+dP/dtmax from baseline atrial pacing compared to the following configurations: BiV pacing with the LV lead in a one of lateral veins, while pacing from the distal, mid, or proximal electrode and all 3 electrodes together (i.e. MSP). All measurements were repeated 4 times at 5 different atrioventricular delays. We also measured QRS-width and individual Q-LV durations. Protocol was completed in 24 patients, all with LBBB (QRS width 171±20 ms) and 58% ischemic aetiology. The percentage change in LV+dP/dtmax for MSP pacing was 31.0±3.3% (Mean±SE), which was not significantly superior to any BiV pacing configuration: 28.9±3.2% (LV-distal), 28.3±2.7% (LV-mid), and 29.5±3.0% (LV-prox), respectively. Correlation between LV+dP/dtmax and either QRS-width or Q-LV ratio was poor.\n\nQuestion:\nDoes in Heart Failure Patients with Left Bundle Branch Block Single Lead MultiSpot Left Ventricular Pacing Improve Acute Hemodynamic Response To Conventional Biventricular Pacing . A Multicenter Prospective , Interventional , Non-Randomized Study?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nAn increasing number of papers have documented the contribution of chronic periodontitis (P) to the pathogenesis of cardiovascular disease. The aim of this study was to answer the question whether there is an association between periodontal inflammation and atherosclerotic processes in hemodialysis patients with chronic kidney disease (CKD). Forty-four hemodialysis patients with CKD were considered. Advanced chronic periodontitis was found in 17, whereas 27 patients had no or moderate chronic periodontitis. In all patients examined, serum C-reactive protein (CRP), TNF-alfa and IL-6 concentrations, as well as intima-media thickness (IMT) of the carotid artery, were assessed. Patients with CKD and advanced periodontitis were characterized by a significantly higher serum CRP concentration (13.2 +/- 11.4 vs. 10.4 +/- 14.4; p<0.05) and IMT (0.742 +/- 0.028 vs. 0.656 +/- 0.019, p<0.05) than CKD patients without periodontitis. In the univariate analysis, a significant correlation between CRP and number of atherosclerotic plaques was revealed; however, it was not confirmed as an independent relationship in the multiple regression analysis.\n\nQuestion:\nIs chronic periodontitis in hemodialysis patients with chronic kidney disease associated with elevated serum C-reactive protein concentration and greater intima-media thickness of the carotid artery?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nAn increasing number of papers have documented the contribution of chronic periodontitis (P) to the pathogenesis of cardiovascular disease. The aim of this study was to answer the question whether there is an association between periodontal inflammation and atherosclerotic processes in hemodialysis patients with chronic kidney disease (CKD). Forty-four hemodialysis patients with CKD were considered. Advanced chronic periodontitis was found in 17, whereas 27 patients had no or moderate chronic periodontitis. In all patients examined, serum C-reactive protein (CRP), TNF-alfa and IL-6 concentrations, as well as intima-media thickness (IMT) of the carotid artery, were assessed. Patients with CKD and advanced periodontitis were characterized by a significantly higher serum CRP concentration (13.2 +/- 11.4 vs. 10.4 +/- 14.4; p<0.05) and IMT (0.742 +/- 0.028 vs. 0.656 +/- 0.019, p<0.05) than CKD patients without periodontitis. In the univariate analysis, a significant correlation between CRP and number of atherosclerotic plaques was revealed; however, it was not confirmed as an independent relationship in the multiple regression analysis.\n\nQuestion:\nIs chronic periodontitis in hemodialysis patients with chronic kidney disease associated with elevated serum C-reactive protein concentration and greater intima-media thickness of the carotid artery?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nAn increasing number of papers have documented the contribution of chronic periodontitis (P) to the pathogenesis of cardiovascular disease. The aim of this study was to answer the question whether there is an association between periodontal inflammation and atherosclerotic processes in hemodialysis patients with chronic kidney disease (CKD). Forty-four hemodialysis patients with CKD were considered. Advanced chronic periodontitis was found in 17, whereas 27 patients had no or moderate chronic periodontitis. In all patients examined, serum C-reactive protein (CRP), TNF-alfa and IL-6 concentrations, as well as intima-media thickness (IMT) of the carotid artery, were assessed. Patients with CKD and advanced periodontitis were characterized by a significantly higher serum CRP concentration (13.2 +/- 11.4 vs. 10.4 +/- 14.4; p<0.05) and IMT (0.742 +/- 0.028 vs. 0.656 +/- 0.019, p<0.05) than CKD patients without periodontitis. In the univariate analysis, a significant correlation between CRP and number of atherosclerotic plaques was revealed; however, it was not confirmed as an independent relationship in the multiple regression analysis.\n\nQuestion:\nIs chronic periodontitis in hemodialysis patients with chronic kidney disease associated with elevated serum C-reactive protein concentration and greater intima-media thickness of the carotid artery?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nThe heme oxygenase-1 (HO-1) system is associated with the rate-limiting step of conversion of heme, one of the most critical roles in cytoprotective mechanisms. Our study investigated its potential role in protection of endothelial cells from T cells. The recombinant plasmid pcDNA3-HO-1 was transfected into endothelial cells. Indirect fluorescent staining was used to examine the expression of HO-1 protein. Then endothelial cells primed by INF-gamma were mixed in culture with Jurkat T cells labeled with carboxyfluorescein diacetate succinimidyl ester (CFSE). The number of adhesive Jurkat T cells was determined using FACS to evaluate the adhesion effect. After being cultured with endothelial cells, the cell cycle of Jurkat T cells was detected using FACS. Expression of HO-1 on endothelial cells conferred significant protection against Jurkat T-cell-mediated adhesion. The rate of Jurkat T-cell adhesions was reduced to 19.06%, in contrast with 31.42% in the control group (P<.05). After using ZnPP, an inhibitor of HO-1, the rate of Jurkat T-cell adhesion recovered to 29.08%. The binding activities between endothelial cells and Jurkat T cells was blocked by HO-1 expression. The proliferation of Jurkat T cells was inhibited after culture with endothelial cells, which had been transfected with HO-1, which blocked cell cycle entry of T cells. More than 60% of Jurkat T cells remained in G0/G1 compared with 40% among the control group.\n\nQuestion:\nDoes heme oxygenase-1 protect INF-gamma primed endothelial cells from Jurkat T-cell adhesion?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nThe heme oxygenase-1 (HO-1) system is associated with the rate-limiting step of conversion of heme, one of the most critical roles in cytoprotective mechanisms. Our study investigated its potential role in protection of endothelial cells from T cells. The recombinant plasmid pcDNA3-HO-1 was transfected into endothelial cells. Indirect fluorescent staining was used to examine the expression of HO-1 protein. Then endothelial cells primed by INF-gamma were mixed in culture with Jurkat T cells labeled with carboxyfluorescein diacetate succinimidyl ester (CFSE). The number of adhesive Jurkat T cells was determined using FACS to evaluate the adhesion effect. After being cultured with endothelial cells, the cell cycle of Jurkat T cells was detected using FACS. Expression of HO-1 on endothelial cells conferred significant protection against Jurkat T-cell-mediated adhesion. The rate of Jurkat T-cell adhesions was reduced to 19.06%, in contrast with 31.42% in the control group (P<.05). After using ZnPP, an inhibitor of HO-1, the rate of Jurkat T-cell adhesion recovered to 29.08%. The binding activities between endothelial cells and Jurkat T cells was blocked by HO-1 expression. The proliferation of Jurkat T cells was inhibited after culture with endothelial cells, which had been transfected with HO-1, which blocked cell cycle entry of T cells. More than 60% of Jurkat T cells remained in G0/G1 compared with 40% among the control group.\n\nQuestion:\nDoes heme oxygenase-1 protect INF-gamma primed endothelial cells from Jurkat T-cell adhesion?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nThe heme oxygenase-1 (HO-1) system is associated with the rate-limiting step of conversion of heme, one of the most critical roles in cytoprotective mechanisms. Our study investigated its potential role in protection of endothelial cells from T cells. The recombinant plasmid pcDNA3-HO-1 was transfected into endothelial cells. Indirect fluorescent staining was used to examine the expression of HO-1 protein. Then endothelial cells primed by INF-gamma were mixed in culture with Jurkat T cells labeled with carboxyfluorescein diacetate succinimidyl ester (CFSE). The number of adhesive Jurkat T cells was determined using FACS to evaluate the adhesion effect. After being cultured with endothelial cells, the cell cycle of Jurkat T cells was detected using FACS. Expression of HO-1 on endothelial cells conferred significant protection against Jurkat T-cell-mediated adhesion. The rate of Jurkat T-cell adhesions was reduced to 19.06%, in contrast with 31.42% in the control group (P<.05). After using ZnPP, an inhibitor of HO-1, the rate of Jurkat T-cell adhesion recovered to 29.08%. The binding activities between endothelial cells and Jurkat T cells was blocked by HO-1 expression. The proliferation of Jurkat T cells was inhibited after culture with endothelial cells, which had been transfected with HO-1, which blocked cell cycle entry of T cells. More than 60% of Jurkat T cells remained in G0/G1 compared with 40% among the control group.\n\nQuestion:\nDoes heme oxygenase-1 protect INF-gamma primed endothelial cells from Jurkat T-cell adhesion?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nMontreal Cognitive Assessment (MoCA) has been proposed as a screening tool in vascular cognitive impairment. Diffusion tensor imaging is sensitive to white matter microstructural damage. We investigated if diffusion tensor imaging-derived indices are more strongly associated with performances on MoCA or on the widely used mini mental state examination in patients with mild cognitive impairment and small vessel disease. Mild cognitive impairment patients with moderate/severe degrees of white matter hyperintensities on MRI were enrolled. Lacunar infarcts, cortical atrophy, medial temporal lobe atrophy and median values of mean diffusivity and fractional anisotropy of the cerebral white matter were studied and correlated with cognitive tests performances. Seventy-six patients (mean age 75.1±6.8 years, mean years of education 8.0±4.3) were assessed. In univariate analyses, a significant association of both MoCA and mini mental state examination scores with age, education, cortical atrophy, and medial temporal lobe atrophy was found, whereas mean diffusivity and fractional anisotropy were associated with MoCA. In partial correlation analyses, adjusting for all demographic and neuroimaging variables, both mean diffusivity and fractional anisotropy were associated only with MoCA (mean diffusivity: r= -0.275, P=0.023; fractional anisotropy: r=0.246, P=0.043).\n\nQuestion:\nIs white matter microstructural damage in small vessel disease associated with Montreal cognitive assessment but not with mini mental state examination performances : vascular mild cognitive impairment Tuscany study?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nMontreal Cognitive Assessment (MoCA) has been proposed as a screening tool in vascular cognitive impairment. Diffusion tensor imaging is sensitive to white matter microstructural damage. We investigated if diffusion tensor imaging-derived indices are more strongly associated with performances on MoCA or on the widely used mini mental state examination in patients with mild cognitive impairment and small vessel disease. Mild cognitive impairment patients with moderate/severe degrees of white matter hyperintensities on MRI were enrolled. Lacunar infarcts, cortical atrophy, medial temporal lobe atrophy and median values of mean diffusivity and fractional anisotropy of the cerebral white matter were studied and correlated with cognitive tests performances. Seventy-six patients (mean age 75.1±6.8 years, mean years of education 8.0±4.3) were assessed. In univariate analyses, a significant association of both MoCA and mini mental state examination scores with age, education, cortical atrophy, and medial temporal lobe atrophy was found, whereas mean diffusivity and fractional anisotropy were associated with MoCA. In partial correlation analyses, adjusting for all demographic and neuroimaging variables, both mean diffusivity and fractional anisotropy were associated only with MoCA (mean diffusivity: r= -0.275, P=0.023; fractional anisotropy: r=0.246, P=0.043).\n\nQuestion:\nIs white matter microstructural damage in small vessel disease associated with Montreal cognitive assessment but not with mini mental state examination performances : vascular mild cognitive impairment Tuscany study?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nMontreal Cognitive Assessment (MoCA) has been proposed as a screening tool in vascular cognitive impairment. Diffusion tensor imaging is sensitive to white matter microstructural damage. We investigated if diffusion tensor imaging-derived indices are more strongly associated with performances on MoCA or on the widely used mini mental state examination in patients with mild cognitive impairment and small vessel disease. Mild cognitive impairment patients with moderate/severe degrees of white matter hyperintensities on MRI were enrolled. Lacunar infarcts, cortical atrophy, medial temporal lobe atrophy and median values of mean diffusivity and fractional anisotropy of the cerebral white matter were studied and correlated with cognitive tests performances. Seventy-six patients (mean age 75.1±6.8 years, mean years of education 8.0±4.3) were assessed. In univariate analyses, a significant association of both MoCA and mini mental state examination scores with age, education, cortical atrophy, and medial temporal lobe atrophy was found, whereas mean diffusivity and fractional anisotropy were associated with MoCA. In partial correlation analyses, adjusting for all demographic and neuroimaging variables, both mean diffusivity and fractional anisotropy were associated only with MoCA (mean diffusivity: r= -0.275, P=0.023; fractional anisotropy: r=0.246, P=0.043).\n\nQuestion:\nIs white matter microstructural damage in small vessel disease associated with Montreal cognitive assessment but not with mini mental state examination performances : vascular mild cognitive impairment Tuscany study?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nAnticytomegalovirus (CMV) prophylaxis prevents the acute disease but its impact on subclinical infection and allograft outcome is unknown. We sought to determine whether CMV prophylaxis administered for three months after heart transplant would improve patient outcomes. This prospective cohort study of 66 heart transplant recipients compared aggressive CMV prophylaxis (n = 21, CMV hyperimmune globulin [CMVIG] plus four weeks of intravenous ganciclovir followed by two months of valganciclovir); with standard prophylaxis (n = 45, intravenous ganciclovir for four weeks). Prophylaxis was based on pretransplant donor (D) and recipient (R) CMV serology: R-/D+ received aggressive prophylaxis; R+ received standard prophylaxis. Outcome measures were: CMV infection assessed by DNA-polymerase chain reaction on peripheral blood polymorphonuclear leukocytes, acute rejection, and cardiac allograft vascular disease (CAV) assessed by intravascular ultrasound. All patients completed one year of follow-up. RESULTS.: CMV infection was subclinical in all but four patients (two in each group). Aggressively treated patients had a lower incidence of CMV infection (73 +/- 10% vs. 94 +/- 4%; P = 0.038), and an independent reduced relative risk for acute rejection graded > or =3A (relative risk [95% CI] = 0.55 [0.26-0.96]; P = 0.03), as compared with the standard prophylaxis group. Aggressively prophylaxed patients also showed a slower progression of CAV, in terms of coronary artery lumen loss (lumen volume change=-21 +/- 13% vs. -10+/-14%; P = 0.05); and vessel shrinkage (vessel volume change = -15 +/- 11% vs. -3 +/- 18%; P = 0.03).\n\nQuestion:\nIs acute rejection and cardiac allograft vascular disease reduced by suppression of subclinical cytomegalovirus infection?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nAnticytomegalovirus (CMV) prophylaxis prevents the acute disease but its impact on subclinical infection and allograft outcome is unknown. We sought to determine whether CMV prophylaxis administered for three months after heart transplant would improve patient outcomes. This prospective cohort study of 66 heart transplant recipients compared aggressive CMV prophylaxis (n = 21, CMV hyperimmune globulin [CMVIG] plus four weeks of intravenous ganciclovir followed by two months of valganciclovir); with standard prophylaxis (n = 45, intravenous ganciclovir for four weeks). Prophylaxis was based on pretransplant donor (D) and recipient (R) CMV serology: R-/D+ received aggressive prophylaxis; R+ received standard prophylaxis. Outcome measures were: CMV infection assessed by DNA-polymerase chain reaction on peripheral blood polymorphonuclear leukocytes, acute rejection, and cardiac allograft vascular disease (CAV) assessed by intravascular ultrasound. All patients completed one year of follow-up. RESULTS.: CMV infection was subclinical in all but four patients (two in each group). Aggressively treated patients had a lower incidence of CMV infection (73 +/- 10% vs. 94 +/- 4%; P = 0.038), and an independent reduced relative risk for acute rejection graded > or =3A (relative risk [95% CI] = 0.55 [0.26-0.96]; P = 0.03), as compared with the standard prophylaxis group. Aggressively prophylaxed patients also showed a slower progression of CAV, in terms of coronary artery lumen loss (lumen volume change=-21 +/- 13% vs. -10+/-14%; P = 0.05); and vessel shrinkage (vessel volume change = -15 +/- 11% vs. -3 +/- 18%; P = 0.03).\n\nQuestion:\nIs acute rejection and cardiac allograft vascular disease reduced by suppression of subclinical cytomegalovirus infection?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nAnticytomegalovirus (CMV) prophylaxis prevents the acute disease but its impact on subclinical infection and allograft outcome is unknown. We sought to determine whether CMV prophylaxis administered for three months after heart transplant would improve patient outcomes. This prospective cohort study of 66 heart transplant recipients compared aggressive CMV prophylaxis (n = 21, CMV hyperimmune globulin [CMVIG] plus four weeks of intravenous ganciclovir followed by two months of valganciclovir); with standard prophylaxis (n = 45, intravenous ganciclovir for four weeks). Prophylaxis was based on pretransplant donor (D) and recipient (R) CMV serology: R-/D+ received aggressive prophylaxis; R+ received standard prophylaxis. Outcome measures were: CMV infection assessed by DNA-polymerase chain reaction on peripheral blood polymorphonuclear leukocytes, acute rejection, and cardiac allograft vascular disease (CAV) assessed by intravascular ultrasound. All patients completed one year of follow-up. RESULTS.: CMV infection was subclinical in all but four patients (two in each group). Aggressively treated patients had a lower incidence of CMV infection (73 +/- 10% vs. 94 +/- 4%; P = 0.038), and an independent reduced relative risk for acute rejection graded > or =3A (relative risk [95% CI] = 0.55 [0.26-0.96]; P = 0.03), as compared with the standard prophylaxis group. Aggressively prophylaxed patients also showed a slower progression of CAV, in terms of coronary artery lumen loss (lumen volume change=-21 +/- 13% vs. -10+/-14%; P = 0.05); and vessel shrinkage (vessel volume change = -15 +/- 11% vs. -3 +/- 18%; P = 0.03).\n\nQuestion:\nIs acute rejection and cardiac allograft vascular disease reduced by suppression of subclinical cytomegalovirus infection?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nThe objective of this study is to evaluate the feasibility of using coated microneedles to deliver vaccines into the oral cavity to induce systemic and mucosal immune responses. Microneedles were coated with sulforhodamine, ovalbumin and two HIV antigens. Coated microneedles were inserted into the inner lower lip and dorsal surface of the tongue of rabbits. Histology was used to confirm microneedle insertion, and systemic and mucosal immune responses were characterized by measuring antigen-specific immunoglobulin G (IgG) in serum and immunoglobulin A (IgA) in saliva, respectively. Histological evaluation of tissues shows that coated microneedles can penetrate the lip and tongue to deliver coatings. Using ovalbumin as a model antigen it was found that the lip and the tongue are equally immunogenic sites for vaccination. Importantly, both sites also induced a significant (p < 0.05) secretory IgA in saliva compared to pre-immune saliva. Microneedle-based oral cavity vaccination was also compared to the intramuscular route using two HIV antigens, a virus-like particle and a DNA vaccine. Microneedle-based delivery to the oral cavity and the intramuscular route exhibited similar (p > 0.05) yet significant (p < 0.05) levels of antigen-specific IgG in serum. However, only the microneedle-based oral cavity vaccination group stimulated a significantly higher (p < 0.05) antigen-specific IgA response in saliva, but not intramuscular injection.\n\nQuestion:\nDoes vaccine delivery to the oral cavity using coated microneedles induce systemic and mucosal immunity?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nThe objective of this study is to evaluate the feasibility of using coated microneedles to deliver vaccines into the oral cavity to induce systemic and mucosal immune responses. Microneedles were coated with sulforhodamine, ovalbumin and two HIV antigens. Coated microneedles were inserted into the inner lower lip and dorsal surface of the tongue of rabbits. Histology was used to confirm microneedle insertion, and systemic and mucosal immune responses were characterized by measuring antigen-specific immunoglobulin G (IgG) in serum and immunoglobulin A (IgA) in saliva, respectively. Histological evaluation of tissues shows that coated microneedles can penetrate the lip and tongue to deliver coatings. Using ovalbumin as a model antigen it was found that the lip and the tongue are equally immunogenic sites for vaccination. Importantly, both sites also induced a significant (p < 0.05) secretory IgA in saliva compared to pre-immune saliva. Microneedle-based oral cavity vaccination was also compared to the intramuscular route using two HIV antigens, a virus-like particle and a DNA vaccine. Microneedle-based delivery to the oral cavity and the intramuscular route exhibited similar (p > 0.05) yet significant (p < 0.05) levels of antigen-specific IgG in serum. However, only the microneedle-based oral cavity vaccination group stimulated a significantly higher (p < 0.05) antigen-specific IgA response in saliva, but not intramuscular injection.\n\nQuestion:\nDoes vaccine delivery to the oral cavity using coated microneedles induce systemic and mucosal immunity?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nThe objective of this study is to evaluate the feasibility of using coated microneedles to deliver vaccines into the oral cavity to induce systemic and mucosal immune responses. Microneedles were coated with sulforhodamine, ovalbumin and two HIV antigens. Coated microneedles were inserted into the inner lower lip and dorsal surface of the tongue of rabbits. Histology was used to confirm microneedle insertion, and systemic and mucosal immune responses were characterized by measuring antigen-specific immunoglobulin G (IgG) in serum and immunoglobulin A (IgA) in saliva, respectively. Histological evaluation of tissues shows that coated microneedles can penetrate the lip and tongue to deliver coatings. Using ovalbumin as a model antigen it was found that the lip and the tongue are equally immunogenic sites for vaccination. Importantly, both sites also induced a significant (p < 0.05) secretory IgA in saliva compared to pre-immune saliva. Microneedle-based oral cavity vaccination was also compared to the intramuscular route using two HIV antigens, a virus-like particle and a DNA vaccine. Microneedle-based delivery to the oral cavity and the intramuscular route exhibited similar (p > 0.05) yet significant (p < 0.05) levels of antigen-specific IgG in serum. However, only the microneedle-based oral cavity vaccination group stimulated a significantly higher (p < 0.05) antigen-specific IgA response in saliva, but not intramuscular injection.\n\nQuestion:\nDoes vaccine delivery to the oral cavity using coated microneedles induce systemic and mucosal immunity?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nTraditional Chinese medicine herbs (TCMHs) are used in medicines as well as in daily dietary supplements in Asia. In this study, we employed pNF-kappaB-Luc or pIFN-gamma-Luc and BALB/c mice peritoneal macrophages or splenocytes to investigate both the immune and inflammatory effects of six selected plant species. Specifically, we used ethyl acetate fractions of Astragalus membranaceus (Fisch.) Bunge var. mongholicus (Bunge) Hsiao (Fabaceae) (AM), Andrographis paniculata (Burm. f.) Nees (Acanthaceae) (AP), Angelica sinensis (Oliv.) Diels (Apiaceae) (AS), Eucommia ulmodes Oliv. (Eucommiaceae) leaves (EU leaves), Isatis indigotica Fort. (Brassicaceae) (II) and Morus alba L. (Moraceae) (MA). We found that ethyl acetate fractions of AP, AS and MA significantly decreased NF-kappaB luciferase activity and also the secretion of NO and PGE(2) in LPS/IFN-gamma stimulated mouse peritoneal macrophages (p<0.05). In contrast, they did not affect IFN-gamma luciferase activity or IFN-gamma production in concanavalin A (Con A)-activated mouse splenocytes. Our results indicated that the anti-inflammatory properties of these plant extracts might be resulted from the inhibition of pro-inflammatory mediators (e.g., NO and PGE(2)), at least in part via suppression of a signaling pathway such as NF-kappaB.\n\nQuestion:\nIs the production of nitric oxide and prostaglandin E2 in peritoneal macrophages inhibited by Andrographis paniculata , Angelica sinensis and Morus alba ethyl acetate fractions?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nTraditional Chinese medicine herbs (TCMHs) are used in medicines as well as in daily dietary supplements in Asia. In this study, we employed pNF-kappaB-Luc or pIFN-gamma-Luc and BALB/c mice peritoneal macrophages or splenocytes to investigate both the immune and inflammatory effects of six selected plant species. Specifically, we used ethyl acetate fractions of Astragalus membranaceus (Fisch.) Bunge var. mongholicus (Bunge) Hsiao (Fabaceae) (AM), Andrographis paniculata (Burm. f.) Nees (Acanthaceae) (AP), Angelica sinensis (Oliv.) Diels (Apiaceae) (AS), Eucommia ulmodes Oliv. (Eucommiaceae) leaves (EU leaves), Isatis indigotica Fort. (Brassicaceae) (II) and Morus alba L. (Moraceae) (MA). We found that ethyl acetate fractions of AP, AS and MA significantly decreased NF-kappaB luciferase activity and also the secretion of NO and PGE(2) in LPS/IFN-gamma stimulated mouse peritoneal macrophages (p<0.05). In contrast, they did not affect IFN-gamma luciferase activity or IFN-gamma production in concanavalin A (Con A)-activated mouse splenocytes. Our results indicated that the anti-inflammatory properties of these plant extracts might be resulted from the inhibition of pro-inflammatory mediators (e.g., NO and PGE(2)), at least in part via suppression of a signaling pathway such as NF-kappaB.\n\nQuestion:\nIs the production of nitric oxide and prostaglandin E2 in peritoneal macrophages inhibited by Andrographis paniculata , Angelica sinensis and Morus alba ethyl acetate fractions?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nTraditional Chinese medicine herbs (TCMHs) are used in medicines as well as in daily dietary supplements in Asia. In this study, we employed pNF-kappaB-Luc or pIFN-gamma-Luc and BALB/c mice peritoneal macrophages or splenocytes to investigate both the immune and inflammatory effects of six selected plant species. Specifically, we used ethyl acetate fractions of Astragalus membranaceus (Fisch.) Bunge var. mongholicus (Bunge) Hsiao (Fabaceae) (AM), Andrographis paniculata (Burm. f.) Nees (Acanthaceae) (AP), Angelica sinensis (Oliv.) Diels (Apiaceae) (AS), Eucommia ulmodes Oliv. (Eucommiaceae) leaves (EU leaves), Isatis indigotica Fort. (Brassicaceae) (II) and Morus alba L. (Moraceae) (MA). We found that ethyl acetate fractions of AP, AS and MA significantly decreased NF-kappaB luciferase activity and also the secretion of NO and PGE(2) in LPS/IFN-gamma stimulated mouse peritoneal macrophages (p<0.05). In contrast, they did not affect IFN-gamma luciferase activity or IFN-gamma production in concanavalin A (Con A)-activated mouse splenocytes. Our results indicated that the anti-inflammatory properties of these plant extracts might be resulted from the inhibition of pro-inflammatory mediators (e.g., NO and PGE(2)), at least in part via suppression of a signaling pathway such as NF-kappaB.\n\nQuestion:\nIs the production of nitric oxide and prostaglandin E2 in peritoneal macrophages inhibited by Andrographis paniculata , Angelica sinensis and Morus alba ethyl acetate fractions?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nTo investigate the pattern of presentation of cervical cancer and to identify the characteristics of women who present symptomatically with cervical cancer. A retrospective study of all cervical cancer cases diagnosed over a 4-year period. Details of mode of presentation, stage at diagnosis and cytological/gynaecological history were collated. In total, 148 cases were identified with a median age of 46 years (range, 20-91 years). In this population, 112 (75.7%) women were within the screening age range. Forty-eight (33.6%) were asymptomatic at diagnosis and presented through the colposcopy clinic. All asymptomatic women (100%) had stage I disease at diagnosis, compared with 37.2% of the symptomatic group (P < 0.001). Postmenopausal bleeding was the most common presenting symptom (33%), followed by postcoital bleeding (14.2%), intermenstrual bleeding (12.2%) and increased vaginal discharge (3.4%). The majority of symptomatic women presented through colposcopy, gynaecological oncology or gynaecology clinics (87.6%); however, 6.5% presented through the emergency department. Women who presented symptomatically were significantly older than asymptomatic women (54.9 versus 38.1 years, P < 0.001). Women at risk of social isolation (non-English speakers, alcohol abusers, heavy smokers, receiving treatment for psychiatric disease) were more likely to present with symptoms, through the emergency department and with advanced disease at diagnosis (stage II+) (P < 0.001).\n\nQuestion:\nDoes cervical cancer still present symptomatically 20 years after the introduction of a structured national screening programme?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nTo investigate the pattern of presentation of cervical cancer and to identify the characteristics of women who present symptomatically with cervical cancer. A retrospective study of all cervical cancer cases diagnosed over a 4-year period. Details of mode of presentation, stage at diagnosis and cytological/gynaecological history were collated. In total, 148 cases were identified with a median age of 46 years (range, 20-91 years). In this population, 112 (75.7%) women were within the screening age range. Forty-eight (33.6%) were asymptomatic at diagnosis and presented through the colposcopy clinic. All asymptomatic women (100%) had stage I disease at diagnosis, compared with 37.2% of the symptomatic group (P < 0.001). Postmenopausal bleeding was the most common presenting symptom (33%), followed by postcoital bleeding (14.2%), intermenstrual bleeding (12.2%) and increased vaginal discharge (3.4%). The majority of symptomatic women presented through colposcopy, gynaecological oncology or gynaecology clinics (87.6%); however, 6.5% presented through the emergency department. Women who presented symptomatically were significantly older than asymptomatic women (54.9 versus 38.1 years, P < 0.001). Women at risk of social isolation (non-English speakers, alcohol abusers, heavy smokers, receiving treatment for psychiatric disease) were more likely to present with symptoms, through the emergency department and with advanced disease at diagnosis (stage II+) (P < 0.001).\n\nQuestion:\nDoes cervical cancer still present symptomatically 20 years after the introduction of a structured national screening programme?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nTo investigate the pattern of presentation of cervical cancer and to identify the characteristics of women who present symptomatically with cervical cancer. A retrospective study of all cervical cancer cases diagnosed over a 4-year period. Details of mode of presentation, stage at diagnosis and cytological/gynaecological history were collated. In total, 148 cases were identified with a median age of 46 years (range, 20-91 years). In this population, 112 (75.7%) women were within the screening age range. Forty-eight (33.6%) were asymptomatic at diagnosis and presented through the colposcopy clinic. All asymptomatic women (100%) had stage I disease at diagnosis, compared with 37.2% of the symptomatic group (P < 0.001). Postmenopausal bleeding was the most common presenting symptom (33%), followed by postcoital bleeding (14.2%), intermenstrual bleeding (12.2%) and increased vaginal discharge (3.4%). The majority of symptomatic women presented through colposcopy, gynaecological oncology or gynaecology clinics (87.6%); however, 6.5% presented through the emergency department. Women who presented symptomatically were significantly older than asymptomatic women (54.9 versus 38.1 years, P < 0.001). Women at risk of social isolation (non-English speakers, alcohol abusers, heavy smokers, receiving treatment for psychiatric disease) were more likely to present with symptoms, through the emergency department and with advanced disease at diagnosis (stage II+) (P < 0.001).\n\nQuestion:\nDoes cervical cancer still present symptomatically 20 years after the introduction of a structured national screening programme?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nThe generation of mature cell types during pancreatic development depends on the expression of many regulatory and signaling proteins. In this study, we tested the hypothesis that the transcriptional regulator Islet-1 (Isl-1), whose expression is first detected in the mesenchyme and epithelium of the developing pancreas and is later restricted to mature islet cells, is involved in the terminal differentiation of islet cells and maintenance of islet mass. To investigate the role of Isl-1 in the pancreatic epithelium during the secondary transition, Isl-1 was conditionally and specifically deleted from embryonic day 13.5 onward using Cre/LoxP technology. Isl-1-deficient endocrine precursors failed to mature into functional islet cells. The postnatal expansion of endocrine cell mass was impaired, and consequently Isl-1 deficient mice were diabetic. In addition, MafA, a potent regulator of the Insulin gene and beta-cell function, was identified as a direct transcriptional target of Isl-1.\n\nQuestion:\nIs islet-1 required for the maturation , proliferation , and survival of the endocrine pancreas?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nThe generation of mature cell types during pancreatic development depends on the expression of many regulatory and signaling proteins. In this study, we tested the hypothesis that the transcriptional regulator Islet-1 (Isl-1), whose expression is first detected in the mesenchyme and epithelium of the developing pancreas and is later restricted to mature islet cells, is involved in the terminal differentiation of islet cells and maintenance of islet mass. To investigate the role of Isl-1 in the pancreatic epithelium during the secondary transition, Isl-1 was conditionally and specifically deleted from embryonic day 13.5 onward using Cre/LoxP technology. Isl-1-deficient endocrine precursors failed to mature into functional islet cells. The postnatal expansion of endocrine cell mass was impaired, and consequently Isl-1 deficient mice were diabetic. In addition, MafA, a potent regulator of the Insulin gene and beta-cell function, was identified as a direct transcriptional target of Isl-1.\n\nQuestion:\nIs islet-1 required for the maturation , proliferation , and survival of the endocrine pancreas?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nThe generation of mature cell types during pancreatic development depends on the expression of many regulatory and signaling proteins. In this study, we tested the hypothesis that the transcriptional regulator Islet-1 (Isl-1), whose expression is first detected in the mesenchyme and epithelium of the developing pancreas and is later restricted to mature islet cells, is involved in the terminal differentiation of islet cells and maintenance of islet mass. To investigate the role of Isl-1 in the pancreatic epithelium during the secondary transition, Isl-1 was conditionally and specifically deleted from embryonic day 13.5 onward using Cre/LoxP technology. Isl-1-deficient endocrine precursors failed to mature into functional islet cells. The postnatal expansion of endocrine cell mass was impaired, and consequently Isl-1 deficient mice were diabetic. In addition, MafA, a potent regulator of the Insulin gene and beta-cell function, was identified as a direct transcriptional target of Isl-1.\n\nQuestion:\nIs islet-1 required for the maturation , proliferation , and survival of the endocrine pancreas?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nMany smokers report smoking because it helps them modulate their negative affect (NA). The stress induction model of smoking suggests, however, that smoking causes stress and concomitant NA. Empirical support for the stress induction model has primarily derived from retrospective reports and experimental manipulations with non-representative samples of smokers. Moreover, prior studies have typically not considered contextual factors (e.g., daily stressors) that may impact the smoking-NA relationship. The aim of this study was to assess the stress induction model of smoking using a prospective design in a nationally representative sample of smokers while simultaneously examining the impact of daily stressors on the relationship between smoking and NA. We hypothesized that smoking and NA would be positively related, and this relationship would be intensified by exposure to daily stressors. A national sample of middle-aged smokers (N = 256) were called on eight consecutive evenings to assess stressor exposure and intensity. Participants also reported on their daily NA and indicated the number of cigarettes they smoked. Analyses were conducted using hierarchical linear modeling to determine the relationship between daily smoking, NA, and stress. Smoking more than usual was associated with increased NA on days when respondents were exposed to any stressors. Smoking more than usual had no effect on NA on days when no stressors were encountered. Moreover, the moderating effect of stressor exposure remained significant even after controlling for the number and intensity of daily stressors reported.\n\nQuestion:\nIs smoking associated with worse mood on stressful days : results from a national diary study?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nMany smokers report smoking because it helps them modulate their negative affect (NA). The stress induction model of smoking suggests, however, that smoking causes stress and concomitant NA. Empirical support for the stress induction model has primarily derived from retrospective reports and experimental manipulations with non-representative samples of smokers. Moreover, prior studies have typically not considered contextual factors (e.g., daily stressors) that may impact the smoking-NA relationship. The aim of this study was to assess the stress induction model of smoking using a prospective design in a nationally representative sample of smokers while simultaneously examining the impact of daily stressors on the relationship between smoking and NA. We hypothesized that smoking and NA would be positively related, and this relationship would be intensified by exposure to daily stressors. A national sample of middle-aged smokers (N = 256) were called on eight consecutive evenings to assess stressor exposure and intensity. Participants also reported on their daily NA and indicated the number of cigarettes they smoked. Analyses were conducted using hierarchical linear modeling to determine the relationship between daily smoking, NA, and stress. Smoking more than usual was associated with increased NA on days when respondents were exposed to any stressors. Smoking more than usual had no effect on NA on days when no stressors were encountered. Moreover, the moderating effect of stressor exposure remained significant even after controlling for the number and intensity of daily stressors reported.\n\nQuestion:\nIs smoking associated with worse mood on stressful days : results from a national diary study?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nMany smokers report smoking because it helps them modulate their negative affect (NA). The stress induction model of smoking suggests, however, that smoking causes stress and concomitant NA. Empirical support for the stress induction model has primarily derived from retrospective reports and experimental manipulations with non-representative samples of smokers. Moreover, prior studies have typically not considered contextual factors (e.g., daily stressors) that may impact the smoking-NA relationship. The aim of this study was to assess the stress induction model of smoking using a prospective design in a nationally representative sample of smokers while simultaneously examining the impact of daily stressors on the relationship between smoking and NA. We hypothesized that smoking and NA would be positively related, and this relationship would be intensified by exposure to daily stressors. A national sample of middle-aged smokers (N = 256) were called on eight consecutive evenings to assess stressor exposure and intensity. Participants also reported on their daily NA and indicated the number of cigarettes they smoked. Analyses were conducted using hierarchical linear modeling to determine the relationship between daily smoking, NA, and stress. Smoking more than usual was associated with increased NA on days when respondents were exposed to any stressors. Smoking more than usual had no effect on NA on days when no stressors were encountered. Moreover, the moderating effect of stressor exposure remained significant even after controlling for the number and intensity of daily stressors reported.\n\nQuestion:\nIs smoking associated with worse mood on stressful days : results from a national diary study?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nCopper toxicosis (CT) in Bedlington terriers is an autosomal recessive disorder characterized by massive lysosomal copper accumulation in livers of affected dogs, and a defect in the biliary excretion of this metal. We propose that MURR1, the gene defective in canine CT, has a role in the regulation of copper excretion into bile during copper overload. Polyclonal antibodies raised against full-length recombinant human MURR1 were used for immunoblot analysis and indirect immunofluorescence studies. Using Western blot analysis, these antibodies abundantly detected MURR1 as a 23 kDa protein in liver extracts of mice and dogs, but MURR1 was undetectable in the livers of affected Bedlington terriers. MURR1 was also detected in different tissues and cell lines; in cell lines the protein was found both in cytosol and membrane preparations. Consistent with this observation, indirect immunofluorescence staining revealed that in some cells MURR1 was associated with a vesicular compartment diffusely localized throughout the cell.\n\nQuestion:\nIs the ubiquitously expressed MURR1 protein absent in canine copper toxicosis?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nCopper toxicosis (CT) in Bedlington terriers is an autosomal recessive disorder characterized by massive lysosomal copper accumulation in livers of affected dogs, and a defect in the biliary excretion of this metal. We propose that MURR1, the gene defective in canine CT, has a role in the regulation of copper excretion into bile during copper overload. Polyclonal antibodies raised against full-length recombinant human MURR1 were used for immunoblot analysis and indirect immunofluorescence studies. Using Western blot analysis, these antibodies abundantly detected MURR1 as a 23 kDa protein in liver extracts of mice and dogs, but MURR1 was undetectable in the livers of affected Bedlington terriers. MURR1 was also detected in different tissues and cell lines; in cell lines the protein was found both in cytosol and membrane preparations. Consistent with this observation, indirect immunofluorescence staining revealed that in some cells MURR1 was associated with a vesicular compartment diffusely localized throughout the cell.\n\nQuestion:\nIs the ubiquitously expressed MURR1 protein absent in canine copper toxicosis?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nCopper toxicosis (CT) in Bedlington terriers is an autosomal recessive disorder characterized by massive lysosomal copper accumulation in livers of affected dogs, and a defect in the biliary excretion of this metal. We propose that MURR1, the gene defective in canine CT, has a role in the regulation of copper excretion into bile during copper overload. Polyclonal antibodies raised against full-length recombinant human MURR1 were used for immunoblot analysis and indirect immunofluorescence studies. Using Western blot analysis, these antibodies abundantly detected MURR1 as a 23 kDa protein in liver extracts of mice and dogs, but MURR1 was undetectable in the livers of affected Bedlington terriers. MURR1 was also detected in different tissues and cell lines; in cell lines the protein was found both in cytosol and membrane preparations. Consistent with this observation, indirect immunofluorescence staining revealed that in some cells MURR1 was associated with a vesicular compartment diffusely localized throughout the cell.\n\nQuestion:\nIs the ubiquitously expressed MURR1 protein absent in canine copper toxicosis?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nTo assess if predefined variables in study design, instrument type, and patient characteristics account for variance in reported retest reliability for the Oswestry Disability Index (ODI) and Roland-Morris Questionnaire (RMQ). A second aim was a more precise estimate of instrument reliability. A systematic literature search of MEDLINE, EMBASE, AMED, PsycINFO, and CINAHL was performed from inception to January 2011. Hand search, gray literature, and reference retrieval completed the search. Two blinded reviewers extracted the data. Original authors were contacted for the missing data. A meta-analysis was performed with the intraclass correlation coefficient as the outcome measure. Fifty studies on 31 ODI and 28 RMQ cohorts were retrieved that met the inclusion criteria. Meta-analysis found the ODI more reliable than the RMQ (coefficient, -0.2840; P = 0.009) and lower reliability on increased days to retest (coefficient, -0.0089; P = 0.005) and in low back pain (LBP) with leg pain than LBP only cohorts (coefficient, -0.2194; P = 0.046). The use of a transition item to identify stable patients and percentage of cohort not included at retest were significant only on single variable analysis.\n\nQuestion:\nDoes meta-analysis identify Back Pain Questionnaire reliability influenced more by instrument than study design or population?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nTo assess if predefined variables in study design, instrument type, and patient characteristics account for variance in reported retest reliability for the Oswestry Disability Index (ODI) and Roland-Morris Questionnaire (RMQ). A second aim was a more precise estimate of instrument reliability. A systematic literature search of MEDLINE, EMBASE, AMED, PsycINFO, and CINAHL was performed from inception to January 2011. Hand search, gray literature, and reference retrieval completed the search. Two blinded reviewers extracted the data. Original authors were contacted for the missing data. A meta-analysis was performed with the intraclass correlation coefficient as the outcome measure. Fifty studies on 31 ODI and 28 RMQ cohorts were retrieved that met the inclusion criteria. Meta-analysis found the ODI more reliable than the RMQ (coefficient, -0.2840; P = 0.009) and lower reliability on increased days to retest (coefficient, -0.0089; P = 0.005) and in low back pain (LBP) with leg pain than LBP only cohorts (coefficient, -0.2194; P = 0.046). The use of a transition item to identify stable patients and percentage of cohort not included at retest were significant only on single variable analysis.\n\nQuestion:\nDoes meta-analysis identify Back Pain Questionnaire reliability influenced more by instrument than study design or population?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nTo assess if predefined variables in study design, instrument type, and patient characteristics account for variance in reported retest reliability for the Oswestry Disability Index (ODI) and Roland-Morris Questionnaire (RMQ). A second aim was a more precise estimate of instrument reliability. A systematic literature search of MEDLINE, EMBASE, AMED, PsycINFO, and CINAHL was performed from inception to January 2011. Hand search, gray literature, and reference retrieval completed the search. Two blinded reviewers extracted the data. Original authors were contacted for the missing data. A meta-analysis was performed with the intraclass correlation coefficient as the outcome measure. Fifty studies on 31 ODI and 28 RMQ cohorts were retrieved that met the inclusion criteria. Meta-analysis found the ODI more reliable than the RMQ (coefficient, -0.2840; P = 0.009) and lower reliability on increased days to retest (coefficient, -0.0089; P = 0.005) and in low back pain (LBP) with leg pain than LBP only cohorts (coefficient, -0.2194; P = 0.046). The use of a transition item to identify stable patients and percentage of cohort not included at retest were significant only on single variable analysis.\n\nQuestion:\nDoes meta-analysis identify Back Pain Questionnaire reliability influenced more by instrument than study design or population?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nIn this study, we have assessed the potential of antigen-specific immunotherapy against hepatocellular carcinoma (HCC) in conditions of low tumour burden, in an autochthonous HCC model. Diethylnitrosamine (DEN) injected into infant mice results in the development of multi-nodular HCC in which alpha-fetoprotein (AFP) is re-expressed. DEN-injected animals received an antigen-specific immunization with a synthetic vector consisting of a low dose of AFP-encoding plasmid formulated with the amphiphilic block copolymer 704 (DNAmAFP/704). Animals were treated at 4 and 5 months, before macroscopic nodules were detected, and were sacrificed at 8 months. The tumour burden, as well as liver histology, was assessed. AFP and MHC class I molecule expression in the nodules were monitored by qRT-PCR. The AFP-specific immunotherapy led to a significant (65%) reduction in tumour size. The reduced expression of AFP and MHC class I molecules was measured in the remaining nodules taken from the DNAmAFP/704-treated group.\n\nQuestion:\nDoes aFP-specific immunotherapy impair growth of autochthonous hepatocellular carcinoma in mice?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nIn this study, we have assessed the potential of antigen-specific immunotherapy against hepatocellular carcinoma (HCC) in conditions of low tumour burden, in an autochthonous HCC model. Diethylnitrosamine (DEN) injected into infant mice results in the development of multi-nodular HCC in which alpha-fetoprotein (AFP) is re-expressed. DEN-injected animals received an antigen-specific immunization with a synthetic vector consisting of a low dose of AFP-encoding plasmid formulated with the amphiphilic block copolymer 704 (DNAmAFP/704). Animals were treated at 4 and 5 months, before macroscopic nodules were detected, and were sacrificed at 8 months. The tumour burden, as well as liver histology, was assessed. AFP and MHC class I molecule expression in the nodules were monitored by qRT-PCR. The AFP-specific immunotherapy led to a significant (65%) reduction in tumour size. The reduced expression of AFP and MHC class I molecules was measured in the remaining nodules taken from the DNAmAFP/704-treated group.\n\nQuestion:\nDoes aFP-specific immunotherapy impair growth of autochthonous hepatocellular carcinoma in mice?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nIn this study, we have assessed the potential of antigen-specific immunotherapy against hepatocellular carcinoma (HCC) in conditions of low tumour burden, in an autochthonous HCC model. Diethylnitrosamine (DEN) injected into infant mice results in the development of multi-nodular HCC in which alpha-fetoprotein (AFP) is re-expressed. DEN-injected animals received an antigen-specific immunization with a synthetic vector consisting of a low dose of AFP-encoding plasmid formulated with the amphiphilic block copolymer 704 (DNAmAFP/704). Animals were treated at 4 and 5 months, before macroscopic nodules were detected, and were sacrificed at 8 months. The tumour burden, as well as liver histology, was assessed. AFP and MHC class I molecule expression in the nodules were monitored by qRT-PCR. The AFP-specific immunotherapy led to a significant (65%) reduction in tumour size. The reduced expression of AFP and MHC class I molecules was measured in the remaining nodules taken from the DNAmAFP/704-treated group.\n\nQuestion:\nDoes aFP-specific immunotherapy impair growth of autochthonous hepatocellular carcinoma in mice?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nA reclassification of the International Union Against Cancer (UICC) staging system for adrenocortical carcinoma (ACC) patients has recently been proposed by the European Network for the Study of Adrenal Tumors (ENSAT) to better discriminate between cancer-specific mortality (CSM) risk strata. We formally tested the validity of the modified staging system in a large North American population-based cohort. Kaplan-Meier survival curves depicted CSM rates in the overall population and after stratification according to the 2004 UICC or the 2008 ENSAT-staging system. Cox regression models addressing CSM tested the prognostic value of respectively the UICC or the ENSAT-staging system. Harrell's concordance index quantified the accuracy of the standard versus the modified staging system. In the overall population (n=573), the CSM-free survival rates at 1, 3, and 5 years were, respectively, 62.9%, 47.0%, and 38.1%. No statistically significant differences in survival were recorded between 2004 UICC stages II and III patients (p=0.1). Conversely, a statistically significant difference was observed between 2008 ENSAT stage II and stage III patients (p<0.001). The 2008 ENSAT-staging system showed higher accuracy (83.0%) in predicting 3-year CSM rates, relative to the 2004 UICC-staging system (79.5%) (p<0.001).\n\nQuestion:\nIs the European Network for the Study of Adrenal Tumors staging system prognostically superior to the international union against cancer-staging system : a North American validation?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nA reclassification of the International Union Against Cancer (UICC) staging system for adrenocortical carcinoma (ACC) patients has recently been proposed by the European Network for the Study of Adrenal Tumors (ENSAT) to better discriminate between cancer-specific mortality (CSM) risk strata. We formally tested the validity of the modified staging system in a large North American population-based cohort. Kaplan-Meier survival curves depicted CSM rates in the overall population and after stratification according to the 2004 UICC or the 2008 ENSAT-staging system. Cox regression models addressing CSM tested the prognostic value of respectively the UICC or the ENSAT-staging system. Harrell's concordance index quantified the accuracy of the standard versus the modified staging system. In the overall population (n=573), the CSM-free survival rates at 1, 3, and 5 years were, respectively, 62.9%, 47.0%, and 38.1%. No statistically significant differences in survival were recorded between 2004 UICC stages II and III patients (p=0.1). Conversely, a statistically significant difference was observed between 2008 ENSAT stage II and stage III patients (p<0.001). The 2008 ENSAT-staging system showed higher accuracy (83.0%) in predicting 3-year CSM rates, relative to the 2004 UICC-staging system (79.5%) (p<0.001).\n\nQuestion:\nIs the European Network for the Study of Adrenal Tumors staging system prognostically superior to the international union against cancer-staging system : a North American validation?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nA reclassification of the International Union Against Cancer (UICC) staging system for adrenocortical carcinoma (ACC) patients has recently been proposed by the European Network for the Study of Adrenal Tumors (ENSAT) to better discriminate between cancer-specific mortality (CSM) risk strata. We formally tested the validity of the modified staging system in a large North American population-based cohort. Kaplan-Meier survival curves depicted CSM rates in the overall population and after stratification according to the 2004 UICC or the 2008 ENSAT-staging system. Cox regression models addressing CSM tested the prognostic value of respectively the UICC or the ENSAT-staging system. Harrell's concordance index quantified the accuracy of the standard versus the modified staging system. In the overall population (n=573), the CSM-free survival rates at 1, 3, and 5 years were, respectively, 62.9%, 47.0%, and 38.1%. No statistically significant differences in survival were recorded between 2004 UICC stages II and III patients (p=0.1). Conversely, a statistically significant difference was observed between 2008 ENSAT stage II and stage III patients (p<0.001). The 2008 ENSAT-staging system showed higher accuracy (83.0%) in predicting 3-year CSM rates, relative to the 2004 UICC-staging system (79.5%) (p<0.001).\n\nQuestion:\nIs the European Network for the Study of Adrenal Tumors staging system prognostically superior to the international union against cancer-staging system : a North American validation?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nDrug challenges in \"intact\" and p-chlorophenylalanine (p-CPA)-treated animals can be used to distinguish agents that act as direct serotonin (5-HT) agonists from agents that function as 5-HT releasers. The objective of the study was to investigate the effect of p-CPA treatment on the capacity of racemic 3,4-methylenedioxymethamphetamine (MDMA) and its stereoisomers to induce the head twitch response, hyperthermia, and locomotor stimulation in mice. Pretreatments with either 100 mg/kg p-CPA or equivolume saline were administered for three consecutive days. The following day, mice were either euthanized (to quantify 5-HT tone), tested with various doses of racemic MDMA or one of its enantiomers in the head twitch assay, or challenged with 32 mg/kg racemic MDMA or one of its enantiomers, while temperature and locomotor activity were monitored via radiotelemetry. p-CPA reduced cortical 5-HT turnover by >70% without altering dopamine turnover. Racemic MDMA did not induce a significant head twitch response in intact or p-CPA-treated mice. S(+)-MDMA and R(-)-MDMA elicited similar head twitch curves in intact mice; p-CPA treatment attenuated this response when induced by S(+)-MDMA but not when elicited by R(-)-MDMA. Neither the hyperthermic nor locomotor-stimulant effects of racemic MDMA were altered by p-CPA treatment. The hyperthermic effects, but not the locomotor-stimulant effects, of S(+)-MDMA were attenuated in mice treated with p-CPA. R(-)-MDMA did not alter core temperature or induce significant locomotor stimulation in intact or p-CPA-treated mice.\n\nQuestion:\nDoes serotonin synthesis inhibition reveal distinct mechanisms of action for MDMA and its enantiomers in the mouse?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nDrug challenges in \"intact\" and p-chlorophenylalanine (p-CPA)-treated animals can be used to distinguish agents that act as direct serotonin (5-HT) agonists from agents that function as 5-HT releasers. The objective of the study was to investigate the effect of p-CPA treatment on the capacity of racemic 3,4-methylenedioxymethamphetamine (MDMA) and its stereoisomers to induce the head twitch response, hyperthermia, and locomotor stimulation in mice. Pretreatments with either 100 mg/kg p-CPA or equivolume saline were administered for three consecutive days. The following day, mice were either euthanized (to quantify 5-HT tone), tested with various doses of racemic MDMA or one of its enantiomers in the head twitch assay, or challenged with 32 mg/kg racemic MDMA or one of its enantiomers, while temperature and locomotor activity were monitored via radiotelemetry. p-CPA reduced cortical 5-HT turnover by >70% without altering dopamine turnover. Racemic MDMA did not induce a significant head twitch response in intact or p-CPA-treated mice. S(+)-MDMA and R(-)-MDMA elicited similar head twitch curves in intact mice; p-CPA treatment attenuated this response when induced by S(+)-MDMA but not when elicited by R(-)-MDMA. Neither the hyperthermic nor locomotor-stimulant effects of racemic MDMA were altered by p-CPA treatment. The hyperthermic effects, but not the locomotor-stimulant effects, of S(+)-MDMA were attenuated in mice treated with p-CPA. R(-)-MDMA did not alter core temperature or induce significant locomotor stimulation in intact or p-CPA-treated mice.\n\nQuestion:\nDoes serotonin synthesis inhibition reveal distinct mechanisms of action for MDMA and its enantiomers in the mouse?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nDrug challenges in \"intact\" and p-chlorophenylalanine (p-CPA)-treated animals can be used to distinguish agents that act as direct serotonin (5-HT) agonists from agents that function as 5-HT releasers. The objective of the study was to investigate the effect of p-CPA treatment on the capacity of racemic 3,4-methylenedioxymethamphetamine (MDMA) and its stereoisomers to induce the head twitch response, hyperthermia, and locomotor stimulation in mice. Pretreatments with either 100 mg/kg p-CPA or equivolume saline were administered for three consecutive days. The following day, mice were either euthanized (to quantify 5-HT tone), tested with various doses of racemic MDMA or one of its enantiomers in the head twitch assay, or challenged with 32 mg/kg racemic MDMA or one of its enantiomers, while temperature and locomotor activity were monitored via radiotelemetry. p-CPA reduced cortical 5-HT turnover by >70% without altering dopamine turnover. Racemic MDMA did not induce a significant head twitch response in intact or p-CPA-treated mice. S(+)-MDMA and R(-)-MDMA elicited similar head twitch curves in intact mice; p-CPA treatment attenuated this response when induced by S(+)-MDMA but not when elicited by R(-)-MDMA. Neither the hyperthermic nor locomotor-stimulant effects of racemic MDMA were altered by p-CPA treatment. The hyperthermic effects, but not the locomotor-stimulant effects, of S(+)-MDMA were attenuated in mice treated with p-CPA. R(-)-MDMA did not alter core temperature or induce significant locomotor stimulation in intact or p-CPA-treated mice.\n\nQuestion:\nDoes serotonin synthesis inhibition reveal distinct mechanisms of action for MDMA and its enantiomers in the mouse?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nStatins are prescribed for their preventative effects within atherosclerosis development. To our knowledge, no study focusing on very low-dose (non-hypolipidemic effect) and long-term atorvastatin treatment in vivo was available. Our aim was to assess the effect of such atorvastatin treatment on the mechanical and functional characteristics of arteries in the context of primary prevention. An atorvastatin treatment (2.5 mg/kg/day) was tested against controls on 34 male 3 to 12 month-old WHHL rabbits. No effect on total cholesterol, triglycerides, HDL or LDL was observed. The arterial stiffness was evaluated on vigil animals by pulse wave velocity (PWV) measurement. Then, in vitro measurements were made to evaluate (1) the endothelial and vascular smooth muscle function, (2) the elasticity of the arterial wall and (3) the composition in collagen and elastin in the aorta. The PWV increasing observed with age in control group was canceled by treatment, creating a significance difference between groups at 12 months (5.17 ± 0.50 vs 2.14 ± 0.34 m s(-1) in control and treated groups respectively). Vasoreactivity modifications can't explain this result but maintain of elasticity with treatment in large arteries was confirm by a static tensile test. A first possible explanation is the change of wall composition with treatment, validated by the percentage of elastin at 12 months, 4.4% lower in the control group compared to the treated group (p < 0.05).\n\nQuestion:\nDoes a non-hypocholesterolemic atorvastatin treatment improve vessel elasticity by acting on elastin composition in WHHL rabbits?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nStatins are prescribed for their preventative effects within atherosclerosis development. To our knowledge, no study focusing on very low-dose (non-hypolipidemic effect) and long-term atorvastatin treatment in vivo was available. Our aim was to assess the effect of such atorvastatin treatment on the mechanical and functional characteristics of arteries in the context of primary prevention. An atorvastatin treatment (2.5 mg/kg/day) was tested against controls on 34 male 3 to 12 month-old WHHL rabbits. No effect on total cholesterol, triglycerides, HDL or LDL was observed. The arterial stiffness was evaluated on vigil animals by pulse wave velocity (PWV) measurement. Then, in vitro measurements were made to evaluate (1) the endothelial and vascular smooth muscle function, (2) the elasticity of the arterial wall and (3) the composition in collagen and elastin in the aorta. The PWV increasing observed with age in control group was canceled by treatment, creating a significance difference between groups at 12 months (5.17 ± 0.50 vs 2.14 ± 0.34 m s(-1) in control and treated groups respectively). Vasoreactivity modifications can't explain this result but maintain of elasticity with treatment in large arteries was confirm by a static tensile test. A first possible explanation is the change of wall composition with treatment, validated by the percentage of elastin at 12 months, 4.4% lower in the control group compared to the treated group (p < 0.05).\n\nQuestion:\nDoes a non-hypocholesterolemic atorvastatin treatment improve vessel elasticity by acting on elastin composition in WHHL rabbits?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nStatins are prescribed for their preventative effects within atherosclerosis development. To our knowledge, no study focusing on very low-dose (non-hypolipidemic effect) and long-term atorvastatin treatment in vivo was available. Our aim was to assess the effect of such atorvastatin treatment on the mechanical and functional characteristics of arteries in the context of primary prevention. An atorvastatin treatment (2.5 mg/kg/day) was tested against controls on 34 male 3 to 12 month-old WHHL rabbits. No effect on total cholesterol, triglycerides, HDL or LDL was observed. The arterial stiffness was evaluated on vigil animals by pulse wave velocity (PWV) measurement. Then, in vitro measurements were made to evaluate (1) the endothelial and vascular smooth muscle function, (2) the elasticity of the arterial wall and (3) the composition in collagen and elastin in the aorta. The PWV increasing observed with age in control group was canceled by treatment, creating a significance difference between groups at 12 months (5.17 ± 0.50 vs 2.14 ± 0.34 m s(-1) in control and treated groups respectively). Vasoreactivity modifications can't explain this result but maintain of elasticity with treatment in large arteries was confirm by a static tensile test. A first possible explanation is the change of wall composition with treatment, validated by the percentage of elastin at 12 months, 4.4% lower in the control group compared to the treated group (p < 0.05).\n\nQuestion:\nDoes a non-hypocholesterolemic atorvastatin treatment improve vessel elasticity by acting on elastin composition in WHHL rabbits?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nMalignant pleural mesotheliomas (MPMs) are aggressive tumors with a poor prognosis. We aimed to clarify the mechanisms of epithelial-to-mesenchymal transition (EMT) in MPMs by analyzing the expressions of EMT-associated transcription factors and E-cadherin in relation to tumor proliferation rates and patient survival. One hundred nine patients with MPMs were investigated. Among these patients, there were 61 epithelioid tumors, 21 sarcomatoid tumors, 20 biphasic tumors, and 7 desmoplastic tumors. Immunohistochemical analyses were performed to evaluate the expressions of Snail, ZEB1, Twist, E-cadherin, and the Ki-67 proliferation index. The expressions of Snail and ZEB1 were significantly higher in the nonepithelioid tumors than in the epithelioid tumors (p<0.0001 and p=0.0051, respectively). Furthermore, the E-cadherin expression was significantly lower in the Snail-high tumors than in the Snail-low tumors (p=0.0423). The E-cadherin expression was significantly lower in the nonepithelioid tumors than in the epithelioid tumors (p=0.0126). The Ki-67 proliferation index was significantly higher in the nonepithelioid tumors than in the epithelioid tumors (p=0.025). Patient survival was significantly lower in patients with Snail-high MPMs than in those with Snail-low MPMs (p=0.0016), especially in patients with nonepithelioid tumors (p=0.0089). The multivariate analysis also demonstrated that nuclear Snail expression was a significant predictor of poor prognosis in patients with MPMs (p=0.0142).\n\nQuestion:\nIs snail expression associated with a poor prognosis in malignant pleural mesotheliomas?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nMalignant pleural mesotheliomas (MPMs) are aggressive tumors with a poor prognosis. We aimed to clarify the mechanisms of epithelial-to-mesenchymal transition (EMT) in MPMs by analyzing the expressions of EMT-associated transcription factors and E-cadherin in relation to tumor proliferation rates and patient survival. One hundred nine patients with MPMs were investigated. Among these patients, there were 61 epithelioid tumors, 21 sarcomatoid tumors, 20 biphasic tumors, and 7 desmoplastic tumors. Immunohistochemical analyses were performed to evaluate the expressions of Snail, ZEB1, Twist, E-cadherin, and the Ki-67 proliferation index. The expressions of Snail and ZEB1 were significantly higher in the nonepithelioid tumors than in the epithelioid tumors (p<0.0001 and p=0.0051, respectively). Furthermore, the E-cadherin expression was significantly lower in the Snail-high tumors than in the Snail-low tumors (p=0.0423). The E-cadherin expression was significantly lower in the nonepithelioid tumors than in the epithelioid tumors (p=0.0126). The Ki-67 proliferation index was significantly higher in the nonepithelioid tumors than in the epithelioid tumors (p=0.025). Patient survival was significantly lower in patients with Snail-high MPMs than in those with Snail-low MPMs (p=0.0016), especially in patients with nonepithelioid tumors (p=0.0089). The multivariate analysis also demonstrated that nuclear Snail expression was a significant predictor of poor prognosis in patients with MPMs (p=0.0142).\n\nQuestion:\nIs snail expression associated with a poor prognosis in malignant pleural mesotheliomas?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nMalignant pleural mesotheliomas (MPMs) are aggressive tumors with a poor prognosis. We aimed to clarify the mechanisms of epithelial-to-mesenchymal transition (EMT) in MPMs by analyzing the expressions of EMT-associated transcription factors and E-cadherin in relation to tumor proliferation rates and patient survival. One hundred nine patients with MPMs were investigated. Among these patients, there were 61 epithelioid tumors, 21 sarcomatoid tumors, 20 biphasic tumors, and 7 desmoplastic tumors. Immunohistochemical analyses were performed to evaluate the expressions of Snail, ZEB1, Twist, E-cadherin, and the Ki-67 proliferation index. The expressions of Snail and ZEB1 were significantly higher in the nonepithelioid tumors than in the epithelioid tumors (p<0.0001 and p=0.0051, respectively). Furthermore, the E-cadherin expression was significantly lower in the Snail-high tumors than in the Snail-low tumors (p=0.0423). The E-cadherin expression was significantly lower in the nonepithelioid tumors than in the epithelioid tumors (p=0.0126). The Ki-67 proliferation index was significantly higher in the nonepithelioid tumors than in the epithelioid tumors (p=0.025). Patient survival was significantly lower in patients with Snail-high MPMs than in those with Snail-low MPMs (p=0.0016), especially in patients with nonepithelioid tumors (p=0.0089). The multivariate analysis also demonstrated that nuclear Snail expression was a significant predictor of poor prognosis in patients with MPMs (p=0.0142).\n\nQuestion:\nIs snail expression associated with a poor prognosis in malignant pleural mesotheliomas?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nTransplacental transfer of nutritive and inhalant allergens has been described being potentially responsible for a series of events leading to antigen-specific immune responses in the fetus. As such, cord blood T cell responses appear ubiquitously. However, studies failed to reveal a consistent dose-response relationship between antenatal allergen exposure and allergen-specific cellular reactivity in cord blood. To examine the transfer process of allergens (ovalbumin (OVA), beta-lactoglobulin (BLG), birch pollen allergen Bet v1) in placental tissue (BeWo cell line, ex vivo placenta model). The choriocarcinoma cell line BeWo was used to study the allergen uptake and transfer experiments in vitro. In the ex vivo placenta model the contribution of different placental compartments was evaluated. For this, immuno-histochemistry, immuno-electronmicroscopy and ELISA techniques were applied using monoclonal antibodies to Bet v1, OVA and -BLG. In vitro transfer studies on a BeWo cell-layer revealed an intracellular allergen uptake and a trans-trophoblastic allergen transfer, which was temperature- and concentration dependent, pH sensitive and asymmetric. Allergen-specific staining of placental tissue after allergen perfusion (BLG) demonstrated bulk of the allergen in the syncytio-trophoblastic cell layer and minor staining in the villous stroma and in the endothelium of fetal vessels. Immunogold staining revealed an accumulation of the perfused allergen in the trophoblastic basement membrane.\n\nQuestion:\nIs most of diaplacentally transferred allergen retained in the placenta?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nTransplacental transfer of nutritive and inhalant allergens has been described being potentially responsible for a series of events leading to antigen-specific immune responses in the fetus. As such, cord blood T cell responses appear ubiquitously. However, studies failed to reveal a consistent dose-response relationship between antenatal allergen exposure and allergen-specific cellular reactivity in cord blood. To examine the transfer process of allergens (ovalbumin (OVA), beta-lactoglobulin (BLG), birch pollen allergen Bet v1) in placental tissue (BeWo cell line, ex vivo placenta model). The choriocarcinoma cell line BeWo was used to study the allergen uptake and transfer experiments in vitro. In the ex vivo placenta model the contribution of different placental compartments was evaluated. For this, immuno-histochemistry, immuno-electronmicroscopy and ELISA techniques were applied using monoclonal antibodies to Bet v1, OVA and -BLG. In vitro transfer studies on a BeWo cell-layer revealed an intracellular allergen uptake and a trans-trophoblastic allergen transfer, which was temperature- and concentration dependent, pH sensitive and asymmetric. Allergen-specific staining of placental tissue after allergen perfusion (BLG) demonstrated bulk of the allergen in the syncytio-trophoblastic cell layer and minor staining in the villous stroma and in the endothelium of fetal vessels. Immunogold staining revealed an accumulation of the perfused allergen in the trophoblastic basement membrane.\n\nQuestion:\nIs most of diaplacentally transferred allergen retained in the placenta?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nTransplacental transfer of nutritive and inhalant allergens has been described being potentially responsible for a series of events leading to antigen-specific immune responses in the fetus. As such, cord blood T cell responses appear ubiquitously. However, studies failed to reveal a consistent dose-response relationship between antenatal allergen exposure and allergen-specific cellular reactivity in cord blood. To examine the transfer process of allergens (ovalbumin (OVA), beta-lactoglobulin (BLG), birch pollen allergen Bet v1) in placental tissue (BeWo cell line, ex vivo placenta model). The choriocarcinoma cell line BeWo was used to study the allergen uptake and transfer experiments in vitro. In the ex vivo placenta model the contribution of different placental compartments was evaluated. For this, immuno-histochemistry, immuno-electronmicroscopy and ELISA techniques were applied using monoclonal antibodies to Bet v1, OVA and -BLG. In vitro transfer studies on a BeWo cell-layer revealed an intracellular allergen uptake and a trans-trophoblastic allergen transfer, which was temperature- and concentration dependent, pH sensitive and asymmetric. Allergen-specific staining of placental tissue after allergen perfusion (BLG) demonstrated bulk of the allergen in the syncytio-trophoblastic cell layer and minor staining in the villous stroma and in the endothelium of fetal vessels. Immunogold staining revealed an accumulation of the perfused allergen in the trophoblastic basement membrane.\n\nQuestion:\nIs most of diaplacentally transferred allergen retained in the placenta?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nDelirium is an organically caused acute dysfunction of the brain associated with increased morbidity, mortality, cost of care and poor cognitive recovery. This point prevalence study of delirium was conducted at Hvidovre Hospital, Copenhagen, Denmark at two separate occasions. Patients were examined with the Brief Confusion Assessment Method (bCAM) in both, but in the second survey bCAM was supplemented with a psychiatric assessment using the Diagnostic and Statistical Manual of Mental Disorders, fourth ed. In all, 126 patients were assessed and eight patients were excluded. The delirious patients' charts were examined. Out of the 118 patients included in the study, 38 (32%) were delirious and in 18 (47%) patients, the diagnosis was documented. Furthermore, in 18 (47%) patients, a pharmacological treatment plan for agitation was prepared (in 89% of those diagnosed with delirium and in 10% of those without the diagnosis). In 26 (68%), a plan to increase care existed (in 78% of those with a diagnosis of delirium and in 60% without the diagnosis). In 11 patients (29%), there was a plan for reducing stress (in 44% of those with a diagnosis of delirium and in 15% without the diagnosis).\n\nQuestion:\nIs delirium seen in one-third of patients in an acute hospital setting . Identification , pharmacologic and non-pharmacologic treatment is inadequate?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nDelirium is an organically caused acute dysfunction of the brain associated with increased morbidity, mortality, cost of care and poor cognitive recovery. This point prevalence study of delirium was conducted at Hvidovre Hospital, Copenhagen, Denmark at two separate occasions. Patients were examined with the Brief Confusion Assessment Method (bCAM) in both, but in the second survey bCAM was supplemented with a psychiatric assessment using the Diagnostic and Statistical Manual of Mental Disorders, fourth ed. In all, 126 patients were assessed and eight patients were excluded. The delirious patients' charts were examined. Out of the 118 patients included in the study, 38 (32%) were delirious and in 18 (47%) patients, the diagnosis was documented. Furthermore, in 18 (47%) patients, a pharmacological treatment plan for agitation was prepared (in 89% of those diagnosed with delirium and in 10% of those without the diagnosis). In 26 (68%), a plan to increase care existed (in 78% of those with a diagnosis of delirium and in 60% without the diagnosis). In 11 patients (29%), there was a plan for reducing stress (in 44% of those with a diagnosis of delirium and in 15% without the diagnosis).\n\nQuestion:\nIs delirium seen in one-third of patients in an acute hospital setting . Identification , pharmacologic and non-pharmacologic treatment is inadequate?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nDelirium is an organically caused acute dysfunction of the brain associated with increased morbidity, mortality, cost of care and poor cognitive recovery. This point prevalence study of delirium was conducted at Hvidovre Hospital, Copenhagen, Denmark at two separate occasions. Patients were examined with the Brief Confusion Assessment Method (bCAM) in both, but in the second survey bCAM was supplemented with a psychiatric assessment using the Diagnostic and Statistical Manual of Mental Disorders, fourth ed. In all, 126 patients were assessed and eight patients were excluded. The delirious patients' charts were examined. Out of the 118 patients included in the study, 38 (32%) were delirious and in 18 (47%) patients, the diagnosis was documented. Furthermore, in 18 (47%) patients, a pharmacological treatment plan for agitation was prepared (in 89% of those diagnosed with delirium and in 10% of those without the diagnosis). In 26 (68%), a plan to increase care existed (in 78% of those with a diagnosis of delirium and in 60% without the diagnosis). In 11 patients (29%), there was a plan for reducing stress (in 44% of those with a diagnosis of delirium and in 15% without the diagnosis).\n\nQuestion:\nIs delirium seen in one-third of patients in an acute hospital setting . Identification , pharmacologic and non-pharmacologic treatment is inadequate?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nThe objective of this study is to investigate the characteristics of esophageal motor activity responsible for the development of gastroesophageal reflux (GER) in patients with esophageal atresia (EA). The subjects consisted of 29 patients with EA (1 month to 19 years). Computerized esophageal manometry was conducted to investigate esophageal contractions at swallow. A topographic esophageal manometric analysis was conducted in each subject, providing 3-dimensional displays to reveal the pressure continuum representing esophageal contractions. Significant contractions in the middle esophagus just below the anastomosis were absent in all subjects. Contractions in the distal esophagus were conspicuously absent in 17 subjects. Of these 17, 6 had already undergone fundoplication, and 9 had symptomatic GER requiring fundoplication subsequent to this study. The remaining 12 patients had contractions in the distal esophagus and did not require medical/surgical intervention. A lack of distal esophageal contractions was significantly correlated with the development of GER (P < .001). There was a significant difference in esophageal acid exposure between the 2 groups (median, 38% vs 4%, P < .001).\n\nQuestion:\nIs lack of distal esophageal contractions a key determinant of gastroesophageal reflux disease after repair of esophageal atresia?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nThe objective of this study is to investigate the characteristics of esophageal motor activity responsible for the development of gastroesophageal reflux (GER) in patients with esophageal atresia (EA). The subjects consisted of 29 patients with EA (1 month to 19 years). Computerized esophageal manometry was conducted to investigate esophageal contractions at swallow. A topographic esophageal manometric analysis was conducted in each subject, providing 3-dimensional displays to reveal the pressure continuum representing esophageal contractions. Significant contractions in the middle esophagus just below the anastomosis were absent in all subjects. Contractions in the distal esophagus were conspicuously absent in 17 subjects. Of these 17, 6 had already undergone fundoplication, and 9 had symptomatic GER requiring fundoplication subsequent to this study. The remaining 12 patients had contractions in the distal esophagus and did not require medical/surgical intervention. A lack of distal esophageal contractions was significantly correlated with the development of GER (P < .001). There was a significant difference in esophageal acid exposure between the 2 groups (median, 38% vs 4%, P < .001).\n\nQuestion:\nIs lack of distal esophageal contractions a key determinant of gastroesophageal reflux disease after repair of esophageal atresia?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nThe objective of this study is to investigate the characteristics of esophageal motor activity responsible for the development of gastroesophageal reflux (GER) in patients with esophageal atresia (EA). The subjects consisted of 29 patients with EA (1 month to 19 years). Computerized esophageal manometry was conducted to investigate esophageal contractions at swallow. A topographic esophageal manometric analysis was conducted in each subject, providing 3-dimensional displays to reveal the pressure continuum representing esophageal contractions. Significant contractions in the middle esophagus just below the anastomosis were absent in all subjects. Contractions in the distal esophagus were conspicuously absent in 17 subjects. Of these 17, 6 had already undergone fundoplication, and 9 had symptomatic GER requiring fundoplication subsequent to this study. The remaining 12 patients had contractions in the distal esophagus and did not require medical/surgical intervention. A lack of distal esophageal contractions was significantly correlated with the development of GER (P < .001). There was a significant difference in esophageal acid exposure between the 2 groups (median, 38% vs 4%, P < .001).\n\nQuestion:\nIs lack of distal esophageal contractions a key determinant of gastroesophageal reflux disease after repair of esophageal atresia?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nCardiac disease accounts for a large burden of premature mortality and morbidity in patients with type 1 myotonic dystrophy (MD). However, little is known about structural cardiac abnormalities particularly in asymptomatic patients with MD. We sought to describe the prevalence and extent of structural cardiac abnormalities in patients with MD and to assess their association with functional, electrical, biochemical and genetic disturbances. In this case-control study, 40 adults with MD who had no contraindications to cardiac MRI (CMR) were identified from the Grampian region genetic database. Forty-one age-and-gender-matched healthy volunteers were also recruited. All subjects underwent detailed assessment including CMR, echocardiography, electrocardiography, signal-averaged electrocardiography, Holter monitoring and quantification of serum B-type natriuretic peptide (BNP). Genetic testing of patients with MD was performed with quantification of CTG trinucleotide repeat sequences. Results of clinical, electrical, genetic and biochemical investigations were correlated with cardiac structural and functional abnormalities detected on CMR. Electrical disturbances including prolongation of PR (187±29 vs 156±23 ms, p<0.001) and QRS intervals (99±11 vs 89±9 ms, p<0.001) were the most prevalent abnormality. Patients with MD had a significantly lower left ventricular (LV) mass (142±44 vs 172±73 g, p=0.03) and lower right ventricular (RV) ejection fraction (46±9 vs 50±7%, p=0.02) compared with controls, although LV ejection fraction was similar between the groups (58±8 vs 59±6%, p=0.34). LV non-compaction was also significantly more prevalent in the MD cohort (35% vs 12%, p=0.019). Late gadolinium enhancement was present in 13% of patients with MD. Muscular disability scores correlated with electrical changes (r=0.529, p<0.001); however, the number of CTG repeat sequences did not correlate with either electrical or structural abnormalities.\n\nQuestion:\nAre structural and electrical cardiac abnormalities prevalent in asymptomatic adults with myotonic dystrophy?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nCardiac disease accounts for a large burden of premature mortality and morbidity in patients with type 1 myotonic dystrophy (MD). However, little is known about structural cardiac abnormalities particularly in asymptomatic patients with MD. We sought to describe the prevalence and extent of structural cardiac abnormalities in patients with MD and to assess their association with functional, electrical, biochemical and genetic disturbances. In this case-control study, 40 adults with MD who had no contraindications to cardiac MRI (CMR) were identified from the Grampian region genetic database. Forty-one age-and-gender-matched healthy volunteers were also recruited. All subjects underwent detailed assessment including CMR, echocardiography, electrocardiography, signal-averaged electrocardiography, Holter monitoring and quantification of serum B-type natriuretic peptide (BNP). Genetic testing of patients with MD was performed with quantification of CTG trinucleotide repeat sequences. Results of clinical, electrical, genetic and biochemical investigations were correlated with cardiac structural and functional abnormalities detected on CMR. Electrical disturbances including prolongation of PR (187±29 vs 156±23 ms, p<0.001) and QRS intervals (99±11 vs 89±9 ms, p<0.001) were the most prevalent abnormality. Patients with MD had a significantly lower left ventricular (LV) mass (142±44 vs 172±73 g, p=0.03) and lower right ventricular (RV) ejection fraction (46±9 vs 50±7%, p=0.02) compared with controls, although LV ejection fraction was similar between the groups (58±8 vs 59±6%, p=0.34). LV non-compaction was also significantly more prevalent in the MD cohort (35% vs 12%, p=0.019). Late gadolinium enhancement was present in 13% of patients with MD. Muscular disability scores correlated with electrical changes (r=0.529, p<0.001); however, the number of CTG repeat sequences did not correlate with either electrical or structural abnormalities.\n\nQuestion:\nAre structural and electrical cardiac abnormalities prevalent in asymptomatic adults with myotonic dystrophy?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nCardiac disease accounts for a large burden of premature mortality and morbidity in patients with type 1 myotonic dystrophy (MD). However, little is known about structural cardiac abnormalities particularly in asymptomatic patients with MD. We sought to describe the prevalence and extent of structural cardiac abnormalities in patients with MD and to assess their association with functional, electrical, biochemical and genetic disturbances. In this case-control study, 40 adults with MD who had no contraindications to cardiac MRI (CMR) were identified from the Grampian region genetic database. Forty-one age-and-gender-matched healthy volunteers were also recruited. All subjects underwent detailed assessment including CMR, echocardiography, electrocardiography, signal-averaged electrocardiography, Holter monitoring and quantification of serum B-type natriuretic peptide (BNP). Genetic testing of patients with MD was performed with quantification of CTG trinucleotide repeat sequences. Results of clinical, electrical, genetic and biochemical investigations were correlated with cardiac structural and functional abnormalities detected on CMR. Electrical disturbances including prolongation of PR (187±29 vs 156±23 ms, p<0.001) and QRS intervals (99±11 vs 89±9 ms, p<0.001) were the most prevalent abnormality. Patients with MD had a significantly lower left ventricular (LV) mass (142±44 vs 172±73 g, p=0.03) and lower right ventricular (RV) ejection fraction (46±9 vs 50±7%, p=0.02) compared with controls, although LV ejection fraction was similar between the groups (58±8 vs 59±6%, p=0.34). LV non-compaction was also significantly more prevalent in the MD cohort (35% vs 12%, p=0.019). Late gadolinium enhancement was present in 13% of patients with MD. Muscular disability scores correlated with electrical changes (r=0.529, p<0.001); however, the number of CTG repeat sequences did not correlate with either electrical or structural abnormalities.\n\nQuestion:\nAre structural and electrical cardiac abnormalities prevalent in asymptomatic adults with myotonic dystrophy?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nTo study the effects of introducing an Enhanced Recovery After Surgery (ERAS) protocol, modified for gynecological surgery, on length of stay and complications following abdominal hysterectomy. Observational study. Department of Obstetrics and Gynecology, Örebro University Hospital, Sweden. Eighty-five patients undergoing abdominal hysterectomy for benign or malignant indications between January and December 2012, with or without salpingo-oophorectomy. Outcomes were compared with all consecutive patients who had undergone the same surgery from January to December 2011, immediately before establishing the ERAS protocol (n = 120). The ERAS protocol was initiated in January 2012 as part of a targeted implementation program. Data were extracted from patient records and from a specific database. Length of stay and the proportion of patients achieving target length of stay (2 days). Length of stay was significantly reduced in the study population after introducing the ERAS protocol from a mean of 2.6 (SD 1.1) days to a mean of 2.3 (SD 1.2) days (p = 0.011). The proportion of patients discharged at 2 days was significantly increased from 56% pre-ERAS to 73% after ERAS (p = 0.012). No differences were found in complications (5% vs. 3.5% in primary stay, 12% vs. 15% within 30 days after discharge), reoperations (2% vs. 1%) or readmission (4% vs. 4%).\n\nQuestion:\nDoes implementing a structured Enhanced Recovery After Surgery ( ERAS ) protocol reduce length of stay after abdominal hysterectomy?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nTo study the effects of introducing an Enhanced Recovery After Surgery (ERAS) protocol, modified for gynecological surgery, on length of stay and complications following abdominal hysterectomy. Observational study. Department of Obstetrics and Gynecology, Örebro University Hospital, Sweden. Eighty-five patients undergoing abdominal hysterectomy for benign or malignant indications between January and December 2012, with or without salpingo-oophorectomy. Outcomes were compared with all consecutive patients who had undergone the same surgery from January to December 2011, immediately before establishing the ERAS protocol (n = 120). The ERAS protocol was initiated in January 2012 as part of a targeted implementation program. Data were extracted from patient records and from a specific database. Length of stay and the proportion of patients achieving target length of stay (2 days). Length of stay was significantly reduced in the study population after introducing the ERAS protocol from a mean of 2.6 (SD 1.1) days to a mean of 2.3 (SD 1.2) days (p = 0.011). The proportion of patients discharged at 2 days was significantly increased from 56% pre-ERAS to 73% after ERAS (p = 0.012). No differences were found in complications (5% vs. 3.5% in primary stay, 12% vs. 15% within 30 days after discharge), reoperations (2% vs. 1%) or readmission (4% vs. 4%).\n\nQuestion:\nDoes implementing a structured Enhanced Recovery After Surgery ( ERAS ) protocol reduce length of stay after abdominal hysterectomy?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nTo study the effects of introducing an Enhanced Recovery After Surgery (ERAS) protocol, modified for gynecological surgery, on length of stay and complications following abdominal hysterectomy. Observational study. Department of Obstetrics and Gynecology, Örebro University Hospital, Sweden. Eighty-five patients undergoing abdominal hysterectomy for benign or malignant indications between January and December 2012, with or without salpingo-oophorectomy. Outcomes were compared with all consecutive patients who had undergone the same surgery from January to December 2011, immediately before establishing the ERAS protocol (n = 120). The ERAS protocol was initiated in January 2012 as part of a targeted implementation program. Data were extracted from patient records and from a specific database. Length of stay and the proportion of patients achieving target length of stay (2 days). Length of stay was significantly reduced in the study population after introducing the ERAS protocol from a mean of 2.6 (SD 1.1) days to a mean of 2.3 (SD 1.2) days (p = 0.011). The proportion of patients discharged at 2 days was significantly increased from 56% pre-ERAS to 73% after ERAS (p = 0.012). No differences were found in complications (5% vs. 3.5% in primary stay, 12% vs. 15% within 30 days after discharge), reoperations (2% vs. 1%) or readmission (4% vs. 4%).\n\nQuestion:\nDoes implementing a structured Enhanced Recovery After Surgery ( ERAS ) protocol reduce length of stay after abdominal hysterectomy?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nStentless aortic valve prostheses have excellent hemodynamic profiles, but may be associated with an increased postoperative heart block when compared to conventional prostheses. To assess the effect of an alternative subcoronary implantation technique on postoperative complete heart block (CHB) and permanent pacemaker implantation (PPI) following aortic valve replacement (AVR) with stentless tissue valves. A total of 130 consecutive patients undergoing AVR with stentless tissue valves by a single surgeon were studied retrospectively. A stentless tissue valve was implanted into 80 patients using the conventional modified subcoronary implantation technique, and 50 patients received a stentless tissue valve by an alternative subcoronary technique in which the inflow suture line is raised at the level of right-non coronary commissure. Data were collected at the time of hospital discharge and at 6-12 months postoperatively. Independent samples t-test was used to compare continuous variables, and categorical variables were compared with the chi-square test. Use of this new method reduced postoperative CHB (4.0% vs. 16.3%, P = 0.033), with fewer patients requiring PPI in the early postoperative period (6.0% vs. 18.8%, P = 0.041). Echocardiographic examination showed no differences in the effective orifice area, peak and mean aortic valve gradients, or left ventricular mass index between groups. Trivial or mild aortic regurgitation was found in 3.9% of patients with the conventional modified technique and 4.0% of patients undergoing the alternative technique, during follow-up (P > 0.05).\n\nQuestion:\nDoes an alternative subcoronary implantation technique decrease the risk of complete heart block after stentless aortic valve replacement?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nStentless aortic valve prostheses have excellent hemodynamic profiles, but may be associated with an increased postoperative heart block when compared to conventional prostheses. To assess the effect of an alternative subcoronary implantation technique on postoperative complete heart block (CHB) and permanent pacemaker implantation (PPI) following aortic valve replacement (AVR) with stentless tissue valves. A total of 130 consecutive patients undergoing AVR with stentless tissue valves by a single surgeon were studied retrospectively. A stentless tissue valve was implanted into 80 patients using the conventional modified subcoronary implantation technique, and 50 patients received a stentless tissue valve by an alternative subcoronary technique in which the inflow suture line is raised at the level of right-non coronary commissure. Data were collected at the time of hospital discharge and at 6-12 months postoperatively. Independent samples t-test was used to compare continuous variables, and categorical variables were compared with the chi-square test. Use of this new method reduced postoperative CHB (4.0% vs. 16.3%, P = 0.033), with fewer patients requiring PPI in the early postoperative period (6.0% vs. 18.8%, P = 0.041). Echocardiographic examination showed no differences in the effective orifice area, peak and mean aortic valve gradients, or left ventricular mass index between groups. Trivial or mild aortic regurgitation was found in 3.9% of patients with the conventional modified technique and 4.0% of patients undergoing the alternative technique, during follow-up (P > 0.05).\n\nQuestion:\nDoes an alternative subcoronary implantation technique decrease the risk of complete heart block after stentless aortic valve replacement?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nStentless aortic valve prostheses have excellent hemodynamic profiles, but may be associated with an increased postoperative heart block when compared to conventional prostheses. To assess the effect of an alternative subcoronary implantation technique on postoperative complete heart block (CHB) and permanent pacemaker implantation (PPI) following aortic valve replacement (AVR) with stentless tissue valves. A total of 130 consecutive patients undergoing AVR with stentless tissue valves by a single surgeon were studied retrospectively. A stentless tissue valve was implanted into 80 patients using the conventional modified subcoronary implantation technique, and 50 patients received a stentless tissue valve by an alternative subcoronary technique in which the inflow suture line is raised at the level of right-non coronary commissure. Data were collected at the time of hospital discharge and at 6-12 months postoperatively. Independent samples t-test was used to compare continuous variables, and categorical variables were compared with the chi-square test. Use of this new method reduced postoperative CHB (4.0% vs. 16.3%, P = 0.033), with fewer patients requiring PPI in the early postoperative period (6.0% vs. 18.8%, P = 0.041). Echocardiographic examination showed no differences in the effective orifice area, peak and mean aortic valve gradients, or left ventricular mass index between groups. Trivial or mild aortic regurgitation was found in 3.9% of patients with the conventional modified technique and 4.0% of patients undergoing the alternative technique, during follow-up (P > 0.05).\n\nQuestion:\nDoes an alternative subcoronary implantation technique decrease the risk of complete heart block after stentless aortic valve replacement?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nTo compare a new insertion method using an EndoGlide (Angiotech/Network Medical Products) with the standard Busin glide (Moria USA) assisted insertion of the posterior lamellar corneal graft in Descemet stripping endothelial keratoplasty (DSEK). Prospective, consecutive, comparative, nonrandomized study. Surgery was performed between October 2008 and October 2010 in 52 eyes of 52 consecutive patients with endothelial dysfunction suitable for DSEK. Twenty-two consecutive eyes underwent the new EndoGlide-assisted insertion of donor lenticule and 30 eyes underwent the surgery using the Busin glide. Six-month follow-up data are available for all patients. Clinical details, best-corrected visual acuity, manifest refraction, intraoperative and postoperative complications, and corneal endothelial cell loss were assessed at 6 months after DSEK. At 6 months after surgery, the best-corrected visual acuity was similar in both groups (0.13 logarithm of the minimal angle of resolution in the EndoGlide eyes as compared with 0.15 logarithm of the minimal angle of resolution in the Busin group; P = .34). Mean spherical equivalent was 0.65 diopter (D) and 0.51 D, and mean refractory cylinder was 1.39 D and 1.08 D, respectively (P = .40). The endothelial cell loss was much lower in the EndoGlide group (25.76%) as compared with the Busin group (47.46%; P < .0001).\n\nQuestion:\nDo a prospective study comparing EndoGlide and Busin glide insertion techniques in descemet stripping endothelial keratoplasty?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nTo compare a new insertion method using an EndoGlide (Angiotech/Network Medical Products) with the standard Busin glide (Moria USA) assisted insertion of the posterior lamellar corneal graft in Descemet stripping endothelial keratoplasty (DSEK). Prospective, consecutive, comparative, nonrandomized study. Surgery was performed between October 2008 and October 2010 in 52 eyes of 52 consecutive patients with endothelial dysfunction suitable for DSEK. Twenty-two consecutive eyes underwent the new EndoGlide-assisted insertion of donor lenticule and 30 eyes underwent the surgery using the Busin glide. Six-month follow-up data are available for all patients. Clinical details, best-corrected visual acuity, manifest refraction, intraoperative and postoperative complications, and corneal endothelial cell loss were assessed at 6 months after DSEK. At 6 months after surgery, the best-corrected visual acuity was similar in both groups (0.13 logarithm of the minimal angle of resolution in the EndoGlide eyes as compared with 0.15 logarithm of the minimal angle of resolution in the Busin group; P = .34). Mean spherical equivalent was 0.65 diopter (D) and 0.51 D, and mean refractory cylinder was 1.39 D and 1.08 D, respectively (P = .40). The endothelial cell loss was much lower in the EndoGlide group (25.76%) as compared with the Busin group (47.46%; P < .0001).\n\nQuestion:\nDo a prospective study comparing EndoGlide and Busin glide insertion techniques in descemet stripping endothelial keratoplasty?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nTo compare a new insertion method using an EndoGlide (Angiotech/Network Medical Products) with the standard Busin glide (Moria USA) assisted insertion of the posterior lamellar corneal graft in Descemet stripping endothelial keratoplasty (DSEK). Prospective, consecutive, comparative, nonrandomized study. Surgery was performed between October 2008 and October 2010 in 52 eyes of 52 consecutive patients with endothelial dysfunction suitable for DSEK. Twenty-two consecutive eyes underwent the new EndoGlide-assisted insertion of donor lenticule and 30 eyes underwent the surgery using the Busin glide. Six-month follow-up data are available for all patients. Clinical details, best-corrected visual acuity, manifest refraction, intraoperative and postoperative complications, and corneal endothelial cell loss were assessed at 6 months after DSEK. At 6 months after surgery, the best-corrected visual acuity was similar in both groups (0.13 logarithm of the minimal angle of resolution in the EndoGlide eyes as compared with 0.15 logarithm of the minimal angle of resolution in the Busin group; P = .34). Mean spherical equivalent was 0.65 diopter (D) and 0.51 D, and mean refractory cylinder was 1.39 D and 1.08 D, respectively (P = .40). The endothelial cell loss was much lower in the EndoGlide group (25.76%) as compared with the Busin group (47.46%; P < .0001).\n\nQuestion:\nDo a prospective study comparing EndoGlide and Busin glide insertion techniques in descemet stripping endothelial keratoplasty?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nLower-extremity injuries constitute the leading cause of trauma hospitalizations among people under the age of 65 years. Rehabilitation has the potential to favorably influence the outcomes associated with traumatic lower-extremity injuries. The objectives of this study were to explore variability in surgeon and physical therapist assessments of the need for physical therapy in patients with traumatic lower-extremity injuries and to determine the factors associated with assessments of need. This study was a retrospective cohort investigation. Participants were 395 patients treated by reconstruction in the Lower-Extremity Assessment Project. They were evaluated at 8 level I trauma centers at 3, 6, and 12 months after hospitalization by an orthopedic surgeon and a physical therapist to determine the need for physical therapy. Analyses included multilevel logistic regression. Chi-square analyses showed that surgeon and therapist assessments of need differed statistically across trauma centers. Surgeons were more likely to assess a need for therapy at 3 months when participants had low work self-efficacy, impaired knee flexion range of motion (ROM), and weight-bearing limitations and at 6 and 12 months when participants had impaired knee flexion ROM and weight-bearing and balance limitations. Therapists were more likely to assess a need for therapy at 3 months when participants had moderate to severe pain and at 6 and 12 months when participants had low work self-efficacy, pain, impaired knee flexion ROM, and balance limitations.\n\nQuestion:\nDo orthopedic surgeons and physical therapists differ in assessment of need for physical therapy after traumatic lower-extremity injury?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nLower-extremity injuries constitute the leading cause of trauma hospitalizations among people under the age of 65 years. Rehabilitation has the potential to favorably influence the outcomes associated with traumatic lower-extremity injuries. The objectives of this study were to explore variability in surgeon and physical therapist assessments of the need for physical therapy in patients with traumatic lower-extremity injuries and to determine the factors associated with assessments of need. This study was a retrospective cohort investigation. Participants were 395 patients treated by reconstruction in the Lower-Extremity Assessment Project. They were evaluated at 8 level I trauma centers at 3, 6, and 12 months after hospitalization by an orthopedic surgeon and a physical therapist to determine the need for physical therapy. Analyses included multilevel logistic regression. Chi-square analyses showed that surgeon and therapist assessments of need differed statistically across trauma centers. Surgeons were more likely to assess a need for therapy at 3 months when participants had low work self-efficacy, impaired knee flexion range of motion (ROM), and weight-bearing limitations and at 6 and 12 months when participants had impaired knee flexion ROM and weight-bearing and balance limitations. Therapists were more likely to assess a need for therapy at 3 months when participants had moderate to severe pain and at 6 and 12 months when participants had low work self-efficacy, pain, impaired knee flexion ROM, and balance limitations.\n\nQuestion:\nDo orthopedic surgeons and physical therapists differ in assessment of need for physical therapy after traumatic lower-extremity injury?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nLower-extremity injuries constitute the leading cause of trauma hospitalizations among people under the age of 65 years. Rehabilitation has the potential to favorably influence the outcomes associated with traumatic lower-extremity injuries. The objectives of this study were to explore variability in surgeon and physical therapist assessments of the need for physical therapy in patients with traumatic lower-extremity injuries and to determine the factors associated with assessments of need. This study was a retrospective cohort investigation. Participants were 395 patients treated by reconstruction in the Lower-Extremity Assessment Project. They were evaluated at 8 level I trauma centers at 3, 6, and 12 months after hospitalization by an orthopedic surgeon and a physical therapist to determine the need for physical therapy. Analyses included multilevel logistic regression. Chi-square analyses showed that surgeon and therapist assessments of need differed statistically across trauma centers. Surgeons were more likely to assess a need for therapy at 3 months when participants had low work self-efficacy, impaired knee flexion range of motion (ROM), and weight-bearing limitations and at 6 and 12 months when participants had impaired knee flexion ROM and weight-bearing and balance limitations. Therapists were more likely to assess a need for therapy at 3 months when participants had moderate to severe pain and at 6 and 12 months when participants had low work self-efficacy, pain, impaired knee flexion ROM, and balance limitations.\n\nQuestion:\nDo orthopedic surgeons and physical therapists differ in assessment of need for physical therapy after traumatic lower-extremity injury?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nPsm2, one of the pyrrolidinoindoline alkaloids isolated from whole Selaginella moellendorffii plants, has shown a potent antiplatelet activity. In this study, we further evaluated the antiplatelet effects of Psm2, and elucidated the underlying mechanisms. Human platelet aggregation in vitro and rat platelet aggregation ex vivo were investigated. Agonist-induced platelet aggregation was measured using a light transmission aggregometer. The antithrombotic effects of Psm2 were evaluated in arteriovenous shunt thrombosis model in rats. To elucidate the mechanisms underlying the antiplatelet activity of Psm2, ELISAs, Western blotting and molecular docking were performed. The bleeding risk of Psm2 administration was assessed in a mouse tail cutting model, and the cytotoxicity of Psm2 was measured with MTT assay in EA.hy926 cells. Psm2 dose-dependently inhibited human platelet aggregation induced by ADP, U4619, thrombin and collagen with IC50 values of 0.64, 0.37, 0.35 and 0.87 mg/mL, respectively. Psm2 (1, 3, 10 mg/kg) administered to rats significantly inhibited platelet aggregation ex vivo induced by ADP. Psm2 (1, 3, 10 mg/mL, iv) administered to rats with the A-V shunt dose-dependently decreased the thrombus formation. Psm2 inhibited platelet adhesion to fibrinogen and collagen with IC50 values of 84.5 and 96.5 mg/mL, respectively, but did not affect the binding of fibrinogen to GPIIb/IIIa. Furthermore, Psm2 inhibited AktSer473 phosphorylation, but did not affect MAPK signaling and Src kinase activation. Molecular docking showed that Psm2 bound to phosphatidylinositol 3-kinase β (PI3Kβ) with a binding free energy of -13.265 kcal/mol. In addition, Psm2 did not cause toxicity in EA.hy926 cells and produced only slight bleeding in a mouse tail cutting model.\n\nQuestion:\nDoes the pyrrolidinoindoline alkaloid Psm2 inhibit platelet aggregation and thrombus formation by affecting PI3K/Akt signaling?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nPsm2, one of the pyrrolidinoindoline alkaloids isolated from whole Selaginella moellendorffii plants, has shown a potent antiplatelet activity. In this study, we further evaluated the antiplatelet effects of Psm2, and elucidated the underlying mechanisms. Human platelet aggregation in vitro and rat platelet aggregation ex vivo were investigated. Agonist-induced platelet aggregation was measured using a light transmission aggregometer. The antithrombotic effects of Psm2 were evaluated in arteriovenous shunt thrombosis model in rats. To elucidate the mechanisms underlying the antiplatelet activity of Psm2, ELISAs, Western blotting and molecular docking were performed. The bleeding risk of Psm2 administration was assessed in a mouse tail cutting model, and the cytotoxicity of Psm2 was measured with MTT assay in EA.hy926 cells. Psm2 dose-dependently inhibited human platelet aggregation induced by ADP, U4619, thrombin and collagen with IC50 values of 0.64, 0.37, 0.35 and 0.87 mg/mL, respectively. Psm2 (1, 3, 10 mg/kg) administered to rats significantly inhibited platelet aggregation ex vivo induced by ADP. Psm2 (1, 3, 10 mg/mL, iv) administered to rats with the A-V shunt dose-dependently decreased the thrombus formation. Psm2 inhibited platelet adhesion to fibrinogen and collagen with IC50 values of 84.5 and 96.5 mg/mL, respectively, but did not affect the binding of fibrinogen to GPIIb/IIIa. Furthermore, Psm2 inhibited AktSer473 phosphorylation, but did not affect MAPK signaling and Src kinase activation. Molecular docking showed that Psm2 bound to phosphatidylinositol 3-kinase β (PI3Kβ) with a binding free energy of -13.265 kcal/mol. In addition, Psm2 did not cause toxicity in EA.hy926 cells and produced only slight bleeding in a mouse tail cutting model.\n\nQuestion:\nDoes the pyrrolidinoindoline alkaloid Psm2 inhibit platelet aggregation and thrombus formation by affecting PI3K/Akt signaling?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nPsm2, one of the pyrrolidinoindoline alkaloids isolated from whole Selaginella moellendorffii plants, has shown a potent antiplatelet activity. In this study, we further evaluated the antiplatelet effects of Psm2, and elucidated the underlying mechanisms. Human platelet aggregation in vitro and rat platelet aggregation ex vivo were investigated. Agonist-induced platelet aggregation was measured using a light transmission aggregometer. The antithrombotic effects of Psm2 were evaluated in arteriovenous shunt thrombosis model in rats. To elucidate the mechanisms underlying the antiplatelet activity of Psm2, ELISAs, Western blotting and molecular docking were performed. The bleeding risk of Psm2 administration was assessed in a mouse tail cutting model, and the cytotoxicity of Psm2 was measured with MTT assay in EA.hy926 cells. Psm2 dose-dependently inhibited human platelet aggregation induced by ADP, U4619, thrombin and collagen with IC50 values of 0.64, 0.37, 0.35 and 0.87 mg/mL, respectively. Psm2 (1, 3, 10 mg/kg) administered to rats significantly inhibited platelet aggregation ex vivo induced by ADP. Psm2 (1, 3, 10 mg/mL, iv) administered to rats with the A-V shunt dose-dependently decreased the thrombus formation. Psm2 inhibited platelet adhesion to fibrinogen and collagen with IC50 values of 84.5 and 96.5 mg/mL, respectively, but did not affect the binding of fibrinogen to GPIIb/IIIa. Furthermore, Psm2 inhibited AktSer473 phosphorylation, but did not affect MAPK signaling and Src kinase activation. Molecular docking showed that Psm2 bound to phosphatidylinositol 3-kinase β (PI3Kβ) with a binding free energy of -13.265 kcal/mol. In addition, Psm2 did not cause toxicity in EA.hy926 cells and produced only slight bleeding in a mouse tail cutting model.\n\nQuestion:\nDoes the pyrrolidinoindoline alkaloid Psm2 inhibit platelet aggregation and thrombus formation by affecting PI3K/Akt signaling?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nThe release and vasoconstrictor effect of endothelin-1 (ET-1) are increased after myocardial ischemia, suggesting a role for ET-1 in ischemia/reperfusion injury. However, the mechanisms of the increased vasoconstriction by ET-1 are unknown. The aim of this study was to test whether ET-1-induced release of thromboxane A2 (TXA2) contributes to the vasoconstrictor effect of ET-1 in nonischemic hearts and whether such release can increase the vasoconstrictor effect of ET-1 in postischemic reperfused hearts. ET-1-induced release of TXA2 was assessed by measurement of the concentrations of its stable metabolite thromboxane B2 (TXB2) in the coronary effluent of nonischemic and reperfused isolated rat hearts before and after administration of 0.01 nmol ET-1 using an enzyme immunoassay. The contribution of ET-1-induced release of TXA2 to the vasoconstrictor effect of ET-1 was assessed by measurement of the effects of ET-1 with and without the cyclooxygenase inhibitor indomethacin or the TXA2/endoperoxide receptor antagonist SQ 30,741 using 31P magnetic resonance spectroscopy. In nonischemic hearts, ET-1 led to a small increase in TXB2 in the coronary effluent (3.9 +/- 1.5 pg/mL; n = 3), but neither indomethacin nor SQ 30,741 significantly diminished the vasoconstrictor effects of ET-1 (reduction of coronary flow, 4.0 +/- 0.4 and 4.5 +/- 0.3 mL/min, respectively, versus 4.9 +/- 0.5 mL/min for ET-1 alone; n = 8, 6, and 9, respectively). In postischemic reperfused hearts, however, ET-1 led to a greater increase in TXB2 (13.7 +/- 1.5 pg/mL; P < .05 versus nonischemic hearts; n = 3), and both indomethacin and SQ 30,741 diminished the vasoconstrictor effects of ET-1 (reduction of coronary flow, 2.6 +/- 0.3 and 2.2 +/- 0.3 mL/min, respectively, versus 4.0 +/- 0.1 mL/min for ET-1 alone; n = 8, 8, and 6, respectively; P < .05). Furthermore, indomethacin and SQ 30,741 prevented the detrimental effects of ET-1 on left ventricular developed pressure, intracellular pH, and phosphocreatine during reperfusion.\n\nQuestion:\nDoes endothelin-1-induced release of thromboxane A2 increase the vasoconstrictor effect of endothelin-1 in postischemic reperfused rat hearts?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nThe release and vasoconstrictor effect of endothelin-1 (ET-1) are increased after myocardial ischemia, suggesting a role for ET-1 in ischemia/reperfusion injury. However, the mechanisms of the increased vasoconstriction by ET-1 are unknown. The aim of this study was to test whether ET-1-induced release of thromboxane A2 (TXA2) contributes to the vasoconstrictor effect of ET-1 in nonischemic hearts and whether such release can increase the vasoconstrictor effect of ET-1 in postischemic reperfused hearts. ET-1-induced release of TXA2 was assessed by measurement of the concentrations of its stable metabolite thromboxane B2 (TXB2) in the coronary effluent of nonischemic and reperfused isolated rat hearts before and after administration of 0.01 nmol ET-1 using an enzyme immunoassay. The contribution of ET-1-induced release of TXA2 to the vasoconstrictor effect of ET-1 was assessed by measurement of the effects of ET-1 with and without the cyclooxygenase inhibitor indomethacin or the TXA2/endoperoxide receptor antagonist SQ 30,741 using 31P magnetic resonance spectroscopy. In nonischemic hearts, ET-1 led to a small increase in TXB2 in the coronary effluent (3.9 +/- 1.5 pg/mL; n = 3), but neither indomethacin nor SQ 30,741 significantly diminished the vasoconstrictor effects of ET-1 (reduction of coronary flow, 4.0 +/- 0.4 and 4.5 +/- 0.3 mL/min, respectively, versus 4.9 +/- 0.5 mL/min for ET-1 alone; n = 8, 6, and 9, respectively). In postischemic reperfused hearts, however, ET-1 led to a greater increase in TXB2 (13.7 +/- 1.5 pg/mL; P < .05 versus nonischemic hearts; n = 3), and both indomethacin and SQ 30,741 diminished the vasoconstrictor effects of ET-1 (reduction of coronary flow, 2.6 +/- 0.3 and 2.2 +/- 0.3 mL/min, respectively, versus 4.0 +/- 0.1 mL/min for ET-1 alone; n = 8, 8, and 6, respectively; P < .05). Furthermore, indomethacin and SQ 30,741 prevented the detrimental effects of ET-1 on left ventricular developed pressure, intracellular pH, and phosphocreatine during reperfusion.\n\nQuestion:\nDoes endothelin-1-induced release of thromboxane A2 increase the vasoconstrictor effect of endothelin-1 in postischemic reperfused rat hearts?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nThe release and vasoconstrictor effect of endothelin-1 (ET-1) are increased after myocardial ischemia, suggesting a role for ET-1 in ischemia/reperfusion injury. However, the mechanisms of the increased vasoconstriction by ET-1 are unknown. The aim of this study was to test whether ET-1-induced release of thromboxane A2 (TXA2) contributes to the vasoconstrictor effect of ET-1 in nonischemic hearts and whether such release can increase the vasoconstrictor effect of ET-1 in postischemic reperfused hearts. ET-1-induced release of TXA2 was assessed by measurement of the concentrations of its stable metabolite thromboxane B2 (TXB2) in the coronary effluent of nonischemic and reperfused isolated rat hearts before and after administration of 0.01 nmol ET-1 using an enzyme immunoassay. The contribution of ET-1-induced release of TXA2 to the vasoconstrictor effect of ET-1 was assessed by measurement of the effects of ET-1 with and without the cyclooxygenase inhibitor indomethacin or the TXA2/endoperoxide receptor antagonist SQ 30,741 using 31P magnetic resonance spectroscopy. In nonischemic hearts, ET-1 led to a small increase in TXB2 in the coronary effluent (3.9 +/- 1.5 pg/mL; n = 3), but neither indomethacin nor SQ 30,741 significantly diminished the vasoconstrictor effects of ET-1 (reduction of coronary flow, 4.0 +/- 0.4 and 4.5 +/- 0.3 mL/min, respectively, versus 4.9 +/- 0.5 mL/min for ET-1 alone; n = 8, 6, and 9, respectively). In postischemic reperfused hearts, however, ET-1 led to a greater increase in TXB2 (13.7 +/- 1.5 pg/mL; P < .05 versus nonischemic hearts; n = 3), and both indomethacin and SQ 30,741 diminished the vasoconstrictor effects of ET-1 (reduction of coronary flow, 2.6 +/- 0.3 and 2.2 +/- 0.3 mL/min, respectively, versus 4.0 +/- 0.1 mL/min for ET-1 alone; n = 8, 8, and 6, respectively; P < .05). Furthermore, indomethacin and SQ 30,741 prevented the detrimental effects of ET-1 on left ventricular developed pressure, intracellular pH, and phosphocreatine during reperfusion.\n\nQuestion:\nDoes endothelin-1-induced release of thromboxane A2 increase the vasoconstrictor effect of endothelin-1 in postischemic reperfused rat hearts?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nEnterovirus infections are major etiological factors in myocarditis and dilated cardiomyopathy. Using an experimental murine model of this disease, previous studies have shown that myocarditis susceptibility depends upon activation of T lymphocytes expressing the gamma delta T cell receptor (TcR), and that only mouse strains which accumulate gamma delta T cells in the myocardium show apoptosis of myocytes or evidence of dilated cardiomyopathy-like disease. The objective of the present studies is to demonstrate that gamma delta T cells directly induce greater Fas-dependent apoptosis of cultured myocytes than T cells expressing the alpha beta TcR. Bl.Tg.E alpha mice were infected for 7 days with coxsackievirus B3 (CVB3). Hearts were removed and were either formalin-fixed, sectioned and stained with hematoxylin and eosin for inflammation, and using TdT-TUNEL for apoptosis, or were minced and collagenase digested for isolation of gamma delta+ and alpha beta+ T cells using immunomagnetic bead separation. Neonatal cultures of cardiac myocytes were isolated from mice less than 2 days old by collagenase and pancreatin digestion, and were either untreated or infected with virus. Levels of Fas (CD95) were measured using FITC-conjugated hamster anti-mouse Fas monoclonal antibody and flow cytometry. Susceptibility of myocytes to Fas-dependent killing was measured by 51Cr-release by labeled myocytes incubated for 4 h on either 3T3-mock or 3T3-FasL transfected cell monolayers. Killing by T cells was also measured in a 4 h 51Cr-release assay. Fas-dependent and perforin-dependent cytotoxicity was determined by specific blocking using either Fas-Fc or concanamycin A. Virally infected myocyte cultures showed significantly enhanced Fas expression compared to uninfected cells, with maximal upregulation of Fas occurring 18-24 h after virus infection. Both infected and uninfected myocytes were selectively killed by FasL-transfected 3T3 cells but not by mock control cells. Approximately 38% of CD3+ lymphocytes isolated from the heart express the gamma delta TcR with the remainder expressing the alpha beta TcR. Both gamma delta+ and alpha beta+ T cells lysed myocyte targets. Blocking studies indicate that gamma delta+ T cells induced predominantly Fas-mediated killing, while alpha beta+ cell produced more perforin-mediated death, although these effectors were capable of Fas-dependent killing as well.\n\nQuestion:\nDo t cells expressing the gamma delta T cell receptor induce apoptosis in cardiac myocytes?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nEnterovirus infections are major etiological factors in myocarditis and dilated cardiomyopathy. Using an experimental murine model of this disease, previous studies have shown that myocarditis susceptibility depends upon activation of T lymphocytes expressing the gamma delta T cell receptor (TcR), and that only mouse strains which accumulate gamma delta T cells in the myocardium show apoptosis of myocytes or evidence of dilated cardiomyopathy-like disease. The objective of the present studies is to demonstrate that gamma delta T cells directly induce greater Fas-dependent apoptosis of cultured myocytes than T cells expressing the alpha beta TcR. Bl.Tg.E alpha mice were infected for 7 days with coxsackievirus B3 (CVB3). Hearts were removed and were either formalin-fixed, sectioned and stained with hematoxylin and eosin for inflammation, and using TdT-TUNEL for apoptosis, or were minced and collagenase digested for isolation of gamma delta+ and alpha beta+ T cells using immunomagnetic bead separation. Neonatal cultures of cardiac myocytes were isolated from mice less than 2 days old by collagenase and pancreatin digestion, and were either untreated or infected with virus. Levels of Fas (CD95) were measured using FITC-conjugated hamster anti-mouse Fas monoclonal antibody and flow cytometry. Susceptibility of myocytes to Fas-dependent killing was measured by 51Cr-release by labeled myocytes incubated for 4 h on either 3T3-mock or 3T3-FasL transfected cell monolayers. Killing by T cells was also measured in a 4 h 51Cr-release assay. Fas-dependent and perforin-dependent cytotoxicity was determined by specific blocking using either Fas-Fc or concanamycin A. Virally infected myocyte cultures showed significantly enhanced Fas expression compared to uninfected cells, with maximal upregulation of Fas occurring 18-24 h after virus infection. Both infected and uninfected myocytes were selectively killed by FasL-transfected 3T3 cells but not by mock control cells. Approximately 38% of CD3+ lymphocytes isolated from the heart express the gamma delta TcR with the remainder expressing the alpha beta TcR. Both gamma delta+ and alpha beta+ T cells lysed myocyte targets. Blocking studies indicate that gamma delta+ T cells induced predominantly Fas-mediated killing, while alpha beta+ cell produced more perforin-mediated death, although these effectors were capable of Fas-dependent killing as well.\n\nQuestion:\nDo t cells expressing the gamma delta T cell receptor induce apoptosis in cardiac myocytes?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nEnterovirus infections are major etiological factors in myocarditis and dilated cardiomyopathy. Using an experimental murine model of this disease, previous studies have shown that myocarditis susceptibility depends upon activation of T lymphocytes expressing the gamma delta T cell receptor (TcR), and that only mouse strains which accumulate gamma delta T cells in the myocardium show apoptosis of myocytes or evidence of dilated cardiomyopathy-like disease. The objective of the present studies is to demonstrate that gamma delta T cells directly induce greater Fas-dependent apoptosis of cultured myocytes than T cells expressing the alpha beta TcR. Bl.Tg.E alpha mice were infected for 7 days with coxsackievirus B3 (CVB3). Hearts were removed and were either formalin-fixed, sectioned and stained with hematoxylin and eosin for inflammation, and using TdT-TUNEL for apoptosis, or were minced and collagenase digested for isolation of gamma delta+ and alpha beta+ T cells using immunomagnetic bead separation. Neonatal cultures of cardiac myocytes were isolated from mice less than 2 days old by collagenase and pancreatin digestion, and were either untreated or infected with virus. Levels of Fas (CD95) were measured using FITC-conjugated hamster anti-mouse Fas monoclonal antibody and flow cytometry. Susceptibility of myocytes to Fas-dependent killing was measured by 51Cr-release by labeled myocytes incubated for 4 h on either 3T3-mock or 3T3-FasL transfected cell monolayers. Killing by T cells was also measured in a 4 h 51Cr-release assay. Fas-dependent and perforin-dependent cytotoxicity was determined by specific blocking using either Fas-Fc or concanamycin A. Virally infected myocyte cultures showed significantly enhanced Fas expression compared to uninfected cells, with maximal upregulation of Fas occurring 18-24 h after virus infection. Both infected and uninfected myocytes were selectively killed by FasL-transfected 3T3 cells but not by mock control cells. Approximately 38% of CD3+ lymphocytes isolated from the heart express the gamma delta TcR with the remainder expressing the alpha beta TcR. Both gamma delta+ and alpha beta+ T cells lysed myocyte targets. Blocking studies indicate that gamma delta+ T cells induced predominantly Fas-mediated killing, while alpha beta+ cell produced more perforin-mediated death, although these effectors were capable of Fas-dependent killing as well.\n\nQuestion:\nDo t cells expressing the gamma delta T cell receptor induce apoptosis in cardiac myocytes?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nIn normal plasma free cortisol accounts for less than 6% of the total with 80-90% bound to corticosteroid-binding globulin (CBG) and the remainder associated albumin. However little is known about the distribution of free cortisol in plasma where CBG is inactivated or in congenital CBG deficiency. Here we describe ligand binding experiments revealing that while free cortisol in unstressed individuals is less than 6% of total cortisol this rises markedly to 25% when CBG is totally inactivated by heat. Similar elevations of the free cortisol fraction were noted in a patient with a rare genetically determined complete lack of CBG (mean 32% on frequent circadian sampling). Following heat inactivation of CBG or in the congenital absence of CBG, there is a shift in cortisol binding from CBG to albumin. That this shift occurs is further supported by experiments adding [3H]-cortisol to physiological human serum albumin solutions, where 25% of cortisol remained in the free fraction.\n\nQuestion:\nDoes plasma free cortisol fraction reflect levels of functioning corticosteroid-binding globulin?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nIn normal plasma free cortisol accounts for less than 6% of the total with 80-90% bound to corticosteroid-binding globulin (CBG) and the remainder associated albumin. However little is known about the distribution of free cortisol in plasma where CBG is inactivated or in congenital CBG deficiency. Here we describe ligand binding experiments revealing that while free cortisol in unstressed individuals is less than 6% of total cortisol this rises markedly to 25% when CBG is totally inactivated by heat. Similar elevations of the free cortisol fraction were noted in a patient with a rare genetically determined complete lack of CBG (mean 32% on frequent circadian sampling). Following heat inactivation of CBG or in the congenital absence of CBG, there is a shift in cortisol binding from CBG to albumin. That this shift occurs is further supported by experiments adding [3H]-cortisol to physiological human serum albumin solutions, where 25% of cortisol remained in the free fraction.\n\nQuestion:\nDoes plasma free cortisol fraction reflect levels of functioning corticosteroid-binding globulin?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nIn normal plasma free cortisol accounts for less than 6% of the total with 80-90% bound to corticosteroid-binding globulin (CBG) and the remainder associated albumin. However little is known about the distribution of free cortisol in plasma where CBG is inactivated or in congenital CBG deficiency. Here we describe ligand binding experiments revealing that while free cortisol in unstressed individuals is less than 6% of total cortisol this rises markedly to 25% when CBG is totally inactivated by heat. Similar elevations of the free cortisol fraction were noted in a patient with a rare genetically determined complete lack of CBG (mean 32% on frequent circadian sampling). Following heat inactivation of CBG or in the congenital absence of CBG, there is a shift in cortisol binding from CBG to albumin. That this shift occurs is further supported by experiments adding [3H]-cortisol to physiological human serum albumin solutions, where 25% of cortisol remained in the free fraction.\n\nQuestion:\nDoes plasma free cortisol fraction reflect levels of functioning corticosteroid-binding globulin?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nAirway smooth muscle (ASM) hyperplasia is a feature of asthma, and increases with disease severity. We hypothesized that this results from migration of ASM or progenitors in response to chemokines derived from ASM or mast cells within the ASM bundle. To examine expression of the chemokine receptor, CC chemokine receptor (CCR) 7, in vivo by ASM in patients with asthma and healthy control subjects, and by primary cultures of ASM and fibroblasts; to define expression of its ligands, CC chemokine ligand (CCL) 19 and CCL21, in bronchial biopsies, and primary cultures of ASM and mast cells; and to investigate CCR7's role in ASM migration and repair. ASM was isolated from bronchoscopy and resection tissue. Receptor and chemokine expression was examined by immunohistochemistry, immunofluorescence, flow cytometry, ELISA, and reverse transcriptase-polymerase chain reaction. CCR7 function was examined by intracellular calcium measurements, chemotaxis, wound healing assays, and measurement of cell proliferation. ASM, myofibroblasts, and fibroblasts expressed CCR7. CCL19, but not CCL21, was highly expressed in bronchial biopsies by mast cells and vessels in asthma of all severities, ASM in severe disease, and ex vivo ASM and mast cells. ASM CCR7 activation by CCL19-mediated intracellular calcium elevation and concentration-dependent migration, but not proliferation. Importantly, mast cell and ASM-derived CCL19 mediated ASM migration and repair.\n\nQuestion:\nDo airway smooth muscle and mast cell-derived CC chemokine ligand 19 mediate airway smooth muscle migration in asthma?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nAirway smooth muscle (ASM) hyperplasia is a feature of asthma, and increases with disease severity. We hypothesized that this results from migration of ASM or progenitors in response to chemokines derived from ASM or mast cells within the ASM bundle. To examine expression of the chemokine receptor, CC chemokine receptor (CCR) 7, in vivo by ASM in patients with asthma and healthy control subjects, and by primary cultures of ASM and fibroblasts; to define expression of its ligands, CC chemokine ligand (CCL) 19 and CCL21, in bronchial biopsies, and primary cultures of ASM and mast cells; and to investigate CCR7's role in ASM migration and repair. ASM was isolated from bronchoscopy and resection tissue. Receptor and chemokine expression was examined by immunohistochemistry, immunofluorescence, flow cytometry, ELISA, and reverse transcriptase-polymerase chain reaction. CCR7 function was examined by intracellular calcium measurements, chemotaxis, wound healing assays, and measurement of cell proliferation. ASM, myofibroblasts, and fibroblasts expressed CCR7. CCL19, but not CCL21, was highly expressed in bronchial biopsies by mast cells and vessels in asthma of all severities, ASM in severe disease, and ex vivo ASM and mast cells. ASM CCR7 activation by CCL19-mediated intracellular calcium elevation and concentration-dependent migration, but not proliferation. Importantly, mast cell and ASM-derived CCL19 mediated ASM migration and repair.\n\nQuestion:\nDo airway smooth muscle and mast cell-derived CC chemokine ligand 19 mediate airway smooth muscle migration in asthma?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nAirway smooth muscle (ASM) hyperplasia is a feature of asthma, and increases with disease severity. We hypothesized that this results from migration of ASM or progenitors in response to chemokines derived from ASM or mast cells within the ASM bundle. To examine expression of the chemokine receptor, CC chemokine receptor (CCR) 7, in vivo by ASM in patients with asthma and healthy control subjects, and by primary cultures of ASM and fibroblasts; to define expression of its ligands, CC chemokine ligand (CCL) 19 and CCL21, in bronchial biopsies, and primary cultures of ASM and mast cells; and to investigate CCR7's role in ASM migration and repair. ASM was isolated from bronchoscopy and resection tissue. Receptor and chemokine expression was examined by immunohistochemistry, immunofluorescence, flow cytometry, ELISA, and reverse transcriptase-polymerase chain reaction. CCR7 function was examined by intracellular calcium measurements, chemotaxis, wound healing assays, and measurement of cell proliferation. ASM, myofibroblasts, and fibroblasts expressed CCR7. CCL19, but not CCL21, was highly expressed in bronchial biopsies by mast cells and vessels in asthma of all severities, ASM in severe disease, and ex vivo ASM and mast cells. ASM CCR7 activation by CCL19-mediated intracellular calcium elevation and concentration-dependent migration, but not proliferation. Importantly, mast cell and ASM-derived CCL19 mediated ASM migration and repair.\n\nQuestion:\nDo airway smooth muscle and mast cell-derived CC chemokine ligand 19 mediate airway smooth muscle migration in asthma?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nMonotherapy with clopidogrel reduced the formation of transplant arteriosclerosis in a murine aortic allograft model. However, the underlying immunologic mechanisms are still unknown. Fully major histocompatibility complex-mismatched C57BL/6 (H2b) donor aortas were transplanted into CBA.J (H2k) recipients and mice received different doses (1, 10, and 20 mg/kg) of clopidogrel, an antagonist of the P2Y12 ADP receptor on platelets, or control saline for 30 days. Blood was analyzed for changes in adhesion molecule and sCD40L concentrations by ELISA. Grafts were analyzed by histology, morphometry, and immunofluorescence on day 30 after transplantation. Intragraft cytokine mRNA production was analyzed by reverse-transcriptase polymerase chain reaction on day 14 after transplantation. Treatment with clopidogrel resulted in significantly decreased blood concentrations of sCD40L and P-selectin after transplantation. Cellular analysis of the aortic transplant revealed fewer numbers of infiltrating dendritic cells (CD205+) and macrophages (F4/80+) after application of clopidogrel, whereas T-cells within the graft were unaltered. In addition cellular P-/E-selectin, ICAM-1, and platelet-derived-growth-factor (PDGF)-beta surface expression were significantly reduced as compared with untreated controls. Intragraft mRNA expression confirmed these results and showed significant lower production of P-/E-selectin, ICAM-1, and PDGF-beta after treatment with clopidogrel. Antiglycoprotein-Ib and antiglycoprotein VI had no beneficial effect on the development of transplant arteriosclerosis.\n\nQuestion:\nIs attenuation of transplant arteriosclerosis with clopidogrel associated with a reduction of infiltrating dendritic cells and macrophages in murine aortic allografts?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nMonotherapy with clopidogrel reduced the formation of transplant arteriosclerosis in a murine aortic allograft model. However, the underlying immunologic mechanisms are still unknown. Fully major histocompatibility complex-mismatched C57BL/6 (H2b) donor aortas were transplanted into CBA.J (H2k) recipients and mice received different doses (1, 10, and 20 mg/kg) of clopidogrel, an antagonist of the P2Y12 ADP receptor on platelets, or control saline for 30 days. Blood was analyzed for changes in adhesion molecule and sCD40L concentrations by ELISA. Grafts were analyzed by histology, morphometry, and immunofluorescence on day 30 after transplantation. Intragraft cytokine mRNA production was analyzed by reverse-transcriptase polymerase chain reaction on day 14 after transplantation. Treatment with clopidogrel resulted in significantly decreased blood concentrations of sCD40L and P-selectin after transplantation. Cellular analysis of the aortic transplant revealed fewer numbers of infiltrating dendritic cells (CD205+) and macrophages (F4/80+) after application of clopidogrel, whereas T-cells within the graft were unaltered. In addition cellular P-/E-selectin, ICAM-1, and platelet-derived-growth-factor (PDGF)-beta surface expression were significantly reduced as compared with untreated controls. Intragraft mRNA expression confirmed these results and showed significant lower production of P-/E-selectin, ICAM-1, and PDGF-beta after treatment with clopidogrel. Antiglycoprotein-Ib and antiglycoprotein VI had no beneficial effect on the development of transplant arteriosclerosis.\n\nQuestion:\nIs attenuation of transplant arteriosclerosis with clopidogrel associated with a reduction of infiltrating dendritic cells and macrophages in murine aortic allografts?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nMonotherapy with clopidogrel reduced the formation of transplant arteriosclerosis in a murine aortic allograft model. However, the underlying immunologic mechanisms are still unknown. Fully major histocompatibility complex-mismatched C57BL/6 (H2b) donor aortas were transplanted into CBA.J (H2k) recipients and mice received different doses (1, 10, and 20 mg/kg) of clopidogrel, an antagonist of the P2Y12 ADP receptor on platelets, or control saline for 30 days. Blood was analyzed for changes in adhesion molecule and sCD40L concentrations by ELISA. Grafts were analyzed by histology, morphometry, and immunofluorescence on day 30 after transplantation. Intragraft cytokine mRNA production was analyzed by reverse-transcriptase polymerase chain reaction on day 14 after transplantation. Treatment with clopidogrel resulted in significantly decreased blood concentrations of sCD40L and P-selectin after transplantation. Cellular analysis of the aortic transplant revealed fewer numbers of infiltrating dendritic cells (CD205+) and macrophages (F4/80+) after application of clopidogrel, whereas T-cells within the graft were unaltered. In addition cellular P-/E-selectin, ICAM-1, and platelet-derived-growth-factor (PDGF)-beta surface expression were significantly reduced as compared with untreated controls. Intragraft mRNA expression confirmed these results and showed significant lower production of P-/E-selectin, ICAM-1, and PDGF-beta after treatment with clopidogrel. Antiglycoprotein-Ib and antiglycoprotein VI had no beneficial effect on the development of transplant arteriosclerosis.\n\nQuestion:\nIs attenuation of transplant arteriosclerosis with clopidogrel associated with a reduction of infiltrating dendritic cells and macrophages in murine aortic allografts?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nAdvanced pancreatic cancer (PC) has very poor prognosis with present treatments, thus necessitating continued efforts to find improved therapeutic approaches. Both preclinical and preliminary clinical data indicate that cytokine-induced killer (CIK) cells are an effective tool against various types of solid tumors. Here, we conducted a study to determine whether CIK cell-based therapy (CBT) can improve the outcomes of advanced PC. Eighty-two patients with advanced PC, whose predicted survival time was longer than 3 months, were analyzed retrospectively. Of all the patients, 57 individuals were receiving chemotherapy, while the remaining 25 individuals were treated with CBT. The overall survival analysis was based on 48 deaths in the 57 patients in the chemotherapy group (84.2%) and 18 deaths in the 25 patients in the CBT group (72.0%). In the CBT group, the median overall survival time was 13.5 months, as compared to 6.6 months in the chemotherapy group (hazard ratio for death, 0.39; 95% confidence interval, 0.23 to 0.65; p < 0.001). The survival rate was 88.9% in the CBT group versus 54.2% in the chemotherapy group at 6 months, 61.1% versus 12.5% at 12 months, and 38.9% versus 4.2% at 18 months. The disease control rate was 68.0% in the CBT group and 29.8% in the chemotherapy group (p < 0.001).\n\nQuestion:\nDoes autologous cytokine-induced killer cell transfusion increase overall survival in advanced pancreatic cancer?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nAdvanced pancreatic cancer (PC) has very poor prognosis with present treatments, thus necessitating continued efforts to find improved therapeutic approaches. Both preclinical and preliminary clinical data indicate that cytokine-induced killer (CIK) cells are an effective tool against various types of solid tumors. Here, we conducted a study to determine whether CIK cell-based therapy (CBT) can improve the outcomes of advanced PC. Eighty-two patients with advanced PC, whose predicted survival time was longer than 3 months, were analyzed retrospectively. Of all the patients, 57 individuals were receiving chemotherapy, while the remaining 25 individuals were treated with CBT. The overall survival analysis was based on 48 deaths in the 57 patients in the chemotherapy group (84.2%) and 18 deaths in the 25 patients in the CBT group (72.0%). In the CBT group, the median overall survival time was 13.5 months, as compared to 6.6 months in the chemotherapy group (hazard ratio for death, 0.39; 95% confidence interval, 0.23 to 0.65; p < 0.001). The survival rate was 88.9% in the CBT group versus 54.2% in the chemotherapy group at 6 months, 61.1% versus 12.5% at 12 months, and 38.9% versus 4.2% at 18 months. The disease control rate was 68.0% in the CBT group and 29.8% in the chemotherapy group (p < 0.001).\n\nQuestion:\nDoes autologous cytokine-induced killer cell transfusion increase overall survival in advanced pancreatic cancer?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nAdvanced pancreatic cancer (PC) has very poor prognosis with present treatments, thus necessitating continued efforts to find improved therapeutic approaches. Both preclinical and preliminary clinical data indicate that cytokine-induced killer (CIK) cells are an effective tool against various types of solid tumors. Here, we conducted a study to determine whether CIK cell-based therapy (CBT) can improve the outcomes of advanced PC. Eighty-two patients with advanced PC, whose predicted survival time was longer than 3 months, were analyzed retrospectively. Of all the patients, 57 individuals were receiving chemotherapy, while the remaining 25 individuals were treated with CBT. The overall survival analysis was based on 48 deaths in the 57 patients in the chemotherapy group (84.2%) and 18 deaths in the 25 patients in the CBT group (72.0%). In the CBT group, the median overall survival time was 13.5 months, as compared to 6.6 months in the chemotherapy group (hazard ratio for death, 0.39; 95% confidence interval, 0.23 to 0.65; p < 0.001). The survival rate was 88.9% in the CBT group versus 54.2% in the chemotherapy group at 6 months, 61.1% versus 12.5% at 12 months, and 38.9% versus 4.2% at 18 months. The disease control rate was 68.0% in the CBT group and 29.8% in the chemotherapy group (p < 0.001).\n\nQuestion:\nDoes autologous cytokine-induced killer cell transfusion increase overall survival in advanced pancreatic cancer?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nMicrovascular disease is a leading cause of cognitive impairment. Approximately 50% of people with a hip fracture have cognitive impairment. We tested the hypothesis that microvascular diseases of the brain (lacunar infarcts and white matter disease [WMD]), kidney (albuminuria [≥ 30 mg/g creatinine] and albumin creatinine ratio [ACR]), and eye (retinal vascular disorders) attenuate the association of cognitive impairment with hip fracture risk. The Cardiovascular Health Cognition Study. Three thousand, one-hundred six participants (mean age, ∼ 79 y; 8.84 y median follow-up) with cognitive testing. Subsets received ACR testing (n=2389), brain magnetic resonance imaging scans (n = 2094), and retinal photography (n = 1098). Incident hip fracture. There were 488 participants (16%) with mild cognitive impairment (MCI) and 564 (18%) with dementia. There were 337 incident hip fractures, of which 19% occurred in participants with MCI and 26% in participants with dementia. Adjusted hazard ratios (HR) and 95% confidence interval for hip fracture in participants with MCI were 2.45 (1.67-3.61) and for dementia 2.35 (1.57-3.52). With doubling of ACR, the HR for fracture was attenuated in participants with dementia compared with participants with normal cognition [interaction HR 0.70 (0.55-0.91)]. No such effect was found in participants with MCI. Albuminuria, lacunar infarcts, WMD, and retinal vascular disease (RVD) did not modify the association of dementia or MCI with hip fracture risk.\n\nQuestion:\nDoes ratio of urine albumin to creatinine attenuate the association of dementia with hip fracture risk?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nMicrovascular disease is a leading cause of cognitive impairment. Approximately 50% of people with a hip fracture have cognitive impairment. We tested the hypothesis that microvascular diseases of the brain (lacunar infarcts and white matter disease [WMD]), kidney (albuminuria [≥ 30 mg/g creatinine] and albumin creatinine ratio [ACR]), and eye (retinal vascular disorders) attenuate the association of cognitive impairment with hip fracture risk. The Cardiovascular Health Cognition Study. Three thousand, one-hundred six participants (mean age, ∼ 79 y; 8.84 y median follow-up) with cognitive testing. Subsets received ACR testing (n=2389), brain magnetic resonance imaging scans (n = 2094), and retinal photography (n = 1098). Incident hip fracture. There were 488 participants (16%) with mild cognitive impairment (MCI) and 564 (18%) with dementia. There were 337 incident hip fractures, of which 19% occurred in participants with MCI and 26% in participants with dementia. Adjusted hazard ratios (HR) and 95% confidence interval for hip fracture in participants with MCI were 2.45 (1.67-3.61) and for dementia 2.35 (1.57-3.52). With doubling of ACR, the HR for fracture was attenuated in participants with dementia compared with participants with normal cognition [interaction HR 0.70 (0.55-0.91)]. No such effect was found in participants with MCI. Albuminuria, lacunar infarcts, WMD, and retinal vascular disease (RVD) did not modify the association of dementia or MCI with hip fracture risk.\n\nQuestion:\nDoes ratio of urine albumin to creatinine attenuate the association of dementia with hip fracture risk?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nMicrovascular disease is a leading cause of cognitive impairment. Approximately 50% of people with a hip fracture have cognitive impairment. We tested the hypothesis that microvascular diseases of the brain (lacunar infarcts and white matter disease [WMD]), kidney (albuminuria [≥ 30 mg/g creatinine] and albumin creatinine ratio [ACR]), and eye (retinal vascular disorders) attenuate the association of cognitive impairment with hip fracture risk. The Cardiovascular Health Cognition Study. Three thousand, one-hundred six participants (mean age, ∼ 79 y; 8.84 y median follow-up) with cognitive testing. Subsets received ACR testing (n=2389), brain magnetic resonance imaging scans (n = 2094), and retinal photography (n = 1098). Incident hip fracture. There were 488 participants (16%) with mild cognitive impairment (MCI) and 564 (18%) with dementia. There were 337 incident hip fractures, of which 19% occurred in participants with MCI and 26% in participants with dementia. Adjusted hazard ratios (HR) and 95% confidence interval for hip fracture in participants with MCI were 2.45 (1.67-3.61) and for dementia 2.35 (1.57-3.52). With doubling of ACR, the HR for fracture was attenuated in participants with dementia compared with participants with normal cognition [interaction HR 0.70 (0.55-0.91)]. No such effect was found in participants with MCI. Albuminuria, lacunar infarcts, WMD, and retinal vascular disease (RVD) did not modify the association of dementia or MCI with hip fracture risk.\n\nQuestion:\nDoes ratio of urine albumin to creatinine attenuate the association of dementia with hip fracture risk?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nPatients with severe renal dysfunction often have unexplained elevated serum concentrations of cardiac troponin T (cTnT). We investigated whether in vivo fragmentation of cTnT could explain these increases. cTnT, creatine kinase isoenzyme MB, and myoglobin serum concentrations were measured in all 63 dialysis patients of our in-hospital dialysis department. A highly sensitive immunoprecipitation assay, followed by electrophoresis and Western blotting, was used to extract and concentrate cTnT and its possible fragments from serum of these 63 hemodialysis patients. Although creatine kinase isoenzyme MB values excluded recent ischemic myocardial events in 55 of the 63 cases, cTnT fragments ranging in size from 8 to 25 kDa were present in the serum samples of all dialysis patients.\n\nQuestion:\nDoes impaired renal clearance explain elevated troponin T fragments in hemodialysis patients?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nPatients with severe renal dysfunction often have unexplained elevated serum concentrations of cardiac troponin T (cTnT). We investigated whether in vivo fragmentation of cTnT could explain these increases. cTnT, creatine kinase isoenzyme MB, and myoglobin serum concentrations were measured in all 63 dialysis patients of our in-hospital dialysis department. A highly sensitive immunoprecipitation assay, followed by electrophoresis and Western blotting, was used to extract and concentrate cTnT and its possible fragments from serum of these 63 hemodialysis patients. Although creatine kinase isoenzyme MB values excluded recent ischemic myocardial events in 55 of the 63 cases, cTnT fragments ranging in size from 8 to 25 kDa were present in the serum samples of all dialysis patients.\n\nQuestion:\nDoes impaired renal clearance explain elevated troponin T fragments in hemodialysis patients?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nPatients with severe renal dysfunction often have unexplained elevated serum concentrations of cardiac troponin T (cTnT). We investigated whether in vivo fragmentation of cTnT could explain these increases. cTnT, creatine kinase isoenzyme MB, and myoglobin serum concentrations were measured in all 63 dialysis patients of our in-hospital dialysis department. A highly sensitive immunoprecipitation assay, followed by electrophoresis and Western blotting, was used to extract and concentrate cTnT and its possible fragments from serum of these 63 hemodialysis patients. Although creatine kinase isoenzyme MB values excluded recent ischemic myocardial events in 55 of the 63 cases, cTnT fragments ranging in size from 8 to 25 kDa were present in the serum samples of all dialysis patients.\n\nQuestion:\nDoes impaired renal clearance explain elevated troponin T fragments in hemodialysis patients?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nBronchopulmonary dysplasia (BPD) and emphysema are characterized by arrested alveolar development or loss of alveoli; both are significant global health problems and currently lack effective therapy. Bone marrow-derived mesenchymal stem cells (BMSCs) prevent adult lung injury, but their therapeutic potential in neonatal lung disease is unknown. We hypothesized that intratracheal delivery of BMSCs would prevent alveolar destruction in experimental BPD. In vitro, BMSC differentiation and migration were assessed using co-culture assays and a modified Boyden chamber. In vivo, the therapeutic potential of BMSCs was assessed in a chronic hyperoxia-induced model of BPD in newborn rats. In vitro, BMSCs developed immunophenotypic and ultrastructural characteristics of type II alveolar epithelial cells (AEC2) (surfactant protein C expression and lamellar bodies) when co-cultured with lung tissue, but not with culture medium alone or liver. Migration assays revealed preferential attraction of BMSCs toward oxygen-damaged lung versus normal lung. In vivo, chronic hyperoxia in newborn rats led to air space enlargement and loss of lung capillaries, and this was associated with a decrease in circulating and resident lung BMSCs. Intratracheal delivery of BMSCs on Postnatal Day 4 improved survival and exercise tolerance while attenuating alveolar and lung vascular injury and pulmonary hypertension. Engrafted BMSCs coexpressed the AEC2-specific marker surfactant protein C. However, engraftment was disproportionately low for cell replacement to account for the therapeutic benefit, suggesting a paracrine-mediated mechanism. In vitro, BMSC-derived conditioned medium prevented O(2)-induced AEC2 apoptosis, accelerated AEC2 wound healing, and enhanced endothelial cord formation.\n\nQuestion:\nDoes airway delivery of mesenchymal stem cells prevent arrested alveolar growth in neonatal lung injury in rats?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nBronchopulmonary dysplasia (BPD) and emphysema are characterized by arrested alveolar development or loss of alveoli; both are significant global health problems and currently lack effective therapy. Bone marrow-derived mesenchymal stem cells (BMSCs) prevent adult lung injury, but their therapeutic potential in neonatal lung disease is unknown. We hypothesized that intratracheal delivery of BMSCs would prevent alveolar destruction in experimental BPD. In vitro, BMSC differentiation and migration were assessed using co-culture assays and a modified Boyden chamber. In vivo, the therapeutic potential of BMSCs was assessed in a chronic hyperoxia-induced model of BPD in newborn rats. In vitro, BMSCs developed immunophenotypic and ultrastructural characteristics of type II alveolar epithelial cells (AEC2) (surfactant protein C expression and lamellar bodies) when co-cultured with lung tissue, but not with culture medium alone or liver. Migration assays revealed preferential attraction of BMSCs toward oxygen-damaged lung versus normal lung. In vivo, chronic hyperoxia in newborn rats led to air space enlargement and loss of lung capillaries, and this was associated with a decrease in circulating and resident lung BMSCs. Intratracheal delivery of BMSCs on Postnatal Day 4 improved survival and exercise tolerance while attenuating alveolar and lung vascular injury and pulmonary hypertension. Engrafted BMSCs coexpressed the AEC2-specific marker surfactant protein C. However, engraftment was disproportionately low for cell replacement to account for the therapeutic benefit, suggesting a paracrine-mediated mechanism. In vitro, BMSC-derived conditioned medium prevented O(2)-induced AEC2 apoptosis, accelerated AEC2 wound healing, and enhanced endothelial cord formation.\n\nQuestion:\nDoes airway delivery of mesenchymal stem cells prevent arrested alveolar growth in neonatal lung injury in rats?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nBronchopulmonary dysplasia (BPD) and emphysema are characterized by arrested alveolar development or loss of alveoli; both are significant global health problems and currently lack effective therapy. Bone marrow-derived mesenchymal stem cells (BMSCs) prevent adult lung injury, but their therapeutic potential in neonatal lung disease is unknown. We hypothesized that intratracheal delivery of BMSCs would prevent alveolar destruction in experimental BPD. In vitro, BMSC differentiation and migration were assessed using co-culture assays and a modified Boyden chamber. In vivo, the therapeutic potential of BMSCs was assessed in a chronic hyperoxia-induced model of BPD in newborn rats. In vitro, BMSCs developed immunophenotypic and ultrastructural characteristics of type II alveolar epithelial cells (AEC2) (surfactant protein C expression and lamellar bodies) when co-cultured with lung tissue, but not with culture medium alone or liver. Migration assays revealed preferential attraction of BMSCs toward oxygen-damaged lung versus normal lung. In vivo, chronic hyperoxia in newborn rats led to air space enlargement and loss of lung capillaries, and this was associated with a decrease in circulating and resident lung BMSCs. Intratracheal delivery of BMSCs on Postnatal Day 4 improved survival and exercise tolerance while attenuating alveolar and lung vascular injury and pulmonary hypertension. Engrafted BMSCs coexpressed the AEC2-specific marker surfactant protein C. However, engraftment was disproportionately low for cell replacement to account for the therapeutic benefit, suggesting a paracrine-mediated mechanism. In vitro, BMSC-derived conditioned medium prevented O(2)-induced AEC2 apoptosis, accelerated AEC2 wound healing, and enhanced endothelial cord formation.\n\nQuestion:\nDoes airway delivery of mesenchymal stem cells prevent arrested alveolar growth in neonatal lung injury in rats?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nMedtronic's Lead Integrity Alert (LIA) software algorithm is useful for detecting abnormal parameters across various ICD-lead families. However, its utility in the assessment of the Biotronik Linox™ family of high-voltage (HV) leads is unknown. We conducted a retrospective cohort study to assess the performance of the LIA algorithm to detect abnormalities and lead failure in Linox ICD-leads. All LIA-enabled Medtronic devices connected to an active Linox lead were included. The alerts were adjudicated by 2 blinded electrophysiologists and correlated with clinical data. Between 2008 and 2012, data from 208 patients with 564 patient-years of follow-up were available for analysis. The median follow-up duration was 32 (IQR 21-41 months). Twenty-one LIA triggers were noted in 20 different patients. The median delay until a positive LIA was 32 months (IQR 21-41 months) postimplant with a 5-year lead survival free from LIA of 76%. Ninety-five percent (19/20) LIA alerts were true lead failures. The most common LIA triggers were short V-V intervals (85%) and nonsustained ventricular tachycardia (85%). Abrupt changes of the ICD-lead impedance occurred in 5/20 triggers. Inappropriate ICD-shocks were strongly associated with a positive LIA (30% vs. 7.4%; P = 0.006). Of the explanted Linox leads 53% had visible abnormalities. The sensitivity, specificity, and positive predictive value for lead failure in the presence of a LIA trigger were 87%, 99.5%, and 95.2%, respectively.\n\nQuestion:\nDoes lead Integrity Alert be Useful for Assessment of Performance of Biotronik Linox Leads?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nMedtronic's Lead Integrity Alert (LIA) software algorithm is useful for detecting abnormal parameters across various ICD-lead families. However, its utility in the assessment of the Biotronik Linox™ family of high-voltage (HV) leads is unknown. We conducted a retrospective cohort study to assess the performance of the LIA algorithm to detect abnormalities and lead failure in Linox ICD-leads. All LIA-enabled Medtronic devices connected to an active Linox lead were included. The alerts were adjudicated by 2 blinded electrophysiologists and correlated with clinical data. Between 2008 and 2012, data from 208 patients with 564 patient-years of follow-up were available for analysis. The median follow-up duration was 32 (IQR 21-41 months). Twenty-one LIA triggers were noted in 20 different patients. The median delay until a positive LIA was 32 months (IQR 21-41 months) postimplant with a 5-year lead survival free from LIA of 76%. Ninety-five percent (19/20) LIA alerts were true lead failures. The most common LIA triggers were short V-V intervals (85%) and nonsustained ventricular tachycardia (85%). Abrupt changes of the ICD-lead impedance occurred in 5/20 triggers. Inappropriate ICD-shocks were strongly associated with a positive LIA (30% vs. 7.4%; P = 0.006). Of the explanted Linox leads 53% had visible abnormalities. The sensitivity, specificity, and positive predictive value for lead failure in the presence of a LIA trigger were 87%, 99.5%, and 95.2%, respectively.\n\nQuestion:\nDoes lead Integrity Alert be Useful for Assessment of Performance of Biotronik Linox Leads?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nMedtronic's Lead Integrity Alert (LIA) software algorithm is useful for detecting abnormal parameters across various ICD-lead families. However, its utility in the assessment of the Biotronik Linox™ family of high-voltage (HV) leads is unknown. We conducted a retrospective cohort study to assess the performance of the LIA algorithm to detect abnormalities and lead failure in Linox ICD-leads. All LIA-enabled Medtronic devices connected to an active Linox lead were included. The alerts were adjudicated by 2 blinded electrophysiologists and correlated with clinical data. Between 2008 and 2012, data from 208 patients with 564 patient-years of follow-up were available for analysis. The median follow-up duration was 32 (IQR 21-41 months). Twenty-one LIA triggers were noted in 20 different patients. The median delay until a positive LIA was 32 months (IQR 21-41 months) postimplant with a 5-year lead survival free from LIA of 76%. Ninety-five percent (19/20) LIA alerts were true lead failures. The most common LIA triggers were short V-V intervals (85%) and nonsustained ventricular tachycardia (85%). Abrupt changes of the ICD-lead impedance occurred in 5/20 triggers. Inappropriate ICD-shocks were strongly associated with a positive LIA (30% vs. 7.4%; P = 0.006). Of the explanted Linox leads 53% had visible abnormalities. The sensitivity, specificity, and positive predictive value for lead failure in the presence of a LIA trigger were 87%, 99.5%, and 95.2%, respectively.\n\nQuestion:\nDoes lead Integrity Alert be Useful for Assessment of Performance of Biotronik Linox Leads?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nThe goals of this study were to determine whether improvements in metabolic control can ameliorate the cognitive dysfunction associated with type 2 diabetes and evaluate the possibility that such improvements are mediated by changes in circulating insulin or insulin resistance. This randomized double-blind trial enrolled 145 subjects at 18 centers in the U.S. Older adults with type 2 diabetes receiving metformin monotherapy received add-on therapy with either rosiglitazone, a thiazolidinedione insulin sensitizer, or glyburide. Cognitive function was assessed at baseline and week 24 using the Digit Symbol Substitution Test, the Rey Auditory Verbal Learning Test, and the Cambridge Neuropsychological Test Automated Battery. Pretreatment fasting plasma glucose (FPG) in both groups was similar, and after 24 weeks both treatment groups showed similar significant reductions in FPG (2.1-2.3 mmol/l). Working memory improved with both rosiglitazone (P < 0.001) and glyburide (P = 0.017). Improvement (25-31% reduction in errors) was most evident on the Paired Associates Learning Test and was significantly correlated (r = 0.30) with improved glycemic control as measured by FPG.\n\nQuestion:\nDoes improving metabolic control lead to better working memory in adults with type 2 diabetes?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nThe goals of this study were to determine whether improvements in metabolic control can ameliorate the cognitive dysfunction associated with type 2 diabetes and evaluate the possibility that such improvements are mediated by changes in circulating insulin or insulin resistance. This randomized double-blind trial enrolled 145 subjects at 18 centers in the U.S. Older adults with type 2 diabetes receiving metformin monotherapy received add-on therapy with either rosiglitazone, a thiazolidinedione insulin sensitizer, or glyburide. Cognitive function was assessed at baseline and week 24 using the Digit Symbol Substitution Test, the Rey Auditory Verbal Learning Test, and the Cambridge Neuropsychological Test Automated Battery. Pretreatment fasting plasma glucose (FPG) in both groups was similar, and after 24 weeks both treatment groups showed similar significant reductions in FPG (2.1-2.3 mmol/l). Working memory improved with both rosiglitazone (P < 0.001) and glyburide (P = 0.017). Improvement (25-31% reduction in errors) was most evident on the Paired Associates Learning Test and was significantly correlated (r = 0.30) with improved glycemic control as measured by FPG.\n\nQuestion:\nDoes improving metabolic control lead to better working memory in adults with type 2 diabetes?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nThe goals of this study were to determine whether improvements in metabolic control can ameliorate the cognitive dysfunction associated with type 2 diabetes and evaluate the possibility that such improvements are mediated by changes in circulating insulin or insulin resistance. This randomized double-blind trial enrolled 145 subjects at 18 centers in the U.S. Older adults with type 2 diabetes receiving metformin monotherapy received add-on therapy with either rosiglitazone, a thiazolidinedione insulin sensitizer, or glyburide. Cognitive function was assessed at baseline and week 24 using the Digit Symbol Substitution Test, the Rey Auditory Verbal Learning Test, and the Cambridge Neuropsychological Test Automated Battery. Pretreatment fasting plasma glucose (FPG) in both groups was similar, and after 24 weeks both treatment groups showed similar significant reductions in FPG (2.1-2.3 mmol/l). Working memory improved with both rosiglitazone (P < 0.001) and glyburide (P = 0.017). Improvement (25-31% reduction in errors) was most evident on the Paired Associates Learning Test and was significantly correlated (r = 0.30) with improved glycemic control as measured by FPG.\n\nQuestion:\nDoes improving metabolic control lead to better working memory in adults with type 2 diabetes?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nConsidering the referred beneficial effects of protein restriction on diabetic nephropathy (DN) and the role of renal endothelium in its pathogenesis, we evaluated the effect of general control nonderepressible 2 (GCN2) kinase activation, a sensor of amino acid deprivation, on known detrimental molecular pathways in primary human glomerular endothelial cells (GEnC). GEnC were cultured under normal or high-glucose conditions in the presence or not of the GCN2 kinase activator, tryptophanol. Glucose transporter 1 (GLUT1) expression was assessed by western blotting and reactive oxygen species (ROS) using a fluorogenic probe. Activities of glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and protein kinase C (PKC) were assessed by commercial activity assays, sorbitol colorimetrically, methylglyoxal by ELISA and O-linked β-N-acetyl glucosamine (O-GlcNAc)-modified proteins by western blotting. High glucose induced GLUT1 expression, increased ROS and inhibited GAPDH. Also it increased the polyol pathway product sorbitol, PKC activity, the level of the O-GlcNAc-modified proteins that produced by the hexosamine pathway and the advanced glycation endproducts' precursor methylglyoxal. Co-treatment of GEnC with tryptophanol restored the above high-glucose-induced alterations.\n\nQuestion:\nDoes activation of general control nonderepressible 2 kinase protect human glomerular endothelial cells from harmful high-glucose-induced molecular pathways?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nConsidering the referred beneficial effects of protein restriction on diabetic nephropathy (DN) and the role of renal endothelium in its pathogenesis, we evaluated the effect of general control nonderepressible 2 (GCN2) kinase activation, a sensor of amino acid deprivation, on known detrimental molecular pathways in primary human glomerular endothelial cells (GEnC). GEnC were cultured under normal or high-glucose conditions in the presence or not of the GCN2 kinase activator, tryptophanol. Glucose transporter 1 (GLUT1) expression was assessed by western blotting and reactive oxygen species (ROS) using a fluorogenic probe. Activities of glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and protein kinase C (PKC) were assessed by commercial activity assays, sorbitol colorimetrically, methylglyoxal by ELISA and O-linked β-N-acetyl glucosamine (O-GlcNAc)-modified proteins by western blotting. High glucose induced GLUT1 expression, increased ROS and inhibited GAPDH. Also it increased the polyol pathway product sorbitol, PKC activity, the level of the O-GlcNAc-modified proteins that produced by the hexosamine pathway and the advanced glycation endproducts' precursor methylglyoxal. Co-treatment of GEnC with tryptophanol restored the above high-glucose-induced alterations.\n\nQuestion:\nDoes activation of general control nonderepressible 2 kinase protect human glomerular endothelial cells from harmful high-glucose-induced molecular pathways?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nConsidering the referred beneficial effects of protein restriction on diabetic nephropathy (DN) and the role of renal endothelium in its pathogenesis, we evaluated the effect of general control nonderepressible 2 (GCN2) kinase activation, a sensor of amino acid deprivation, on known detrimental molecular pathways in primary human glomerular endothelial cells (GEnC). GEnC were cultured under normal or high-glucose conditions in the presence or not of the GCN2 kinase activator, tryptophanol. Glucose transporter 1 (GLUT1) expression was assessed by western blotting and reactive oxygen species (ROS) using a fluorogenic probe. Activities of glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and protein kinase C (PKC) were assessed by commercial activity assays, sorbitol colorimetrically, methylglyoxal by ELISA and O-linked β-N-acetyl glucosamine (O-GlcNAc)-modified proteins by western blotting. High glucose induced GLUT1 expression, increased ROS and inhibited GAPDH. Also it increased the polyol pathway product sorbitol, PKC activity, the level of the O-GlcNAc-modified proteins that produced by the hexosamine pathway and the advanced glycation endproducts' precursor methylglyoxal. Co-treatment of GEnC with tryptophanol restored the above high-glucose-induced alterations.\n\nQuestion:\nDoes activation of general control nonderepressible 2 kinase protect human glomerular endothelial cells from harmful high-glucose-induced molecular pathways?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nThe mechanisms of osteoclast maturation and the role of rheumatoid arthritis (RA) synovial fibroblasts in the control of osteoclastogenesis remain unclear. The purpose of this study was to determine the humoral factors that influence osteoclast differentiation resulting from mutual interactions between osteoclast progenitor cells and synovial fibroblasts. The cloned mouse macrophage cell line RAW 264.7 or isolated human CD14+ monocytes were cocultured with RA or osteoarthritis (OA) synovial fibroblasts in the presence of RANKL. Osteoclasts were visualized by staining for tartrate-resistant acid phosphatase (TRAP), and their functions were evaluated by bone resorption assay. Transforming growth factor beta (TGFbeta) and osteoprotegerin (OPG) levels were measured by enzyme-linked immunosorbent assay. Expression of pSmad2 and Smad7 was analyzed by Western blotting. RANKL-mediated osteoclast formation was observed in cocultures of RAW cells with RA synovial cells, but not with OA synovial cells. This formation was inhibited by TGFbeta receptor kinase inhibitor or neutralizing TGFbeta antibody. Human CD14+ monocytes showed the same results with RAW 264.7, and bone resorption activity was consistent with osteoclast formation. RA synovial fibroblasts produced TGFbeta in response to cell-cell contact with RAW cells in a RANKL-dependent manner. TGFbeta reduced OPG production by RA synovial fibroblasts, but dose-dependently increased OPG secretion in OA synovial fibroblasts. TGFbeta decreased the expression of pSmad2 and increased the expression of Smad7 in RA synovial fibroblasts, but not OA synovial fibroblasts.\n\nQuestion:\nDoes coculture of osteoclast precursors with rheumatoid synovial fibroblasts induce osteoclastogenesis via transforming growth factor beta-mediated down-regulation of osteoprotegerin?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nThe mechanisms of osteoclast maturation and the role of rheumatoid arthritis (RA) synovial fibroblasts in the control of osteoclastogenesis remain unclear. The purpose of this study was to determine the humoral factors that influence osteoclast differentiation resulting from mutual interactions between osteoclast progenitor cells and synovial fibroblasts. The cloned mouse macrophage cell line RAW 264.7 or isolated human CD14+ monocytes were cocultured with RA or osteoarthritis (OA) synovial fibroblasts in the presence of RANKL. Osteoclasts were visualized by staining for tartrate-resistant acid phosphatase (TRAP), and their functions were evaluated by bone resorption assay. Transforming growth factor beta (TGFbeta) and osteoprotegerin (OPG) levels were measured by enzyme-linked immunosorbent assay. Expression of pSmad2 and Smad7 was analyzed by Western blotting. RANKL-mediated osteoclast formation was observed in cocultures of RAW cells with RA synovial cells, but not with OA synovial cells. This formation was inhibited by TGFbeta receptor kinase inhibitor or neutralizing TGFbeta antibody. Human CD14+ monocytes showed the same results with RAW 264.7, and bone resorption activity was consistent with osteoclast formation. RA synovial fibroblasts produced TGFbeta in response to cell-cell contact with RAW cells in a RANKL-dependent manner. TGFbeta reduced OPG production by RA synovial fibroblasts, but dose-dependently increased OPG secretion in OA synovial fibroblasts. TGFbeta decreased the expression of pSmad2 and increased the expression of Smad7 in RA synovial fibroblasts, but not OA synovial fibroblasts.\n\nQuestion:\nDoes coculture of osteoclast precursors with rheumatoid synovial fibroblasts induce osteoclastogenesis via transforming growth factor beta-mediated down-regulation of osteoprotegerin?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nThe mechanisms of osteoclast maturation and the role of rheumatoid arthritis (RA) synovial fibroblasts in the control of osteoclastogenesis remain unclear. The purpose of this study was to determine the humoral factors that influence osteoclast differentiation resulting from mutual interactions between osteoclast progenitor cells and synovial fibroblasts. The cloned mouse macrophage cell line RAW 264.7 or isolated human CD14+ monocytes were cocultured with RA or osteoarthritis (OA) synovial fibroblasts in the presence of RANKL. Osteoclasts were visualized by staining for tartrate-resistant acid phosphatase (TRAP), and their functions were evaluated by bone resorption assay. Transforming growth factor beta (TGFbeta) and osteoprotegerin (OPG) levels were measured by enzyme-linked immunosorbent assay. Expression of pSmad2 and Smad7 was analyzed by Western blotting. RANKL-mediated osteoclast formation was observed in cocultures of RAW cells with RA synovial cells, but not with OA synovial cells. This formation was inhibited by TGFbeta receptor kinase inhibitor or neutralizing TGFbeta antibody. Human CD14+ monocytes showed the same results with RAW 264.7, and bone resorption activity was consistent with osteoclast formation. RA synovial fibroblasts produced TGFbeta in response to cell-cell contact with RAW cells in a RANKL-dependent manner. TGFbeta reduced OPG production by RA synovial fibroblasts, but dose-dependently increased OPG secretion in OA synovial fibroblasts. TGFbeta decreased the expression of pSmad2 and increased the expression of Smad7 in RA synovial fibroblasts, but not OA synovial fibroblasts.\n\nQuestion:\nDoes coculture of osteoclast precursors with rheumatoid synovial fibroblasts induce osteoclastogenesis via transforming growth factor beta-mediated down-regulation of osteoprotegerin?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nIt is not clear whether risk for hepatocellular carcinoma can be accurately determined from long-term changes in serum levels of hepatitis B virus (HBV) DNA or alanine aminotransferase (ALT). We measured serum levels of HBV DNA and ALT at enrollment and during follow-up analysis of 3160 participants in the REVEAL-HBV study. Development of hepatocellular carcinoma was determined from follow-up examinations and computerized linkage with National Cancer Registry and National Death Certification profiles. Multivariate-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox regression models. During 38,330 person-years of follow-up, 81 participants developed hepatocellular carcinoma (incidence rate, 211.3/100,000 person-years). The risk for hepatocellular carcinoma was only slightly higher for participants whose follow-up levels of HBV DNA spontaneously decreased to <10,000 copies/mL compared with those with baseline levels of HBV DNA<10,000 copies/mL (control group; HR, 2.25; 95% CI, 0.68-7.37). Compared with the control group, the HRs (95% CI) for long-term levels of HBV DNA that persisted at 10,000 to 100,000 copies/mL, decreased to/persisted at 100,000 to 1,000,000 copies/mL, or decreased to/persisted at 1,000,000 to 10,000,000 copies/mL were 3.12 (1.09-8.89), 8.85 (3.85-20.35), and 16.78 (7.33-38.39), respectively. A gradient in ALT level was significantly associated with hepatocellular carcinoma risk: from all low-normal, to ever high-normal, to transient abnormal, to persistent abnormal (Ptrend<.001).\n\nQuestion:\nDo changes in serum levels of HBV DNA and alanine aminotransferase determine risk for hepatocellular carcinoma?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nIt is not clear whether risk for hepatocellular carcinoma can be accurately determined from long-term changes in serum levels of hepatitis B virus (HBV) DNA or alanine aminotransferase (ALT). We measured serum levels of HBV DNA and ALT at enrollment and during follow-up analysis of 3160 participants in the REVEAL-HBV study. Development of hepatocellular carcinoma was determined from follow-up examinations and computerized linkage with National Cancer Registry and National Death Certification profiles. Multivariate-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox regression models. During 38,330 person-years of follow-up, 81 participants developed hepatocellular carcinoma (incidence rate, 211.3/100,000 person-years). The risk for hepatocellular carcinoma was only slightly higher for participants whose follow-up levels of HBV DNA spontaneously decreased to <10,000 copies/mL compared with those with baseline levels of HBV DNA<10,000 copies/mL (control group; HR, 2.25; 95% CI, 0.68-7.37). Compared with the control group, the HRs (95% CI) for long-term levels of HBV DNA that persisted at 10,000 to 100,000 copies/mL, decreased to/persisted at 100,000 to 1,000,000 copies/mL, or decreased to/persisted at 1,000,000 to 10,000,000 copies/mL were 3.12 (1.09-8.89), 8.85 (3.85-20.35), and 16.78 (7.33-38.39), respectively. A gradient in ALT level was significantly associated with hepatocellular carcinoma risk: from all low-normal, to ever high-normal, to transient abnormal, to persistent abnormal (Ptrend<.001).\n\nQuestion:\nDo changes in serum levels of HBV DNA and alanine aminotransferase determine risk for hepatocellular carcinoma?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nIt is not clear whether risk for hepatocellular carcinoma can be accurately determined from long-term changes in serum levels of hepatitis B virus (HBV) DNA or alanine aminotransferase (ALT). We measured serum levels of HBV DNA and ALT at enrollment and during follow-up analysis of 3160 participants in the REVEAL-HBV study. Development of hepatocellular carcinoma was determined from follow-up examinations and computerized linkage with National Cancer Registry and National Death Certification profiles. Multivariate-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox regression models. During 38,330 person-years of follow-up, 81 participants developed hepatocellular carcinoma (incidence rate, 211.3/100,000 person-years). The risk for hepatocellular carcinoma was only slightly higher for participants whose follow-up levels of HBV DNA spontaneously decreased to <10,000 copies/mL compared with those with baseline levels of HBV DNA<10,000 copies/mL (control group; HR, 2.25; 95% CI, 0.68-7.37). Compared with the control group, the HRs (95% CI) for long-term levels of HBV DNA that persisted at 10,000 to 100,000 copies/mL, decreased to/persisted at 100,000 to 1,000,000 copies/mL, or decreased to/persisted at 1,000,000 to 10,000,000 copies/mL were 3.12 (1.09-8.89), 8.85 (3.85-20.35), and 16.78 (7.33-38.39), respectively. A gradient in ALT level was significantly associated with hepatocellular carcinoma risk: from all low-normal, to ever high-normal, to transient abnormal, to persistent abnormal (Ptrend<.001).\n\nQuestion:\nDo changes in serum levels of HBV DNA and alanine aminotransferase determine risk for hepatocellular carcinoma?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nTo evaluate patients' self-assessment of their symptoms and cosmetic appearance after fluorescein-potentiated argon laser treatment (FPAL) for corneal inflammation associated with neovascularization. To describe the objective effects of FPAL therapy on established corneal neovascularization with secondary corneal edema and lipid keratopathy. Fifteen patients with corneal neovascularization resulting from various infectious and traumatic etiologies were enrolled in an open, nonrandomized pilot study. Treatment consisted of repeated sessions of intravenous fluorescein, a photosensitizer, combined with blue-green argon laser applications to abnormal corneal vessels. Patients completed a written survey to grade their symptoms and cosmetic appearance prior to treatment and at the end of the follow-up period. Objective changes in signs after FPAL treatment were described by two nonmasked ophthalmologists after slit-lamp examinations and review of serial corneal photographs. Clinical symptoms of blurred vision (p <or= 0.003), photophobia (p <or= 0.03), and cosmetic appearance ( p <or= 0.02) were found to be significantly improved by the patient's subjective assessment survey. There was a trend toward pain reduction (p <or= 0.06) but no apparent reduction in tearing or foreign body sensation (p <or= ns). Objective signs of corneal edema, neovascularization, and lipid keratopathy appeared to be reduced after FPAL therapy.\n\nQuestion:\nDoes fluorescein-potentiated argon laser therapy improve symptoms and appearance of corneal neovascularization?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nTo evaluate patients' self-assessment of their symptoms and cosmetic appearance after fluorescein-potentiated argon laser treatment (FPAL) for corneal inflammation associated with neovascularization. To describe the objective effects of FPAL therapy on established corneal neovascularization with secondary corneal edema and lipid keratopathy. Fifteen patients with corneal neovascularization resulting from various infectious and traumatic etiologies were enrolled in an open, nonrandomized pilot study. Treatment consisted of repeated sessions of intravenous fluorescein, a photosensitizer, combined with blue-green argon laser applications to abnormal corneal vessels. Patients completed a written survey to grade their symptoms and cosmetic appearance prior to treatment and at the end of the follow-up period. Objective changes in signs after FPAL treatment were described by two nonmasked ophthalmologists after slit-lamp examinations and review of serial corneal photographs. Clinical symptoms of blurred vision (p <or= 0.003), photophobia (p <or= 0.03), and cosmetic appearance ( p <or= 0.02) were found to be significantly improved by the patient's subjective assessment survey. There was a trend toward pain reduction (p <or= 0.06) but no apparent reduction in tearing or foreign body sensation (p <or= ns). Objective signs of corneal edema, neovascularization, and lipid keratopathy appeared to be reduced after FPAL therapy.\n\nQuestion:\nDoes fluorescein-potentiated argon laser therapy improve symptoms and appearance of corneal neovascularization?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nTo evaluate patients' self-assessment of their symptoms and cosmetic appearance after fluorescein-potentiated argon laser treatment (FPAL) for corneal inflammation associated with neovascularization. To describe the objective effects of FPAL therapy on established corneal neovascularization with secondary corneal edema and lipid keratopathy. Fifteen patients with corneal neovascularization resulting from various infectious and traumatic etiologies were enrolled in an open, nonrandomized pilot study. Treatment consisted of repeated sessions of intravenous fluorescein, a photosensitizer, combined with blue-green argon laser applications to abnormal corneal vessels. Patients completed a written survey to grade their symptoms and cosmetic appearance prior to treatment and at the end of the follow-up period. Objective changes in signs after FPAL treatment were described by two nonmasked ophthalmologists after slit-lamp examinations and review of serial corneal photographs. Clinical symptoms of blurred vision (p <or= 0.003), photophobia (p <or= 0.03), and cosmetic appearance ( p <or= 0.02) were found to be significantly improved by the patient's subjective assessment survey. There was a trend toward pain reduction (p <or= 0.06) but no apparent reduction in tearing or foreign body sensation (p <or= ns). Objective signs of corneal edema, neovascularization, and lipid keratopathy appeared to be reduced after FPAL therapy.\n\nQuestion:\nDoes fluorescein-potentiated argon laser therapy improve symptoms and appearance of corneal neovascularization?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nEpithelial-mesenchymal transition (EMT) increases cell migration and is implicated in cancer cell invasion and metastasis. We have previously described the involvement of the transcription factors, nuclear factor I-C2 (NFI-C2) and Forkhead box F1 (FoxF1), in the regulation of EMT and invasion during breast tumor progression. NFI-C2 counteracts these processes and FoxF1 is a directly repressed target of NFI-C2. FoxF1 induces EMT and invasiveness and enhances xenograft tumorigenicity in nude mice. Here we identify oppositely regulated targets of NFI-C2 and FoxF1 involved in these processes and further study a possible role for FoxF1 in tumorigenesis. We used Affymetrix microarray to detect changes in the transcriptome of a mouse mammary epithelial cell line upon overexpression of NFI-C2 or FoxF1. To elucidate the effects and signaling events following FoxF1 overexpression we investigated in vitro invasion capacity and changes in transcription and protein expression resulting from RNAi and inhibitor treatment. The extracellular matrix enzyme lysyl oxidase (LOX) was negatively regulated by NFI-C2 and positively regulated by FoxF1, and upregulation of LOX following FoxF1 overexpression in mouse mammary epithelial cells increased in vitro cell invasion. In the nuclei of FoxF1-overexpressing cells, the phosphorylation of Smad2 decreased, while that of p38 increased. Depletion of LOX by RNAi enhanced phosphorylation of Smad2 by a focal adhesion kinase (FAK)-dependent mechanism. In addition, induced expression of FoxF1 in a non-malignant human mammary epithelial cell line showed that the increase in LOX transcription and the suppression of Smad2 activity are early effects of FoxF1.\n\nQuestion:\nDoes forkhead Box F1 promote breast cancer cell migration by upregulating lysyl oxidase and suppressing Smad2/3 signaling?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nEpithelial-mesenchymal transition (EMT) increases cell migration and is implicated in cancer cell invasion and metastasis. We have previously described the involvement of the transcription factors, nuclear factor I-C2 (NFI-C2) and Forkhead box F1 (FoxF1), in the regulation of EMT and invasion during breast tumor progression. NFI-C2 counteracts these processes and FoxF1 is a directly repressed target of NFI-C2. FoxF1 induces EMT and invasiveness and enhances xenograft tumorigenicity in nude mice. Here we identify oppositely regulated targets of NFI-C2 and FoxF1 involved in these processes and further study a possible role for FoxF1 in tumorigenesis. We used Affymetrix microarray to detect changes in the transcriptome of a mouse mammary epithelial cell line upon overexpression of NFI-C2 or FoxF1. To elucidate the effects and signaling events following FoxF1 overexpression we investigated in vitro invasion capacity and changes in transcription and protein expression resulting from RNAi and inhibitor treatment. The extracellular matrix enzyme lysyl oxidase (LOX) was negatively regulated by NFI-C2 and positively regulated by FoxF1, and upregulation of LOX following FoxF1 overexpression in mouse mammary epithelial cells increased in vitro cell invasion. In the nuclei of FoxF1-overexpressing cells, the phosphorylation of Smad2 decreased, while that of p38 increased. Depletion of LOX by RNAi enhanced phosphorylation of Smad2 by a focal adhesion kinase (FAK)-dependent mechanism. In addition, induced expression of FoxF1 in a non-malignant human mammary epithelial cell line showed that the increase in LOX transcription and the suppression of Smad2 activity are early effects of FoxF1.\n\nQuestion:\nDoes forkhead Box F1 promote breast cancer cell migration by upregulating lysyl oxidase and suppressing Smad2/3 signaling?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nEpithelial-mesenchymal transition (EMT) increases cell migration and is implicated in cancer cell invasion and metastasis. We have previously described the involvement of the transcription factors, nuclear factor I-C2 (NFI-C2) and Forkhead box F1 (FoxF1), in the regulation of EMT and invasion during breast tumor progression. NFI-C2 counteracts these processes and FoxF1 is a directly repressed target of NFI-C2. FoxF1 induces EMT and invasiveness and enhances xenograft tumorigenicity in nude mice. Here we identify oppositely regulated targets of NFI-C2 and FoxF1 involved in these processes and further study a possible role for FoxF1 in tumorigenesis. We used Affymetrix microarray to detect changes in the transcriptome of a mouse mammary epithelial cell line upon overexpression of NFI-C2 or FoxF1. To elucidate the effects and signaling events following FoxF1 overexpression we investigated in vitro invasion capacity and changes in transcription and protein expression resulting from RNAi and inhibitor treatment. The extracellular matrix enzyme lysyl oxidase (LOX) was negatively regulated by NFI-C2 and positively regulated by FoxF1, and upregulation of LOX following FoxF1 overexpression in mouse mammary epithelial cells increased in vitro cell invasion. In the nuclei of FoxF1-overexpressing cells, the phosphorylation of Smad2 decreased, while that of p38 increased. Depletion of LOX by RNAi enhanced phosphorylation of Smad2 by a focal adhesion kinase (FAK)-dependent mechanism. In addition, induced expression of FoxF1 in a non-malignant human mammary epithelial cell line showed that the increase in LOX transcription and the suppression of Smad2 activity are early effects of FoxF1.\n\nQuestion:\nDoes forkhead Box F1 promote breast cancer cell migration by upregulating lysyl oxidase and suppressing Smad2/3 signaling?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nThe V600E BRAF mutant plays an important role in the pathogenesis of papillary thyroid cancer (PTC) and is associated with loss of expression of thyroid iodide-metabolizing genes. This study was done to investigate the restorability of expression of these genes by suppressing the BRAF/extracellular signal-regulated kinase kinase (MEK)/mitogen-activated protein (MAP) kinase pathway in V600E BRAF-harboring thyroid cells and to explore the mechanisms involved. We used inducible expression of V600E BRAF, small interfering RNA transfection, and MEK-specific inhibitor to alter the MAP kinase pathway activities and subsequently examined the changes in expression, promoter activities, and methylation status of thyroid genes. MEK inhibitor U0126 or cessation of V600E BRAF expression in PCCL3 cells restored expression of thyroid genes silenced by induced expression of V600E BRAF. U0126 also restored the expression of these genes in V600E BRAF-harboring PTC-derived NPA cells. Knockdown of BRAF by specific small interfering RNA restored expression of some of these genes in NPA cells. Luciferase reporter assay using thyroid-stimulating hormone receptor gene as a model showed that the promoter activity was modulated by the MAP kinase pathway. Promoter methylation in association with DNA methyltransferase expression played a role in gene silencing by MAP kinase pathway in NPA cells.\n\nQuestion:\nDoes suppression of BRAF/MEK/MAP kinase pathway restore expression of iodide-metabolizing genes in thyroid cells expressing the V600E BRAF mutant?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nThe V600E BRAF mutant plays an important role in the pathogenesis of papillary thyroid cancer (PTC) and is associated with loss of expression of thyroid iodide-metabolizing genes. This study was done to investigate the restorability of expression of these genes by suppressing the BRAF/extracellular signal-regulated kinase kinase (MEK)/mitogen-activated protein (MAP) kinase pathway in V600E BRAF-harboring thyroid cells and to explore the mechanisms involved. We used inducible expression of V600E BRAF, small interfering RNA transfection, and MEK-specific inhibitor to alter the MAP kinase pathway activities and subsequently examined the changes in expression, promoter activities, and methylation status of thyroid genes. MEK inhibitor U0126 or cessation of V600E BRAF expression in PCCL3 cells restored expression of thyroid genes silenced by induced expression of V600E BRAF. U0126 also restored the expression of these genes in V600E BRAF-harboring PTC-derived NPA cells. Knockdown of BRAF by specific small interfering RNA restored expression of some of these genes in NPA cells. Luciferase reporter assay using thyroid-stimulating hormone receptor gene as a model showed that the promoter activity was modulated by the MAP kinase pathway. Promoter methylation in association with DNA methyltransferase expression played a role in gene silencing by MAP kinase pathway in NPA cells.\n\nQuestion:\nDoes suppression of BRAF/MEK/MAP kinase pathway restore expression of iodide-metabolizing genes in thyroid cells expressing the V600E BRAF mutant?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nThe V600E BRAF mutant plays an important role in the pathogenesis of papillary thyroid cancer (PTC) and is associated with loss of expression of thyroid iodide-metabolizing genes. This study was done to investigate the restorability of expression of these genes by suppressing the BRAF/extracellular signal-regulated kinase kinase (MEK)/mitogen-activated protein (MAP) kinase pathway in V600E BRAF-harboring thyroid cells and to explore the mechanisms involved. We used inducible expression of V600E BRAF, small interfering RNA transfection, and MEK-specific inhibitor to alter the MAP kinase pathway activities and subsequently examined the changes in expression, promoter activities, and methylation status of thyroid genes. MEK inhibitor U0126 or cessation of V600E BRAF expression in PCCL3 cells restored expression of thyroid genes silenced by induced expression of V600E BRAF. U0126 also restored the expression of these genes in V600E BRAF-harboring PTC-derived NPA cells. Knockdown of BRAF by specific small interfering RNA restored expression of some of these genes in NPA cells. Luciferase reporter assay using thyroid-stimulating hormone receptor gene as a model showed that the promoter activity was modulated by the MAP kinase pathway. Promoter methylation in association with DNA methyltransferase expression played a role in gene silencing by MAP kinase pathway in NPA cells.\n\nQuestion:\nDoes suppression of BRAF/MEK/MAP kinase pathway restore expression of iodide-metabolizing genes in thyroid cells expressing the V600E BRAF mutant?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nIdentical DNA methylation differences between maternal and paternal alleles in gametes and adults suggest that the inheritance of genomic imprints is strictly due to the embryonic maintenance of DNA methylation. Such maintenance would occur in association with every cycle of DNA replication, including those of preimplantation embryos. The expression of the somatic form of the Dnmt1 cytosine methyltransferase (Dnmt1s) was examined in cleavage-stage preimplantation mouse embryos. Low concentrations of Dnmt1s are found in 1-, 2-, 4-, and 8-cell embryos, as well as in morulae and blastocysts. Dnmt1s is present in the cytoplasm at all stages, and in the nuclei of all stages except the 1-cell, pronuclear-stage embryo. The related oocyte-derived Dnmt1o protein is also present in nuclei of 8-cell embryos, along with embryo-synthesized Dnmt1s. Dnmt1s protein expressed in 1-cell and 2-cell embryos is derived from the oocyte, whereas the embryo synthesizes its own Dnmt1s from the 2-cell stage onward.\n\nQuestion:\nDoes preimplantation expression of the somatic form of Dnmt1 suggest a role in the inheritance of genomic imprints?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nIdentical DNA methylation differences between maternal and paternal alleles in gametes and adults suggest that the inheritance of genomic imprints is strictly due to the embryonic maintenance of DNA methylation. Such maintenance would occur in association with every cycle of DNA replication, including those of preimplantation embryos. The expression of the somatic form of the Dnmt1 cytosine methyltransferase (Dnmt1s) was examined in cleavage-stage preimplantation mouse embryos. Low concentrations of Dnmt1s are found in 1-, 2-, 4-, and 8-cell embryos, as well as in morulae and blastocysts. Dnmt1s is present in the cytoplasm at all stages, and in the nuclei of all stages except the 1-cell, pronuclear-stage embryo. The related oocyte-derived Dnmt1o protein is also present in nuclei of 8-cell embryos, along with embryo-synthesized Dnmt1s. Dnmt1s protein expressed in 1-cell and 2-cell embryos is derived from the oocyte, whereas the embryo synthesizes its own Dnmt1s from the 2-cell stage onward.\n\nQuestion:\nDoes preimplantation expression of the somatic form of Dnmt1 suggest a role in the inheritance of genomic imprints?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nIdentical DNA methylation differences between maternal and paternal alleles in gametes and adults suggest that the inheritance of genomic imprints is strictly due to the embryonic maintenance of DNA methylation. Such maintenance would occur in association with every cycle of DNA replication, including those of preimplantation embryos. The expression of the somatic form of the Dnmt1 cytosine methyltransferase (Dnmt1s) was examined in cleavage-stage preimplantation mouse embryos. Low concentrations of Dnmt1s are found in 1-, 2-, 4-, and 8-cell embryos, as well as in morulae and blastocysts. Dnmt1s is present in the cytoplasm at all stages, and in the nuclei of all stages except the 1-cell, pronuclear-stage embryo. The related oocyte-derived Dnmt1o protein is also present in nuclei of 8-cell embryos, along with embryo-synthesized Dnmt1s. Dnmt1s protein expressed in 1-cell and 2-cell embryos is derived from the oocyte, whereas the embryo synthesizes its own Dnmt1s from the 2-cell stage onward.\n\nQuestion:\nDoes preimplantation expression of the somatic form of Dnmt1 suggest a role in the inheritance of genomic imprints?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nTo investigate the placental expression of angiopoietin (Ang)-1, Ang-2 and their receptor, Tie-2, in preeclampsia (PE) with or without intrauterine growth restriction (IUGR). Case-control study including placentas from 28 PE pregnancies, 30 PE-IUGR pregnancies and 40 controls. The expression status of the genes was evaluated by quantitative real-time PCR. In both PE and PE-IUGR groups, compared to the control group, there was significantly higher expression of Ang-2 (p < 0.001) and Tie-2 (p = 0.008) and lower expression of Ang-1 (p = 0.001). The magnitude of the difference was similar for Ang-1 for both groups, whereas the magnitude of the differences was higher for Ang-2 and Tie-2 in PE-IUGR group compared to controls. Ang-2 and Tie-2 were correlated in both PE (r = 0.8602, p < 0.001) and PE-IUGR (r = 0.6342, p < 0.001) groups. In PE-IUGR group, Ang-1 was associated to Ang-2 (r = 0.3458, p = 0.0452) and Tie-2 (r = 0.4448, p = 0.0084). Log10Ang-1 but not Ang-2 was gestational age dependent (R2 = 0.40, p < 0.001). After conversion in Multiples of the Median (MoM) log10 MoM Ang-1 was reduced in the PE group (mean = -0.8181, p < 0.001) and the PE-IUGR group (mean = -1.2583, p < 0.001) compared to control group (mean = -0.0924).\n\nQuestion:\nIs placental mRNA expression of angiopoietins ( Ang ) -1 , Ang-2 and their receptor Tie-2 altered in pregnancies complicated by preeclampsia?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nTo investigate the placental expression of angiopoietin (Ang)-1, Ang-2 and their receptor, Tie-2, in preeclampsia (PE) with or without intrauterine growth restriction (IUGR). Case-control study including placentas from 28 PE pregnancies, 30 PE-IUGR pregnancies and 40 controls. The expression status of the genes was evaluated by quantitative real-time PCR. In both PE and PE-IUGR groups, compared to the control group, there was significantly higher expression of Ang-2 (p < 0.001) and Tie-2 (p = 0.008) and lower expression of Ang-1 (p = 0.001). The magnitude of the difference was similar for Ang-1 for both groups, whereas the magnitude of the differences was higher for Ang-2 and Tie-2 in PE-IUGR group compared to controls. Ang-2 and Tie-2 were correlated in both PE (r = 0.8602, p < 0.001) and PE-IUGR (r = 0.6342, p < 0.001) groups. In PE-IUGR group, Ang-1 was associated to Ang-2 (r = 0.3458, p = 0.0452) and Tie-2 (r = 0.4448, p = 0.0084). Log10Ang-1 but not Ang-2 was gestational age dependent (R2 = 0.40, p < 0.001). After conversion in Multiples of the Median (MoM) log10 MoM Ang-1 was reduced in the PE group (mean = -0.8181, p < 0.001) and the PE-IUGR group (mean = -1.2583, p < 0.001) compared to control group (mean = -0.0924).\n\nQuestion:\nIs placental mRNA expression of angiopoietins ( Ang ) -1 , Ang-2 and their receptor Tie-2 altered in pregnancies complicated by preeclampsia?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nTo investigate the placental expression of angiopoietin (Ang)-1, Ang-2 and their receptor, Tie-2, in preeclampsia (PE) with or without intrauterine growth restriction (IUGR). Case-control study including placentas from 28 PE pregnancies, 30 PE-IUGR pregnancies and 40 controls. The expression status of the genes was evaluated by quantitative real-time PCR. In both PE and PE-IUGR groups, compared to the control group, there was significantly higher expression of Ang-2 (p < 0.001) and Tie-2 (p = 0.008) and lower expression of Ang-1 (p = 0.001). The magnitude of the difference was similar for Ang-1 for both groups, whereas the magnitude of the differences was higher for Ang-2 and Tie-2 in PE-IUGR group compared to controls. Ang-2 and Tie-2 were correlated in both PE (r = 0.8602, p < 0.001) and PE-IUGR (r = 0.6342, p < 0.001) groups. In PE-IUGR group, Ang-1 was associated to Ang-2 (r = 0.3458, p = 0.0452) and Tie-2 (r = 0.4448, p = 0.0084). Log10Ang-1 but not Ang-2 was gestational age dependent (R2 = 0.40, p < 0.001). After conversion in Multiples of the Median (MoM) log10 MoM Ang-1 was reduced in the PE group (mean = -0.8181, p < 0.001) and the PE-IUGR group (mean = -1.2583, p < 0.001) compared to control group (mean = -0.0924).\n\nQuestion:\nIs placental mRNA expression of angiopoietins ( Ang ) -1 , Ang-2 and their receptor Tie-2 altered in pregnancies complicated by preeclampsia?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nThyroid hormone (TH) is essential for the developing brain, and because the fetal thyroid develops relatively late in gestation, the maternal TH supply is critical for fetal brain development. However, if the mother has hypothyroidism during pregnancy, fetal brain and neuropsychological development may be compromised. Rodents experiencing maternal TH insufficiency show abnormal corpus callosum (CC) morphology, but it is not known if children born to women treated for hypothyroidism (HYPO) show similar effects. The purpose of the current study was to investigate HYPO for CC morphology and morphometry and to determine whether any specific CC abnormalities were associated aspects of maternal hypothyroidism and were correlated with reduced neuropsychological functioning in the children. ANALYZE software was used to trace CCs in archived magnetic resonance imaging scans from 22 HYPO and 22 matched controls. Areas of two sub-regions and six segments and different shape metrics (angles, lengths, ratios) were determined. CC parameters were correlated with maternal thyrotropin (TSH) values and number of hypothyroid trimesters as well as the child's neuropsychological test performance. HYPO showed a smaller anterior CC and genu and larger posterior CC and splenium areas than controls as well as shape abnormalities in genu and splenium. Results were correlated with the duration of maternal hypothyroidism. Executive function skills were positively associated with genu size in HYPO, while verbal comprehension skills were negatively associated with splenium and overall posterior CC sizes.\n\nQuestion:\nDo children born to women treated for hypothyroidism during pregnancy show abnormal corpus callosum development?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nThyroid hormone (TH) is essential for the developing brain, and because the fetal thyroid develops relatively late in gestation, the maternal TH supply is critical for fetal brain development. However, if the mother has hypothyroidism during pregnancy, fetal brain and neuropsychological development may be compromised. Rodents experiencing maternal TH insufficiency show abnormal corpus callosum (CC) morphology, but it is not known if children born to women treated for hypothyroidism (HYPO) show similar effects. The purpose of the current study was to investigate HYPO for CC morphology and morphometry and to determine whether any specific CC abnormalities were associated aspects of maternal hypothyroidism and were correlated with reduced neuropsychological functioning in the children. ANALYZE software was used to trace CCs in archived magnetic resonance imaging scans from 22 HYPO and 22 matched controls. Areas of two sub-regions and six segments and different shape metrics (angles, lengths, ratios) were determined. CC parameters were correlated with maternal thyrotropin (TSH) values and number of hypothyroid trimesters as well as the child's neuropsychological test performance. HYPO showed a smaller anterior CC and genu and larger posterior CC and splenium areas than controls as well as shape abnormalities in genu and splenium. Results were correlated with the duration of maternal hypothyroidism. Executive function skills were positively associated with genu size in HYPO, while verbal comprehension skills were negatively associated with splenium and overall posterior CC sizes.\n\nQuestion:\nDo children born to women treated for hypothyroidism during pregnancy show abnormal corpus callosum development?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nThyroid hormone (TH) is essential for the developing brain, and because the fetal thyroid develops relatively late in gestation, the maternal TH supply is critical for fetal brain development. However, if the mother has hypothyroidism during pregnancy, fetal brain and neuropsychological development may be compromised. Rodents experiencing maternal TH insufficiency show abnormal corpus callosum (CC) morphology, but it is not known if children born to women treated for hypothyroidism (HYPO) show similar effects. The purpose of the current study was to investigate HYPO for CC morphology and morphometry and to determine whether any specific CC abnormalities were associated aspects of maternal hypothyroidism and were correlated with reduced neuropsychological functioning in the children. ANALYZE software was used to trace CCs in archived magnetic resonance imaging scans from 22 HYPO and 22 matched controls. Areas of two sub-regions and six segments and different shape metrics (angles, lengths, ratios) were determined. CC parameters were correlated with maternal thyrotropin (TSH) values and number of hypothyroid trimesters as well as the child's neuropsychological test performance. HYPO showed a smaller anterior CC and genu and larger posterior CC and splenium areas than controls as well as shape abnormalities in genu and splenium. Results were correlated with the duration of maternal hypothyroidism. Executive function skills were positively associated with genu size in HYPO, while verbal comprehension skills were negatively associated with splenium and overall posterior CC sizes.\n\nQuestion:\nDo children born to women treated for hypothyroidism during pregnancy show abnormal corpus callosum development?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nTo examine the effects produced by electroacupuncture (EA) of different frequencies on the expression of morphine conditioned place preference (CPP) in rats. SD rats were given 4 days consecutive trials in a computerized three-chamber \"unbiased\" CPP apparatus. Twenty-four hours later, the time spent on drug-pairing compartment of the rat was examined. Rats trained with CPP paradigms were then given EA of 2 Hz or 100 Hz once a day for 3 days. Twenty-four hours after the final EA session, they were again put to the CPP chamber, and the time spent on drug-pairing compartment was measured. Rats receiving morphine at a dose of 4 mg.kg-1 (i.p.) showed significantly enhanced preference scores in drug-pairing side than that of the control group. In other words, rats preferred the drug-pairing environment to the nondrug-pairing place. In addition, rats that received treatment with EA of 2 Hz or 100 Hz spent significantly less time on the drug pairing side than that of the CPP control group.\n\nQuestion:\nDoes [ Electroacupuncture suppress morphine -- induced conditioned place preference ( CPP ) in rats ]?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nTo examine the effects produced by electroacupuncture (EA) of different frequencies on the expression of morphine conditioned place preference (CPP) in rats. SD rats were given 4 days consecutive trials in a computerized three-chamber \"unbiased\" CPP apparatus. Twenty-four hours later, the time spent on drug-pairing compartment of the rat was examined. Rats trained with CPP paradigms were then given EA of 2 Hz or 100 Hz once a day for 3 days. Twenty-four hours after the final EA session, they were again put to the CPP chamber, and the time spent on drug-pairing compartment was measured. Rats receiving morphine at a dose of 4 mg.kg-1 (i.p.) showed significantly enhanced preference scores in drug-pairing side than that of the control group. In other words, rats preferred the drug-pairing environment to the nondrug-pairing place. In addition, rats that received treatment with EA of 2 Hz or 100 Hz spent significantly less time on the drug pairing side than that of the CPP control group.\n\nQuestion:\nDoes [ Electroacupuncture suppress morphine -- induced conditioned place preference ( CPP ) in rats ]?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nTo examine the effects produced by electroacupuncture (EA) of different frequencies on the expression of morphine conditioned place preference (CPP) in rats. SD rats were given 4 days consecutive trials in a computerized three-chamber \"unbiased\" CPP apparatus. Twenty-four hours later, the time spent on drug-pairing compartment of the rat was examined. Rats trained with CPP paradigms were then given EA of 2 Hz or 100 Hz once a day for 3 days. Twenty-four hours after the final EA session, they were again put to the CPP chamber, and the time spent on drug-pairing compartment was measured. Rats receiving morphine at a dose of 4 mg.kg-1 (i.p.) showed significantly enhanced preference scores in drug-pairing side than that of the control group. In other words, rats preferred the drug-pairing environment to the nondrug-pairing place. In addition, rats that received treatment with EA of 2 Hz or 100 Hz spent significantly less time on the drug pairing side than that of the CPP control group.\n\nQuestion:\nDoes [ Electroacupuncture suppress morphine -- induced conditioned place preference ( CPP ) in rats ]?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nPeripheral clock genes show a circadian rhythm is correlated with the timing of feeding in peripheral tissues. It was reported that these clock genes are strongly regulated by insulin action and that a high-fat diet (HFD) intake in C57BL/6J mice for 21days induced insulin secretion during the dark phase and reduced the circadian rhythm of clock genes. In this study, we examined the circadian expression patterns of these clock genes in insulin-resistant animal models with excess secretion of insulin during the day. We examined whether insulin resistance induced by a HFD intake for 80days altered blood parameters (glucose and insulin concentrations) and expression of mRNA and proteins encoded by clock and functional genes in the liver using male ICR mice. Serum insulin concentrations were continuously higher during the day in mice fed a HFD than control mice. Expression of lipogenesis-related genes (Fas and Accβ) and the transcription factor Chrebp peaked at zeitgeber time (ZT)24 in the liver of control mice. A HFD intake reduced the expression of these genes at ZT24 and disrupted the circadian rhythm. Expression of Bmal1 and Clock, transcription factors that compose the core feedback loop, showed circadian variation and were synchronously associated with Fas gene expression in control mice, but not in those fed a HFD.\n\nQuestion:\nIs loss of circadian rhythm of circulating insulin concentration induced by high-fat diet intake associated with disrupted rhythmic expression of circadian clock genes in the liver?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nPeripheral clock genes show a circadian rhythm is correlated with the timing of feeding in peripheral tissues. It was reported that these clock genes are strongly regulated by insulin action and that a high-fat diet (HFD) intake in C57BL/6J mice for 21days induced insulin secretion during the dark phase and reduced the circadian rhythm of clock genes. In this study, we examined the circadian expression patterns of these clock genes in insulin-resistant animal models with excess secretion of insulin during the day. We examined whether insulin resistance induced by a HFD intake for 80days altered blood parameters (glucose and insulin concentrations) and expression of mRNA and proteins encoded by clock and functional genes in the liver using male ICR mice. Serum insulin concentrations were continuously higher during the day in mice fed a HFD than control mice. Expression of lipogenesis-related genes (Fas and Accβ) and the transcription factor Chrebp peaked at zeitgeber time (ZT)24 in the liver of control mice. A HFD intake reduced the expression of these genes at ZT24 and disrupted the circadian rhythm. Expression of Bmal1 and Clock, transcription factors that compose the core feedback loop, showed circadian variation and were synchronously associated with Fas gene expression in control mice, but not in those fed a HFD.\n\nQuestion:\nIs loss of circadian rhythm of circulating insulin concentration induced by high-fat diet intake associated with disrupted rhythmic expression of circadian clock genes in the liver?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nPeripheral clock genes show a circadian rhythm is correlated with the timing of feeding in peripheral tissues. It was reported that these clock genes are strongly regulated by insulin action and that a high-fat diet (HFD) intake in C57BL/6J mice for 21days induced insulin secretion during the dark phase and reduced the circadian rhythm of clock genes. In this study, we examined the circadian expression patterns of these clock genes in insulin-resistant animal models with excess secretion of insulin during the day. We examined whether insulin resistance induced by a HFD intake for 80days altered blood parameters (glucose and insulin concentrations) and expression of mRNA and proteins encoded by clock and functional genes in the liver using male ICR mice. Serum insulin concentrations were continuously higher during the day in mice fed a HFD than control mice. Expression of lipogenesis-related genes (Fas and Accβ) and the transcription factor Chrebp peaked at zeitgeber time (ZT)24 in the liver of control mice. A HFD intake reduced the expression of these genes at ZT24 and disrupted the circadian rhythm. Expression of Bmal1 and Clock, transcription factors that compose the core feedback loop, showed circadian variation and were synchronously associated with Fas gene expression in control mice, but not in those fed a HFD.\n\nQuestion:\nIs loss of circadian rhythm of circulating insulin concentration induced by high-fat diet intake associated with disrupted rhythmic expression of circadian clock genes in the liver?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nTo examine the prevalence rates of household smoking and ownership of a furred or feathered pet, the intercorrelation of these home environment measures, and their association with sociodemographic, family, and child asthma variables. Children with asthma (n = 152, aged 7-18 years) with asthma and their primary parent were evaluated through the use of reliable and valid questionnaires focusing on exposure to household smoke and furred or feathered pets as well as sociodemographic, family, and asthma variables. Prevalence of household smoking and pet ownership were high and comparable to normal levels in the US population. Smoking and pet ownership were not correlated with each other or with asthma medication adherence. Sociodemographic, family, and asthma variables showed distinct patterns of correlation with smoking and pet status. Household smoking was associated with poorer family resources and greater stress; pet ownership was associated with greater resources.\n\nQuestion:\nDoes prevalence and correlate of household exposures to tobacco smoke and pets in children with asthma?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nTo examine the prevalence rates of household smoking and ownership of a furred or feathered pet, the intercorrelation of these home environment measures, and their association with sociodemographic, family, and child asthma variables. Children with asthma (n = 152, aged 7-18 years) with asthma and their primary parent were evaluated through the use of reliable and valid questionnaires focusing on exposure to household smoke and furred or feathered pets as well as sociodemographic, family, and asthma variables. Prevalence of household smoking and pet ownership were high and comparable to normal levels in the US population. Smoking and pet ownership were not correlated with each other or with asthma medication adherence. Sociodemographic, family, and asthma variables showed distinct patterns of correlation with smoking and pet status. Household smoking was associated with poorer family resources and greater stress; pet ownership was associated with greater resources.\n\nQuestion:\nDoes prevalence and correlate of household exposures to tobacco smoke and pets in children with asthma?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nTo examine the prevalence rates of household smoking and ownership of a furred or feathered pet, the intercorrelation of these home environment measures, and their association with sociodemographic, family, and child asthma variables. Children with asthma (n = 152, aged 7-18 years) with asthma and their primary parent were evaluated through the use of reliable and valid questionnaires focusing on exposure to household smoke and furred or feathered pets as well as sociodemographic, family, and asthma variables. Prevalence of household smoking and pet ownership were high and comparable to normal levels in the US population. Smoking and pet ownership were not correlated with each other or with asthma medication adherence. Sociodemographic, family, and asthma variables showed distinct patterns of correlation with smoking and pet status. Household smoking was associated with poorer family resources and greater stress; pet ownership was associated with greater resources.\n\nQuestion:\nDoes prevalence and correlate of household exposures to tobacco smoke and pets in children with asthma?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nAccumulating evidence supports a role of 4-hydroxynonenal (4HNE) in oxidative-stress related diseases, but its specific contribution to disease development remains to be clarified. Further to our finding of high circulating 4HNE-protein thioether adducts (4HNE-P) in spontaneously hypertensive rats (SHRs), we aimed at correlating 4HNE-P with cardiac function and testing the impact of antioxidant therapy. The lipoperoxidation inhibitor probucol (10 mg/kg/day) or vehicle (corn oil) were administered daily (i.p.) for 4 weeks in 18-week-old SHRs (9 rats/group). Cardiac functions were assessed by echocardiography and 4HNE-P by gas chromatography/mass spectrometry. Diastolic dysfunction worsened in SHRs receiving vehicle as reflected by changes (P < 0.05) in indexes of left ventricular relaxation (increased isovolumic relaxation time) and compliance (increased E-wave deceleration rate; EDR). Higher circulating 4HNE-P correlated with diastolic dysfunction (EDR: R(2) = 0.518; P < 0.001) and heart rate (R(2) = 0.225; P < 0.05). Probucol prevented the deterioration of diastolic function, while lowering the mean and median of circulating 4HNE-P by 21% and 35%, respectively.\n\nQuestion:\nDo higher circulating 4-hydroxynonenal-protein thioether adducts correlate with more severe diastolic dysfunction in spontaneously hypertensive rats?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nAccumulating evidence supports a role of 4-hydroxynonenal (4HNE) in oxidative-stress related diseases, but its specific contribution to disease development remains to be clarified. Further to our finding of high circulating 4HNE-protein thioether adducts (4HNE-P) in spontaneously hypertensive rats (SHRs), we aimed at correlating 4HNE-P with cardiac function and testing the impact of antioxidant therapy. The lipoperoxidation inhibitor probucol (10 mg/kg/day) or vehicle (corn oil) were administered daily (i.p.) for 4 weeks in 18-week-old SHRs (9 rats/group). Cardiac functions were assessed by echocardiography and 4HNE-P by gas chromatography/mass spectrometry. Diastolic dysfunction worsened in SHRs receiving vehicle as reflected by changes (P < 0.05) in indexes of left ventricular relaxation (increased isovolumic relaxation time) and compliance (increased E-wave deceleration rate; EDR). Higher circulating 4HNE-P correlated with diastolic dysfunction (EDR: R(2) = 0.518; P < 0.001) and heart rate (R(2) = 0.225; P < 0.05). Probucol prevented the deterioration of diastolic function, while lowering the mean and median of circulating 4HNE-P by 21% and 35%, respectively.\n\nQuestion:\nDo higher circulating 4-hydroxynonenal-protein thioether adducts correlate with more severe diastolic dysfunction in spontaneously hypertensive rats?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nAccumulating evidence supports a role of 4-hydroxynonenal (4HNE) in oxidative-stress related diseases, but its specific contribution to disease development remains to be clarified. Further to our finding of high circulating 4HNE-protein thioether adducts (4HNE-P) in spontaneously hypertensive rats (SHRs), we aimed at correlating 4HNE-P with cardiac function and testing the impact of antioxidant therapy. The lipoperoxidation inhibitor probucol (10 mg/kg/day) or vehicle (corn oil) were administered daily (i.p.) for 4 weeks in 18-week-old SHRs (9 rats/group). Cardiac functions were assessed by echocardiography and 4HNE-P by gas chromatography/mass spectrometry. Diastolic dysfunction worsened in SHRs receiving vehicle as reflected by changes (P < 0.05) in indexes of left ventricular relaxation (increased isovolumic relaxation time) and compliance (increased E-wave deceleration rate; EDR). Higher circulating 4HNE-P correlated with diastolic dysfunction (EDR: R(2) = 0.518; P < 0.001) and heart rate (R(2) = 0.225; P < 0.05). Probucol prevented the deterioration of diastolic function, while lowering the mean and median of circulating 4HNE-P by 21% and 35%, respectively.\n\nQuestion:\nDo higher circulating 4-hydroxynonenal-protein thioether adducts correlate with more severe diastolic dysfunction in spontaneously hypertensive rats?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nThis study was designed to determine the level of survivin expression and its clinical significance as a prognostic factor in Stage III gastric adenocarcinoma. We performed immunohistochemical staining for survivin, p53 and Bax in formalin-fixed, paraffin-embedded blocks from 157 surgically resected Stage III gastric cancer tissues. To determine the association with clinical course, we reviewed the patients' clinical records. Of the 157 gastric cancer tissues, 63 (40.1%) cases showed positive expression for survivin protein. There was no significant association between survivin expression and p53 or Bax. For clinicopathologic parameters, large tumor size was closely related to survivin expression (P < 0.05). The 5-year survival rate of patients with positive survivin expression was significantly lower compared with that for survivin-negative cancer patients (P < 0.05). Survivin and p53 were independent prognostic factors in Stage III gastric cancer.\n\nQuestion:\nDoes expression of the antiapoptosis gene Survivin predict poor prognosis of stage III gastric adenocarcinoma?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nThis study was designed to determine the level of survivin expression and its clinical significance as a prognostic factor in Stage III gastric adenocarcinoma. We performed immunohistochemical staining for survivin, p53 and Bax in formalin-fixed, paraffin-embedded blocks from 157 surgically resected Stage III gastric cancer tissues. To determine the association with clinical course, we reviewed the patients' clinical records. Of the 157 gastric cancer tissues, 63 (40.1%) cases showed positive expression for survivin protein. There was no significant association between survivin expression and p53 or Bax. For clinicopathologic parameters, large tumor size was closely related to survivin expression (P < 0.05). The 5-year survival rate of patients with positive survivin expression was significantly lower compared with that for survivin-negative cancer patients (P < 0.05). Survivin and p53 were independent prognostic factors in Stage III gastric cancer.\n\nQuestion:\nDoes expression of the antiapoptosis gene Survivin predict poor prognosis of stage III gastric adenocarcinoma?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nThis study was designed to determine the level of survivin expression and its clinical significance as a prognostic factor in Stage III gastric adenocarcinoma. We performed immunohistochemical staining for survivin, p53 and Bax in formalin-fixed, paraffin-embedded blocks from 157 surgically resected Stage III gastric cancer tissues. To determine the association with clinical course, we reviewed the patients' clinical records. Of the 157 gastric cancer tissues, 63 (40.1%) cases showed positive expression for survivin protein. There was no significant association between survivin expression and p53 or Bax. For clinicopathologic parameters, large tumor size was closely related to survivin expression (P < 0.05). The 5-year survival rate of patients with positive survivin expression was significantly lower compared with that for survivin-negative cancer patients (P < 0.05). Survivin and p53 were independent prognostic factors in Stage III gastric cancer.\n\nQuestion:\nDoes expression of the antiapoptosis gene Survivin predict poor prognosis of stage III gastric adenocarcinoma?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nWe have previously demonstrated that human serum can suppress the proliferative response in autologous mixed lymphocyte reaction (AMLR) in which phytohemagglutinin (PHA)-activated T lymphoblasts act as stimulators (T-TPHA AMLR). The aim of the present work was to determine whether pregnancy serum (PS) possesses an inhibitory capacity similar or different in magnitude. Sixteen PS were added to T-TPHA AMLR cultures and the proliferative response was compared with that in the presence of human serum. The effect of PS on the IL-2 dependent proliferation of PHA-activated T Lymphoblasts was examined as well. PS induced a significantly more pronounced suppression of T-TPHA AMLR than human serum (P < 0.05). One PS tested was not inhibitory but rather stimulatory. This PS was obtained from a woman who subsequently had IUGR. The inhibition is related to the existence of a serum inhibitory factor and not to the lack of a serum supporting factor. PS inhibited not only T-TPHA AMLR of the same woman but also T-TPHA AMLR of other individuals as well, implying that the inhibitor is a non-MHC restricted factor. IL-2 dependent cell proliferation was not inhibited by PS, implying that the inhibitor detected in T-TPHA AMLR is not a general cell proliferation inhibitor.\n\nQuestion:\nDoes human pregnancy serum suppress the proliferative response of lymphocytes to autologous PHA-activated T lymphoblasts?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nWe have previously demonstrated that human serum can suppress the proliferative response in autologous mixed lymphocyte reaction (AMLR) in which phytohemagglutinin (PHA)-activated T lymphoblasts act as stimulators (T-TPHA AMLR). The aim of the present work was to determine whether pregnancy serum (PS) possesses an inhibitory capacity similar or different in magnitude. Sixteen PS were added to T-TPHA AMLR cultures and the proliferative response was compared with that in the presence of human serum. The effect of PS on the IL-2 dependent proliferation of PHA-activated T Lymphoblasts was examined as well. PS induced a significantly more pronounced suppression of T-TPHA AMLR than human serum (P < 0.05). One PS tested was not inhibitory but rather stimulatory. This PS was obtained from a woman who subsequently had IUGR. The inhibition is related to the existence of a serum inhibitory factor and not to the lack of a serum supporting factor. PS inhibited not only T-TPHA AMLR of the same woman but also T-TPHA AMLR of other individuals as well, implying that the inhibitor is a non-MHC restricted factor. IL-2 dependent cell proliferation was not inhibited by PS, implying that the inhibitor detected in T-TPHA AMLR is not a general cell proliferation inhibitor.\n\nQuestion:\nDoes human pregnancy serum suppress the proliferative response of lymphocytes to autologous PHA-activated T lymphoblasts?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nWe have previously demonstrated that human serum can suppress the proliferative response in autologous mixed lymphocyte reaction (AMLR) in which phytohemagglutinin (PHA)-activated T lymphoblasts act as stimulators (T-TPHA AMLR). The aim of the present work was to determine whether pregnancy serum (PS) possesses an inhibitory capacity similar or different in magnitude. Sixteen PS were added to T-TPHA AMLR cultures and the proliferative response was compared with that in the presence of human serum. The effect of PS on the IL-2 dependent proliferation of PHA-activated T Lymphoblasts was examined as well. PS induced a significantly more pronounced suppression of T-TPHA AMLR than human serum (P < 0.05). One PS tested was not inhibitory but rather stimulatory. This PS was obtained from a woman who subsequently had IUGR. The inhibition is related to the existence of a serum inhibitory factor and not to the lack of a serum supporting factor. PS inhibited not only T-TPHA AMLR of the same woman but also T-TPHA AMLR of other individuals as well, implying that the inhibitor is a non-MHC restricted factor. IL-2 dependent cell proliferation was not inhibited by PS, implying that the inhibitor detected in T-TPHA AMLR is not a general cell proliferation inhibitor.\n\nQuestion:\nDoes human pregnancy serum suppress the proliferative response of lymphocytes to autologous PHA-activated T lymphoblasts?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nEndometriosis is a gynecological condition that is characterized by extreme abdominal pain and also decreased fertility. Regulatory T cells (Tregs) have immunosuppressive activity critical for embryonic implantation and likewise the acceptance of tissue engraftment. Utilizing the induced non-human primate (Papio anubis) model of endometriosis, we hypothesize that endometriosis decreases the peripheral and endomet rial Treg profile, whereas ectopic lesions have increased Treg localization. Peripheral blood and endometrium were obtained throughout the menstrual cycle prior to and after induction of disease. Animals were randomly assigned to control (n = 7) or diseased (n = 16) treatment groups. Endometriosis was induced by i.p. injection of autologous menstrual tissue for 2 consecutive months during menses. Peripheral blood and endometrial tissue were collected at d9-11PO at 1, 3, 6, 9, 12 and 15 months post-induction of disease for fluorescence-activated cell sorting, quantitative RT-PCR and immunohistochemistry. Ectopic lesions were excised at 1 and 6 months post-inoculation and also harvested at necropsy (15 months) and processed for RNA of IHC. Identification of Tregs through analysis of FOXP3 expression was conducted utlilizing several methodologies. Differences were determined by non-parametric statistical analysis between all treatment groups and time points. In control animals, the proportion of peripheral natural Tregs (nTregs) was reduced (P < 0.05) during the mid- and late secretory stages of the menstrual cycle compared with menses. The induction of disease decreased peripheral Treg expression at early time points (P < 0.05) and this remained low throughout the time course, compared with the pre-inoculatory level of an individual. FOXP3 gene expression and Treg populations were also decreased in the eutopic endometrium (P < 0.05) compared with control animals, whereas these parameters were increased in ectopic lesions (P < 0.05), compared with the eutopic endometrium.\n\nQuestion:\nDoes induction of endometriosis alter the peripheral and endometrial regulatory T cell population in the non-human primate?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nEndometriosis is a gynecological condition that is characterized by extreme abdominal pain and also decreased fertility. Regulatory T cells (Tregs) have immunosuppressive activity critical for embryonic implantation and likewise the acceptance of tissue engraftment. Utilizing the induced non-human primate (Papio anubis) model of endometriosis, we hypothesize that endometriosis decreases the peripheral and endomet rial Treg profile, whereas ectopic lesions have increased Treg localization. Peripheral blood and endometrium were obtained throughout the menstrual cycle prior to and after induction of disease. Animals were randomly assigned to control (n = 7) or diseased (n = 16) treatment groups. Endometriosis was induced by i.p. injection of autologous menstrual tissue for 2 consecutive months during menses. Peripheral blood and endometrial tissue were collected at d9-11PO at 1, 3, 6, 9, 12 and 15 months post-induction of disease for fluorescence-activated cell sorting, quantitative RT-PCR and immunohistochemistry. Ectopic lesions were excised at 1 and 6 months post-inoculation and also harvested at necropsy (15 months) and processed for RNA of IHC. Identification of Tregs through analysis of FOXP3 expression was conducted utlilizing several methodologies. Differences were determined by non-parametric statistical analysis between all treatment groups and time points. In control animals, the proportion of peripheral natural Tregs (nTregs) was reduced (P < 0.05) during the mid- and late secretory stages of the menstrual cycle compared with menses. The induction of disease decreased peripheral Treg expression at early time points (P < 0.05) and this remained low throughout the time course, compared with the pre-inoculatory level of an individual. FOXP3 gene expression and Treg populations were also decreased in the eutopic endometrium (P < 0.05) compared with control animals, whereas these parameters were increased in ectopic lesions (P < 0.05), compared with the eutopic endometrium.\n\nQuestion:\nDoes induction of endometriosis alter the peripheral and endometrial regulatory T cell population in the non-human primate?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nEndometriosis is a gynecological condition that is characterized by extreme abdominal pain and also decreased fertility. Regulatory T cells (Tregs) have immunosuppressive activity critical for embryonic implantation and likewise the acceptance of tissue engraftment. Utilizing the induced non-human primate (Papio anubis) model of endometriosis, we hypothesize that endometriosis decreases the peripheral and endomet rial Treg profile, whereas ectopic lesions have increased Treg localization. Peripheral blood and endometrium were obtained throughout the menstrual cycle prior to and after induction of disease. Animals were randomly assigned to control (n = 7) or diseased (n = 16) treatment groups. Endometriosis was induced by i.p. injection of autologous menstrual tissue for 2 consecutive months during menses. Peripheral blood and endometrial tissue were collected at d9-11PO at 1, 3, 6, 9, 12 and 15 months post-induction of disease for fluorescence-activated cell sorting, quantitative RT-PCR and immunohistochemistry. Ectopic lesions were excised at 1 and 6 months post-inoculation and also harvested at necropsy (15 months) and processed for RNA of IHC. Identification of Tregs through analysis of FOXP3 expression was conducted utlilizing several methodologies. Differences were determined by non-parametric statistical analysis between all treatment groups and time points. In control animals, the proportion of peripheral natural Tregs (nTregs) was reduced (P < 0.05) during the mid- and late secretory stages of the menstrual cycle compared with menses. The induction of disease decreased peripheral Treg expression at early time points (P < 0.05) and this remained low throughout the time course, compared with the pre-inoculatory level of an individual. FOXP3 gene expression and Treg populations were also decreased in the eutopic endometrium (P < 0.05) compared with control animals, whereas these parameters were increased in ectopic lesions (P < 0.05), compared with the eutopic endometrium.\n\nQuestion:\nDoes induction of endometriosis alter the peripheral and endometrial regulatory T cell population in the non-human primate?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nTo examine the association of blood antioxidants with cataract. Cross-sectional study of people aged >or=50 years identified from a household enumeration of 11 randomly sampled villages in North India. Participants were interviewed for putative risk factors (tobacco, alcohol, biomass fuel use, sunlight exposure, and socioeconomic status) and underwent lens photography and blood sampling. Lens photographs (nuclear, cortical, and posterior subcapsular) were graded according to the Lens Opacities Classification System (LOCS II). Cataract was defined as LOCS II grade >or=2 for any opacity or ungradable, because of dense opacification or history of cataract surgery. People without cataract were defined as LOCS II <2 on all three types of opacity, with absence of previous surgery. Of 1443 people aged >or=50 years, 94% were interviewed, 87% attended an eye examination, and 78% gave a blood sample; 1112 (77%) were included in the analyses. Compared with levels in Western populations, antioxidants were low, especially vitamin C. Vitamin C was inversely associated with cataract. Odds ratios (OR) for the highest (>or=15 micromol/L) compared with the lowest (<or=6.3 micromol/L) tertile were 0.64, (95% confidence interval [CI] 0.48-0.85; P < 0.01). Tertiles of zeaxanthin (P < 0.03), alpha-carotene (P < 0.05), and retinol (P < 0.02) were associated with decreased odds of cataract. In analysis of continuous data, significant inverse associations were found for vitamin C, zeaxanthin, lutein, lycopene, alpha- and beta-carotene, and beta-cryptoxanthin, but not for alpha- or gamma-tocopherol.\n\nQuestion:\nAre blood levels of vitamin C , carotenoids and retinol inversely associated with cataract in a North Indian population?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nTo examine the association of blood antioxidants with cataract. Cross-sectional study of people aged >or=50 years identified from a household enumeration of 11 randomly sampled villages in North India. Participants were interviewed for putative risk factors (tobacco, alcohol, biomass fuel use, sunlight exposure, and socioeconomic status) and underwent lens photography and blood sampling. Lens photographs (nuclear, cortical, and posterior subcapsular) were graded according to the Lens Opacities Classification System (LOCS II). Cataract was defined as LOCS II grade >or=2 for any opacity or ungradable, because of dense opacification or history of cataract surgery. People without cataract were defined as LOCS II <2 on all three types of opacity, with absence of previous surgery. Of 1443 people aged >or=50 years, 94% were interviewed, 87% attended an eye examination, and 78% gave a blood sample; 1112 (77%) were included in the analyses. Compared with levels in Western populations, antioxidants were low, especially vitamin C. Vitamin C was inversely associated with cataract. Odds ratios (OR) for the highest (>or=15 micromol/L) compared with the lowest (<or=6.3 micromol/L) tertile were 0.64, (95% confidence interval [CI] 0.48-0.85; P < 0.01). Tertiles of zeaxanthin (P < 0.03), alpha-carotene (P < 0.05), and retinol (P < 0.02) were associated with decreased odds of cataract. In analysis of continuous data, significant inverse associations were found for vitamin C, zeaxanthin, lutein, lycopene, alpha- and beta-carotene, and beta-cryptoxanthin, but not for alpha- or gamma-tocopherol.\n\nQuestion:\nAre blood levels of vitamin C , carotenoids and retinol inversely associated with cataract in a North Indian population?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nTo examine the association of blood antioxidants with cataract. Cross-sectional study of people aged >or=50 years identified from a household enumeration of 11 randomly sampled villages in North India. Participants were interviewed for putative risk factors (tobacco, alcohol, biomass fuel use, sunlight exposure, and socioeconomic status) and underwent lens photography and blood sampling. Lens photographs (nuclear, cortical, and posterior subcapsular) were graded according to the Lens Opacities Classification System (LOCS II). Cataract was defined as LOCS II grade >or=2 for any opacity or ungradable, because of dense opacification or history of cataract surgery. People without cataract were defined as LOCS II <2 on all three types of opacity, with absence of previous surgery. Of 1443 people aged >or=50 years, 94% were interviewed, 87% attended an eye examination, and 78% gave a blood sample; 1112 (77%) were included in the analyses. Compared with levels in Western populations, antioxidants were low, especially vitamin C. Vitamin C was inversely associated with cataract. Odds ratios (OR) for the highest (>or=15 micromol/L) compared with the lowest (<or=6.3 micromol/L) tertile were 0.64, (95% confidence interval [CI] 0.48-0.85; P < 0.01). Tertiles of zeaxanthin (P < 0.03), alpha-carotene (P < 0.05), and retinol (P < 0.02) were associated with decreased odds of cataract. In analysis of continuous data, significant inverse associations were found for vitamin C, zeaxanthin, lutein, lycopene, alpha- and beta-carotene, and beta-cryptoxanthin, but not for alpha- or gamma-tocopherol.\n\nQuestion:\nAre blood levels of vitamin C , carotenoids and retinol inversely associated with cataract in a North Indian population?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nThe purpose of the study was to assess ongoing pregnancy rates across groups of patients treated by IVF, which were defined according to criteria aimed at the prevention of premature LH surge and used for initiating GnRH antagonist. This is a prospective observational cohort study. During the last 3 years, in IVF-ICSI patients undergoing controlled ovarian stimulation (COS) with the antagonist protocol, the antagonist administration was initiated according to at least one of the following patient-specific criteria: (i) at least one follicle measuring >14 mm; (ii) estradiol levels >600 pg/ml; and (iii) LH levels >10 IU/l. Based upon these criteria, 208 cases of normal responders were analysed and categorized into three groups according to the starting day of the regimen: group D4 (n = 40) for day 4, group D5 (n = 98) for day 5 and group D6 (n = 70) for day 6. The main outcome measure was the ongoing pregnancy rate per started cycle. The total number of patients in the D4 and D5 groups (138 out of 208), who received the antagonist earlier, was considerably larger compared with that of D6 (70 out of 208). Ongoing pregnancy rates were 37.5, 34.7 and 18.6% for groups D4, D5 and D6, respectively. Patients who initiated the GnRH antagonist on days 4 and 5 had statistically significant higher pregnancy rates compared with day 6. Rapid response, causing earlier antagonist administration initiation, according to the proposed criteria for the prevention of premature LH surges, and the absence of premature luteinization, as evidenced by normal progesterone levels on HCG day, were found to be independent positive predictive factors for favourable IVF outcome.\n\nQuestion:\nIs in a flexible antagonist protocol , earlier , criteria-based initiation of GnRH antagonist associated with increased pregnancy rates in IVF?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nThe purpose of the study was to assess ongoing pregnancy rates across groups of patients treated by IVF, which were defined according to criteria aimed at the prevention of premature LH surge and used for initiating GnRH antagonist. This is a prospective observational cohort study. During the last 3 years, in IVF-ICSI patients undergoing controlled ovarian stimulation (COS) with the antagonist protocol, the antagonist administration was initiated according to at least one of the following patient-specific criteria: (i) at least one follicle measuring >14 mm; (ii) estradiol levels >600 pg/ml; and (iii) LH levels >10 IU/l. Based upon these criteria, 208 cases of normal responders were analysed and categorized into three groups according to the starting day of the regimen: group D4 (n = 40) for day 4, group D5 (n = 98) for day 5 and group D6 (n = 70) for day 6. The main outcome measure was the ongoing pregnancy rate per started cycle. The total number of patients in the D4 and D5 groups (138 out of 208), who received the antagonist earlier, was considerably larger compared with that of D6 (70 out of 208). Ongoing pregnancy rates were 37.5, 34.7 and 18.6% for groups D4, D5 and D6, respectively. Patients who initiated the GnRH antagonist on days 4 and 5 had statistically significant higher pregnancy rates compared with day 6. Rapid response, causing earlier antagonist administration initiation, according to the proposed criteria for the prevention of premature LH surges, and the absence of premature luteinization, as evidenced by normal progesterone levels on HCG day, were found to be independent positive predictive factors for favourable IVF outcome.\n\nQuestion:\nIs in a flexible antagonist protocol , earlier , criteria-based initiation of GnRH antagonist associated with increased pregnancy rates in IVF?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nThe purpose of the study was to assess ongoing pregnancy rates across groups of patients treated by IVF, which were defined according to criteria aimed at the prevention of premature LH surge and used for initiating GnRH antagonist. This is a prospective observational cohort study. During the last 3 years, in IVF-ICSI patients undergoing controlled ovarian stimulation (COS) with the antagonist protocol, the antagonist administration was initiated according to at least one of the following patient-specific criteria: (i) at least one follicle measuring >14 mm; (ii) estradiol levels >600 pg/ml; and (iii) LH levels >10 IU/l. Based upon these criteria, 208 cases of normal responders were analysed and categorized into three groups according to the starting day of the regimen: group D4 (n = 40) for day 4, group D5 (n = 98) for day 5 and group D6 (n = 70) for day 6. The main outcome measure was the ongoing pregnancy rate per started cycle. The total number of patients in the D4 and D5 groups (138 out of 208), who received the antagonist earlier, was considerably larger compared with that of D6 (70 out of 208). Ongoing pregnancy rates were 37.5, 34.7 and 18.6% for groups D4, D5 and D6, respectively. Patients who initiated the GnRH antagonist on days 4 and 5 had statistically significant higher pregnancy rates compared with day 6. Rapid response, causing earlier antagonist administration initiation, according to the proposed criteria for the prevention of premature LH surges, and the absence of premature luteinization, as evidenced by normal progesterone levels on HCG day, were found to be independent positive predictive factors for favourable IVF outcome.\n\nQuestion:\nIs in a flexible antagonist protocol , earlier , criteria-based initiation of GnRH antagonist associated with increased pregnancy rates in IVF?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nMean platelet volume (MPV), an indicator of platelet activation, has been shown to be elevated in patients with coronary artery disease (CAD) in some studies. Insulin resistance contributes to increased platelet activation and it is one of the risk factors for CAD. The aim of this study was to assess the relationship between insulin resistance and MPV in non-obese, non-diabetic patients with CAD. Seventy-seven non-obese, non-diabetic CAD patients were divided into two groups, insulin resistant and insulin sensitive according to the homeostasis model assessment insulin resistance index (HOMA-IR). The insulin-resistant group was composed of 45 patients (30 males/15 females; mean age 59.8±11.1 years). The insulin-sensitive group was composed of 32 patients (17 males/15 females; mean age 58.9±12.2 years). Insulin and HOMA-IR values were significantly higher in insulin-resistant CAD patients than in insulin-sensitive CAD patients. The MPV values were significantly higher in insulin-resistant CAD patients than in insulin-sensitive CAD patients (8.6±1.0 fl vs. 8.0±0.7 fl; respectively, p=0.01). The MPV was poorly correlated with HOMA-IR (r=0.30, p=0.054) and insulin (r=0.22, p=0.053).\n\nQuestion:\nIs mean platelet volume associated with insulin resistance in non-obese , non-diabetic patients with coronary artery disease?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nMean platelet volume (MPV), an indicator of platelet activation, has been shown to be elevated in patients with coronary artery disease (CAD) in some studies. Insulin resistance contributes to increased platelet activation and it is one of the risk factors for CAD. The aim of this study was to assess the relationship between insulin resistance and MPV in non-obese, non-diabetic patients with CAD. Seventy-seven non-obese, non-diabetic CAD patients were divided into two groups, insulin resistant and insulin sensitive according to the homeostasis model assessment insulin resistance index (HOMA-IR). The insulin-resistant group was composed of 45 patients (30 males/15 females; mean age 59.8±11.1 years). The insulin-sensitive group was composed of 32 patients (17 males/15 females; mean age 58.9±12.2 years). Insulin and HOMA-IR values were significantly higher in insulin-resistant CAD patients than in insulin-sensitive CAD patients. The MPV values were significantly higher in insulin-resistant CAD patients than in insulin-sensitive CAD patients (8.6±1.0 fl vs. 8.0±0.7 fl; respectively, p=0.01). The MPV was poorly correlated with HOMA-IR (r=0.30, p=0.054) and insulin (r=0.22, p=0.053).\n\nQuestion:\nIs mean platelet volume associated with insulin resistance in non-obese , non-diabetic patients with coronary artery disease?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nMean platelet volume (MPV), an indicator of platelet activation, has been shown to be elevated in patients with coronary artery disease (CAD) in some studies. Insulin resistance contributes to increased platelet activation and it is one of the risk factors for CAD. The aim of this study was to assess the relationship between insulin resistance and MPV in non-obese, non-diabetic patients with CAD. Seventy-seven non-obese, non-diabetic CAD patients were divided into two groups, insulin resistant and insulin sensitive according to the homeostasis model assessment insulin resistance index (HOMA-IR). The insulin-resistant group was composed of 45 patients (30 males/15 females; mean age 59.8±11.1 years). The insulin-sensitive group was composed of 32 patients (17 males/15 females; mean age 58.9±12.2 years). Insulin and HOMA-IR values were significantly higher in insulin-resistant CAD patients than in insulin-sensitive CAD patients. The MPV values were significantly higher in insulin-resistant CAD patients than in insulin-sensitive CAD patients (8.6±1.0 fl vs. 8.0±0.7 fl; respectively, p=0.01). The MPV was poorly correlated with HOMA-IR (r=0.30, p=0.054) and insulin (r=0.22, p=0.053).\n\nQuestion:\nIs mean platelet volume associated with insulin resistance in non-obese , non-diabetic patients with coronary artery disease?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nThe objective of this work was to determine the effect of an androgen agonist, R1881, on intracellular cholesterol synthesis and esterification in androgen-sensitive (AS) prostate cancer (LNCaP) cells. We investigated the activity and expression of cholesterol metabolism enzymes, HMG-CoA-reductase and ACAT in the LNCaP and PC-3 (androgen-independent control) models. Microsomal PC-3 HMG-CoA-reductase activity was increased with R1881 despite having similar cholesterol levels while increased cholesterol levels in microsomes from LNCaPs treated with R1881 (L+) were associated with increased HMG-CoA reductase activity. Increased intracellular cholesteryl esters (CE) found in (L+) were not associated with an increased ACAT1 activity. There was no effect from androgen treatment on ACAT1 protein expression in theses cells; however, ACAT2 expression was induced upon R1881 treatment. In contrast, we found an increase in the in vitro ACAT1 activity in PC-3 cells treated with androgen (P+). Only ACAT1 expression was induced in P+. We further assessed the expression of STAT1 alpha, a transcriptional activator that modulates ACAT1 expression. STAT1 alpha expression and phosphorylation were induced in P+. To determine the role of the AR on ACAT1 expression and esterification, we treated PC-3 cells overexpressing the androgen receptor with R1881 (PAR+). AR expression was decreased in PAR+ cells; ACAT1 protein expression and cholesterol ester levels were also decreased, however, ACAT2 remained unchanged. STAT1 alpha expression was decreased in PAR+.\n\nQuestion:\nIs androgen-mediated cholesterol metabolism in LNCaP and PC-3 cell lines regulated through two different isoforms of acyl-coenzyme A : Cholesterol Acyltransferase ( ACAT )?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nThe objective of this work was to determine the effect of an androgen agonist, R1881, on intracellular cholesterol synthesis and esterification in androgen-sensitive (AS) prostate cancer (LNCaP) cells. We investigated the activity and expression of cholesterol metabolism enzymes, HMG-CoA-reductase and ACAT in the LNCaP and PC-3 (androgen-independent control) models. Microsomal PC-3 HMG-CoA-reductase activity was increased with R1881 despite having similar cholesterol levels while increased cholesterol levels in microsomes from LNCaPs treated with R1881 (L+) were associated with increased HMG-CoA reductase activity. Increased intracellular cholesteryl esters (CE) found in (L+) were not associated with an increased ACAT1 activity. There was no effect from androgen treatment on ACAT1 protein expression in theses cells; however, ACAT2 expression was induced upon R1881 treatment. In contrast, we found an increase in the in vitro ACAT1 activity in PC-3 cells treated with androgen (P+). Only ACAT1 expression was induced in P+. We further assessed the expression of STAT1 alpha, a transcriptional activator that modulates ACAT1 expression. STAT1 alpha expression and phosphorylation were induced in P+. To determine the role of the AR on ACAT1 expression and esterification, we treated PC-3 cells overexpressing the androgen receptor with R1881 (PAR+). AR expression was decreased in PAR+ cells; ACAT1 protein expression and cholesterol ester levels were also decreased, however, ACAT2 remained unchanged. STAT1 alpha expression was decreased in PAR+.\n\nQuestion:\nIs androgen-mediated cholesterol metabolism in LNCaP and PC-3 cell lines regulated through two different isoforms of acyl-coenzyme A : Cholesterol Acyltransferase ( ACAT )?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nThe objective of this work was to determine the effect of an androgen agonist, R1881, on intracellular cholesterol synthesis and esterification in androgen-sensitive (AS) prostate cancer (LNCaP) cells. We investigated the activity and expression of cholesterol metabolism enzymes, HMG-CoA-reductase and ACAT in the LNCaP and PC-3 (androgen-independent control) models. Microsomal PC-3 HMG-CoA-reductase activity was increased with R1881 despite having similar cholesterol levels while increased cholesterol levels in microsomes from LNCaPs treated with R1881 (L+) were associated with increased HMG-CoA reductase activity. Increased intracellular cholesteryl esters (CE) found in (L+) were not associated with an increased ACAT1 activity. There was no effect from androgen treatment on ACAT1 protein expression in theses cells; however, ACAT2 expression was induced upon R1881 treatment. In contrast, we found an increase in the in vitro ACAT1 activity in PC-3 cells treated with androgen (P+). Only ACAT1 expression was induced in P+. We further assessed the expression of STAT1 alpha, a transcriptional activator that modulates ACAT1 expression. STAT1 alpha expression and phosphorylation were induced in P+. To determine the role of the AR on ACAT1 expression and esterification, we treated PC-3 cells overexpressing the androgen receptor with R1881 (PAR+). AR expression was decreased in PAR+ cells; ACAT1 protein expression and cholesterol ester levels were also decreased, however, ACAT2 remained unchanged. STAT1 alpha expression was decreased in PAR+.\n\nQuestion:\nIs androgen-mediated cholesterol metabolism in LNCaP and PC-3 cell lines regulated through two different isoforms of acyl-coenzyme A : Cholesterol Acyltransferase ( ACAT )?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nWe aimed to investigate whether high-sensitive cardiac troponin T (hs-cTnT) is associated with all-cause and cardiovascular mortality in stable type 2 diabetes (T2D) outpatients treated in primary care. Cardiac troponin T was measured with a high-sensitive assay at baseline in patients with T2D participating in the observational ZODIAC study. Cox proportional hazards models were used to investigate the relationship between hs-cTnT and mortality with adjustment for selected confounders. Risk prediction capabilities of hs-cTnT were assessed with Harrell C statistics. Complete baseline data were available for 1,133 patients. During median follow-up of 11 (7-14) years, 513 (45%) patients died, of which 218 (42%) died of cardiovascular causes. Of the patients with undetectable hs-cTnT levels (<3 ng/L), only 23% died, compared with 58% with low detectable levels (3-14 ng/L) and 84% with raised levels (≥14 ng/L). Natural log hs-cTnT was significantly associated with all-cause mortality (hazard ratio 1.30, 95% CI 1.19-1.42) and cardiovascular mortality (hazard ratio 1.33, 95% CI 1.15-1.53), independent of potential confounders. The Harrell C statistic for the crude model of hs-cTnT was 0.72 (95% CI 0.70-0.75) for all-cause mortality and 0.74 (95% CI 0.71-0.77) for cardiovascular mortality.\n\nQuestion:\nIs high-sensitive troponin T associated with all-cause and cardiovascular mortality in stable outpatients with type 2 diabetes ( ZODIAC-37 )?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nWe aimed to investigate whether high-sensitive cardiac troponin T (hs-cTnT) is associated with all-cause and cardiovascular mortality in stable type 2 diabetes (T2D) outpatients treated in primary care. Cardiac troponin T was measured with a high-sensitive assay at baseline in patients with T2D participating in the observational ZODIAC study. Cox proportional hazards models were used to investigate the relationship between hs-cTnT and mortality with adjustment for selected confounders. Risk prediction capabilities of hs-cTnT were assessed with Harrell C statistics. Complete baseline data were available for 1,133 patients. During median follow-up of 11 (7-14) years, 513 (45%) patients died, of which 218 (42%) died of cardiovascular causes. Of the patients with undetectable hs-cTnT levels (<3 ng/L), only 23% died, compared with 58% with low detectable levels (3-14 ng/L) and 84% with raised levels (≥14 ng/L). Natural log hs-cTnT was significantly associated with all-cause mortality (hazard ratio 1.30, 95% CI 1.19-1.42) and cardiovascular mortality (hazard ratio 1.33, 95% CI 1.15-1.53), independent of potential confounders. The Harrell C statistic for the crude model of hs-cTnT was 0.72 (95% CI 0.70-0.75) for all-cause mortality and 0.74 (95% CI 0.71-0.77) for cardiovascular mortality.\n\nQuestion:\nIs high-sensitive troponin T associated with all-cause and cardiovascular mortality in stable outpatients with type 2 diabetes ( ZODIAC-37 )?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nWe aimed to investigate whether high-sensitive cardiac troponin T (hs-cTnT) is associated with all-cause and cardiovascular mortality in stable type 2 diabetes (T2D) outpatients treated in primary care. Cardiac troponin T was measured with a high-sensitive assay at baseline in patients with T2D participating in the observational ZODIAC study. Cox proportional hazards models were used to investigate the relationship between hs-cTnT and mortality with adjustment for selected confounders. Risk prediction capabilities of hs-cTnT were assessed with Harrell C statistics. Complete baseline data were available for 1,133 patients. During median follow-up of 11 (7-14) years, 513 (45%) patients died, of which 218 (42%) died of cardiovascular causes. Of the patients with undetectable hs-cTnT levels (<3 ng/L), only 23% died, compared with 58% with low detectable levels (3-14 ng/L) and 84% with raised levels (≥14 ng/L). Natural log hs-cTnT was significantly associated with all-cause mortality (hazard ratio 1.30, 95% CI 1.19-1.42) and cardiovascular mortality (hazard ratio 1.33, 95% CI 1.15-1.53), independent of potential confounders. The Harrell C statistic for the crude model of hs-cTnT was 0.72 (95% CI 0.70-0.75) for all-cause mortality and 0.74 (95% CI 0.71-0.77) for cardiovascular mortality.\n\nQuestion:\nIs high-sensitive troponin T associated with all-cause and cardiovascular mortality in stable outpatients with type 2 diabetes ( ZODIAC-37 )?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nOrganic cation transporters 1-3 (OCT1-3; Slc22a1-3) mediate the membrane transport of organic cations in the kidney. We previously reported that rat (r)OCT2 expression in the kidney was regulated by testosterone. In this study, we examined the transcriptional mechanisms underlying the testosterone-dependent regulation of rOCT2 expression. Approximately 3000-bp fragments of the rOCT1-3 promoter region were isolated, and promoter activities were measured in the renal epithelial cell line LLC-PK1 with the coexpression of rat androgen receptor. Among reporter constructs tested, only rOCT2 promoter activity was stimulated by testosterone. This stimulation was suppressed by nilutamide, an antiandrogen drug. Reporter assays using deletion constructs and mutational constructs of putative androgen response elements (ARE) in the rOCT2 promoter region suggested that two AREs, located at approximately -3000 and -1300, respectively, play an important role in the induction by testosterone.\n\nQuestion:\nIs androgen receptor responsible for rat organic cation transporter 2 gene regulation but not for rOCT1 and rOCT3?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nOrganic cation transporters 1-3 (OCT1-3; Slc22a1-3) mediate the membrane transport of organic cations in the kidney. We previously reported that rat (r)OCT2 expression in the kidney was regulated by testosterone. In this study, we examined the transcriptional mechanisms underlying the testosterone-dependent regulation of rOCT2 expression. Approximately 3000-bp fragments of the rOCT1-3 promoter region were isolated, and promoter activities were measured in the renal epithelial cell line LLC-PK1 with the coexpression of rat androgen receptor. Among reporter constructs tested, only rOCT2 promoter activity was stimulated by testosterone. This stimulation was suppressed by nilutamide, an antiandrogen drug. Reporter assays using deletion constructs and mutational constructs of putative androgen response elements (ARE) in the rOCT2 promoter region suggested that two AREs, located at approximately -3000 and -1300, respectively, play an important role in the induction by testosterone.\n\nQuestion:\nIs androgen receptor responsible for rat organic cation transporter 2 gene regulation but not for rOCT1 and rOCT3?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nOrganic cation transporters 1-3 (OCT1-3; Slc22a1-3) mediate the membrane transport of organic cations in the kidney. We previously reported that rat (r)OCT2 expression in the kidney was regulated by testosterone. In this study, we examined the transcriptional mechanisms underlying the testosterone-dependent regulation of rOCT2 expression. Approximately 3000-bp fragments of the rOCT1-3 promoter region were isolated, and promoter activities were measured in the renal epithelial cell line LLC-PK1 with the coexpression of rat androgen receptor. Among reporter constructs tested, only rOCT2 promoter activity was stimulated by testosterone. This stimulation was suppressed by nilutamide, an antiandrogen drug. Reporter assays using deletion constructs and mutational constructs of putative androgen response elements (ARE) in the rOCT2 promoter region suggested that two AREs, located at approximately -3000 and -1300, respectively, play an important role in the induction by testosterone.\n\nQuestion:\nIs androgen receptor responsible for rat organic cation transporter 2 gene regulation but not for rOCT1 and rOCT3?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nGOALS, BACKGROUND: The elderly population has been increasing during the last half a century and it would be important to know how aging influences the occurrence and biologic behavior of cancers. We investigated clinicopathologic characteristics of colorectal cancer in 1354 patients who underwent colorectal cancer resection and compared the results between extremely elderly patients (over 80 years old) and middle-aged/elderly patients (40 to less than 80 years old). Furthermore, we also examined expression of tumor suppressor genes and Cox-2 using frozen samples of colorectal cancer obtained from 62 patients ranging in age from 45 to 87 years. The results obtained in the extremely aged patients were: (1) higher ratio of women, (2) higher incidence at the proximal site, (3) higher incidence of cases with deeper invasion, (4) higher incidence of cases with lymph node metastasis (5) poorer survival rate as compared with middle-aged/elderly patients, and (6) lower mRNA expression levels of p27 and p53.\n\nQuestion:\nIs poor prognosis of colorectal cancer in patients over 80 years old associated with down-regulation of tumor suppressor genes?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nGOALS, BACKGROUND: The elderly population has been increasing during the last half a century and it would be important to know how aging influences the occurrence and biologic behavior of cancers. We investigated clinicopathologic characteristics of colorectal cancer in 1354 patients who underwent colorectal cancer resection and compared the results between extremely elderly patients (over 80 years old) and middle-aged/elderly patients (40 to less than 80 years old). Furthermore, we also examined expression of tumor suppressor genes and Cox-2 using frozen samples of colorectal cancer obtained from 62 patients ranging in age from 45 to 87 years. The results obtained in the extremely aged patients were: (1) higher ratio of women, (2) higher incidence at the proximal site, (3) higher incidence of cases with deeper invasion, (4) higher incidence of cases with lymph node metastasis (5) poorer survival rate as compared with middle-aged/elderly patients, and (6) lower mRNA expression levels of p27 and p53.\n\nQuestion:\nIs poor prognosis of colorectal cancer in patients over 80 years old associated with down-regulation of tumor suppressor genes?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nGOALS, BACKGROUND: The elderly population has been increasing during the last half a century and it would be important to know how aging influences the occurrence and biologic behavior of cancers. We investigated clinicopathologic characteristics of colorectal cancer in 1354 patients who underwent colorectal cancer resection and compared the results between extremely elderly patients (over 80 years old) and middle-aged/elderly patients (40 to less than 80 years old). Furthermore, we also examined expression of tumor suppressor genes and Cox-2 using frozen samples of colorectal cancer obtained from 62 patients ranging in age from 45 to 87 years. The results obtained in the extremely aged patients were: (1) higher ratio of women, (2) higher incidence at the proximal site, (3) higher incidence of cases with deeper invasion, (4) higher incidence of cases with lymph node metastasis (5) poorer survival rate as compared with middle-aged/elderly patients, and (6) lower mRNA expression levels of p27 and p53.\n\nQuestion:\nIs poor prognosis of colorectal cancer in patients over 80 years old associated with down-regulation of tumor suppressor genes?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nUsing a diet-induced obesity (DIO) mouse model, we investigated the antidiabetic effect of Labrador tea [Rhododendron groenlandicum (Oeder) Kron and Judd], a beverage and medicinal tea used by the Cree Nations of northern Quebec. C57BL6 mice were divided into five groups and given standard chow (~4 % of lipids) or high-fat diet (~35 % of lipids) for 8 weeks until they became obese and insulin resistant. Treatment began by adding the plant extract at three doses (125, 250 and 500 mg/kg) to the high-fat diet for another 8 weeks. At the end of the study, insulin-sensitive tissues (liver, skeletal muscle, adipose tissue) were collected to investigate the plant's molecular mechanisms. Labrador tea significantly reduced blood glucose (13 %), the response to an oral glucose tolerance test (18.2 %) and plasma insulin (65 %) while preventing hepatic steatosis (42 % reduction in hepatic triglyceride levels) in DIO mice. It stimulated insulin-dependent Akt pathway (55 %) and increased the expression of GLUT4 (53 %) in skeletal muscle. In the liver, Labrador tea stimulated the insulin-dependent Akt and the insulin-independent AMP-activated protein kinase pathways. The improvement in hepatic steatosis observed in DIO-treated mice was associated with a reduction in inflammation (through the IKK α/β) and a decrease in the hepatic content of SREBP-1 (39 %).\n\nQuestion:\nDoes labrador tea ( Rhododendron groenlandicum ) attenuate insulin resistance in a diet-induced obesity mouse model?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nUsing a diet-induced obesity (DIO) mouse model, we investigated the antidiabetic effect of Labrador tea [Rhododendron groenlandicum (Oeder) Kron and Judd], a beverage and medicinal tea used by the Cree Nations of northern Quebec. C57BL6 mice were divided into five groups and given standard chow (~4 % of lipids) or high-fat diet (~35 % of lipids) for 8 weeks until they became obese and insulin resistant. Treatment began by adding the plant extract at three doses (125, 250 and 500 mg/kg) to the high-fat diet for another 8 weeks. At the end of the study, insulin-sensitive tissues (liver, skeletal muscle, adipose tissue) were collected to investigate the plant's molecular mechanisms. Labrador tea significantly reduced blood glucose (13 %), the response to an oral glucose tolerance test (18.2 %) and plasma insulin (65 %) while preventing hepatic steatosis (42 % reduction in hepatic triglyceride levels) in DIO mice. It stimulated insulin-dependent Akt pathway (55 %) and increased the expression of GLUT4 (53 %) in skeletal muscle. In the liver, Labrador tea stimulated the insulin-dependent Akt and the insulin-independent AMP-activated protein kinase pathways. The improvement in hepatic steatosis observed in DIO-treated mice was associated with a reduction in inflammation (through the IKK α/β) and a decrease in the hepatic content of SREBP-1 (39 %).\n\nQuestion:\nDoes labrador tea ( Rhododendron groenlandicum ) attenuate insulin resistance in a diet-induced obesity mouse model?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nUsing a diet-induced obesity (DIO) mouse model, we investigated the antidiabetic effect of Labrador tea [Rhododendron groenlandicum (Oeder) Kron and Judd], a beverage and medicinal tea used by the Cree Nations of northern Quebec. C57BL6 mice were divided into five groups and given standard chow (~4 % of lipids) or high-fat diet (~35 % of lipids) for 8 weeks until they became obese and insulin resistant. Treatment began by adding the plant extract at three doses (125, 250 and 500 mg/kg) to the high-fat diet for another 8 weeks. At the end of the study, insulin-sensitive tissues (liver, skeletal muscle, adipose tissue) were collected to investigate the plant's molecular mechanisms. Labrador tea significantly reduced blood glucose (13 %), the response to an oral glucose tolerance test (18.2 %) and plasma insulin (65 %) while preventing hepatic steatosis (42 % reduction in hepatic triglyceride levels) in DIO mice. It stimulated insulin-dependent Akt pathway (55 %) and increased the expression of GLUT4 (53 %) in skeletal muscle. In the liver, Labrador tea stimulated the insulin-dependent Akt and the insulin-independent AMP-activated protein kinase pathways. The improvement in hepatic steatosis observed in DIO-treated mice was associated with a reduction in inflammation (through the IKK α/β) and a decrease in the hepatic content of SREBP-1 (39 %).\n\nQuestion:\nDoes labrador tea ( Rhododendron groenlandicum ) attenuate insulin resistance in a diet-induced obesity mouse model?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nTo determine the ability of voriconazole to inhibit the formation of biofilms. A total of 38 blood isolates of Candida spp. (8 Candida albicans, 10 Candida tropicalis, 10 Candida glabrata, 7 Candida parapsilosis sensu stricto and 3 Candida orthopsilosis) and C. albicans ATCC 90028 and ATCC 64548 were assessed. Biofilm formation was quantified using XTT reduction assays. The inhibition of biofilm formation was determined (i) in the presence of 0.06 and 0.25 mg/L voriconazole, and (ii) on surfaces previously coated with 0.06, 0.25, 1, 4 and 16 mg/L voriconazole. Voriconazole reduced biofilm formation under both conditions, the extent depending on the species, isolate and drug concentration. In the presence of 0.25 mg/L, the highest reduction was found for C. parapsilosis (79% ± 8.6%), followed by C. albicans (64.5% ± 6.3%), C. tropicalis (53.3% ± 13.1%) and C. glabrata (23.8% ± 11.2%). This reduction was significant (P < 0.05) for all isolates tested. After coating the wells with voriconazole, biofilm formation was reduced in all Candida spp. examined, C. albicans being the species with the highest reduction (68.8% with 16 mg/L) and C. parapsilosis complex and C. glabrata the lowest.\n\nQuestion:\nDoes voriconazole inhibit biofilm formation in different species of the genus Candida?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nTo determine the ability of voriconazole to inhibit the formation of biofilms. A total of 38 blood isolates of Candida spp. (8 Candida albicans, 10 Candida tropicalis, 10 Candida glabrata, 7 Candida parapsilosis sensu stricto and 3 Candida orthopsilosis) and C. albicans ATCC 90028 and ATCC 64548 were assessed. Biofilm formation was quantified using XTT reduction assays. The inhibition of biofilm formation was determined (i) in the presence of 0.06 and 0.25 mg/L voriconazole, and (ii) on surfaces previously coated with 0.06, 0.25, 1, 4 and 16 mg/L voriconazole. Voriconazole reduced biofilm formation under both conditions, the extent depending on the species, isolate and drug concentration. In the presence of 0.25 mg/L, the highest reduction was found for C. parapsilosis (79% ± 8.6%), followed by C. albicans (64.5% ± 6.3%), C. tropicalis (53.3% ± 13.1%) and C. glabrata (23.8% ± 11.2%). This reduction was significant (P < 0.05) for all isolates tested. After coating the wells with voriconazole, biofilm formation was reduced in all Candida spp. examined, C. albicans being the species with the highest reduction (68.8% with 16 mg/L) and C. parapsilosis complex and C. glabrata the lowest.\n\nQuestion:\nDoes voriconazole inhibit biofilm formation in different species of the genus Candida?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nTo determine the ability of voriconazole to inhibit the formation of biofilms. A total of 38 blood isolates of Candida spp. (8 Candida albicans, 10 Candida tropicalis, 10 Candida glabrata, 7 Candida parapsilosis sensu stricto and 3 Candida orthopsilosis) and C. albicans ATCC 90028 and ATCC 64548 were assessed. Biofilm formation was quantified using XTT reduction assays. The inhibition of biofilm formation was determined (i) in the presence of 0.06 and 0.25 mg/L voriconazole, and (ii) on surfaces previously coated with 0.06, 0.25, 1, 4 and 16 mg/L voriconazole. Voriconazole reduced biofilm formation under both conditions, the extent depending on the species, isolate and drug concentration. In the presence of 0.25 mg/L, the highest reduction was found for C. parapsilosis (79% ± 8.6%), followed by C. albicans (64.5% ± 6.3%), C. tropicalis (53.3% ± 13.1%) and C. glabrata (23.8% ± 11.2%). This reduction was significant (P < 0.05) for all isolates tested. After coating the wells with voriconazole, biofilm formation was reduced in all Candida spp. examined, C. albicans being the species with the highest reduction (68.8% with 16 mg/L) and C. parapsilosis complex and C. glabrata the lowest.\n\nQuestion:\nDoes voriconazole inhibit biofilm formation in different species of the genus Candida?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nObstructive nephropathy is a primary cause of renal failure in infancy. Chronic unilateral ureteral obstruction (UUO) in the neonatal rat results in reduced renal expression of epidermal growth factor (EGF), renal tubular epithelial (RTE) cell apoptosis and interstitial fibrosis. We wished to determine whether these changes could be prevented by exogenous administration of EGF. Thirty-three Sprague-Dawley rats underwent UUO within the first 48 hours of life, and received daily injections of either EGF (0.1 mg/kg/day) or saline (control) for the following seven days, after which obstructed and intact opposite kidneys were removed for study. These were compared to 11 sham-operated rats that received either no injections, EGF injections, or saline injections. Renal cell proliferation was determined by proliferating cell nuclear antigen, apoptosis was measured by the TUNEL technique, and the distribution of vimentin, clusterin, transforming growth factor-beta 1 (TGF-beta 1), and alpha-smooth muscle actin were determined by immunohistochemistry. Tubular dilation, tubular atrophy, and interstitial collagen deposition were quantitated by histomorphometry. Compared to controls, EGF treatment increased RTE cell proliferation in the obstructed kidney by 76%, decreased apoptosis by 80%, and reduced vimentin, clusterin and TGF-beta 1 immunostaining (all P < 0.05). EGF treatment reduced tubular dilation by 50%, atrophic tubules by 30%, and interstitial fibrosis by 50% (all P < 0.05). There was no significant effect of EGF on renal alpha smooth muscle actin distribution. There was no effect of saline or EGF injections on kidneys from sham-operated rats for any of the parameters studied.\n\nQuestion:\nIs obstructive nephropathy in the neonatal rat attenuated by epidermal growth factor?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nObstructive nephropathy is a primary cause of renal failure in infancy. Chronic unilateral ureteral obstruction (UUO) in the neonatal rat results in reduced renal expression of epidermal growth factor (EGF), renal tubular epithelial (RTE) cell apoptosis and interstitial fibrosis. We wished to determine whether these changes could be prevented by exogenous administration of EGF. Thirty-three Sprague-Dawley rats underwent UUO within the first 48 hours of life, and received daily injections of either EGF (0.1 mg/kg/day) or saline (control) for the following seven days, after which obstructed and intact opposite kidneys were removed for study. These were compared to 11 sham-operated rats that received either no injections, EGF injections, or saline injections. Renal cell proliferation was determined by proliferating cell nuclear antigen, apoptosis was measured by the TUNEL technique, and the distribution of vimentin, clusterin, transforming growth factor-beta 1 (TGF-beta 1), and alpha-smooth muscle actin were determined by immunohistochemistry. Tubular dilation, tubular atrophy, and interstitial collagen deposition were quantitated by histomorphometry. Compared to controls, EGF treatment increased RTE cell proliferation in the obstructed kidney by 76%, decreased apoptosis by 80%, and reduced vimentin, clusterin and TGF-beta 1 immunostaining (all P < 0.05). EGF treatment reduced tubular dilation by 50%, atrophic tubules by 30%, and interstitial fibrosis by 50% (all P < 0.05). There was no significant effect of EGF on renal alpha smooth muscle actin distribution. There was no effect of saline or EGF injections on kidneys from sham-operated rats for any of the parameters studied.\n\nQuestion:\nIs obstructive nephropathy in the neonatal rat attenuated by epidermal growth factor?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nObstructive nephropathy is a primary cause of renal failure in infancy. Chronic unilateral ureteral obstruction (UUO) in the neonatal rat results in reduced renal expression of epidermal growth factor (EGF), renal tubular epithelial (RTE) cell apoptosis and interstitial fibrosis. We wished to determine whether these changes could be prevented by exogenous administration of EGF. Thirty-three Sprague-Dawley rats underwent UUO within the first 48 hours of life, and received daily injections of either EGF (0.1 mg/kg/day) or saline (control) for the following seven days, after which obstructed and intact opposite kidneys were removed for study. These were compared to 11 sham-operated rats that received either no injections, EGF injections, or saline injections. Renal cell proliferation was determined by proliferating cell nuclear antigen, apoptosis was measured by the TUNEL technique, and the distribution of vimentin, clusterin, transforming growth factor-beta 1 (TGF-beta 1), and alpha-smooth muscle actin were determined by immunohistochemistry. Tubular dilation, tubular atrophy, and interstitial collagen deposition were quantitated by histomorphometry. Compared to controls, EGF treatment increased RTE cell proliferation in the obstructed kidney by 76%, decreased apoptosis by 80%, and reduced vimentin, clusterin and TGF-beta 1 immunostaining (all P < 0.05). EGF treatment reduced tubular dilation by 50%, atrophic tubules by 30%, and interstitial fibrosis by 50% (all P < 0.05). There was no significant effect of EGF on renal alpha smooth muscle actin distribution. There was no effect of saline or EGF injections on kidneys from sham-operated rats for any of the parameters studied.\n\nQuestion:\nIs obstructive nephropathy in the neonatal rat attenuated by epidermal growth factor?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nTo assess drug-compliance observed among patients with suspected streptococcal pharyngitis treated with twice-daily antibiotic regimens (b.i.d.) and others with thrice-daily regimens (t.i.d.). A prospective study in the primary care setting was designed in which patients with pharyngitis and three or more Centor criteria, non-allergic to beta-lactam agents, treated with several b.i.d and t.i.d antibiotic regimens based on doctor's choice, were recruited. Patient compliance was assessed with electronic monitoring. A total of 113 patients were enrolled (64 in the t.i.d. group and 49 in the b.i.d. group). Mean openings ranged from 70.3 to 83.3% of the total amount of pills. All the parameters analysed indicated significantly worse compliance with the t.i.d. regimens. Eleven patients allocated to the t.i.d. group took at least 80% of the pills (17.2%), this being significantly lower than those who received b.i.d. antibiotics (59.2%; p < 0.001). The percentage of patients who opened the Medication Event Monitoring System (MEMS) container the satisfactory number of times a day was systematically lower among t.i.d. regimens, this being statistically significant from day three (p < 0.05). Patients assigned to t.i.d. regimens more frequently forgot the afternoon dose.\n\nQuestion:\nIs [ Compliance rate of antibiotic therapy in patients with acute pharyngitis very low , mainly when thrice-daily antibiotics are given ]?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nTo assess drug-compliance observed among patients with suspected streptococcal pharyngitis treated with twice-daily antibiotic regimens (b.i.d.) and others with thrice-daily regimens (t.i.d.). A prospective study in the primary care setting was designed in which patients with pharyngitis and three or more Centor criteria, non-allergic to beta-lactam agents, treated with several b.i.d and t.i.d antibiotic regimens based on doctor's choice, were recruited. Patient compliance was assessed with electronic monitoring. A total of 113 patients were enrolled (64 in the t.i.d. group and 49 in the b.i.d. group). Mean openings ranged from 70.3 to 83.3% of the total amount of pills. All the parameters analysed indicated significantly worse compliance with the t.i.d. regimens. Eleven patients allocated to the t.i.d. group took at least 80% of the pills (17.2%), this being significantly lower than those who received b.i.d. antibiotics (59.2%; p < 0.001). The percentage of patients who opened the Medication Event Monitoring System (MEMS) container the satisfactory number of times a day was systematically lower among t.i.d. regimens, this being statistically significant from day three (p < 0.05). Patients assigned to t.i.d. regimens more frequently forgot the afternoon dose.\n\nQuestion:\nIs [ Compliance rate of antibiotic therapy in patients with acute pharyngitis very low , mainly when thrice-daily antibiotics are given ]?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nTo assess drug-compliance observed among patients with suspected streptococcal pharyngitis treated with twice-daily antibiotic regimens (b.i.d.) and others with thrice-daily regimens (t.i.d.). A prospective study in the primary care setting was designed in which patients with pharyngitis and three or more Centor criteria, non-allergic to beta-lactam agents, treated with several b.i.d and t.i.d antibiotic regimens based on doctor's choice, were recruited. Patient compliance was assessed with electronic monitoring. A total of 113 patients were enrolled (64 in the t.i.d. group and 49 in the b.i.d. group). Mean openings ranged from 70.3 to 83.3% of the total amount of pills. All the parameters analysed indicated significantly worse compliance with the t.i.d. regimens. Eleven patients allocated to the t.i.d. group took at least 80% of the pills (17.2%), this being significantly lower than those who received b.i.d. antibiotics (59.2%; p < 0.001). The percentage of patients who opened the Medication Event Monitoring System (MEMS) container the satisfactory number of times a day was systematically lower among t.i.d. regimens, this being statistically significant from day three (p < 0.05). Patients assigned to t.i.d. regimens more frequently forgot the afternoon dose.\n\nQuestion:\nIs [ Compliance rate of antibiotic therapy in patients with acute pharyngitis very low , mainly when thrice-daily antibiotics are given ]?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nPatients affected by chronic lymphocytic leukemia (CLL) have an increased risk of developing a second cancer. There is not a definitive explanation for this phenomenon, although some hypotheses have been postulated. The aim of the present work was to assess the presence of second cancer in untreated patients with CLL who were cytogenetically characterized, and secondly to investigate if there is a correlation between the genetics of CLL and the emergence of second cancer. We performed conventional cytogenetics and Fluorescent in situ hybridization analyses in a series of 106 patients. We observed that nearly 8% of cases developed second cancer, mostly epithelial tumors. The majority of them presented two common features, del(13)(q14.3) and the presence of at least two genetic alterations.\n\nQuestion:\nDoes genetics of lymphocytes influence the emergence of second cancer in chronic lymphocytic leukemia?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nPatients affected by chronic lymphocytic leukemia (CLL) have an increased risk of developing a second cancer. There is not a definitive explanation for this phenomenon, although some hypotheses have been postulated. The aim of the present work was to assess the presence of second cancer in untreated patients with CLL who were cytogenetically characterized, and secondly to investigate if there is a correlation between the genetics of CLL and the emergence of second cancer. We performed conventional cytogenetics and Fluorescent in situ hybridization analyses in a series of 106 patients. We observed that nearly 8% of cases developed second cancer, mostly epithelial tumors. The majority of them presented two common features, del(13)(q14.3) and the presence of at least two genetic alterations.\n\nQuestion:\nDoes genetics of lymphocytes influence the emergence of second cancer in chronic lymphocytic leukemia?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nPatients affected by chronic lymphocytic leukemia (CLL) have an increased risk of developing a second cancer. There is not a definitive explanation for this phenomenon, although some hypotheses have been postulated. The aim of the present work was to assess the presence of second cancer in untreated patients with CLL who were cytogenetically characterized, and secondly to investigate if there is a correlation between the genetics of CLL and the emergence of second cancer. We performed conventional cytogenetics and Fluorescent in situ hybridization analyses in a series of 106 patients. We observed that nearly 8% of cases developed second cancer, mostly epithelial tumors. The majority of them presented two common features, del(13)(q14.3) and the presence of at least two genetic alterations.\n\nQuestion:\nDoes genetics of lymphocytes influence the emergence of second cancer in chronic lymphocytic leukemia?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nBreast milk has been shown to be associated with greater success with regard to weaning children with intestinal failure off parenteral nutrition (PN). There are only a few studies investigating the role of breast milk in decreasing PN-associated liver disease (PNALD). The aim of our study was to determine whether breast milk is better than formula milk in preventing PNALD in infants receiving PN for >4 weeks. We conducted a retrospective analysis of newborns requiring prolonged parenteral nutrition. We divided the sample into 3 different groups (exclusive breast-feeding, exclusive formula-feeding, and mixed feeding. We compared baseline characteristics, feeding profiles and liver function tests, and liver enzymes among the 3 groups. Among infants receiving PN for >4 weeks, we found that infants who were fed only breast milk were significantly less likely to develop PNALD (34.6%) compared with those who were fed only formula milk (72.7%; P = 0.008). The mean maximum conjugated bilirubin (P = 0.03) and the mean maximum aspartate aminotransferase were significantly lower in the breast-fed group (P = 0.04) compared with the formula-fed group. Among the mixed-feeding group, infants who received a higher percentage of breast milk showed a significant negative correlation with the mean maximum conjugated bilirubin. (Pearson correlation -0.517, P = 0.027). The mean number of days receiving PN and the average daily lipid intake in the 2 groups was not significantly different.\n\nQuestion:\nIs breast milk better than formula milk in preventing parenteral nutrition-associated liver disease in infants receiving prolonged parenteral nutrition?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nBreast milk has been shown to be associated with greater success with regard to weaning children with intestinal failure off parenteral nutrition (PN). There are only a few studies investigating the role of breast milk in decreasing PN-associated liver disease (PNALD). The aim of our study was to determine whether breast milk is better than formula milk in preventing PNALD in infants receiving PN for >4 weeks. We conducted a retrospective analysis of newborns requiring prolonged parenteral nutrition. We divided the sample into 3 different groups (exclusive breast-feeding, exclusive formula-feeding, and mixed feeding. We compared baseline characteristics, feeding profiles and liver function tests, and liver enzymes among the 3 groups. Among infants receiving PN for >4 weeks, we found that infants who were fed only breast milk were significantly less likely to develop PNALD (34.6%) compared with those who were fed only formula milk (72.7%; P = 0.008). The mean maximum conjugated bilirubin (P = 0.03) and the mean maximum aspartate aminotransferase were significantly lower in the breast-fed group (P = 0.04) compared with the formula-fed group. Among the mixed-feeding group, infants who received a higher percentage of breast milk showed a significant negative correlation with the mean maximum conjugated bilirubin. (Pearson correlation -0.517, P = 0.027). The mean number of days receiving PN and the average daily lipid intake in the 2 groups was not significantly different.\n\nQuestion:\nIs breast milk better than formula milk in preventing parenteral nutrition-associated liver disease in infants receiving prolonged parenteral nutrition?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nBreast milk has been shown to be associated with greater success with regard to weaning children with intestinal failure off parenteral nutrition (PN). There are only a few studies investigating the role of breast milk in decreasing PN-associated liver disease (PNALD). The aim of our study was to determine whether breast milk is better than formula milk in preventing PNALD in infants receiving PN for >4 weeks. We conducted a retrospective analysis of newborns requiring prolonged parenteral nutrition. We divided the sample into 3 different groups (exclusive breast-feeding, exclusive formula-feeding, and mixed feeding. We compared baseline characteristics, feeding profiles and liver function tests, and liver enzymes among the 3 groups. Among infants receiving PN for >4 weeks, we found that infants who were fed only breast milk were significantly less likely to develop PNALD (34.6%) compared with those who were fed only formula milk (72.7%; P = 0.008). The mean maximum conjugated bilirubin (P = 0.03) and the mean maximum aspartate aminotransferase were significantly lower in the breast-fed group (P = 0.04) compared with the formula-fed group. Among the mixed-feeding group, infants who received a higher percentage of breast milk showed a significant negative correlation with the mean maximum conjugated bilirubin. (Pearson correlation -0.517, P = 0.027). The mean number of days receiving PN and the average daily lipid intake in the 2 groups was not significantly different.\n\nQuestion:\nIs breast milk better than formula milk in preventing parenteral nutrition-associated liver disease in infants receiving prolonged parenteral nutrition?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nEpithelial cells cultured from prostatic acini do not demonstrate significant (P > 0.05) growth response to the testosterone metabolite dihydrotestosterone (DHT) at concentrations of 0.001-10.0 nM. In addition, the nonsteroidal antiandrogen hydroxyflutamide (HO-F) does not influence primary epithelial cell proliferation in this concentration range. Northern blotting carried out with an androgen reception (AR)-specific cDNA probe indicated that the extent of AR gene expression in six unpassaged primary prostatic epithelial cell cultures was insufficient to elicit a detectable signal upon autoradiography. However, RT/PCR analysis of total RNA using two sets of intron-spanning androgen receptor (AR) primers demonstrates the presence of full-length receptor transcripts in two BPH-derived epithelial cell cultures (BPH1 and BPH2) as well as a carcinoma-derived culture (CaP1). AR-positive LNCaP cells transfected with the AR reporter plasmid pMMTV/SPAP exhibit significant increases (P < 0.05) in SPAP production upon treatment with DHT. pMMTV/SPAP-transfected primary epithelial cells exhibit no such response when pulsed with either androgen or anti-androgen.\n\nQuestion:\nIs androgen independence of primary epithelial cultures of the prostate associated with a down-regulation of androgen receptor gene expression?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nEpithelial cells cultured from prostatic acini do not demonstrate significant (P > 0.05) growth response to the testosterone metabolite dihydrotestosterone (DHT) at concentrations of 0.001-10.0 nM. In addition, the nonsteroidal antiandrogen hydroxyflutamide (HO-F) does not influence primary epithelial cell proliferation in this concentration range. Northern blotting carried out with an androgen reception (AR)-specific cDNA probe indicated that the extent of AR gene expression in six unpassaged primary prostatic epithelial cell cultures was insufficient to elicit a detectable signal upon autoradiography. However, RT/PCR analysis of total RNA using two sets of intron-spanning androgen receptor (AR) primers demonstrates the presence of full-length receptor transcripts in two BPH-derived epithelial cell cultures (BPH1 and BPH2) as well as a carcinoma-derived culture (CaP1). AR-positive LNCaP cells transfected with the AR reporter plasmid pMMTV/SPAP exhibit significant increases (P < 0.05) in SPAP production upon treatment with DHT. pMMTV/SPAP-transfected primary epithelial cells exhibit no such response when pulsed with either androgen or anti-androgen.\n\nQuestion:\nIs androgen independence of primary epithelial cultures of the prostate associated with a down-regulation of androgen receptor gene expression?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nEpithelial cells cultured from prostatic acini do not demonstrate significant (P > 0.05) growth response to the testosterone metabolite dihydrotestosterone (DHT) at concentrations of 0.001-10.0 nM. In addition, the nonsteroidal antiandrogen hydroxyflutamide (HO-F) does not influence primary epithelial cell proliferation in this concentration range. Northern blotting carried out with an androgen reception (AR)-specific cDNA probe indicated that the extent of AR gene expression in six unpassaged primary prostatic epithelial cell cultures was insufficient to elicit a detectable signal upon autoradiography. However, RT/PCR analysis of total RNA using two sets of intron-spanning androgen receptor (AR) primers demonstrates the presence of full-length receptor transcripts in two BPH-derived epithelial cell cultures (BPH1 and BPH2) as well as a carcinoma-derived culture (CaP1). AR-positive LNCaP cells transfected with the AR reporter plasmid pMMTV/SPAP exhibit significant increases (P < 0.05) in SPAP production upon treatment with DHT. pMMTV/SPAP-transfected primary epithelial cells exhibit no such response when pulsed with either androgen or anti-androgen.\n\nQuestion:\nIs androgen independence of primary epithelial cultures of the prostate associated with a down-regulation of androgen receptor gene expression?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nActivity of the tumour-suppressor gene PTEN is reduced in different types of cancer and implicates non-responsiveness to targeted therapy. This study evaluates the gene and protein status of PTEN in salivary gland carcinomas. A total of 287 carcinomas of the major and minor salivary glands were investigated for phosphatase and tensin homologue located on chromosome 10 (PTEN) deletion and loss of PTEN expression using fluorescence in situ hybridisation (FISH) and immunohistochemistry (IHC), respectively. Results were correlated to clinicopathological parameters, long-term survival, epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2) (IHC and FISH) status of the tumours. Hemizygous deletions of PTEN were found in 35 out of 232 (15.1%) carcinomas, while homozygous deletions were observed in 17 out of 232 (7.3%) tumours. Phosphatase and tensin homologue located on chromosome 10 deletion was common in certain histological subtypes and especially homozygous deletion was associated with high-grade malignancy, lymph node metastases and unfavourable long-term prognosis (P<0.001). Loss of PTEN expression was present in 59 out of 273 (21.6%) carcinomas and was significantly correlated to genomic PTEN deletion, high-grade malignancy (P<0.001), increased tumour size (P=0.036), lymph node metastases (P=0.007) and worse disease-specific survival (P=0.002). Genomic PTEN deletion, in particular homogenous deletion (P<0.001) predominantly occurred in tumours with increased gene copy number of EGFR (60.0%) and/or amplification of HER2 (63.6%). Loss of PTEN expression was frequently found in tumours overexpressing EGFR (28.6%) and/or HER2 (52.6%).\n\nQuestion:\nIs loss of PTEN associated with elevated EGFR and HER2 expression and worse prognosis in salivary gland cancer?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nActivity of the tumour-suppressor gene PTEN is reduced in different types of cancer and implicates non-responsiveness to targeted therapy. This study evaluates the gene and protein status of PTEN in salivary gland carcinomas. A total of 287 carcinomas of the major and minor salivary glands were investigated for phosphatase and tensin homologue located on chromosome 10 (PTEN) deletion and loss of PTEN expression using fluorescence in situ hybridisation (FISH) and immunohistochemistry (IHC), respectively. Results were correlated to clinicopathological parameters, long-term survival, epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2) (IHC and FISH) status of the tumours. Hemizygous deletions of PTEN were found in 35 out of 232 (15.1%) carcinomas, while homozygous deletions were observed in 17 out of 232 (7.3%) tumours. Phosphatase and tensin homologue located on chromosome 10 deletion was common in certain histological subtypes and especially homozygous deletion was associated with high-grade malignancy, lymph node metastases and unfavourable long-term prognosis (P<0.001). Loss of PTEN expression was present in 59 out of 273 (21.6%) carcinomas and was significantly correlated to genomic PTEN deletion, high-grade malignancy (P<0.001), increased tumour size (P=0.036), lymph node metastases (P=0.007) and worse disease-specific survival (P=0.002). Genomic PTEN deletion, in particular homogenous deletion (P<0.001) predominantly occurred in tumours with increased gene copy number of EGFR (60.0%) and/or amplification of HER2 (63.6%). Loss of PTEN expression was frequently found in tumours overexpressing EGFR (28.6%) and/or HER2 (52.6%).\n\nQuestion:\nIs loss of PTEN associated with elevated EGFR and HER2 expression and worse prognosis in salivary gland cancer?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nActivity of the tumour-suppressor gene PTEN is reduced in different types of cancer and implicates non-responsiveness to targeted therapy. This study evaluates the gene and protein status of PTEN in salivary gland carcinomas. A total of 287 carcinomas of the major and minor salivary glands were investigated for phosphatase and tensin homologue located on chromosome 10 (PTEN) deletion and loss of PTEN expression using fluorescence in situ hybridisation (FISH) and immunohistochemistry (IHC), respectively. Results were correlated to clinicopathological parameters, long-term survival, epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2) (IHC and FISH) status of the tumours. Hemizygous deletions of PTEN were found in 35 out of 232 (15.1%) carcinomas, while homozygous deletions were observed in 17 out of 232 (7.3%) tumours. Phosphatase and tensin homologue located on chromosome 10 deletion was common in certain histological subtypes and especially homozygous deletion was associated with high-grade malignancy, lymph node metastases and unfavourable long-term prognosis (P<0.001). Loss of PTEN expression was present in 59 out of 273 (21.6%) carcinomas and was significantly correlated to genomic PTEN deletion, high-grade malignancy (P<0.001), increased tumour size (P=0.036), lymph node metastases (P=0.007) and worse disease-specific survival (P=0.002). Genomic PTEN deletion, in particular homogenous deletion (P<0.001) predominantly occurred in tumours with increased gene copy number of EGFR (60.0%) and/or amplification of HER2 (63.6%). Loss of PTEN expression was frequently found in tumours overexpressing EGFR (28.6%) and/or HER2 (52.6%).\n\nQuestion:\nIs loss of PTEN associated with elevated EGFR and HER2 expression and worse prognosis in salivary gland cancer?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nLong QT syndrome type 3 (LQT3) is a lethal disease caused by gain-of-function mutations in the SCN5A gene, coding for the alpha-subunit of the sodium channel NaV1.5. Mexiletine is used to block late sodium current and to shorten QT interval in LQT3 patients. The aim of this study was to determine whether mexiletine prevents arrhythmic events (arrhythmic syncope, aborted cardiac arrest, or sudden cardiac death) in LQT3 patients. The endpoint of this retrospective cohort study, which studied consecutive LQT3 patients who were referred to our center and treated with mexiletine, was to evaluate the antiarrhythmic efficacy of mexiletine by comparing the number of arrhythmic events per patient and the annual rate of arrhythmic events during observation periods of equal duration before and after the beginning of therapy with mexiletine. The study population comprised 34 LQT3 patients, 19 (56%) of whom were male. The median age at beginning of treatment with mexiletine was 22 years, and median QTc interval before therapy 509 ms. The median duration of oral mexiletine therapy was 36 months, at an average daily dose of 8 ± 0.5 mg/kg. Mexiletine significantly shortened QTc (by 63 ± 6 ms; p < 0.0001) and reduced the percentage of patients with arrhythmic events (from 22% to 3%; p = 0.031), the mean number of arrhythmic events per patient (from 0.43 ± 0.17 to 0.03 ± 0.03; p = 0.027), and the annual rate of arrhythmic events (from 10.3% to 0.7%; p = 0.0097).\n\nQuestion:\nDoes gene-Specific Therapy With Mexiletine reduce Arrhythmic Events in Patients With Long QT Syndrome Type 3?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nLong QT syndrome type 3 (LQT3) is a lethal disease caused by gain-of-function mutations in the SCN5A gene, coding for the alpha-subunit of the sodium channel NaV1.5. Mexiletine is used to block late sodium current and to shorten QT interval in LQT3 patients. The aim of this study was to determine whether mexiletine prevents arrhythmic events (arrhythmic syncope, aborted cardiac arrest, or sudden cardiac death) in LQT3 patients. The endpoint of this retrospective cohort study, which studied consecutive LQT3 patients who were referred to our center and treated with mexiletine, was to evaluate the antiarrhythmic efficacy of mexiletine by comparing the number of arrhythmic events per patient and the annual rate of arrhythmic events during observation periods of equal duration before and after the beginning of therapy with mexiletine. The study population comprised 34 LQT3 patients, 19 (56%) of whom were male. The median age at beginning of treatment with mexiletine was 22 years, and median QTc interval before therapy 509 ms. The median duration of oral mexiletine therapy was 36 months, at an average daily dose of 8 ± 0.5 mg/kg. Mexiletine significantly shortened QTc (by 63 ± 6 ms; p < 0.0001) and reduced the percentage of patients with arrhythmic events (from 22% to 3%; p = 0.031), the mean number of arrhythmic events per patient (from 0.43 ± 0.17 to 0.03 ± 0.03; p = 0.027), and the annual rate of arrhythmic events (from 10.3% to 0.7%; p = 0.0097).\n\nQuestion:\nDoes gene-Specific Therapy With Mexiletine reduce Arrhythmic Events in Patients With Long QT Syndrome Type 3?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nLong QT syndrome type 3 (LQT3) is a lethal disease caused by gain-of-function mutations in the SCN5A gene, coding for the alpha-subunit of the sodium channel NaV1.5. Mexiletine is used to block late sodium current and to shorten QT interval in LQT3 patients. The aim of this study was to determine whether mexiletine prevents arrhythmic events (arrhythmic syncope, aborted cardiac arrest, or sudden cardiac death) in LQT3 patients. The endpoint of this retrospective cohort study, which studied consecutive LQT3 patients who were referred to our center and treated with mexiletine, was to evaluate the antiarrhythmic efficacy of mexiletine by comparing the number of arrhythmic events per patient and the annual rate of arrhythmic events during observation periods of equal duration before and after the beginning of therapy with mexiletine. The study population comprised 34 LQT3 patients, 19 (56%) of whom were male. The median age at beginning of treatment with mexiletine was 22 years, and median QTc interval before therapy 509 ms. The median duration of oral mexiletine therapy was 36 months, at an average daily dose of 8 ± 0.5 mg/kg. Mexiletine significantly shortened QTc (by 63 ± 6 ms; p < 0.0001) and reduced the percentage of patients with arrhythmic events (from 22% to 3%; p = 0.031), the mean number of arrhythmic events per patient (from 0.43 ± 0.17 to 0.03 ± 0.03; p = 0.027), and the annual rate of arrhythmic events (from 10.3% to 0.7%; p = 0.0097).\n\nQuestion:\nDoes gene-Specific Therapy With Mexiletine reduce Arrhythmic Events in Patients With Long QT Syndrome Type 3?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nIntra-arterial (IA) nicardipine is often used to treat cerebral vasospasm associated with subarachnoid hemorrhage (SAH). While hypotension has been noted to be a dose-limiting side effect of intravenous infusions, this has seldom been reported for IA administration. We reviewed a consecutive series of patients who received IA nicardipine for SAH-associated vasospasm. Nicardipine was titrated to angiographic response, with blood pressure and intracranial pressure monitoring. We analyzed data using Wilcoxon signed rank, Student's t-test, Spearman's correlation, and χ(2) statistics as appropriate. A P value <0.05 was considered significant. Thirty patients underwent 50 procedures in which nicardipine was the sole chemical vasodilator (median dose, 15 mg). Median mean arterial pressures (MAP) decreased from 118 to 100 mmHg (P < 0.001), with an intra-operative low of 80 mmHg. Both intra-operative and post-operative decreases in MAP were directly related to nicardipine dose (r (s) = 0.352, P = 0.022 and r (s) = 0.308, P = 0.047, respectively). Hypotension (MAP < 70 mmHg) occurred in 22%, and 44% required initiation of or increases in vasopressor therapy. After the first treatment, 11 of 16 patients treated with vasodilator therapy alone, and 5 of 14 patients who underwent additional balloon angioplasty (68.8 vs. 35.7%, P = 0.141), required further endovascular treatments due to recurrent vasospasm on subsequent days.\n\nQuestion:\nDoes high-dose intra-arterial nicardipine result in hypotension following vasospasm treatment in subarachnoid hemorrhage?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nIntra-arterial (IA) nicardipine is often used to treat cerebral vasospasm associated with subarachnoid hemorrhage (SAH). While hypotension has been noted to be a dose-limiting side effect of intravenous infusions, this has seldom been reported for IA administration. We reviewed a consecutive series of patients who received IA nicardipine for SAH-associated vasospasm. Nicardipine was titrated to angiographic response, with blood pressure and intracranial pressure monitoring. We analyzed data using Wilcoxon signed rank, Student's t-test, Spearman's correlation, and χ(2) statistics as appropriate. A P value <0.05 was considered significant. Thirty patients underwent 50 procedures in which nicardipine was the sole chemical vasodilator (median dose, 15 mg). Median mean arterial pressures (MAP) decreased from 118 to 100 mmHg (P < 0.001), with an intra-operative low of 80 mmHg. Both intra-operative and post-operative decreases in MAP were directly related to nicardipine dose (r (s) = 0.352, P = 0.022 and r (s) = 0.308, P = 0.047, respectively). Hypotension (MAP < 70 mmHg) occurred in 22%, and 44% required initiation of or increases in vasopressor therapy. After the first treatment, 11 of 16 patients treated with vasodilator therapy alone, and 5 of 14 patients who underwent additional balloon angioplasty (68.8 vs. 35.7%, P = 0.141), required further endovascular treatments due to recurrent vasospasm on subsequent days.\n\nQuestion:\nDoes high-dose intra-arterial nicardipine result in hypotension following vasospasm treatment in subarachnoid hemorrhage?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nIntra-arterial (IA) nicardipine is often used to treat cerebral vasospasm associated with subarachnoid hemorrhage (SAH). While hypotension has been noted to be a dose-limiting side effect of intravenous infusions, this has seldom been reported for IA administration. We reviewed a consecutive series of patients who received IA nicardipine for SAH-associated vasospasm. Nicardipine was titrated to angiographic response, with blood pressure and intracranial pressure monitoring. We analyzed data using Wilcoxon signed rank, Student's t-test, Spearman's correlation, and χ(2) statistics as appropriate. A P value <0.05 was considered significant. Thirty patients underwent 50 procedures in which nicardipine was the sole chemical vasodilator (median dose, 15 mg). Median mean arterial pressures (MAP) decreased from 118 to 100 mmHg (P < 0.001), with an intra-operative low of 80 mmHg. Both intra-operative and post-operative decreases in MAP were directly related to nicardipine dose (r (s) = 0.352, P = 0.022 and r (s) = 0.308, P = 0.047, respectively). Hypotension (MAP < 70 mmHg) occurred in 22%, and 44% required initiation of or increases in vasopressor therapy. After the first treatment, 11 of 16 patients treated with vasodilator therapy alone, and 5 of 14 patients who underwent additional balloon angioplasty (68.8 vs. 35.7%, P = 0.141), required further endovascular treatments due to recurrent vasospasm on subsequent days.\n\nQuestion:\nDoes high-dose intra-arterial nicardipine result in hypotension following vasospasm treatment in subarachnoid hemorrhage?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nThe gut microbiome, a dynamic bacterial community that interacts with the host, is integral to human health because it regulates energy metabolism and immune functions. The gut microbiome may also play a role in risks from environmental toxicants. We investigated the effects of polychlorinated biphenyls (PCBs) and exercise on the composition and structure of the gut microbiome in mice. After mice exercised voluntarily for 5 weeks, they were treated by oral gavage with a mixture of environmentally relevant PCB congeners (PCB153, PCB138, and PCB180; total PCB dose, 150 µmol/kg) for 2 days. We then assessed the microbiome by determination of 16S rRNA using microarray analysis. Oral exposure to PCBs significantly altered the abundance of the gut microbiome in mice primarily by decreasing the levels of Proteobacteria. The activity level of the mice correlated with a substantial shift in abundance, biodiversity, and composition of the microbiome. Importantly, exercise attenuated PCB-induced changes in the gut microbiome.\n\nQuestion:\nDoes exercise attenuate PCB-induced changes in the mouse gut microbiome?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nThe gut microbiome, a dynamic bacterial community that interacts with the host, is integral to human health because it regulates energy metabolism and immune functions. The gut microbiome may also play a role in risks from environmental toxicants. We investigated the effects of polychlorinated biphenyls (PCBs) and exercise on the composition and structure of the gut microbiome in mice. After mice exercised voluntarily for 5 weeks, they were treated by oral gavage with a mixture of environmentally relevant PCB congeners (PCB153, PCB138, and PCB180; total PCB dose, 150 µmol/kg) for 2 days. We then assessed the microbiome by determination of 16S rRNA using microarray analysis. Oral exposure to PCBs significantly altered the abundance of the gut microbiome in mice primarily by decreasing the levels of Proteobacteria. The activity level of the mice correlated with a substantial shift in abundance, biodiversity, and composition of the microbiome. Importantly, exercise attenuated PCB-induced changes in the gut microbiome.\n\nQuestion:\nDoes exercise attenuate PCB-induced changes in the mouse gut microbiome?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nThe gut microbiome, a dynamic bacterial community that interacts with the host, is integral to human health because it regulates energy metabolism and immune functions. The gut microbiome may also play a role in risks from environmental toxicants. We investigated the effects of polychlorinated biphenyls (PCBs) and exercise on the composition and structure of the gut microbiome in mice. After mice exercised voluntarily for 5 weeks, they were treated by oral gavage with a mixture of environmentally relevant PCB congeners (PCB153, PCB138, and PCB180; total PCB dose, 150 µmol/kg) for 2 days. We then assessed the microbiome by determination of 16S rRNA using microarray analysis. Oral exposure to PCBs significantly altered the abundance of the gut microbiome in mice primarily by decreasing the levels of Proteobacteria. The activity level of the mice correlated with a substantial shift in abundance, biodiversity, and composition of the microbiome. Importantly, exercise attenuated PCB-induced changes in the gut microbiome.\n\nQuestion:\nDoes exercise attenuate PCB-induced changes in the mouse gut microbiome?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nEndothelial dysfunction is an early step in the development of atherosclerosis. Increased formation of superoxide anions by NADPH oxidase Nox1, 2, and 5 reduces nitric oxide availability and can promote endothelial dysfunction. In contrast, recent evidence supports a vasoprotective role of H2O2 produced by main endothelial isoform Nox4. Therefore, we analysed the impact of genetic deletion of Nox4 on endothelial dysfunction and atherosclerosis in the low-density lipoprotein receptor (Ldlr) knockout model. Ex vivo analysis of endothelial function by Mulvany myograph showed impaired endothelial function in thoracic aorta of Nox4(-/-)/Ldlr(-/-) mice. Further progression of endothelial dysfunction due to high-fat diet increased atherosclerotic plaque burden and galectin-3 staining in Nox4(-/-)/Ldlr(-/-) mice compared with Ldlr(-/-) mice. Under physiological conditions, loss of Nox4 does not influence aortic vascular function. In this setting, loss of Nox4-derived H2O2 production could be partially compensated for by nNOS upregulation. Using an innovative optical coherence tomography approach, we were able to analyse endothelial function by flow-mediated vasodilation in the murine saphenous artery in vivo. This new approach revealed an altered flow-mediated dilation in Nox4(-/-) mice, indicating a role for Nox4 under physiological conditions in peripheral arteries in vivo.\n\nQuestion:\nDoes nADPH oxidase 4 protect against development of endothelial dysfunction and atherosclerosis in LDL receptor deficient mice?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nEndothelial dysfunction is an early step in the development of atherosclerosis. Increased formation of superoxide anions by NADPH oxidase Nox1, 2, and 5 reduces nitric oxide availability and can promote endothelial dysfunction. In contrast, recent evidence supports a vasoprotective role of H2O2 produced by main endothelial isoform Nox4. Therefore, we analysed the impact of genetic deletion of Nox4 on endothelial dysfunction and atherosclerosis in the low-density lipoprotein receptor (Ldlr) knockout model. Ex vivo analysis of endothelial function by Mulvany myograph showed impaired endothelial function in thoracic aorta of Nox4(-/-)/Ldlr(-/-) mice. Further progression of endothelial dysfunction due to high-fat diet increased atherosclerotic plaque burden and galectin-3 staining in Nox4(-/-)/Ldlr(-/-) mice compared with Ldlr(-/-) mice. Under physiological conditions, loss of Nox4 does not influence aortic vascular function. In this setting, loss of Nox4-derived H2O2 production could be partially compensated for by nNOS upregulation. Using an innovative optical coherence tomography approach, we were able to analyse endothelial function by flow-mediated vasodilation in the murine saphenous artery in vivo. This new approach revealed an altered flow-mediated dilation in Nox4(-/-) mice, indicating a role for Nox4 under physiological conditions in peripheral arteries in vivo.\n\nQuestion:\nDoes nADPH oxidase 4 protect against development of endothelial dysfunction and atherosclerosis in LDL receptor deficient mice?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nEndothelial dysfunction is an early step in the development of atherosclerosis. Increased formation of superoxide anions by NADPH oxidase Nox1, 2, and 5 reduces nitric oxide availability and can promote endothelial dysfunction. In contrast, recent evidence supports a vasoprotective role of H2O2 produced by main endothelial isoform Nox4. Therefore, we analysed the impact of genetic deletion of Nox4 on endothelial dysfunction and atherosclerosis in the low-density lipoprotein receptor (Ldlr) knockout model. Ex vivo analysis of endothelial function by Mulvany myograph showed impaired endothelial function in thoracic aorta of Nox4(-/-)/Ldlr(-/-) mice. Further progression of endothelial dysfunction due to high-fat diet increased atherosclerotic plaque burden and galectin-3 staining in Nox4(-/-)/Ldlr(-/-) mice compared with Ldlr(-/-) mice. Under physiological conditions, loss of Nox4 does not influence aortic vascular function. In this setting, loss of Nox4-derived H2O2 production could be partially compensated for by nNOS upregulation. Using an innovative optical coherence tomography approach, we were able to analyse endothelial function by flow-mediated vasodilation in the murine saphenous artery in vivo. This new approach revealed an altered flow-mediated dilation in Nox4(-/-) mice, indicating a role for Nox4 under physiological conditions in peripheral arteries in vivo.\n\nQuestion:\nDoes nADPH oxidase 4 protect against development of endothelial dysfunction and atherosclerosis in LDL receptor deficient mice?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nWe aimed to evaluate if anterior colporrhaphy causes incomplete voiding due to bladder outlet obstruction. Women scheduled for anterior colporrhaphy were asked to undergo multichannel urodynamic investigation before surgery and the first postoperative day. Bladder outlet obstruction was assessed using the Blaivas–Groutz voiding nomogram. Maximum flow rate, detrusor pressure and residual volume were compared between pre- and postoperative measurements and between women with and without an abnormal post-void residual volume (PVR; volume exceeding 150 ml). Seventeen women participated. One woman who was unobstructed before surgery was obstructed after surgery. Overall, detrusor pressure and maximum flow rate before and after surgery did not differ. After surgery, six women had an abnormal PVR, one was unable to void, four were mildly obstructed and one moderately obstructed.\n\nQuestion:\nDoes anterior colporrhaphy induce bladder outlet obstruction?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nWe aimed to evaluate if anterior colporrhaphy causes incomplete voiding due to bladder outlet obstruction. Women scheduled for anterior colporrhaphy were asked to undergo multichannel urodynamic investigation before surgery and the first postoperative day. Bladder outlet obstruction was assessed using the Blaivas–Groutz voiding nomogram. Maximum flow rate, detrusor pressure and residual volume were compared between pre- and postoperative measurements and between women with and without an abnormal post-void residual volume (PVR; volume exceeding 150 ml). Seventeen women participated. One woman who was unobstructed before surgery was obstructed after surgery. Overall, detrusor pressure and maximum flow rate before and after surgery did not differ. After surgery, six women had an abnormal PVR, one was unable to void, four were mildly obstructed and one moderately obstructed.\n\nQuestion:\nDoes anterior colporrhaphy induce bladder outlet obstruction?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nWe aimed to evaluate if anterior colporrhaphy causes incomplete voiding due to bladder outlet obstruction. Women scheduled for anterior colporrhaphy were asked to undergo multichannel urodynamic investigation before surgery and the first postoperative day. Bladder outlet obstruction was assessed using the Blaivas–Groutz voiding nomogram. Maximum flow rate, detrusor pressure and residual volume were compared between pre- and postoperative measurements and between women with and without an abnormal post-void residual volume (PVR; volume exceeding 150 ml). Seventeen women participated. One woman who was unobstructed before surgery was obstructed after surgery. Overall, detrusor pressure and maximum flow rate before and after surgery did not differ. After surgery, six women had an abnormal PVR, one was unable to void, four were mildly obstructed and one moderately obstructed.\n\nQuestion:\nDoes anterior colporrhaphy induce bladder outlet obstruction?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nArterial stiffness may contribute to left ventricular hypertrophy (LVH). This study was conducted to evaluate the independent factor of LVH and the quantification of LVH by electrocardiogram (ECG) to predict the degree of aortic stiffness using brachial-ankle pulse wave velocity (baPWV) in subjects with hypertension. A total of 984 consecutive patients who were diagnosed as having essential hypertension were entered into the study. baPWV determination, ECG and blood sampling were performed after a 12-hour overnight fast. LVH was diagnosed using electrocardiography; Romhilt-Estes point score was subsequently calculated. Participants were separated into LVH and non-LVH groups. Additional factors associated with LVH were examined using multivariate analyses. The non-LVH groups were younger (P = 0.001), had less men (P = 0.001), lower systolic and diastolic blood pressure and pulse pressure (P < 0.001 for each) and lower baPWV (P < 0.001). Stepwise multiple logistic regression analysis demonstrated that sex, age, systolic blood pressure and baPWV are independent factors. Using a baPWV value of 1825 cm/sec, the area under the receiver operating characteristic curve was 0.644 and the highest discriminating sensitivity and specificity were 60% and 65%, respectively.\n\nQuestion:\nIs arterial stiffness the independent factor of left ventricular hypertrophy determined by electrocardiogram?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nArterial stiffness may contribute to left ventricular hypertrophy (LVH). This study was conducted to evaluate the independent factor of LVH and the quantification of LVH by electrocardiogram (ECG) to predict the degree of aortic stiffness using brachial-ankle pulse wave velocity (baPWV) in subjects with hypertension. A total of 984 consecutive patients who were diagnosed as having essential hypertension were entered into the study. baPWV determination, ECG and blood sampling were performed after a 12-hour overnight fast. LVH was diagnosed using electrocardiography; Romhilt-Estes point score was subsequently calculated. Participants were separated into LVH and non-LVH groups. Additional factors associated with LVH were examined using multivariate analyses. The non-LVH groups were younger (P = 0.001), had less men (P = 0.001), lower systolic and diastolic blood pressure and pulse pressure (P < 0.001 for each) and lower baPWV (P < 0.001). Stepwise multiple logistic regression analysis demonstrated that sex, age, systolic blood pressure and baPWV are independent factors. Using a baPWV value of 1825 cm/sec, the area under the receiver operating characteristic curve was 0.644 and the highest discriminating sensitivity and specificity were 60% and 65%, respectively.\n\nQuestion:\nIs arterial stiffness the independent factor of left ventricular hypertrophy determined by electrocardiogram?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nArterial stiffness may contribute to left ventricular hypertrophy (LVH). This study was conducted to evaluate the independent factor of LVH and the quantification of LVH by electrocardiogram (ECG) to predict the degree of aortic stiffness using brachial-ankle pulse wave velocity (baPWV) in subjects with hypertension. A total of 984 consecutive patients who were diagnosed as having essential hypertension were entered into the study. baPWV determination, ECG and blood sampling were performed after a 12-hour overnight fast. LVH was diagnosed using electrocardiography; Romhilt-Estes point score was subsequently calculated. Participants were separated into LVH and non-LVH groups. Additional factors associated with LVH were examined using multivariate analyses. The non-LVH groups were younger (P = 0.001), had less men (P = 0.001), lower systolic and diastolic blood pressure and pulse pressure (P < 0.001 for each) and lower baPWV (P < 0.001). Stepwise multiple logistic regression analysis demonstrated that sex, age, systolic blood pressure and baPWV are independent factors. Using a baPWV value of 1825 cm/sec, the area under the receiver operating characteristic curve was 0.644 and the highest discriminating sensitivity and specificity were 60% and 65%, respectively.\n\nQuestion:\nIs arterial stiffness the independent factor of left ventricular hypertrophy determined by electrocardiogram?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nTo characterize the effect of systemically administered AGP on early leukocyte recruitment in the livers of endotoxemic or septic mice and to determine whether this is influenced by LPS sequestration. Endotoxemia was induced in C57Bl/6 mice via intraperitoneal injection of LPS. Sepsis was induced in mice by cecal ligation and perforation. AGP (165 mg/kg) or saline (20 mL/kg) or HAS (200 mg/kg) was administered immediately after surgery or LPS injection and the hepatic microcirculation was examined by intravital microscopy at four hour. Leukocyte adhesion in the PSV was reduced by treatment with AGP in mice subjected to either LPS or CLP protocols compared to either saline or HAS treatment. AGP-treated mice also had significantly higher sinusoidal flow in both models. Pre-incubation of LPS with AGP reduced the ability of LPS to recruit leukocytes to the liver microcirculation.\n\nQuestion:\nDoes alpha-1 acid glycoprotein reduce hepatic leukocyte recruitment in murine models of either early endotoxemia or early sepsis?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nTo characterize the effect of systemically administered AGP on early leukocyte recruitment in the livers of endotoxemic or septic mice and to determine whether this is influenced by LPS sequestration. Endotoxemia was induced in C57Bl/6 mice via intraperitoneal injection of LPS. Sepsis was induced in mice by cecal ligation and perforation. AGP (165 mg/kg) or saline (20 mL/kg) or HAS (200 mg/kg) was administered immediately after surgery or LPS injection and the hepatic microcirculation was examined by intravital microscopy at four hour. Leukocyte adhesion in the PSV was reduced by treatment with AGP in mice subjected to either LPS or CLP protocols compared to either saline or HAS treatment. AGP-treated mice also had significantly higher sinusoidal flow in both models. Pre-incubation of LPS with AGP reduced the ability of LPS to recruit leukocytes to the liver microcirculation.\n\nQuestion:\nDoes alpha-1 acid glycoprotein reduce hepatic leukocyte recruitment in murine models of either early endotoxemia or early sepsis?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nTo characterize the effect of systemically administered AGP on early leukocyte recruitment in the livers of endotoxemic or septic mice and to determine whether this is influenced by LPS sequestration. Endotoxemia was induced in C57Bl/6 mice via intraperitoneal injection of LPS. Sepsis was induced in mice by cecal ligation and perforation. AGP (165 mg/kg) or saline (20 mL/kg) or HAS (200 mg/kg) was administered immediately after surgery or LPS injection and the hepatic microcirculation was examined by intravital microscopy at four hour. Leukocyte adhesion in the PSV was reduced by treatment with AGP in mice subjected to either LPS or CLP protocols compared to either saline or HAS treatment. AGP-treated mice also had significantly higher sinusoidal flow in both models. Pre-incubation of LPS with AGP reduced the ability of LPS to recruit leukocytes to the liver microcirculation.\n\nQuestion:\nDoes alpha-1 acid glycoprotein reduce hepatic leukocyte recruitment in murine models of either early endotoxemia or early sepsis?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nTo compare oncologic outcomes in a contemporary series of patients undergoing radical cystectomy (RCX) by the laparoscopic or open approach. Laparoscopic RCX with extracorporeally constructed urinary diversion is a safe and effective operation for appropriate patients with bladder cancer. Perioperative and functional outcomes are comparable with open surgery. Worldwide experience continues to increase; more than 1000 surgeries have already been performed. Intermediate-term oncologic outcomes appear to be comparable to open approach.\n\nQuestion:\nAre the oncologic results of laparoscopic radical cystectomy ( yet ) equivalent to open cystectomy?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nTo compare oncologic outcomes in a contemporary series of patients undergoing radical cystectomy (RCX) by the laparoscopic or open approach. Laparoscopic RCX with extracorporeally constructed urinary diversion is a safe and effective operation for appropriate patients with bladder cancer. Perioperative and functional outcomes are comparable with open surgery. Worldwide experience continues to increase; more than 1000 surgeries have already been performed. Intermediate-term oncologic outcomes appear to be comparable to open approach.\n\nQuestion:\nAre the oncologic results of laparoscopic radical cystectomy ( yet ) equivalent to open cystectomy?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nTo compare oncologic outcomes in a contemporary series of patients undergoing radical cystectomy (RCX) by the laparoscopic or open approach. Laparoscopic RCX with extracorporeally constructed urinary diversion is a safe and effective operation for appropriate patients with bladder cancer. Perioperative and functional outcomes are comparable with open surgery. Worldwide experience continues to increase; more than 1000 surgeries have already been performed. Intermediate-term oncologic outcomes appear to be comparable to open approach.\n\nQuestion:\nAre the oncologic results of laparoscopic radical cystectomy ( yet ) equivalent to open cystectomy?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nEndothelial progenitor cells (EPCs) comprise a heterogeneous population of cells, which improve therapeutic neovascularization after ischemia. The neovascularization-promoting potential of progenitor cells depends on survival and retention of the infused cells to the tissue. Caspases mediate apoptosis but are also involved in other critical biological processes. Therefore, we aimed to address the role of caspases in proangiogenic cells. The caspase-8 inhibitor zIETD abrogated the ex vivo formation of EPCs, inhibited EPC adhesion and migration, and reduced their capacity to improve neovascularization in vivo. Consistently, cells isolated from caspase-8-deficient mice exhibited a reduced capacity for enhancing neovascularization when transplanted into mice after hindlimb ischemia. Because inhibition of Caspase-8 reduced the adhesion and homing functions of EPCs, we further determined the surface expression of integrins and receptors involved in cell recruitment to ischemic tissues. Pharmacological inhibition of caspase-8 and genetic depletion of caspase-8 reduced the expression of the fibronectin receptor subunits alpha5 and beta1 and the SDF-1 receptor CXCR4. Moreover, we identified the E3 ubiquitin ligase Cbl-b, which negatively regulates integrin and receptor-mediated signaling, as a potential Caspase-8 substrate.\n\nQuestion:\nIs caspase-8 involved in neovascularization-promoting progenitor cell functions?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nEndothelial progenitor cells (EPCs) comprise a heterogeneous population of cells, which improve therapeutic neovascularization after ischemia. The neovascularization-promoting potential of progenitor cells depends on survival and retention of the infused cells to the tissue. Caspases mediate apoptosis but are also involved in other critical biological processes. Therefore, we aimed to address the role of caspases in proangiogenic cells. The caspase-8 inhibitor zIETD abrogated the ex vivo formation of EPCs, inhibited EPC adhesion and migration, and reduced their capacity to improve neovascularization in vivo. Consistently, cells isolated from caspase-8-deficient mice exhibited a reduced capacity for enhancing neovascularization when transplanted into mice after hindlimb ischemia. Because inhibition of Caspase-8 reduced the adhesion and homing functions of EPCs, we further determined the surface expression of integrins and receptors involved in cell recruitment to ischemic tissues. Pharmacological inhibition of caspase-8 and genetic depletion of caspase-8 reduced the expression of the fibronectin receptor subunits alpha5 and beta1 and the SDF-1 receptor CXCR4. Moreover, we identified the E3 ubiquitin ligase Cbl-b, which negatively regulates integrin and receptor-mediated signaling, as a potential Caspase-8 substrate.\n\nQuestion:\nIs caspase-8 involved in neovascularization-promoting progenitor cell functions?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nEndothelial progenitor cells (EPCs) comprise a heterogeneous population of cells, which improve therapeutic neovascularization after ischemia. The neovascularization-promoting potential of progenitor cells depends on survival and retention of the infused cells to the tissue. Caspases mediate apoptosis but are also involved in other critical biological processes. Therefore, we aimed to address the role of caspases in proangiogenic cells. The caspase-8 inhibitor zIETD abrogated the ex vivo formation of EPCs, inhibited EPC adhesion and migration, and reduced their capacity to improve neovascularization in vivo. Consistently, cells isolated from caspase-8-deficient mice exhibited a reduced capacity for enhancing neovascularization when transplanted into mice after hindlimb ischemia. Because inhibition of Caspase-8 reduced the adhesion and homing functions of EPCs, we further determined the surface expression of integrins and receptors involved in cell recruitment to ischemic tissues. Pharmacological inhibition of caspase-8 and genetic depletion of caspase-8 reduced the expression of the fibronectin receptor subunits alpha5 and beta1 and the SDF-1 receptor CXCR4. Moreover, we identified the E3 ubiquitin ligase Cbl-b, which negatively regulates integrin and receptor-mediated signaling, as a potential Caspase-8 substrate.\n\nQuestion:\nIs caspase-8 involved in neovascularization-promoting progenitor cell functions?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nExposure to air pollution is associated with increased cardiovascular morbidity, although the underlying mechanisms are unclear. Vascular dysfunction reduces arterial compliance and increases central arterial pressure and left ventricular after-load. We determined the effect of diesel exhaust exposure on arterial compliance using a validated non-invasive measure of arterial stiffness. In a double-blind randomized fashion, 12 healthy volunteers were exposed to diesel exhaust (approximately 350 mug/m3) or filtered air for one hour during moderate exercise. Arterial stiffness was measured using applanation tonometry at the radial artery for pulse wave analysis (PWA), as well as at the femoral and carotid arteries for pulse wave velocity (PWV). PWA was performed 10, 20 and 30 min, and carotid-femoral PWV 40 min, post-exposure. Augmentation pressure (AP), augmentation index (AIx) and time to wave reflection (Tr) were calculated. Blood pressure, AP and AIx were generally low reflecting compliant arteries. In comparison to filtered air, diesel exhaust exposure induced an increase in AP of 2.5 mmHg (p = 0.02) and in AIx of 7.8% (p = 0.01), along with a 16 ms reduction in Tr (p = 0.03), 10 minutes post-exposure.\n\nQuestion:\nDoes experimental exposure to diesel exhaust increase arterial stiffness in man?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nExposure to air pollution is associated with increased cardiovascular morbidity, although the underlying mechanisms are unclear. Vascular dysfunction reduces arterial compliance and increases central arterial pressure and left ventricular after-load. We determined the effect of diesel exhaust exposure on arterial compliance using a validated non-invasive measure of arterial stiffness. In a double-blind randomized fashion, 12 healthy volunteers were exposed to diesel exhaust (approximately 350 mug/m3) or filtered air for one hour during moderate exercise. Arterial stiffness was measured using applanation tonometry at the radial artery for pulse wave analysis (PWA), as well as at the femoral and carotid arteries for pulse wave velocity (PWV). PWA was performed 10, 20 and 30 min, and carotid-femoral PWV 40 min, post-exposure. Augmentation pressure (AP), augmentation index (AIx) and time to wave reflection (Tr) were calculated. Blood pressure, AP and AIx were generally low reflecting compliant arteries. In comparison to filtered air, diesel exhaust exposure induced an increase in AP of 2.5 mmHg (p = 0.02) and in AIx of 7.8% (p = 0.01), along with a 16 ms reduction in Tr (p = 0.03), 10 minutes post-exposure.\n\nQuestion:\nDoes experimental exposure to diesel exhaust increase arterial stiffness in man?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nExposure to air pollution is associated with increased cardiovascular morbidity, although the underlying mechanisms are unclear. Vascular dysfunction reduces arterial compliance and increases central arterial pressure and left ventricular after-load. We determined the effect of diesel exhaust exposure on arterial compliance using a validated non-invasive measure of arterial stiffness. In a double-blind randomized fashion, 12 healthy volunteers were exposed to diesel exhaust (approximately 350 mug/m3) or filtered air for one hour during moderate exercise. Arterial stiffness was measured using applanation tonometry at the radial artery for pulse wave analysis (PWA), as well as at the femoral and carotid arteries for pulse wave velocity (PWV). PWA was performed 10, 20 and 30 min, and carotid-femoral PWV 40 min, post-exposure. Augmentation pressure (AP), augmentation index (AIx) and time to wave reflection (Tr) were calculated. Blood pressure, AP and AIx were generally low reflecting compliant arteries. In comparison to filtered air, diesel exhaust exposure induced an increase in AP of 2.5 mmHg (p = 0.02) and in AIx of 7.8% (p = 0.01), along with a 16 ms reduction in Tr (p = 0.03), 10 minutes post-exposure.\n\nQuestion:\nDoes experimental exposure to diesel exhaust increase arterial stiffness in man?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nMetastatic bone disease is one of the major causes of morbidity and mortality in prostate cancer patients. Bisphosphonates are currently used to inhibit bone resorption and reduce tumor-induced skeletal complications. More effective bisphosphonates would enhance their clinical value. We tested several bisphosphonates in a green fluorescent protein (GFP)-expressing human prostate cancer nude mouse model. The in vivo effects of four bisphosphonates, including pamidronate, etidronic acid, and olpadronate, on bone tumor burden in mice intratibially inoculated with PC-3-GFP human prostate cancer cells were visualized by whole-body fluorescence imaging and X-ray. The PC-3-GFP cells produced extensive bone lesions when injected into the tibia of immunocompromised mice. The skeletal progression of the PC-3-GFP cell growth was monitored by GFP fluorescence and the bone destruction was evaluated by X-ray. We showed that 3,3-dimethylaminopropane-1-hydroxy-1,1-diphosphonic acid (olpadronate) was the most effective bisphosphonate treatment in reducing tumor burden as assessed by GFP imaging and radiography. The GFP tumor area and X-ray score significantly correlated. Reduced tumor growth in the bone was accompanied by reduced serum calcium, parathyroid hormone-related protein, and osteoprotegerin.\n\nQuestion:\nDoes the bisphosphonate olpadronate inhibit skeletal prostate cancer progression in a green fluorescent protein nude mouse model?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nMetastatic bone disease is one of the major causes of morbidity and mortality in prostate cancer patients. Bisphosphonates are currently used to inhibit bone resorption and reduce tumor-induced skeletal complications. More effective bisphosphonates would enhance their clinical value. We tested several bisphosphonates in a green fluorescent protein (GFP)-expressing human prostate cancer nude mouse model. The in vivo effects of four bisphosphonates, including pamidronate, etidronic acid, and olpadronate, on bone tumor burden in mice intratibially inoculated with PC-3-GFP human prostate cancer cells were visualized by whole-body fluorescence imaging and X-ray. The PC-3-GFP cells produced extensive bone lesions when injected into the tibia of immunocompromised mice. The skeletal progression of the PC-3-GFP cell growth was monitored by GFP fluorescence and the bone destruction was evaluated by X-ray. We showed that 3,3-dimethylaminopropane-1-hydroxy-1,1-diphosphonic acid (olpadronate) was the most effective bisphosphonate treatment in reducing tumor burden as assessed by GFP imaging and radiography. The GFP tumor area and X-ray score significantly correlated. Reduced tumor growth in the bone was accompanied by reduced serum calcium, parathyroid hormone-related protein, and osteoprotegerin.\n\nQuestion:\nDoes the bisphosphonate olpadronate inhibit skeletal prostate cancer progression in a green fluorescent protein nude mouse model?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nMetastatic bone disease is one of the major causes of morbidity and mortality in prostate cancer patients. Bisphosphonates are currently used to inhibit bone resorption and reduce tumor-induced skeletal complications. More effective bisphosphonates would enhance their clinical value. We tested several bisphosphonates in a green fluorescent protein (GFP)-expressing human prostate cancer nude mouse model. The in vivo effects of four bisphosphonates, including pamidronate, etidronic acid, and olpadronate, on bone tumor burden in mice intratibially inoculated with PC-3-GFP human prostate cancer cells were visualized by whole-body fluorescence imaging and X-ray. The PC-3-GFP cells produced extensive bone lesions when injected into the tibia of immunocompromised mice. The skeletal progression of the PC-3-GFP cell growth was monitored by GFP fluorescence and the bone destruction was evaluated by X-ray. We showed that 3,3-dimethylaminopropane-1-hydroxy-1,1-diphosphonic acid (olpadronate) was the most effective bisphosphonate treatment in reducing tumor burden as assessed by GFP imaging and radiography. The GFP tumor area and X-ray score significantly correlated. Reduced tumor growth in the bone was accompanied by reduced serum calcium, parathyroid hormone-related protein, and osteoprotegerin.\n\nQuestion:\nDoes the bisphosphonate olpadronate inhibit skeletal prostate cancer progression in a green fluorescent protein nude mouse model?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nLumbar spinal manipulation (SM) is a popular, effective treatment for low back pain but the physiological mechanisms remain elusive. During SM, mechanoreceptors innervating the facet joint capsule (FJC) may receive a novel stimulus, contributing to the neurophysiological benefits of SM. The biomechanics of SM and physiological axial rotations were compared to determine whether speed or loading site affected FJC strain magnitudes or patterns. Human lumbar spine specimens were tested during physiological rotations and simulated SM while measuring applied torque, vertebral motion, and FJC strain. During physiological rotations, specimens were actuated at T12 to 20 degrees left and right axial rotation at 2 degrees to 125 degrees per second. During SM simulations, a 7-mm impulse displacement was applied to L3, L4, or L5 at 5 to 50 mm per second. Physiological rotations. Increasing displacement rate resulted in significantly larger torque magnitudes (P < .001), whereas vertebral kinematics and FJC strain magnitudes were unchanged (P > .05). Physiological rotations vs SM. Applied torque and vertebral rotation magnitudes were similar across speed and vertebral level. Total vertebral translations were slightly larger during physiological rotations vs SM at a given loading rate (P < .05). Patterns of vertebral motions and FJC strain during SM and physiological rotations varied significantly with loading rate (P < .05) but not with actuation site (P > .15).\n\nQuestion:\nDoes high loading rate during spinal manipulation produce unique facet joint capsule strain patterns compared with axial rotations?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nLumbar spinal manipulation (SM) is a popular, effective treatment for low back pain but the physiological mechanisms remain elusive. During SM, mechanoreceptors innervating the facet joint capsule (FJC) may receive a novel stimulus, contributing to the neurophysiological benefits of SM. The biomechanics of SM and physiological axial rotations were compared to determine whether speed or loading site affected FJC strain magnitudes or patterns. Human lumbar spine specimens were tested during physiological rotations and simulated SM while measuring applied torque, vertebral motion, and FJC strain. During physiological rotations, specimens were actuated at T12 to 20 degrees left and right axial rotation at 2 degrees to 125 degrees per second. During SM simulations, a 7-mm impulse displacement was applied to L3, L4, or L5 at 5 to 50 mm per second. Physiological rotations. Increasing displacement rate resulted in significantly larger torque magnitudes (P < .001), whereas vertebral kinematics and FJC strain magnitudes were unchanged (P > .05). Physiological rotations vs SM. Applied torque and vertebral rotation magnitudes were similar across speed and vertebral level. Total vertebral translations were slightly larger during physiological rotations vs SM at a given loading rate (P < .05). Patterns of vertebral motions and FJC strain during SM and physiological rotations varied significantly with loading rate (P < .05) but not with actuation site (P > .15).\n\nQuestion:\nDoes high loading rate during spinal manipulation produce unique facet joint capsule strain patterns compared with axial rotations?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nLumbar spinal manipulation (SM) is a popular, effective treatment for low back pain but the physiological mechanisms remain elusive. During SM, mechanoreceptors innervating the facet joint capsule (FJC) may receive a novel stimulus, contributing to the neurophysiological benefits of SM. The biomechanics of SM and physiological axial rotations were compared to determine whether speed or loading site affected FJC strain magnitudes or patterns. Human lumbar spine specimens were tested during physiological rotations and simulated SM while measuring applied torque, vertebral motion, and FJC strain. During physiological rotations, specimens were actuated at T12 to 20 degrees left and right axial rotation at 2 degrees to 125 degrees per second. During SM simulations, a 7-mm impulse displacement was applied to L3, L4, or L5 at 5 to 50 mm per second. Physiological rotations. Increasing displacement rate resulted in significantly larger torque magnitudes (P < .001), whereas vertebral kinematics and FJC strain magnitudes were unchanged (P > .05). Physiological rotations vs SM. Applied torque and vertebral rotation magnitudes were similar across speed and vertebral level. Total vertebral translations were slightly larger during physiological rotations vs SM at a given loading rate (P < .05). Patterns of vertebral motions and FJC strain during SM and physiological rotations varied significantly with loading rate (P < .05) but not with actuation site (P > .15).\n\nQuestion:\nDoes high loading rate during spinal manipulation produce unique facet joint capsule strain patterns compared with axial rotations?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nEndothelial chimerism occurs in renal transplants, but factors involved in its development and its impact on outcome, are unknown. Most studies on chimerism are restricted to gender-mismatched combinations of female donor organs into male recipients. By using blood group antigen mismatches to detect chimeric cells, we circumvented this restriction. We determined which factors predispose for the development of endothelial chimerism, and how it influences graft survival. We studied 85 renal transplant biopsies of 24 patients with either blood group A or B, who received a blood group O kidney. Biopsies were scored according to BANFF '97. Blood group antigens were stained by immunohistochemistry. Semiquantitative scoring was performed by four independent observers. Endothelial chimerism was found in 27/85 biopsies from 16/24 patients. All female recipients, but only half of the male recipients, had endothelial chimerism in their grafts (P < 0.025). In female recipients, endothelial chimerism occurred significantly earlier than in male recipients (P < 0.02). The presence of endothelial chimerism was not associated with: rejection, outcome, original renal disease, previous transplantations, age, warm/cold ischemia time, pretransplantation blood urea levels, or erythropoietin therapy.\n\nQuestion:\nDoes endothelial cell chimerism occur more often and earlier in female than in male recipients of kidney transplants?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nEndothelial chimerism occurs in renal transplants, but factors involved in its development and its impact on outcome, are unknown. Most studies on chimerism are restricted to gender-mismatched combinations of female donor organs into male recipients. By using blood group antigen mismatches to detect chimeric cells, we circumvented this restriction. We determined which factors predispose for the development of endothelial chimerism, and how it influences graft survival. We studied 85 renal transplant biopsies of 24 patients with either blood group A or B, who received a blood group O kidney. Biopsies were scored according to BANFF '97. Blood group antigens were stained by immunohistochemistry. Semiquantitative scoring was performed by four independent observers. Endothelial chimerism was found in 27/85 biopsies from 16/24 patients. All female recipients, but only half of the male recipients, had endothelial chimerism in their grafts (P < 0.025). In female recipients, endothelial chimerism occurred significantly earlier than in male recipients (P < 0.02). The presence of endothelial chimerism was not associated with: rejection, outcome, original renal disease, previous transplantations, age, warm/cold ischemia time, pretransplantation blood urea levels, or erythropoietin therapy.\n\nQuestion:\nDoes endothelial cell chimerism occur more often and earlier in female than in male recipients of kidney transplants?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nEndothelial chimerism occurs in renal transplants, but factors involved in its development and its impact on outcome, are unknown. Most studies on chimerism are restricted to gender-mismatched combinations of female donor organs into male recipients. By using blood group antigen mismatches to detect chimeric cells, we circumvented this restriction. We determined which factors predispose for the development of endothelial chimerism, and how it influences graft survival. We studied 85 renal transplant biopsies of 24 patients with either blood group A or B, who received a blood group O kidney. Biopsies were scored according to BANFF '97. Blood group antigens were stained by immunohistochemistry. Semiquantitative scoring was performed by four independent observers. Endothelial chimerism was found in 27/85 biopsies from 16/24 patients. All female recipients, but only half of the male recipients, had endothelial chimerism in their grafts (P < 0.025). In female recipients, endothelial chimerism occurred significantly earlier than in male recipients (P < 0.02). The presence of endothelial chimerism was not associated with: rejection, outcome, original renal disease, previous transplantations, age, warm/cold ischemia time, pretransplantation blood urea levels, or erythropoietin therapy.\n\nQuestion:\nDoes endothelial cell chimerism occur more often and earlier in female than in male recipients of kidney transplants?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nFood habits, nutrient needs and intakes differ between males and females, although few nutritional studies on patients with coeliac disease (CD) have reported results stratified by gender. To compare energy and nutrient intakes among 13-year olds diagnosed with CD in early childhood with those of a non-coeliac (NC) age- and gender-matched control group, and also with estimated average requirements (EAR). A case-control study was conducted in Sweden 2006-2007 within the coeliac screening study ETICS (Exploring The Iceberg of Coeliacs in Sweden). Dietary intake was assessed among 37 adolescents (23 girls) diagnosed with CD at median age 1.7 years (CD group) and 805 (430 girls) NC controls (NC group) using a food-frequency questionnaire covering 4 weeks. Reported energy intake was validated by comparison with the calculated physical activity level (PAL). Regardless of CD status, most adolescents reported an intake above EAR for most nutrients. However, both groups had a low intake of vitamin C, with 13% in the CD-group and 25% in the NC-group below EAR, and 21% of boys in the CD-group below EAR for thiamine. The intake of fatty acids was unbalanced, with a high intake of saturated and a low intake of unsaturated fats. Girls and boys in the CD-group had an overall lower nutrient density in reported food intake compared to girls and boys in the NC-group.\n\nQuestion:\nIs nutrient intake in adolescent girls and boys diagnosed with coeliac disease at an early age mostly comparable to their non-coeliac contemporaries?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nFood habits, nutrient needs and intakes differ between males and females, although few nutritional studies on patients with coeliac disease (CD) have reported results stratified by gender. To compare energy and nutrient intakes among 13-year olds diagnosed with CD in early childhood with those of a non-coeliac (NC) age- and gender-matched control group, and also with estimated average requirements (EAR). A case-control study was conducted in Sweden 2006-2007 within the coeliac screening study ETICS (Exploring The Iceberg of Coeliacs in Sweden). Dietary intake was assessed among 37 adolescents (23 girls) diagnosed with CD at median age 1.7 years (CD group) and 805 (430 girls) NC controls (NC group) using a food-frequency questionnaire covering 4 weeks. Reported energy intake was validated by comparison with the calculated physical activity level (PAL). Regardless of CD status, most adolescents reported an intake above EAR for most nutrients. However, both groups had a low intake of vitamin C, with 13% in the CD-group and 25% in the NC-group below EAR, and 21% of boys in the CD-group below EAR for thiamine. The intake of fatty acids was unbalanced, with a high intake of saturated and a low intake of unsaturated fats. Girls and boys in the CD-group had an overall lower nutrient density in reported food intake compared to girls and boys in the NC-group.\n\nQuestion:\nIs nutrient intake in adolescent girls and boys diagnosed with coeliac disease at an early age mostly comparable to their non-coeliac contemporaries?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nFood habits, nutrient needs and intakes differ between males and females, although few nutritional studies on patients with coeliac disease (CD) have reported results stratified by gender. To compare energy and nutrient intakes among 13-year olds diagnosed with CD in early childhood with those of a non-coeliac (NC) age- and gender-matched control group, and also with estimated average requirements (EAR). A case-control study was conducted in Sweden 2006-2007 within the coeliac screening study ETICS (Exploring The Iceberg of Coeliacs in Sweden). Dietary intake was assessed among 37 adolescents (23 girls) diagnosed with CD at median age 1.7 years (CD group) and 805 (430 girls) NC controls (NC group) using a food-frequency questionnaire covering 4 weeks. Reported energy intake was validated by comparison with the calculated physical activity level (PAL). Regardless of CD status, most adolescents reported an intake above EAR for most nutrients. However, both groups had a low intake of vitamin C, with 13% in the CD-group and 25% in the NC-group below EAR, and 21% of boys in the CD-group below EAR for thiamine. The intake of fatty acids was unbalanced, with a high intake of saturated and a low intake of unsaturated fats. Girls and boys in the CD-group had an overall lower nutrient density in reported food intake compared to girls and boys in the NC-group.\n\nQuestion:\nIs nutrient intake in adolescent girls and boys diagnosed with coeliac disease at an early age mostly comparable to their non-coeliac contemporaries?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nFolium Hibisci Mutabilis was one of the traditional Chinese medicines with pharmacological activities of wound healing, antibacterial and anti-inflammatory, normally applied to the clinical treatment of local purulent infection, scald, and epidemic parotitis. However, few people reported that its effects of extracts on RAW264.7, cells and TNF-α, IL-6, and NO levels in rats serum of inflammation rats. We mainly adopted the RAW264.7, macrophage cell line which was intervened by lipopolysaccharide (L PS), to establish the model of inflammatory cells. The secretion changes of TNF, and IL-6, level in the model cell acted by the FHMAEs, were detected by ELISA, NO level changes were determined by nitrate reductase method; Arthritis model induced by Collagen Type II were chose, and regulatory role of FHMAEs on IL-6 and NO level in serum were observed, FHMAEs mechanism of action were investigated in the treatment of rheumatoid arthritis. The states of the model rats were recorded. Release of TNF-α, IL-6, and NO in LPS-induced RAW264.7, cells were significantly inhibited and has a clear dose-response relationship; The TNF-α, IL-6 and NO levels were reduced by FHMAEs in experimental arthritis rats serum, and the status of rats were improved. At last, we found that IL-6, NO and TNF-α levels in the inflammatory cells could be reduced by FHMAEs greatly.\n\nQuestion:\nDoes in vitro anti-inflammatory mechanism of Folium Hibisci Mutabilis leave ethanol extracts?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nFolium Hibisci Mutabilis was one of the traditional Chinese medicines with pharmacological activities of wound healing, antibacterial and anti-inflammatory, normally applied to the clinical treatment of local purulent infection, scald, and epidemic parotitis. However, few people reported that its effects of extracts on RAW264.7, cells and TNF-α, IL-6, and NO levels in rats serum of inflammation rats. We mainly adopted the RAW264.7, macrophage cell line which was intervened by lipopolysaccharide (L PS), to establish the model of inflammatory cells. The secretion changes of TNF, and IL-6, level in the model cell acted by the FHMAEs, were detected by ELISA, NO level changes were determined by nitrate reductase method; Arthritis model induced by Collagen Type II were chose, and regulatory role of FHMAEs on IL-6 and NO level in serum were observed, FHMAEs mechanism of action were investigated in the treatment of rheumatoid arthritis. The states of the model rats were recorded. Release of TNF-α, IL-6, and NO in LPS-induced RAW264.7, cells were significantly inhibited and has a clear dose-response relationship; The TNF-α, IL-6 and NO levels were reduced by FHMAEs in experimental arthritis rats serum, and the status of rats were improved. At last, we found that IL-6, NO and TNF-α levels in the inflammatory cells could be reduced by FHMAEs greatly.\n\nQuestion:\nDoes in vitro anti-inflammatory mechanism of Folium Hibisci Mutabilis leave ethanol extracts?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nFolium Hibisci Mutabilis was one of the traditional Chinese medicines with pharmacological activities of wound healing, antibacterial and anti-inflammatory, normally applied to the clinical treatment of local purulent infection, scald, and epidemic parotitis. However, few people reported that its effects of extracts on RAW264.7, cells and TNF-α, IL-6, and NO levels in rats serum of inflammation rats. We mainly adopted the RAW264.7, macrophage cell line which was intervened by lipopolysaccharide (L PS), to establish the model of inflammatory cells. The secretion changes of TNF, and IL-6, level in the model cell acted by the FHMAEs, were detected by ELISA, NO level changes were determined by nitrate reductase method; Arthritis model induced by Collagen Type II were chose, and regulatory role of FHMAEs on IL-6 and NO level in serum were observed, FHMAEs mechanism of action were investigated in the treatment of rheumatoid arthritis. The states of the model rats were recorded. Release of TNF-α, IL-6, and NO in LPS-induced RAW264.7, cells were significantly inhibited and has a clear dose-response relationship; The TNF-α, IL-6 and NO levels were reduced by FHMAEs in experimental arthritis rats serum, and the status of rats were improved. At last, we found that IL-6, NO and TNF-α levels in the inflammatory cells could be reduced by FHMAEs greatly.\n\nQuestion:\nDoes in vitro anti-inflammatory mechanism of Folium Hibisci Mutabilis leave ethanol extracts?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nOxidative stress has been advocated as a major cause for cardiovascular disease (CVD), and low plasma antioxidant concentrations are associated with endothelial dysfunction, the first step towards atherosclerosis. However, although the antioxidant content in fruits and vegetables may explain at least in part their protective effect against CVD, supplementation with antioxidant vitamins fails to improve endothelial function and reduce CVD risk. The aim of this study was to investigate the impact of a diet rich in antioxidants on endothelial function measured by flow-mediated dilatation (FMD) in volunteers at low cardiovascular risk. In a crossover trial, 24 subjects (13 women, mean age 61 ± 3 years), received, in a randomised order, a 14-day high (HT) and a 14-day low (LT) antioxidant diets, with a 2-week wash-out (WO) in between. Both diets were comparable in daily portions of fruits and vegetables, and in alcohol, fibre and macronutrient intake, but differed in their total antioxidant capacity. Before and after each diet, anthropometrics, blood pressure, fasting plasma glucose, lipid profile, hepatic enzymes, circulating antioxidant concentrations, high sensitivity C-reactive protein (hs-CRP) and FMD were assessed. FMD increased significantly during the HT diet compared to the LT (p < 0.000). FMD values were 2.3% higher after HT compared with LT (p < 0.001) after adjustment for age, gender and diet order. α-tocopherol increased significantly (p < 0.05) and hs-CRP and of γ-glutamyltranspeptidase decreased significantly (p < 0.05 and p < 0.01, respectively) during the HT diet, compared with the LT diet.\n\nQuestion:\nDoes food selection based on high total antioxidant capacity improve endothelial function in a low cardiovascular risk population?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nOxidative stress has been advocated as a major cause for cardiovascular disease (CVD), and low plasma antioxidant concentrations are associated with endothelial dysfunction, the first step towards atherosclerosis. However, although the antioxidant content in fruits and vegetables may explain at least in part their protective effect against CVD, supplementation with antioxidant vitamins fails to improve endothelial function and reduce CVD risk. The aim of this study was to investigate the impact of a diet rich in antioxidants on endothelial function measured by flow-mediated dilatation (FMD) in volunteers at low cardiovascular risk. In a crossover trial, 24 subjects (13 women, mean age 61 ± 3 years), received, in a randomised order, a 14-day high (HT) and a 14-day low (LT) antioxidant diets, with a 2-week wash-out (WO) in between. Both diets were comparable in daily portions of fruits and vegetables, and in alcohol, fibre and macronutrient intake, but differed in their total antioxidant capacity. Before and after each diet, anthropometrics, blood pressure, fasting plasma glucose, lipid profile, hepatic enzymes, circulating antioxidant concentrations, high sensitivity C-reactive protein (hs-CRP) and FMD were assessed. FMD increased significantly during the HT diet compared to the LT (p < 0.000). FMD values were 2.3% higher after HT compared with LT (p < 0.001) after adjustment for age, gender and diet order. α-tocopherol increased significantly (p < 0.05) and hs-CRP and of γ-glutamyltranspeptidase decreased significantly (p < 0.05 and p < 0.01, respectively) during the HT diet, compared with the LT diet.\n\nQuestion:\nDoes food selection based on high total antioxidant capacity improve endothelial function in a low cardiovascular risk population?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nOxidative stress has been advocated as a major cause for cardiovascular disease (CVD), and low plasma antioxidant concentrations are associated with endothelial dysfunction, the first step towards atherosclerosis. However, although the antioxidant content in fruits and vegetables may explain at least in part their protective effect against CVD, supplementation with antioxidant vitamins fails to improve endothelial function and reduce CVD risk. The aim of this study was to investigate the impact of a diet rich in antioxidants on endothelial function measured by flow-mediated dilatation (FMD) in volunteers at low cardiovascular risk. In a crossover trial, 24 subjects (13 women, mean age 61 ± 3 years), received, in a randomised order, a 14-day high (HT) and a 14-day low (LT) antioxidant diets, with a 2-week wash-out (WO) in between. Both diets were comparable in daily portions of fruits and vegetables, and in alcohol, fibre and macronutrient intake, but differed in their total antioxidant capacity. Before and after each diet, anthropometrics, blood pressure, fasting plasma glucose, lipid profile, hepatic enzymes, circulating antioxidant concentrations, high sensitivity C-reactive protein (hs-CRP) and FMD were assessed. FMD increased significantly during the HT diet compared to the LT (p < 0.000). FMD values were 2.3% higher after HT compared with LT (p < 0.001) after adjustment for age, gender and diet order. α-tocopherol increased significantly (p < 0.05) and hs-CRP and of γ-glutamyltranspeptidase decreased significantly (p < 0.05 and p < 0.01, respectively) during the HT diet, compared with the LT diet.\n\nQuestion:\nDoes food selection based on high total antioxidant capacity improve endothelial function in a low cardiovascular risk population?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nDuring endocytosis in yeast, a choreographed series of discrete local events at the plasma membrane lead to a rapid burst of actin polymerization and the subsequent internalization of an endocytic vesicle. What initiates Arp2/3-dependent actin polymerization in this process is not well understood. The Schizosaccharomyces pombe WISH/DIP/SPIN90 ortholog dip1p is an actin-patch protein that regulates the temporal sequence of endocytic events. dip1Δ mutants exhibit a novel phenotype in which early events such as WASp localization occur normally but arrival of Arp2/3, actin polymerization, and subsequent steps are delayed and occur with apparently random timing. In studying this mutant, we demonstrate that positive feedback loops of WASp, rapid actin assembly, and Arp2/3 contribute to switch-like behavior that initiates actin polymerization. In the absence of dip1p, a subset of patches is activated concurrently with the \"touch\" of a neighboring endocytic vesicle.\n\nQuestion:\nDoes characterization of dip1p reveal a switch in Arp2/3-dependent actin assembly for fission yeast endocytosis?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nDuring endocytosis in yeast, a choreographed series of discrete local events at the plasma membrane lead to a rapid burst of actin polymerization and the subsequent internalization of an endocytic vesicle. What initiates Arp2/3-dependent actin polymerization in this process is not well understood. The Schizosaccharomyces pombe WISH/DIP/SPIN90 ortholog dip1p is an actin-patch protein that regulates the temporal sequence of endocytic events. dip1Δ mutants exhibit a novel phenotype in which early events such as WASp localization occur normally but arrival of Arp2/3, actin polymerization, and subsequent steps are delayed and occur with apparently random timing. In studying this mutant, we demonstrate that positive feedback loops of WASp, rapid actin assembly, and Arp2/3 contribute to switch-like behavior that initiates actin polymerization. In the absence of dip1p, a subset of patches is activated concurrently with the \"touch\" of a neighboring endocytic vesicle.\n\nQuestion:\nDoes characterization of dip1p reveal a switch in Arp2/3-dependent actin assembly for fission yeast endocytosis?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nDuring endocytosis in yeast, a choreographed series of discrete local events at the plasma membrane lead to a rapid burst of actin polymerization and the subsequent internalization of an endocytic vesicle. What initiates Arp2/3-dependent actin polymerization in this process is not well understood. The Schizosaccharomyces pombe WISH/DIP/SPIN90 ortholog dip1p is an actin-patch protein that regulates the temporal sequence of endocytic events. dip1Δ mutants exhibit a novel phenotype in which early events such as WASp localization occur normally but arrival of Arp2/3, actin polymerization, and subsequent steps are delayed and occur with apparently random timing. In studying this mutant, we demonstrate that positive feedback loops of WASp, rapid actin assembly, and Arp2/3 contribute to switch-like behavior that initiates actin polymerization. In the absence of dip1p, a subset of patches is activated concurrently with the \"touch\" of a neighboring endocytic vesicle.\n\nQuestion:\nDoes characterization of dip1p reveal a switch in Arp2/3-dependent actin assembly for fission yeast endocytosis?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nWe evaluated the endothelial and vascular smooth muscle function in patients with chronic severe anemia to determine whether increased basal nitric oxide levels contribute to the systemic vasodilation and high cardiac output seen in these patients. Patients with chronic severe anemia have a high output state due to a low systemic vascular resistance. However, the cause of the low vascular resistance is unclear. Because hemoglobin is a potent inhibitor of endothelium-derived relaxing factor, we postulated that in chronic severe anemia, low circulating hemoglobin results in reduced inhibition of endothelium-derived relaxing factor. The basal endothelium-derived relaxing factor activity therefore increases, and this contributes significantly to the low systemic vascular resistance and the hyperdynamic state seen in this condition. Hemodynamic variables and forearm blood flow (using plethysmography) were measured in eight patients with chronic severe anemia before (hematocrit 16 +/- 2% [mean +/- SD]) and within 24 h of red blood cell transfusion (n = 6, hematocrit 30 +/- 1%) and in six control subjects. The effect on baseline blood flow of blocking endothelium-derived relaxing factor activity with NG-monomethyl-L-arginine was investigated. In addition, the effects of both endothelium-dependent and endothelium-independent vasodilators on forearm blood flow were tested. Baseline forearm blood flow was markedly increased in untreated patients (6.5 +/- 1.2 ml/min per 100 ml) compared with that in control subjects (2.8 +/- 0.7 ml/min per 100 ml, p < 0.0001, 95% confidence interval [CI] for difference -5 to -2.5). Red blood cell transfusion significantly reduced blood flow in the anemic patients to 3.5 +/- 1.1 ml/min per 100 ml (p < 0.001, 95% CI for difference -4.9 to -1.9), which was not significantly different from that in control subjects; increased systemic vascular resistance (796 +/- 141 to 1,230 +/- 151 dynes.s.cm-5, p < 0.001); and decreased cardiac output (4.9 +/- 0.6 to 3.5 +/- 0.5 liters/min per m2, p < 0.001). NG-monomethyl-L-arginine (16 mumol/min), a specific inhibitor of endothelium-derived relaxing factor, reduced forearm blood flow by an equal amount (p = 0.9, 95% CI for difference -0.7 to 0.8) in control subjects (0.98 +/- 0.39 ml/min) and treated patients (1.03 +/- 0.8 ml/min) but caused a threefold greater decrease in flow (2.9 +/- 0.9 ml/min) in untreated patients (p = 0.0003, 95% CI for difference between untreated patients and control subjects 1.1 to 2.7). These findings suggest increased basal endothelium-derived relaxing factor activity in patients with anemia. Stimulated forearm blood flows (both endothelium dependent and endothelium independent) were similar in all groups, confirming normal endothelial and smooth-muscle function.\n\nQuestion:\nIs endothelium-derived relaxing factor important in mediating the high output state in chronic severe anemia?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nWe evaluated the endothelial and vascular smooth muscle function in patients with chronic severe anemia to determine whether increased basal nitric oxide levels contribute to the systemic vasodilation and high cardiac output seen in these patients. Patients with chronic severe anemia have a high output state due to a low systemic vascular resistance. However, the cause of the low vascular resistance is unclear. Because hemoglobin is a potent inhibitor of endothelium-derived relaxing factor, we postulated that in chronic severe anemia, low circulating hemoglobin results in reduced inhibition of endothelium-derived relaxing factor. The basal endothelium-derived relaxing factor activity therefore increases, and this contributes significantly to the low systemic vascular resistance and the hyperdynamic state seen in this condition. Hemodynamic variables and forearm blood flow (using plethysmography) were measured in eight patients with chronic severe anemia before (hematocrit 16 +/- 2% [mean +/- SD]) and within 24 h of red blood cell transfusion (n = 6, hematocrit 30 +/- 1%) and in six control subjects. The effect on baseline blood flow of blocking endothelium-derived relaxing factor activity with NG-monomethyl-L-arginine was investigated. In addition, the effects of both endothelium-dependent and endothelium-independent vasodilators on forearm blood flow were tested. Baseline forearm blood flow was markedly increased in untreated patients (6.5 +/- 1.2 ml/min per 100 ml) compared with that in control subjects (2.8 +/- 0.7 ml/min per 100 ml, p < 0.0001, 95% confidence interval [CI] for difference -5 to -2.5). Red blood cell transfusion significantly reduced blood flow in the anemic patients to 3.5 +/- 1.1 ml/min per 100 ml (p < 0.001, 95% CI for difference -4.9 to -1.9), which was not significantly different from that in control subjects; increased systemic vascular resistance (796 +/- 141 to 1,230 +/- 151 dynes.s.cm-5, p < 0.001); and decreased cardiac output (4.9 +/- 0.6 to 3.5 +/- 0.5 liters/min per m2, p < 0.001). NG-monomethyl-L-arginine (16 mumol/min), a specific inhibitor of endothelium-derived relaxing factor, reduced forearm blood flow by an equal amount (p = 0.9, 95% CI for difference -0.7 to 0.8) in control subjects (0.98 +/- 0.39 ml/min) and treated patients (1.03 +/- 0.8 ml/min) but caused a threefold greater decrease in flow (2.9 +/- 0.9 ml/min) in untreated patients (p = 0.0003, 95% CI for difference between untreated patients and control subjects 1.1 to 2.7). These findings suggest increased basal endothelium-derived relaxing factor activity in patients with anemia. Stimulated forearm blood flows (both endothelium dependent and endothelium independent) were similar in all groups, confirming normal endothelial and smooth-muscle function.\n\nQuestion:\nIs endothelium-derived relaxing factor important in mediating the high output state in chronic severe anemia?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nWe evaluated the endothelial and vascular smooth muscle function in patients with chronic severe anemia to determine whether increased basal nitric oxide levels contribute to the systemic vasodilation and high cardiac output seen in these patients. Patients with chronic severe anemia have a high output state due to a low systemic vascular resistance. However, the cause of the low vascular resistance is unclear. Because hemoglobin is a potent inhibitor of endothelium-derived relaxing factor, we postulated that in chronic severe anemia, low circulating hemoglobin results in reduced inhibition of endothelium-derived relaxing factor. The basal endothelium-derived relaxing factor activity therefore increases, and this contributes significantly to the low systemic vascular resistance and the hyperdynamic state seen in this condition. Hemodynamic variables and forearm blood flow (using plethysmography) were measured in eight patients with chronic severe anemia before (hematocrit 16 +/- 2% [mean +/- SD]) and within 24 h of red blood cell transfusion (n = 6, hematocrit 30 +/- 1%) and in six control subjects. The effect on baseline blood flow of blocking endothelium-derived relaxing factor activity with NG-monomethyl-L-arginine was investigated. In addition, the effects of both endothelium-dependent and endothelium-independent vasodilators on forearm blood flow were tested. Baseline forearm blood flow was markedly increased in untreated patients (6.5 +/- 1.2 ml/min per 100 ml) compared with that in control subjects (2.8 +/- 0.7 ml/min per 100 ml, p < 0.0001, 95% confidence interval [CI] for difference -5 to -2.5). Red blood cell transfusion significantly reduced blood flow in the anemic patients to 3.5 +/- 1.1 ml/min per 100 ml (p < 0.001, 95% CI for difference -4.9 to -1.9), which was not significantly different from that in control subjects; increased systemic vascular resistance (796 +/- 141 to 1,230 +/- 151 dynes.s.cm-5, p < 0.001); and decreased cardiac output (4.9 +/- 0.6 to 3.5 +/- 0.5 liters/min per m2, p < 0.001). NG-monomethyl-L-arginine (16 mumol/min), a specific inhibitor of endothelium-derived relaxing factor, reduced forearm blood flow by an equal amount (p = 0.9, 95% CI for difference -0.7 to 0.8) in control subjects (0.98 +/- 0.39 ml/min) and treated patients (1.03 +/- 0.8 ml/min) but caused a threefold greater decrease in flow (2.9 +/- 0.9 ml/min) in untreated patients (p = 0.0003, 95% CI for difference between untreated patients and control subjects 1.1 to 2.7). These findings suggest increased basal endothelium-derived relaxing factor activity in patients with anemia. Stimulated forearm blood flows (both endothelium dependent and endothelium independent) were similar in all groups, confirming normal endothelial and smooth-muscle function.\n\nQuestion:\nIs endothelium-derived relaxing factor important in mediating the high output state in chronic severe anemia?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nDental plaque has been suggested as a permanent reservoir of Helicobacter pylori (H. pylori) and a potential source of reinfection. The aims of this study were to investigate the presence of H. pylori in both dental plaque and the stomach and to evaluate the therapeutic effect of triple therapy on H. pylori in dental plaque. Dental plaque and gastric biopsy samples were obtained from 65 patients with dyspeptic symptoms for endoscopic examination. The prevalence of H. pylori in dental plaque and stomach was determined with rapid urease test, histologic examinations and polymerase chain reaction assay based on the primer pair derived from the cagA gene of H. pylori. Triple therapy was administered to patients infected with H. pylori. H. pylori status was re-evaluated after eradication therapy. Prior to treatment, H. pylori was found in the stomach in 38 of 65 (58%) patients and in dental plaque in 28 of 65 (43%) patients. The coexisting infection rate of H. pylori in both stomach and dental plaque was 74%. After triple therapy, H. pylori was eradicated from the stomach in 32 of 38 (84%) patients, but only 2 of 28 (7%) patients with coexisting H. pylori infections of stomach and dental plaque showed the elimination of H. pylori from dental plaque.\n\nQuestion:\nIs it difficult to eradicate Helicobacter pylori from dental plaque by triple therapy?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nDental plaque has been suggested as a permanent reservoir of Helicobacter pylori (H. pylori) and a potential source of reinfection. The aims of this study were to investigate the presence of H. pylori in both dental plaque and the stomach and to evaluate the therapeutic effect of triple therapy on H. pylori in dental plaque. Dental plaque and gastric biopsy samples were obtained from 65 patients with dyspeptic symptoms for endoscopic examination. The prevalence of H. pylori in dental plaque and stomach was determined with rapid urease test, histologic examinations and polymerase chain reaction assay based on the primer pair derived from the cagA gene of H. pylori. Triple therapy was administered to patients infected with H. pylori. H. pylori status was re-evaluated after eradication therapy. Prior to treatment, H. pylori was found in the stomach in 38 of 65 (58%) patients and in dental plaque in 28 of 65 (43%) patients. The coexisting infection rate of H. pylori in both stomach and dental plaque was 74%. After triple therapy, H. pylori was eradicated from the stomach in 32 of 38 (84%) patients, but only 2 of 28 (7%) patients with coexisting H. pylori infections of stomach and dental plaque showed the elimination of H. pylori from dental plaque.\n\nQuestion:\nIs it difficult to eradicate Helicobacter pylori from dental plaque by triple therapy?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nDental plaque has been suggested as a permanent reservoir of Helicobacter pylori (H. pylori) and a potential source of reinfection. The aims of this study were to investigate the presence of H. pylori in both dental plaque and the stomach and to evaluate the therapeutic effect of triple therapy on H. pylori in dental plaque. Dental plaque and gastric biopsy samples were obtained from 65 patients with dyspeptic symptoms for endoscopic examination. The prevalence of H. pylori in dental plaque and stomach was determined with rapid urease test, histologic examinations and polymerase chain reaction assay based on the primer pair derived from the cagA gene of H. pylori. Triple therapy was administered to patients infected with H. pylori. H. pylori status was re-evaluated after eradication therapy. Prior to treatment, H. pylori was found in the stomach in 38 of 65 (58%) patients and in dental plaque in 28 of 65 (43%) patients. The coexisting infection rate of H. pylori in both stomach and dental plaque was 74%. After triple therapy, H. pylori was eradicated from the stomach in 32 of 38 (84%) patients, but only 2 of 28 (7%) patients with coexisting H. pylori infections of stomach and dental plaque showed the elimination of H. pylori from dental plaque.\n\nQuestion:\nIs it difficult to eradicate Helicobacter pylori from dental plaque by triple therapy?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nTo construct a eukaryotic expression vector containing human cannabinoid receptor 2 (hCB2R) gene and investigate its expression, location and the influence on the apoptosis of cervical cancer Caski cells. The eukaryotic expression vector GV230-hCB2R was constructed and identified by double enzyme digestion and DNA sequencing analysis. Then it was transfected into HEK293 cells and Caski cells by Lipofectamine(TM) 2000. The expression and cellular localization of hCB2R protein were detected by Western blotting and immunofluorescent cytochemistry combined with laser scanning confocal microscopy, the apoptosis rate was tested by flow cytometry. The mRNA and protein expressions of hCB2R, Bcl-2, Bax and Bad were examined by real-time fluorescent quantitative PCR (qRT-PCR) and Western blotting, respectively. The gene fragment of 1128 bp was obtained by double enzyme digestion, it had 99% homology with human hCB2R gene nucleic acid sequence reported (NM_001841.2). After transfected into HEK293 cells, hCB2R protein, with the relative molecular mass (Mr) being 40 000, was expressed in both cytoplasm and cellular membrane. The over-expression of hCB2R promoted apoptosis of Caski cells via up-regulating the Bax, Bad expressions and down-regulating the Bcl-2 expression.\n\nQuestion:\nDoes [ Over-expression of cannabinoid receptor 2 induce the apoptosis of cervical carcinoma Caski cells ]?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nTo construct a eukaryotic expression vector containing human cannabinoid receptor 2 (hCB2R) gene and investigate its expression, location and the influence on the apoptosis of cervical cancer Caski cells. The eukaryotic expression vector GV230-hCB2R was constructed and identified by double enzyme digestion and DNA sequencing analysis. Then it was transfected into HEK293 cells and Caski cells by Lipofectamine(TM) 2000. The expression and cellular localization of hCB2R protein were detected by Western blotting and immunofluorescent cytochemistry combined with laser scanning confocal microscopy, the apoptosis rate was tested by flow cytometry. The mRNA and protein expressions of hCB2R, Bcl-2, Bax and Bad were examined by real-time fluorescent quantitative PCR (qRT-PCR) and Western blotting, respectively. The gene fragment of 1128 bp was obtained by double enzyme digestion, it had 99% homology with human hCB2R gene nucleic acid sequence reported (NM_001841.2). After transfected into HEK293 cells, hCB2R protein, with the relative molecular mass (Mr) being 40 000, was expressed in both cytoplasm and cellular membrane. The over-expression of hCB2R promoted apoptosis of Caski cells via up-regulating the Bax, Bad expressions and down-regulating the Bcl-2 expression.\n\nQuestion:\nDoes [ Over-expression of cannabinoid receptor 2 induce the apoptosis of cervical carcinoma Caski cells ]?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nTo construct a eukaryotic expression vector containing human cannabinoid receptor 2 (hCB2R) gene and investigate its expression, location and the influence on the apoptosis of cervical cancer Caski cells. The eukaryotic expression vector GV230-hCB2R was constructed and identified by double enzyme digestion and DNA sequencing analysis. Then it was transfected into HEK293 cells and Caski cells by Lipofectamine(TM) 2000. The expression and cellular localization of hCB2R protein were detected by Western blotting and immunofluorescent cytochemistry combined with laser scanning confocal microscopy, the apoptosis rate was tested by flow cytometry. The mRNA and protein expressions of hCB2R, Bcl-2, Bax and Bad were examined by real-time fluorescent quantitative PCR (qRT-PCR) and Western blotting, respectively. The gene fragment of 1128 bp was obtained by double enzyme digestion, it had 99% homology with human hCB2R gene nucleic acid sequence reported (NM_001841.2). After transfected into HEK293 cells, hCB2R protein, with the relative molecular mass (Mr) being 40 000, was expressed in both cytoplasm and cellular membrane. The over-expression of hCB2R promoted apoptosis of Caski cells via up-regulating the Bax, Bad expressions and down-regulating the Bcl-2 expression.\n\nQuestion:\nDoes [ Over-expression of cannabinoid receptor 2 induce the apoptosis of cervical carcinoma Caski cells ]?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nTo evaluate the impact of body mass index (BMI) on perioperative outcomes and radiation exposure for ultrasound (US)-guided percutaneous nephrolithotomy (PCNL). Data were prospectively collected for consecutive patients who underwent PCNL at the University of California, San Francisco, from July 2013 to November 2015. Patients were divided into 3 groups according to their BMI: <25 (normal weight), 25-29.9 (overweight), and >30 (obese) kg/m One hundred thirty-five patients were enrolled; 93 cases were performed under US and 42 under fluoroscopic guidance. US successfully guided renal access in 76.9% of normal weight, 79.0% of overweight, and 45.7% of obese patients (P < .05). Mean fluoroscopic screening time and radiation exposure dose were reduced for US compared to fluoroscopy cases across all BMI categories (P < .05). As BMI increased, radiation exposure dose rose disproportionately faster compared to screening time (P < .001). No significant differences among the BMI groups were found with regard to complication rate, hospital stay, and stone-free status.\n\nQuestion:\nDoes ultrasound Guidance to Assist Percutaneous Nephrolithotomy reduce Radiation Exposure in Obese Patients?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nTo evaluate the impact of body mass index (BMI) on perioperative outcomes and radiation exposure for ultrasound (US)-guided percutaneous nephrolithotomy (PCNL). Data were prospectively collected for consecutive patients who underwent PCNL at the University of California, San Francisco, from July 2013 to November 2015. Patients were divided into 3 groups according to their BMI: <25 (normal weight), 25-29.9 (overweight), and >30 (obese) kg/m One hundred thirty-five patients were enrolled; 93 cases were performed under US and 42 under fluoroscopic guidance. US successfully guided renal access in 76.9% of normal weight, 79.0% of overweight, and 45.7% of obese patients (P < .05). Mean fluoroscopic screening time and radiation exposure dose were reduced for US compared to fluoroscopy cases across all BMI categories (P < .05). As BMI increased, radiation exposure dose rose disproportionately faster compared to screening time (P < .001). No significant differences among the BMI groups were found with regard to complication rate, hospital stay, and stone-free status.\n\nQuestion:\nDoes ultrasound Guidance to Assist Percutaneous Nephrolithotomy reduce Radiation Exposure in Obese Patients?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nTo evaluate the impact of body mass index (BMI) on perioperative outcomes and radiation exposure for ultrasound (US)-guided percutaneous nephrolithotomy (PCNL). Data were prospectively collected for consecutive patients who underwent PCNL at the University of California, San Francisco, from July 2013 to November 2015. Patients were divided into 3 groups according to their BMI: <25 (normal weight), 25-29.9 (overweight), and >30 (obese) kg/m One hundred thirty-five patients were enrolled; 93 cases were performed under US and 42 under fluoroscopic guidance. US successfully guided renal access in 76.9% of normal weight, 79.0% of overweight, and 45.7% of obese patients (P < .05). Mean fluoroscopic screening time and radiation exposure dose were reduced for US compared to fluoroscopy cases across all BMI categories (P < .05). As BMI increased, radiation exposure dose rose disproportionately faster compared to screening time (P < .001). No significant differences among the BMI groups were found with regard to complication rate, hospital stay, and stone-free status.\n\nQuestion:\nDoes ultrasound Guidance to Assist Percutaneous Nephrolithotomy reduce Radiation Exposure in Obese Patients?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nTAZ (Transcriptional co-Activator with PDZ-binding motif), is a biologically potent transcriptional coactivator and functions by binding to the PPXY motif present in several transcription factors. Notably, TAZ behaves as a transducer linking cytoplasmic signaling events to transcriptional regulation in the nucleus. Several different factors regulate TAZ expression and/or function. In particular, a major regulation of TAZ activity occurs through the Hippo pathway by a phosphorylation-mediated mechanism that causes its cytoplasmic sequestration or degradation. Here we demonstrate that AMOTL2 robustly co-immunoprecipitates with TAZ, and their interaction is dependent on the WW domain of TAZ and the PPXY motif in the N-terminus of AMOTL2. Furthermore, we show that AMOTL2 colocalizes with TAZ in the cytoplasm of H441 human lung cells and regulates TAZ cytoplasm-to-nucleus translocation through direct protein-protein interaction. Interestingly, the overexpression of AMOTL2 inhibits the functional cooperation between the transcription factor TTF-1 and TAZ on the Surfactant C gene promoter, as well as the expression of other known target genes of these regulatory factors.\n\nQuestion:\nDoes aMOTL2 interaction with TAZ cause the inhibition of surfactant proteins expression in lung cells?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nTAZ (Transcriptional co-Activator with PDZ-binding motif), is a biologically potent transcriptional coactivator and functions by binding to the PPXY motif present in several transcription factors. Notably, TAZ behaves as a transducer linking cytoplasmic signaling events to transcriptional regulation in the nucleus. Several different factors regulate TAZ expression and/or function. In particular, a major regulation of TAZ activity occurs through the Hippo pathway by a phosphorylation-mediated mechanism that causes its cytoplasmic sequestration or degradation. Here we demonstrate that AMOTL2 robustly co-immunoprecipitates with TAZ, and their interaction is dependent on the WW domain of TAZ and the PPXY motif in the N-terminus of AMOTL2. Furthermore, we show that AMOTL2 colocalizes with TAZ in the cytoplasm of H441 human lung cells and regulates TAZ cytoplasm-to-nucleus translocation through direct protein-protein interaction. Interestingly, the overexpression of AMOTL2 inhibits the functional cooperation between the transcription factor TTF-1 and TAZ on the Surfactant C gene promoter, as well as the expression of other known target genes of these regulatory factors.\n\nQuestion:\nDoes aMOTL2 interaction with TAZ cause the inhibition of surfactant proteins expression in lung cells?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nTAZ (Transcriptional co-Activator with PDZ-binding motif), is a biologically potent transcriptional coactivator and functions by binding to the PPXY motif present in several transcription factors. Notably, TAZ behaves as a transducer linking cytoplasmic signaling events to transcriptional regulation in the nucleus. Several different factors regulate TAZ expression and/or function. In particular, a major regulation of TAZ activity occurs through the Hippo pathway by a phosphorylation-mediated mechanism that causes its cytoplasmic sequestration or degradation. Here we demonstrate that AMOTL2 robustly co-immunoprecipitates with TAZ, and their interaction is dependent on the WW domain of TAZ and the PPXY motif in the N-terminus of AMOTL2. Furthermore, we show that AMOTL2 colocalizes with TAZ in the cytoplasm of H441 human lung cells and regulates TAZ cytoplasm-to-nucleus translocation through direct protein-protein interaction. Interestingly, the overexpression of AMOTL2 inhibits the functional cooperation between the transcription factor TTF-1 and TAZ on the Surfactant C gene promoter, as well as the expression of other known target genes of these regulatory factors.\n\nQuestion:\nDoes aMOTL2 interaction with TAZ cause the inhibition of surfactant proteins expression in lung cells?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nAlthough several kinds of evidence suggest that glycosaminoglycans (GAGs) and proteoglycans (PGs) may contribute to the development of beta2-microglobulin-related (Abeta2m) amyloidosis, the precise roles of these molecules for the development of Abeta2m amyloidosis are poorly understood. We investigated the effects of GAGs and PGs on the depolymerization of Abeta2m amyloid fibrils at a neutral pH, as well as on the formation of the fibrils at an acidic pH in vitro, using fluorescence spectroscopy with thioflavin T and electron microscopy. Depolymerization of Abeta2m amyloid fibrils at pH 7.5 at 37 degrees C was inhibited dose-dependently by the presence of some GAGs (heparin, dermatan sulfate, or heparan sulfate) or PGs (biglycan, decorin, or keratan sulfate proteoglycan). Electron microscopy revealed that a significant amount of Abeta2m amyloid fibrils remained in the reaction mixture with some lateral aggregation. Second, when monomeric beta2m was incubated with aggrecan, biglycan, decorin, or heparin at pH 2.5 at 37 degrees C for up to 21 days, the thioflavin T fluorescence increased depending on dose and time. Electron microscopy revealed the formation of rigid and straight fibrils similar to Abeta2m amyloid fibrils in beta2m incubated with biglycan for 21 days.\n\nQuestion:\nDo glycosaminoglycan and proteoglycan inhibit the depolymerization of beta2-microglobulin amyloid fibrils in vitro?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nAlthough several kinds of evidence suggest that glycosaminoglycans (GAGs) and proteoglycans (PGs) may contribute to the development of beta2-microglobulin-related (Abeta2m) amyloidosis, the precise roles of these molecules for the development of Abeta2m amyloidosis are poorly understood. We investigated the effects of GAGs and PGs on the depolymerization of Abeta2m amyloid fibrils at a neutral pH, as well as on the formation of the fibrils at an acidic pH in vitro, using fluorescence spectroscopy with thioflavin T and electron microscopy. Depolymerization of Abeta2m amyloid fibrils at pH 7.5 at 37 degrees C was inhibited dose-dependently by the presence of some GAGs (heparin, dermatan sulfate, or heparan sulfate) or PGs (biglycan, decorin, or keratan sulfate proteoglycan). Electron microscopy revealed that a significant amount of Abeta2m amyloid fibrils remained in the reaction mixture with some lateral aggregation. Second, when monomeric beta2m was incubated with aggrecan, biglycan, decorin, or heparin at pH 2.5 at 37 degrees C for up to 21 days, the thioflavin T fluorescence increased depending on dose and time. Electron microscopy revealed the formation of rigid and straight fibrils similar to Abeta2m amyloid fibrils in beta2m incubated with biglycan for 21 days.\n\nQuestion:\nDo glycosaminoglycan and proteoglycan inhibit the depolymerization of beta2-microglobulin amyloid fibrils in vitro?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nAlthough several kinds of evidence suggest that glycosaminoglycans (GAGs) and proteoglycans (PGs) may contribute to the development of beta2-microglobulin-related (Abeta2m) amyloidosis, the precise roles of these molecules for the development of Abeta2m amyloidosis are poorly understood. We investigated the effects of GAGs and PGs on the depolymerization of Abeta2m amyloid fibrils at a neutral pH, as well as on the formation of the fibrils at an acidic pH in vitro, using fluorescence spectroscopy with thioflavin T and electron microscopy. Depolymerization of Abeta2m amyloid fibrils at pH 7.5 at 37 degrees C was inhibited dose-dependently by the presence of some GAGs (heparin, dermatan sulfate, or heparan sulfate) or PGs (biglycan, decorin, or keratan sulfate proteoglycan). Electron microscopy revealed that a significant amount of Abeta2m amyloid fibrils remained in the reaction mixture with some lateral aggregation. Second, when monomeric beta2m was incubated with aggrecan, biglycan, decorin, or heparin at pH 2.5 at 37 degrees C for up to 21 days, the thioflavin T fluorescence increased depending on dose and time. Electron microscopy revealed the formation of rigid and straight fibrils similar to Abeta2m amyloid fibrils in beta2m incubated with biglycan for 21 days.\n\nQuestion:\nDo glycosaminoglycan and proteoglycan inhibit the depolymerization of beta2-microglobulin amyloid fibrils in vitro?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nOral tongue squamous cell carcinoma (OTSCC) is one of the most aggressive forms of head and neck/oral cancer (HNOC), and is a complex disease with extensive genetic and epigenetic defects, including microRNA deregulation. Identifying the deregulation of microRNA-mRNA regulatory modules (MRMs) is crucial for understanding the role of microRNA in OTSCC. A comprehensive bioinformatics analysis was performed to identify MRMs in HNOC by examining the correlation among differentially expressed microRNA and mRNA profiling datasets and integrating with 12 different sequence-based microRNA target prediction algorithms. Confirmation experiments were performed to further assess the correlation among MRMs using OTSCC patient samples and HNOC cell lines. Functional analyses were performed to validate one of the identified MRMs: miR-21-15-Hydroxyprostaglandin Dehydrogenase (HPGD) regulatory module. Our bioinformatics analysis revealed 53 MRMs that are deregulated in HNOC. Four high confidence MRMs were further defined by confirmation experiments using OTSCC patient samples and HNOC cell lines, including miR-21-HPGD regulatory module. HPGD is a known anti-tumorigenic effecter, and it regulates the tumorigenic actions of Prostaglandin E2 (PGE2) by converts PGE2 to its biologically inactive metabolite. Ectopic transfection of miR-21 reduced the expression of HPGD in OTSCC cell lines, and the direct targeting of the miR-21 to the HPGD mRNA was confirmed using a luciferase reporter gene assay. The PGE2-mediated upregulation of miR-21 was also confirmed which suggested the existence of a positive feed-forward loop that involves miR-21, HPGD and PGE2 in OTSCC cells that contribute to tumorigenesis.\n\nQuestion:\nDoes microRNA-21 regulate prostaglandin E2 signaling pathway by targeting 15-hydroxyprostaglandin dehydrogenase in tongue squamous cell carcinoma?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nOral tongue squamous cell carcinoma (OTSCC) is one of the most aggressive forms of head and neck/oral cancer (HNOC), and is a complex disease with extensive genetic and epigenetic defects, including microRNA deregulation. Identifying the deregulation of microRNA-mRNA regulatory modules (MRMs) is crucial for understanding the role of microRNA in OTSCC. A comprehensive bioinformatics analysis was performed to identify MRMs in HNOC by examining the correlation among differentially expressed microRNA and mRNA profiling datasets and integrating with 12 different sequence-based microRNA target prediction algorithms. Confirmation experiments were performed to further assess the correlation among MRMs using OTSCC patient samples and HNOC cell lines. Functional analyses were performed to validate one of the identified MRMs: miR-21-15-Hydroxyprostaglandin Dehydrogenase (HPGD) regulatory module. Our bioinformatics analysis revealed 53 MRMs that are deregulated in HNOC. Four high confidence MRMs were further defined by confirmation experiments using OTSCC patient samples and HNOC cell lines, including miR-21-HPGD regulatory module. HPGD is a known anti-tumorigenic effecter, and it regulates the tumorigenic actions of Prostaglandin E2 (PGE2) by converts PGE2 to its biologically inactive metabolite. Ectopic transfection of miR-21 reduced the expression of HPGD in OTSCC cell lines, and the direct targeting of the miR-21 to the HPGD mRNA was confirmed using a luciferase reporter gene assay. The PGE2-mediated upregulation of miR-21 was also confirmed which suggested the existence of a positive feed-forward loop that involves miR-21, HPGD and PGE2 in OTSCC cells that contribute to tumorigenesis.\n\nQuestion:\nDoes microRNA-21 regulate prostaglandin E2 signaling pathway by targeting 15-hydroxyprostaglandin dehydrogenase in tongue squamous cell carcinoma?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nOral tongue squamous cell carcinoma (OTSCC) is one of the most aggressive forms of head and neck/oral cancer (HNOC), and is a complex disease with extensive genetic and epigenetic defects, including microRNA deregulation. Identifying the deregulation of microRNA-mRNA regulatory modules (MRMs) is crucial for understanding the role of microRNA in OTSCC. A comprehensive bioinformatics analysis was performed to identify MRMs in HNOC by examining the correlation among differentially expressed microRNA and mRNA profiling datasets and integrating with 12 different sequence-based microRNA target prediction algorithms. Confirmation experiments were performed to further assess the correlation among MRMs using OTSCC patient samples and HNOC cell lines. Functional analyses were performed to validate one of the identified MRMs: miR-21-15-Hydroxyprostaglandin Dehydrogenase (HPGD) regulatory module. Our bioinformatics analysis revealed 53 MRMs that are deregulated in HNOC. Four high confidence MRMs were further defined by confirmation experiments using OTSCC patient samples and HNOC cell lines, including miR-21-HPGD regulatory module. HPGD is a known anti-tumorigenic effecter, and it regulates the tumorigenic actions of Prostaglandin E2 (PGE2) by converts PGE2 to its biologically inactive metabolite. Ectopic transfection of miR-21 reduced the expression of HPGD in OTSCC cell lines, and the direct targeting of the miR-21 to the HPGD mRNA was confirmed using a luciferase reporter gene assay. The PGE2-mediated upregulation of miR-21 was also confirmed which suggested the existence of a positive feed-forward loop that involves miR-21, HPGD and PGE2 in OTSCC cells that contribute to tumorigenesis.\n\nQuestion:\nDoes microRNA-21 regulate prostaglandin E2 signaling pathway by targeting 15-hydroxyprostaglandin dehydrogenase in tongue squamous cell carcinoma?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nThis observational study examines changes in paediatric hospital-seeking behaviour at Kolding Hospital in The Region of Southern Denmark (RSD) following a major change in administrative units in Denmark on 1 January 2007. Data on the paediatric admissions from 2004 to 2009 reported by department of paediatrics and municipalities were drawn from the Danish National Hospital Registration. Patient hospital-seeking behaviour was related to changes in the political/administrative units. Changes in number of admissions were compared with distances to the corresponding departments. From 2006 to 2009, the number of acute and planned admissions at the Department of Paediatrics in Kolding for children living in the RSD increased by 46.1% and 65.0%, respectively. The corresponding changes for children living in the neighboring region, the Central Denmark Region (CDR), were -69.9% and -78.6%.\n\nQuestion:\nDoes referral of paediatric patients follow geographic borders of administrative units?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nThis observational study examines changes in paediatric hospital-seeking behaviour at Kolding Hospital in The Region of Southern Denmark (RSD) following a major change in administrative units in Denmark on 1 January 2007. Data on the paediatric admissions from 2004 to 2009 reported by department of paediatrics and municipalities were drawn from the Danish National Hospital Registration. Patient hospital-seeking behaviour was related to changes in the political/administrative units. Changes in number of admissions were compared with distances to the corresponding departments. From 2006 to 2009, the number of acute and planned admissions at the Department of Paediatrics in Kolding for children living in the RSD increased by 46.1% and 65.0%, respectively. The corresponding changes for children living in the neighboring region, the Central Denmark Region (CDR), were -69.9% and -78.6%.\n\nQuestion:\nDoes referral of paediatric patients follow geographic borders of administrative units?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nThis observational study examines changes in paediatric hospital-seeking behaviour at Kolding Hospital in The Region of Southern Denmark (RSD) following a major change in administrative units in Denmark on 1 January 2007. Data on the paediatric admissions from 2004 to 2009 reported by department of paediatrics and municipalities were drawn from the Danish National Hospital Registration. Patient hospital-seeking behaviour was related to changes in the political/administrative units. Changes in number of admissions were compared with distances to the corresponding departments. From 2006 to 2009, the number of acute and planned admissions at the Department of Paediatrics in Kolding for children living in the RSD increased by 46.1% and 65.0%, respectively. The corresponding changes for children living in the neighboring region, the Central Denmark Region (CDR), were -69.9% and -78.6%.\n\nQuestion:\nDoes referral of paediatric patients follow geographic borders of administrative units?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nNuclear factor (NF)-kappaB is a key transcription factor that regulates inflammatory processes. In the present study, we assessed the hypothesis that blockade of NF-kappaB may ameliorate ventricular hypertrophy in response to chronic infusion of angiotensin II. Mice with targeted disruption of the p50 subunit of NF-kappaB (KO) were used to block the activation of NF-kappaB. Male KO and age-matched wild-type (WT) mice were chronically infused with angiotensin II at the rate of 0.2 (low dose) or 2 microg/kg/min (high dose) for 4 weeks. High- but not low-dose angiotensin II significantly increased systemic blood pressure and left ventricular weight in WT mice. In contrast, although the pressor response was slightly but significantly augmented, the hypertrophic effect of angiotensin II was significantly attenuated in KO mice. The attenuated hypertrophic responsiveness was confirmed histologically (cross-sectional area) and transcriptionally (atrial natriuretic peptide). Echocardiography revealed no evidence of cardiac dysfunction in angiotensin II-treated KO mice. Although phosphorylation of MAPKs, including ERK, JNK, or p38-MAPK, was not affected after 4 weeks of angiotensin II treatment in WT mice, phosphorylation of JNK was specifically abrogated in KO mice. Angiotensin II increased myocardial expression of proinflammatory cytokines and chemokines in WT mice, while expression of TNF-alpha and RANTES was paradoxically augmented in KO mice.\n\nQuestion:\nDoes blockade of NF-kappaB ameliorate myocardial hypertrophy in response to chronic infusion of angiotensin II?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nNuclear factor (NF)-kappaB is a key transcription factor that regulates inflammatory processes. In the present study, we assessed the hypothesis that blockade of NF-kappaB may ameliorate ventricular hypertrophy in response to chronic infusion of angiotensin II. Mice with targeted disruption of the p50 subunit of NF-kappaB (KO) were used to block the activation of NF-kappaB. Male KO and age-matched wild-type (WT) mice were chronically infused with angiotensin II at the rate of 0.2 (low dose) or 2 microg/kg/min (high dose) for 4 weeks. High- but not low-dose angiotensin II significantly increased systemic blood pressure and left ventricular weight in WT mice. In contrast, although the pressor response was slightly but significantly augmented, the hypertrophic effect of angiotensin II was significantly attenuated in KO mice. The attenuated hypertrophic responsiveness was confirmed histologically (cross-sectional area) and transcriptionally (atrial natriuretic peptide). Echocardiography revealed no evidence of cardiac dysfunction in angiotensin II-treated KO mice. Although phosphorylation of MAPKs, including ERK, JNK, or p38-MAPK, was not affected after 4 weeks of angiotensin II treatment in WT mice, phosphorylation of JNK was specifically abrogated in KO mice. Angiotensin II increased myocardial expression of proinflammatory cytokines and chemokines in WT mice, while expression of TNF-alpha and RANTES was paradoxically augmented in KO mice.\n\nQuestion:\nDoes blockade of NF-kappaB ameliorate myocardial hypertrophy in response to chronic infusion of angiotensin II?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nNuclear factor (NF)-kappaB is a key transcription factor that regulates inflammatory processes. In the present study, we assessed the hypothesis that blockade of NF-kappaB may ameliorate ventricular hypertrophy in response to chronic infusion of angiotensin II. Mice with targeted disruption of the p50 subunit of NF-kappaB (KO) were used to block the activation of NF-kappaB. Male KO and age-matched wild-type (WT) mice were chronically infused with angiotensin II at the rate of 0.2 (low dose) or 2 microg/kg/min (high dose) for 4 weeks. High- but not low-dose angiotensin II significantly increased systemic blood pressure and left ventricular weight in WT mice. In contrast, although the pressor response was slightly but significantly augmented, the hypertrophic effect of angiotensin II was significantly attenuated in KO mice. The attenuated hypertrophic responsiveness was confirmed histologically (cross-sectional area) and transcriptionally (atrial natriuretic peptide). Echocardiography revealed no evidence of cardiac dysfunction in angiotensin II-treated KO mice. Although phosphorylation of MAPKs, including ERK, JNK, or p38-MAPK, was not affected after 4 weeks of angiotensin II treatment in WT mice, phosphorylation of JNK was specifically abrogated in KO mice. Angiotensin II increased myocardial expression of proinflammatory cytokines and chemokines in WT mice, while expression of TNF-alpha and RANTES was paradoxically augmented in KO mice.\n\nQuestion:\nDoes blockade of NF-kappaB ameliorate myocardial hypertrophy in response to chronic infusion of angiotensin II?", "role": "user" } ]