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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:\nResistance to Fas-mediated apoptosis limits the efficacy of currently available chemotherapy regimens. We identified CD74, which is known to be overexpressed in hematological malignancies, as one of the factors interfering with Fas-mediated apoptosis. CD74 expression was suppressed in human B-lymphoma cell lines, BJAB and Raji, by either transduction with lentivirus particles or transfection with episomal vector, both encoding CD74-specific shRNAs or non-target shRNA. Effect of CD74 expression on Fas signaling was evaluated by comparing survival of mice hydrodynamically transfected with vector encoding full-length CD74 or empty vector. Sensitivity of cells with suppressed CD74 expression to FasL, edelfosine, doxorubicin, and a humanized CD74-specific antibody, milatuzumab, was evaluated by flow cytometry and compared to control cells. Fas signaling in response to FasL stimulation and the expression of Fas signaling components were evaluated by Western blot. Surface expression of Fas was detected by flow cytometry. We determined that cells with suppressed CD74 are more sensitive to FasL-induced apoptosis and Fas signaling-dependent chemotherapies, edelfosine and doxorubicin, than control CD74-expressing cells. On the other hand, expression of full-length CD74 in livers protected the mice from a lethal challenge with agonistic anti-Fas antibody Jo2. A detailed analysis of Fas signaling in cells lacking CD74 and control cells revealed increased cleavage/activation of pro-caspase-8 and corresponding enhancement of caspase-3 activation in the absence of CD74, suggesting that CD74 affects the immediate early steps in Fas signaling at the plasma membrane. Cells with suppressed CD74 expression showed increased staining of Fas receptor on their surface. Pre-treatment with milatuzumab sensitized BJAB cells to Fas-mediated apoptosis.\n\nQuestion:\nDoes cD74 interfere with the expression of fas receptor on the surface of lymphoma 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:\nResistance to Fas-mediated apoptosis limits the efficacy of currently available chemotherapy regimens. We identified CD74, which is known to be overexpressed in hematological malignancies, as one of the factors interfering with Fas-mediated apoptosis. CD74 expression was suppressed in human B-lymphoma cell lines, BJAB and Raji, by either transduction with lentivirus particles or transfection with episomal vector, both encoding CD74-specific shRNAs or non-target shRNA. Effect of CD74 expression on Fas signaling was evaluated by comparing survival of mice hydrodynamically transfected with vector encoding full-length CD74 or empty vector. Sensitivity of cells with suppressed CD74 expression to FasL, edelfosine, doxorubicin, and a humanized CD74-specific antibody, milatuzumab, was evaluated by flow cytometry and compared to control cells. Fas signaling in response to FasL stimulation and the expression of Fas signaling components were evaluated by Western blot. Surface expression of Fas was detected by flow cytometry. We determined that cells with suppressed CD74 are more sensitive to FasL-induced apoptosis and Fas signaling-dependent chemotherapies, edelfosine and doxorubicin, than control CD74-expressing cells. On the other hand, expression of full-length CD74 in livers protected the mice from a lethal challenge with agonistic anti-Fas antibody Jo2. A detailed analysis of Fas signaling in cells lacking CD74 and control cells revealed increased cleavage/activation of pro-caspase-8 and corresponding enhancement of caspase-3 activation in the absence of CD74, suggesting that CD74 affects the immediate early steps in Fas signaling at the plasma membrane. Cells with suppressed CD74 expression showed increased staining of Fas receptor on their surface. Pre-treatment with milatuzumab sensitized BJAB cells to Fas-mediated apoptosis.\n\nQuestion:\nDoes cD74 interfere with the expression of fas receptor on the surface of lymphoma 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:\nResistance to Fas-mediated apoptosis limits the efficacy of currently available chemotherapy regimens. We identified CD74, which is known to be overexpressed in hematological malignancies, as one of the factors interfering with Fas-mediated apoptosis. CD74 expression was suppressed in human B-lymphoma cell lines, BJAB and Raji, by either transduction with lentivirus particles or transfection with episomal vector, both encoding CD74-specific shRNAs or non-target shRNA. Effect of CD74 expression on Fas signaling was evaluated by comparing survival of mice hydrodynamically transfected with vector encoding full-length CD74 or empty vector. Sensitivity of cells with suppressed CD74 expression to FasL, edelfosine, doxorubicin, and a humanized CD74-specific antibody, milatuzumab, was evaluated by flow cytometry and compared to control cells. Fas signaling in response to FasL stimulation and the expression of Fas signaling components were evaluated by Western blot. Surface expression of Fas was detected by flow cytometry. We determined that cells with suppressed CD74 are more sensitive to FasL-induced apoptosis and Fas signaling-dependent chemotherapies, edelfosine and doxorubicin, than control CD74-expressing cells. On the other hand, expression of full-length CD74 in livers protected the mice from a lethal challenge with agonistic anti-Fas antibody Jo2. A detailed analysis of Fas signaling in cells lacking CD74 and control cells revealed increased cleavage/activation of pro-caspase-8 and corresponding enhancement of caspase-3 activation in the absence of CD74, suggesting that CD74 affects the immediate early steps in Fas signaling at the plasma membrane. Cells with suppressed CD74 expression showed increased staining of Fas receptor on their surface. Pre-treatment with milatuzumab sensitized BJAB cells to Fas-mediated apoptosis.\n\nQuestion:\nDoes cD74 interfere with the expression of fas receptor on the surface of lymphoma 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:\nArterial hypertension is an important risk factor for cerebrovascular diseases, such as transient ischemic attacks or stroke, and represents a major global health issue. The effects of hypertension on cerebral blood flow, particularly at the microvascular level, remain unknown. Using the spontaneously hypertensive rat (SHR) model, we examined cortical hemodynamic responses on whisker stimulation applying a multimodal imaging approach (multiwavelength spectroscopy, laser speckle imaging, and 2-photon microscopy). We assessed the effects of hypertension in 10-, 20-, and 40-week-old male SHRs and age-matched male Wistar Kyoto rats (CTRL) on hemodynamic responses, histology, and biochemical parameters. In 40-week-old animals, losartan or verapamil was administered for 10 weeks to test the reversibility of hypertension-induced impairments. Increased arterial blood pressure was associated with a progressive impairment in functional hyperemia in 20- and 40-week-old SHRs; baseline capillary red blood cell velocity was increased in 40-week-old SHRs compared with age-matched CTRLs. Antihypertensive treatment reduced baseline capillary cerebral blood flow almost to CTRL values, whereas functional hyperemic signals did not improve after 10 weeks of drug therapy. Structural analyses of the microvascular network revealed no differences between normo- and hypertensive animals, whereas expression analyses of cerebral lysates showed signs of increased oxidative stress and signs of impaired endothelial homeostasis upon early hypertension.\n\nQuestion:\nDoes multimodal imaging in rats reveal impaired neurovascular coupling in sustained hypertension?", "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 hypertension is an important risk factor for cerebrovascular diseases, such as transient ischemic attacks or stroke, and represents a major global health issue. The effects of hypertension on cerebral blood flow, particularly at the microvascular level, remain unknown. Using the spontaneously hypertensive rat (SHR) model, we examined cortical hemodynamic responses on whisker stimulation applying a multimodal imaging approach (multiwavelength spectroscopy, laser speckle imaging, and 2-photon microscopy). We assessed the effects of hypertension in 10-, 20-, and 40-week-old male SHRs and age-matched male Wistar Kyoto rats (CTRL) on hemodynamic responses, histology, and biochemical parameters. In 40-week-old animals, losartan or verapamil was administered for 10 weeks to test the reversibility of hypertension-induced impairments. Increased arterial blood pressure was associated with a progressive impairment in functional hyperemia in 20- and 40-week-old SHRs; baseline capillary red blood cell velocity was increased in 40-week-old SHRs compared with age-matched CTRLs. Antihypertensive treatment reduced baseline capillary cerebral blood flow almost to CTRL values, whereas functional hyperemic signals did not improve after 10 weeks of drug therapy. Structural analyses of the microvascular network revealed no differences between normo- and hypertensive animals, whereas expression analyses of cerebral lysates showed signs of increased oxidative stress and signs of impaired endothelial homeostasis upon early hypertension.\n\nQuestion:\nDoes multimodal imaging in rats reveal impaired neurovascular coupling in sustained hypertension?", "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 hypertension is an important risk factor for cerebrovascular diseases, such as transient ischemic attacks or stroke, and represents a major global health issue. The effects of hypertension on cerebral blood flow, particularly at the microvascular level, remain unknown. Using the spontaneously hypertensive rat (SHR) model, we examined cortical hemodynamic responses on whisker stimulation applying a multimodal imaging approach (multiwavelength spectroscopy, laser speckle imaging, and 2-photon microscopy). We assessed the effects of hypertension in 10-, 20-, and 40-week-old male SHRs and age-matched male Wistar Kyoto rats (CTRL) on hemodynamic responses, histology, and biochemical parameters. In 40-week-old animals, losartan or verapamil was administered for 10 weeks to test the reversibility of hypertension-induced impairments. Increased arterial blood pressure was associated with a progressive impairment in functional hyperemia in 20- and 40-week-old SHRs; baseline capillary red blood cell velocity was increased in 40-week-old SHRs compared with age-matched CTRLs. Antihypertensive treatment reduced baseline capillary cerebral blood flow almost to CTRL values, whereas functional hyperemic signals did not improve after 10 weeks of drug therapy. Structural analyses of the microvascular network revealed no differences between normo- and hypertensive animals, whereas expression analyses of cerebral lysates showed signs of increased oxidative stress and signs of impaired endothelial homeostasis upon early hypertension.\n\nQuestion:\nDoes multimodal imaging in rats reveal impaired neurovascular coupling in sustained hypertension?", "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 brain-derived neurotrophic factor (BDNF) gene is involved in mechanisms of synaptic plasticity in the adult brain. It has been demonstrated that BDNF also plays a significant role in shaping externally induced human brain plasticity. Plasticity induced in the human motor cortex by intermittent theta-burst stimulation (iTBS) was impaired in individuals expressing the Val66Met polymorphism. To explore whether this polymorphism is also important for other neuroplasticity-inducing tools in humans with modes of action differing from that of iTBS, namely, transcranial direct current (tDCS) and random noise stimulation (tRNS), we retrospectively analyzed the data of 64 subjects studied in our laboratory with regard to BDNF genotype. Fifteen subjects with the Val66Met allele, 46 subjects with the Val66Val allele, and 3 Met66Met carriers were identified. The response of the Val66Met allele carriers to stimulation differed in two protocols compared with the response of Val66Val individuals. For iTBS (15 subjects, 5 heterozygotes), plasticity could be only induced in the Val66Val allele carriers. However, for facilitatory tDCS (24 subjects, 10 heterozygotes), as well as for inhibitory tDCS, (19 subjects, 8 heterozygotes), carriers of the Val66Met allele displayed enhanced plasticity, whereas for transcranial random noise stimulation (29 subjects, 8 heterozygotes), the difference between groups was not so pronounced.\n\nQuestion:\nDo brain-derived neurotrophic factor ( BDNF ) gene polymorphisms shape cortical plasticity in humans?", "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 brain-derived neurotrophic factor (BDNF) gene is involved in mechanisms of synaptic plasticity in the adult brain. It has been demonstrated that BDNF also plays a significant role in shaping externally induced human brain plasticity. Plasticity induced in the human motor cortex by intermittent theta-burst stimulation (iTBS) was impaired in individuals expressing the Val66Met polymorphism. To explore whether this polymorphism is also important for other neuroplasticity-inducing tools in humans with modes of action differing from that of iTBS, namely, transcranial direct current (tDCS) and random noise stimulation (tRNS), we retrospectively analyzed the data of 64 subjects studied in our laboratory with regard to BDNF genotype. Fifteen subjects with the Val66Met allele, 46 subjects with the Val66Val allele, and 3 Met66Met carriers were identified. The response of the Val66Met allele carriers to stimulation differed in two protocols compared with the response of Val66Val individuals. For iTBS (15 subjects, 5 heterozygotes), plasticity could be only induced in the Val66Val allele carriers. However, for facilitatory tDCS (24 subjects, 10 heterozygotes), as well as for inhibitory tDCS, (19 subjects, 8 heterozygotes), carriers of the Val66Met allele displayed enhanced plasticity, whereas for transcranial random noise stimulation (29 subjects, 8 heterozygotes), the difference between groups was not so pronounced.\n\nQuestion:\nDo brain-derived neurotrophic factor ( BDNF ) gene polymorphisms shape cortical plasticity in humans?", "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 brain-derived neurotrophic factor (BDNF) gene is involved in mechanisms of synaptic plasticity in the adult brain. It has been demonstrated that BDNF also plays a significant role in shaping externally induced human brain plasticity. Plasticity induced in the human motor cortex by intermittent theta-burst stimulation (iTBS) was impaired in individuals expressing the Val66Met polymorphism. To explore whether this polymorphism is also important for other neuroplasticity-inducing tools in humans with modes of action differing from that of iTBS, namely, transcranial direct current (tDCS) and random noise stimulation (tRNS), we retrospectively analyzed the data of 64 subjects studied in our laboratory with regard to BDNF genotype. Fifteen subjects with the Val66Met allele, 46 subjects with the Val66Val allele, and 3 Met66Met carriers were identified. The response of the Val66Met allele carriers to stimulation differed in two protocols compared with the response of Val66Val individuals. For iTBS (15 subjects, 5 heterozygotes), plasticity could be only induced in the Val66Val allele carriers. However, for facilitatory tDCS (24 subjects, 10 heterozygotes), as well as for inhibitory tDCS, (19 subjects, 8 heterozygotes), carriers of the Val66Met allele displayed enhanced plasticity, whereas for transcranial random noise stimulation (29 subjects, 8 heterozygotes), the difference between groups was not so pronounced.\n\nQuestion:\nDo brain-derived neurotrophic factor ( BDNF ) gene polymorphisms shape cortical plasticity in humans?", "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:\nDeregulation of the cell cycle machinery is often found in human cancers. Modulations in the cell cycle regulator function and expression result not only in proliferative advantages, but also lead to tumor progression and invasiveness of the cancer. In particular, cyclin D1 and p21 are often over-expressed in human cancers, correlating with high tumor grade, poor prognosis and increased metastasis. This prompted us to investigate the role of the cyclin D1/p21 signaling axis downstream of transforming growth factor beta (TGFβ) in breast cancer progression. Cyclins mRNA and protein expressions were assessed by quantitative real-time PCR and Western blot in triple negative breast cancer cell lines. Co-localization and interaction between cyclin D1 and p21 were performed by immunocytochemistry and co-immunoprecipitation, respectively. Cell migration was assessed by wound healing and quantitative time-lapse imaging assays. In addition, the effects of cyclin D1 on cellular structure and actin organization were examined by staining with F-actin marker phalloidin and mesenchymal intermediate filament vimentin. Finally, a mammary fat pad xenograft mouse model was used to assess mammary tumor growth and local invasion. We found TGFβ to specifically up-regulate the expression of cyclin D1 in triple negative breast cancer cells. Induction of cyclin D1 is also required for TGFβ-mediated cell migration. Suppression of cyclin D1 expression not only resulted in a rounded and epithelial-like phenotype, but also prevented TGFβ-induced vimentin and F-actin co-localization at the cell edge as well as invadopodia formation. Furthermore, TGFβ promoted the nuclear co-localization and physical interaction between cyclin D1 and p21. The co-expression of cyclin D1 and p21 proteins are required for the initial steps of tumor development, as double knockdown of these two molecules prevented primary tumor formation in a Xenograft mouse model. Moreover, the in vivo studies indicated that locally advanced features of the invasive tumors, including skeletal muscle, mammary fat pad and lymphovascular invasion, as well as ulcerated skin, were attenuated in the absence of cyclin D1 and p21.\n\nQuestion:\nDoes cyclin D1 cooperate with p21 to regulate TGFβ-mediated breast cancer cell migration and tumor local invasion?", "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:\nDeregulation of the cell cycle machinery is often found in human cancers. Modulations in the cell cycle regulator function and expression result not only in proliferative advantages, but also lead to tumor progression and invasiveness of the cancer. In particular, cyclin D1 and p21 are often over-expressed in human cancers, correlating with high tumor grade, poor prognosis and increased metastasis. This prompted us to investigate the role of the cyclin D1/p21 signaling axis downstream of transforming growth factor beta (TGFβ) in breast cancer progression. Cyclins mRNA and protein expressions were assessed by quantitative real-time PCR and Western blot in triple negative breast cancer cell lines. Co-localization and interaction between cyclin D1 and p21 were performed by immunocytochemistry and co-immunoprecipitation, respectively. Cell migration was assessed by wound healing and quantitative time-lapse imaging assays. In addition, the effects of cyclin D1 on cellular structure and actin organization were examined by staining with F-actin marker phalloidin and mesenchymal intermediate filament vimentin. Finally, a mammary fat pad xenograft mouse model was used to assess mammary tumor growth and local invasion. We found TGFβ to specifically up-regulate the expression of cyclin D1 in triple negative breast cancer cells. Induction of cyclin D1 is also required for TGFβ-mediated cell migration. Suppression of cyclin D1 expression not only resulted in a rounded and epithelial-like phenotype, but also prevented TGFβ-induced vimentin and F-actin co-localization at the cell edge as well as invadopodia formation. Furthermore, TGFβ promoted the nuclear co-localization and physical interaction between cyclin D1 and p21. The co-expression of cyclin D1 and p21 proteins are required for the initial steps of tumor development, as double knockdown of these two molecules prevented primary tumor formation in a Xenograft mouse model. Moreover, the in vivo studies indicated that locally advanced features of the invasive tumors, including skeletal muscle, mammary fat pad and lymphovascular invasion, as well as ulcerated skin, were attenuated in the absence of cyclin D1 and p21.\n\nQuestion:\nDoes cyclin D1 cooperate with p21 to regulate TGFβ-mediated breast cancer cell migration and tumor local invasion?", "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:\nDeregulation of the cell cycle machinery is often found in human cancers. Modulations in the cell cycle regulator function and expression result not only in proliferative advantages, but also lead to tumor progression and invasiveness of the cancer. In particular, cyclin D1 and p21 are often over-expressed in human cancers, correlating with high tumor grade, poor prognosis and increased metastasis. This prompted us to investigate the role of the cyclin D1/p21 signaling axis downstream of transforming growth factor beta (TGFβ) in breast cancer progression. Cyclins mRNA and protein expressions were assessed by quantitative real-time PCR and Western blot in triple negative breast cancer cell lines. Co-localization and interaction between cyclin D1 and p21 were performed by immunocytochemistry and co-immunoprecipitation, respectively. Cell migration was assessed by wound healing and quantitative time-lapse imaging assays. In addition, the effects of cyclin D1 on cellular structure and actin organization were examined by staining with F-actin marker phalloidin and mesenchymal intermediate filament vimentin. Finally, a mammary fat pad xenograft mouse model was used to assess mammary tumor growth and local invasion. We found TGFβ to specifically up-regulate the expression of cyclin D1 in triple negative breast cancer cells. Induction of cyclin D1 is also required for TGFβ-mediated cell migration. Suppression of cyclin D1 expression not only resulted in a rounded and epithelial-like phenotype, but also prevented TGFβ-induced vimentin and F-actin co-localization at the cell edge as well as invadopodia formation. Furthermore, TGFβ promoted the nuclear co-localization and physical interaction between cyclin D1 and p21. The co-expression of cyclin D1 and p21 proteins are required for the initial steps of tumor development, as double knockdown of these two molecules prevented primary tumor formation in a Xenograft mouse model. Moreover, the in vivo studies indicated that locally advanced features of the invasive tumors, including skeletal muscle, mammary fat pad and lymphovascular invasion, as well as ulcerated skin, were attenuated in the absence of cyclin D1 and p21.\n\nQuestion:\nDoes cyclin D1 cooperate with p21 to regulate TGFβ-mediated breast cancer cell migration and tumor local invasion?", "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 if dopamine (D3) receptor genotypes are associated with anovulation and response to ovulation induction with clomiphene citrate. Clinical and laboratory characteristics of anovulatory patients and ovulatory controls were compared with findings at the DNA level. An outpatient clinic at an university medical center. One hundred eighty human Hispanic female volunteers (130 of these with documented ovulatory status) were studied. Genomic DNAs were extracted from each patient. Polymerase chain reaction with subsequent restriction digest was performed to analyze the D3 receptor allele status (two possible alleles). Menstrual history, serum T, and midluteal serum Ps from spontaneous and clomiphene cycles were correlated with D3 receptor genotype. Hispanic females with the 22 genotype compared with the other genotypes (11 and 12) were more likely to have irregular menses, an elevated serum T (> or = 70 ng/dL [conversion factor to SI unit, 3.467]), and hyperandrogenic chronic anovulation. These patients tended to be resistant to ovulation induction requiring a significantly higher dose of clomiphene to achieve an ovulatory response (22 genotype [mean +/- SEM] [140.0 +/- 19.0 mg] versus 11 [77.1 +/- 17.5 mg] or 12 [69.2 +/- 13.1 mg]). This effect was independent of patient age, weight, or serum T level.\n\nQuestion:\nIs a dopamine D3 receptor genotype associated with hyperandrogenic chronic anovulation and resistant to ovulation induction with clomiphene citrate in female Hispanics?", "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 if dopamine (D3) receptor genotypes are associated with anovulation and response to ovulation induction with clomiphene citrate. Clinical and laboratory characteristics of anovulatory patients and ovulatory controls were compared with findings at the DNA level. An outpatient clinic at an university medical center. One hundred eighty human Hispanic female volunteers (130 of these with documented ovulatory status) were studied. Genomic DNAs were extracted from each patient. Polymerase chain reaction with subsequent restriction digest was performed to analyze the D3 receptor allele status (two possible alleles). Menstrual history, serum T, and midluteal serum Ps from spontaneous and clomiphene cycles were correlated with D3 receptor genotype. Hispanic females with the 22 genotype compared with the other genotypes (11 and 12) were more likely to have irregular menses, an elevated serum T (> or = 70 ng/dL [conversion factor to SI unit, 3.467]), and hyperandrogenic chronic anovulation. These patients tended to be resistant to ovulation induction requiring a significantly higher dose of clomiphene to achieve an ovulatory response (22 genotype [mean +/- SEM] [140.0 +/- 19.0 mg] versus 11 [77.1 +/- 17.5 mg] or 12 [69.2 +/- 13.1 mg]). This effect was independent of patient age, weight, or serum T level.\n\nQuestion:\nIs a dopamine D3 receptor genotype associated with hyperandrogenic chronic anovulation and resistant to ovulation induction with clomiphene citrate in female Hispanics?", "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 if dopamine (D3) receptor genotypes are associated with anovulation and response to ovulation induction with clomiphene citrate. Clinical and laboratory characteristics of anovulatory patients and ovulatory controls were compared with findings at the DNA level. An outpatient clinic at an university medical center. One hundred eighty human Hispanic female volunteers (130 of these with documented ovulatory status) were studied. Genomic DNAs were extracted from each patient. Polymerase chain reaction with subsequent restriction digest was performed to analyze the D3 receptor allele status (two possible alleles). Menstrual history, serum T, and midluteal serum Ps from spontaneous and clomiphene cycles were correlated with D3 receptor genotype. Hispanic females with the 22 genotype compared with the other genotypes (11 and 12) were more likely to have irregular menses, an elevated serum T (> or = 70 ng/dL [conversion factor to SI unit, 3.467]), and hyperandrogenic chronic anovulation. These patients tended to be resistant to ovulation induction requiring a significantly higher dose of clomiphene to achieve an ovulatory response (22 genotype [mean +/- SEM] [140.0 +/- 19.0 mg] versus 11 [77.1 +/- 17.5 mg] or 12 [69.2 +/- 13.1 mg]). This effect was independent of patient age, weight, or serum T level.\n\nQuestion:\nIs a dopamine D3 receptor genotype associated with hyperandrogenic chronic anovulation and resistant to ovulation induction with clomiphene citrate in female Hispanics?", "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:\nCyclooxygenase-2 (COX-2) is an enzyme that catalyses the synthesis of prostaglandins and is over-expressed in a variety of premalignant and malignant conditions. The human embryonic lethal abnormal vision (ELAV)-like protein, HuR, is an mRNA stability protein that can regulate COX-2 expression. Because the regulation of gene expression through the post-transcriptional modification of the mRNA stability is an important mechanism in the control of cellular growth, this study investigated the expression and cellular localisation of the HuR protein and the relationships between COX-2 and HuR in laryngeal epithelium. The expression patterns of HuR and COX-2 in 39 laryngeal squamous cell carcinomas and paired samples of 38 normal and/or 30 dysplastic mucosa adjacent to an infiltrating carcinoma were analysed by immunohistochemistry and compared. An immunohistochemical evaluation of the specimens revealed high nuclear and cytoplasmic immunoreactivity for HuR in 39 (100%) and 26 (66.6%) of 39 lesions with laryngeal squamous cell carcinoma, 27 (90.0%) and one (3.3%) of 30 lesions with epithelial dysplasia, and 19 (50.0%) and 0 (0%) of 38 specimens with normal-appearing laryngeal epithelium, respectively. High levels of COX-2 expression were observed in 66.6% and 6.7% of laryngeal squamous cell carcinoma and epithelial dysplasia, respectively, but no COX-2 expression was detected in the normal epithelium. There was no significant correlation between HuR expression and the other clinicopathological parameters such as age, site, tumour size, or nodal status as well as histological differentiation. There was a statistically significant correlation between COX-2 immunoreactivity and the cytoplasmic HuR expression level in laryngeal squamous cell carcinoma.\n\nQuestion:\nIs cytoplasmic HuR over-expression associated with increased cyclooxygenase-2 expression in laryngeal squamous cell carcinomas?", "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:\nCyclooxygenase-2 (COX-2) is an enzyme that catalyses the synthesis of prostaglandins and is over-expressed in a variety of premalignant and malignant conditions. The human embryonic lethal abnormal vision (ELAV)-like protein, HuR, is an mRNA stability protein that can regulate COX-2 expression. Because the regulation of gene expression through the post-transcriptional modification of the mRNA stability is an important mechanism in the control of cellular growth, this study investigated the expression and cellular localisation of the HuR protein and the relationships between COX-2 and HuR in laryngeal epithelium. The expression patterns of HuR and COX-2 in 39 laryngeal squamous cell carcinomas and paired samples of 38 normal and/or 30 dysplastic mucosa adjacent to an infiltrating carcinoma were analysed by immunohistochemistry and compared. An immunohistochemical evaluation of the specimens revealed high nuclear and cytoplasmic immunoreactivity for HuR in 39 (100%) and 26 (66.6%) of 39 lesions with laryngeal squamous cell carcinoma, 27 (90.0%) and one (3.3%) of 30 lesions with epithelial dysplasia, and 19 (50.0%) and 0 (0%) of 38 specimens with normal-appearing laryngeal epithelium, respectively. High levels of COX-2 expression were observed in 66.6% and 6.7% of laryngeal squamous cell carcinoma and epithelial dysplasia, respectively, but no COX-2 expression was detected in the normal epithelium. There was no significant correlation between HuR expression and the other clinicopathological parameters such as age, site, tumour size, or nodal status as well as histological differentiation. There was a statistically significant correlation between COX-2 immunoreactivity and the cytoplasmic HuR expression level in laryngeal squamous cell carcinoma.\n\nQuestion:\nIs cytoplasmic HuR over-expression associated with increased cyclooxygenase-2 expression in laryngeal squamous cell carcinomas?", "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:\nCyclooxygenase-2 (COX-2) is an enzyme that catalyses the synthesis of prostaglandins and is over-expressed in a variety of premalignant and malignant conditions. The human embryonic lethal abnormal vision (ELAV)-like protein, HuR, is an mRNA stability protein that can regulate COX-2 expression. Because the regulation of gene expression through the post-transcriptional modification of the mRNA stability is an important mechanism in the control of cellular growth, this study investigated the expression and cellular localisation of the HuR protein and the relationships between COX-2 and HuR in laryngeal epithelium. The expression patterns of HuR and COX-2 in 39 laryngeal squamous cell carcinomas and paired samples of 38 normal and/or 30 dysplastic mucosa adjacent to an infiltrating carcinoma were analysed by immunohistochemistry and compared. An immunohistochemical evaluation of the specimens revealed high nuclear and cytoplasmic immunoreactivity for HuR in 39 (100%) and 26 (66.6%) of 39 lesions with laryngeal squamous cell carcinoma, 27 (90.0%) and one (3.3%) of 30 lesions with epithelial dysplasia, and 19 (50.0%) and 0 (0%) of 38 specimens with normal-appearing laryngeal epithelium, respectively. High levels of COX-2 expression were observed in 66.6% and 6.7% of laryngeal squamous cell carcinoma and epithelial dysplasia, respectively, but no COX-2 expression was detected in the normal epithelium. There was no significant correlation between HuR expression and the other clinicopathological parameters such as age, site, tumour size, or nodal status as well as histological differentiation. There was a statistically significant correlation between COX-2 immunoreactivity and the cytoplasmic HuR expression level in laryngeal squamous cell carcinoma.\n\nQuestion:\nIs cytoplasmic HuR over-expression associated with increased cyclooxygenase-2 expression in laryngeal squamous cell carcinomas?", "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:\nSingle chain Fvs (scFvs) are widely applied in research, diagnostics and therapeutic settings. Display and selection from combinatorial libraries is the main route to their discovery and many factors influence the success of this process. They exhibit low thermodynamic stability, resulting in low levels of premature cytosolic folding or aggregation which facilitates sec YEG-mediated translocation and phage in E. coli. However, there is little data analysing how this is related to and influenced by scFv protein expression. We characterised the relationship between overall scFv expression and display propensity for a panel of 15 anti-tetanus toxin scFvs and found a strong positive correlation (Rho = 0.88, p < 0.005) between the two parameters. Display propensity, overall expression and soluble localisation to the periplasm and extracellular fractions were clone specific characteristics which varied despite high levels of sequence homology. There was no correlation between display of scFv or its expression in non-fused (free) form with soluble scFv localisation to the periplasm or culture supernatant. This suggests that divergence in the fate of scFv-pIII and non-fused scFv after translocation to the periplasm accounts for the observed disparity. Differential degrees of periplasmic aggregation of non-fused scFv between clones may affect the partitioning of scFv in the periplasm and culture supernatant abrogating any correlation. We suggest that these factors do not apply to the scFv-pIII fusion since it remains anchored to the bacterial inner membrane as part of the innate phage packaging and budding process.\n\nQuestion:\nDoes single-chain Fv phage display propensity exhibit strong positive correlation with overall expression levels?", "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:\nSingle chain Fvs (scFvs) are widely applied in research, diagnostics and therapeutic settings. Display and selection from combinatorial libraries is the main route to their discovery and many factors influence the success of this process. They exhibit low thermodynamic stability, resulting in low levels of premature cytosolic folding or aggregation which facilitates sec YEG-mediated translocation and phage in E. coli. However, there is little data analysing how this is related to and influenced by scFv protein expression. We characterised the relationship between overall scFv expression and display propensity for a panel of 15 anti-tetanus toxin scFvs and found a strong positive correlation (Rho = 0.88, p < 0.005) between the two parameters. Display propensity, overall expression and soluble localisation to the periplasm and extracellular fractions were clone specific characteristics which varied despite high levels of sequence homology. There was no correlation between display of scFv or its expression in non-fused (free) form with soluble scFv localisation to the periplasm or culture supernatant. This suggests that divergence in the fate of scFv-pIII and non-fused scFv after translocation to the periplasm accounts for the observed disparity. Differential degrees of periplasmic aggregation of non-fused scFv between clones may affect the partitioning of scFv in the periplasm and culture supernatant abrogating any correlation. We suggest that these factors do not apply to the scFv-pIII fusion since it remains anchored to the bacterial inner membrane as part of the innate phage packaging and budding process.\n\nQuestion:\nDoes single-chain Fv phage display propensity exhibit strong positive correlation with overall expression levels?", "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:\nSingle chain Fvs (scFvs) are widely applied in research, diagnostics and therapeutic settings. Display and selection from combinatorial libraries is the main route to their discovery and many factors influence the success of this process. They exhibit low thermodynamic stability, resulting in low levels of premature cytosolic folding or aggregation which facilitates sec YEG-mediated translocation and phage in E. coli. However, there is little data analysing how this is related to and influenced by scFv protein expression. We characterised the relationship between overall scFv expression and display propensity for a panel of 15 anti-tetanus toxin scFvs and found a strong positive correlation (Rho = 0.88, p < 0.005) between the two parameters. Display propensity, overall expression and soluble localisation to the periplasm and extracellular fractions were clone specific characteristics which varied despite high levels of sequence homology. There was no correlation between display of scFv or its expression in non-fused (free) form with soluble scFv localisation to the periplasm or culture supernatant. This suggests that divergence in the fate of scFv-pIII and non-fused scFv after translocation to the periplasm accounts for the observed disparity. Differential degrees of periplasmic aggregation of non-fused scFv between clones may affect the partitioning of scFv in the periplasm and culture supernatant abrogating any correlation. We suggest that these factors do not apply to the scFv-pIII fusion since it remains anchored to the bacterial inner membrane as part of the innate phage packaging and budding process.\n\nQuestion:\nDoes single-chain Fv phage display propensity exhibit strong positive correlation with overall expression levels?", "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:\nSecretoglobin 1A1 (SCGB 1A1), also called Clara cell secretory protein, is the most abundantly secreted protein of the airway. The SCGB1A1 gene has been characterized in mammals as a single copy in the genome. However, analysis of the equine genome suggested that horses might have multiple SCGB1A1 gene copies. Non-ciliated lung epithelial cells produce SCGB 1A1 during inhalation of noxious substances to counter airway inflammation. Airway fluid and lung tissue of horses with recurrent airway obstruction (RAO), a chronic inflammatory lung disease affecting mature horses similar to environmentally induced asthma of humans, have reduced total SCGB 1A1 concentration. Herein, we investigated whether horses have distinct expressed SCGB1A1 genes; whether the transcripts are differentially expressed in tissues and in inflammatory lung disease; and whether there is cell specific protein expression in tissues. We identified three SCGB1A1 gene copies on equine chromosome 12, contained within a 512-kilobase region. Bioinformatic analysis showed that SCGB1A1 genes differ from each other by 8 to 10 nucleotides, and that they code for different proteins. Transcripts were detected for SCGB1A1 and SCGB1A1A, but not for SCGB1A1P. The SCGB1A1P gene had most inter-individual variability and contained a non-sense mutation in many animals, suggesting that SCGB1A1P has evolved into a pseudogene. Analysis of SCGB1A1 and SCGB1A1A sequences by endpoint-limiting dilution PCR identified a consistent difference affecting 3 bp within exon 2, which served as a gene-specific \"signature\". Assessment of gene- and organ-specific expression by semiquantitative RT-PCR of 33 tissues showed strong expression of SCGB1A1 and SCGB1A1A in lung, uterus, Fallopian tube and mammary gland, which correlated with detection of SCGB 1A1 protein by immunohistochemistry. Significantly altered expression of the ratio of SCGB1A1A to SCGB1A1 was detected in RAO-affected animals compared to controls, suggesting different roles for SCGB 1A1 and SCGB 1A1A in this inflammatory condition.\n\nQuestion:\nAre multiple secretoglobin 1A1 genes differentially expressed in horses?", "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:\nSecretoglobin 1A1 (SCGB 1A1), also called Clara cell secretory protein, is the most abundantly secreted protein of the airway. The SCGB1A1 gene has been characterized in mammals as a single copy in the genome. However, analysis of the equine genome suggested that horses might have multiple SCGB1A1 gene copies. Non-ciliated lung epithelial cells produce SCGB 1A1 during inhalation of noxious substances to counter airway inflammation. Airway fluid and lung tissue of horses with recurrent airway obstruction (RAO), a chronic inflammatory lung disease affecting mature horses similar to environmentally induced asthma of humans, have reduced total SCGB 1A1 concentration. Herein, we investigated whether horses have distinct expressed SCGB1A1 genes; whether the transcripts are differentially expressed in tissues and in inflammatory lung disease; and whether there is cell specific protein expression in tissues. We identified three SCGB1A1 gene copies on equine chromosome 12, contained within a 512-kilobase region. Bioinformatic analysis showed that SCGB1A1 genes differ from each other by 8 to 10 nucleotides, and that they code for different proteins. Transcripts were detected for SCGB1A1 and SCGB1A1A, but not for SCGB1A1P. The SCGB1A1P gene had most inter-individual variability and contained a non-sense mutation in many animals, suggesting that SCGB1A1P has evolved into a pseudogene. Analysis of SCGB1A1 and SCGB1A1A sequences by endpoint-limiting dilution PCR identified a consistent difference affecting 3 bp within exon 2, which served as a gene-specific \"signature\". Assessment of gene- and organ-specific expression by semiquantitative RT-PCR of 33 tissues showed strong expression of SCGB1A1 and SCGB1A1A in lung, uterus, Fallopian tube and mammary gland, which correlated with detection of SCGB 1A1 protein by immunohistochemistry. Significantly altered expression of the ratio of SCGB1A1A to SCGB1A1 was detected in RAO-affected animals compared to controls, suggesting different roles for SCGB 1A1 and SCGB 1A1A in this inflammatory condition.\n\nQuestion:\nAre multiple secretoglobin 1A1 genes differentially expressed in horses?", "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:\nSecretoglobin 1A1 (SCGB 1A1), also called Clara cell secretory protein, is the most abundantly secreted protein of the airway. The SCGB1A1 gene has been characterized in mammals as a single copy in the genome. However, analysis of the equine genome suggested that horses might have multiple SCGB1A1 gene copies. Non-ciliated lung epithelial cells produce SCGB 1A1 during inhalation of noxious substances to counter airway inflammation. Airway fluid and lung tissue of horses with recurrent airway obstruction (RAO), a chronic inflammatory lung disease affecting mature horses similar to environmentally induced asthma of humans, have reduced total SCGB 1A1 concentration. Herein, we investigated whether horses have distinct expressed SCGB1A1 genes; whether the transcripts are differentially expressed in tissues and in inflammatory lung disease; and whether there is cell specific protein expression in tissues. We identified three SCGB1A1 gene copies on equine chromosome 12, contained within a 512-kilobase region. Bioinformatic analysis showed that SCGB1A1 genes differ from each other by 8 to 10 nucleotides, and that they code for different proteins. Transcripts were detected for SCGB1A1 and SCGB1A1A, but not for SCGB1A1P. The SCGB1A1P gene had most inter-individual variability and contained a non-sense mutation in many animals, suggesting that SCGB1A1P has evolved into a pseudogene. Analysis of SCGB1A1 and SCGB1A1A sequences by endpoint-limiting dilution PCR identified a consistent difference affecting 3 bp within exon 2, which served as a gene-specific \"signature\". Assessment of gene- and organ-specific expression by semiquantitative RT-PCR of 33 tissues showed strong expression of SCGB1A1 and SCGB1A1A in lung, uterus, Fallopian tube and mammary gland, which correlated with detection of SCGB 1A1 protein by immunohistochemistry. Significantly altered expression of the ratio of SCGB1A1A to SCGB1A1 was detected in RAO-affected animals compared to controls, suggesting different roles for SCGB 1A1 and SCGB 1A1A in this inflammatory condition.\n\nQuestion:\nAre multiple secretoglobin 1A1 genes differentially expressed in horses?", "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 efficacy of the 8-aminoquinoline (8AQ) drug primaquine (PQ) has been historically linked to CYP-mediated metabolism. Although to date no clear evidence exists in the literature that unambiguously assigns the metabolic pathway or specific metabolites necessary for activity, recent literature suggests a role for CYP 2D6 in the generation of redox active metabolites. In the present study, the specific CYP 2D6 inhibitor paroxetine was used to assess its effects on the production of specific phenolic metabolites thought to be involved in PQ efficacy. Further, PQ causal prophylactic (developing liver stage) efficacy against Plasmodium berghei in CYP 2D knockout mice was assessed in comparison with a normal C57 background and with humanized CYP 2D6 mice to determine the direct effects of CYP 2D6 metabolism on PQ activity. PQ exhibited no activity at 20 or 40 mg/kg in CYP 2D knockout mice, compared to 5/5 cures in normal mice at 20 mg/kg. The activity against developing liver stages was partially restored in humanized CYP 2D6 mice.\n\nQuestion:\nIs the metabolism of primaquine to its active metabolite dependent on CYP 2D6?", "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 efficacy of the 8-aminoquinoline (8AQ) drug primaquine (PQ) has been historically linked to CYP-mediated metabolism. Although to date no clear evidence exists in the literature that unambiguously assigns the metabolic pathway or specific metabolites necessary for activity, recent literature suggests a role for CYP 2D6 in the generation of redox active metabolites. In the present study, the specific CYP 2D6 inhibitor paroxetine was used to assess its effects on the production of specific phenolic metabolites thought to be involved in PQ efficacy. Further, PQ causal prophylactic (developing liver stage) efficacy against Plasmodium berghei in CYP 2D knockout mice was assessed in comparison with a normal C57 background and with humanized CYP 2D6 mice to determine the direct effects of CYP 2D6 metabolism on PQ activity. PQ exhibited no activity at 20 or 40 mg/kg in CYP 2D knockout mice, compared to 5/5 cures in normal mice at 20 mg/kg. The activity against developing liver stages was partially restored in humanized CYP 2D6 mice.\n\nQuestion:\nIs the metabolism of primaquine to its active metabolite dependent on CYP 2D6?", "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 efficacy of the 8-aminoquinoline (8AQ) drug primaquine (PQ) has been historically linked to CYP-mediated metabolism. Although to date no clear evidence exists in the literature that unambiguously assigns the metabolic pathway or specific metabolites necessary for activity, recent literature suggests a role for CYP 2D6 in the generation of redox active metabolites. In the present study, the specific CYP 2D6 inhibitor paroxetine was used to assess its effects on the production of specific phenolic metabolites thought to be involved in PQ efficacy. Further, PQ causal prophylactic (developing liver stage) efficacy against Plasmodium berghei in CYP 2D knockout mice was assessed in comparison with a normal C57 background and with humanized CYP 2D6 mice to determine the direct effects of CYP 2D6 metabolism on PQ activity. PQ exhibited no activity at 20 or 40 mg/kg in CYP 2D knockout mice, compared to 5/5 cures in normal mice at 20 mg/kg. The activity against developing liver stages was partially restored in humanized CYP 2D6 mice.\n\nQuestion:\nIs the metabolism of primaquine to its active metabolite dependent on CYP 2D6?", "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 three-wave longitudinal study was twofold. First, prevalence data on alcohol characteristics (e.g., drinks per day, heavy episodic drinking [HED]) were provided for a community sample of middle-aged adults. Aggregate (or group) and individual levels of stability of these characteristics across a 10-year interval were a major focus. Second, an actor-partner interdependence model (APIM) was used to test husbands' and wives' mutual influences on each other's alcohol use. Prospective data were collected from the middle-aged parents of a cohort study that originally targeted adolescents. Three measurement occasions occurred at baseline, 5 years later, and an additional 5 years later. Data from 597 men and 847 women were used to derive prevalence data on alcohol use, and 489 intact marital dyads were used to test spouses' interdependence on alcohol use and HED in the APIMs. The majority of men and women reported alcohol use at each measurement occasion, and the average number of drinks per day was highly similar across time, as was the percentage reporting HED. There was substantial stability at the individual level in the amount of alcohol consumed and HED between waves of measurement. Marital partners had significant but modest effects on each other's alcohol use. Wives had a somewhat greater influence on their husbands' drinking than vice versa.\n\nQuestion:\nDoes a prospective study of alcohol use among middle-aged adults and marital partner influence on drinking?", "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 three-wave longitudinal study was twofold. First, prevalence data on alcohol characteristics (e.g., drinks per day, heavy episodic drinking [HED]) were provided for a community sample of middle-aged adults. Aggregate (or group) and individual levels of stability of these characteristics across a 10-year interval were a major focus. Second, an actor-partner interdependence model (APIM) was used to test husbands' and wives' mutual influences on each other's alcohol use. Prospective data were collected from the middle-aged parents of a cohort study that originally targeted adolescents. Three measurement occasions occurred at baseline, 5 years later, and an additional 5 years later. Data from 597 men and 847 women were used to derive prevalence data on alcohol use, and 489 intact marital dyads were used to test spouses' interdependence on alcohol use and HED in the APIMs. The majority of men and women reported alcohol use at each measurement occasion, and the average number of drinks per day was highly similar across time, as was the percentage reporting HED. There was substantial stability at the individual level in the amount of alcohol consumed and HED between waves of measurement. Marital partners had significant but modest effects on each other's alcohol use. Wives had a somewhat greater influence on their husbands' drinking than vice versa.\n\nQuestion:\nDoes a prospective study of alcohol use among middle-aged adults and marital partner influence on drinking?", "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 three-wave longitudinal study was twofold. First, prevalence data on alcohol characteristics (e.g., drinks per day, heavy episodic drinking [HED]) were provided for a community sample of middle-aged adults. Aggregate (or group) and individual levels of stability of these characteristics across a 10-year interval were a major focus. Second, an actor-partner interdependence model (APIM) was used to test husbands' and wives' mutual influences on each other's alcohol use. Prospective data were collected from the middle-aged parents of a cohort study that originally targeted adolescents. Three measurement occasions occurred at baseline, 5 years later, and an additional 5 years later. Data from 597 men and 847 women were used to derive prevalence data on alcohol use, and 489 intact marital dyads were used to test spouses' interdependence on alcohol use and HED in the APIMs. The majority of men and women reported alcohol use at each measurement occasion, and the average number of drinks per day was highly similar across time, as was the percentage reporting HED. There was substantial stability at the individual level in the amount of alcohol consumed and HED between waves of measurement. Marital partners had significant but modest effects on each other's alcohol use. Wives had a somewhat greater influence on their husbands' drinking than vice versa.\n\nQuestion:\nDoes a prospective study of alcohol use among middle-aged adults and marital partner influence on drinking?", "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 tissue plasminogen activator (t-PA) thrombolysis in patients without major arterial occlusion is effective or safe. Consecutive anterior circulation stroke patients treated with t-PA within 3 h of onset were studied. The patients were divided into three groups according to magnetic resonance angiography findings before t-PA infusion: ICA group, ICA occlusion; MCA group, M1 and M2 occlusion, and no occlusion group. Clinical characteristics, the presence of hemorrhagic transformation on T₂* at 24 h after t-PA thrombolysis, and outcome at 3 months were compared among the three groups. 112 patients were enrolled. The no occlusion group had 21 (18.8%) patients, the ICA group had 29 (25.9%), and the MCA group had 62 (55.4%). The frequency of hemorrhagic transformation was only 4.8% in the no occlusion group (31.0% for the ICA group, and 48.4% for the MCA group, p = 0.0012). At 3 months after t-PA therapy, 61.5% of the no occlusion group had a favorable outcome (modified Rankin score 0-1), which was the highest among the three groups (15.0% for the ICA group, and 41.5% for the MCA group, p = 0.0203).\n\nQuestion:\nDoes intravenous tissue plasminogen activator thrombolysis in patients without major arterial occlusion seem to be safe and effective?", "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 tissue plasminogen activator (t-PA) thrombolysis in patients without major arterial occlusion is effective or safe. Consecutive anterior circulation stroke patients treated with t-PA within 3 h of onset were studied. The patients were divided into three groups according to magnetic resonance angiography findings before t-PA infusion: ICA group, ICA occlusion; MCA group, M1 and M2 occlusion, and no occlusion group. Clinical characteristics, the presence of hemorrhagic transformation on T₂* at 24 h after t-PA thrombolysis, and outcome at 3 months were compared among the three groups. 112 patients were enrolled. The no occlusion group had 21 (18.8%) patients, the ICA group had 29 (25.9%), and the MCA group had 62 (55.4%). The frequency of hemorrhagic transformation was only 4.8% in the no occlusion group (31.0% for the ICA group, and 48.4% for the MCA group, p = 0.0012). At 3 months after t-PA therapy, 61.5% of the no occlusion group had a favorable outcome (modified Rankin score 0-1), which was the highest among the three groups (15.0% for the ICA group, and 41.5% for the MCA group, p = 0.0203).\n\nQuestion:\nDoes intravenous tissue plasminogen activator thrombolysis in patients without major arterial occlusion seem to be safe and effective?", "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 tissue plasminogen activator (t-PA) thrombolysis in patients without major arterial occlusion is effective or safe. Consecutive anterior circulation stroke patients treated with t-PA within 3 h of onset were studied. The patients were divided into three groups according to magnetic resonance angiography findings before t-PA infusion: ICA group, ICA occlusion; MCA group, M1 and M2 occlusion, and no occlusion group. Clinical characteristics, the presence of hemorrhagic transformation on T₂* at 24 h after t-PA thrombolysis, and outcome at 3 months were compared among the three groups. 112 patients were enrolled. The no occlusion group had 21 (18.8%) patients, the ICA group had 29 (25.9%), and the MCA group had 62 (55.4%). The frequency of hemorrhagic transformation was only 4.8% in the no occlusion group (31.0% for the ICA group, and 48.4% for the MCA group, p = 0.0012). At 3 months after t-PA therapy, 61.5% of the no occlusion group had a favorable outcome (modified Rankin score 0-1), which was the highest among the three groups (15.0% for the ICA group, and 41.5% for the MCA group, p = 0.0203).\n\nQuestion:\nDoes intravenous tissue plasminogen activator thrombolysis in patients without major arterial occlusion seem to be safe and effective?", "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 represents a key event in the pathogenesis of Alzheimer's disease (AD). Low circulating concentrations of vitamin E, quantitatively the major lipophilic antioxidant in the brain, are frequently observed in AD patients, suggesting that supplementation with vitamin E may delay the development of AD. To assess the value of therapeutic use of vitamin E in AD. Search of the PubMed and Medline online libraries for relevant English-language publications between 1966 and 2007.\n\nQuestion:\nDo an update on using vitamin E in Alzheimer 's 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:\nOxidative stress represents a key event in the pathogenesis of Alzheimer's disease (AD). Low circulating concentrations of vitamin E, quantitatively the major lipophilic antioxidant in the brain, are frequently observed in AD patients, suggesting that supplementation with vitamin E may delay the development of AD. To assess the value of therapeutic use of vitamin E in AD. Search of the PubMed and Medline online libraries for relevant English-language publications between 1966 and 2007.\n\nQuestion:\nDo an update on using vitamin E in Alzheimer 's 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:\nOxidative stress represents a key event in the pathogenesis of Alzheimer's disease (AD). Low circulating concentrations of vitamin E, quantitatively the major lipophilic antioxidant in the brain, are frequently observed in AD patients, suggesting that supplementation with vitamin E may delay the development of AD. To assess the value of therapeutic use of vitamin E in AD. Search of the PubMed and Medline online libraries for relevant English-language publications between 1966 and 2007.\n\nQuestion:\nDo an update on using vitamin E in Alzheimer 's 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:\nHepatitis B e antigen (HBeAg) status and serum hepatitis B virus (HBV) DNA levels are major factors affecting the prognosis of adult HBV carriers; however, the impact of viral load on long-term outcomes after spontaneous HBeAg seroconversion remains unclear. A total of 390 spontaneous HBeAg seroconverters with a long-term follow-up were enrolled. Serum HBV-DNA levels at 1 year after HBeAg seroconversion were determined, and their correlation with long-term adverse outcomes was explored. In a mean follow-up of 6.8 years, the average annual incidence rates were 4.4% and 1.9% for HBeAg-negative hepatitis and hepatitis flare, respectively. Compared with patients with HBV-DNA levels <200 IU/mL, the adjusted hazard ratios of HBeAg-negative hepatitis were 2.4 (95% confidence interval, 1.3-4.4), 3.6 (1.8-7.2), and 5.3 (2.8-10.0), respectively, for serum HBV-DNA level of 2000 -2 × 10(4), 2 × 10(4) -2 × 10(5), and ≥2 × 10(5) IU/mL. In addition, serum HBV-DNA levels were independently associated with HBeAg-negative hepatitis flare, which confirmed their impact on the immune active hepatitis after HBeAg seroconversion.\n\nQuestion:\nDo serum hepatitis B virus-DNA levels correlate with long-term adverse outcomes in spontaneous hepatitis B e antigen seroconverters?", "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:\nHepatitis B e antigen (HBeAg) status and serum hepatitis B virus (HBV) DNA levels are major factors affecting the prognosis of adult HBV carriers; however, the impact of viral load on long-term outcomes after spontaneous HBeAg seroconversion remains unclear. A total of 390 spontaneous HBeAg seroconverters with a long-term follow-up were enrolled. Serum HBV-DNA levels at 1 year after HBeAg seroconversion were determined, and their correlation with long-term adverse outcomes was explored. In a mean follow-up of 6.8 years, the average annual incidence rates were 4.4% and 1.9% for HBeAg-negative hepatitis and hepatitis flare, respectively. Compared with patients with HBV-DNA levels <200 IU/mL, the adjusted hazard ratios of HBeAg-negative hepatitis were 2.4 (95% confidence interval, 1.3-4.4), 3.6 (1.8-7.2), and 5.3 (2.8-10.0), respectively, for serum HBV-DNA level of 2000 -2 × 10(4), 2 × 10(4) -2 × 10(5), and ≥2 × 10(5) IU/mL. In addition, serum HBV-DNA levels were independently associated with HBeAg-negative hepatitis flare, which confirmed their impact on the immune active hepatitis after HBeAg seroconversion.\n\nQuestion:\nDo serum hepatitis B virus-DNA levels correlate with long-term adverse outcomes in spontaneous hepatitis B e antigen seroconverters?", "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:\nHepatitis B e antigen (HBeAg) status and serum hepatitis B virus (HBV) DNA levels are major factors affecting the prognosis of adult HBV carriers; however, the impact of viral load on long-term outcomes after spontaneous HBeAg seroconversion remains unclear. A total of 390 spontaneous HBeAg seroconverters with a long-term follow-up were enrolled. Serum HBV-DNA levels at 1 year after HBeAg seroconversion were determined, and their correlation with long-term adverse outcomes was explored. In a mean follow-up of 6.8 years, the average annual incidence rates were 4.4% and 1.9% for HBeAg-negative hepatitis and hepatitis flare, respectively. Compared with patients with HBV-DNA levels <200 IU/mL, the adjusted hazard ratios of HBeAg-negative hepatitis were 2.4 (95% confidence interval, 1.3-4.4), 3.6 (1.8-7.2), and 5.3 (2.8-10.0), respectively, for serum HBV-DNA level of 2000 -2 × 10(4), 2 × 10(4) -2 × 10(5), and ≥2 × 10(5) IU/mL. In addition, serum HBV-DNA levels were independently associated with HBeAg-negative hepatitis flare, which confirmed their impact on the immune active hepatitis after HBeAg seroconversion.\n\nQuestion:\nDo serum hepatitis B virus-DNA levels correlate with long-term adverse outcomes in spontaneous hepatitis B e antigen seroconverters?", "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 enhancer of zeste homologue 2 (EZH2) is a catalytic subunit of the polycomb repressive complex 2, a highly conserved histone methyltransferase. EZH2 overexpression has been implicated in various malignancies, including breast cancer, where is associated with poor outcomes. This study aims to clarify nuclear EZH2 expression levels in breast cancers using immunohistochemistry (IHC) and correlate these findings with clinicopathologic variables, including prognostic significance. IHC was performed on tissue microarrays of 432 invasive ductal carcinoma (IDC) tumors. Associations between EZH2 expression, clinicopathologic characteristics, and molecular subtype were retrospectively analyzed. The relationship between EZH2 protein expression in normal breast tissue and ductal carcinoma in situ (DCIS) was also assessed. High EZH2 expression was demonstrated in 215 of 432 tumors (49.8%). EZH2 was more frequently expressed in DCIS and IDC than in normal breast tissue (p=0.001). High EZH2 expression significantly correlated with high histologic grade (p<0.001), large tumor size (p=0.014), advanced pathologic stage (p=0.006), negative estrogen receptor status (p<0.001), positive human epidermal growth factor receptor 2 (HER2) status (p<0.001), high Ki-67 staining index (p<0.001), positive cytokeratin 5/6 status (p=0.003), positive epidermal growth factor receptor status (p<0.001), and positive p53 status (p<0.001). Based on molecular subtypes, high EZH2 expression was significantly associated with HER2-negative luminal B, HER2-positive luminal B, and HER2 type and triple-negative basal cancers (p<0.001). In patients with luminal A, there was a significant trend toward shorter overall survival for those with tumors having high EZH2 expression compared to those with tumors having low EZH2 expression (p=0.045).\n\nQuestion:\nDoes high EZH2 Protein Expression be Associated with Poor Overall Survival in Patients with Luminal A Breast 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:\nThe enhancer of zeste homologue 2 (EZH2) is a catalytic subunit of the polycomb repressive complex 2, a highly conserved histone methyltransferase. EZH2 overexpression has been implicated in various malignancies, including breast cancer, where is associated with poor outcomes. This study aims to clarify nuclear EZH2 expression levels in breast cancers using immunohistochemistry (IHC) and correlate these findings with clinicopathologic variables, including prognostic significance. IHC was performed on tissue microarrays of 432 invasive ductal carcinoma (IDC) tumors. Associations between EZH2 expression, clinicopathologic characteristics, and molecular subtype were retrospectively analyzed. The relationship between EZH2 protein expression in normal breast tissue and ductal carcinoma in situ (DCIS) was also assessed. High EZH2 expression was demonstrated in 215 of 432 tumors (49.8%). EZH2 was more frequently expressed in DCIS and IDC than in normal breast tissue (p=0.001). High EZH2 expression significantly correlated with high histologic grade (p<0.001), large tumor size (p=0.014), advanced pathologic stage (p=0.006), negative estrogen receptor status (p<0.001), positive human epidermal growth factor receptor 2 (HER2) status (p<0.001), high Ki-67 staining index (p<0.001), positive cytokeratin 5/6 status (p=0.003), positive epidermal growth factor receptor status (p<0.001), and positive p53 status (p<0.001). Based on molecular subtypes, high EZH2 expression was significantly associated with HER2-negative luminal B, HER2-positive luminal B, and HER2 type and triple-negative basal cancers (p<0.001). In patients with luminal A, there was a significant trend toward shorter overall survival for those with tumors having high EZH2 expression compared to those with tumors having low EZH2 expression (p=0.045).\n\nQuestion:\nDoes high EZH2 Protein Expression be Associated with Poor Overall Survival in Patients with Luminal A Breast 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:\nThe enhancer of zeste homologue 2 (EZH2) is a catalytic subunit of the polycomb repressive complex 2, a highly conserved histone methyltransferase. EZH2 overexpression has been implicated in various malignancies, including breast cancer, where is associated with poor outcomes. This study aims to clarify nuclear EZH2 expression levels in breast cancers using immunohistochemistry (IHC) and correlate these findings with clinicopathologic variables, including prognostic significance. IHC was performed on tissue microarrays of 432 invasive ductal carcinoma (IDC) tumors. Associations between EZH2 expression, clinicopathologic characteristics, and molecular subtype were retrospectively analyzed. The relationship between EZH2 protein expression in normal breast tissue and ductal carcinoma in situ (DCIS) was also assessed. High EZH2 expression was demonstrated in 215 of 432 tumors (49.8%). EZH2 was more frequently expressed in DCIS and IDC than in normal breast tissue (p=0.001). High EZH2 expression significantly correlated with high histologic grade (p<0.001), large tumor size (p=0.014), advanced pathologic stage (p=0.006), negative estrogen receptor status (p<0.001), positive human epidermal growth factor receptor 2 (HER2) status (p<0.001), high Ki-67 staining index (p<0.001), positive cytokeratin 5/6 status (p=0.003), positive epidermal growth factor receptor status (p<0.001), and positive p53 status (p<0.001). Based on molecular subtypes, high EZH2 expression was significantly associated with HER2-negative luminal B, HER2-positive luminal B, and HER2 type and triple-negative basal cancers (p<0.001). In patients with luminal A, there was a significant trend toward shorter overall survival for those with tumors having high EZH2 expression compared to those with tumors having low EZH2 expression (p=0.045).\n\nQuestion:\nDoes high EZH2 Protein Expression be Associated with Poor Overall Survival in Patients with Luminal A Breast 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:\nIdentifying Hunner lesions in patients with interstitial cystitis/bladder pain syndrome presents an opportunity for objective classification into Hunner lesion interstitial cystitis/bladder pain syndrome (classic interstitial cystitis) and nonHunner lesion bladder pain syndrome. While currently the former diagnosis requires cystoscopy, limited data suggest that these subtypes can be distinguished without endoscopy based on the degree of bladder focused centricity and the infrequent association with generalized pain conditions. Patients in a prospective, single center database of interstitial cystitis/bladder pain syndrome who had documented cystoscopic findings were categorized with Hunner lesion interstitial cystitis/bladder pain syndrome or nonHunner lesion bladder pain syndrome. Demographics, pain and symptom scores, voiding symptoms, irritable bowel syndrome and clinical UPOINT (urinary, psychosocial, organ specific, infection, neurological and tenderness) scoring were comparatively analyzed. We reviewed the records of 469 patients, including 359 with documented local anesthetic cystoscopic findings, 44 (12.3%) with Hunner lesion interstitial cystitis/bladder pain syndrome and 315 (87.7%) with nonHunner bladder pain syndrome. Patients with Hunner lesions were older (p = 0.004) and had greater urinary frequency (p = 0.013), more nocturia (p = 0.0004) and higher ICSI (Interstitial Cystitis Symptom Index) scores (p = 0.017). Hunner lesion prevalence was significantly lower in those younger than 50 years vs those 50 years old or older (7.8% vs 14.9%, p = 0.0095). There was no difference in the number of UPOINT phenotype domains reported, overall UPOINT scores or the prevalence of irritable bowel syndrome between the groups.\n\nQuestion:\nDoes clinical Phenotyping Differentiate Hunner Lesion Subtype of Interstitial Cystitis/Bladder Pain Syndrome : A Relook at the Role of Cystoscopy?", "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:\nIdentifying Hunner lesions in patients with interstitial cystitis/bladder pain syndrome presents an opportunity for objective classification into Hunner lesion interstitial cystitis/bladder pain syndrome (classic interstitial cystitis) and nonHunner lesion bladder pain syndrome. While currently the former diagnosis requires cystoscopy, limited data suggest that these subtypes can be distinguished without endoscopy based on the degree of bladder focused centricity and the infrequent association with generalized pain conditions. Patients in a prospective, single center database of interstitial cystitis/bladder pain syndrome who had documented cystoscopic findings were categorized with Hunner lesion interstitial cystitis/bladder pain syndrome or nonHunner lesion bladder pain syndrome. Demographics, pain and symptom scores, voiding symptoms, irritable bowel syndrome and clinical UPOINT (urinary, psychosocial, organ specific, infection, neurological and tenderness) scoring were comparatively analyzed. We reviewed the records of 469 patients, including 359 with documented local anesthetic cystoscopic findings, 44 (12.3%) with Hunner lesion interstitial cystitis/bladder pain syndrome and 315 (87.7%) with nonHunner bladder pain syndrome. Patients with Hunner lesions were older (p = 0.004) and had greater urinary frequency (p = 0.013), more nocturia (p = 0.0004) and higher ICSI (Interstitial Cystitis Symptom Index) scores (p = 0.017). Hunner lesion prevalence was significantly lower in those younger than 50 years vs those 50 years old or older (7.8% vs 14.9%, p = 0.0095). There was no difference in the number of UPOINT phenotype domains reported, overall UPOINT scores or the prevalence of irritable bowel syndrome between the groups.\n\nQuestion:\nDoes clinical Phenotyping Differentiate Hunner Lesion Subtype of Interstitial Cystitis/Bladder Pain Syndrome : A Relook at the Role of Cystoscopy?", "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:\nIdentifying Hunner lesions in patients with interstitial cystitis/bladder pain syndrome presents an opportunity for objective classification into Hunner lesion interstitial cystitis/bladder pain syndrome (classic interstitial cystitis) and nonHunner lesion bladder pain syndrome. While currently the former diagnosis requires cystoscopy, limited data suggest that these subtypes can be distinguished without endoscopy based on the degree of bladder focused centricity and the infrequent association with generalized pain conditions. Patients in a prospective, single center database of interstitial cystitis/bladder pain syndrome who had documented cystoscopic findings were categorized with Hunner lesion interstitial cystitis/bladder pain syndrome or nonHunner lesion bladder pain syndrome. Demographics, pain and symptom scores, voiding symptoms, irritable bowel syndrome and clinical UPOINT (urinary, psychosocial, organ specific, infection, neurological and tenderness) scoring were comparatively analyzed. We reviewed the records of 469 patients, including 359 with documented local anesthetic cystoscopic findings, 44 (12.3%) with Hunner lesion interstitial cystitis/bladder pain syndrome and 315 (87.7%) with nonHunner bladder pain syndrome. Patients with Hunner lesions were older (p = 0.004) and had greater urinary frequency (p = 0.013), more nocturia (p = 0.0004) and higher ICSI (Interstitial Cystitis Symptom Index) scores (p = 0.017). Hunner lesion prevalence was significantly lower in those younger than 50 years vs those 50 years old or older (7.8% vs 14.9%, p = 0.0095). There was no difference in the number of UPOINT phenotype domains reported, overall UPOINT scores or the prevalence of irritable bowel syndrome between the groups.\n\nQuestion:\nDoes clinical Phenotyping Differentiate Hunner Lesion Subtype of Interstitial Cystitis/Bladder Pain Syndrome : A Relook at the Role of Cystoscopy?", "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:\nThrombogenicity associated with the induction of leukocyte procoagulant activity (PCA) is a common complication in sepsis and cancer. Since nanoparticles are increasingly used for drug delivery, their interaction with coagulation systems is an important part of the safety assessment. The purpose of this study was to investigate the effects of nanoparticle physicochemical properties on leukocyte PCA, and to get insight into the mechanism of PCA induction. A total of 12 formulations of polyamidoamine (PAMAM) dendrimers, varying in size and surface charge, were studied in vitro using recalcification time assay. Irrespective of their size, anionic and neutral dendrimers did not induce leukocyte PCA in vitro. Cationic particles induced PCA in a size- and charge-dependent manner. The mechanism of PCA induction was similar to that of doxorubicin. Cationic dendrimers were also found to exacerbate endotoxin-induced PCA.\n\nQuestion:\nDoes dendrimer-induced leukocyte procoagulant activity depend on particle size and surface charge?", "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:\nThrombogenicity associated with the induction of leukocyte procoagulant activity (PCA) is a common complication in sepsis and cancer. Since nanoparticles are increasingly used for drug delivery, their interaction with coagulation systems is an important part of the safety assessment. The purpose of this study was to investigate the effects of nanoparticle physicochemical properties on leukocyte PCA, and to get insight into the mechanism of PCA induction. A total of 12 formulations of polyamidoamine (PAMAM) dendrimers, varying in size and surface charge, were studied in vitro using recalcification time assay. Irrespective of their size, anionic and neutral dendrimers did not induce leukocyte PCA in vitro. Cationic particles induced PCA in a size- and charge-dependent manner. The mechanism of PCA induction was similar to that of doxorubicin. Cationic dendrimers were also found to exacerbate endotoxin-induced PCA.\n\nQuestion:\nDoes dendrimer-induced leukocyte procoagulant activity depend on particle size and surface charge?", "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:\nThrombogenicity associated with the induction of leukocyte procoagulant activity (PCA) is a common complication in sepsis and cancer. Since nanoparticles are increasingly used for drug delivery, their interaction with coagulation systems is an important part of the safety assessment. The purpose of this study was to investigate the effects of nanoparticle physicochemical properties on leukocyte PCA, and to get insight into the mechanism of PCA induction. A total of 12 formulations of polyamidoamine (PAMAM) dendrimers, varying in size and surface charge, were studied in vitro using recalcification time assay. Irrespective of their size, anionic and neutral dendrimers did not induce leukocyte PCA in vitro. Cationic particles induced PCA in a size- and charge-dependent manner. The mechanism of PCA induction was similar to that of doxorubicin. Cationic dendrimers were also found to exacerbate endotoxin-induced PCA.\n\nQuestion:\nDoes dendrimer-induced leukocyte procoagulant activity depend on particle size and surface charge?", "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:\nMechanical injury to the skin by scratching is an important feature of atopic dermatitis (AD). To investigate the role of COX-2 in allergic skin inflammation elicited by epicutaneous (EC) sensitization via introduction of ovalbumin through shaved tape-stripped skin. COX-2 mRNA was measured by quantitative PCR, and COX-2 protein was measured by Western blotting. We investigated the effect of administration of the COX-2 selective inhibitor NS-398 during EC sensitization with ovalbumin in a mouse model of AD characterized by eosinophil skin infiltration, elevated total and antigen specific IgE, and a systemic TH2 response to antigen. We further examined the response of COX-2-deficient mice to EC immunization with ovalbumin. Tape stripping caused a transient increase in skin COX-2 mRNA. In contrast, COX-2 mRNA was not increased after ovalbumin sensitization. Infiltration by eosinophils and expression of IL-4 mRNA in ovalbumin-sensitized skin sites, ovalbumin specific IgE and IgG1 antibody responses, and IL-4 secretion by splenocytes after ovalbumin stimulation were all significantly increased in EC mice that received NS-398. In contrast, ovalbumin specific IgG 2a antibody response and IFN-gamma secretion by splenocytes after ovalbumin stimulation were significantly decreased in these mice. COX-2-deficient mice also exhibited an enhanced systemic TH2 response to EC sensitization.\n\nQuestion:\nDoes cOX-2 inhibition enhance the TH2 immune response to epicutaneous sensitization?", "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:\nMechanical injury to the skin by scratching is an important feature of atopic dermatitis (AD). To investigate the role of COX-2 in allergic skin inflammation elicited by epicutaneous (EC) sensitization via introduction of ovalbumin through shaved tape-stripped skin. COX-2 mRNA was measured by quantitative PCR, and COX-2 protein was measured by Western blotting. We investigated the effect of administration of the COX-2 selective inhibitor NS-398 during EC sensitization with ovalbumin in a mouse model of AD characterized by eosinophil skin infiltration, elevated total and antigen specific IgE, and a systemic TH2 response to antigen. We further examined the response of COX-2-deficient mice to EC immunization with ovalbumin. Tape stripping caused a transient increase in skin COX-2 mRNA. In contrast, COX-2 mRNA was not increased after ovalbumin sensitization. Infiltration by eosinophils and expression of IL-4 mRNA in ovalbumin-sensitized skin sites, ovalbumin specific IgE and IgG1 antibody responses, and IL-4 secretion by splenocytes after ovalbumin stimulation were all significantly increased in EC mice that received NS-398. In contrast, ovalbumin specific IgG 2a antibody response and IFN-gamma secretion by splenocytes after ovalbumin stimulation were significantly decreased in these mice. COX-2-deficient mice also exhibited an enhanced systemic TH2 response to EC sensitization.\n\nQuestion:\nDoes cOX-2 inhibition enhance the TH2 immune response to epicutaneous sensitization?", "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:\nMechanical injury to the skin by scratching is an important feature of atopic dermatitis (AD). To investigate the role of COX-2 in allergic skin inflammation elicited by epicutaneous (EC) sensitization via introduction of ovalbumin through shaved tape-stripped skin. COX-2 mRNA was measured by quantitative PCR, and COX-2 protein was measured by Western blotting. We investigated the effect of administration of the COX-2 selective inhibitor NS-398 during EC sensitization with ovalbumin in a mouse model of AD characterized by eosinophil skin infiltration, elevated total and antigen specific IgE, and a systemic TH2 response to antigen. We further examined the response of COX-2-deficient mice to EC immunization with ovalbumin. Tape stripping caused a transient increase in skin COX-2 mRNA. In contrast, COX-2 mRNA was not increased after ovalbumin sensitization. Infiltration by eosinophils and expression of IL-4 mRNA in ovalbumin-sensitized skin sites, ovalbumin specific IgE and IgG1 antibody responses, and IL-4 secretion by splenocytes after ovalbumin stimulation were all significantly increased in EC mice that received NS-398. In contrast, ovalbumin specific IgG 2a antibody response and IFN-gamma secretion by splenocytes after ovalbumin stimulation were significantly decreased in these mice. COX-2-deficient mice also exhibited an enhanced systemic TH2 response to EC sensitization.\n\nQuestion:\nDoes cOX-2 inhibition enhance the TH2 immune response to epicutaneous sensitization?", "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 whether weight loss could reverse excessive sleep in high-fat diet-induced obesity. Three groups of mice participated in the study. A weight gain/loss group was fed with high-fat food for 6 weeks (weight gain), and regular food again for 4 weeks (weight loss). A control group and a weight gain only group were fed with regular food and high-fat food, respectively, for 10 weeks after the baseline. Adult male C57BL/6 mice. The amounts of wake, rapid eye movement sleep (REMS) and non-REM sleep (NREMS) were determined at week 0 (baseline), week 6, and week 10. The weight gain/loss group displayed a significant decrease in wakefulness and increases in NREMS and episodes of NREMS during 6 weeks of weight gain, which were reversed during subsequent 4 weeks of weight loss. The weight gain only group displayed significant decrease in wakefulness and increase of NREMS and REMS at both week 6 and week 10. The control group did not show significant sleep alterations during the experiment.\n\nQuestion:\nIs sleep increased by weight gain and decreased by weight loss 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:\nTo determine whether weight loss could reverse excessive sleep in high-fat diet-induced obesity. Three groups of mice participated in the study. A weight gain/loss group was fed with high-fat food for 6 weeks (weight gain), and regular food again for 4 weeks (weight loss). A control group and a weight gain only group were fed with regular food and high-fat food, respectively, for 10 weeks after the baseline. Adult male C57BL/6 mice. The amounts of wake, rapid eye movement sleep (REMS) and non-REM sleep (NREMS) were determined at week 0 (baseline), week 6, and week 10. The weight gain/loss group displayed a significant decrease in wakefulness and increases in NREMS and episodes of NREMS during 6 weeks of weight gain, which were reversed during subsequent 4 weeks of weight loss. The weight gain only group displayed significant decrease in wakefulness and increase of NREMS and REMS at both week 6 and week 10. The control group did not show significant sleep alterations during the experiment.\n\nQuestion:\nIs sleep increased by weight gain and decreased by weight loss 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:\nTo determine whether weight loss could reverse excessive sleep in high-fat diet-induced obesity. Three groups of mice participated in the study. A weight gain/loss group was fed with high-fat food for 6 weeks (weight gain), and regular food again for 4 weeks (weight loss). A control group and a weight gain only group were fed with regular food and high-fat food, respectively, for 10 weeks after the baseline. Adult male C57BL/6 mice. The amounts of wake, rapid eye movement sleep (REMS) and non-REM sleep (NREMS) were determined at week 0 (baseline), week 6, and week 10. The weight gain/loss group displayed a significant decrease in wakefulness and increases in NREMS and episodes of NREMS during 6 weeks of weight gain, which were reversed during subsequent 4 weeks of weight loss. The weight gain only group displayed significant decrease in wakefulness and increase of NREMS and REMS at both week 6 and week 10. The control group did not show significant sleep alterations during the experiment.\n\nQuestion:\nIs sleep increased by weight gain and decreased by weight loss 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:\nAs EPO treatment of chronic anemia of advanced renal disease is now the standard of care we examined if such treatment may slow the progression of renal function decline. Data of 18 pre-ESRD patients were analyzed retrospectively 12 months prior and prospectively 12 months after the initiation of EPO. Mean creatinine was 5.0 +/- 1.8 mg/dL (Mean +/- SEM) when starting EPO at a weekly dose of 5000 +/- 500 units once the hematocrit was below 30 %. EPO dose was titrated monthly for a hematocrit between 33.0% and 37.0%. Metabolic complications and hypertension were controlled. At month_0 the average blood pressure was 148/76 +/- 5/4 mmHg and at month_12 it was 145/73 +/- 6/3 mmHg (p = 0.75 by 2 tailed paired Student's t test). 12/18 patients were on an ACE-i or ARB before month_0 and 14/18 were on it after (p = 0.71 by Fisher's 2 tailed exact test). The average hematocrit rose from 26.9% +/- 0.6 to 33.1 % +/- 0.1. When linear regression analysis was applied to pre- and post-EPO 1/creatinine data the mean rate of decline was -0.0140 +/- 0.0119 (mean +/- SD) and -0.0017 +/- 0.0090 (non-parametric Wilcoxon matched pairs signed rank sum test: Z value: -2.91; P = 0.004) respectively. 5/18 patients did not require dialysis 12 months after starting EPO (month_0).\n\nQuestion:\nDoes r.hu-erythropoietin ( EPO ) treatment of pre-ESRD patients slow the rate of progression of renal decline?", "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:\nAs EPO treatment of chronic anemia of advanced renal disease is now the standard of care we examined if such treatment may slow the progression of renal function decline. Data of 18 pre-ESRD patients were analyzed retrospectively 12 months prior and prospectively 12 months after the initiation of EPO. Mean creatinine was 5.0 +/- 1.8 mg/dL (Mean +/- SEM) when starting EPO at a weekly dose of 5000 +/- 500 units once the hematocrit was below 30 %. EPO dose was titrated monthly for a hematocrit between 33.0% and 37.0%. Metabolic complications and hypertension were controlled. At month_0 the average blood pressure was 148/76 +/- 5/4 mmHg and at month_12 it was 145/73 +/- 6/3 mmHg (p = 0.75 by 2 tailed paired Student's t test). 12/18 patients were on an ACE-i or ARB before month_0 and 14/18 were on it after (p = 0.71 by Fisher's 2 tailed exact test). The average hematocrit rose from 26.9% +/- 0.6 to 33.1 % +/- 0.1. When linear regression analysis was applied to pre- and post-EPO 1/creatinine data the mean rate of decline was -0.0140 +/- 0.0119 (mean +/- SD) and -0.0017 +/- 0.0090 (non-parametric Wilcoxon matched pairs signed rank sum test: Z value: -2.91; P = 0.004) respectively. 5/18 patients did not require dialysis 12 months after starting EPO (month_0).\n\nQuestion:\nDoes r.hu-erythropoietin ( EPO ) treatment of pre-ESRD patients slow the rate of progression of renal decline?", "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:\nAs EPO treatment of chronic anemia of advanced renal disease is now the standard of care we examined if such treatment may slow the progression of renal function decline. Data of 18 pre-ESRD patients were analyzed retrospectively 12 months prior and prospectively 12 months after the initiation of EPO. Mean creatinine was 5.0 +/- 1.8 mg/dL (Mean +/- SEM) when starting EPO at a weekly dose of 5000 +/- 500 units once the hematocrit was below 30 %. EPO dose was titrated monthly for a hematocrit between 33.0% and 37.0%. Metabolic complications and hypertension were controlled. At month_0 the average blood pressure was 148/76 +/- 5/4 mmHg and at month_12 it was 145/73 +/- 6/3 mmHg (p = 0.75 by 2 tailed paired Student's t test). 12/18 patients were on an ACE-i or ARB before month_0 and 14/18 were on it after (p = 0.71 by Fisher's 2 tailed exact test). The average hematocrit rose from 26.9% +/- 0.6 to 33.1 % +/- 0.1. When linear regression analysis was applied to pre- and post-EPO 1/creatinine data the mean rate of decline was -0.0140 +/- 0.0119 (mean +/- SD) and -0.0017 +/- 0.0090 (non-parametric Wilcoxon matched pairs signed rank sum test: Z value: -2.91; P = 0.004) respectively. 5/18 patients did not require dialysis 12 months after starting EPO (month_0).\n\nQuestion:\nDoes r.hu-erythropoietin ( EPO ) treatment of pre-ESRD patients slow the rate of progression of renal decline?", "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 has been suggested that modestly elevated circulating D-dimer values may be associated with acute ischemic stroke (AIS). Thus, the purpose of this study was to investigate the association between plasma D-dimer level at admission and AIS in Chinese population. In a prospective observational study, plasma D-dimer levels were measured using a particle-enhanced, immunoturbidimetric assay on admission in 240 Chinese patients with AIS. The National Institutes of Health Stroke Scale (NIHSS) score was assessed on admission blinded to D-dimer levels. Plasma median D-dimer levels were significantly (P = 0.000) higher in AIS patients as compared to healthy controls (0.88; interquartiler range [IQR], 0.28-2.11 mg/L and 0.31; IQR, 0.17-0.74 mg/L). D-dimer levels increased with increasing severity of stroke as defined by the NIHSS score(r = 0.179, p = 0.005) and infarct volume(r = 0.425, p = 0.000). Those positive trends still existed even after correcting for possible confounding factors (P = 0.012, 0.000; respectively). Based on the Receiver operating characteristic (ROC) curve, the optimal cut-off value of plasma D-dimer levels as an indicator for diagnosis of cardioembolic strokes was projected to be 0.91 mg/L, which yielded a sensitivity of 83.7% and a specificity of 81.5%, the area under the curve was 0.862(95% confidence interval [CI], 0.811-0.912).\n\nQuestion:\nAre plasma D-dimer levels associated with stroke subtypes and infarction volume in patients with acute ischemic stroke?", "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 has been suggested that modestly elevated circulating D-dimer values may be associated with acute ischemic stroke (AIS). Thus, the purpose of this study was to investigate the association between plasma D-dimer level at admission and AIS in Chinese population. In a prospective observational study, plasma D-dimer levels were measured using a particle-enhanced, immunoturbidimetric assay on admission in 240 Chinese patients with AIS. The National Institutes of Health Stroke Scale (NIHSS) score was assessed on admission blinded to D-dimer levels. Plasma median D-dimer levels were significantly (P = 0.000) higher in AIS patients as compared to healthy controls (0.88; interquartiler range [IQR], 0.28-2.11 mg/L and 0.31; IQR, 0.17-0.74 mg/L). D-dimer levels increased with increasing severity of stroke as defined by the NIHSS score(r = 0.179, p = 0.005) and infarct volume(r = 0.425, p = 0.000). Those positive trends still existed even after correcting for possible confounding factors (P = 0.012, 0.000; respectively). Based on the Receiver operating characteristic (ROC) curve, the optimal cut-off value of plasma D-dimer levels as an indicator for diagnosis of cardioembolic strokes was projected to be 0.91 mg/L, which yielded a sensitivity of 83.7% and a specificity of 81.5%, the area under the curve was 0.862(95% confidence interval [CI], 0.811-0.912).\n\nQuestion:\nAre plasma D-dimer levels associated with stroke subtypes and infarction volume in patients with acute ischemic stroke?", "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 has been suggested that modestly elevated circulating D-dimer values may be associated with acute ischemic stroke (AIS). Thus, the purpose of this study was to investigate the association between plasma D-dimer level at admission and AIS in Chinese population. In a prospective observational study, plasma D-dimer levels were measured using a particle-enhanced, immunoturbidimetric assay on admission in 240 Chinese patients with AIS. The National Institutes of Health Stroke Scale (NIHSS) score was assessed on admission blinded to D-dimer levels. Plasma median D-dimer levels were significantly (P = 0.000) higher in AIS patients as compared to healthy controls (0.88; interquartiler range [IQR], 0.28-2.11 mg/L and 0.31; IQR, 0.17-0.74 mg/L). D-dimer levels increased with increasing severity of stroke as defined by the NIHSS score(r = 0.179, p = 0.005) and infarct volume(r = 0.425, p = 0.000). Those positive trends still existed even after correcting for possible confounding factors (P = 0.012, 0.000; respectively). Based on the Receiver operating characteristic (ROC) curve, the optimal cut-off value of plasma D-dimer levels as an indicator for diagnosis of cardioembolic strokes was projected to be 0.91 mg/L, which yielded a sensitivity of 83.7% and a specificity of 81.5%, the area under the curve was 0.862(95% confidence interval [CI], 0.811-0.912).\n\nQuestion:\nAre plasma D-dimer levels associated with stroke subtypes and infarction volume in patients with acute ischemic stroke?", "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:\nDietary modifications may play an important role in the prevention of diabetes. We aimed to assess the temporal association between diet quality and both impaired fasting glucose and Type 2 diabetes among older adults. A total of 2564 participants aged 49+ years at baseline were examined between 1992 and 1994 and 2002-2004 and had their fasting blood glucose measured. Dietary data were collected using a semi-quantitative food frequency questionnaire. A modified version of the Healthy Eating Index for Australians was developed to determine Total Diet Score. Incident diabetes (or impaired fasting glucose) was defined in participants at risk who were newly diagnosed by a physician during the follow-up or found to have a fasting blood glucose level ≥ 7.0 mmol/l (or 6.1-6.9 mmol/l). After adjusting for age, sex, current smoking, body mass index, hypertension and serum triglycerides, comparing highest with lowest tertile of total diet score, a significant 75% decrease in risk of incident impaired fasting glucose was observed in men (P(trend) = 0.02). Also, in men, each two-point increase in Total Diet Score was associated with a 52% reduction in the 10-year incidence of impaired fasting glucose, (OR 0.48, 95% CI 0.33-0.69). No significant associations were observed among women or with the 10-year incidence of diabetes.\n\nQuestion:\nIs diet quality prospectively associated with incident impaired fasting glucose in older adults?", "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:\nDietary modifications may play an important role in the prevention of diabetes. We aimed to assess the temporal association between diet quality and both impaired fasting glucose and Type 2 diabetes among older adults. A total of 2564 participants aged 49+ years at baseline were examined between 1992 and 1994 and 2002-2004 and had their fasting blood glucose measured. Dietary data were collected using a semi-quantitative food frequency questionnaire. A modified version of the Healthy Eating Index for Australians was developed to determine Total Diet Score. Incident diabetes (or impaired fasting glucose) was defined in participants at risk who were newly diagnosed by a physician during the follow-up or found to have a fasting blood glucose level ≥ 7.0 mmol/l (or 6.1-6.9 mmol/l). After adjusting for age, sex, current smoking, body mass index, hypertension and serum triglycerides, comparing highest with lowest tertile of total diet score, a significant 75% decrease in risk of incident impaired fasting glucose was observed in men (P(trend) = 0.02). Also, in men, each two-point increase in Total Diet Score was associated with a 52% reduction in the 10-year incidence of impaired fasting glucose, (OR 0.48, 95% CI 0.33-0.69). No significant associations were observed among women or with the 10-year incidence of diabetes.\n\nQuestion:\nIs diet quality prospectively associated with incident impaired fasting glucose in older adults?", "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:\nDietary modifications may play an important role in the prevention of diabetes. We aimed to assess the temporal association between diet quality and both impaired fasting glucose and Type 2 diabetes among older adults. A total of 2564 participants aged 49+ years at baseline were examined between 1992 and 1994 and 2002-2004 and had their fasting blood glucose measured. Dietary data were collected using a semi-quantitative food frequency questionnaire. A modified version of the Healthy Eating Index for Australians was developed to determine Total Diet Score. Incident diabetes (or impaired fasting glucose) was defined in participants at risk who were newly diagnosed by a physician during the follow-up or found to have a fasting blood glucose level ≥ 7.0 mmol/l (or 6.1-6.9 mmol/l). After adjusting for age, sex, current smoking, body mass index, hypertension and serum triglycerides, comparing highest with lowest tertile of total diet score, a significant 75% decrease in risk of incident impaired fasting glucose was observed in men (P(trend) = 0.02). Also, in men, each two-point increase in Total Diet Score was associated with a 52% reduction in the 10-year incidence of impaired fasting glucose, (OR 0.48, 95% CI 0.33-0.69). No significant associations were observed among women or with the 10-year incidence of diabetes.\n\nQuestion:\nIs diet quality prospectively associated with incident impaired fasting glucose in older adults?", "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:\nElectroacupuncture (EA) is reported to be an effective treatment for obesity, but its mechanism is unclear. This study aimed to investigate the relationship between hypothalamic LKB1-AMPK-ACC signaling and EA. Fifty male Sprague-Dawley rats were divided into two groups fed either chow (chow-fed group) or high-fat diet (HF group). After 4 weeks of feeding, obese rats in the HF group (defined as weighing 20% or more than rats in the chow-fed group) were randomly allocated into an EA or Diet-induced obesity (DIO) group. The EA group was given EA on bilateral ST25-ST36 for 4 weeks, while the DIO group received no further intervention. Body weight of the chow-fed, DIO, and EA groups were measured weekly. mRNA and protein levels of the hypothalamic LKB1-AMPK-ACC signaling pathway were detected using real-time (RT)-PCR and western blot, respectively. After 4 weeks of EA treatment, the weight growth trend of rats in the EA group was inhibited compared with those in the DIO group. RT-PCR and western blotting showed that EA upregulated the transcription of Adenosine 5'-monophosphate-activated protein kinase α2 (AMPKα2), promoted protein expression of Liver kinase B1 (LKB1) and AMPKα1, and inhibited acetyl-CoA carboxylase (ACC) protein expression in the hypothalamus.\n\nQuestion:\nDoes electroacupuncture inhibit weight gain in diet-induced obese rats by activating hypothalamic LKB1-AMPK 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:\nElectroacupuncture (EA) is reported to be an effective treatment for obesity, but its mechanism is unclear. This study aimed to investigate the relationship between hypothalamic LKB1-AMPK-ACC signaling and EA. Fifty male Sprague-Dawley rats were divided into two groups fed either chow (chow-fed group) or high-fat diet (HF group). After 4 weeks of feeding, obese rats in the HF group (defined as weighing 20% or more than rats in the chow-fed group) were randomly allocated into an EA or Diet-induced obesity (DIO) group. The EA group was given EA on bilateral ST25-ST36 for 4 weeks, while the DIO group received no further intervention. Body weight of the chow-fed, DIO, and EA groups were measured weekly. mRNA and protein levels of the hypothalamic LKB1-AMPK-ACC signaling pathway were detected using real-time (RT)-PCR and western blot, respectively. After 4 weeks of EA treatment, the weight growth trend of rats in the EA group was inhibited compared with those in the DIO group. RT-PCR and western blotting showed that EA upregulated the transcription of Adenosine 5'-monophosphate-activated protein kinase α2 (AMPKα2), promoted protein expression of Liver kinase B1 (LKB1) and AMPKα1, and inhibited acetyl-CoA carboxylase (ACC) protein expression in the hypothalamus.\n\nQuestion:\nDoes electroacupuncture inhibit weight gain in diet-induced obese rats by activating hypothalamic LKB1-AMPK 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:\nElectroacupuncture (EA) is reported to be an effective treatment for obesity, but its mechanism is unclear. This study aimed to investigate the relationship between hypothalamic LKB1-AMPK-ACC signaling and EA. Fifty male Sprague-Dawley rats were divided into two groups fed either chow (chow-fed group) or high-fat diet (HF group). After 4 weeks of feeding, obese rats in the HF group (defined as weighing 20% or more than rats in the chow-fed group) were randomly allocated into an EA or Diet-induced obesity (DIO) group. The EA group was given EA on bilateral ST25-ST36 for 4 weeks, while the DIO group received no further intervention. Body weight of the chow-fed, DIO, and EA groups were measured weekly. mRNA and protein levels of the hypothalamic LKB1-AMPK-ACC signaling pathway were detected using real-time (RT)-PCR and western blot, respectively. After 4 weeks of EA treatment, the weight growth trend of rats in the EA group was inhibited compared with those in the DIO group. RT-PCR and western blotting showed that EA upregulated the transcription of Adenosine 5'-monophosphate-activated protein kinase α2 (AMPKα2), promoted protein expression of Liver kinase B1 (LKB1) and AMPKα1, and inhibited acetyl-CoA carboxylase (ACC) protein expression in the hypothalamus.\n\nQuestion:\nDoes electroacupuncture inhibit weight gain in diet-induced obese rats by activating hypothalamic LKB1-AMPK 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 esophagus of blood-feeding schistosomes has been largely neglected although its posterior portion was designated as a gland decades ago. However, we recently showed it plays a pivotal role in blood processing. It is clearly demarcated into anterior and posterior compartments, both surrounded by a mass of cell bodies. Feeding movies revealed that erythrocytes accumulate in the anterior compartment before entering the posterior, indicating that a distinct process is executed there. We therefore investigated ultrastructural aspects and possible functions of the anterior region. The heads of adult Schistosoma japonicum were detached and prepared for both transmission and scanning electron microscopy to define the detailed ultrastructure of the anterior esophagus. Cryosections of heads were also prepared for immunocytochemistry and confocal microscopy to define the pattern of intrinsic host antibody binding in the anterior esophageal lining. The anterior syncytial lining of the esophagus is highly extended by long, thin corrugations of cytoplasm projecting towards the lumen. Strikingly in the male worm, the tips of the corrugations are further expanded by numerous threads of cytoplasm, producing a spaghetti-like appearance in the central lumen. Flattened, pitted cytoplasmic plates are interspersed in the tangled mass of threads. Abundant, morphologically distinct light vesicles of varied size and contents are manufactured in the cell bodies, from where they traffic through cytoplasmic connections to the corrugations and out to the tips. Clusters of vesicles accumulate in expanded tips in males, together with occasional mitochondria whilst females have more mitochondria but fewer vesicles. The membranous contents of light vesicles are secreted mainly from the tips, but also from the sides of the corrugations. They coat the surfaces and then form organised self-adherent membrane figures when shed into the lumen. Host antibody binds strongly in a characteristic pattern to the anterior esophageal lining indicating that the secretions are highly immunogenic.\n\nQuestion:\nIs the anterior esophageal region of Schistosoma japonicum a secretory organ?", "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 esophagus of blood-feeding schistosomes has been largely neglected although its posterior portion was designated as a gland decades ago. However, we recently showed it plays a pivotal role in blood processing. It is clearly demarcated into anterior and posterior compartments, both surrounded by a mass of cell bodies. Feeding movies revealed that erythrocytes accumulate in the anterior compartment before entering the posterior, indicating that a distinct process is executed there. We therefore investigated ultrastructural aspects and possible functions of the anterior region. The heads of adult Schistosoma japonicum were detached and prepared for both transmission and scanning electron microscopy to define the detailed ultrastructure of the anterior esophagus. Cryosections of heads were also prepared for immunocytochemistry and confocal microscopy to define the pattern of intrinsic host antibody binding in the anterior esophageal lining. The anterior syncytial lining of the esophagus is highly extended by long, thin corrugations of cytoplasm projecting towards the lumen. Strikingly in the male worm, the tips of the corrugations are further expanded by numerous threads of cytoplasm, producing a spaghetti-like appearance in the central lumen. Flattened, pitted cytoplasmic plates are interspersed in the tangled mass of threads. Abundant, morphologically distinct light vesicles of varied size and contents are manufactured in the cell bodies, from where they traffic through cytoplasmic connections to the corrugations and out to the tips. Clusters of vesicles accumulate in expanded tips in males, together with occasional mitochondria whilst females have more mitochondria but fewer vesicles. The membranous contents of light vesicles are secreted mainly from the tips, but also from the sides of the corrugations. They coat the surfaces and then form organised self-adherent membrane figures when shed into the lumen. Host antibody binds strongly in a characteristic pattern to the anterior esophageal lining indicating that the secretions are highly immunogenic.\n\nQuestion:\nIs the anterior esophageal region of Schistosoma japonicum a secretory organ?", "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 esophagus of blood-feeding schistosomes has been largely neglected although its posterior portion was designated as a gland decades ago. However, we recently showed it plays a pivotal role in blood processing. It is clearly demarcated into anterior and posterior compartments, both surrounded by a mass of cell bodies. Feeding movies revealed that erythrocytes accumulate in the anterior compartment before entering the posterior, indicating that a distinct process is executed there. We therefore investigated ultrastructural aspects and possible functions of the anterior region. The heads of adult Schistosoma japonicum were detached and prepared for both transmission and scanning electron microscopy to define the detailed ultrastructure of the anterior esophagus. Cryosections of heads were also prepared for immunocytochemistry and confocal microscopy to define the pattern of intrinsic host antibody binding in the anterior esophageal lining. The anterior syncytial lining of the esophagus is highly extended by long, thin corrugations of cytoplasm projecting towards the lumen. Strikingly in the male worm, the tips of the corrugations are further expanded by numerous threads of cytoplasm, producing a spaghetti-like appearance in the central lumen. Flattened, pitted cytoplasmic plates are interspersed in the tangled mass of threads. Abundant, morphologically distinct light vesicles of varied size and contents are manufactured in the cell bodies, from where they traffic through cytoplasmic connections to the corrugations and out to the tips. Clusters of vesicles accumulate in expanded tips in males, together with occasional mitochondria whilst females have more mitochondria but fewer vesicles. The membranous contents of light vesicles are secreted mainly from the tips, but also from the sides of the corrugations. They coat the surfaces and then form organised self-adherent membrane figures when shed into the lumen. Host antibody binds strongly in a characteristic pattern to the anterior esophageal lining indicating that the secretions are highly immunogenic.\n\nQuestion:\nIs the anterior esophageal region of Schistosoma japonicum a secretory organ?", "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 aimed to evaluate the adverse effects of various doses of nicotine and protective effects of different concentrations of gamma-tocotrienol (gamma-TCT) on in vitro embryonic development and lipid peroxidation in mice. A) Effects of various doses of nicotine on in vitro embryonic development: Female mice were treated with 1.0, 3.0, or 5.0 mg/kg/day nicotine for 7 consecutive days. Animals were superovulated, cohabited overnight, and sacrificed. Embryos were cultured in vitro. Plasma was assayed. B) Effects of concomitant treatment of nicotine concurrently with various doses of gamma-TCT on in vitro embryonic development: Female mice were treated with nicotine (5.0 mg/kg/day), gavaged gamma-TCT of 30, 60, or 90 mg/kg/day or nicotine concurrently with gamma-TCT of 3 different doses for 7 consecutive days. Animals were superovulated, cohabited overnight, and sacrificed. Embryos were cultured and plasma was assayed. A) Effects of various doses of nicotine on in vitro embryonic development: Number of hatched blastocysts decreased in 1.0 and 3.0 mg/kg/day nicotine groups. Nicotine at 5.0 mg/kg/day stopped embryo development at morula. MDA concentrations increased following all nicotine doses. B) Effects of concomitant treatment of nicotine concurrently with various doses of gamma-TCT on in vitro embryonic development: Embryo development was completed in all groups. MDA concentration increased only in the group treated with nicotine concurrently with 30 mg/kg/day gamma-TCT.\n\nQuestion:\nIs nicotine-induced cessation of embryonic development reversed by γ-tocotrienol 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:\nThis study aimed to evaluate the adverse effects of various doses of nicotine and protective effects of different concentrations of gamma-tocotrienol (gamma-TCT) on in vitro embryonic development and lipid peroxidation in mice. A) Effects of various doses of nicotine on in vitro embryonic development: Female mice were treated with 1.0, 3.0, or 5.0 mg/kg/day nicotine for 7 consecutive days. Animals were superovulated, cohabited overnight, and sacrificed. Embryos were cultured in vitro. Plasma was assayed. B) Effects of concomitant treatment of nicotine concurrently with various doses of gamma-TCT on in vitro embryonic development: Female mice were treated with nicotine (5.0 mg/kg/day), gavaged gamma-TCT of 30, 60, or 90 mg/kg/day or nicotine concurrently with gamma-TCT of 3 different doses for 7 consecutive days. Animals were superovulated, cohabited overnight, and sacrificed. Embryos were cultured and plasma was assayed. A) Effects of various doses of nicotine on in vitro embryonic development: Number of hatched blastocysts decreased in 1.0 and 3.0 mg/kg/day nicotine groups. Nicotine at 5.0 mg/kg/day stopped embryo development at morula. MDA concentrations increased following all nicotine doses. B) Effects of concomitant treatment of nicotine concurrently with various doses of gamma-TCT on in vitro embryonic development: Embryo development was completed in all groups. MDA concentration increased only in the group treated with nicotine concurrently with 30 mg/kg/day gamma-TCT.\n\nQuestion:\nIs nicotine-induced cessation of embryonic development reversed by γ-tocotrienol 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:\nThis study aimed to evaluate the adverse effects of various doses of nicotine and protective effects of different concentrations of gamma-tocotrienol (gamma-TCT) on in vitro embryonic development and lipid peroxidation in mice. A) Effects of various doses of nicotine on in vitro embryonic development: Female mice were treated with 1.0, 3.0, or 5.0 mg/kg/day nicotine for 7 consecutive days. Animals were superovulated, cohabited overnight, and sacrificed. Embryos were cultured in vitro. Plasma was assayed. B) Effects of concomitant treatment of nicotine concurrently with various doses of gamma-TCT on in vitro embryonic development: Female mice were treated with nicotine (5.0 mg/kg/day), gavaged gamma-TCT of 30, 60, or 90 mg/kg/day or nicotine concurrently with gamma-TCT of 3 different doses for 7 consecutive days. Animals were superovulated, cohabited overnight, and sacrificed. Embryos were cultured and plasma was assayed. A) Effects of various doses of nicotine on in vitro embryonic development: Number of hatched blastocysts decreased in 1.0 and 3.0 mg/kg/day nicotine groups. Nicotine at 5.0 mg/kg/day stopped embryo development at morula. MDA concentrations increased following all nicotine doses. B) Effects of concomitant treatment of nicotine concurrently with various doses of gamma-TCT on in vitro embryonic development: Embryo development was completed in all groups. MDA concentration increased only in the group treated with nicotine concurrently with 30 mg/kg/day gamma-TCT.\n\nQuestion:\nIs nicotine-induced cessation of embryonic development reversed by γ-tocotrienol 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:\nDosimetry studies have shown that activities of 131I as small as 10-20 MBq may cause a stunning effect. A result of this stunning effect may be a lower success rate of the ablative 131I therapy for differentiated thyroid carcinoma (DTC). The aim of this study was to determine whether pre-therapeutic uptake measurement with 40 MBq 131I causes a lower success rate of ablation. retrospective chart review study. In two hospitals the ablation protocols differed in one respect only: in the one hospital no diagnostic 131I was applied before ablation (group 1, n = 48), whereas in the other hospital a 24-h uptake-measurement with 40 MBq 131I was performed (group 2, n = 51). Included were all DTC patients without distant metastases who had undergone 131I ablation between July 2002 and December 2005, and who had returned for 131I follow-up. Successful ablation was defined as absence of pathological 131I uptake on diagnostic whole-body scintigraphy and undetectable thyroglobulin-levels under TSH stimulation. Overall, ablation was successful in 31/48 patients (65%) in group 1 and in 17/51 patients (33%) in group 2 (p=0.002). Multivariate analysis showed that pre-therapeutic uptake measurement using 40 MBq 131I was an independent determinant for success of ablation (p = 0.002).\n\nQuestion:\nIs the success of 131I ablation in thyroid cancer patients significantly reduced after a diagnostic activity of 40 MBq 131I?", "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:\nDosimetry studies have shown that activities of 131I as small as 10-20 MBq may cause a stunning effect. A result of this stunning effect may be a lower success rate of the ablative 131I therapy for differentiated thyroid carcinoma (DTC). The aim of this study was to determine whether pre-therapeutic uptake measurement with 40 MBq 131I causes a lower success rate of ablation. retrospective chart review study. In two hospitals the ablation protocols differed in one respect only: in the one hospital no diagnostic 131I was applied before ablation (group 1, n = 48), whereas in the other hospital a 24-h uptake-measurement with 40 MBq 131I was performed (group 2, n = 51). Included were all DTC patients without distant metastases who had undergone 131I ablation between July 2002 and December 2005, and who had returned for 131I follow-up. Successful ablation was defined as absence of pathological 131I uptake on diagnostic whole-body scintigraphy and undetectable thyroglobulin-levels under TSH stimulation. Overall, ablation was successful in 31/48 patients (65%) in group 1 and in 17/51 patients (33%) in group 2 (p=0.002). Multivariate analysis showed that pre-therapeutic uptake measurement using 40 MBq 131I was an independent determinant for success of ablation (p = 0.002).\n\nQuestion:\nIs the success of 131I ablation in thyroid cancer patients significantly reduced after a diagnostic activity of 40 MBq 131I?", "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:\nDosimetry studies have shown that activities of 131I as small as 10-20 MBq may cause a stunning effect. A result of this stunning effect may be a lower success rate of the ablative 131I therapy for differentiated thyroid carcinoma (DTC). The aim of this study was to determine whether pre-therapeutic uptake measurement with 40 MBq 131I causes a lower success rate of ablation. retrospective chart review study. In two hospitals the ablation protocols differed in one respect only: in the one hospital no diagnostic 131I was applied before ablation (group 1, n = 48), whereas in the other hospital a 24-h uptake-measurement with 40 MBq 131I was performed (group 2, n = 51). Included were all DTC patients without distant metastases who had undergone 131I ablation between July 2002 and December 2005, and who had returned for 131I follow-up. Successful ablation was defined as absence of pathological 131I uptake on diagnostic whole-body scintigraphy and undetectable thyroglobulin-levels under TSH stimulation. Overall, ablation was successful in 31/48 patients (65%) in group 1 and in 17/51 patients (33%) in group 2 (p=0.002). Multivariate analysis showed that pre-therapeutic uptake measurement using 40 MBq 131I was an independent determinant for success of ablation (p = 0.002).\n\nQuestion:\nIs the success of 131I ablation in thyroid cancer patients significantly reduced after a diagnostic activity of 40 MBq 131I?", "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:\nApc mutant (Apc(Min)) mice develop multiple adenomas in their intestines and are widely used to study colorectal carcinogenesis and chemopreventive approaches. Molecular imaging of intestinal adenomas could potentially provide noninvasive longitudinal evaluation of these lesions in living mice. Therefore, the aim of this study was to investigate the role of (18)F-FDG PET in the Apc(Min) mouse model. Apc(Min) mice (n = 8) fed a purified diet were imaged serially after injection of (18)F-FDG at age 9 and 12 wk using a small-animal PET scanner. Abdominal uptake of the tracer was quantified. After dissection, intestines were imaged separately, and intestinal tracer uptake was quantified. Tracer distribution was compared with results from microscopic examination regarding adenoma number and size. Thereafter, findings were validated serially in 20 Apc(Min) mice aged 6, 8, 10, and 12 wk that received standard chow to increase adenoma numbers. In vivo abdominal (18)F-FDG uptake was correlated with microscopy results. Microscopic examination showed that the mice developed 25-35 intestinal adenomas at age 12 wk. Ex vivo (18)F-FDG PET of the dissected intestines visualized all large adenomas and most small adenomas. Ex vivo total intestinal (18)F-FDG uptake correlated with in vivo total abdominal uptake and with the number of large adenomas at age 9 and 12 wk. At 12 wk, there was a clear correlation between in vivo abdominal tracer uptake and the number of large adenomas but not the total number of lesions.\n\nQuestion:\nDoes total abdominal 18F-FDG uptake reflect intestinal adenoma burden in Apc mutant 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:\nApc mutant (Apc(Min)) mice develop multiple adenomas in their intestines and are widely used to study colorectal carcinogenesis and chemopreventive approaches. Molecular imaging of intestinal adenomas could potentially provide noninvasive longitudinal evaluation of these lesions in living mice. Therefore, the aim of this study was to investigate the role of (18)F-FDG PET in the Apc(Min) mouse model. Apc(Min) mice (n = 8) fed a purified diet were imaged serially after injection of (18)F-FDG at age 9 and 12 wk using a small-animal PET scanner. Abdominal uptake of the tracer was quantified. After dissection, intestines were imaged separately, and intestinal tracer uptake was quantified. Tracer distribution was compared with results from microscopic examination regarding adenoma number and size. Thereafter, findings were validated serially in 20 Apc(Min) mice aged 6, 8, 10, and 12 wk that received standard chow to increase adenoma numbers. In vivo abdominal (18)F-FDG uptake was correlated with microscopy results. Microscopic examination showed that the mice developed 25-35 intestinal adenomas at age 12 wk. Ex vivo (18)F-FDG PET of the dissected intestines visualized all large adenomas and most small adenomas. Ex vivo total intestinal (18)F-FDG uptake correlated with in vivo total abdominal uptake and with the number of large adenomas at age 9 and 12 wk. At 12 wk, there was a clear correlation between in vivo abdominal tracer uptake and the number of large adenomas but not the total number of lesions.\n\nQuestion:\nDoes total abdominal 18F-FDG uptake reflect intestinal adenoma burden in Apc mutant 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:\nApc mutant (Apc(Min)) mice develop multiple adenomas in their intestines and are widely used to study colorectal carcinogenesis and chemopreventive approaches. Molecular imaging of intestinal adenomas could potentially provide noninvasive longitudinal evaluation of these lesions in living mice. Therefore, the aim of this study was to investigate the role of (18)F-FDG PET in the Apc(Min) mouse model. Apc(Min) mice (n = 8) fed a purified diet were imaged serially after injection of (18)F-FDG at age 9 and 12 wk using a small-animal PET scanner. Abdominal uptake of the tracer was quantified. After dissection, intestines were imaged separately, and intestinal tracer uptake was quantified. Tracer distribution was compared with results from microscopic examination regarding adenoma number and size. Thereafter, findings were validated serially in 20 Apc(Min) mice aged 6, 8, 10, and 12 wk that received standard chow to increase adenoma numbers. In vivo abdominal (18)F-FDG uptake was correlated with microscopy results. Microscopic examination showed that the mice developed 25-35 intestinal adenomas at age 12 wk. Ex vivo (18)F-FDG PET of the dissected intestines visualized all large adenomas and most small adenomas. Ex vivo total intestinal (18)F-FDG uptake correlated with in vivo total abdominal uptake and with the number of large adenomas at age 9 and 12 wk. At 12 wk, there was a clear correlation between in vivo abdominal tracer uptake and the number of large adenomas but not the total number of lesions.\n\nQuestion:\nDoes total abdominal 18F-FDG uptake reflect intestinal adenoma burden in Apc mutant 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:\nSurgical and systemic treatment modalities for breast cancer (BC) patients with micrometastatic disease in the sentinel lymph node biopsy (SNB) are controversial. The aim of this study was to evaluate decisional factors associated with assignment of adjuvant chemotherapy (CT). In a retrospective multicentric European study we evaluated cases of primary BC patients who underwent SNB. Logistic regression (LR) and recursive partitioning analyses (RPA) were performed to determine factors associated with CT. Of the 172 patients with micrometastatic disease, 39.5% received adjuvant CT. In the group treated with CT, patients tended to be younger (P = 0.001), with higher grade (P = 0.001) and HER2 positive tumors (P = 0.006) compared to patients without CT. In multivariate LR, age (P = 0.0027), high grading (P = 0.01) HER2 positivity (P = 0.03), and positive non-SN status (P = 0.03) were significantly associated with CT. RPA demonstrated that tumor grade, and not the non-SN status, was the first split in the partition tree followed by HER2 status, and non-SN status influencing the probability for CT administration.\n\nQuestion:\nIs the positive non-sentinel status the main decisional factor for chemotherapy assignment in breast cancer with micrometastatic disease in the sentinel lymph node?", "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:\nSurgical and systemic treatment modalities for breast cancer (BC) patients with micrometastatic disease in the sentinel lymph node biopsy (SNB) are controversial. The aim of this study was to evaluate decisional factors associated with assignment of adjuvant chemotherapy (CT). In a retrospective multicentric European study we evaluated cases of primary BC patients who underwent SNB. Logistic regression (LR) and recursive partitioning analyses (RPA) were performed to determine factors associated with CT. Of the 172 patients with micrometastatic disease, 39.5% received adjuvant CT. In the group treated with CT, patients tended to be younger (P = 0.001), with higher grade (P = 0.001) and HER2 positive tumors (P = 0.006) compared to patients without CT. In multivariate LR, age (P = 0.0027), high grading (P = 0.01) HER2 positivity (P = 0.03), and positive non-SN status (P = 0.03) were significantly associated with CT. RPA demonstrated that tumor grade, and not the non-SN status, was the first split in the partition tree followed by HER2 status, and non-SN status influencing the probability for CT administration.\n\nQuestion:\nIs the positive non-sentinel status the main decisional factor for chemotherapy assignment in breast cancer with micrometastatic disease in the sentinel lymph node?", "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:\nSurgical and systemic treatment modalities for breast cancer (BC) patients with micrometastatic disease in the sentinel lymph node biopsy (SNB) are controversial. The aim of this study was to evaluate decisional factors associated with assignment of adjuvant chemotherapy (CT). In a retrospective multicentric European study we evaluated cases of primary BC patients who underwent SNB. Logistic regression (LR) and recursive partitioning analyses (RPA) were performed to determine factors associated with CT. Of the 172 patients with micrometastatic disease, 39.5% received adjuvant CT. In the group treated with CT, patients tended to be younger (P = 0.001), with higher grade (P = 0.001) and HER2 positive tumors (P = 0.006) compared to patients without CT. In multivariate LR, age (P = 0.0027), high grading (P = 0.01) HER2 positivity (P = 0.03), and positive non-SN status (P = 0.03) were significantly associated with CT. RPA demonstrated that tumor grade, and not the non-SN status, was the first split in the partition tree followed by HER2 status, and non-SN status influencing the probability for CT administration.\n\nQuestion:\nIs the positive non-sentinel status the main decisional factor for chemotherapy assignment in breast cancer with micrometastatic disease in the sentinel lymph node?", "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 oxidation protein products (AOPPs), a novel marker for oxidative protein damage, regulated cell behavior in many cell types. Although previous reports have revealed that oxidative stress resulted in an increased AOPPs content in cultured osteoblast-like cells, the effects of AOPPs on osteoblast-like cell function remain unclear. This study aimed to investigate the effect of AOPPs on the proliferation and differentiation of rat osteoblast-like (ROB) cells in vitro. ROB cells isolated from calvarias of newborn rats were incubated with AOPPs-modified rat serum albumin (AOPPs-RSA) prepared in vitro by incubation of RSA with hypochlorous acid. Cell proliferation was evaluated by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay. Alkaline phosphatase activity was measured. Expression of osteocalcin mRNA and protein were examined using reverse transcriptase-polymerase chain reaction and Western blot, respectively. Reactive oxygen species (ROS) generation was detected by flow cytometry and fluorescent microscope. Phosphorylation of nuclear factor (NF)- kappaB p65 subunit was detected by Western blot. Exposure of ROB cells to AOPPs-RSA significantly inhibited cell proliferation, decreased alkaline phosphatase activity, down-regulated the expression of osteocalcin mRNA and protein in both a concentration- and time-dependent manner. AOPPs challenge induced ROS generation and NF-kappaB p65 phosphorylation, which were inhibited by superoxide dismutase, catalase and NADPH oxidase inhibitors diphenyleneiodonium and apocynin. Furthermore, NF-kappaB inhibitor SN50 could reverse the AOPPs-induced inhibition of ROB cell proliferation and differentiation.\n\nQuestion:\nDo advanced oxidation protein products inhibit proliferation and differentiation of rat osteoblast-like cells via NF-kappaB 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:\nAdvanced oxidation protein products (AOPPs), a novel marker for oxidative protein damage, regulated cell behavior in many cell types. Although previous reports have revealed that oxidative stress resulted in an increased AOPPs content in cultured osteoblast-like cells, the effects of AOPPs on osteoblast-like cell function remain unclear. This study aimed to investigate the effect of AOPPs on the proliferation and differentiation of rat osteoblast-like (ROB) cells in vitro. ROB cells isolated from calvarias of newborn rats were incubated with AOPPs-modified rat serum albumin (AOPPs-RSA) prepared in vitro by incubation of RSA with hypochlorous acid. Cell proliferation was evaluated by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay. Alkaline phosphatase activity was measured. Expression of osteocalcin mRNA and protein were examined using reverse transcriptase-polymerase chain reaction and Western blot, respectively. Reactive oxygen species (ROS) generation was detected by flow cytometry and fluorescent microscope. Phosphorylation of nuclear factor (NF)- kappaB p65 subunit was detected by Western blot. Exposure of ROB cells to AOPPs-RSA significantly inhibited cell proliferation, decreased alkaline phosphatase activity, down-regulated the expression of osteocalcin mRNA and protein in both a concentration- and time-dependent manner. AOPPs challenge induced ROS generation and NF-kappaB p65 phosphorylation, which were inhibited by superoxide dismutase, catalase and NADPH oxidase inhibitors diphenyleneiodonium and apocynin. Furthermore, NF-kappaB inhibitor SN50 could reverse the AOPPs-induced inhibition of ROB cell proliferation and differentiation.\n\nQuestion:\nDo advanced oxidation protein products inhibit proliferation and differentiation of rat osteoblast-like cells via NF-kappaB 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:\nAdvanced oxidation protein products (AOPPs), a novel marker for oxidative protein damage, regulated cell behavior in many cell types. Although previous reports have revealed that oxidative stress resulted in an increased AOPPs content in cultured osteoblast-like cells, the effects of AOPPs on osteoblast-like cell function remain unclear. This study aimed to investigate the effect of AOPPs on the proliferation and differentiation of rat osteoblast-like (ROB) cells in vitro. ROB cells isolated from calvarias of newborn rats were incubated with AOPPs-modified rat serum albumin (AOPPs-RSA) prepared in vitro by incubation of RSA with hypochlorous acid. Cell proliferation was evaluated by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay. Alkaline phosphatase activity was measured. Expression of osteocalcin mRNA and protein were examined using reverse transcriptase-polymerase chain reaction and Western blot, respectively. Reactive oxygen species (ROS) generation was detected by flow cytometry and fluorescent microscope. Phosphorylation of nuclear factor (NF)- kappaB p65 subunit was detected by Western blot. Exposure of ROB cells to AOPPs-RSA significantly inhibited cell proliferation, decreased alkaline phosphatase activity, down-regulated the expression of osteocalcin mRNA and protein in both a concentration- and time-dependent manner. AOPPs challenge induced ROS generation and NF-kappaB p65 phosphorylation, which were inhibited by superoxide dismutase, catalase and NADPH oxidase inhibitors diphenyleneiodonium and apocynin. Furthermore, NF-kappaB inhibitor SN50 could reverse the AOPPs-induced inhibition of ROB cell proliferation and differentiation.\n\nQuestion:\nDo advanced oxidation protein products inhibit proliferation and differentiation of rat osteoblast-like cells via NF-kappaB 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:\nOesophageal pH monitoring is considered to be the gold standard investigation in the diagnosis of gastro-oesophageal reflux disease. Results of pH monitoring in regurgitating infants, however, may be within normal ranges. Therefore it was hypothesized that prolonged buffering of gastric acidity caused by milk-feeding may falsely normalize the pH data. Therefore, it may be relevant to omit the periods of gastric acid buffering in the analysis of the oesophageal pH monitoring data. Combined gastric and oesophageal pH monitoring (Digitrapper Mark III, two-channel antimony electrode, Synectics) was performed in 90 consecutive infants, 0.5-10 months old, who were referred to the unit by outdoor paediatricians for pH measurement. The data were analysed in three different ways. The reflux index (RI), or the percentage time that the pH in the oesophagus was < 4.0, was calculated in three different ways: (i) the total duration of the investigation; (ii) excluding 90-min postprandial periods, starting from the beginning of a feeding; and (iii) excluding all periods with a gastric pH > 4.0, which are the periods of gastric buffering with a theoretical impossibility of recording an oesophageal pH < 4.0. The mean duration of the pHmetries was 19.20+/-2.01h (A; mean +/- 1 SD), with a RI of 5.38+/-5.39% (B; median 3.45%). If the 90-min postprandial periods were not considered, the mean duration decreased to 12.21+/-2.41h (C; P(A vs C) < 0.001), with an oesophageal RI of 6.82+/-6.57% (D; median: 4.65; P(B vs D) = NS; r (B vs D) = 0.97). If all periods with a gastric pH > 4.0 were elminated, the duration available for analysis of the data with a gastric pH < 4.0 was 12.53+/-4.00 h (E; P(A vs E) < 0.001; P(C vs E) = NS), with an oesophageal RI of 7.06+/-7.52% (F; median: 4.50; P(B vs D vs F) = NS; r(B vs F), (D vs F) = 0.96).\n\nQuestion:\nDoes oesophageal pH monitoring in infants : elimination of gastric buffering modify reflux index?", "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:\nOesophageal pH monitoring is considered to be the gold standard investigation in the diagnosis of gastro-oesophageal reflux disease. Results of pH monitoring in regurgitating infants, however, may be within normal ranges. Therefore it was hypothesized that prolonged buffering of gastric acidity caused by milk-feeding may falsely normalize the pH data. Therefore, it may be relevant to omit the periods of gastric acid buffering in the analysis of the oesophageal pH monitoring data. Combined gastric and oesophageal pH monitoring (Digitrapper Mark III, two-channel antimony electrode, Synectics) was performed in 90 consecutive infants, 0.5-10 months old, who were referred to the unit by outdoor paediatricians for pH measurement. The data were analysed in three different ways. The reflux index (RI), or the percentage time that the pH in the oesophagus was < 4.0, was calculated in three different ways: (i) the total duration of the investigation; (ii) excluding 90-min postprandial periods, starting from the beginning of a feeding; and (iii) excluding all periods with a gastric pH > 4.0, which are the periods of gastric buffering with a theoretical impossibility of recording an oesophageal pH < 4.0. The mean duration of the pHmetries was 19.20+/-2.01h (A; mean +/- 1 SD), with a RI of 5.38+/-5.39% (B; median 3.45%). If the 90-min postprandial periods were not considered, the mean duration decreased to 12.21+/-2.41h (C; P(A vs C) < 0.001), with an oesophageal RI of 6.82+/-6.57% (D; median: 4.65; P(B vs D) = NS; r (B vs D) = 0.97). If all periods with a gastric pH > 4.0 were elminated, the duration available for analysis of the data with a gastric pH < 4.0 was 12.53+/-4.00 h (E; P(A vs E) < 0.001; P(C vs E) = NS), with an oesophageal RI of 7.06+/-7.52% (F; median: 4.50; P(B vs D vs F) = NS; r(B vs F), (D vs F) = 0.96).\n\nQuestion:\nDoes oesophageal pH monitoring in infants : elimination of gastric buffering modify reflux index?", "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:\nOesophageal pH monitoring is considered to be the gold standard investigation in the diagnosis of gastro-oesophageal reflux disease. Results of pH monitoring in regurgitating infants, however, may be within normal ranges. Therefore it was hypothesized that prolonged buffering of gastric acidity caused by milk-feeding may falsely normalize the pH data. Therefore, it may be relevant to omit the periods of gastric acid buffering in the analysis of the oesophageal pH monitoring data. Combined gastric and oesophageal pH monitoring (Digitrapper Mark III, two-channel antimony electrode, Synectics) was performed in 90 consecutive infants, 0.5-10 months old, who were referred to the unit by outdoor paediatricians for pH measurement. The data were analysed in three different ways. The reflux index (RI), or the percentage time that the pH in the oesophagus was < 4.0, was calculated in three different ways: (i) the total duration of the investigation; (ii) excluding 90-min postprandial periods, starting from the beginning of a feeding; and (iii) excluding all periods with a gastric pH > 4.0, which are the periods of gastric buffering with a theoretical impossibility of recording an oesophageal pH < 4.0. The mean duration of the pHmetries was 19.20+/-2.01h (A; mean +/- 1 SD), with a RI of 5.38+/-5.39% (B; median 3.45%). If the 90-min postprandial periods were not considered, the mean duration decreased to 12.21+/-2.41h (C; P(A vs C) < 0.001), with an oesophageal RI of 6.82+/-6.57% (D; median: 4.65; P(B vs D) = NS; r (B vs D) = 0.97). If all periods with a gastric pH > 4.0 were elminated, the duration available for analysis of the data with a gastric pH < 4.0 was 12.53+/-4.00 h (E; P(A vs E) < 0.001; P(C vs E) = NS), with an oesophageal RI of 7.06+/-7.52% (F; median: 4.50; P(B vs D vs F) = NS; r(B vs F), (D vs F) = 0.96).\n\nQuestion:\nDoes oesophageal pH monitoring in infants : elimination of gastric buffering modify reflux index?", "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:\nHIV-1 transcription is activated by the viral Tat protein that recruits host positive transcription elongation factor-b (P-TEFb) containing CDK9/cyclin T1 to the HIV-1 promoter. P-TEFb in the cells exists as a lower molecular weight CDK9/cyclin T1 dimer and a high molecular weight complex of 7SK RNA, CDK9/cyclin T1, HEXIM1 dimer and several additional proteins. Our previous studies implicated CDK2 in HIV-1 transcription regulation. We also found that inhibition of CDK2 by iron chelators leads to the inhibition of CDK9 activity, suggesting a functional link between CDK2 and CDK9. Here, we investigate whether CDK2 phosphorylates CDK9 and regulates its activity. The siRNA-mediated knockdown of CDK2 inhibited CDK9 kinase activity and reduced CDK9 phosphorylation. Stable shRNA-mediated CDK2 knockdown inhibited HIV-1 transcription, but also increased the overall level of 7SK RNA. CDK9 contains a motif (90SPYNR94) that is consensus CDK2 phosphorylation site. CDK9 was phosphorylated on Ser90 by CDK2 in vitro. In cultured cells, CDK9 phosphorylation was reduced when Ser90 was mutated to an Ala. Phosphorylation of CDK9 on Ser90 was also detected with phospho-specific antibodies and it was reduced after the knockdown of CDK2. CDK9 expression decreased in the large complex for the CDK9-S90A mutant and was correlated with a reduced activity and an inhibition of HIV-1 transcription. In contrast, the CDK9-S90D mutant showed a slight decrease in CDK9 expression in both the large and small complexes but induced Tat-dependent HIV-1 transcription. Molecular modeling showed that Ser 90 of CDK9 is located on a flexible loop exposed to solvent, suggesting its availability for phosphorylation.\n\nQuestion:\nDoes cDK2 regulate HIV-1 transcription by phosphorylation of CDK9 on serine 90?", "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:\nHIV-1 transcription is activated by the viral Tat protein that recruits host positive transcription elongation factor-b (P-TEFb) containing CDK9/cyclin T1 to the HIV-1 promoter. P-TEFb in the cells exists as a lower molecular weight CDK9/cyclin T1 dimer and a high molecular weight complex of 7SK RNA, CDK9/cyclin T1, HEXIM1 dimer and several additional proteins. Our previous studies implicated CDK2 in HIV-1 transcription regulation. We also found that inhibition of CDK2 by iron chelators leads to the inhibition of CDK9 activity, suggesting a functional link between CDK2 and CDK9. Here, we investigate whether CDK2 phosphorylates CDK9 and regulates its activity. The siRNA-mediated knockdown of CDK2 inhibited CDK9 kinase activity and reduced CDK9 phosphorylation. Stable shRNA-mediated CDK2 knockdown inhibited HIV-1 transcription, but also increased the overall level of 7SK RNA. CDK9 contains a motif (90SPYNR94) that is consensus CDK2 phosphorylation site. CDK9 was phosphorylated on Ser90 by CDK2 in vitro. In cultured cells, CDK9 phosphorylation was reduced when Ser90 was mutated to an Ala. Phosphorylation of CDK9 on Ser90 was also detected with phospho-specific antibodies and it was reduced after the knockdown of CDK2. CDK9 expression decreased in the large complex for the CDK9-S90A mutant and was correlated with a reduced activity and an inhibition of HIV-1 transcription. In contrast, the CDK9-S90D mutant showed a slight decrease in CDK9 expression in both the large and small complexes but induced Tat-dependent HIV-1 transcription. Molecular modeling showed that Ser 90 of CDK9 is located on a flexible loop exposed to solvent, suggesting its availability for phosphorylation.\n\nQuestion:\nDoes cDK2 regulate HIV-1 transcription by phosphorylation of CDK9 on serine 90?", "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:\nHIV-1 transcription is activated by the viral Tat protein that recruits host positive transcription elongation factor-b (P-TEFb) containing CDK9/cyclin T1 to the HIV-1 promoter. P-TEFb in the cells exists as a lower molecular weight CDK9/cyclin T1 dimer and a high molecular weight complex of 7SK RNA, CDK9/cyclin T1, HEXIM1 dimer and several additional proteins. Our previous studies implicated CDK2 in HIV-1 transcription regulation. We also found that inhibition of CDK2 by iron chelators leads to the inhibition of CDK9 activity, suggesting a functional link between CDK2 and CDK9. Here, we investigate whether CDK2 phosphorylates CDK9 and regulates its activity. The siRNA-mediated knockdown of CDK2 inhibited CDK9 kinase activity and reduced CDK9 phosphorylation. Stable shRNA-mediated CDK2 knockdown inhibited HIV-1 transcription, but also increased the overall level of 7SK RNA. CDK9 contains a motif (90SPYNR94) that is consensus CDK2 phosphorylation site. CDK9 was phosphorylated on Ser90 by CDK2 in vitro. In cultured cells, CDK9 phosphorylation was reduced when Ser90 was mutated to an Ala. Phosphorylation of CDK9 on Ser90 was also detected with phospho-specific antibodies and it was reduced after the knockdown of CDK2. CDK9 expression decreased in the large complex for the CDK9-S90A mutant and was correlated with a reduced activity and an inhibition of HIV-1 transcription. In contrast, the CDK9-S90D mutant showed a slight decrease in CDK9 expression in both the large and small complexes but induced Tat-dependent HIV-1 transcription. Molecular modeling showed that Ser 90 of CDK9 is located on a flexible loop exposed to solvent, suggesting its availability for phosphorylation.\n\nQuestion:\nDoes cDK2 regulate HIV-1 transcription by phosphorylation of CDK9 on serine 90?", "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:\nWall shear stress, arterial wall elasticity, and intimal hyperplasia are related. The aim of this study was to investigate the in vitro mechanical properties of ovine femoral arteries, jugular veins, and expanded polytetrafluoroethylene conduits, and to evaluate postoperative intimal hyperplasia. Arterial, venous, and ePTFE mechanical properties were studied in a circulating loop at isobaric systemic pressures. Histological studies of intimal hyperplasia in ePTFE-bypassed femoral arteries with and without Miller cuffs were performed at the 40th and 120th day. The incremental elastic modulus of veins was significantly higher than that of femoral arteries (P < 0.05), but significantly lower than that of ePTFE graft conduits (P < 0.05). Intimal hyperplasia was significantly less in Miller-cuff-bypassed arteries both at the 40th and 120th day (P < 0.01).\n\nQuestion:\nDoes reduced elastic mismatch achieved by interposing vein cuff in expanded polytetrafluoroethylene femoral bypass decrease intimal hyperplasia?", "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:\nWall shear stress, arterial wall elasticity, and intimal hyperplasia are related. The aim of this study was to investigate the in vitro mechanical properties of ovine femoral arteries, jugular veins, and expanded polytetrafluoroethylene conduits, and to evaluate postoperative intimal hyperplasia. Arterial, venous, and ePTFE mechanical properties were studied in a circulating loop at isobaric systemic pressures. Histological studies of intimal hyperplasia in ePTFE-bypassed femoral arteries with and without Miller cuffs were performed at the 40th and 120th day. The incremental elastic modulus of veins was significantly higher than that of femoral arteries (P < 0.05), but significantly lower than that of ePTFE graft conduits (P < 0.05). Intimal hyperplasia was significantly less in Miller-cuff-bypassed arteries both at the 40th and 120th day (P < 0.01).\n\nQuestion:\nDoes reduced elastic mismatch achieved by interposing vein cuff in expanded polytetrafluoroethylene femoral bypass decrease intimal hyperplasia?", "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:\nWall shear stress, arterial wall elasticity, and intimal hyperplasia are related. The aim of this study was to investigate the in vitro mechanical properties of ovine femoral arteries, jugular veins, and expanded polytetrafluoroethylene conduits, and to evaluate postoperative intimal hyperplasia. Arterial, venous, and ePTFE mechanical properties were studied in a circulating loop at isobaric systemic pressures. Histological studies of intimal hyperplasia in ePTFE-bypassed femoral arteries with and without Miller cuffs were performed at the 40th and 120th day. The incremental elastic modulus of veins was significantly higher than that of femoral arteries (P < 0.05), but significantly lower than that of ePTFE graft conduits (P < 0.05). Intimal hyperplasia was significantly less in Miller-cuff-bypassed arteries both at the 40th and 120th day (P < 0.01).\n\nQuestion:\nDoes reduced elastic mismatch achieved by interposing vein cuff in expanded polytetrafluoroethylene femoral bypass decrease intimal hyperplasia?", "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 U12-type spliceosome is responsible for the removal of a subset of introns from eukaryotic mRNAs. U12-type introns are spliced less efficiently than normal U2-type introns, which suggests a rate-limiting role in gene expression. The Drosophila genome contains about 20 U12-type introns, many of them in essential genes, and the U12-type spliceosome has previously been shown to be essential in the fly. We have used a Drosophila line with a P-element insertion in U6atac snRNA, an essential component of the U12-type spliceosome, to investigate the impact of U12-type introns on gene expression at the organismal level during fly development. This line exhibits progressive accumulation of unspliced U12-type introns during larval development and the death of larvae at the third instar stage. Surprisingly, microarray and RT-PCR analyses revealed that most genes containing U12-type introns showed only mild perturbations in the splicing of U12-type introns. In contrast, we detected widespread downstream effects on genes that do not contain U12-type introns, with genes related to various metabolic pathways constituting the largest group.\n\nQuestion:\nDoes gene expression profiling of U12-type spliceosome mutant Drosophila reveal widespread changes in metabolic 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:\nThe U12-type spliceosome is responsible for the removal of a subset of introns from eukaryotic mRNAs. U12-type introns are spliced less efficiently than normal U2-type introns, which suggests a rate-limiting role in gene expression. The Drosophila genome contains about 20 U12-type introns, many of them in essential genes, and the U12-type spliceosome has previously been shown to be essential in the fly. We have used a Drosophila line with a P-element insertion in U6atac snRNA, an essential component of the U12-type spliceosome, to investigate the impact of U12-type introns on gene expression at the organismal level during fly development. This line exhibits progressive accumulation of unspliced U12-type introns during larval development and the death of larvae at the third instar stage. Surprisingly, microarray and RT-PCR analyses revealed that most genes containing U12-type introns showed only mild perturbations in the splicing of U12-type introns. In contrast, we detected widespread downstream effects on genes that do not contain U12-type introns, with genes related to various metabolic pathways constituting the largest group.\n\nQuestion:\nDoes gene expression profiling of U12-type spliceosome mutant Drosophila reveal widespread changes in metabolic 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:\nThe U12-type spliceosome is responsible for the removal of a subset of introns from eukaryotic mRNAs. U12-type introns are spliced less efficiently than normal U2-type introns, which suggests a rate-limiting role in gene expression. The Drosophila genome contains about 20 U12-type introns, many of them in essential genes, and the U12-type spliceosome has previously been shown to be essential in the fly. We have used a Drosophila line with a P-element insertion in U6atac snRNA, an essential component of the U12-type spliceosome, to investigate the impact of U12-type introns on gene expression at the organismal level during fly development. This line exhibits progressive accumulation of unspliced U12-type introns during larval development and the death of larvae at the third instar stage. Surprisingly, microarray and RT-PCR analyses revealed that most genes containing U12-type introns showed only mild perturbations in the splicing of U12-type introns. In contrast, we detected widespread downstream effects on genes that do not contain U12-type introns, with genes related to various metabolic pathways constituting the largest group.\n\nQuestion:\nDoes gene expression profiling of U12-type spliceosome mutant Drosophila reveal widespread changes in metabolic 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:\nBacterial adherence to the upper airway epithelium is considered to be an important phenomenon in the pathogenesis of infections. However, the evidence for the hypothesis that bacterial adherence to mucosal epithelial cells has significance for pathogenesis of mucosal infections is based on studies using indirect techniques. We could find no biopsy studies with direct ocular observations of significant numbers of bacteria adhering to upper airway mucosal epithelial cells either in health or during disease. We studied specimens from healthy and infected tonsillar epithelium and specimens from the soft palate epithelium obtained by surgery. The specimens were examined by TEM. In the vast majority of specimens, we found no bacteria adhering to the epithelial cells in the mucosal line regardless of whether the patient was infected or not. Bacteria adhering to shed epithelial cells were seen in higher numbers. Furthermore, as bacteria are small compared to epithelial cells, we calculated the risk of overlooking every adhered bacteria in a section if bacterial adherence was such a significant phenomenon as earlier suggested. We found this risk to be very small.\n\nQuestion:\nDoes bacterial adherence to mucosal epithelium in the upper airways have less significance than believed?", "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:\nBacterial adherence to the upper airway epithelium is considered to be an important phenomenon in the pathogenesis of infections. However, the evidence for the hypothesis that bacterial adherence to mucosal epithelial cells has significance for pathogenesis of mucosal infections is based on studies using indirect techniques. We could find no biopsy studies with direct ocular observations of significant numbers of bacteria adhering to upper airway mucosal epithelial cells either in health or during disease. We studied specimens from healthy and infected tonsillar epithelium and specimens from the soft palate epithelium obtained by surgery. The specimens were examined by TEM. In the vast majority of specimens, we found no bacteria adhering to the epithelial cells in the mucosal line regardless of whether the patient was infected or not. Bacteria adhering to shed epithelial cells were seen in higher numbers. Furthermore, as bacteria are small compared to epithelial cells, we calculated the risk of overlooking every adhered bacteria in a section if bacterial adherence was such a significant phenomenon as earlier suggested. We found this risk to be very small.\n\nQuestion:\nDoes bacterial adherence to mucosal epithelium in the upper airways have less significance than believed?", "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:\nBacterial adherence to the upper airway epithelium is considered to be an important phenomenon in the pathogenesis of infections. However, the evidence for the hypothesis that bacterial adherence to mucosal epithelial cells has significance for pathogenesis of mucosal infections is based on studies using indirect techniques. We could find no biopsy studies with direct ocular observations of significant numbers of bacteria adhering to upper airway mucosal epithelial cells either in health or during disease. We studied specimens from healthy and infected tonsillar epithelium and specimens from the soft palate epithelium obtained by surgery. The specimens were examined by TEM. In the vast majority of specimens, we found no bacteria adhering to the epithelial cells in the mucosal line regardless of whether the patient was infected or not. Bacteria adhering to shed epithelial cells were seen in higher numbers. Furthermore, as bacteria are small compared to epithelial cells, we calculated the risk of overlooking every adhered bacteria in a section if bacterial adherence was such a significant phenomenon as earlier suggested. We found this risk to be very small.\n\nQuestion:\nDoes bacterial adherence to mucosal epithelium in the upper airways have less significance than believed?", "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:\nFew have studied how personal activities of daily living (P-ADL) develop over time in nursing home residents with dementia. Thus, the aim was to study variables associated with the development of P-ADL functioning over a 52-month follow-up period, with a particular focus on the importance of the degree of dementia. In all, 932 nursing home residents with dementia (Clinical Dementia Rating-CDR- Scale ≥ 1) were included in a longitudinal study with four assessments of P-ADL functioning during 52 months. P-ADL was measured using the Lawton and Brody's Physical Self-Maintenance Scale. Degree of dementia (CDR), neuropsychiatric symptoms and use of psychotropic medication were assessed at the same four time points. Demographic information and information about physical health was included at baseline. Linear regression models for longitudinal data were estimated. Follow-up time was positively associated with a decline in P-ADL functioning. Degree of dementia at baseline was associated with a decline in P-ADL functioning over time. The association between degree of dementia and P-ADL functioning was strongest at baseline, and then flattened over time. A higher level of neuropsychiatric symptoms such as agitation and apathy and no use of anxiolytics and antidementia medication were associated with a decline in P-ADL functioning at four time points. Higher physical co-morbidity at baseline was associated with a decline in P-ADL functioning.\n\nQuestion:\nDoes a 52 month follow-up of functional decline in nursing home residents - degree of dementia contribute?", "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:\nFew have studied how personal activities of daily living (P-ADL) develop over time in nursing home residents with dementia. Thus, the aim was to study variables associated with the development of P-ADL functioning over a 52-month follow-up period, with a particular focus on the importance of the degree of dementia. In all, 932 nursing home residents with dementia (Clinical Dementia Rating-CDR- Scale ≥ 1) were included in a longitudinal study with four assessments of P-ADL functioning during 52 months. P-ADL was measured using the Lawton and Brody's Physical Self-Maintenance Scale. Degree of dementia (CDR), neuropsychiatric symptoms and use of psychotropic medication were assessed at the same four time points. Demographic information and information about physical health was included at baseline. Linear regression models for longitudinal data were estimated. Follow-up time was positively associated with a decline in P-ADL functioning. Degree of dementia at baseline was associated with a decline in P-ADL functioning over time. The association between degree of dementia and P-ADL functioning was strongest at baseline, and then flattened over time. A higher level of neuropsychiatric symptoms such as agitation and apathy and no use of anxiolytics and antidementia medication were associated with a decline in P-ADL functioning at four time points. Higher physical co-morbidity at baseline was associated with a decline in P-ADL functioning.\n\nQuestion:\nDoes a 52 month follow-up of functional decline in nursing home residents - degree of dementia contribute?", "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:\nFew have studied how personal activities of daily living (P-ADL) develop over time in nursing home residents with dementia. Thus, the aim was to study variables associated with the development of P-ADL functioning over a 52-month follow-up period, with a particular focus on the importance of the degree of dementia. In all, 932 nursing home residents with dementia (Clinical Dementia Rating-CDR- Scale ≥ 1) were included in a longitudinal study with four assessments of P-ADL functioning during 52 months. P-ADL was measured using the Lawton and Brody's Physical Self-Maintenance Scale. Degree of dementia (CDR), neuropsychiatric symptoms and use of psychotropic medication were assessed at the same four time points. Demographic information and information about physical health was included at baseline. Linear regression models for longitudinal data were estimated. Follow-up time was positively associated with a decline in P-ADL functioning. Degree of dementia at baseline was associated with a decline in P-ADL functioning over time. The association between degree of dementia and P-ADL functioning was strongest at baseline, and then flattened over time. A higher level of neuropsychiatric symptoms such as agitation and apathy and no use of anxiolytics and antidementia medication were associated with a decline in P-ADL functioning at four time points. Higher physical co-morbidity at baseline was associated with a decline in P-ADL functioning.\n\nQuestion:\nDoes a 52 month follow-up of functional decline in nursing home residents - degree of dementia contribute?", "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 efficacy of topical tissue plasminogen activator (tPA) for the resolution of postoperative or inflammatory intraocular fibrinous exudates. Each treatment consisted of drops of 1 mg/ml tPA given 9 times 5 minutes apart. Records were reviewed and the results at 24 and 48 hours were recorded. Sixty-two patients had a total of 94 treatments. Fibrin exudates following intraocular surgery in 34 patients were treated 44 times. In 6 patients there was a positive result. Fibrin associated with intraocular infection was treated in 9 patients. None showed clear improvement. Nineteen patients had a total of 34 treatments for poorly controlled intraocular pressure (IOP) after glaucoma surgery. Five patients showed adequate control of the IOP, 12 did not change, and 2 had a questionable improvement. Eleven patients had adequate IOP control after additional treatment. Seven required suture lysis, 2 ab interno bleb revision, and 2 YAG capsulotomy or iridotomy to reduce the IOP to an acceptable level.\n\nQuestion:\nDoes topical tissue plasminogen activator appear ineffective for the clearance of intraocular fibrin?", "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 efficacy of topical tissue plasminogen activator (tPA) for the resolution of postoperative or inflammatory intraocular fibrinous exudates. Each treatment consisted of drops of 1 mg/ml tPA given 9 times 5 minutes apart. Records were reviewed and the results at 24 and 48 hours were recorded. Sixty-two patients had a total of 94 treatments. Fibrin exudates following intraocular surgery in 34 patients were treated 44 times. In 6 patients there was a positive result. Fibrin associated with intraocular infection was treated in 9 patients. None showed clear improvement. Nineteen patients had a total of 34 treatments for poorly controlled intraocular pressure (IOP) after glaucoma surgery. Five patients showed adequate control of the IOP, 12 did not change, and 2 had a questionable improvement. Eleven patients had adequate IOP control after additional treatment. Seven required suture lysis, 2 ab interno bleb revision, and 2 YAG capsulotomy or iridotomy to reduce the IOP to an acceptable level.\n\nQuestion:\nDoes topical tissue plasminogen activator appear ineffective for the clearance of intraocular fibrin?", "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 efficacy of topical tissue plasminogen activator (tPA) for the resolution of postoperative or inflammatory intraocular fibrinous exudates. Each treatment consisted of drops of 1 mg/ml tPA given 9 times 5 minutes apart. Records were reviewed and the results at 24 and 48 hours were recorded. Sixty-two patients had a total of 94 treatments. Fibrin exudates following intraocular surgery in 34 patients were treated 44 times. In 6 patients there was a positive result. Fibrin associated with intraocular infection was treated in 9 patients. None showed clear improvement. Nineteen patients had a total of 34 treatments for poorly controlled intraocular pressure (IOP) after glaucoma surgery. Five patients showed adequate control of the IOP, 12 did not change, and 2 had a questionable improvement. Eleven patients had adequate IOP control after additional treatment. Seven required suture lysis, 2 ab interno bleb revision, and 2 YAG capsulotomy or iridotomy to reduce the IOP to an acceptable level.\n\nQuestion:\nDoes topical tissue plasminogen activator appear ineffective for the clearance of intraocular fibrin?", "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 goal of the current studies was to elucidate the role of the principal poly(ADP-ribose)polymerase isoform, PARP1 in the regulation of cellular energetics in endothelial cells under resting conditions and during oxidative stress. We utilized bEnd.3 endothelial cells and A549 human transformed epithelial cells. PARP1 was inhibited either by pharmacological inhibitors or by siRNA silencing. The Seahorse XF24 Extracellular Flux Analyzer was used to measure indices of mitochondrial respiration (oxygen consumption rate) and of glycolysis (extracellular acidification rate). Cell viability, cellular and mitochondrial NAD(+) levels and mitochondrial biogenesis were also measured. Silencing of PARP1 increased basal cellular parameters of oxidative phosphorylation, providing direct evidence that PARP1 is a regulator of mitochondrial function in resting cells. Pharmacological inhibitors of PARP1 and siRNA silencing of PARP1 protected against the development of mitochondrial dysfunction and elevated the respiratory reserve capacity in endothelial and epithelial cells exposed to oxidative stress. The observed effects were unrelated to an effect on mitochondrial biogenesis. Isolated mitochondria of A549 human transformed epithelial cells exhibited an improved resting bioenergetic status after stable lentiviral silencing of PARP1; these effects were associated with elevated resting mitochondrial NAD+ levels in PARP1 silenced cells.\n\nQuestion:\nIs cellular bioenergetics regulated by PARP1 under resting conditions and during oxidative stress?", "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 goal of the current studies was to elucidate the role of the principal poly(ADP-ribose)polymerase isoform, PARP1 in the regulation of cellular energetics in endothelial cells under resting conditions and during oxidative stress. We utilized bEnd.3 endothelial cells and A549 human transformed epithelial cells. PARP1 was inhibited either by pharmacological inhibitors or by siRNA silencing. The Seahorse XF24 Extracellular Flux Analyzer was used to measure indices of mitochondrial respiration (oxygen consumption rate) and of glycolysis (extracellular acidification rate). Cell viability, cellular and mitochondrial NAD(+) levels and mitochondrial biogenesis were also measured. Silencing of PARP1 increased basal cellular parameters of oxidative phosphorylation, providing direct evidence that PARP1 is a regulator of mitochondrial function in resting cells. Pharmacological inhibitors of PARP1 and siRNA silencing of PARP1 protected against the development of mitochondrial dysfunction and elevated the respiratory reserve capacity in endothelial and epithelial cells exposed to oxidative stress. The observed effects were unrelated to an effect on mitochondrial biogenesis. Isolated mitochondria of A549 human transformed epithelial cells exhibited an improved resting bioenergetic status after stable lentiviral silencing of PARP1; these effects were associated with elevated resting mitochondrial NAD+ levels in PARP1 silenced cells.\n\nQuestion:\nIs cellular bioenergetics regulated by PARP1 under resting conditions and during oxidative stress?", "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 goal of the current studies was to elucidate the role of the principal poly(ADP-ribose)polymerase isoform, PARP1 in the regulation of cellular energetics in endothelial cells under resting conditions and during oxidative stress. We utilized bEnd.3 endothelial cells and A549 human transformed epithelial cells. PARP1 was inhibited either by pharmacological inhibitors or by siRNA silencing. The Seahorse XF24 Extracellular Flux Analyzer was used to measure indices of mitochondrial respiration (oxygen consumption rate) and of glycolysis (extracellular acidification rate). Cell viability, cellular and mitochondrial NAD(+) levels and mitochondrial biogenesis were also measured. Silencing of PARP1 increased basal cellular parameters of oxidative phosphorylation, providing direct evidence that PARP1 is a regulator of mitochondrial function in resting cells. Pharmacological inhibitors of PARP1 and siRNA silencing of PARP1 protected against the development of mitochondrial dysfunction and elevated the respiratory reserve capacity in endothelial and epithelial cells exposed to oxidative stress. The observed effects were unrelated to an effect on mitochondrial biogenesis. Isolated mitochondria of A549 human transformed epithelial cells exhibited an improved resting bioenergetic status after stable lentiviral silencing of PARP1; these effects were associated with elevated resting mitochondrial NAD+ levels in PARP1 silenced cells.\n\nQuestion:\nIs cellular bioenergetics regulated by PARP1 under resting conditions and during oxidative stress?", "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:\nAutoantibodies recognizing 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) are found in patients with statin-associated immune-mediated necrotizing myopathy and, less commonly, in statin-unexposed patients with autoimmune myopathy. The main objective of this study was to define the association of anti-HMGCR antibody levels with disease activity. Anti-HMGCR levels, creatine kinase (CK) levels, and strength were assessed in anti-HMGCR-positive patients. Associations of antibody level with CK level and strength at visit 1 were analyzed in 55 patients, 40 of whom were exposed to statins. In 12 statin-exposed and 5 statin-unexposed patients with serum from 5 serial visits, the evolution of antibody levels, CK levels, and strength was investigated. Antibody levels were associated with CK levels (P < 0.001), arm strength (P < 0.05), and leg strength (P < 0.05) at visit 1, but these associations were only significant among statin-exposed patients in stratified analyses. With immunosuppressive treatment over 26.2 ± 12.6 months (mean ± SD), antibody levels declined (P < 0.05) and arm abduction strength improved (P < 0.05) in the 17 patients followed up longitudinally. The separate analysis showed that statin-exposed patients developed decreased antibody levels (P < 0.01), decreased CK levels (P < 0.001), improved arm strength (P < 0.05), and improved hip flexion strength (P < 0.05) with treatment. Anti-HMGCR antibody levels did not normalize in any patient.\n\nQuestion:\nDo antibody levels correlate with creatine kinase levels and strength in anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase-associated autoimmune myopathy?", "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:\nAutoantibodies recognizing 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) are found in patients with statin-associated immune-mediated necrotizing myopathy and, less commonly, in statin-unexposed patients with autoimmune myopathy. The main objective of this study was to define the association of anti-HMGCR antibody levels with disease activity. Anti-HMGCR levels, creatine kinase (CK) levels, and strength were assessed in anti-HMGCR-positive patients. Associations of antibody level with CK level and strength at visit 1 were analyzed in 55 patients, 40 of whom were exposed to statins. In 12 statin-exposed and 5 statin-unexposed patients with serum from 5 serial visits, the evolution of antibody levels, CK levels, and strength was investigated. Antibody levels were associated with CK levels (P < 0.001), arm strength (P < 0.05), and leg strength (P < 0.05) at visit 1, but these associations were only significant among statin-exposed patients in stratified analyses. With immunosuppressive treatment over 26.2 ± 12.6 months (mean ± SD), antibody levels declined (P < 0.05) and arm abduction strength improved (P < 0.05) in the 17 patients followed up longitudinally. The separate analysis showed that statin-exposed patients developed decreased antibody levels (P < 0.01), decreased CK levels (P < 0.001), improved arm strength (P < 0.05), and improved hip flexion strength (P < 0.05) with treatment. Anti-HMGCR antibody levels did not normalize in any patient.\n\nQuestion:\nDo antibody levels correlate with creatine kinase levels and strength in anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase-associated autoimmune myopathy?", "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:\nAutoantibodies recognizing 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) are found in patients with statin-associated immune-mediated necrotizing myopathy and, less commonly, in statin-unexposed patients with autoimmune myopathy. The main objective of this study was to define the association of anti-HMGCR antibody levels with disease activity. Anti-HMGCR levels, creatine kinase (CK) levels, and strength were assessed in anti-HMGCR-positive patients. Associations of antibody level with CK level and strength at visit 1 were analyzed in 55 patients, 40 of whom were exposed to statins. In 12 statin-exposed and 5 statin-unexposed patients with serum from 5 serial visits, the evolution of antibody levels, CK levels, and strength was investigated. Antibody levels were associated with CK levels (P < 0.001), arm strength (P < 0.05), and leg strength (P < 0.05) at visit 1, but these associations were only significant among statin-exposed patients in stratified analyses. With immunosuppressive treatment over 26.2 ± 12.6 months (mean ± SD), antibody levels declined (P < 0.05) and arm abduction strength improved (P < 0.05) in the 17 patients followed up longitudinally. The separate analysis showed that statin-exposed patients developed decreased antibody levels (P < 0.01), decreased CK levels (P < 0.001), improved arm strength (P < 0.05), and improved hip flexion strength (P < 0.05) with treatment. Anti-HMGCR antibody levels did not normalize in any patient.\n\nQuestion:\nDo antibody levels correlate with creatine kinase levels and strength in anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase-associated autoimmune myopathy?", "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:\nSpinal cord ischaemia with resulting paraplegia remains a devastating and unpredictable complication after thoraco-abdominal aortic surgery. With the advent of stem cell therapy and its potential to induce nervous tissue regeneration processes, the interest in the use of these cells as a treatment for neurological disorders has increased. Human stem cells, derived from the umbilical cord, are one of the strong candidates used in cell therapy for spinal cord injury because of weak immunogenicity and ready availability. We sought to evaluate the use of human umbilical cord blood stem cells (HUCBSCs) to attenuate the neurological effects of spinal cord ischaemia induced by high thoracic aorta occlusion. Forty Wistar rats were randomized to receive intrathecal injection of 10 µl phosphate buffered saline (PBS) solution containing 1 × 10(4) HUCBSCs, 30 min before (Tpre group: n = 10) and 30 min after (Tpos group: n = 10) descending thoracic aorta occlusion by intraluminal balloon during 12 min. Control groups received only PBS solution (Cpre group: n = 10; and Cpos group: n = 10). During a 28-day observational period, motor function was assessed by a functional grading scale (Basso, Beattie and Bresnahan). Segments of thoracolumbar spinal cord specimens were analysed for histological and immunohistochemical assessment for detection and quantification of human haematopoietic cells (CD45(+)) and apoptosis (transferase-mediated deoxyuridine triphosphate-biotin nick-end labelling). Overall mortality was 12 animals (30%). Therefore, the observational sample was composed of 28 animals. All groups showed similar incidence of paraplegia and mortality. The mean motor function scores showed no difference during time between the animals of each group, excepting for the Tpos group, which improved from 8.14 (±8.6) to 14.28 (±9.8) (P < 0.01). A treatment-by-time interaction was detected among animals that received HUCBSCs 30 min after ischaemia, with BBB scores higher from Days 14 to 28 compared with the first observational day with statistical difference (P = 0.01). Number of viable neurons was higher in the Tpos group (P = 0.14) and the incidence of apoptosis was lower in the same animals (P = 0.048), but showed no difference with its respective control. We confirmed the presence of CD45(+) cells 4 weeks after intrathecal injection in both therapeutic groups but mainly in the Tpos group.\n\nQuestion:\nDoes intrathecal injection of human umbilical cord blood stem cells attenuate spinal cord ischaemic compromise 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:\nSpinal cord ischaemia with resulting paraplegia remains a devastating and unpredictable complication after thoraco-abdominal aortic surgery. With the advent of stem cell therapy and its potential to induce nervous tissue regeneration processes, the interest in the use of these cells as a treatment for neurological disorders has increased. Human stem cells, derived from the umbilical cord, are one of the strong candidates used in cell therapy for spinal cord injury because of weak immunogenicity and ready availability. We sought to evaluate the use of human umbilical cord blood stem cells (HUCBSCs) to attenuate the neurological effects of spinal cord ischaemia induced by high thoracic aorta occlusion. Forty Wistar rats were randomized to receive intrathecal injection of 10 µl phosphate buffered saline (PBS) solution containing 1 × 10(4) HUCBSCs, 30 min before (Tpre group: n = 10) and 30 min after (Tpos group: n = 10) descending thoracic aorta occlusion by intraluminal balloon during 12 min. Control groups received only PBS solution (Cpre group: n = 10; and Cpos group: n = 10). During a 28-day observational period, motor function was assessed by a functional grading scale (Basso, Beattie and Bresnahan). Segments of thoracolumbar spinal cord specimens were analysed for histological and immunohistochemical assessment for detection and quantification of human haematopoietic cells (CD45(+)) and apoptosis (transferase-mediated deoxyuridine triphosphate-biotin nick-end labelling). Overall mortality was 12 animals (30%). Therefore, the observational sample was composed of 28 animals. All groups showed similar incidence of paraplegia and mortality. The mean motor function scores showed no difference during time between the animals of each group, excepting for the Tpos group, which improved from 8.14 (±8.6) to 14.28 (±9.8) (P < 0.01). A treatment-by-time interaction was detected among animals that received HUCBSCs 30 min after ischaemia, with BBB scores higher from Days 14 to 28 compared with the first observational day with statistical difference (P = 0.01). Number of viable neurons was higher in the Tpos group (P = 0.14) and the incidence of apoptosis was lower in the same animals (P = 0.048), but showed no difference with its respective control. We confirmed the presence of CD45(+) cells 4 weeks after intrathecal injection in both therapeutic groups but mainly in the Tpos group.\n\nQuestion:\nDoes intrathecal injection of human umbilical cord blood stem cells attenuate spinal cord ischaemic compromise 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:\nSpinal cord ischaemia with resulting paraplegia remains a devastating and unpredictable complication after thoraco-abdominal aortic surgery. With the advent of stem cell therapy and its potential to induce nervous tissue regeneration processes, the interest in the use of these cells as a treatment for neurological disorders has increased. Human stem cells, derived from the umbilical cord, are one of the strong candidates used in cell therapy for spinal cord injury because of weak immunogenicity and ready availability. We sought to evaluate the use of human umbilical cord blood stem cells (HUCBSCs) to attenuate the neurological effects of spinal cord ischaemia induced by high thoracic aorta occlusion. Forty Wistar rats were randomized to receive intrathecal injection of 10 µl phosphate buffered saline (PBS) solution containing 1 × 10(4) HUCBSCs, 30 min before (Tpre group: n = 10) and 30 min after (Tpos group: n = 10) descending thoracic aorta occlusion by intraluminal balloon during 12 min. Control groups received only PBS solution (Cpre group: n = 10; and Cpos group: n = 10). During a 28-day observational period, motor function was assessed by a functional grading scale (Basso, Beattie and Bresnahan). Segments of thoracolumbar spinal cord specimens were analysed for histological and immunohistochemical assessment for detection and quantification of human haematopoietic cells (CD45(+)) and apoptosis (transferase-mediated deoxyuridine triphosphate-biotin nick-end labelling). Overall mortality was 12 animals (30%). Therefore, the observational sample was composed of 28 animals. All groups showed similar incidence of paraplegia and mortality. The mean motor function scores showed no difference during time between the animals of each group, excepting for the Tpos group, which improved from 8.14 (±8.6) to 14.28 (±9.8) (P < 0.01). A treatment-by-time interaction was detected among animals that received HUCBSCs 30 min after ischaemia, with BBB scores higher from Days 14 to 28 compared with the first observational day with statistical difference (P = 0.01). Number of viable neurons was higher in the Tpos group (P = 0.14) and the incidence of apoptosis was lower in the same animals (P = 0.048), but showed no difference with its respective control. We confirmed the presence of CD45(+) cells 4 weeks after intrathecal injection in both therapeutic groups but mainly in the Tpos group.\n\nQuestion:\nDoes intrathecal injection of human umbilical cord blood stem cells attenuate spinal cord ischaemic compromise 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:\nPeriodontitis is a chronic infectious disease associated with Gram-negative subgingival microflora. In pregnant women, periodontitis is thought to be associated with adverse pregnancy outcomes, although the pathophysiology is unknown. Additionally, smoking is an established risk factor for adverse pregnancy outcomes. In the present study, we examined the direct effects of Porphyromonas gingivalis lipopolysaccharides (PGLPS) and nicotine on a trophoblast cell line. HTR-8/SVneo cells were plated on Matrigel chambers with or without PGLPS and nicotine. The invasive activity of the cells was directly evaluated using microscopy. PGLPS alone did not reduce the invasive activity of the HTR-8/SVneo cells. The co-administration of nicotine with PGLPS significantly reduced the invasive activity of the cells.\n\nQuestion:\nDoes porphyromonas gingivalis lipopolysaccharide inhibit trophoblast invasion in the presence of nicotine?", "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:\nPeriodontitis is a chronic infectious disease associated with Gram-negative subgingival microflora. In pregnant women, periodontitis is thought to be associated with adverse pregnancy outcomes, although the pathophysiology is unknown. Additionally, smoking is an established risk factor for adverse pregnancy outcomes. In the present study, we examined the direct effects of Porphyromonas gingivalis lipopolysaccharides (PGLPS) and nicotine on a trophoblast cell line. HTR-8/SVneo cells were plated on Matrigel chambers with or without PGLPS and nicotine. The invasive activity of the cells was directly evaluated using microscopy. PGLPS alone did not reduce the invasive activity of the HTR-8/SVneo cells. The co-administration of nicotine with PGLPS significantly reduced the invasive activity of the cells.\n\nQuestion:\nDoes porphyromonas gingivalis lipopolysaccharide inhibit trophoblast invasion in the presence of nicotine?", "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:\nPeriodontitis is a chronic infectious disease associated with Gram-negative subgingival microflora. In pregnant women, periodontitis is thought to be associated with adverse pregnancy outcomes, although the pathophysiology is unknown. Additionally, smoking is an established risk factor for adverse pregnancy outcomes. In the present study, we examined the direct effects of Porphyromonas gingivalis lipopolysaccharides (PGLPS) and nicotine on a trophoblast cell line. HTR-8/SVneo cells were plated on Matrigel chambers with or without PGLPS and nicotine. The invasive activity of the cells was directly evaluated using microscopy. PGLPS alone did not reduce the invasive activity of the HTR-8/SVneo cells. The co-administration of nicotine with PGLPS significantly reduced the invasive activity of the cells.\n\nQuestion:\nDoes porphyromonas gingivalis lipopolysaccharide inhibit trophoblast invasion in the presence of nicotine?", "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:\nHypomagnesemia has been associated with an increased risk of postoperative atrial fibrillation (POAF). Although previous studies have suggested a beneficial effect of magnesium (Mg) therapy, almost all of these are limited by small sample size and relatively low Mg dose. We hypothesized that high-dose Mg decreases the occurrence of new-onset POAF, and we tested this hypothesis by using data from a prospective trial that assessed the effect of Mg on cognitive outcomes in patients undergoing cardiac surgery. A total of 389 patients undergoing cardiac surgery were enrolled in this double-blind, placebo-controlled trial. Subjects were randomized to receive Mg as a 50-mg/kg bolus immediately after induction of anesthesia followed by another 50 mg/kg as an infusion given over 3 hours (total dose, 100 mg/kg) or placebo. We tested the effect of Mg therapy on POAF with logistic regression, adjusting for the risk of atrial fibrillation (AF) by using the Multicenter Study of Perioperative Ischemia risk index for Atrial Fibrillation after Cardiac Surgery. Among the 363 patients analyzed, after we excluded patients with chronic or acute preoperative AF (placebo: n = 177; Mg: n = 186), the incidence of new-onset POAF was 42.5% (95% confidence interval [CI], 35%-50%) in the Mg group compared with 37.9% (95% CI, 31%-45%) in the placebo group (P = 0.40). The 95% CI for this absolute risk difference of 4.6% is -5.5% to 14.7%. The time to onset of POAF also was identical between the groups, and no significant effect of Mg was found in logistic regression analysis after we adjusted for AF risk (odds ratio, 1.09; 95% CI, 0.69-1.72; P = 0.73).\n\nQuestion:\nDoes intraoperative Magnesium Administration Reduce Postoperative Atrial Fibrillation After Cardiac Surgery?", "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:\nHypomagnesemia has been associated with an increased risk of postoperative atrial fibrillation (POAF). Although previous studies have suggested a beneficial effect of magnesium (Mg) therapy, almost all of these are limited by small sample size and relatively low Mg dose. We hypothesized that high-dose Mg decreases the occurrence of new-onset POAF, and we tested this hypothesis by using data from a prospective trial that assessed the effect of Mg on cognitive outcomes in patients undergoing cardiac surgery. A total of 389 patients undergoing cardiac surgery were enrolled in this double-blind, placebo-controlled trial. Subjects were randomized to receive Mg as a 50-mg/kg bolus immediately after induction of anesthesia followed by another 50 mg/kg as an infusion given over 3 hours (total dose, 100 mg/kg) or placebo. We tested the effect of Mg therapy on POAF with logistic regression, adjusting for the risk of atrial fibrillation (AF) by using the Multicenter Study of Perioperative Ischemia risk index for Atrial Fibrillation after Cardiac Surgery. Among the 363 patients analyzed, after we excluded patients with chronic or acute preoperative AF (placebo: n = 177; Mg: n = 186), the incidence of new-onset POAF was 42.5% (95% confidence interval [CI], 35%-50%) in the Mg group compared with 37.9% (95% CI, 31%-45%) in the placebo group (P = 0.40). The 95% CI for this absolute risk difference of 4.6% is -5.5% to 14.7%. The time to onset of POAF also was identical between the groups, and no significant effect of Mg was found in logistic regression analysis after we adjusted for AF risk (odds ratio, 1.09; 95% CI, 0.69-1.72; P = 0.73).\n\nQuestion:\nDoes intraoperative Magnesium Administration Reduce Postoperative Atrial Fibrillation After Cardiac Surgery?", "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:\nHypomagnesemia has been associated with an increased risk of postoperative atrial fibrillation (POAF). Although previous studies have suggested a beneficial effect of magnesium (Mg) therapy, almost all of these are limited by small sample size and relatively low Mg dose. We hypothesized that high-dose Mg decreases the occurrence of new-onset POAF, and we tested this hypothesis by using data from a prospective trial that assessed the effect of Mg on cognitive outcomes in patients undergoing cardiac surgery. A total of 389 patients undergoing cardiac surgery were enrolled in this double-blind, placebo-controlled trial. Subjects were randomized to receive Mg as a 50-mg/kg bolus immediately after induction of anesthesia followed by another 50 mg/kg as an infusion given over 3 hours (total dose, 100 mg/kg) or placebo. We tested the effect of Mg therapy on POAF with logistic regression, adjusting for the risk of atrial fibrillation (AF) by using the Multicenter Study of Perioperative Ischemia risk index for Atrial Fibrillation after Cardiac Surgery. Among the 363 patients analyzed, after we excluded patients with chronic or acute preoperative AF (placebo: n = 177; Mg: n = 186), the incidence of new-onset POAF was 42.5% (95% confidence interval [CI], 35%-50%) in the Mg group compared with 37.9% (95% CI, 31%-45%) in the placebo group (P = 0.40). The 95% CI for this absolute risk difference of 4.6% is -5.5% to 14.7%. The time to onset of POAF also was identical between the groups, and no significant effect of Mg was found in logistic regression analysis after we adjusted for AF risk (odds ratio, 1.09; 95% CI, 0.69-1.72; P = 0.73).\n\nQuestion:\nDoes intraoperative Magnesium Administration Reduce Postoperative Atrial Fibrillation After Cardiac Surgery?", "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:\nTotal food intake is a function of meal size and meal frequency, and adjustments to these parameters allow animals to maintain a stable energy balance in changing environmental conditions. The physiological mechanisms that regulate meal size have been studied in blowflies but have not been previously examined in Drosophila. Here we show that mutations in the leucokinin neuropeptide (leuc) and leucokinin receptor (lkr) genes cause phenotypes in which Drosophila adults have an increase in meal size and a compensatory reduction in meal frequency. Because mutant flies take larger but fewer meals, their caloric intake is the same as that of wild-type flies. The expression patterns of the leuc and lkr genes identify small groups of brain neurons that regulate this behavior. Leuc-containing presynaptic terminals are found close to Lkr neurons in the brain and ventral ganglia, suggesting that they deliver Leuc peptide to these neurons. Lkr neurons innervate the foregut. Flies in which Leuc or Lkr neurons are ablated have defects identical to those of leucokinin pathway mutants.\n\nQuestion:\nDo the leucokinin pathway and its neurons regulate meal size in Drosophila?", "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:\nTotal food intake is a function of meal size and meal frequency, and adjustments to these parameters allow animals to maintain a stable energy balance in changing environmental conditions. The physiological mechanisms that regulate meal size have been studied in blowflies but have not been previously examined in Drosophila. Here we show that mutations in the leucokinin neuropeptide (leuc) and leucokinin receptor (lkr) genes cause phenotypes in which Drosophila adults have an increase in meal size and a compensatory reduction in meal frequency. Because mutant flies take larger but fewer meals, their caloric intake is the same as that of wild-type flies. The expression patterns of the leuc and lkr genes identify small groups of brain neurons that regulate this behavior. Leuc-containing presynaptic terminals are found close to Lkr neurons in the brain and ventral ganglia, suggesting that they deliver Leuc peptide to these neurons. Lkr neurons innervate the foregut. Flies in which Leuc or Lkr neurons are ablated have defects identical to those of leucokinin pathway mutants.\n\nQuestion:\nDo the leucokinin pathway and its neurons regulate meal size in Drosophila?", "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:\nTotal food intake is a function of meal size and meal frequency, and adjustments to these parameters allow animals to maintain a stable energy balance in changing environmental conditions. The physiological mechanisms that regulate meal size have been studied in blowflies but have not been previously examined in Drosophila. Here we show that mutations in the leucokinin neuropeptide (leuc) and leucokinin receptor (lkr) genes cause phenotypes in which Drosophila adults have an increase in meal size and a compensatory reduction in meal frequency. Because mutant flies take larger but fewer meals, their caloric intake is the same as that of wild-type flies. The expression patterns of the leuc and lkr genes identify small groups of brain neurons that regulate this behavior. Leuc-containing presynaptic terminals are found close to Lkr neurons in the brain and ventral ganglia, suggesting that they deliver Leuc peptide to these neurons. Lkr neurons innervate the foregut. Flies in which Leuc or Lkr neurons are ablated have defects identical to those of leucokinin pathway mutants.\n\nQuestion:\nDo the leucokinin pathway and its neurons regulate meal size in Drosophila?", "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 define whether immunosuppressive agents that block the interleukin (IL)-2 pathway could prevent activation-induced cell death of activated T cells in the graft, we measured expression of IL-2, IL-2 receptor alpha chain (CD25), IL-15, Fas, and Fas ligand by real time reverse transcription-polymerase chain reaction in cardiac allografts. We characterized the phenotype of the infiltrating cells (CD3, CD68, CD25) by immunohistochemistry. The proportion of apoptotic graft-infiltrating cells was determined by TUNEL (terminal deoxynucleotidyl transferase dUTP nick-end labeling) staining. We analyzed endomyocardial biopsy specimens from cardiac allograft recipients who were treated with anti-CD25 monoclonal antibody (mAb) induction therapy (daclizumab) or with matching placebo in combination with cyclosporine, steroids, and mycophenolate mofetil. Treatment with anti-CD25 mAb affected the number of infiltrating CD3 and CD68 cells and the IL-2-regulated apoptotic pathway. During anti-CD25 mAb treatment, significantly lower intragraft IL-2 and CD25 mRNA transcription levels and decreased numbers of CD25+ T cells were found compared with the levels measured in endomyocardial biopsy specimens from placebo-treated patients (5- to 10-fold, P=0.002 and P<0.0001, respectively). In these samples the intragraft mRNA expression levels of IL-15 were also lower (P=0.02). Inhibition of the IL-2 pathway by anti-CD25 mAb therapy was accompanied by reduced mRNA and protein of Fas ligand and not by reduced Fas expression (P=0.001 and P=0.03). TUNEL staining revealed that the proportion of graft-infiltrating cells was lower in the anti-CD25 mAb patient group than the proportion of apoptotic cells in patients receiving placebo (P=0.06).\n\nQuestion:\nDoes anti-CD25 monoclonal antibody therapy affect the death signals of graft-infiltrating cells after clinical heart transplantation?", "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 define whether immunosuppressive agents that block the interleukin (IL)-2 pathway could prevent activation-induced cell death of activated T cells in the graft, we measured expression of IL-2, IL-2 receptor alpha chain (CD25), IL-15, Fas, and Fas ligand by real time reverse transcription-polymerase chain reaction in cardiac allografts. We characterized the phenotype of the infiltrating cells (CD3, CD68, CD25) by immunohistochemistry. The proportion of apoptotic graft-infiltrating cells was determined by TUNEL (terminal deoxynucleotidyl transferase dUTP nick-end labeling) staining. We analyzed endomyocardial biopsy specimens from cardiac allograft recipients who were treated with anti-CD25 monoclonal antibody (mAb) induction therapy (daclizumab) or with matching placebo in combination with cyclosporine, steroids, and mycophenolate mofetil. Treatment with anti-CD25 mAb affected the number of infiltrating CD3 and CD68 cells and the IL-2-regulated apoptotic pathway. During anti-CD25 mAb treatment, significantly lower intragraft IL-2 and CD25 mRNA transcription levels and decreased numbers of CD25+ T cells were found compared with the levels measured in endomyocardial biopsy specimens from placebo-treated patients (5- to 10-fold, P=0.002 and P<0.0001, respectively). In these samples the intragraft mRNA expression levels of IL-15 were also lower (P=0.02). Inhibition of the IL-2 pathway by anti-CD25 mAb therapy was accompanied by reduced mRNA and protein of Fas ligand and not by reduced Fas expression (P=0.001 and P=0.03). TUNEL staining revealed that the proportion of graft-infiltrating cells was lower in the anti-CD25 mAb patient group than the proportion of apoptotic cells in patients receiving placebo (P=0.06).\n\nQuestion:\nDoes anti-CD25 monoclonal antibody therapy affect the death signals of graft-infiltrating cells after clinical heart transplantation?", "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 define whether immunosuppressive agents that block the interleukin (IL)-2 pathway could prevent activation-induced cell death of activated T cells in the graft, we measured expression of IL-2, IL-2 receptor alpha chain (CD25), IL-15, Fas, and Fas ligand by real time reverse transcription-polymerase chain reaction in cardiac allografts. We characterized the phenotype of the infiltrating cells (CD3, CD68, CD25) by immunohistochemistry. The proportion of apoptotic graft-infiltrating cells was determined by TUNEL (terminal deoxynucleotidyl transferase dUTP nick-end labeling) staining. We analyzed endomyocardial biopsy specimens from cardiac allograft recipients who were treated with anti-CD25 monoclonal antibody (mAb) induction therapy (daclizumab) or with matching placebo in combination with cyclosporine, steroids, and mycophenolate mofetil. Treatment with anti-CD25 mAb affected the number of infiltrating CD3 and CD68 cells and the IL-2-regulated apoptotic pathway. During anti-CD25 mAb treatment, significantly lower intragraft IL-2 and CD25 mRNA transcription levels and decreased numbers of CD25+ T cells were found compared with the levels measured in endomyocardial biopsy specimens from placebo-treated patients (5- to 10-fold, P=0.002 and P<0.0001, respectively). In these samples the intragraft mRNA expression levels of IL-15 were also lower (P=0.02). Inhibition of the IL-2 pathway by anti-CD25 mAb therapy was accompanied by reduced mRNA and protein of Fas ligand and not by reduced Fas expression (P=0.001 and P=0.03). TUNEL staining revealed that the proportion of graft-infiltrating cells was lower in the anti-CD25 mAb patient group than the proportion of apoptotic cells in patients receiving placebo (P=0.06).\n\nQuestion:\nDoes anti-CD25 monoclonal antibody therapy affect the death signals of graft-infiltrating cells after clinical heart transplantation?", "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:\nCarnosine is a naturally occurring dipeptide with multiple neuroprotective properties. In addition, it is well tolerated in high doses with minimal side effects. The purposes of this study were to determine whether carnosine is neuroprotective in permanent focal cerebral ischemia and to determine potential mechanisms of neuroprotection. We investigated the efficacy of carnosine in a mouse model of permanent focal cerebral ischemia. The effects of carnosine were investigated with respect to neuronal damage and infarct formation, endogenous antioxidant status, and matrix metalloproteinase activity. Carnosine significantly decreased infarct size and neuronal damage when administered at time points both before and after the induction of ischemia. Carnosine also decreased reactive oxygen species levels in the ischemic brain, preserved normal glutathione levels, and decreased matrix metalloproteinase protein levels and activity.\n\nQuestion:\nIs carnosine neuroprotective against permanent focal cerebral ischemia 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:\nCarnosine is a naturally occurring dipeptide with multiple neuroprotective properties. In addition, it is well tolerated in high doses with minimal side effects. The purposes of this study were to determine whether carnosine is neuroprotective in permanent focal cerebral ischemia and to determine potential mechanisms of neuroprotection. We investigated the efficacy of carnosine in a mouse model of permanent focal cerebral ischemia. The effects of carnosine were investigated with respect to neuronal damage and infarct formation, endogenous antioxidant status, and matrix metalloproteinase activity. Carnosine significantly decreased infarct size and neuronal damage when administered at time points both before and after the induction of ischemia. Carnosine also decreased reactive oxygen species levels in the ischemic brain, preserved normal glutathione levels, and decreased matrix metalloproteinase protein levels and activity.\n\nQuestion:\nIs carnosine neuroprotective against permanent focal cerebral ischemia 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:\nCarnosine is a naturally occurring dipeptide with multiple neuroprotective properties. In addition, it is well tolerated in high doses with minimal side effects. The purposes of this study were to determine whether carnosine is neuroprotective in permanent focal cerebral ischemia and to determine potential mechanisms of neuroprotection. We investigated the efficacy of carnosine in a mouse model of permanent focal cerebral ischemia. The effects of carnosine were investigated with respect to neuronal damage and infarct formation, endogenous antioxidant status, and matrix metalloproteinase activity. Carnosine significantly decreased infarct size and neuronal damage when administered at time points both before and after the induction of ischemia. Carnosine also decreased reactive oxygen species levels in the ischemic brain, preserved normal glutathione levels, and decreased matrix metalloproteinase protein levels and activity.\n\nQuestion:\nIs carnosine neuroprotective against permanent focal cerebral ischemia 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:\nOxidative stress is causally associated with the pathogenesis of Parkinson's disease (PD). Oxygen generates a large amount of reactive oxygen species (ROS). ROS including hydroxyl radicals and H(2)O(2) react with guanine residues in DNA and produce 8-hydroxydeoxyguanosine (8-OHdG). 8-OHdG serves as a biomarker for oxidative stress in various diseases. We investigated urinary 8-OHdG levels in 61 PD patients and 28 normal subjects to evaluate the correlation with various clinical features. We quantified disease severity using the Unified Parkinson's Disease Rating Scale for motor symptoms (UPDRS part 3), the Mini-Mental State Examination (MMSE) for mental function, and the Tottori University Hallucination Rating Scale (TUHARS) for quantifying hallucinations. There were significant correlations between 8-OHdG and all the examined parameters, but the partial correlation coefficients excluding contributions of all the other parameters showed that only TUHARS and UPDRS part 3 are significantly related to 8-OHdG. In particular, TUHARS correlates best with urinary 8-OHdG levels.\n\nQuestion:\nDo urinary 8-hydroxydeoxyguanosine correlate with hallucinations rather than motor symptoms in Parkinson 's 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:\nOxidative stress is causally associated with the pathogenesis of Parkinson's disease (PD). Oxygen generates a large amount of reactive oxygen species (ROS). ROS including hydroxyl radicals and H(2)O(2) react with guanine residues in DNA and produce 8-hydroxydeoxyguanosine (8-OHdG). 8-OHdG serves as a biomarker for oxidative stress in various diseases. We investigated urinary 8-OHdG levels in 61 PD patients and 28 normal subjects to evaluate the correlation with various clinical features. We quantified disease severity using the Unified Parkinson's Disease Rating Scale for motor symptoms (UPDRS part 3), the Mini-Mental State Examination (MMSE) for mental function, and the Tottori University Hallucination Rating Scale (TUHARS) for quantifying hallucinations. There were significant correlations between 8-OHdG and all the examined parameters, but the partial correlation coefficients excluding contributions of all the other parameters showed that only TUHARS and UPDRS part 3 are significantly related to 8-OHdG. In particular, TUHARS correlates best with urinary 8-OHdG levels.\n\nQuestion:\nDo urinary 8-hydroxydeoxyguanosine correlate with hallucinations rather than motor symptoms in Parkinson 's 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:\nOxidative stress is causally associated with the pathogenesis of Parkinson's disease (PD). Oxygen generates a large amount of reactive oxygen species (ROS). ROS including hydroxyl radicals and H(2)O(2) react with guanine residues in DNA and produce 8-hydroxydeoxyguanosine (8-OHdG). 8-OHdG serves as a biomarker for oxidative stress in various diseases. We investigated urinary 8-OHdG levels in 61 PD patients and 28 normal subjects to evaluate the correlation with various clinical features. We quantified disease severity using the Unified Parkinson's Disease Rating Scale for motor symptoms (UPDRS part 3), the Mini-Mental State Examination (MMSE) for mental function, and the Tottori University Hallucination Rating Scale (TUHARS) for quantifying hallucinations. There were significant correlations between 8-OHdG and all the examined parameters, but the partial correlation coefficients excluding contributions of all the other parameters showed that only TUHARS and UPDRS part 3 are significantly related to 8-OHdG. In particular, TUHARS correlates best with urinary 8-OHdG levels.\n\nQuestion:\nDo urinary 8-hydroxydeoxyguanosine correlate with hallucinations rather than motor symptoms in Parkinson 's 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:\nAlthough chronic rhinosinusitis (CRS) with nasal polyps (CRSwNP) is characterized by T(H)2 inflammation, the role of mast cells is poorly understood. The objective of this study was to investigate the presence, localization, and phenotype of mast cells in patients with CRS. We collected nasal tissue and nasal lavage fluid from patients with CRS and control subjects. We analyzed mRNA for the mast cell proteases tryptase, chymase, and carboxypeptidase A3 by using real-time PCR and measured mast cell protease proteins by using ELISA, immunohistochemistry, and immunofluorescence. Tryptase mRNA was significantly increased in nasal polyps (NPs) from patients with CRSwNP (P< .001) compared with uncinate tissue from patients with CRS or control subjects. Tryptase protein was also elevated in NPs and in nasal lavage fluids from patients with CRSwNP. Immnohistochemistry showed increased numbers of mast cells in epithelium and glands but not within the lamina propria in NPs. The mast cells detected in the epithelium in NPs were characterized by the expression of tryptase and carboxypeptidase A3 but not chymase. Mast cells expressing all the 3 proteases were abundant within the glandular epithelium of NPs but were not found in normal glandular structures.\n\nQuestion:\nAre glandular mast cells with distinct phenotype highly elevated in chronic rhinosinusitis with nasal polyps?", "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 chronic rhinosinusitis (CRS) with nasal polyps (CRSwNP) is characterized by T(H)2 inflammation, the role of mast cells is poorly understood. The objective of this study was to investigate the presence, localization, and phenotype of mast cells in patients with CRS. We collected nasal tissue and nasal lavage fluid from patients with CRS and control subjects. We analyzed mRNA for the mast cell proteases tryptase, chymase, and carboxypeptidase A3 by using real-time PCR and measured mast cell protease proteins by using ELISA, immunohistochemistry, and immunofluorescence. Tryptase mRNA was significantly increased in nasal polyps (NPs) from patients with CRSwNP (P< .001) compared with uncinate tissue from patients with CRS or control subjects. Tryptase protein was also elevated in NPs and in nasal lavage fluids from patients with CRSwNP. Immnohistochemistry showed increased numbers of mast cells in epithelium and glands but not within the lamina propria in NPs. The mast cells detected in the epithelium in NPs were characterized by the expression of tryptase and carboxypeptidase A3 but not chymase. Mast cells expressing all the 3 proteases were abundant within the glandular epithelium of NPs but were not found in normal glandular structures.\n\nQuestion:\nAre glandular mast cells with distinct phenotype highly elevated in chronic rhinosinusitis with nasal polyps?", "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 chronic rhinosinusitis (CRS) with nasal polyps (CRSwNP) is characterized by T(H)2 inflammation, the role of mast cells is poorly understood. The objective of this study was to investigate the presence, localization, and phenotype of mast cells in patients with CRS. We collected nasal tissue and nasal lavage fluid from patients with CRS and control subjects. We analyzed mRNA for the mast cell proteases tryptase, chymase, and carboxypeptidase A3 by using real-time PCR and measured mast cell protease proteins by using ELISA, immunohistochemistry, and immunofluorescence. Tryptase mRNA was significantly increased in nasal polyps (NPs) from patients with CRSwNP (P< .001) compared with uncinate tissue from patients with CRS or control subjects. Tryptase protein was also elevated in NPs and in nasal lavage fluids from patients with CRSwNP. Immnohistochemistry showed increased numbers of mast cells in epithelium and glands but not within the lamina propria in NPs. The mast cells detected in the epithelium in NPs were characterized by the expression of tryptase and carboxypeptidase A3 but not chymase. Mast cells expressing all the 3 proteases were abundant within the glandular epithelium of NPs but were not found in normal glandular structures.\n\nQuestion:\nAre glandular mast cells with distinct phenotype highly elevated in chronic rhinosinusitis with nasal polyps?", "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) is the key process driving cancer metastasis. Oncogene/self renewal factor BMI-1 has been shown to induce EMT in cancer cells. Recent studies have implied that noncoding microRNAs (miRNAs) act as crucial modulators for EMT. The aims of this study was to determine the roles of BMI-1 in inducing EMT of endometrial cancer (EC) cells and the possible role of miRNA in controlling BMI-1 expression. We evaluated the expression of BMI-1 gene in a panel of EC cell lines, and detected a strong association with invasive capability. Stable silencing of BMI-1 in invasive mesenchymal-type EC cells up-regulated the epithelial marker E-cadherin, down-regulated mesenchymal marker Vimentin, and significantly reduced cell invasion in vitro. Furthermore, we discovered that the expression of BMI-1 was suppressed by miR-194 via direct binding to the BMI-1 3'-untranslated region 3'-UTR). Ectopic expression of miR-194 in EC cells induced a mesenchymal to epithelial transition (MET) by restoring E-cadherin, reducing Vimentin expression, and inhibiting cell invasion in vitro. Moreover, BMI-1 knockdown inhibited in vitro EC cell proliferation and clone growth, correlated with either increased p16 expression or decreased expression of stem cell and chemoresistance markers (SOX-2, KLF4 and MRP-1).\n\nQuestion:\nDoes microRNA-194 inhibit epithelial to mesenchymal transition of endometrial cancer cells by targeting oncogene BMI-1?", "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) is the key process driving cancer metastasis. Oncogene/self renewal factor BMI-1 has been shown to induce EMT in cancer cells. Recent studies have implied that noncoding microRNAs (miRNAs) act as crucial modulators for EMT. The aims of this study was to determine the roles of BMI-1 in inducing EMT of endometrial cancer (EC) cells and the possible role of miRNA in controlling BMI-1 expression. We evaluated the expression of BMI-1 gene in a panel of EC cell lines, and detected a strong association with invasive capability. Stable silencing of BMI-1 in invasive mesenchymal-type EC cells up-regulated the epithelial marker E-cadherin, down-regulated mesenchymal marker Vimentin, and significantly reduced cell invasion in vitro. Furthermore, we discovered that the expression of BMI-1 was suppressed by miR-194 via direct binding to the BMI-1 3'-untranslated region 3'-UTR). Ectopic expression of miR-194 in EC cells induced a mesenchymal to epithelial transition (MET) by restoring E-cadherin, reducing Vimentin expression, and inhibiting cell invasion in vitro. Moreover, BMI-1 knockdown inhibited in vitro EC cell proliferation and clone growth, correlated with either increased p16 expression or decreased expression of stem cell and chemoresistance markers (SOX-2, KLF4 and MRP-1).\n\nQuestion:\nDoes microRNA-194 inhibit epithelial to mesenchymal transition of endometrial cancer cells by targeting oncogene BMI-1?", "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) is the key process driving cancer metastasis. Oncogene/self renewal factor BMI-1 has been shown to induce EMT in cancer cells. Recent studies have implied that noncoding microRNAs (miRNAs) act as crucial modulators for EMT. The aims of this study was to determine the roles of BMI-1 in inducing EMT of endometrial cancer (EC) cells and the possible role of miRNA in controlling BMI-1 expression. We evaluated the expression of BMI-1 gene in a panel of EC cell lines, and detected a strong association with invasive capability. Stable silencing of BMI-1 in invasive mesenchymal-type EC cells up-regulated the epithelial marker E-cadherin, down-regulated mesenchymal marker Vimentin, and significantly reduced cell invasion in vitro. Furthermore, we discovered that the expression of BMI-1 was suppressed by miR-194 via direct binding to the BMI-1 3'-untranslated region 3'-UTR). Ectopic expression of miR-194 in EC cells induced a mesenchymal to epithelial transition (MET) by restoring E-cadherin, reducing Vimentin expression, and inhibiting cell invasion in vitro. Moreover, BMI-1 knockdown inhibited in vitro EC cell proliferation and clone growth, correlated with either increased p16 expression or decreased expression of stem cell and chemoresistance markers (SOX-2, KLF4 and MRP-1).\n\nQuestion:\nDoes microRNA-194 inhibit epithelial to mesenchymal transition of endometrial cancer cells by targeting oncogene BMI-1?", "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:\nTwo endophenotypes of arterial calcification, calcification on arterial wall and calcification in atherosclerotic plaques, are associated with different types of cardiovascular events. Mgp-deficient mice showed matrix Gla protein (MGP) is strongly associated with calcification on arterial wall without atherosclerotic plaques, and MGP variants were not significantly associated with myocardial infarction. MGP may play different roles in the 2 endophenotypes. We analyzed the associations of MGP variants rs4236, rs1800801, and rs1800802 with the 2 endophenotypes determined by multidetector computed tomography angiography. A total of 585 with calcification on coronary artery wall, 675 with calcification in coronary atherosclerotic plaques, 454 with calcification on aortic wall, and 725 controls were enrolled. After Bonferroni correction, rs4236 and rs1800801 were still associated with calcification on arterial wall, the odds ratios were 0.708 (95% confidence interval, 0.540-0.928) for rs4236 and 0.652 (95% confidence interval, 0.479-0.888) for rs1800801 in coronary artery wall calcification, and 0.699 (95% confidence interval, 0.525-0.931) for rs4236 and 0.650 (95% confidence interval, 0.467-0.905) for rs1800801 in aortic wall calcification, respectively. The variants were correlated with calcification severity by ln(CAC Agatston score+1) in coronary artery wall calcification but not in atherosclerotic plaque calcification. In accordance with their associations with calcification on arterial wall, rs4236C and rs1800801A were associated with higher MGP plasma levels, whereas rs1800802C was associated with lower MGP levels in normal controls. Because of the role of calcification in plaque vulnerability, their associations with acute myocardial infarction were also determined in 771 controls and 752 patients, no association was found.\n\nQuestion:\nAre common genetic variants of MGP associated with calcification on the arterial wall but not with calcification present in the atherosclerotic plaques?", "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:\nTwo endophenotypes of arterial calcification, calcification on arterial wall and calcification in atherosclerotic plaques, are associated with different types of cardiovascular events. Mgp-deficient mice showed matrix Gla protein (MGP) is strongly associated with calcification on arterial wall without atherosclerotic plaques, and MGP variants were not significantly associated with myocardial infarction. MGP may play different roles in the 2 endophenotypes. We analyzed the associations of MGP variants rs4236, rs1800801, and rs1800802 with the 2 endophenotypes determined by multidetector computed tomography angiography. A total of 585 with calcification on coronary artery wall, 675 with calcification in coronary atherosclerotic plaques, 454 with calcification on aortic wall, and 725 controls were enrolled. After Bonferroni correction, rs4236 and rs1800801 were still associated with calcification on arterial wall, the odds ratios were 0.708 (95% confidence interval, 0.540-0.928) for rs4236 and 0.652 (95% confidence interval, 0.479-0.888) for rs1800801 in coronary artery wall calcification, and 0.699 (95% confidence interval, 0.525-0.931) for rs4236 and 0.650 (95% confidence interval, 0.467-0.905) for rs1800801 in aortic wall calcification, respectively. The variants were correlated with calcification severity by ln(CAC Agatston score+1) in coronary artery wall calcification but not in atherosclerotic plaque calcification. In accordance with their associations with calcification on arterial wall, rs4236C and rs1800801A were associated with higher MGP plasma levels, whereas rs1800802C was associated with lower MGP levels in normal controls. Because of the role of calcification in plaque vulnerability, their associations with acute myocardial infarction were also determined in 771 controls and 752 patients, no association was found.\n\nQuestion:\nAre common genetic variants of MGP associated with calcification on the arterial wall but not with calcification present in the atherosclerotic plaques?", "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:\nTwo endophenotypes of arterial calcification, calcification on arterial wall and calcification in atherosclerotic plaques, are associated with different types of cardiovascular events. Mgp-deficient mice showed matrix Gla protein (MGP) is strongly associated with calcification on arterial wall without atherosclerotic plaques, and MGP variants were not significantly associated with myocardial infarction. MGP may play different roles in the 2 endophenotypes. We analyzed the associations of MGP variants rs4236, rs1800801, and rs1800802 with the 2 endophenotypes determined by multidetector computed tomography angiography. A total of 585 with calcification on coronary artery wall, 675 with calcification in coronary atherosclerotic plaques, 454 with calcification on aortic wall, and 725 controls were enrolled. After Bonferroni correction, rs4236 and rs1800801 were still associated with calcification on arterial wall, the odds ratios were 0.708 (95% confidence interval, 0.540-0.928) for rs4236 and 0.652 (95% confidence interval, 0.479-0.888) for rs1800801 in coronary artery wall calcification, and 0.699 (95% confidence interval, 0.525-0.931) for rs4236 and 0.650 (95% confidence interval, 0.467-0.905) for rs1800801 in aortic wall calcification, respectively. The variants were correlated with calcification severity by ln(CAC Agatston score+1) in coronary artery wall calcification but not in atherosclerotic plaque calcification. In accordance with their associations with calcification on arterial wall, rs4236C and rs1800801A were associated with higher MGP plasma levels, whereas rs1800802C was associated with lower MGP levels in normal controls. Because of the role of calcification in plaque vulnerability, their associations with acute myocardial infarction were also determined in 771 controls and 752 patients, no association was found.\n\nQuestion:\nAre common genetic variants of MGP associated with calcification on the arterial wall but not with calcification present in the atherosclerotic plaques?", "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:\nBased on in vitro studies, it has been hypothesized that 1,25-dihydroxy vitamin D (1,25-vit D) may promote weight gain in humans, but previous studies have demonstrated conflicting results regarding the association between serum 1,25-vit D and body mass index (BMI). To evaluate the relation between serum 1,25-vit D and BMI. Two thousand one hundred and eighty-seven subjects, recruited from a metabolic and medical lifestyle management clinic, were included in a cross-sectional study. BMI, 25-hydroxy vitamin D (25-OH-vit D) and 1,25-vit D were measured. The cohort was divided according to BMI in five groups (<25, 25-29.9, 30-34.9, 35-39.9 and >39.9 kg/m(2)). Statistical analyses were performed with multiple linear regression models. Age and gender were used as explanatory covariates. With increasing BMI group, there was a significant decrease in both serum 25-OH-vit D and 1,25-vit D (P<0.001). Those with BMI >39.9 kg/m(2) had 24% lower serum 25-OH-vit D levels and 18% lower 1,25-vit D levels than those with BMI <25 kg/m(2).\n\nQuestion:\nIs serum 1,25-dihydroxy vitamin D inversely associated with body mass index?", "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:\nBased on in vitro studies, it has been hypothesized that 1,25-dihydroxy vitamin D (1,25-vit D) may promote weight gain in humans, but previous studies have demonstrated conflicting results regarding the association between serum 1,25-vit D and body mass index (BMI). To evaluate the relation between serum 1,25-vit D and BMI. Two thousand one hundred and eighty-seven subjects, recruited from a metabolic and medical lifestyle management clinic, were included in a cross-sectional study. BMI, 25-hydroxy vitamin D (25-OH-vit D) and 1,25-vit D were measured. The cohort was divided according to BMI in five groups (<25, 25-29.9, 30-34.9, 35-39.9 and >39.9 kg/m(2)). Statistical analyses were performed with multiple linear regression models. Age and gender were used as explanatory covariates. With increasing BMI group, there was a significant decrease in both serum 25-OH-vit D and 1,25-vit D (P<0.001). Those with BMI >39.9 kg/m(2) had 24% lower serum 25-OH-vit D levels and 18% lower 1,25-vit D levels than those with BMI <25 kg/m(2).\n\nQuestion:\nIs serum 1,25-dihydroxy vitamin D inversely associated with body mass index?", "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:\nBased on in vitro studies, it has been hypothesized that 1,25-dihydroxy vitamin D (1,25-vit D) may promote weight gain in humans, but previous studies have demonstrated conflicting results regarding the association between serum 1,25-vit D and body mass index (BMI). To evaluate the relation between serum 1,25-vit D and BMI. Two thousand one hundred and eighty-seven subjects, recruited from a metabolic and medical lifestyle management clinic, were included in a cross-sectional study. BMI, 25-hydroxy vitamin D (25-OH-vit D) and 1,25-vit D were measured. The cohort was divided according to BMI in five groups (<25, 25-29.9, 30-34.9, 35-39.9 and >39.9 kg/m(2)). Statistical analyses were performed with multiple linear regression models. Age and gender were used as explanatory covariates. With increasing BMI group, there was a significant decrease in both serum 25-OH-vit D and 1,25-vit D (P<0.001). Those with BMI >39.9 kg/m(2) had 24% lower serum 25-OH-vit D levels and 18% lower 1,25-vit D levels than those with BMI <25 kg/m(2).\n\nQuestion:\nIs serum 1,25-dihydroxy vitamin D inversely associated with body mass index?", "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:\nFemales with the neurological disorder Rett syndrome are heterozygous for mutations in X-linked MECP2 that encodes methyl-CpG binding protein 2 (MeCP2) thought to act as a transcriptional repressor. To identify target genes for MeCP2 modulation, we studied global gene expression in single cell-derived wild-type and mutant MECP2 expressing fibroblast clones with four common mutations (R106W, R306C, 705delG, 1155del32) and in lymphoblastoid cell lines (LCLs) that included four mutant MeCP2 (T158M, 803delG, R168X and 1159del28) expressing, and five (1159del28, R106W, R255X, 803delG, 803delG) wild-type MeCP2 expressing lines. Clonality and mutation status were verified by androgen receptor methylation assays for X-inactivation and by sequencing MECP2 transcripts. Expression studies were done with oligonucleotide microarrays (Affymetrix U95) and verified with real-time quantitative RT-PCR using Sybr Green. Expression of 49 transcripts was increased, and expression of 21 transcripts was decreased, in at least 3 of 4 mutant/wild-type fibroblast comparisons. Transcript levels of 11 genes, determined by quantitative RT-PCR, were highly correlated with the microarray data. Therefore, multiple additional clones from two Rett individuals were tested by RT-PCR only. Striking expression differences were found in both mutant and wildtype MeCP2 expressing clones. Comparing expression profiles of lymphoblastoid cell lines yielded 16 differentially expressed genes.\n\nQuestion:\nDo gene expression patterns vary in clonal cell cultures from Rett syndrome females with eight different MECP2 mutations?", "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:\nFemales with the neurological disorder Rett syndrome are heterozygous for mutations in X-linked MECP2 that encodes methyl-CpG binding protein 2 (MeCP2) thought to act as a transcriptional repressor. To identify target genes for MeCP2 modulation, we studied global gene expression in single cell-derived wild-type and mutant MECP2 expressing fibroblast clones with four common mutations (R106W, R306C, 705delG, 1155del32) and in lymphoblastoid cell lines (LCLs) that included four mutant MeCP2 (T158M, 803delG, R168X and 1159del28) expressing, and five (1159del28, R106W, R255X, 803delG, 803delG) wild-type MeCP2 expressing lines. Clonality and mutation status were verified by androgen receptor methylation assays for X-inactivation and by sequencing MECP2 transcripts. Expression studies were done with oligonucleotide microarrays (Affymetrix U95) and verified with real-time quantitative RT-PCR using Sybr Green. Expression of 49 transcripts was increased, and expression of 21 transcripts was decreased, in at least 3 of 4 mutant/wild-type fibroblast comparisons. Transcript levels of 11 genes, determined by quantitative RT-PCR, were highly correlated with the microarray data. Therefore, multiple additional clones from two Rett individuals were tested by RT-PCR only. Striking expression differences were found in both mutant and wildtype MeCP2 expressing clones. Comparing expression profiles of lymphoblastoid cell lines yielded 16 differentially expressed genes.\n\nQuestion:\nDo gene expression patterns vary in clonal cell cultures from Rett syndrome females with eight different MECP2 mutations?", "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:\nFemales with the neurological disorder Rett syndrome are heterozygous for mutations in X-linked MECP2 that encodes methyl-CpG binding protein 2 (MeCP2) thought to act as a transcriptional repressor. To identify target genes for MeCP2 modulation, we studied global gene expression in single cell-derived wild-type and mutant MECP2 expressing fibroblast clones with four common mutations (R106W, R306C, 705delG, 1155del32) and in lymphoblastoid cell lines (LCLs) that included four mutant MeCP2 (T158M, 803delG, R168X and 1159del28) expressing, and five (1159del28, R106W, R255X, 803delG, 803delG) wild-type MeCP2 expressing lines. Clonality and mutation status were verified by androgen receptor methylation assays for X-inactivation and by sequencing MECP2 transcripts. Expression studies were done with oligonucleotide microarrays (Affymetrix U95) and verified with real-time quantitative RT-PCR using Sybr Green. Expression of 49 transcripts was increased, and expression of 21 transcripts was decreased, in at least 3 of 4 mutant/wild-type fibroblast comparisons. Transcript levels of 11 genes, determined by quantitative RT-PCR, were highly correlated with the microarray data. Therefore, multiple additional clones from two Rett individuals were tested by RT-PCR only. Striking expression differences were found in both mutant and wildtype MeCP2 expressing clones. Comparing expression profiles of lymphoblastoid cell lines yielded 16 differentially expressed genes.\n\nQuestion:\nDo gene expression patterns vary in clonal cell cultures from Rett syndrome females with eight different MECP2 mutations?", "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 primary purpose of this study was to determine the impact of bone mineral content (BMC) from QDR 1000/W and DPX-L dual-energy x-ray absorptiometers (DXA(QDR) and DXA(DPX-L) on percent fat (%fat) estimates from a four-component model. A secondary purpose was to test the accuracy of %fat estimates from DXA(QDR) and DXA(DPX-L) using %fat estimates from a four-component model as the criterion. Percent fat, fat mass, and fat-free mass (FFM) were determined from DXA(QDR) and DXA(DPX-L) and from a four-component model based on measures of body density from underwater weighing, body water from deuterium dilution, and BMC from DXA(QDR) (4C(QDR)) or DXA(DPX-L) (4C(DPX-L)) in young men (N = 14) and women (N = 10). BMC was significantly lower using DXA(QDR) compared with DXA(DPX-L) (approximately 11%), resulting in slightly lower estimates of %fat and fat mass and slightly higher estimates of FFM from 4C(QDR) than 4C(DPX-L). Although estimates of %fat, fat mass, and FFM from DXA(QDR) and DXA(DPX-L) were not different than those from a four-component model, there was considerable individual variability between methods. Furthermore, %fat from DXA(QDR) was lower than %fat from 4C(DPX-L).\n\nQuestion:\nDoes impact of bone mineral estimate on percent fat estimates from a four-component 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:\nThe primary purpose of this study was to determine the impact of bone mineral content (BMC) from QDR 1000/W and DPX-L dual-energy x-ray absorptiometers (DXA(QDR) and DXA(DPX-L) on percent fat (%fat) estimates from a four-component model. A secondary purpose was to test the accuracy of %fat estimates from DXA(QDR) and DXA(DPX-L) using %fat estimates from a four-component model as the criterion. Percent fat, fat mass, and fat-free mass (FFM) were determined from DXA(QDR) and DXA(DPX-L) and from a four-component model based on measures of body density from underwater weighing, body water from deuterium dilution, and BMC from DXA(QDR) (4C(QDR)) or DXA(DPX-L) (4C(DPX-L)) in young men (N = 14) and women (N = 10). BMC was significantly lower using DXA(QDR) compared with DXA(DPX-L) (approximately 11%), resulting in slightly lower estimates of %fat and fat mass and slightly higher estimates of FFM from 4C(QDR) than 4C(DPX-L). Although estimates of %fat, fat mass, and FFM from DXA(QDR) and DXA(DPX-L) were not different than those from a four-component model, there was considerable individual variability between methods. Furthermore, %fat from DXA(QDR) was lower than %fat from 4C(DPX-L).\n\nQuestion:\nDoes impact of bone mineral estimate on percent fat estimates from a four-component 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:\nThe primary purpose of this study was to determine the impact of bone mineral content (BMC) from QDR 1000/W and DPX-L dual-energy x-ray absorptiometers (DXA(QDR) and DXA(DPX-L) on percent fat (%fat) estimates from a four-component model. A secondary purpose was to test the accuracy of %fat estimates from DXA(QDR) and DXA(DPX-L) using %fat estimates from a four-component model as the criterion. Percent fat, fat mass, and fat-free mass (FFM) were determined from DXA(QDR) and DXA(DPX-L) and from a four-component model based on measures of body density from underwater weighing, body water from deuterium dilution, and BMC from DXA(QDR) (4C(QDR)) or DXA(DPX-L) (4C(DPX-L)) in young men (N = 14) and women (N = 10). BMC was significantly lower using DXA(QDR) compared with DXA(DPX-L) (approximately 11%), resulting in slightly lower estimates of %fat and fat mass and slightly higher estimates of FFM from 4C(QDR) than 4C(DPX-L). Although estimates of %fat, fat mass, and FFM from DXA(QDR) and DXA(DPX-L) were not different than those from a four-component model, there was considerable individual variability between methods. Furthermore, %fat from DXA(QDR) was lower than %fat from 4C(DPX-L).\n\nQuestion:\nDoes impact of bone mineral estimate on percent fat estimates from a four-component 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:\nDespite increasing interest in the renin-angiotensin system in cancer, little is known about angiotensin II (Ang II) expression in human prostate tumors. Using immunohistochemistry, we examined Ang II expression in prostate cancer (Gleason grades 2-5), benign prostatic hyperplasia (BPH), and high-grade prostatic intraepithelial neoplasia (HGPIN). Ang II was present in proliferating neoplastic cells in HGPIN, in malignant cells in all grades of prostate cancer examined, in basal but not luminal epithelial cells in BPH, and in the cytoplasm of LNCaP, DU145, and PC3 prostate cancer cells.\n\nQuestion:\nIs appearance of angiotensin II expression in non-basal epithelial cells an early feature of malignant change in human prostate?", "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:\nDespite increasing interest in the renin-angiotensin system in cancer, little is known about angiotensin II (Ang II) expression in human prostate tumors. Using immunohistochemistry, we examined Ang II expression in prostate cancer (Gleason grades 2-5), benign prostatic hyperplasia (BPH), and high-grade prostatic intraepithelial neoplasia (HGPIN). Ang II was present in proliferating neoplastic cells in HGPIN, in malignant cells in all grades of prostate cancer examined, in basal but not luminal epithelial cells in BPH, and in the cytoplasm of LNCaP, DU145, and PC3 prostate cancer cells.\n\nQuestion:\nIs appearance of angiotensin II expression in non-basal epithelial cells an early feature of malignant change in human prostate?", "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:\nDespite increasing interest in the renin-angiotensin system in cancer, little is known about angiotensin II (Ang II) expression in human prostate tumors. Using immunohistochemistry, we examined Ang II expression in prostate cancer (Gleason grades 2-5), benign prostatic hyperplasia (BPH), and high-grade prostatic intraepithelial neoplasia (HGPIN). Ang II was present in proliferating neoplastic cells in HGPIN, in malignant cells in all grades of prostate cancer examined, in basal but not luminal epithelial cells in BPH, and in the cytoplasm of LNCaP, DU145, and PC3 prostate cancer cells.\n\nQuestion:\nIs appearance of angiotensin II expression in non-basal epithelial cells an early feature of malignant change in human prostate?", "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:\nCystatin SN is a secreted protein and a cysteine proteinase inhibitor. It has been considered to be a tumor marker for gastrointestinal tract cancer in several functional researches. However, the clinicopathological and prognostic significance of Cystatin SN expression in esophageal squamous cell carcinoma (ESCC) has not been elucidated. In our study, the expression of Cystatin SN was detected in 209 surgically resected ESCC tissues and 170 peritumoral normal esophageal mucosae by immunohistochemistry. The prognostic significance of Cystatin SN expression was analysed with Kaplan-Meier plots and the Cox proportional hazards regression models. The results showed that the immunostaining of Cystatin SN in ESCC tissues was less intense than that in the normal control tissue (P < 0.001). Compared with patients with low tumoral Cystatin SN expression, ESCC patients with tumors high-expression Cystatin SN exhibited increased disease-free survival (DFS) and overall survival (OS) (P < 0.001 and P < 0.001, respectively). Furthermore, the expression level of Cystatin SN could further stratify the ESCC patients by survival (DFS and OS) in the stage II subgroup (P < 0.001 and P < 0.001, respectively). Multivariate analyses showed that Cystatin SN expression, N status and differentiation were independent and significant predictors of survival.\n\nQuestion:\nDoes overexpression of cystatin SN positively affect survival of patients with surgically resected esophageal 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:\nCystatin SN is a secreted protein and a cysteine proteinase inhibitor. It has been considered to be a tumor marker for gastrointestinal tract cancer in several functional researches. However, the clinicopathological and prognostic significance of Cystatin SN expression in esophageal squamous cell carcinoma (ESCC) has not been elucidated. In our study, the expression of Cystatin SN was detected in 209 surgically resected ESCC tissues and 170 peritumoral normal esophageal mucosae by immunohistochemistry. The prognostic significance of Cystatin SN expression was analysed with Kaplan-Meier plots and the Cox proportional hazards regression models. The results showed that the immunostaining of Cystatin SN in ESCC tissues was less intense than that in the normal control tissue (P < 0.001). Compared with patients with low tumoral Cystatin SN expression, ESCC patients with tumors high-expression Cystatin SN exhibited increased disease-free survival (DFS) and overall survival (OS) (P < 0.001 and P < 0.001, respectively). Furthermore, the expression level of Cystatin SN could further stratify the ESCC patients by survival (DFS and OS) in the stage II subgroup (P < 0.001 and P < 0.001, respectively). Multivariate analyses showed that Cystatin SN expression, N status and differentiation were independent and significant predictors of survival.\n\nQuestion:\nDoes overexpression of cystatin SN positively affect survival of patients with surgically resected esophageal 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:\nCystatin SN is a secreted protein and a cysteine proteinase inhibitor. It has been considered to be a tumor marker for gastrointestinal tract cancer in several functional researches. However, the clinicopathological and prognostic significance of Cystatin SN expression in esophageal squamous cell carcinoma (ESCC) has not been elucidated. In our study, the expression of Cystatin SN was detected in 209 surgically resected ESCC tissues and 170 peritumoral normal esophageal mucosae by immunohistochemistry. The prognostic significance of Cystatin SN expression was analysed with Kaplan-Meier plots and the Cox proportional hazards regression models. The results showed that the immunostaining of Cystatin SN in ESCC tissues was less intense than that in the normal control tissue (P < 0.001). Compared with patients with low tumoral Cystatin SN expression, ESCC patients with tumors high-expression Cystatin SN exhibited increased disease-free survival (DFS) and overall survival (OS) (P < 0.001 and P < 0.001, respectively). Furthermore, the expression level of Cystatin SN could further stratify the ESCC patients by survival (DFS and OS) in the stage II subgroup (P < 0.001 and P < 0.001, respectively). Multivariate analyses showed that Cystatin SN expression, N status and differentiation were independent and significant predictors of survival.\n\nQuestion:\nDoes overexpression of cystatin SN positively affect survival of patients with surgically resected esophageal 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:\nWnt/β-catenin signaling is known to play an important role in colorectal cancer (CRC). Niclosamide, a salicylamide derivative used in the treatment of tapeworm infections, targets the Wnt/β-catenin pathway. The objective of this study was to investigate niclosamide as a therapeutic agent against CRC. The antiproliferative effects of 1, 3, 10, and 50 μM concentrations of niclosamide on human (SW480 and SW620) and rodent (CC531) CRC cell lines were determined by MTS assay and direct cell count. The lymphoid enhancer-binding factor 1/transcription factor (LEF/TCF) reporter assay monitored the activity of Wnt signaling. Immunofluorescence staining demonstrated the expression pattern of active β-catenin. Gene expression of canonical and noncanonical Wnt signaling components was analyzed using qRT-PCR. Western blot analysis was performed with antibodies detecting nuclear localization of β-catenin and c-jun. Cell proliferation in CRC cell lines was blocked dose dependently after 12 and 24 h of incubation. The Wnt promoter activity of LEF/TCF significantly decreased with niclosamide concentrations of 10 and 50 μM after 12 h of incubation. Active β-catenin did not shift from the nuclear to the cytosolic pool. However, canonical target genes (met, MMP7, and cyclin D1) as well as the coactivating factor Bcl9 were downregulated, whereas the noncanonical key player c-jun was clearly activated.\n\nQuestion:\nDoes the anthelmintic niclosamide inhibit colorectal cancer cell lines via modulation of the canonical and noncanonical Wnt signaling 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:\nWnt/β-catenin signaling is known to play an important role in colorectal cancer (CRC). Niclosamide, a salicylamide derivative used in the treatment of tapeworm infections, targets the Wnt/β-catenin pathway. The objective of this study was to investigate niclosamide as a therapeutic agent against CRC. The antiproliferative effects of 1, 3, 10, and 50 μM concentrations of niclosamide on human (SW480 and SW620) and rodent (CC531) CRC cell lines were determined by MTS assay and direct cell count. The lymphoid enhancer-binding factor 1/transcription factor (LEF/TCF) reporter assay monitored the activity of Wnt signaling. Immunofluorescence staining demonstrated the expression pattern of active β-catenin. Gene expression of canonical and noncanonical Wnt signaling components was analyzed using qRT-PCR. Western blot analysis was performed with antibodies detecting nuclear localization of β-catenin and c-jun. Cell proliferation in CRC cell lines was blocked dose dependently after 12 and 24 h of incubation. The Wnt promoter activity of LEF/TCF significantly decreased with niclosamide concentrations of 10 and 50 μM after 12 h of incubation. Active β-catenin did not shift from the nuclear to the cytosolic pool. However, canonical target genes (met, MMP7, and cyclin D1) as well as the coactivating factor Bcl9 were downregulated, whereas the noncanonical key player c-jun was clearly activated.\n\nQuestion:\nDoes the anthelmintic niclosamide inhibit colorectal cancer cell lines via modulation of the canonical and noncanonical Wnt signaling 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:\nWnt/β-catenin signaling is known to play an important role in colorectal cancer (CRC). Niclosamide, a salicylamide derivative used in the treatment of tapeworm infections, targets the Wnt/β-catenin pathway. The objective of this study was to investigate niclosamide as a therapeutic agent against CRC. The antiproliferative effects of 1, 3, 10, and 50 μM concentrations of niclosamide on human (SW480 and SW620) and rodent (CC531) CRC cell lines were determined by MTS assay and direct cell count. The lymphoid enhancer-binding factor 1/transcription factor (LEF/TCF) reporter assay monitored the activity of Wnt signaling. Immunofluorescence staining demonstrated the expression pattern of active β-catenin. Gene expression of canonical and noncanonical Wnt signaling components was analyzed using qRT-PCR. Western blot analysis was performed with antibodies detecting nuclear localization of β-catenin and c-jun. Cell proliferation in CRC cell lines was blocked dose dependently after 12 and 24 h of incubation. The Wnt promoter activity of LEF/TCF significantly decreased with niclosamide concentrations of 10 and 50 μM after 12 h of incubation. Active β-catenin did not shift from the nuclear to the cytosolic pool. However, canonical target genes (met, MMP7, and cyclin D1) as well as the coactivating factor Bcl9 were downregulated, whereas the noncanonical key player c-jun was clearly activated.\n\nQuestion:\nDoes the anthelmintic niclosamide inhibit colorectal cancer cell lines via modulation of the canonical and noncanonical Wnt signaling 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:\nRecent studies have revealed the existence of bone marrow-derived endothelial progenitor cells (EPCs). The number of circulating EPCs might reflect the pathogenesis of atherosclerosis and progression of cardiovascular diseases (CVDs). The purpose of this study was to evaluate the relationship between the number of EPCs and cardiovascular risk factors. Flow cytometry analysis was used to quantify the number of EPCs (CD34(+)AC133(+)CD45(low)) in 135 consecutive hospitalized patients with CVD and 25 healthy subjects. The number of EPCs was less in the patients than in the healthy subjects (1,047.4 +/- 521.1 vs. 612.8 +/- 461.6/ml, P < 0.0001). The number of EPCs significantly correlated with the number of risk factors (r = 0.424, P < 0.0001). The numbers of EPCs in patients with hypertension and diabetes mellitus were less than those in patients without those diseases (762.6 +/- 579.5 vs. 495.2 +/- 297.7/ml, P < 0.01 and 666.8 +/- 505.5 vs. 477.0 +/- 290.4/ml, P < 0.05, respectively). In healthy subjects a reduced number of EPCs was found in smokers compared with nonsmokers (833.3 +/- 347.5 vs. 1,274.6 +/- 560.9/ml, P < 0.05), whereas smoking did not alter the number of EPCs in the patients group. In multivariate analysis, hypertension and age were independent predictors of reduced number of EPCs. Renin-angiotensin system (RAS) inhibitors increased the number of EPCs (464.7 +/- 252.1/ml vs. 617.5 +/- 343.5/ml, P < 0.05), while calcium antagonists, diuretics, and beta-blockers did not alter the number of EPCs in patients with hypertension.\n\nQuestion:\nAre aging and hypertension independent risk factors for reduced number of circulating endothelial progenitor 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:\nRecent studies have revealed the existence of bone marrow-derived endothelial progenitor cells (EPCs). The number of circulating EPCs might reflect the pathogenesis of atherosclerosis and progression of cardiovascular diseases (CVDs). The purpose of this study was to evaluate the relationship between the number of EPCs and cardiovascular risk factors. Flow cytometry analysis was used to quantify the number of EPCs (CD34(+)AC133(+)CD45(low)) in 135 consecutive hospitalized patients with CVD and 25 healthy subjects. The number of EPCs was less in the patients than in the healthy subjects (1,047.4 +/- 521.1 vs. 612.8 +/- 461.6/ml, P < 0.0001). The number of EPCs significantly correlated with the number of risk factors (r = 0.424, P < 0.0001). The numbers of EPCs in patients with hypertension and diabetes mellitus were less than those in patients without those diseases (762.6 +/- 579.5 vs. 495.2 +/- 297.7/ml, P < 0.01 and 666.8 +/- 505.5 vs. 477.0 +/- 290.4/ml, P < 0.05, respectively). In healthy subjects a reduced number of EPCs was found in smokers compared with nonsmokers (833.3 +/- 347.5 vs. 1,274.6 +/- 560.9/ml, P < 0.05), whereas smoking did not alter the number of EPCs in the patients group. In multivariate analysis, hypertension and age were independent predictors of reduced number of EPCs. Renin-angiotensin system (RAS) inhibitors increased the number of EPCs (464.7 +/- 252.1/ml vs. 617.5 +/- 343.5/ml, P < 0.05), while calcium antagonists, diuretics, and beta-blockers did not alter the number of EPCs in patients with hypertension.\n\nQuestion:\nAre aging and hypertension independent risk factors for reduced number of circulating endothelial progenitor 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:\nRecent studies have revealed the existence of bone marrow-derived endothelial progenitor cells (EPCs). The number of circulating EPCs might reflect the pathogenesis of atherosclerosis and progression of cardiovascular diseases (CVDs). The purpose of this study was to evaluate the relationship between the number of EPCs and cardiovascular risk factors. Flow cytometry analysis was used to quantify the number of EPCs (CD34(+)AC133(+)CD45(low)) in 135 consecutive hospitalized patients with CVD and 25 healthy subjects. The number of EPCs was less in the patients than in the healthy subjects (1,047.4 +/- 521.1 vs. 612.8 +/- 461.6/ml, P < 0.0001). The number of EPCs significantly correlated with the number of risk factors (r = 0.424, P < 0.0001). The numbers of EPCs in patients with hypertension and diabetes mellitus were less than those in patients without those diseases (762.6 +/- 579.5 vs. 495.2 +/- 297.7/ml, P < 0.01 and 666.8 +/- 505.5 vs. 477.0 +/- 290.4/ml, P < 0.05, respectively). In healthy subjects a reduced number of EPCs was found in smokers compared with nonsmokers (833.3 +/- 347.5 vs. 1,274.6 +/- 560.9/ml, P < 0.05), whereas smoking did not alter the number of EPCs in the patients group. In multivariate analysis, hypertension and age were independent predictors of reduced number of EPCs. Renin-angiotensin system (RAS) inhibitors increased the number of EPCs (464.7 +/- 252.1/ml vs. 617.5 +/- 343.5/ml, P < 0.05), while calcium antagonists, diuretics, and beta-blockers did not alter the number of EPCs in patients with hypertension.\n\nQuestion:\nAre aging and hypertension independent risk factors for reduced number of circulating endothelial progenitor 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:\nNeuronal circuit assembly comprises a number of developmental processes that ultimately underlie function. Identifying the molecular events that dictate these processes can give key insights into how neuronal circuit formation is coordinated. To begin to identify such molecular mechanisms, we have analysed the expression of a candidate gene of entirely unknown function within the nervous system. Here we reveal the spatial and temporal distribution of Lzts1 in mouse and chick embryonic spinal cord and propose potential biological functions. Lzts1 mRNA is transiently expressed at the border of the ventricular and mantle zones in subsets of sensory and motor spinal neurons. The protein is localized to the cell body, axon, and trailing process of motor, commissural, and dorsal root neurons during development.\n\nQuestion:\nDoes the expression profile of the tumor suppressor gene Lzts1 suggest a role in neuronal 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:\nNeuronal circuit assembly comprises a number of developmental processes that ultimately underlie function. Identifying the molecular events that dictate these processes can give key insights into how neuronal circuit formation is coordinated. To begin to identify such molecular mechanisms, we have analysed the expression of a candidate gene of entirely unknown function within the nervous system. Here we reveal the spatial and temporal distribution of Lzts1 in mouse and chick embryonic spinal cord and propose potential biological functions. Lzts1 mRNA is transiently expressed at the border of the ventricular and mantle zones in subsets of sensory and motor spinal neurons. The protein is localized to the cell body, axon, and trailing process of motor, commissural, and dorsal root neurons during development.\n\nQuestion:\nDoes the expression profile of the tumor suppressor gene Lzts1 suggest a role in neuronal 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:\nNeuronal circuit assembly comprises a number of developmental processes that ultimately underlie function. Identifying the molecular events that dictate these processes can give key insights into how neuronal circuit formation is coordinated. To begin to identify such molecular mechanisms, we have analysed the expression of a candidate gene of entirely unknown function within the nervous system. Here we reveal the spatial and temporal distribution of Lzts1 in mouse and chick embryonic spinal cord and propose potential biological functions. Lzts1 mRNA is transiently expressed at the border of the ventricular and mantle zones in subsets of sensory and motor spinal neurons. The protein is localized to the cell body, axon, and trailing process of motor, commissural, and dorsal root neurons during development.\n\nQuestion:\nDoes the expression profile of the tumor suppressor gene Lzts1 suggest a role in neuronal 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 assess the hemodynamic effects of high mean proximal airway pressures (Paw) during high-frequency oscillatory ventilation (HFOV) in non-neonatal pediatrics patients with severe respiratory failure. Prospective and retrospective study. Pediatric ICU in a university-affiliated hospital. 8 non-neonatal pediatric patients with severe respiratory failure ventilated with HFOV at our institution between July 1991 and February 1994. All patients had a pulmonary artery catheter. HFOV. Higher Paw was required during HFOV to obtain adequate lung expansion during the first 24 h (median 20.9 cmH2O, range 16.9-30.0 cmH2O in CMV, versus median 30.0 cmH2O, range 21.0-33.0 cmH2O in HFOV, p = 0.008), resulting in improved oxygenation as evaluated by alveolar-arterial oxygen difference (median of 557.2 mmHg, range 360.4-607.8 mmHg in CMV, versus median of 410.5 mmHg, range 282.9-550.2 mmHg after 24 h of HFOV, p = 0.03). The only observed effect on the cardiovascular system was a decrease in heart rate (median of 162, range 129-178 in CMV, versus median of 142, range 104-195 after 24 h of HFOV, p = 0.03). Oxygen delivery, cardiac index, mean systemic arterial blood pressure, and pulmonary and systemic vascular resistances did not change significantly before and after HFOV in the patients as a group, although in one case a decrease in cardiac index and oxygen delivery was observed.\n\nQuestion:\nDo hemodynamic effects of high-frequency oscillatory ventilation in severe pediatric respiratory failure?", "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 the hemodynamic effects of high mean proximal airway pressures (Paw) during high-frequency oscillatory ventilation (HFOV) in non-neonatal pediatrics patients with severe respiratory failure. Prospective and retrospective study. Pediatric ICU in a university-affiliated hospital. 8 non-neonatal pediatric patients with severe respiratory failure ventilated with HFOV at our institution between July 1991 and February 1994. All patients had a pulmonary artery catheter. HFOV. Higher Paw was required during HFOV to obtain adequate lung expansion during the first 24 h (median 20.9 cmH2O, range 16.9-30.0 cmH2O in CMV, versus median 30.0 cmH2O, range 21.0-33.0 cmH2O in HFOV, p = 0.008), resulting in improved oxygenation as evaluated by alveolar-arterial oxygen difference (median of 557.2 mmHg, range 360.4-607.8 mmHg in CMV, versus median of 410.5 mmHg, range 282.9-550.2 mmHg after 24 h of HFOV, p = 0.03). The only observed effect on the cardiovascular system was a decrease in heart rate (median of 162, range 129-178 in CMV, versus median of 142, range 104-195 after 24 h of HFOV, p = 0.03). Oxygen delivery, cardiac index, mean systemic arterial blood pressure, and pulmonary and systemic vascular resistances did not change significantly before and after HFOV in the patients as a group, although in one case a decrease in cardiac index and oxygen delivery was observed.\n\nQuestion:\nDo hemodynamic effects of high-frequency oscillatory ventilation in severe pediatric respiratory failure?", "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 the hemodynamic effects of high mean proximal airway pressures (Paw) during high-frequency oscillatory ventilation (HFOV) in non-neonatal pediatrics patients with severe respiratory failure. Prospective and retrospective study. Pediatric ICU in a university-affiliated hospital. 8 non-neonatal pediatric patients with severe respiratory failure ventilated with HFOV at our institution between July 1991 and February 1994. All patients had a pulmonary artery catheter. HFOV. Higher Paw was required during HFOV to obtain adequate lung expansion during the first 24 h (median 20.9 cmH2O, range 16.9-30.0 cmH2O in CMV, versus median 30.0 cmH2O, range 21.0-33.0 cmH2O in HFOV, p = 0.008), resulting in improved oxygenation as evaluated by alveolar-arterial oxygen difference (median of 557.2 mmHg, range 360.4-607.8 mmHg in CMV, versus median of 410.5 mmHg, range 282.9-550.2 mmHg after 24 h of HFOV, p = 0.03). The only observed effect on the cardiovascular system was a decrease in heart rate (median of 162, range 129-178 in CMV, versus median of 142, range 104-195 after 24 h of HFOV, p = 0.03). Oxygen delivery, cardiac index, mean systemic arterial blood pressure, and pulmonary and systemic vascular resistances did not change significantly before and after HFOV in the patients as a group, although in one case a decrease in cardiac index and oxygen delivery was observed.\n\nQuestion:\nDo hemodynamic effects of high-frequency oscillatory ventilation in severe pediatric respiratory failure?", "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:\nAberrant regulation of the proliferation, survival, and migration of endothelial cells (ECs) is closely related to the abnormal angiogenesis that occurs in hypoxia-induced pathological situations, such as cancer and vascular retinopathy. Hypoxic conditions and the subsequent upregulation of hypoxia-inducible factor-1α and target genes are important for the angiogenic functions of ECs. Phospholipase D2 (PLD2) is a crucial signaling mediator that stimulates the production of the second messenger phosphatidic acid. PLD2 is involved in various cellular functions; however, its specific roles in ECs under hypoxia and in vivo angiogenesis remain unclear. In the present study, we investigated the potential roles of PLD2 in ECs under hypoxia and in hypoxia-induced pathological angiogenesis in vivo. Pld2 knockout ECs exhibited decreased hypoxia-induced cellular responses in survival, migration, and thus vessel sprouting. Analysis of hypoxia-induced gene expression revealed that PLD2 deficiency disrupted the upregulation of hypoxia-inducible factor-1α target genes, including VEGF, PFKFB3, HMOX-1, and NTRK2. Consistent with this, PLD2 contributed to hypoxia-induced hypoxia-inducible factor-1α expression at the translational level. The roles of PLD2 in hypoxia-induced in vivo pathological angiogenesis were assessed using oxygen-induced retinopathy and tumor implantation models in endothelial-specific Pld2 knockout mice. Pld2 endothelial-specific knockout retinae showed decreased neovascular tuft formation, despite a larger avascular region. Tumor growth and tumor blood vessel formation were also reduced in Pld2 endothelial-specific knockout mice.\n\nQuestion:\nDoes endothelial deletion of phospholipase D2 reduce hypoxic response and pathological angiogenesis?", "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:\nAberrant regulation of the proliferation, survival, and migration of endothelial cells (ECs) is closely related to the abnormal angiogenesis that occurs in hypoxia-induced pathological situations, such as cancer and vascular retinopathy. Hypoxic conditions and the subsequent upregulation of hypoxia-inducible factor-1α and target genes are important for the angiogenic functions of ECs. Phospholipase D2 (PLD2) is a crucial signaling mediator that stimulates the production of the second messenger phosphatidic acid. PLD2 is involved in various cellular functions; however, its specific roles in ECs under hypoxia and in vivo angiogenesis remain unclear. In the present study, we investigated the potential roles of PLD2 in ECs under hypoxia and in hypoxia-induced pathological angiogenesis in vivo. Pld2 knockout ECs exhibited decreased hypoxia-induced cellular responses in survival, migration, and thus vessel sprouting. Analysis of hypoxia-induced gene expression revealed that PLD2 deficiency disrupted the upregulation of hypoxia-inducible factor-1α target genes, including VEGF, PFKFB3, HMOX-1, and NTRK2. Consistent with this, PLD2 contributed to hypoxia-induced hypoxia-inducible factor-1α expression at the translational level. The roles of PLD2 in hypoxia-induced in vivo pathological angiogenesis were assessed using oxygen-induced retinopathy and tumor implantation models in endothelial-specific Pld2 knockout mice. Pld2 endothelial-specific knockout retinae showed decreased neovascular tuft formation, despite a larger avascular region. Tumor growth and tumor blood vessel formation were also reduced in Pld2 endothelial-specific knockout mice.\n\nQuestion:\nDoes endothelial deletion of phospholipase D2 reduce hypoxic response and pathological angiogenesis?", "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:\nAberrant regulation of the proliferation, survival, and migration of endothelial cells (ECs) is closely related to the abnormal angiogenesis that occurs in hypoxia-induced pathological situations, such as cancer and vascular retinopathy. Hypoxic conditions and the subsequent upregulation of hypoxia-inducible factor-1α and target genes are important for the angiogenic functions of ECs. Phospholipase D2 (PLD2) is a crucial signaling mediator that stimulates the production of the second messenger phosphatidic acid. PLD2 is involved in various cellular functions; however, its specific roles in ECs under hypoxia and in vivo angiogenesis remain unclear. In the present study, we investigated the potential roles of PLD2 in ECs under hypoxia and in hypoxia-induced pathological angiogenesis in vivo. Pld2 knockout ECs exhibited decreased hypoxia-induced cellular responses in survival, migration, and thus vessel sprouting. Analysis of hypoxia-induced gene expression revealed that PLD2 deficiency disrupted the upregulation of hypoxia-inducible factor-1α target genes, including VEGF, PFKFB3, HMOX-1, and NTRK2. Consistent with this, PLD2 contributed to hypoxia-induced hypoxia-inducible factor-1α expression at the translational level. The roles of PLD2 in hypoxia-induced in vivo pathological angiogenesis were assessed using oxygen-induced retinopathy and tumor implantation models in endothelial-specific Pld2 knockout mice. Pld2 endothelial-specific knockout retinae showed decreased neovascular tuft formation, despite a larger avascular region. Tumor growth and tumor blood vessel formation were also reduced in Pld2 endothelial-specific knockout mice.\n\nQuestion:\nDoes endothelial deletion of phospholipase D2 reduce hypoxic response and pathological angiogenesis?", "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:\nReceptor-like kinases are well-known to play key roles in disease resistance. Among them, the Wall-associated kinases (WAKs) have been shown to be positive regulators of fungal disease resistance in several plant species. WAK genes are often transcriptionally regulated during infection but the pathways involved in this regulation are not known. In rice, the OsWAK gene family is significantly amplified compared to Arabidopsis. The possibility that several WAKs participate in different ways to basal defense has not been addressed. Moreover, the direct requirement of rice OSWAK genes in regulating defense has not been explored. Here we show using rice (Oryza sativa) loss-of-function mutants of four selected OsWAK genes, that individual OsWAKs are required for quantitative resistance to the rice blast fungus, Magnaporthe oryzae. While OsWAK14, OsWAK91 and OsWAK92 positively regulate quantitative resistance, OsWAK112d is a negative regulator of blast resistance. In addition, we show that the very early transcriptional regulation of the rice OsWAK genes is triggered by chitin and is partially under the control of the chitin receptor CEBiP. Finally, we show that OsWAK91 is required for H2O2 production and sufficient to enhance defense gene expression during infection.\n\nQuestion:\nDo several wall-associated kinases participate positively and negatively in basal defense against rice blast fungus?", "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:\nReceptor-like kinases are well-known to play key roles in disease resistance. Among them, the Wall-associated kinases (WAKs) have been shown to be positive regulators of fungal disease resistance in several plant species. WAK genes are often transcriptionally regulated during infection but the pathways involved in this regulation are not known. In rice, the OsWAK gene family is significantly amplified compared to Arabidopsis. The possibility that several WAKs participate in different ways to basal defense has not been addressed. Moreover, the direct requirement of rice OSWAK genes in regulating defense has not been explored. Here we show using rice (Oryza sativa) loss-of-function mutants of four selected OsWAK genes, that individual OsWAKs are required for quantitative resistance to the rice blast fungus, Magnaporthe oryzae. While OsWAK14, OsWAK91 and OsWAK92 positively regulate quantitative resistance, OsWAK112d is a negative regulator of blast resistance. In addition, we show that the very early transcriptional regulation of the rice OsWAK genes is triggered by chitin and is partially under the control of the chitin receptor CEBiP. Finally, we show that OsWAK91 is required for H2O2 production and sufficient to enhance defense gene expression during infection.\n\nQuestion:\nDo several wall-associated kinases participate positively and negatively in basal defense against rice blast fungus?", "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:\nReceptor-like kinases are well-known to play key roles in disease resistance. Among them, the Wall-associated kinases (WAKs) have been shown to be positive regulators of fungal disease resistance in several plant species. WAK genes are often transcriptionally regulated during infection but the pathways involved in this regulation are not known. In rice, the OsWAK gene family is significantly amplified compared to Arabidopsis. The possibility that several WAKs participate in different ways to basal defense has not been addressed. Moreover, the direct requirement of rice OSWAK genes in regulating defense has not been explored. Here we show using rice (Oryza sativa) loss-of-function mutants of four selected OsWAK genes, that individual OsWAKs are required for quantitative resistance to the rice blast fungus, Magnaporthe oryzae. While OsWAK14, OsWAK91 and OsWAK92 positively regulate quantitative resistance, OsWAK112d is a negative regulator of blast resistance. In addition, we show that the very early transcriptional regulation of the rice OsWAK genes is triggered by chitin and is partially under the control of the chitin receptor CEBiP. Finally, we show that OsWAK91 is required for H2O2 production and sufficient to enhance defense gene expression during infection.\n\nQuestion:\nDo several wall-associated kinases participate positively and negatively in basal defense against rice blast fungus?", "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 preconditioning by tumour necrosis factor-alpha (TNFalpha), activation of the signal transducer and activator of transcription-3 (STAT-3) but not Akt, is essential, whereas ischaemic cardiac preconditioning (IPC) requires both STAT-3 and Akt at the time of reperfusion. However, it is not known whether the same signalling pattern occurs during the preconditioning stimulus (trigger phase) and whether links exist between STAT-3 and Akt. Hence, our hypothesis is that concomitant activation or co-interaction between these two key signals is required during the trigger phase for IPC. Conversely, we proposed that there would be no such interaction when preconditioning was induced by TNFalpha (TNF-PC). Cardiomyocytes, isolated from adult wild-type (WT) and cardiac-specific STAT-3 knockout (KO) mice, were exposed to simulated ischaemia (SI) reperfusion. Cells were preconditioned either by 30 min SI or by 30 min TNFalpha (0.5 ng/mL) in the presence or absence of AG490 (100 nM) or wortmannin (100 nM) to inhibit STAT-3 or Akt, respectively. Cell viability was evaluated by trypan blue, and phosphorylation levels of STAT-3 and Akt were measured by Western blot analysis. Similar experiments were conducted in isolated rat hearts subjected to an ischaemia-reperfusion insult. Both preconditioning stimuli failed to protect KO cardiomyocytes, and addition of AG490 abolished preconditioning in WT cardiomyocytes or isolated hearts. Wortmannin abolished the protection afforded by IPC, but did not affect TNF-PC in both models. Western blot analysis demonstrated that added wortmannin during IPC stimulus decreased STAT-3 phosphorylation while, conversely, AG490 reduced Akt phosphorylation.\n\nQuestion:\nIs dual activation of STAT-3 and Akt required during the trigger phase of ischaemic preconditioning?", "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 preconditioning by tumour necrosis factor-alpha (TNFalpha), activation of the signal transducer and activator of transcription-3 (STAT-3) but not Akt, is essential, whereas ischaemic cardiac preconditioning (IPC) requires both STAT-3 and Akt at the time of reperfusion. However, it is not known whether the same signalling pattern occurs during the preconditioning stimulus (trigger phase) and whether links exist between STAT-3 and Akt. Hence, our hypothesis is that concomitant activation or co-interaction between these two key signals is required during the trigger phase for IPC. Conversely, we proposed that there would be no such interaction when preconditioning was induced by TNFalpha (TNF-PC). Cardiomyocytes, isolated from adult wild-type (WT) and cardiac-specific STAT-3 knockout (KO) mice, were exposed to simulated ischaemia (SI) reperfusion. Cells were preconditioned either by 30 min SI or by 30 min TNFalpha (0.5 ng/mL) in the presence or absence of AG490 (100 nM) or wortmannin (100 nM) to inhibit STAT-3 or Akt, respectively. Cell viability was evaluated by trypan blue, and phosphorylation levels of STAT-3 and Akt were measured by Western blot analysis. Similar experiments were conducted in isolated rat hearts subjected to an ischaemia-reperfusion insult. Both preconditioning stimuli failed to protect KO cardiomyocytes, and addition of AG490 abolished preconditioning in WT cardiomyocytes or isolated hearts. Wortmannin abolished the protection afforded by IPC, but did not affect TNF-PC in both models. Western blot analysis demonstrated that added wortmannin during IPC stimulus decreased STAT-3 phosphorylation while, conversely, AG490 reduced Akt phosphorylation.\n\nQuestion:\nIs dual activation of STAT-3 and Akt required during the trigger phase of ischaemic preconditioning?", "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 preconditioning by tumour necrosis factor-alpha (TNFalpha), activation of the signal transducer and activator of transcription-3 (STAT-3) but not Akt, is essential, whereas ischaemic cardiac preconditioning (IPC) requires both STAT-3 and Akt at the time of reperfusion. However, it is not known whether the same signalling pattern occurs during the preconditioning stimulus (trigger phase) and whether links exist between STAT-3 and Akt. Hence, our hypothesis is that concomitant activation or co-interaction between these two key signals is required during the trigger phase for IPC. Conversely, we proposed that there would be no such interaction when preconditioning was induced by TNFalpha (TNF-PC). Cardiomyocytes, isolated from adult wild-type (WT) and cardiac-specific STAT-3 knockout (KO) mice, were exposed to simulated ischaemia (SI) reperfusion. Cells were preconditioned either by 30 min SI or by 30 min TNFalpha (0.5 ng/mL) in the presence or absence of AG490 (100 nM) or wortmannin (100 nM) to inhibit STAT-3 or Akt, respectively. Cell viability was evaluated by trypan blue, and phosphorylation levels of STAT-3 and Akt were measured by Western blot analysis. Similar experiments were conducted in isolated rat hearts subjected to an ischaemia-reperfusion insult. Both preconditioning stimuli failed to protect KO cardiomyocytes, and addition of AG490 abolished preconditioning in WT cardiomyocytes or isolated hearts. Wortmannin abolished the protection afforded by IPC, but did not affect TNF-PC in both models. Western blot analysis demonstrated that added wortmannin during IPC stimulus decreased STAT-3 phosphorylation while, conversely, AG490 reduced Akt phosphorylation.\n\nQuestion:\nIs dual activation of STAT-3 and Akt required during the trigger phase of ischaemic preconditioning?", "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:\nPten plays a crucial role in the stem cell maintenance in a few organs. Pten defect also causes the premature oocytes and ovary aging. We and other groups have found that the phosphatidylinositol-3-OH kinase (PI3K)-Akt signaling regulates the proliferation and differentiation of spermatogonial stem cells (SSCs). PTEN functions as a negative regulator of the PI3K pathway. Thus, we thought that the fate of SSCs might be controlled by Pten. We report that promyelocytic leukaemia zinc finger (PLZF) and undifferentiated embryonic cell transcription factor 1 (UTF1), both of which are germ cell-specific transcriptional factors, are regulated by Pten. Conditional deletion of Pten leads to reduction in PLZF expression but induction of UTF1, which is associated with SSCs depletion and infertility in males with age.\n\nQuestion:\nIs pTEN signaling required for the maintenance of spermatogonial stem cells in mouse , by regulating the expressions of PLZF and UTF1?", "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:\nPten plays a crucial role in the stem cell maintenance in a few organs. Pten defect also causes the premature oocytes and ovary aging. We and other groups have found that the phosphatidylinositol-3-OH kinase (PI3K)-Akt signaling regulates the proliferation and differentiation of spermatogonial stem cells (SSCs). PTEN functions as a negative regulator of the PI3K pathway. Thus, we thought that the fate of SSCs might be controlled by Pten. We report that promyelocytic leukaemia zinc finger (PLZF) and undifferentiated embryonic cell transcription factor 1 (UTF1), both of which are germ cell-specific transcriptional factors, are regulated by Pten. Conditional deletion of Pten leads to reduction in PLZF expression but induction of UTF1, which is associated with SSCs depletion and infertility in males with age.\n\nQuestion:\nIs pTEN signaling required for the maintenance of spermatogonial stem cells in mouse , by regulating the expressions of PLZF and UTF1?", "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:\nPten plays a crucial role in the stem cell maintenance in a few organs. Pten defect also causes the premature oocytes and ovary aging. We and other groups have found that the phosphatidylinositol-3-OH kinase (PI3K)-Akt signaling regulates the proliferation and differentiation of spermatogonial stem cells (SSCs). PTEN functions as a negative regulator of the PI3K pathway. Thus, we thought that the fate of SSCs might be controlled by Pten. We report that promyelocytic leukaemia zinc finger (PLZF) and undifferentiated embryonic cell transcription factor 1 (UTF1), both of which are germ cell-specific transcriptional factors, are regulated by Pten. Conditional deletion of Pten leads to reduction in PLZF expression but induction of UTF1, which is associated with SSCs depletion and infertility in males with age.\n\nQuestion:\nIs pTEN signaling required for the maintenance of spermatogonial stem cells in mouse , by regulating the expressions of PLZF and UTF1?", "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:\nEsophageal pH monitoring using a wireless pH capsule has been suggested to generate less adverse symptoms resulting in improved patient acceptance compared with the catheter-based method although evidence to support this assumption is lacking. The aim of this study was to evaluate and compare the subjective experience of patients undergoing both techniques for esophageal pH monitoring. Using a randomized study design, patients referred for esophageal pH testing underwent both wireless and traditional catheter-based 24-h pH recording with a 7-day interval. The wireless pH capsule was placed during endoscopy and followed by 48-h pH recording. All patients answered a questionnaire, including a 10-cm visual analog scale (VAS), which described the perceived severity of symptoms and the degree of interference with normal daily activities during the pH tests. Thirty-one patients, 16 women and 15 men, were included in the analysis. The severity of all adverse symptoms associated with the wireless technique was significantly lower compared with the catheter-based technique (median VAS 2.1 vs 5.1, P < 0.001). Wireless pH recording was associated with less interference with off-work activities and normal daily life, median VAS 0.6 and 0.7 compared with 5.0 and 5.7, respectively, for the catheter-based technique (P < 0.0001). Patients actively working during both tests reported less interference with normal work during the capsule-based test than during the catheter-based pH test (median VAS 0.3 vs 6.8, P= 0.005). Twenty-seven patients (87%) stated that, if they had to undergo esophageal pH monitoring again, they preferred the wireless test over the catheter-based pH test (P < 0.0001).\n\nQuestion:\nIs wireless esophageal pH monitoring better tolerated than the catheter-based technique : results from a randomized cross-over trial?", "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:\nEsophageal pH monitoring using a wireless pH capsule has been suggested to generate less adverse symptoms resulting in improved patient acceptance compared with the catheter-based method although evidence to support this assumption is lacking. The aim of this study was to evaluate and compare the subjective experience of patients undergoing both techniques for esophageal pH monitoring. Using a randomized study design, patients referred for esophageal pH testing underwent both wireless and traditional catheter-based 24-h pH recording with a 7-day interval. The wireless pH capsule was placed during endoscopy and followed by 48-h pH recording. All patients answered a questionnaire, including a 10-cm visual analog scale (VAS), which described the perceived severity of symptoms and the degree of interference with normal daily activities during the pH tests. Thirty-one patients, 16 women and 15 men, were included in the analysis. The severity of all adverse symptoms associated with the wireless technique was significantly lower compared with the catheter-based technique (median VAS 2.1 vs 5.1, P < 0.001). Wireless pH recording was associated with less interference with off-work activities and normal daily life, median VAS 0.6 and 0.7 compared with 5.0 and 5.7, respectively, for the catheter-based technique (P < 0.0001). Patients actively working during both tests reported less interference with normal work during the capsule-based test than during the catheter-based pH test (median VAS 0.3 vs 6.8, P= 0.005). Twenty-seven patients (87%) stated that, if they had to undergo esophageal pH monitoring again, they preferred the wireless test over the catheter-based pH test (P < 0.0001).\n\nQuestion:\nIs wireless esophageal pH monitoring better tolerated than the catheter-based technique : results from a randomized cross-over trial?", "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:\nEsophageal pH monitoring using a wireless pH capsule has been suggested to generate less adverse symptoms resulting in improved patient acceptance compared with the catheter-based method although evidence to support this assumption is lacking. The aim of this study was to evaluate and compare the subjective experience of patients undergoing both techniques for esophageal pH monitoring. Using a randomized study design, patients referred for esophageal pH testing underwent both wireless and traditional catheter-based 24-h pH recording with a 7-day interval. The wireless pH capsule was placed during endoscopy and followed by 48-h pH recording. All patients answered a questionnaire, including a 10-cm visual analog scale (VAS), which described the perceived severity of symptoms and the degree of interference with normal daily activities during the pH tests. Thirty-one patients, 16 women and 15 men, were included in the analysis. The severity of all adverse symptoms associated with the wireless technique was significantly lower compared with the catheter-based technique (median VAS 2.1 vs 5.1, P < 0.001). Wireless pH recording was associated with less interference with off-work activities and normal daily life, median VAS 0.6 and 0.7 compared with 5.0 and 5.7, respectively, for the catheter-based technique (P < 0.0001). Patients actively working during both tests reported less interference with normal work during the capsule-based test than during the catheter-based pH test (median VAS 0.3 vs 6.8, P= 0.005). Twenty-seven patients (87%) stated that, if they had to undergo esophageal pH monitoring again, they preferred the wireless test over the catheter-based pH test (P < 0.0001).\n\nQuestion:\nIs wireless esophageal pH monitoring better tolerated than the catheter-based technique : results from a randomized cross-over trial?", "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 analyzed the involvement of thromboxane (TX) A2/prostaglandin (PG) H2 (TP) receptor in ischemia-induced neovascularization in mice. Unilateral hindlimb ischemia was induced by right femoral artery ligature in male C57BL/6J mice (n=7 per group). Animals were then treated with or without TP receptor antagonist (S18886, 5 or 10 mg/kg per day; ramatroban, 10 mg/kg per day) or aspirin (30 mg/kg per day) in drinking water for 21 days. Hindlimb ischemia raised plasma level of TXB2, the stable metabolite of TXA2, by 4.7-fold. This increase was blocked by aspirin treatment whereas S18886 (5 or 10 mg/kg per day) had no effect. However, neither S 18886 nor aspirin affected postischemic neovascularization. We next assessed the putative involvement of TXA2 signaling in angiotensin II (Ang II) proangiogenic pathway. Ang II (0.3 mg/kg per day) enhanced TXB2 plasma levels by 2.6-fold over that of control (P<0.01). Ang II-induced TXB2 upregulation was reduced by cotreatment with Ang II type I receptor antagonist (candesartan, 20 mg/kg per day). Angiographic score, capillary number, and foot perfusion were improved by 1.7-, 1.7-, and 1.4-fold, respectively, in Ang II-treated mice compared with controls (P<0.05). Ang II proangiogenic effect was associated with a 1.6-fold increase in VEGF-A protein content (P<0.05) and a 1.4-fold increase in the number of Mac-3-positive cells (ie, macrophages) in ischemic areas (P<0.05). Interestingly, treatments with TP receptor antagonists or aspirin hampered the proangiogenic effects of Ang II.\n\nQuestion:\nDoes thromboxane A2/prostaglandin H2 receptor activation mediate angiotensin II-induced postischemic 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:\nWe analyzed the involvement of thromboxane (TX) A2/prostaglandin (PG) H2 (TP) receptor in ischemia-induced neovascularization in mice. Unilateral hindlimb ischemia was induced by right femoral artery ligature in male C57BL/6J mice (n=7 per group). Animals were then treated with or without TP receptor antagonist (S18886, 5 or 10 mg/kg per day; ramatroban, 10 mg/kg per day) or aspirin (30 mg/kg per day) in drinking water for 21 days. Hindlimb ischemia raised plasma level of TXB2, the stable metabolite of TXA2, by 4.7-fold. This increase was blocked by aspirin treatment whereas S18886 (5 or 10 mg/kg per day) had no effect. However, neither S 18886 nor aspirin affected postischemic neovascularization. We next assessed the putative involvement of TXA2 signaling in angiotensin II (Ang II) proangiogenic pathway. Ang II (0.3 mg/kg per day) enhanced TXB2 plasma levels by 2.6-fold over that of control (P<0.01). Ang II-induced TXB2 upregulation was reduced by cotreatment with Ang II type I receptor antagonist (candesartan, 20 mg/kg per day). Angiographic score, capillary number, and foot perfusion were improved by 1.7-, 1.7-, and 1.4-fold, respectively, in Ang II-treated mice compared with controls (P<0.05). Ang II proangiogenic effect was associated with a 1.6-fold increase in VEGF-A protein content (P<0.05) and a 1.4-fold increase in the number of Mac-3-positive cells (ie, macrophages) in ischemic areas (P<0.05). Interestingly, treatments with TP receptor antagonists or aspirin hampered the proangiogenic effects of Ang II.\n\nQuestion:\nDoes thromboxane A2/prostaglandin H2 receptor activation mediate angiotensin II-induced postischemic 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:\nWe analyzed the involvement of thromboxane (TX) A2/prostaglandin (PG) H2 (TP) receptor in ischemia-induced neovascularization in mice. Unilateral hindlimb ischemia was induced by right femoral artery ligature in male C57BL/6J mice (n=7 per group). Animals were then treated with or without TP receptor antagonist (S18886, 5 or 10 mg/kg per day; ramatroban, 10 mg/kg per day) or aspirin (30 mg/kg per day) in drinking water for 21 days. Hindlimb ischemia raised plasma level of TXB2, the stable metabolite of TXA2, by 4.7-fold. This increase was blocked by aspirin treatment whereas S18886 (5 or 10 mg/kg per day) had no effect. However, neither S 18886 nor aspirin affected postischemic neovascularization. We next assessed the putative involvement of TXA2 signaling in angiotensin II (Ang II) proangiogenic pathway. Ang II (0.3 mg/kg per day) enhanced TXB2 plasma levels by 2.6-fold over that of control (P<0.01). Ang II-induced TXB2 upregulation was reduced by cotreatment with Ang II type I receptor antagonist (candesartan, 20 mg/kg per day). Angiographic score, capillary number, and foot perfusion were improved by 1.7-, 1.7-, and 1.4-fold, respectively, in Ang II-treated mice compared with controls (P<0.05). Ang II proangiogenic effect was associated with a 1.6-fold increase in VEGF-A protein content (P<0.05) and a 1.4-fold increase in the number of Mac-3-positive cells (ie, macrophages) in ischemic areas (P<0.05). Interestingly, treatments with TP receptor antagonists or aspirin hampered the proangiogenic effects of Ang II.\n\nQuestion:\nDoes thromboxane A2/prostaglandin H2 receptor activation mediate angiotensin II-induced postischemic 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:\nIntraventricular fibrinolysis (IVF) in subarachnoid hemorrhage (SAH) is an emerging strategy aiming to hasten clot lysis, treat hydrocephalus, and reduce permanent shunt rates. Because of clinical heterogeneity of investigated patient effects of IVF on permanent shunt incidence and functional outcome are widely debated. The present study is the first to investigate solely endovascular-treated SAH patients. Overall, 88 consecutive patients with aneurysmal SAH requiring external ventricular drain placement and endovascular aneurysm closure were included. Functional outcome and shunt dependency were assessed 90 days after event. A matched controlled sub-analysis was carried out to investigate the effects of IVF treatment (n = 14; matching criteria: age, neuro-status and imaging). Multivariate modeling was performed to identify independent predictors for permanent shunt dependency. In IVF-patients neurological status was significantly poorer [Hunt&Hess: IVF = 4(3-5) vs. non-IVF = 3(1-5); p = 0.035] and the extent of ventricular hemorrhage was increased [Graeb Score: IVF = 7(6-8) vs. non-IVF = 3(1-4); p ≤ 0.001]. Consecutive matched controlled sub-analysis revealed no significant therapeutic effect of IVF with respect to shunt dependency rate and functional outcome. Multivariate analysis revealed Graeb score [OR = 1.34(1.02-1.76); p = 0.035] and sepsis [OR = 11.23(2.28-55.27); p = 0.003] as independent predictors for shunt dependency, whereas IVF did not exert significant effects (p = 0.820).\n\nQuestion:\nDoes intraventricular fibrinolysis have no effects on shunt dependency and functional outcome in endovascular-treated aneurysmal SAH?", "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:\nIntraventricular fibrinolysis (IVF) in subarachnoid hemorrhage (SAH) is an emerging strategy aiming to hasten clot lysis, treat hydrocephalus, and reduce permanent shunt rates. Because of clinical heterogeneity of investigated patient effects of IVF on permanent shunt incidence and functional outcome are widely debated. The present study is the first to investigate solely endovascular-treated SAH patients. Overall, 88 consecutive patients with aneurysmal SAH requiring external ventricular drain placement and endovascular aneurysm closure were included. Functional outcome and shunt dependency were assessed 90 days after event. A matched controlled sub-analysis was carried out to investigate the effects of IVF treatment (n = 14; matching criteria: age, neuro-status and imaging). Multivariate modeling was performed to identify independent predictors for permanent shunt dependency. In IVF-patients neurological status was significantly poorer [Hunt&Hess: IVF = 4(3-5) vs. non-IVF = 3(1-5); p = 0.035] and the extent of ventricular hemorrhage was increased [Graeb Score: IVF = 7(6-8) vs. non-IVF = 3(1-4); p ≤ 0.001]. Consecutive matched controlled sub-analysis revealed no significant therapeutic effect of IVF with respect to shunt dependency rate and functional outcome. Multivariate analysis revealed Graeb score [OR = 1.34(1.02-1.76); p = 0.035] and sepsis [OR = 11.23(2.28-55.27); p = 0.003] as independent predictors for shunt dependency, whereas IVF did not exert significant effects (p = 0.820).\n\nQuestion:\nDoes intraventricular fibrinolysis have no effects on shunt dependency and functional outcome in endovascular-treated aneurysmal SAH?", "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:\nIntraventricular fibrinolysis (IVF) in subarachnoid hemorrhage (SAH) is an emerging strategy aiming to hasten clot lysis, treat hydrocephalus, and reduce permanent shunt rates. Because of clinical heterogeneity of investigated patient effects of IVF on permanent shunt incidence and functional outcome are widely debated. The present study is the first to investigate solely endovascular-treated SAH patients. Overall, 88 consecutive patients with aneurysmal SAH requiring external ventricular drain placement and endovascular aneurysm closure were included. Functional outcome and shunt dependency were assessed 90 days after event. A matched controlled sub-analysis was carried out to investigate the effects of IVF treatment (n = 14; matching criteria: age, neuro-status and imaging). Multivariate modeling was performed to identify independent predictors for permanent shunt dependency. In IVF-patients neurological status was significantly poorer [Hunt&Hess: IVF = 4(3-5) vs. non-IVF = 3(1-5); p = 0.035] and the extent of ventricular hemorrhage was increased [Graeb Score: IVF = 7(6-8) vs. non-IVF = 3(1-4); p ≤ 0.001]. Consecutive matched controlled sub-analysis revealed no significant therapeutic effect of IVF with respect to shunt dependency rate and functional outcome. Multivariate analysis revealed Graeb score [OR = 1.34(1.02-1.76); p = 0.035] and sepsis [OR = 11.23(2.28-55.27); p = 0.003] as independent predictors for shunt dependency, whereas IVF did not exert significant effects (p = 0.820).\n\nQuestion:\nDoes intraventricular fibrinolysis have no effects on shunt dependency and functional outcome in endovascular-treated aneurysmal SAH?", "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 present study examined the role of cystathionine γ-lyase (CSE) in CCl4- induced liver damage. A CSE gene knock-out and luciferase gene knock-in mouse model was constructed to study the function of CSE and trace its expression in living status. CCl4 or LPS markedly downregulated CSE expression in the liver of mice. CSE-deficient mice showed increased serum alanine aminotransferase and aspartate aminotransferase levels, and liver damage after CCl4 challenge, whereas albumin and endogenous H2S levels decreased significantly. CSE knockout mice showed increased serum homocysteine levels, upregulation of inflammatory cytokines, and increased autophagy and IκB-α degradation in the liver in response to CCl4 treatment. The increase in pro-inflammatory cytokines including TNF-α in CSE-deficient mice after CCl4 challenge was accompanied by a significant increase in liver tissue hydroxyproline and α-SMA and histopathologic changes in the liver. However, H2S donor pretreatment effectively attenuated most of these imbalances. Here, a CSE knock-out and luciferase knock-in mouse model was established for the first time to study the transcriptional regulation of CSE expression in real-time in a non-invasive manner, providing information on the effects and potential mechanisms of CSE on CCl4-induced liver injury.\n\nQuestion:\nDoes cystathionine γ-lyase Deficiency exacerbate CCl4-induced Acute Hepatitis and Fibrosis in the Mouse 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:\nThe present study examined the role of cystathionine γ-lyase (CSE) in CCl4- induced liver damage. A CSE gene knock-out and luciferase gene knock-in mouse model was constructed to study the function of CSE and trace its expression in living status. CCl4 or LPS markedly downregulated CSE expression in the liver of mice. CSE-deficient mice showed increased serum alanine aminotransferase and aspartate aminotransferase levels, and liver damage after CCl4 challenge, whereas albumin and endogenous H2S levels decreased significantly. CSE knockout mice showed increased serum homocysteine levels, upregulation of inflammatory cytokines, and increased autophagy and IκB-α degradation in the liver in response to CCl4 treatment. The increase in pro-inflammatory cytokines including TNF-α in CSE-deficient mice after CCl4 challenge was accompanied by a significant increase in liver tissue hydroxyproline and α-SMA and histopathologic changes in the liver. However, H2S donor pretreatment effectively attenuated most of these imbalances. Here, a CSE knock-out and luciferase knock-in mouse model was established for the first time to study the transcriptional regulation of CSE expression in real-time in a non-invasive manner, providing information on the effects and potential mechanisms of CSE on CCl4-induced liver injury.\n\nQuestion:\nDoes cystathionine γ-lyase Deficiency exacerbate CCl4-induced Acute Hepatitis and Fibrosis in the Mouse 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:\nThe present study examined the role of cystathionine γ-lyase (CSE) in CCl4- induced liver damage. A CSE gene knock-out and luciferase gene knock-in mouse model was constructed to study the function of CSE and trace its expression in living status. CCl4 or LPS markedly downregulated CSE expression in the liver of mice. CSE-deficient mice showed increased serum alanine aminotransferase and aspartate aminotransferase levels, and liver damage after CCl4 challenge, whereas albumin and endogenous H2S levels decreased significantly. CSE knockout mice showed increased serum homocysteine levels, upregulation of inflammatory cytokines, and increased autophagy and IκB-α degradation in the liver in response to CCl4 treatment. The increase in pro-inflammatory cytokines including TNF-α in CSE-deficient mice after CCl4 challenge was accompanied by a significant increase in liver tissue hydroxyproline and α-SMA and histopathologic changes in the liver. However, H2S donor pretreatment effectively attenuated most of these imbalances. Here, a CSE knock-out and luciferase knock-in mouse model was established for the first time to study the transcriptional regulation of CSE expression in real-time in a non-invasive manner, providing information on the effects and potential mechanisms of CSE on CCl4-induced liver injury.\n\nQuestion:\nDoes cystathionine γ-lyase Deficiency exacerbate CCl4-induced Acute Hepatitis and Fibrosis in the Mouse 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:\nApnea of prematurity remains among the most commonly diagnosed conditions in the Newborn Intensive Care Unit and may prolong hospital stays in some infants. Because survival of extremely premature infants has improved markedly, the natural history of apnea in this population needs to be reassessed. To document the natural history of recurrent apnea and/or bradycardia events in infants delivered at 24 to 28 weeks' gestation. Medical records of all infants delivered at 24 to 28 weeks' gestation admitted to the Brigham and Women's Hospital Newborn Intensive Care Unit between January 1989 and March 1994 were reviewed to document the clinical course of apnea of prematurity. Subjects were included in the study sample if they were discharged home from the Brigham and Women's Hospital or after transfer to an affiliated hospital. Recordings of apnea and/or bradycardia events were based on nursing observations of monitor alarms and assessment of the infant's condition. Of 457 eligible infants, 226 were included in the study sample and stratified by gestational age at birth assigned by the attending neonatologist. The time to resolution of recurrent apnea/bradycardia events was longer with lower gestational age at birth. Apnea/bradycardia events were frequently observed beyond 36 weeks' postconceptional age in all gestational age groups. The incidence of apnea persisting beyond 38 weeks postconceptional age was significantly higher in the 24- to 27-week infants combined compared with the 28-week infants.\n\nQuestion:\nDoes apnea frequently persist beyond term gestation in infants delivered at 24 to 28 weeks?", "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:\nApnea of prematurity remains among the most commonly diagnosed conditions in the Newborn Intensive Care Unit and may prolong hospital stays in some infants. Because survival of extremely premature infants has improved markedly, the natural history of apnea in this population needs to be reassessed. To document the natural history of recurrent apnea and/or bradycardia events in infants delivered at 24 to 28 weeks' gestation. Medical records of all infants delivered at 24 to 28 weeks' gestation admitted to the Brigham and Women's Hospital Newborn Intensive Care Unit between January 1989 and March 1994 were reviewed to document the clinical course of apnea of prematurity. Subjects were included in the study sample if they were discharged home from the Brigham and Women's Hospital or after transfer to an affiliated hospital. Recordings of apnea and/or bradycardia events were based on nursing observations of monitor alarms and assessment of the infant's condition. Of 457 eligible infants, 226 were included in the study sample and stratified by gestational age at birth assigned by the attending neonatologist. The time to resolution of recurrent apnea/bradycardia events was longer with lower gestational age at birth. Apnea/bradycardia events were frequently observed beyond 36 weeks' postconceptional age in all gestational age groups. The incidence of apnea persisting beyond 38 weeks postconceptional age was significantly higher in the 24- to 27-week infants combined compared with the 28-week infants.\n\nQuestion:\nDoes apnea frequently persist beyond term gestation in infants delivered at 24 to 28 weeks?", "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:\nApnea of prematurity remains among the most commonly diagnosed conditions in the Newborn Intensive Care Unit and may prolong hospital stays in some infants. Because survival of extremely premature infants has improved markedly, the natural history of apnea in this population needs to be reassessed. To document the natural history of recurrent apnea and/or bradycardia events in infants delivered at 24 to 28 weeks' gestation. Medical records of all infants delivered at 24 to 28 weeks' gestation admitted to the Brigham and Women's Hospital Newborn Intensive Care Unit between January 1989 and March 1994 were reviewed to document the clinical course of apnea of prematurity. Subjects were included in the study sample if they were discharged home from the Brigham and Women's Hospital or after transfer to an affiliated hospital. Recordings of apnea and/or bradycardia events were based on nursing observations of monitor alarms and assessment of the infant's condition. Of 457 eligible infants, 226 were included in the study sample and stratified by gestational age at birth assigned by the attending neonatologist. The time to resolution of recurrent apnea/bradycardia events was longer with lower gestational age at birth. Apnea/bradycardia events were frequently observed beyond 36 weeks' postconceptional age in all gestational age groups. The incidence of apnea persisting beyond 38 weeks postconceptional age was significantly higher in the 24- to 27-week infants combined compared with the 28-week infants.\n\nQuestion:\nDoes apnea frequently persist beyond term gestation in infants delivered at 24 to 28 weeks?", "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 Bispectral Index (BIS) is a mathematically derived electroencephalographic (EEG) derivative that has been introduced to monitor depth of anesthesia (1,2). The A-2000 BIS monitoring system (Aspect Medical Systems, Inc., Newton, MA) is currently the only commercially available system to monitor depth of anesthesia. In several studies, its propensity to optimize the use of hypnotics to maintain and achieve a certain depth of anesthesia has been described (3,4). Some studies have even proposed that the routine use of the monitoring system can decrease awareness (1,5), an increasing factor in malpractice claims. The cost-benefit calculations for BIS monitoring suffer from the fact that like its predecessor, the 1000-A BIS monitor, the A-2000 BIS monitoring system demands the use of expensive, special electrodes (6). Although the application of the single-use BIS sensor is very comfortable and easy to use, its high price of approximately $10-20 US prevents many anesthesiologists from using it. Furthermore, whereas the former model of the monitor (1000-A BIS monitor; Aspect Medical Systems, Inc.) used standardized connectors, which allowed the use of other electrodes such as electrocardiogram (ECG), the new monitoring system makes this very difficult because of special connectors that match the equivalent connector at the proximal BIS sensor site. The purpose of this prospective study was to compare BIS values derived from the original BIS sensor with BIS values derived from commercially available ECG electrodes. This comparison was made possible by designing and manufacturing a connector allowing the use of ECG electrodes.\n\nQuestion:\nDo electrocardiographic electrodes provide the same results as expensive special sensors in the routine monitoring of anesthetic depth?", "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 Bispectral Index (BIS) is a mathematically derived electroencephalographic (EEG) derivative that has been introduced to monitor depth of anesthesia (1,2). The A-2000 BIS monitoring system (Aspect Medical Systems, Inc., Newton, MA) is currently the only commercially available system to monitor depth of anesthesia. In several studies, its propensity to optimize the use of hypnotics to maintain and achieve a certain depth of anesthesia has been described (3,4). Some studies have even proposed that the routine use of the monitoring system can decrease awareness (1,5), an increasing factor in malpractice claims. The cost-benefit calculations for BIS monitoring suffer from the fact that like its predecessor, the 1000-A BIS monitor, the A-2000 BIS monitoring system demands the use of expensive, special electrodes (6). Although the application of the single-use BIS sensor is very comfortable and easy to use, its high price of approximately $10-20 US prevents many anesthesiologists from using it. Furthermore, whereas the former model of the monitor (1000-A BIS monitor; Aspect Medical Systems, Inc.) used standardized connectors, which allowed the use of other electrodes such as electrocardiogram (ECG), the new monitoring system makes this very difficult because of special connectors that match the equivalent connector at the proximal BIS sensor site. The purpose of this prospective study was to compare BIS values derived from the original BIS sensor with BIS values derived from commercially available ECG electrodes. This comparison was made possible by designing and manufacturing a connector allowing the use of ECG electrodes.\n\nQuestion:\nDo electrocardiographic electrodes provide the same results as expensive special sensors in the routine monitoring of anesthetic depth?", "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 Bispectral Index (BIS) is a mathematically derived electroencephalographic (EEG) derivative that has been introduced to monitor depth of anesthesia (1,2). The A-2000 BIS monitoring system (Aspect Medical Systems, Inc., Newton, MA) is currently the only commercially available system to monitor depth of anesthesia. In several studies, its propensity to optimize the use of hypnotics to maintain and achieve a certain depth of anesthesia has been described (3,4). Some studies have even proposed that the routine use of the monitoring system can decrease awareness (1,5), an increasing factor in malpractice claims. The cost-benefit calculations for BIS monitoring suffer from the fact that like its predecessor, the 1000-A BIS monitor, the A-2000 BIS monitoring system demands the use of expensive, special electrodes (6). Although the application of the single-use BIS sensor is very comfortable and easy to use, its high price of approximately $10-20 US prevents many anesthesiologists from using it. Furthermore, whereas the former model of the monitor (1000-A BIS monitor; Aspect Medical Systems, Inc.) used standardized connectors, which allowed the use of other electrodes such as electrocardiogram (ECG), the new monitoring system makes this very difficult because of special connectors that match the equivalent connector at the proximal BIS sensor site. The purpose of this prospective study was to compare BIS values derived from the original BIS sensor with BIS values derived from commercially available ECG electrodes. This comparison was made possible by designing and manufacturing a connector allowing the use of ECG electrodes.\n\nQuestion:\nDo electrocardiographic electrodes provide the same results as expensive special sensors in the routine monitoring of anesthetic depth?", "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:\nSurgical site infection (SSI) can be a problematic complication of Mohs micrographic surgery (MMS). Previous reports have cited nasal Staphylococcus aureus (S. aureus) carriage as a risk factor for SSI, but none thus far in dermatologic surgery. The aim was to determine the difference in infection rates between nasal carriers of S. aureus and non-carriers, and whether decolonisation with intranasal mupirocin ointment and chlorhexidine wash would reduce the infection rate in nasal carriers. In all, 738 patients presenting for MMS at the Oxford Day Surgery and Dermatology underwent a nasal swab to determine their S. aureus carriage status. S. aureus carriers were randomised for decolonisation with intranasal mupirocin ointment and chlorhexidine body wash. Non-carriers were untreated. All patients were followed up for SSI. The rate of SSI was 11 per cent in untreated S. aureus carriers, 4 per cent in treated carriers, and 3 per cent in non-carriers. The difference in infection rate between carriers and non-carriers was significant (P < 0.001). The difference between treated and untreated carriers was also significant (P = 0.05).\n\nQuestion:\nIs nasal carriage of Staphylococcus aureus in patients undergoing Mohs micrographic surgery an important risk factor for postoperative surgical site infection : a prospective randomised 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:\nSurgical site infection (SSI) can be a problematic complication of Mohs micrographic surgery (MMS). Previous reports have cited nasal Staphylococcus aureus (S. aureus) carriage as a risk factor for SSI, but none thus far in dermatologic surgery. The aim was to determine the difference in infection rates between nasal carriers of S. aureus and non-carriers, and whether decolonisation with intranasal mupirocin ointment and chlorhexidine wash would reduce the infection rate in nasal carriers. In all, 738 patients presenting for MMS at the Oxford Day Surgery and Dermatology underwent a nasal swab to determine their S. aureus carriage status. S. aureus carriers were randomised for decolonisation with intranasal mupirocin ointment and chlorhexidine body wash. Non-carriers were untreated. All patients were followed up for SSI. The rate of SSI was 11 per cent in untreated S. aureus carriers, 4 per cent in treated carriers, and 3 per cent in non-carriers. The difference in infection rate between carriers and non-carriers was significant (P < 0.001). The difference between treated and untreated carriers was also significant (P = 0.05).\n\nQuestion:\nIs nasal carriage of Staphylococcus aureus in patients undergoing Mohs micrographic surgery an important risk factor for postoperative surgical site infection : a prospective randomised 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:\nSurgical site infection (SSI) can be a problematic complication of Mohs micrographic surgery (MMS). Previous reports have cited nasal Staphylococcus aureus (S. aureus) carriage as a risk factor for SSI, but none thus far in dermatologic surgery. The aim was to determine the difference in infection rates between nasal carriers of S. aureus and non-carriers, and whether decolonisation with intranasal mupirocin ointment and chlorhexidine wash would reduce the infection rate in nasal carriers. In all, 738 patients presenting for MMS at the Oxford Day Surgery and Dermatology underwent a nasal swab to determine their S. aureus carriage status. S. aureus carriers were randomised for decolonisation with intranasal mupirocin ointment and chlorhexidine body wash. Non-carriers were untreated. All patients were followed up for SSI. The rate of SSI was 11 per cent in untreated S. aureus carriers, 4 per cent in treated carriers, and 3 per cent in non-carriers. The difference in infection rate between carriers and non-carriers was significant (P < 0.001). The difference between treated and untreated carriers was also significant (P = 0.05).\n\nQuestion:\nIs nasal carriage of Staphylococcus aureus in patients undergoing Mohs micrographic surgery an important risk factor for postoperative surgical site infection : a prospective randomised 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:\nAmylin, a 37-amino-acid peptide hormone, is a potent inhibitor of gastric emptying. It is co-secreted by the pancreatic beta cells in response to enteral nutrient intake. Feed intolerance is common in preterm neonates and often presents as increased gastric residual volume (GRV). It is therefore hypothesised that serum amylin concentrations are raised in preterm neonates with poor gastric emptying, which may contribute to this observed feed intolerance. To determine serum amylin concentrations in feed-intolerant preterm neonates. Feed-intolerant (nTOL) preterm neonates (GRV >50% of a previous 4 h feed volume on two consecutive occasions) were matched for gestation, birth weight and postnatal age with feed-tolerant (TOL) neonates. Blood samples were analysed for amylin concentration. Seventy neonates were studied with median (interquartile range) gestation of 29 weeks (28-33) and birth weight of 1.3 kg (1.0-1.8). Serum amylin concentration and percentage GRV (median (interquartile range)) were significantly higher in the nTOL (47.9 pmol/l (21.4-79.8), 150% (100-350)) than the TOL (8.7 pmol/l (5.7-16), 5% (0-5)) group (p<0.001). In the nTOL group, a positive correlation was observed between serum amylin and GRV (r = 0.78, 95% CI 0.59 to 0.89, p<0.001), days to reach full enteral feeds (r = 0.40, 95% CI 0.08 to 0.68, p = 0.02), and days to discharge (r = 0.43, 95% CI 0.09 to 0.68, p = 0.01).\n\nQuestion:\nIs amylin peptide increased in preterm neonates with feed intolerance?", "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:\nAmylin, a 37-amino-acid peptide hormone, is a potent inhibitor of gastric emptying. It is co-secreted by the pancreatic beta cells in response to enteral nutrient intake. Feed intolerance is common in preterm neonates and often presents as increased gastric residual volume (GRV). It is therefore hypothesised that serum amylin concentrations are raised in preterm neonates with poor gastric emptying, which may contribute to this observed feed intolerance. To determine serum amylin concentrations in feed-intolerant preterm neonates. Feed-intolerant (nTOL) preterm neonates (GRV >50% of a previous 4 h feed volume on two consecutive occasions) were matched for gestation, birth weight and postnatal age with feed-tolerant (TOL) neonates. Blood samples were analysed for amylin concentration. Seventy neonates were studied with median (interquartile range) gestation of 29 weeks (28-33) and birth weight of 1.3 kg (1.0-1.8). Serum amylin concentration and percentage GRV (median (interquartile range)) were significantly higher in the nTOL (47.9 pmol/l (21.4-79.8), 150% (100-350)) than the TOL (8.7 pmol/l (5.7-16), 5% (0-5)) group (p<0.001). In the nTOL group, a positive correlation was observed between serum amylin and GRV (r = 0.78, 95% CI 0.59 to 0.89, p<0.001), days to reach full enteral feeds (r = 0.40, 95% CI 0.08 to 0.68, p = 0.02), and days to discharge (r = 0.43, 95% CI 0.09 to 0.68, p = 0.01).\n\nQuestion:\nIs amylin peptide increased in preterm neonates with feed intolerance?", "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:\nAmylin, a 37-amino-acid peptide hormone, is a potent inhibitor of gastric emptying. It is co-secreted by the pancreatic beta cells in response to enteral nutrient intake. Feed intolerance is common in preterm neonates and often presents as increased gastric residual volume (GRV). It is therefore hypothesised that serum amylin concentrations are raised in preterm neonates with poor gastric emptying, which may contribute to this observed feed intolerance. To determine serum amylin concentrations in feed-intolerant preterm neonates. Feed-intolerant (nTOL) preterm neonates (GRV >50% of a previous 4 h feed volume on two consecutive occasions) were matched for gestation, birth weight and postnatal age with feed-tolerant (TOL) neonates. Blood samples were analysed for amylin concentration. Seventy neonates were studied with median (interquartile range) gestation of 29 weeks (28-33) and birth weight of 1.3 kg (1.0-1.8). Serum amylin concentration and percentage GRV (median (interquartile range)) were significantly higher in the nTOL (47.9 pmol/l (21.4-79.8), 150% (100-350)) than the TOL (8.7 pmol/l (5.7-16), 5% (0-5)) group (p<0.001). In the nTOL group, a positive correlation was observed between serum amylin and GRV (r = 0.78, 95% CI 0.59 to 0.89, p<0.001), days to reach full enteral feeds (r = 0.40, 95% CI 0.08 to 0.68, p = 0.02), and days to discharge (r = 0.43, 95% CI 0.09 to 0.68, p = 0.01).\n\nQuestion:\nIs amylin peptide increased in preterm neonates with feed intolerance?", "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:\nVasopeptidase inhibitors are a new class of cardiovascular compounds that inhibit both angiotensin-converting enzyme (ACE) and neutral endopeptidase (NEP). The aim of the present study was to explore the effects of omapatrilat, a vasopeptidase inhibitor, on renal function and pathology in subtotally nephrectomized (STNx) rats. STNx rats were randomized to four groups and treated for 12 weeks: no treatment (N = 14); omapatrilat at a low dose of 10 mg/kg (L, N = 12) and at a high dose of 40 mg/kg (H, N = 10); or an ACE inhibitor, fosinopril, at a dose of 10 mg/kg (N = 12). Sham-operated rats were used as control animals (N = 12). Elevated blood pressure in STNx rats (174 +/- 9 mm Hg) was reduced by omapatrilat in a dose-dependent manner (L, 121 +/- 3 mm Hg; H, 110 +/- 3 mm Hg) and by fosinopril (149 +/- 5 mm Hg). Proteinuria in STNx rats (246 +/- 73 mg/day) was reduced by treatment with fosinopril (88 +/- 21 mg/day) and was normalized by treatment with omapatrilat (L, 30 +/- 4 mg/day; H, 20 +/- 2 mg/day vs. control 25 +/- 1 mg/day). Decreased glomerular filtration rates, elevated plasma urea and creatinine and glomerulosclerosis, and tubulointerstitial fibrosis were ameliorated by omapatrilat and fosinopril to a similar degree. Compared with fosinopril, omapatrilat treatment was associated with increased plasma renin activity and decreased renal ACE and NEP binding in a dose-dependent manner.\n\nQuestion:\nDoes vasopeptidase inhibition attenuate the progression of renal injury in subtotal nephrectomized 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:\nVasopeptidase inhibitors are a new class of cardiovascular compounds that inhibit both angiotensin-converting enzyme (ACE) and neutral endopeptidase (NEP). The aim of the present study was to explore the effects of omapatrilat, a vasopeptidase inhibitor, on renal function and pathology in subtotally nephrectomized (STNx) rats. STNx rats were randomized to four groups and treated for 12 weeks: no treatment (N = 14); omapatrilat at a low dose of 10 mg/kg (L, N = 12) and at a high dose of 40 mg/kg (H, N = 10); or an ACE inhibitor, fosinopril, at a dose of 10 mg/kg (N = 12). Sham-operated rats were used as control animals (N = 12). Elevated blood pressure in STNx rats (174 +/- 9 mm Hg) was reduced by omapatrilat in a dose-dependent manner (L, 121 +/- 3 mm Hg; H, 110 +/- 3 mm Hg) and by fosinopril (149 +/- 5 mm Hg). Proteinuria in STNx rats (246 +/- 73 mg/day) was reduced by treatment with fosinopril (88 +/- 21 mg/day) and was normalized by treatment with omapatrilat (L, 30 +/- 4 mg/day; H, 20 +/- 2 mg/day vs. control 25 +/- 1 mg/day). Decreased glomerular filtration rates, elevated plasma urea and creatinine and glomerulosclerosis, and tubulointerstitial fibrosis were ameliorated by omapatrilat and fosinopril to a similar degree. Compared with fosinopril, omapatrilat treatment was associated with increased plasma renin activity and decreased renal ACE and NEP binding in a dose-dependent manner.\n\nQuestion:\nDoes vasopeptidase inhibition attenuate the progression of renal injury in subtotal nephrectomized 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:\nVasopeptidase inhibitors are a new class of cardiovascular compounds that inhibit both angiotensin-converting enzyme (ACE) and neutral endopeptidase (NEP). The aim of the present study was to explore the effects of omapatrilat, a vasopeptidase inhibitor, on renal function and pathology in subtotally nephrectomized (STNx) rats. STNx rats were randomized to four groups and treated for 12 weeks: no treatment (N = 14); omapatrilat at a low dose of 10 mg/kg (L, N = 12) and at a high dose of 40 mg/kg (H, N = 10); or an ACE inhibitor, fosinopril, at a dose of 10 mg/kg (N = 12). Sham-operated rats were used as control animals (N = 12). Elevated blood pressure in STNx rats (174 +/- 9 mm Hg) was reduced by omapatrilat in a dose-dependent manner (L, 121 +/- 3 mm Hg; H, 110 +/- 3 mm Hg) and by fosinopril (149 +/- 5 mm Hg). Proteinuria in STNx rats (246 +/- 73 mg/day) was reduced by treatment with fosinopril (88 +/- 21 mg/day) and was normalized by treatment with omapatrilat (L, 30 +/- 4 mg/day; H, 20 +/- 2 mg/day vs. control 25 +/- 1 mg/day). Decreased glomerular filtration rates, elevated plasma urea and creatinine and glomerulosclerosis, and tubulointerstitial fibrosis were ameliorated by omapatrilat and fosinopril to a similar degree. Compared with fosinopril, omapatrilat treatment was associated with increased plasma renin activity and decreased renal ACE and NEP binding in a dose-dependent manner.\n\nQuestion:\nDoes vasopeptidase inhibition attenuate the progression of renal injury in subtotal nephrectomized 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:\nEsophagectomy is one of the most invasive surgical treatments for digestive tract cancer, and the blood levels of inflammatory cytokines such as interleukin-1, interleukin-6, and interleukin-8 are increased for several hours after surgery or in patients experiencing postoperative complications. CXCR2, an interleukin-8 receptor, is reportedly expressed in several carcinomas, and interleukin-8 signaling promotes cancer cell proliferation. The impact of postoperative complications following esophagectomy on long-term survival is controversial. In this study, we demonstrate the significance of CXCR2 expression and validate the effects of CXCR2 expression and postoperative complications on long-term prognosis of esophageal squamous cell carcinoma using resected specimens. Eighty-two specimens were sectioned from archived, paraffin-embedded tumor tissues obtained from patients with esophageal squamous cell carcinoma who underwent esophagectomy and extended lymphadenectomy for complete resection of cancer in our institute between 1997 and 2002. Immunohistochemistry was performed using a polyclonal antibody to CXCR2, and the correlation of stainability with clinicopathological factors and long-term survival was examined. CXCR2 was expressed in 33 of 82 (40.2 %) specimens. In the CXCR2-positive group, the recurrence-free survival and overall survival rates of patients who developed postoperative complications were both significantly lower than those for patients who did not develop any complications. In contrast, in the CXCR2-negative group, there was no significant difference in long-term prognosis between patients with and without complications. CXCR2 positivity combined with postoperative complications was an independent risk factor for subsequent tumor recurrence, showing the highest hazard ratio.\n\nQuestion:\nDo cXCR2 expression and postoperative complications affect long-term survival in patients with esophageal 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:\nEsophagectomy is one of the most invasive surgical treatments for digestive tract cancer, and the blood levels of inflammatory cytokines such as interleukin-1, interleukin-6, and interleukin-8 are increased for several hours after surgery or in patients experiencing postoperative complications. CXCR2, an interleukin-8 receptor, is reportedly expressed in several carcinomas, and interleukin-8 signaling promotes cancer cell proliferation. The impact of postoperative complications following esophagectomy on long-term survival is controversial. In this study, we demonstrate the significance of CXCR2 expression and validate the effects of CXCR2 expression and postoperative complications on long-term prognosis of esophageal squamous cell carcinoma using resected specimens. Eighty-two specimens were sectioned from archived, paraffin-embedded tumor tissues obtained from patients with esophageal squamous cell carcinoma who underwent esophagectomy and extended lymphadenectomy for complete resection of cancer in our institute between 1997 and 2002. Immunohistochemistry was performed using a polyclonal antibody to CXCR2, and the correlation of stainability with clinicopathological factors and long-term survival was examined. CXCR2 was expressed in 33 of 82 (40.2 %) specimens. In the CXCR2-positive group, the recurrence-free survival and overall survival rates of patients who developed postoperative complications were both significantly lower than those for patients who did not develop any complications. In contrast, in the CXCR2-negative group, there was no significant difference in long-term prognosis between patients with and without complications. CXCR2 positivity combined with postoperative complications was an independent risk factor for subsequent tumor recurrence, showing the highest hazard ratio.\n\nQuestion:\nDo cXCR2 expression and postoperative complications affect long-term survival in patients with esophageal 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:\nEsophagectomy is one of the most invasive surgical treatments for digestive tract cancer, and the blood levels of inflammatory cytokines such as interleukin-1, interleukin-6, and interleukin-8 are increased for several hours after surgery or in patients experiencing postoperative complications. CXCR2, an interleukin-8 receptor, is reportedly expressed in several carcinomas, and interleukin-8 signaling promotes cancer cell proliferation. The impact of postoperative complications following esophagectomy on long-term survival is controversial. In this study, we demonstrate the significance of CXCR2 expression and validate the effects of CXCR2 expression and postoperative complications on long-term prognosis of esophageal squamous cell carcinoma using resected specimens. Eighty-two specimens were sectioned from archived, paraffin-embedded tumor tissues obtained from patients with esophageal squamous cell carcinoma who underwent esophagectomy and extended lymphadenectomy for complete resection of cancer in our institute between 1997 and 2002. Immunohistochemistry was performed using a polyclonal antibody to CXCR2, and the correlation of stainability with clinicopathological factors and long-term survival was examined. CXCR2 was expressed in 33 of 82 (40.2 %) specimens. In the CXCR2-positive group, the recurrence-free survival and overall survival rates of patients who developed postoperative complications were both significantly lower than those for patients who did not develop any complications. In contrast, in the CXCR2-negative group, there was no significant difference in long-term prognosis between patients with and without complications. CXCR2 positivity combined with postoperative complications was an independent risk factor for subsequent tumor recurrence, showing the highest hazard ratio.\n\nQuestion:\nDo cXCR2 expression and postoperative complications affect long-term survival in patients with esophageal 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:\nCardiac surgery causes induction and release of inflammatory mediators that may be regulated by genetic background. Macrophage migration inhibitory factor (MIF) is a proinflammatory mediator that is known to be up-regulated in patients undergoing cardiac operations. Here we analyzed genotype distribution and allele frequency of the MIF-173*G/C single nucleotide polymorphism (SNP) and MIF plasma levels in patients undergoing surgical revascularization with (on-pump, n=45) and without (off-pump, n=34) cardiopulmonary bypass (CPB). Genotyping was performed using a real-time PCR-based system with a hybridization probe system specific for the MIF-173*G/C SNP. In on-pump patients, blood samples were drawn before start of CPB, after termination of CPB and 12h postoperatively. In off-pump patients, blood samples were collected before stabilizer placement, after removal of the stabilizer and 12h postoperatively. MIF levels were measured using ELISA technique. Genotype distribution and allele frequencies were comparable between on-pump and off-pump patients. When comparing patients according to MIF genotype, a significant increase of MIF plasma levels after completed coronary bypass grafting using CPB was found in patients heterozygous for the MIF-173*G/C SNP (p<0.05). Moreover, on-pump patients showed significantly decreased MIF plasma levels after 12h postoperatively (p<0.05). In off-pump patients, MIF plasma levels were not significantly different over the time-course and were independent of the genotype.\n\nQuestion:\nIs a single nucleotide polymorphism of macrophage migration inhibitory factor related to inflammatory response in coronary bypass surgery using cardiopulmonary bypass?", "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 surgery causes induction and release of inflammatory mediators that may be regulated by genetic background. Macrophage migration inhibitory factor (MIF) is a proinflammatory mediator that is known to be up-regulated in patients undergoing cardiac operations. Here we analyzed genotype distribution and allele frequency of the MIF-173*G/C single nucleotide polymorphism (SNP) and MIF plasma levels in patients undergoing surgical revascularization with (on-pump, n=45) and without (off-pump, n=34) cardiopulmonary bypass (CPB). Genotyping was performed using a real-time PCR-based system with a hybridization probe system specific for the MIF-173*G/C SNP. In on-pump patients, blood samples were drawn before start of CPB, after termination of CPB and 12h postoperatively. In off-pump patients, blood samples were collected before stabilizer placement, after removal of the stabilizer and 12h postoperatively. MIF levels were measured using ELISA technique. Genotype distribution and allele frequencies were comparable between on-pump and off-pump patients. When comparing patients according to MIF genotype, a significant increase of MIF plasma levels after completed coronary bypass grafting using CPB was found in patients heterozygous for the MIF-173*G/C SNP (p<0.05). Moreover, on-pump patients showed significantly decreased MIF plasma levels after 12h postoperatively (p<0.05). In off-pump patients, MIF plasma levels were not significantly different over the time-course and were independent of the genotype.\n\nQuestion:\nIs a single nucleotide polymorphism of macrophage migration inhibitory factor related to inflammatory response in coronary bypass surgery using cardiopulmonary bypass?", "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 surgery causes induction and release of inflammatory mediators that may be regulated by genetic background. Macrophage migration inhibitory factor (MIF) is a proinflammatory mediator that is known to be up-regulated in patients undergoing cardiac operations. Here we analyzed genotype distribution and allele frequency of the MIF-173*G/C single nucleotide polymorphism (SNP) and MIF plasma levels in patients undergoing surgical revascularization with (on-pump, n=45) and without (off-pump, n=34) cardiopulmonary bypass (CPB). Genotyping was performed using a real-time PCR-based system with a hybridization probe system specific for the MIF-173*G/C SNP. In on-pump patients, blood samples were drawn before start of CPB, after termination of CPB and 12h postoperatively. In off-pump patients, blood samples were collected before stabilizer placement, after removal of the stabilizer and 12h postoperatively. MIF levels were measured using ELISA technique. Genotype distribution and allele frequencies were comparable between on-pump and off-pump patients. When comparing patients according to MIF genotype, a significant increase of MIF plasma levels after completed coronary bypass grafting using CPB was found in patients heterozygous for the MIF-173*G/C SNP (p<0.05). Moreover, on-pump patients showed significantly decreased MIF plasma levels after 12h postoperatively (p<0.05). In off-pump patients, MIF plasma levels were not significantly different over the time-course and were independent of the genotype.\n\nQuestion:\nIs a single nucleotide polymorphism of macrophage migration inhibitory factor related to inflammatory response in coronary bypass surgery using cardiopulmonary bypass?", "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:\nProgranulin (PGRN) was recently introduced as a novel marker of chronic inflammatory response in obesity and type 2 diabetes capable of directly affecting the insulin signaling pathway. This study aimed to investigate the correlation between PGRN and type 2 diabetics with microvascular complications. PGRN serum levels and glucose metabolism related substance were measured in 84 type 2 diabetic patients with or without microangiopathies and 12 health persons. Further analyses of serum PGRN in different stages of diabetic microangiopathies were conducted. Serum levels of PGRN were markedly higher in type 2 diabetic patients with microangiopathies. PGRN serum levels increased with the progress of diabetic microangiopathies with significantly highest values detectable in clinical diabetic nephropathy (CDN) and proliferative diabetic retinopathy (PDR) groups. Serum PGRN concentrations in all individuals positively and markedly correlated with systolic blood pressure (SBP), diastolic blood pressure (DBP), body mass index (BMI), triglyceride (TG), urinary albumin excretion rate (UAER), blood urea nitrogen (BUN), creatinine (CRE), white blood cell (WBC), disease duration, IL-6, and TNF-α, while correlating negatively and significantly with eGFR. Multiple linear regression analysis showed that only UAER and CRE were independently associated with serum PGRN.\n\nQuestion:\nDo serum Levels of Progranulin Are Closely Associated with Microvascular Complication in 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:\nProgranulin (PGRN) was recently introduced as a novel marker of chronic inflammatory response in obesity and type 2 diabetes capable of directly affecting the insulin signaling pathway. This study aimed to investigate the correlation between PGRN and type 2 diabetics with microvascular complications. PGRN serum levels and glucose metabolism related substance were measured in 84 type 2 diabetic patients with or without microangiopathies and 12 health persons. Further analyses of serum PGRN in different stages of diabetic microangiopathies were conducted. Serum levels of PGRN were markedly higher in type 2 diabetic patients with microangiopathies. PGRN serum levels increased with the progress of diabetic microangiopathies with significantly highest values detectable in clinical diabetic nephropathy (CDN) and proliferative diabetic retinopathy (PDR) groups. Serum PGRN concentrations in all individuals positively and markedly correlated with systolic blood pressure (SBP), diastolic blood pressure (DBP), body mass index (BMI), triglyceride (TG), urinary albumin excretion rate (UAER), blood urea nitrogen (BUN), creatinine (CRE), white blood cell (WBC), disease duration, IL-6, and TNF-α, while correlating negatively and significantly with eGFR. Multiple linear regression analysis showed that only UAER and CRE were independently associated with serum PGRN.\n\nQuestion:\nDo serum Levels of Progranulin Are Closely Associated with Microvascular Complication in 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:\nProgranulin (PGRN) was recently introduced as a novel marker of chronic inflammatory response in obesity and type 2 diabetes capable of directly affecting the insulin signaling pathway. This study aimed to investigate the correlation between PGRN and type 2 diabetics with microvascular complications. PGRN serum levels and glucose metabolism related substance were measured in 84 type 2 diabetic patients with or without microangiopathies and 12 health persons. Further analyses of serum PGRN in different stages of diabetic microangiopathies were conducted. Serum levels of PGRN were markedly higher in type 2 diabetic patients with microangiopathies. PGRN serum levels increased with the progress of diabetic microangiopathies with significantly highest values detectable in clinical diabetic nephropathy (CDN) and proliferative diabetic retinopathy (PDR) groups. Serum PGRN concentrations in all individuals positively and markedly correlated with systolic blood pressure (SBP), diastolic blood pressure (DBP), body mass index (BMI), triglyceride (TG), urinary albumin excretion rate (UAER), blood urea nitrogen (BUN), creatinine (CRE), white blood cell (WBC), disease duration, IL-6, and TNF-α, while correlating negatively and significantly with eGFR. Multiple linear regression analysis showed that only UAER and CRE were independently associated with serum PGRN.\n\nQuestion:\nDo serum Levels of Progranulin Are Closely Associated with Microvascular Complication in 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:\nRacemic albuterol is a 50:50 mixture of the R-isomer, levalbuterol, and the S-isomer, S-albuterol. S-Albuterol increases airway hyperresponsiveness to spasmogens, exacerbates asthmatic conditions and stimulates cell growth, whereas levalbuterol attenuates cell growth in culture. The mechanisms of S-albuterol-induced cell proliferation are not well understood. We studied the role of albuterol isomers and intracellular cell cycle regulators on proliferation of human bronchial smooth muscle cells. Serum-starved cells (72 h) were fed test agents for 24 h and cell proliferation was measured. The expression of nuclear factor-kappaB inhibitory protein IkappaBalpha, nuclear factor-kappaB, cyclin-dependent kinases 2 and 4, interleukin (IL)-6, and retinoblastoma and platelet-activating factor (PAF) receptor protein were measured by Western blotting. S-Albuterol, PAF and platelet-derived growth factor stimulated cell proliferation, but levalbuterol and the racemic mixture inhibited cell proliferation compared with the effect of 5% fetal bovine serum alone. The proliferative effect of platelet-derived growth factor on S-albuterol was not additive, suggesting that the 2 mediators act by different mechanisms. S-Albuterol induced greater expression of all the measured proteins than either levalbuterol, the racemic mixture or 5% fetal bovine serum. S-Albuterol stimulated IL-6 secretion and abolished the ability of levalbuterol to inhibit IL-6 secretion.\n\nQuestion:\nDoes mechanisms by which S-albuterol induce human bronchial smooth muscle cell proliferation?", "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:\nRacemic albuterol is a 50:50 mixture of the R-isomer, levalbuterol, and the S-isomer, S-albuterol. S-Albuterol increases airway hyperresponsiveness to spasmogens, exacerbates asthmatic conditions and stimulates cell growth, whereas levalbuterol attenuates cell growth in culture. The mechanisms of S-albuterol-induced cell proliferation are not well understood. We studied the role of albuterol isomers and intracellular cell cycle regulators on proliferation of human bronchial smooth muscle cells. Serum-starved cells (72 h) were fed test agents for 24 h and cell proliferation was measured. The expression of nuclear factor-kappaB inhibitory protein IkappaBalpha, nuclear factor-kappaB, cyclin-dependent kinases 2 and 4, interleukin (IL)-6, and retinoblastoma and platelet-activating factor (PAF) receptor protein were measured by Western blotting. S-Albuterol, PAF and platelet-derived growth factor stimulated cell proliferation, but levalbuterol and the racemic mixture inhibited cell proliferation compared with the effect of 5% fetal bovine serum alone. The proliferative effect of platelet-derived growth factor on S-albuterol was not additive, suggesting that the 2 mediators act by different mechanisms. S-Albuterol induced greater expression of all the measured proteins than either levalbuterol, the racemic mixture or 5% fetal bovine serum. S-Albuterol stimulated IL-6 secretion and abolished the ability of levalbuterol to inhibit IL-6 secretion.\n\nQuestion:\nDoes mechanisms by which S-albuterol induce human bronchial smooth muscle cell proliferation?", "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:\nRacemic albuterol is a 50:50 mixture of the R-isomer, levalbuterol, and the S-isomer, S-albuterol. S-Albuterol increases airway hyperresponsiveness to spasmogens, exacerbates asthmatic conditions and stimulates cell growth, whereas levalbuterol attenuates cell growth in culture. The mechanisms of S-albuterol-induced cell proliferation are not well understood. We studied the role of albuterol isomers and intracellular cell cycle regulators on proliferation of human bronchial smooth muscle cells. Serum-starved cells (72 h) were fed test agents for 24 h and cell proliferation was measured. The expression of nuclear factor-kappaB inhibitory protein IkappaBalpha, nuclear factor-kappaB, cyclin-dependent kinases 2 and 4, interleukin (IL)-6, and retinoblastoma and platelet-activating factor (PAF) receptor protein were measured by Western blotting. S-Albuterol, PAF and platelet-derived growth factor stimulated cell proliferation, but levalbuterol and the racemic mixture inhibited cell proliferation compared with the effect of 5% fetal bovine serum alone. The proliferative effect of platelet-derived growth factor on S-albuterol was not additive, suggesting that the 2 mediators act by different mechanisms. S-Albuterol induced greater expression of all the measured proteins than either levalbuterol, the racemic mixture or 5% fetal bovine serum. S-Albuterol stimulated IL-6 secretion and abolished the ability of levalbuterol to inhibit IL-6 secretion.\n\nQuestion:\nDoes mechanisms by which S-albuterol induce human bronchial smooth muscle cell proliferation?", "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:\nHsp90-β and annexin A1 have been demonstrated to be associated with tumorigenesis. However, the effect of Hsp90-β and annexin A1 in lung cancer remains poorly understood. In this research, the correlation of Hsp90-β and annexin A1 in lung cancer patients were analyzed. The expression levels of Hsp90-β and annexin A1 were examined by immunohistochemistry and ELISA. Lung cancer tissues and serum exhibited higher co-expression of Hsp90-β and annexin A1 than control groups (p < 0.05). Hsp90-β and annexin A1 could discriminate lung cancer from the control groups (sensitivity of Hsp90-β was 80.2% in tissues and 96% in serum; specificity of Hsp90-β was 80% in tissues and 83.33% in serum; sensitivity of annexin A1 was 68.76% in tissues and 95.23% in serum; specificity of annexin A1 was 75% in tissues and 85.7% in serum) and multi-index combined detection had a better diagnostic value.\n\nQuestion:\nDoes co-overexpression of Hsp90-β and annexin A1 with a significantly positive correlation contribute to the diagnosis of lung 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:\nHsp90-β and annexin A1 have been demonstrated to be associated with tumorigenesis. However, the effect of Hsp90-β and annexin A1 in lung cancer remains poorly understood. In this research, the correlation of Hsp90-β and annexin A1 in lung cancer patients were analyzed. The expression levels of Hsp90-β and annexin A1 were examined by immunohistochemistry and ELISA. Lung cancer tissues and serum exhibited higher co-expression of Hsp90-β and annexin A1 than control groups (p < 0.05). Hsp90-β and annexin A1 could discriminate lung cancer from the control groups (sensitivity of Hsp90-β was 80.2% in tissues and 96% in serum; specificity of Hsp90-β was 80% in tissues and 83.33% in serum; sensitivity of annexin A1 was 68.76% in tissues and 95.23% in serum; specificity of annexin A1 was 75% in tissues and 85.7% in serum) and multi-index combined detection had a better diagnostic value.\n\nQuestion:\nDoes co-overexpression of Hsp90-β and annexin A1 with a significantly positive correlation contribute to the diagnosis of lung 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:\nHsp90-β and annexin A1 have been demonstrated to be associated with tumorigenesis. However, the effect of Hsp90-β and annexin A1 in lung cancer remains poorly understood. In this research, the correlation of Hsp90-β and annexin A1 in lung cancer patients were analyzed. The expression levels of Hsp90-β and annexin A1 were examined by immunohistochemistry and ELISA. Lung cancer tissues and serum exhibited higher co-expression of Hsp90-β and annexin A1 than control groups (p < 0.05). Hsp90-β and annexin A1 could discriminate lung cancer from the control groups (sensitivity of Hsp90-β was 80.2% in tissues and 96% in serum; specificity of Hsp90-β was 80% in tissues and 83.33% in serum; sensitivity of annexin A1 was 68.76% in tissues and 95.23% in serum; specificity of annexin A1 was 75% in tissues and 85.7% in serum) and multi-index combined detection had a better diagnostic value.\n\nQuestion:\nDoes co-overexpression of Hsp90-β and annexin A1 with a significantly positive correlation contribute to the diagnosis of lung 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:\nThe tetraspanin CD81 is one of the main receptors involved in hepatitis C virus entry. Herein, we aimed to explore the role of microRNAs in regulating CD81 receptor expression and function. Bioinformatics analysis was carried out to select potential mircroRNAs that binds CD81 3'untranslated region. Liver biopsies taken from 28 HCV genotype- 4 patients and 10 healthy donors were screened. Naïve, JFH1 and ED43/JFH1- infected- Huh7 cells were transfected with mimics and inhibitors followed by analyzing CD81 protein and mRNA expression. This was done using flow cytometry and Q-RT PCR, respectively. HCV entry into Huh7 cells was investigated post-transfection. Binding confirmation was done using luciferase reporter vector harboring wild/mutant target sites of microRNA. The impact of Epigallocatechin-gallate on modulating microRNA/CD81 expression was assessed. Bioinformatics revealed that CD81 is a potential down-stream target for miR-194. A significant inverse correlation was found between miR-194 and CD81 expression in liver biopsies of HCV patients. Forcing the expression of miR-194 showed a down-regulation of CD81 protein, mRNA expression and significantly abrogated the HCV infectivity of Huh7 cells. Stimulation with EGCG enhanced mir-194 expression and down-regulated CD81 expression.\n\nQuestion:\nIs mir-194 a hepatocyte gate keeper hindering HCV entry through targeting CD81 receptor?", "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 tetraspanin CD81 is one of the main receptors involved in hepatitis C virus entry. Herein, we aimed to explore the role of microRNAs in regulating CD81 receptor expression and function. Bioinformatics analysis was carried out to select potential mircroRNAs that binds CD81 3'untranslated region. Liver biopsies taken from 28 HCV genotype- 4 patients and 10 healthy donors were screened. Naïve, JFH1 and ED43/JFH1- infected- Huh7 cells were transfected with mimics and inhibitors followed by analyzing CD81 protein and mRNA expression. This was done using flow cytometry and Q-RT PCR, respectively. HCV entry into Huh7 cells was investigated post-transfection. Binding confirmation was done using luciferase reporter vector harboring wild/mutant target sites of microRNA. The impact of Epigallocatechin-gallate on modulating microRNA/CD81 expression was assessed. Bioinformatics revealed that CD81 is a potential down-stream target for miR-194. A significant inverse correlation was found between miR-194 and CD81 expression in liver biopsies of HCV patients. Forcing the expression of miR-194 showed a down-regulation of CD81 protein, mRNA expression and significantly abrogated the HCV infectivity of Huh7 cells. Stimulation with EGCG enhanced mir-194 expression and down-regulated CD81 expression.\n\nQuestion:\nIs mir-194 a hepatocyte gate keeper hindering HCV entry through targeting CD81 receptor?", "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 tetraspanin CD81 is one of the main receptors involved in hepatitis C virus entry. Herein, we aimed to explore the role of microRNAs in regulating CD81 receptor expression and function. Bioinformatics analysis was carried out to select potential mircroRNAs that binds CD81 3'untranslated region. Liver biopsies taken from 28 HCV genotype- 4 patients and 10 healthy donors were screened. Naïve, JFH1 and ED43/JFH1- infected- Huh7 cells were transfected with mimics and inhibitors followed by analyzing CD81 protein and mRNA expression. This was done using flow cytometry and Q-RT PCR, respectively. HCV entry into Huh7 cells was investigated post-transfection. Binding confirmation was done using luciferase reporter vector harboring wild/mutant target sites of microRNA. The impact of Epigallocatechin-gallate on modulating microRNA/CD81 expression was assessed. Bioinformatics revealed that CD81 is a potential down-stream target for miR-194. A significant inverse correlation was found between miR-194 and CD81 expression in liver biopsies of HCV patients. Forcing the expression of miR-194 showed a down-regulation of CD81 protein, mRNA expression and significantly abrogated the HCV infectivity of Huh7 cells. Stimulation with EGCG enhanced mir-194 expression and down-regulated CD81 expression.\n\nQuestion:\nIs mir-194 a hepatocyte gate keeper hindering HCV entry through targeting CD81 receptor?", "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 molecular basis of autosomal recessive non-syndromic mental retardation (NSMR) is poorly understood, mostly owing to heterogeneity and absence of clinical criteria for grouping families for linkage analysis. Only two autosomal genes, the PRSS12 gene on chromosome 4q26 and the CRBN on chromosome 3p26, have been shown to cause autosomal recessive NSMR, each gene in only one family. To identify the gene causing autosomal recessive NSMR on chromosome 19p13.12. The candidate region established by homozygosity mapping was narrowed down from 2.4 Mb to 0.9 Mb on chromosome 19p13.12. A protein truncating mutation was identified in the gene CC2D1A in nine consanguineous families with severe autosomal recessive NSMR. The absence of the wild type protein in the lymphoblastoid cells of the patients was confirmed. CC2D1A is a member of a previously uncharacterised gene family that carries two conserved motifs, a C2 domain and a DM14 domain. The C2 domain is found in proteins which function in calcium dependent phospholipid binding; the DM14 domain is unique to the CC2D1A protein family and its role is unknown. CC2D1A is a putative signal transducer participating in positive regulation of I-kappaB kinase/NFkappaB cascade. Expression of CC2D1A mRNA was shown in the embryonic ventricular zone and developing cortical plate in staged mouse embryos, persisting into adulthood, with highest expression in the cerebral cortex and hippocampus.\n\nQuestion:\nIs the CC2D1A , a member of a new gene family with C2 domains , involved in autosomal recessive non-syndromic mental retardation?", "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 molecular basis of autosomal recessive non-syndromic mental retardation (NSMR) is poorly understood, mostly owing to heterogeneity and absence of clinical criteria for grouping families for linkage analysis. Only two autosomal genes, the PRSS12 gene on chromosome 4q26 and the CRBN on chromosome 3p26, have been shown to cause autosomal recessive NSMR, each gene in only one family. To identify the gene causing autosomal recessive NSMR on chromosome 19p13.12. The candidate region established by homozygosity mapping was narrowed down from 2.4 Mb to 0.9 Mb on chromosome 19p13.12. A protein truncating mutation was identified in the gene CC2D1A in nine consanguineous families with severe autosomal recessive NSMR. The absence of the wild type protein in the lymphoblastoid cells of the patients was confirmed. CC2D1A is a member of a previously uncharacterised gene family that carries two conserved motifs, a C2 domain and a DM14 domain. The C2 domain is found in proteins which function in calcium dependent phospholipid binding; the DM14 domain is unique to the CC2D1A protein family and its role is unknown. CC2D1A is a putative signal transducer participating in positive regulation of I-kappaB kinase/NFkappaB cascade. Expression of CC2D1A mRNA was shown in the embryonic ventricular zone and developing cortical plate in staged mouse embryos, persisting into adulthood, with highest expression in the cerebral cortex and hippocampus.\n\nQuestion:\nIs the CC2D1A , a member of a new gene family with C2 domains , involved in autosomal recessive non-syndromic mental retardation?", "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 molecular basis of autosomal recessive non-syndromic mental retardation (NSMR) is poorly understood, mostly owing to heterogeneity and absence of clinical criteria for grouping families for linkage analysis. Only two autosomal genes, the PRSS12 gene on chromosome 4q26 and the CRBN on chromosome 3p26, have been shown to cause autosomal recessive NSMR, each gene in only one family. To identify the gene causing autosomal recessive NSMR on chromosome 19p13.12. The candidate region established by homozygosity mapping was narrowed down from 2.4 Mb to 0.9 Mb on chromosome 19p13.12. A protein truncating mutation was identified in the gene CC2D1A in nine consanguineous families with severe autosomal recessive NSMR. The absence of the wild type protein in the lymphoblastoid cells of the patients was confirmed. CC2D1A is a member of a previously uncharacterised gene family that carries two conserved motifs, a C2 domain and a DM14 domain. The C2 domain is found in proteins which function in calcium dependent phospholipid binding; the DM14 domain is unique to the CC2D1A protein family and its role is unknown. CC2D1A is a putative signal transducer participating in positive regulation of I-kappaB kinase/NFkappaB cascade. Expression of CC2D1A mRNA was shown in the embryonic ventricular zone and developing cortical plate in staged mouse embryos, persisting into adulthood, with highest expression in the cerebral cortex and hippocampus.\n\nQuestion:\nIs the CC2D1A , a member of a new gene family with C2 domains , involved in autosomal recessive non-syndromic mental retardation?", "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:\nHyperkinetic pulmonary arterial hypertension (PAH) is a common complication in congenital heart disease, and affects operations, indications, and prognoses for patients. Gene-based stem cell transplantation is an alternative treatment that can attenuate PAH. Hyperkinetic PAH rabbit models were successfully established, using common carotid artery and jugular vein anastomosis. Endothelial progenitor cells (EPCs) were isolated from the bone marrow, cultured, and transfected with human hypoxia inducible factor-1 alpha (hHIF-1α), using lentiviruses. Two weeks after the transfected EPCs were transplanted into the rabbits, catheterization was applied to collect hemodynamic data. The hypertrophy of the right ventricle and pulmonary vascular remodeling were evaluated by measuring the right ventricle hypertrophy index, the medial wall thickness, and the medial wall area. Western blot and immunohistochemistry analyses were used to detect the expression of hHIF-1α in the pulmonary small arteries. Two weeks after transplantation, systolic pulmonary arterial pressure and mean pulmonary arterial pressure were both attenuated. The hypertrophy of the right ventricle, and pulmonary vascular remodeling were reversed. Expression of hHIF-1α in the hHIF-1α-transfected EPCs that had been transplanted was high, and the number of pulmonary small arteries had increased. In addition, combined HIF-1α and homogeneous EPC therapy was more effective at attenuating PAH and increasing the density of pulmonary small arteries, compared with EPC transplantation alone.\n\nQuestion:\nDoes combined hypoxia inducible factor-1α and homogeneous endothelial progenitor cell therapy attenuate shunt flow-induced pulmonary arterial hypertension in 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:\nHyperkinetic pulmonary arterial hypertension (PAH) is a common complication in congenital heart disease, and affects operations, indications, and prognoses for patients. Gene-based stem cell transplantation is an alternative treatment that can attenuate PAH. Hyperkinetic PAH rabbit models were successfully established, using common carotid artery and jugular vein anastomosis. Endothelial progenitor cells (EPCs) were isolated from the bone marrow, cultured, and transfected with human hypoxia inducible factor-1 alpha (hHIF-1α), using lentiviruses. Two weeks after the transfected EPCs were transplanted into the rabbits, catheterization was applied to collect hemodynamic data. The hypertrophy of the right ventricle and pulmonary vascular remodeling were evaluated by measuring the right ventricle hypertrophy index, the medial wall thickness, and the medial wall area. Western blot and immunohistochemistry analyses were used to detect the expression of hHIF-1α in the pulmonary small arteries. Two weeks after transplantation, systolic pulmonary arterial pressure and mean pulmonary arterial pressure were both attenuated. The hypertrophy of the right ventricle, and pulmonary vascular remodeling were reversed. Expression of hHIF-1α in the hHIF-1α-transfected EPCs that had been transplanted was high, and the number of pulmonary small arteries had increased. In addition, combined HIF-1α and homogeneous EPC therapy was more effective at attenuating PAH and increasing the density of pulmonary small arteries, compared with EPC transplantation alone.\n\nQuestion:\nDoes combined hypoxia inducible factor-1α and homogeneous endothelial progenitor cell therapy attenuate shunt flow-induced pulmonary arterial hypertension in 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:\nHyperkinetic pulmonary arterial hypertension (PAH) is a common complication in congenital heart disease, and affects operations, indications, and prognoses for patients. Gene-based stem cell transplantation is an alternative treatment that can attenuate PAH. Hyperkinetic PAH rabbit models were successfully established, using common carotid artery and jugular vein anastomosis. Endothelial progenitor cells (EPCs) were isolated from the bone marrow, cultured, and transfected with human hypoxia inducible factor-1 alpha (hHIF-1α), using lentiviruses. Two weeks after the transfected EPCs were transplanted into the rabbits, catheterization was applied to collect hemodynamic data. The hypertrophy of the right ventricle and pulmonary vascular remodeling were evaluated by measuring the right ventricle hypertrophy index, the medial wall thickness, and the medial wall area. Western blot and immunohistochemistry analyses were used to detect the expression of hHIF-1α in the pulmonary small arteries. Two weeks after transplantation, systolic pulmonary arterial pressure and mean pulmonary arterial pressure were both attenuated. The hypertrophy of the right ventricle, and pulmonary vascular remodeling were reversed. Expression of hHIF-1α in the hHIF-1α-transfected EPCs that had been transplanted was high, and the number of pulmonary small arteries had increased. In addition, combined HIF-1α and homogeneous EPC therapy was more effective at attenuating PAH and increasing the density of pulmonary small arteries, compared with EPC transplantation alone.\n\nQuestion:\nDoes combined hypoxia inducible factor-1α and homogeneous endothelial progenitor cell therapy attenuate shunt flow-induced pulmonary arterial hypertension in 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:\nFractional tissue oxygen extraction (FTOE) is a measure derived from cerebral near-infrared spectroscopy (NIRS) and simultaneous pulse oximetry (SpO Infants born before <30 weeks and weighing <1500 g underwent synchronized SpO A total of 63 infants were included with a mean±s.d. gestational age of 25.8±1.5 weeks and birth weight of 898.5±206.9 g; 13/63 (20%) had severe ROP. SpO\n\nQuestion:\nIs early hyperoxia burden detected by cerebral near-infrared spectroscopy superior to pulse oximetry for prediction of severe retinopathy of prematurity?", "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:\nFractional tissue oxygen extraction (FTOE) is a measure derived from cerebral near-infrared spectroscopy (NIRS) and simultaneous pulse oximetry (SpO Infants born before <30 weeks and weighing <1500 g underwent synchronized SpO A total of 63 infants were included with a mean±s.d. gestational age of 25.8±1.5 weeks and birth weight of 898.5±206.9 g; 13/63 (20%) had severe ROP. SpO\n\nQuestion:\nIs early hyperoxia burden detected by cerebral near-infrared spectroscopy superior to pulse oximetry for prediction of severe retinopathy of prematurity?", "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:\nFractional tissue oxygen extraction (FTOE) is a measure derived from cerebral near-infrared spectroscopy (NIRS) and simultaneous pulse oximetry (SpO Infants born before <30 weeks and weighing <1500 g underwent synchronized SpO A total of 63 infants were included with a mean±s.d. gestational age of 25.8±1.5 weeks and birth weight of 898.5±206.9 g; 13/63 (20%) had severe ROP. SpO\n\nQuestion:\nIs early hyperoxia burden detected by cerebral near-infrared spectroscopy superior to pulse oximetry for prediction of severe retinopathy of prematurity?", "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 see if humorally mediated negative inotropism contributes to the cardiac output (CO) depression seen during positive end-expiratory pressure (PEEP) ventilation. 8 pairs of piglets were used and a combined blood circulation was established between the two animals in each pair. One animal was ventilated with a PEEP of 15 cmH20 (donor) and the other was ventilated without PEEP (recipient). CO and stroke volume deteriorated in the donors by 32% and 44%, respectively, while no change was seen in the recipients.\n\nQuestion:\nDoes pEEP ventilation cause humorally mediated cardiac output depression in pigs?", "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 see if humorally mediated negative inotropism contributes to the cardiac output (CO) depression seen during positive end-expiratory pressure (PEEP) ventilation. 8 pairs of piglets were used and a combined blood circulation was established between the two animals in each pair. One animal was ventilated with a PEEP of 15 cmH20 (donor) and the other was ventilated without PEEP (recipient). CO and stroke volume deteriorated in the donors by 32% and 44%, respectively, while no change was seen in the recipients.\n\nQuestion:\nDoes pEEP ventilation cause humorally mediated cardiac output depression in pigs?", "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 see if humorally mediated negative inotropism contributes to the cardiac output (CO) depression seen during positive end-expiratory pressure (PEEP) ventilation. 8 pairs of piglets were used and a combined blood circulation was established between the two animals in each pair. One animal was ventilated with a PEEP of 15 cmH20 (donor) and the other was ventilated without PEEP (recipient). CO and stroke volume deteriorated in the donors by 32% and 44%, respectively, while no change was seen in the recipients.\n\nQuestion:\nDoes pEEP ventilation cause humorally mediated cardiac output depression in pigs?", "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 establish the cytochrome P450 (CYP) isozymes involved in the metabolism of the alkylating agent, thiotepa, to the pharmacologically active metabolite, TEPA. In vitro chemical inhibition studies were conducted by incubating thiotepa and pooled human hepatic microsomes in the presence of known inhibitors to CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4. Studies were also performed with cloned, expressed CYP3A4, CYP2A6, CYP2E1 and CYP2B6 microsomes, and anti-CYP2B6 monoclonal antibody. Known CYP3A4 inhibitors reduced TEPA production. Inhibition with CYP2E1 inhibitors was inconsistent. All other inhibitors produced little or no change in TEPA formation. Cloned, expressed CYP2B6 and CYP3A4 microsomes catalyzed TEPA formation, whereas CYP2A6 and CYP2E1 did not. Incubation of thiotepa with anti-CYP2B6 antibody and cloned, expressed CYP2B6 microsomes resulted in reductions in the formation of TEPA, but no change in TEPA formation occurred in human liver microsomes.\n\nQuestion:\nAre cytochrome P450 isozymes 3A4 and 2B6 involved in the in vitro human metabolism of thiotepa to TEPA?", "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 establish the cytochrome P450 (CYP) isozymes involved in the metabolism of the alkylating agent, thiotepa, to the pharmacologically active metabolite, TEPA. In vitro chemical inhibition studies were conducted by incubating thiotepa and pooled human hepatic microsomes in the presence of known inhibitors to CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4. Studies were also performed with cloned, expressed CYP3A4, CYP2A6, CYP2E1 and CYP2B6 microsomes, and anti-CYP2B6 monoclonal antibody. Known CYP3A4 inhibitors reduced TEPA production. Inhibition with CYP2E1 inhibitors was inconsistent. All other inhibitors produced little or no change in TEPA formation. Cloned, expressed CYP2B6 and CYP3A4 microsomes catalyzed TEPA formation, whereas CYP2A6 and CYP2E1 did not. Incubation of thiotepa with anti-CYP2B6 antibody and cloned, expressed CYP2B6 microsomes resulted in reductions in the formation of TEPA, but no change in TEPA formation occurred in human liver microsomes.\n\nQuestion:\nAre cytochrome P450 isozymes 3A4 and 2B6 involved in the in vitro human metabolism of thiotepa to TEPA?", "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 establish the cytochrome P450 (CYP) isozymes involved in the metabolism of the alkylating agent, thiotepa, to the pharmacologically active metabolite, TEPA. In vitro chemical inhibition studies were conducted by incubating thiotepa and pooled human hepatic microsomes in the presence of known inhibitors to CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4. Studies were also performed with cloned, expressed CYP3A4, CYP2A6, CYP2E1 and CYP2B6 microsomes, and anti-CYP2B6 monoclonal antibody. Known CYP3A4 inhibitors reduced TEPA production. Inhibition with CYP2E1 inhibitors was inconsistent. All other inhibitors produced little or no change in TEPA formation. Cloned, expressed CYP2B6 and CYP3A4 microsomes catalyzed TEPA formation, whereas CYP2A6 and CYP2E1 did not. Incubation of thiotepa with anti-CYP2B6 antibody and cloned, expressed CYP2B6 microsomes resulted in reductions in the formation of TEPA, but no change in TEPA formation occurred in human liver microsomes.\n\nQuestion:\nAre cytochrome P450 isozymes 3A4 and 2B6 involved in the in vitro human metabolism of thiotepa to TEPA?", "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:\nRickettsioses are endemic in sub-Sahara Africa. Burden of disease, risk factors and transmission are hitherto sparsely described. From the EMINI (Evaluating and Monitoring the Impact of New Interventions) population cohort, we randomly selected 1,228 persons above the age of 5 years from the nine participating communities in Mbeya region, Southwestern Tanzania, stratified by age, altitude of residence and ownership of domestic mammals, to conduct a cross-sectional seroprevalence study in. The aim was to estimate the seroprevalence of IgG antibodies against Spotted Fever Group (SFG) rickettsiae and to assess socioeconomic and environmental risk factors. Serology (indirect immunofluorescence) was performed at a dilution of 1:64. SFG-seropositivity in the cohort was found to be 67.9% (range among nine sites: 42.8-91.4%). Multivariable analysis revealed an association with age (prevalence ratio, PR per 10 years: 1.08; 95% CI 1.06-1.10), warmer temperatures (PR per °C: 1.38; 1.11-1.71), male gender (PR 1.08; 1.00-1.16), and low population density (PR per 1.000 persons/km²increase 0.96; 0.94-0.99). At higher elevations, higher cattle density was associated with higher seroprevalence.\n\nQuestion:\nIs high seroprevalence for spotted fever group rickettsiae , associated with higher temperatures and rural environment in Mbeya region , Southwestern Tanzania?", "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:\nRickettsioses are endemic in sub-Sahara Africa. Burden of disease, risk factors and transmission are hitherto sparsely described. From the EMINI (Evaluating and Monitoring the Impact of New Interventions) population cohort, we randomly selected 1,228 persons above the age of 5 years from the nine participating communities in Mbeya region, Southwestern Tanzania, stratified by age, altitude of residence and ownership of domestic mammals, to conduct a cross-sectional seroprevalence study in. The aim was to estimate the seroprevalence of IgG antibodies against Spotted Fever Group (SFG) rickettsiae and to assess socioeconomic and environmental risk factors. Serology (indirect immunofluorescence) was performed at a dilution of 1:64. SFG-seropositivity in the cohort was found to be 67.9% (range among nine sites: 42.8-91.4%). Multivariable analysis revealed an association with age (prevalence ratio, PR per 10 years: 1.08; 95% CI 1.06-1.10), warmer temperatures (PR per °C: 1.38; 1.11-1.71), male gender (PR 1.08; 1.00-1.16), and low population density (PR per 1.000 persons/km²increase 0.96; 0.94-0.99). At higher elevations, higher cattle density was associated with higher seroprevalence.\n\nQuestion:\nIs high seroprevalence for spotted fever group rickettsiae , associated with higher temperatures and rural environment in Mbeya region , Southwestern Tanzania?", "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:\nRickettsioses are endemic in sub-Sahara Africa. Burden of disease, risk factors and transmission are hitherto sparsely described. From the EMINI (Evaluating and Monitoring the Impact of New Interventions) population cohort, we randomly selected 1,228 persons above the age of 5 years from the nine participating communities in Mbeya region, Southwestern Tanzania, stratified by age, altitude of residence and ownership of domestic mammals, to conduct a cross-sectional seroprevalence study in. The aim was to estimate the seroprevalence of IgG antibodies against Spotted Fever Group (SFG) rickettsiae and to assess socioeconomic and environmental risk factors. Serology (indirect immunofluorescence) was performed at a dilution of 1:64. SFG-seropositivity in the cohort was found to be 67.9% (range among nine sites: 42.8-91.4%). Multivariable analysis revealed an association with age (prevalence ratio, PR per 10 years: 1.08; 95% CI 1.06-1.10), warmer temperatures (PR per °C: 1.38; 1.11-1.71), male gender (PR 1.08; 1.00-1.16), and low population density (PR per 1.000 persons/km²increase 0.96; 0.94-0.99). At higher elevations, higher cattle density was associated with higher seroprevalence.\n\nQuestion:\nIs high seroprevalence for spotted fever group rickettsiae , associated with higher temperatures and rural environment in Mbeya region , Southwestern Tanzania?", "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:\nMultiple myeloma is an incurable malignancy of bone marrow plasma cells. Progression of multiple myeloma is accompanied by an increase in bone marrow angiogenesis. Studies from our laboratory suggest a role for the CXCL12 chemokine in this process, with circulating levels of CXCL12 correlating with bone marrow angiogenesis in patients with multiple myeloma. While the mechanisms responsible for aberrant plasma cell expression of CXCL12 remain to be determined, studies in other systems suggest a role for hypoxia and hypoxia-inducible transcription factors. The expression of hypoxia-inducible factor protein was examined in patients' bone marrow biopsy specimens using immunohistochemistry. The hypoxic regulation of CXCL12 was examined in multiple myeloma plasma cell lines using polymerase chain reaction and western blotting. The role of hypoxia-inducible factors-1 and -2 in the regulation of CXCL12 expression was examined using over-expression and short hairpin RNA knockdown constructs, electrophoretic mobility shift assays and chromatin immunoprecipitation. The contribution of CXCL12 to hypoxia-induced angiogenesis was examined in vivo using a subcutaneous murine model of neovascularization. Strong hypoxia-inducible factor-2 protein expression was detected in CD138(+) multiple myeloma plasma cells in patients' biopsy specimens. Prolonged exposure to hypoxia strongly up-regulated CXCL12 expression in multiple myeloma plasma cells and hypoxia-inducible factor-2 was found to play a key role in this response. Promoter analyses revealed increased hypoxia-inducible factor-2 binding to the CXCL12 promoter under hypoxic conditions. Over-expression of hypoxia-inducible factor in multiple myeloma plasma cells strongly induced in vivo angiogenesis, and administration of a CXCL12 antagonist decreased hypoxia-inducible factor-induced angiogenesis.\n\nQuestion:\nIs hypoxia-inducible factor-2 a novel regulator of aberrant CXCL12 expression in multiple myeloma plasma 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:\nMultiple myeloma is an incurable malignancy of bone marrow plasma cells. Progression of multiple myeloma is accompanied by an increase in bone marrow angiogenesis. Studies from our laboratory suggest a role for the CXCL12 chemokine in this process, with circulating levels of CXCL12 correlating with bone marrow angiogenesis in patients with multiple myeloma. While the mechanisms responsible for aberrant plasma cell expression of CXCL12 remain to be determined, studies in other systems suggest a role for hypoxia and hypoxia-inducible transcription factors. The expression of hypoxia-inducible factor protein was examined in patients' bone marrow biopsy specimens using immunohistochemistry. The hypoxic regulation of CXCL12 was examined in multiple myeloma plasma cell lines using polymerase chain reaction and western blotting. The role of hypoxia-inducible factors-1 and -2 in the regulation of CXCL12 expression was examined using over-expression and short hairpin RNA knockdown constructs, electrophoretic mobility shift assays and chromatin immunoprecipitation. The contribution of CXCL12 to hypoxia-induced angiogenesis was examined in vivo using a subcutaneous murine model of neovascularization. Strong hypoxia-inducible factor-2 protein expression was detected in CD138(+) multiple myeloma plasma cells in patients' biopsy specimens. Prolonged exposure to hypoxia strongly up-regulated CXCL12 expression in multiple myeloma plasma cells and hypoxia-inducible factor-2 was found to play a key role in this response. Promoter analyses revealed increased hypoxia-inducible factor-2 binding to the CXCL12 promoter under hypoxic conditions. Over-expression of hypoxia-inducible factor in multiple myeloma plasma cells strongly induced in vivo angiogenesis, and administration of a CXCL12 antagonist decreased hypoxia-inducible factor-induced angiogenesis.\n\nQuestion:\nIs hypoxia-inducible factor-2 a novel regulator of aberrant CXCL12 expression in multiple myeloma plasma 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:\nMultiple myeloma is an incurable malignancy of bone marrow plasma cells. Progression of multiple myeloma is accompanied by an increase in bone marrow angiogenesis. Studies from our laboratory suggest a role for the CXCL12 chemokine in this process, with circulating levels of CXCL12 correlating with bone marrow angiogenesis in patients with multiple myeloma. While the mechanisms responsible for aberrant plasma cell expression of CXCL12 remain to be determined, studies in other systems suggest a role for hypoxia and hypoxia-inducible transcription factors. The expression of hypoxia-inducible factor protein was examined in patients' bone marrow biopsy specimens using immunohistochemistry. The hypoxic regulation of CXCL12 was examined in multiple myeloma plasma cell lines using polymerase chain reaction and western blotting. The role of hypoxia-inducible factors-1 and -2 in the regulation of CXCL12 expression was examined using over-expression and short hairpin RNA knockdown constructs, electrophoretic mobility shift assays and chromatin immunoprecipitation. The contribution of CXCL12 to hypoxia-induced angiogenesis was examined in vivo using a subcutaneous murine model of neovascularization. Strong hypoxia-inducible factor-2 protein expression was detected in CD138(+) multiple myeloma plasma cells in patients' biopsy specimens. Prolonged exposure to hypoxia strongly up-regulated CXCL12 expression in multiple myeloma plasma cells and hypoxia-inducible factor-2 was found to play a key role in this response. Promoter analyses revealed increased hypoxia-inducible factor-2 binding to the CXCL12 promoter under hypoxic conditions. Over-expression of hypoxia-inducible factor in multiple myeloma plasma cells strongly induced in vivo angiogenesis, and administration of a CXCL12 antagonist decreased hypoxia-inducible factor-induced angiogenesis.\n\nQuestion:\nIs hypoxia-inducible factor-2 a novel regulator of aberrant CXCL12 expression in multiple myeloma plasma 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:\nDuring the long-term treatment of patients with hereditary haemochromatosis (HH) the authors observed that proton pump inhibitors (PPI) reduced the requirement for maintenance phlebotomy. Gastric acid plays a crucial role in non-haem iron absorption and the authors performed a case review and intervention study to investigate if PPI-induced suppression of gastric acid would reduce dietary iron absorption in C282Y homozygous patients. Phlebotomy requirements to keep serum ferritin approximately 50 microg/l before (mean 6.1 (SE 0.6) years) and during (3.8 (0.9) years) administration of a PPI were evaluated in seven patients and a post-prandial study was performed to determine whether PPIs reduce absorption of non-haem iron (14.5 mg) from a test meal in a further 14 phlebotomised patients with normal iron stores. There was a significant reduction (p<0.001) in the volume of blood removed annually before (2.5 (0.25) l) and while taking (0.5 (0.25) l) a PPI. Administration of a PPI for 7d suppressed absorption of non-haem iron from the meal as shown by a significant reduction (all p<0.01) in: area under the serum curve (2145 (374) versus 1059 (219)), % recovery of administered iron at peak serum iron (20.5 (3.2) versus 11.0 (2.0)%) and peak serum iron (13.6 (2.4) vs 6.1 (1.2) micromol/l) (all values are before vs during PPI).\n\nQuestion:\nDo proton pump inhibitors suppress absorption of dietary non-haem iron in hereditary haemochromatosis?", "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 the long-term treatment of patients with hereditary haemochromatosis (HH) the authors observed that proton pump inhibitors (PPI) reduced the requirement for maintenance phlebotomy. Gastric acid plays a crucial role in non-haem iron absorption and the authors performed a case review and intervention study to investigate if PPI-induced suppression of gastric acid would reduce dietary iron absorption in C282Y homozygous patients. Phlebotomy requirements to keep serum ferritin approximately 50 microg/l before (mean 6.1 (SE 0.6) years) and during (3.8 (0.9) years) administration of a PPI were evaluated in seven patients and a post-prandial study was performed to determine whether PPIs reduce absorption of non-haem iron (14.5 mg) from a test meal in a further 14 phlebotomised patients with normal iron stores. There was a significant reduction (p<0.001) in the volume of blood removed annually before (2.5 (0.25) l) and while taking (0.5 (0.25) l) a PPI. Administration of a PPI for 7d suppressed absorption of non-haem iron from the meal as shown by a significant reduction (all p<0.01) in: area under the serum curve (2145 (374) versus 1059 (219)), % recovery of administered iron at peak serum iron (20.5 (3.2) versus 11.0 (2.0)%) and peak serum iron (13.6 (2.4) vs 6.1 (1.2) micromol/l) (all values are before vs during PPI).\n\nQuestion:\nDo proton pump inhibitors suppress absorption of dietary non-haem iron in hereditary haemochromatosis?", "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 the long-term treatment of patients with hereditary haemochromatosis (HH) the authors observed that proton pump inhibitors (PPI) reduced the requirement for maintenance phlebotomy. Gastric acid plays a crucial role in non-haem iron absorption and the authors performed a case review and intervention study to investigate if PPI-induced suppression of gastric acid would reduce dietary iron absorption in C282Y homozygous patients. Phlebotomy requirements to keep serum ferritin approximately 50 microg/l before (mean 6.1 (SE 0.6) years) and during (3.8 (0.9) years) administration of a PPI were evaluated in seven patients and a post-prandial study was performed to determine whether PPIs reduce absorption of non-haem iron (14.5 mg) from a test meal in a further 14 phlebotomised patients with normal iron stores. There was a significant reduction (p<0.001) in the volume of blood removed annually before (2.5 (0.25) l) and while taking (0.5 (0.25) l) a PPI. Administration of a PPI for 7d suppressed absorption of non-haem iron from the meal as shown by a significant reduction (all p<0.01) in: area under the serum curve (2145 (374) versus 1059 (219)), % recovery of administered iron at peak serum iron (20.5 (3.2) versus 11.0 (2.0)%) and peak serum iron (13.6 (2.4) vs 6.1 (1.2) micromol/l) (all values are before vs during PPI).\n\nQuestion:\nDo proton pump inhibitors suppress absorption of dietary non-haem iron in hereditary haemochromatosis?", "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 role of Helicobacter pylori infection in the development of oesophageal malignancies was investigated through a multivariate conditional logistic regression analysis in a nested case-control study. Blood samples and a questionnaire on smoking and alcohol habits were collected from a cohort of 32,906 city residents during a health-screening programme between 1974 and 1992. Forty-four cases of oesophageal cancer and 149 matched controls were selected. The mean interval between screening and cancer diagnosis was 11.9 years. H. pylori seropositivity was determined by an enzyme-linked immunosorbant assay measuring IgG. Occupation was included in the statistical analysis as an indicator of socio-economic status. Helicobacter pylori seropositivity was present in 10 of the cases (22.7%) and 67 of the controls (45.0%). In a multivariate model, with adjustment for occupation, tobacco and alcohol consumption, the odds ratio for developing an oesophageal malignancy when infected with H. pylori was 0.29 (95% confidence interval (CI): 0.12-0.67). Current smokers had an odds ratio of 17.3 (95% CI: 3.0-99.4) and the odds ratio for ex-smokers was 5.9 (95% CI: 1.15-29.9). High alcohol consumption was no longer significantly associated with oesophageal neoplasms after tobacco smoking was included into the model, odds ratio 1.22 (95% CI: 0.46-3.2). The protective effect of H. pylori was more pronounced for oesophageal adenocarcinoma (seven cases, odds ratio 0.16, 95% CI: 0.00-1.06) than for squamous-cell carcinoma (29 cases, odds ratio 0.41, 95% CI: 0.14-1.2).\n\nQuestion:\nIs helicobacter pylori infection associated with a decreased risk of developing oesophageal neoplasms?", "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 role of Helicobacter pylori infection in the development of oesophageal malignancies was investigated through a multivariate conditional logistic regression analysis in a nested case-control study. Blood samples and a questionnaire on smoking and alcohol habits were collected from a cohort of 32,906 city residents during a health-screening programme between 1974 and 1992. Forty-four cases of oesophageal cancer and 149 matched controls were selected. The mean interval between screening and cancer diagnosis was 11.9 years. H. pylori seropositivity was determined by an enzyme-linked immunosorbant assay measuring IgG. Occupation was included in the statistical analysis as an indicator of socio-economic status. Helicobacter pylori seropositivity was present in 10 of the cases (22.7%) and 67 of the controls (45.0%). In a multivariate model, with adjustment for occupation, tobacco and alcohol consumption, the odds ratio for developing an oesophageal malignancy when infected with H. pylori was 0.29 (95% confidence interval (CI): 0.12-0.67). Current smokers had an odds ratio of 17.3 (95% CI: 3.0-99.4) and the odds ratio for ex-smokers was 5.9 (95% CI: 1.15-29.9). High alcohol consumption was no longer significantly associated with oesophageal neoplasms after tobacco smoking was included into the model, odds ratio 1.22 (95% CI: 0.46-3.2). The protective effect of H. pylori was more pronounced for oesophageal adenocarcinoma (seven cases, odds ratio 0.16, 95% CI: 0.00-1.06) than for squamous-cell carcinoma (29 cases, odds ratio 0.41, 95% CI: 0.14-1.2).\n\nQuestion:\nIs helicobacter pylori infection associated with a decreased risk of developing oesophageal neoplasms?", "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 role of Helicobacter pylori infection in the development of oesophageal malignancies was investigated through a multivariate conditional logistic regression analysis in a nested case-control study. Blood samples and a questionnaire on smoking and alcohol habits were collected from a cohort of 32,906 city residents during a health-screening programme between 1974 and 1992. Forty-four cases of oesophageal cancer and 149 matched controls were selected. The mean interval between screening and cancer diagnosis was 11.9 years. H. pylori seropositivity was determined by an enzyme-linked immunosorbant assay measuring IgG. Occupation was included in the statistical analysis as an indicator of socio-economic status. Helicobacter pylori seropositivity was present in 10 of the cases (22.7%) and 67 of the controls (45.0%). In a multivariate model, with adjustment for occupation, tobacco and alcohol consumption, the odds ratio for developing an oesophageal malignancy when infected with H. pylori was 0.29 (95% confidence interval (CI): 0.12-0.67). Current smokers had an odds ratio of 17.3 (95% CI: 3.0-99.4) and the odds ratio for ex-smokers was 5.9 (95% CI: 1.15-29.9). High alcohol consumption was no longer significantly associated with oesophageal neoplasms after tobacco smoking was included into the model, odds ratio 1.22 (95% CI: 0.46-3.2). The protective effect of H. pylori was more pronounced for oesophageal adenocarcinoma (seven cases, odds ratio 0.16, 95% CI: 0.00-1.06) than for squamous-cell carcinoma (29 cases, odds ratio 0.41, 95% CI: 0.14-1.2).\n\nQuestion:\nIs helicobacter pylori infection associated with a decreased risk of developing oesophageal neoplasms?", "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:\nImmune challenge of mice with Bacille Calmette-Guérin (BCG) has been reported to cause transient weight loss and a behavioural sickness response. Although BCG-induced depression involves the kynurenine pathway, weight loss occurs independently of this factor. Because neuropeptide Y (NPY) and peptide YY (PYY) are involved in the regulation of food intake, we hypothesized that they play a role in the BCG-induced weight loss. Male wild-type, PYY knockout (PYY-/-), NPY knockout (NPY-/-) and NPY-/-;PYY-/- double knockout mice were injected with vehicle or BCG (approximately 10(8) colony-forming units per mouse), and their weight, locomotion, exploration and ingestion were recorded for 2 weeks post-treatment. Deletion of PYY and NPY aggravated the BCG-induced loss of body weight, which was most pronounced in NPY-/-;PYY-/- mice (maximum loss: 15%). The weight loss in NPY-/-;PYY-/- mice did not normalize during the 2 week observation period. BCG suppressed the circadian pattern of locomotion, exploration and food intake. However, these changes took a different time course than the prolonged weight loss caused by BCG in NPY-/-;PYY-/- mice. The effect of BCG to increase circulating IL-6 (measured 16 days post-treatment) remained unaltered by knockout of PYY, NPY or NPY plus PYY.\n\nQuestion:\nDo neuropeptide Y and peptide YY protect from weight loss caused by Bacille Calmette-Guérin 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:\nImmune challenge of mice with Bacille Calmette-Guérin (BCG) has been reported to cause transient weight loss and a behavioural sickness response. Although BCG-induced depression involves the kynurenine pathway, weight loss occurs independently of this factor. Because neuropeptide Y (NPY) and peptide YY (PYY) are involved in the regulation of food intake, we hypothesized that they play a role in the BCG-induced weight loss. Male wild-type, PYY knockout (PYY-/-), NPY knockout (NPY-/-) and NPY-/-;PYY-/- double knockout mice were injected with vehicle or BCG (approximately 10(8) colony-forming units per mouse), and their weight, locomotion, exploration and ingestion were recorded for 2 weeks post-treatment. Deletion of PYY and NPY aggravated the BCG-induced loss of body weight, which was most pronounced in NPY-/-;PYY-/- mice (maximum loss: 15%). The weight loss in NPY-/-;PYY-/- mice did not normalize during the 2 week observation period. BCG suppressed the circadian pattern of locomotion, exploration and food intake. However, these changes took a different time course than the prolonged weight loss caused by BCG in NPY-/-;PYY-/- mice. The effect of BCG to increase circulating IL-6 (measured 16 days post-treatment) remained unaltered by knockout of PYY, NPY or NPY plus PYY.\n\nQuestion:\nDo neuropeptide Y and peptide YY protect from weight loss caused by Bacille Calmette-Guérin 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:\nImmune challenge of mice with Bacille Calmette-Guérin (BCG) has been reported to cause transient weight loss and a behavioural sickness response. Although BCG-induced depression involves the kynurenine pathway, weight loss occurs independently of this factor. Because neuropeptide Y (NPY) and peptide YY (PYY) are involved in the regulation of food intake, we hypothesized that they play a role in the BCG-induced weight loss. Male wild-type, PYY knockout (PYY-/-), NPY knockout (NPY-/-) and NPY-/-;PYY-/- double knockout mice were injected with vehicle or BCG (approximately 10(8) colony-forming units per mouse), and their weight, locomotion, exploration and ingestion were recorded for 2 weeks post-treatment. Deletion of PYY and NPY aggravated the BCG-induced loss of body weight, which was most pronounced in NPY-/-;PYY-/- mice (maximum loss: 15%). The weight loss in NPY-/-;PYY-/- mice did not normalize during the 2 week observation period. BCG suppressed the circadian pattern of locomotion, exploration and food intake. However, these changes took a different time course than the prolonged weight loss caused by BCG in NPY-/-;PYY-/- mice. The effect of BCG to increase circulating IL-6 (measured 16 days post-treatment) remained unaltered by knockout of PYY, NPY or NPY plus PYY.\n\nQuestion:\nDo neuropeptide Y and peptide YY protect from weight loss caused by Bacille Calmette-Guérin 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:\nTo test the hypothesis that left-ventricular hypertrophy (LVH) is better associated with aortic, than brachial, 24-h average blood pressure (BP) in individuals with hypertension. The office aortic BP is associated better with organ damage, such as LVH, than the office brachial BP; whether the 24-h average aortic BP associates better with LVH, than the 24-h average brachial BP, has never been tested. Aortic ambulatory BP monitoring (ABPM) was performed with a novel validated oscillometric cuff-based BP recording device, also used for simultaneous brachial ABPM, and the application of pulse wave analysis method. Office brachial and aortic BP were assessed with validated oscillometric recording device and pulse wave analysis, respectively; left-ventricular mass was measured by ultrasound. Regression analysis performed in 229 individuals (aged 54.3 ± 14.6 years; 56% men; 75% hypertensive patients) showed that the 24-h average aortic SBP was significantly better associated with left-ventricular mass index and LVH than the 24-h average brachial, as well as, office (brachial or aortic) SBP, independently of age, sex, obesity or treatment. Receiver operator characteristics curve analysis showed a higher discriminatory ability of 24-h average aortic than brachial SBP to detect the presence of LVH (area under the curve: 0.73 versus 0.69; P = 0.007). A high degree of interindividual overlap regarding aortic 24-h average SBP level was found in individuals in whom the corresponding brachial measurements denoted different hypertension levels.\n\nQuestion:\nIs left-ventricular hypertrophy associated better with 24-h aortic pressure than 24-h brachial pressure in hypertensive patients : the SAFAR 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:\nTo test the hypothesis that left-ventricular hypertrophy (LVH) is better associated with aortic, than brachial, 24-h average blood pressure (BP) in individuals with hypertension. The office aortic BP is associated better with organ damage, such as LVH, than the office brachial BP; whether the 24-h average aortic BP associates better with LVH, than the 24-h average brachial BP, has never been tested. Aortic ambulatory BP monitoring (ABPM) was performed with a novel validated oscillometric cuff-based BP recording device, also used for simultaneous brachial ABPM, and the application of pulse wave analysis method. Office brachial and aortic BP were assessed with validated oscillometric recording device and pulse wave analysis, respectively; left-ventricular mass was measured by ultrasound. Regression analysis performed in 229 individuals (aged 54.3 ± 14.6 years; 56% men; 75% hypertensive patients) showed that the 24-h average aortic SBP was significantly better associated with left-ventricular mass index and LVH than the 24-h average brachial, as well as, office (brachial or aortic) SBP, independently of age, sex, obesity or treatment. Receiver operator characteristics curve analysis showed a higher discriminatory ability of 24-h average aortic than brachial SBP to detect the presence of LVH (area under the curve: 0.73 versus 0.69; P = 0.007). A high degree of interindividual overlap regarding aortic 24-h average SBP level was found in individuals in whom the corresponding brachial measurements denoted different hypertension levels.\n\nQuestion:\nIs left-ventricular hypertrophy associated better with 24-h aortic pressure than 24-h brachial pressure in hypertensive patients : the SAFAR 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:\nTo test the hypothesis that left-ventricular hypertrophy (LVH) is better associated with aortic, than brachial, 24-h average blood pressure (BP) in individuals with hypertension. The office aortic BP is associated better with organ damage, such as LVH, than the office brachial BP; whether the 24-h average aortic BP associates better with LVH, than the 24-h average brachial BP, has never been tested. Aortic ambulatory BP monitoring (ABPM) was performed with a novel validated oscillometric cuff-based BP recording device, also used for simultaneous brachial ABPM, and the application of pulse wave analysis method. Office brachial and aortic BP were assessed with validated oscillometric recording device and pulse wave analysis, respectively; left-ventricular mass was measured by ultrasound. Regression analysis performed in 229 individuals (aged 54.3 ± 14.6 years; 56% men; 75% hypertensive patients) showed that the 24-h average aortic SBP was significantly better associated with left-ventricular mass index and LVH than the 24-h average brachial, as well as, office (brachial or aortic) SBP, independently of age, sex, obesity or treatment. Receiver operator characteristics curve analysis showed a higher discriminatory ability of 24-h average aortic than brachial SBP to detect the presence of LVH (area under the curve: 0.73 versus 0.69; P = 0.007). A high degree of interindividual overlap regarding aortic 24-h average SBP level was found in individuals in whom the corresponding brachial measurements denoted different hypertension levels.\n\nQuestion:\nIs left-ventricular hypertrophy associated better with 24-h aortic pressure than 24-h brachial pressure in hypertensive patients : the SAFAR 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:\nThis study examined whether problematic Internet use was associated with substance use among young adolescents and assessed whether this association accounted for the use of tobacco, alcohol, cannabis and other drugs. Using the Internet Addiction Test, we divided a representative sample of 3067 adolescents in Switzerland (mean age 14 years) into regular and problematic Internet users. We performed a bivariate analysis and two logistic regression models, to analyse substances separately and simultaneously, and developed a log-linear model to define the associations between significant variables. Problematic Internet users were more likely to be female, to use substances, to come from nonintact families, to report poor emotional well-being and to be below average students. The first model showed significant associations between problematic users and each substance, with adjusted odds ratios of 2.05 for tobacco, 1.72 for alcohol, 1.94 for cannabis and 2.73 for other drugs. Only smoking remained significant in the second model, with an adjusted odds ratio of 1.71.\n\nQuestion:\nIs problematic Internet use associated with substance use in young adolescents?", "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 examined whether problematic Internet use was associated with substance use among young adolescents and assessed whether this association accounted for the use of tobacco, alcohol, cannabis and other drugs. Using the Internet Addiction Test, we divided a representative sample of 3067 adolescents in Switzerland (mean age 14 years) into regular and problematic Internet users. We performed a bivariate analysis and two logistic regression models, to analyse substances separately and simultaneously, and developed a log-linear model to define the associations between significant variables. Problematic Internet users were more likely to be female, to use substances, to come from nonintact families, to report poor emotional well-being and to be below average students. The first model showed significant associations between problematic users and each substance, with adjusted odds ratios of 2.05 for tobacco, 1.72 for alcohol, 1.94 for cannabis and 2.73 for other drugs. Only smoking remained significant in the second model, with an adjusted odds ratio of 1.71.\n\nQuestion:\nIs problematic Internet use associated with substance use in young adolescents?", "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 examined whether problematic Internet use was associated with substance use among young adolescents and assessed whether this association accounted for the use of tobacco, alcohol, cannabis and other drugs. Using the Internet Addiction Test, we divided a representative sample of 3067 adolescents in Switzerland (mean age 14 years) into regular and problematic Internet users. We performed a bivariate analysis and two logistic regression models, to analyse substances separately and simultaneously, and developed a log-linear model to define the associations between significant variables. Problematic Internet users were more likely to be female, to use substances, to come from nonintact families, to report poor emotional well-being and to be below average students. The first model showed significant associations between problematic users and each substance, with adjusted odds ratios of 2.05 for tobacco, 1.72 for alcohol, 1.94 for cannabis and 2.73 for other drugs. Only smoking remained significant in the second model, with an adjusted odds ratio of 1.71.\n\nQuestion:\nIs problematic Internet use associated with substance use in young adolescents?", "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:\nDeep venous thrombosis (DVT) confers vein wall injury associated with fibrosis and extracellular matrix (ECM) turnover, likely mediated by matrix proteases. This study investigated the expression of proteases and collagen involved in early vein wall remodeling. In the mouse, DVT was produced by ligation of the infrarenal inferior vena cava (IVC) or sham operation, and tissue was harvested at 4, 8, and 12 days. The vein wall tissue was processed for real-time reverse transcriptase-polymerase chain reaction (6 to 8 per time point), Western immunoblotting (5 per time point), and gelatin zymography (5 per time point). Analysis of variance was used for multiple comparisons, and a P < .05 was significant. Thrombus resolution was documented by a 38% decrease in the thrombosed IVC weight from day 4 to day 12 (P = .007). Total vein wall collagen increased over time, with a corresponding increase in procollagen I and III, and expression peaked at 12 days (24-fold and 6.1-fold, respectively, P < .02). Matrix metalloproteinase-2 (MMP-2) gene expression was 23-fold greater at 12 days after thrombus formation compared with sham or 4 days after thrombosis (P < .05). Total MMP-2 activity was also significantly elevated at 12 days compared with sham (P < .05). MMP-9 expression was 19-fold and 27-fold higher at days 4 and 8, respectively, relative to sham (P < .05), with no difference in activity. MMP-14 expression was twofold to 3.6-fold greater at day 12 compared with earlier time points and shams (P < .001), but no differences in protein levels were found. Urokinase-type plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1) protein levels were not significantly different from sham over time; however, the ratio of uPA to PAI-1 was decreased through 8 days.\n\nQuestion:\nDoes vein wall remodeling after deep vein thrombosis involve matrix metalloproteinases and late fibrosis in a 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:\nDeep venous thrombosis (DVT) confers vein wall injury associated with fibrosis and extracellular matrix (ECM) turnover, likely mediated by matrix proteases. This study investigated the expression of proteases and collagen involved in early vein wall remodeling. In the mouse, DVT was produced by ligation of the infrarenal inferior vena cava (IVC) or sham operation, and tissue was harvested at 4, 8, and 12 days. The vein wall tissue was processed for real-time reverse transcriptase-polymerase chain reaction (6 to 8 per time point), Western immunoblotting (5 per time point), and gelatin zymography (5 per time point). Analysis of variance was used for multiple comparisons, and a P < .05 was significant. Thrombus resolution was documented by a 38% decrease in the thrombosed IVC weight from day 4 to day 12 (P = .007). Total vein wall collagen increased over time, with a corresponding increase in procollagen I and III, and expression peaked at 12 days (24-fold and 6.1-fold, respectively, P < .02). Matrix metalloproteinase-2 (MMP-2) gene expression was 23-fold greater at 12 days after thrombus formation compared with sham or 4 days after thrombosis (P < .05). Total MMP-2 activity was also significantly elevated at 12 days compared with sham (P < .05). MMP-9 expression was 19-fold and 27-fold higher at days 4 and 8, respectively, relative to sham (P < .05), with no difference in activity. MMP-14 expression was twofold to 3.6-fold greater at day 12 compared with earlier time points and shams (P < .001), but no differences in protein levels were found. Urokinase-type plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1) protein levels were not significantly different from sham over time; however, the ratio of uPA to PAI-1 was decreased through 8 days.\n\nQuestion:\nDoes vein wall remodeling after deep vein thrombosis involve matrix metalloproteinases and late fibrosis in a 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:\nDeep venous thrombosis (DVT) confers vein wall injury associated with fibrosis and extracellular matrix (ECM) turnover, likely mediated by matrix proteases. This study investigated the expression of proteases and collagen involved in early vein wall remodeling. In the mouse, DVT was produced by ligation of the infrarenal inferior vena cava (IVC) or sham operation, and tissue was harvested at 4, 8, and 12 days. The vein wall tissue was processed for real-time reverse transcriptase-polymerase chain reaction (6 to 8 per time point), Western immunoblotting (5 per time point), and gelatin zymography (5 per time point). Analysis of variance was used for multiple comparisons, and a P < .05 was significant. Thrombus resolution was documented by a 38% decrease in the thrombosed IVC weight from day 4 to day 12 (P = .007). Total vein wall collagen increased over time, with a corresponding increase in procollagen I and III, and expression peaked at 12 days (24-fold and 6.1-fold, respectively, P < .02). Matrix metalloproteinase-2 (MMP-2) gene expression was 23-fold greater at 12 days after thrombus formation compared with sham or 4 days after thrombosis (P < .05). Total MMP-2 activity was also significantly elevated at 12 days compared with sham (P < .05). MMP-9 expression was 19-fold and 27-fold higher at days 4 and 8, respectively, relative to sham (P < .05), with no difference in activity. MMP-14 expression was twofold to 3.6-fold greater at day 12 compared with earlier time points and shams (P < .001), but no differences in protein levels were found. Urokinase-type plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1) protein levels were not significantly different from sham over time; however, the ratio of uPA to PAI-1 was decreased through 8 days.\n\nQuestion:\nDoes vein wall remodeling after deep vein thrombosis involve matrix metalloproteinases and late fibrosis in a 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:\nGhrelin and its receptor, growth hormone secretagogue (GHS) receptor (GHSR), are expressed in the normal pituitary gland and various types of pituitary adenoma. Somatic mutations in the subunit of Gs alpha protein (gsp), which led to a constitutive activation of adenylyl cyclase, are reported in GH-producing pituitary adenomas. We analysed the relationship between ghrelin mRNA and GHSR mRNA expression levels in gsp mutation-positive and -negative GH-producing pituitary adenomas. Pituitary adenoma tissue was obtained at surgery from 20 patients with acromegaly. The expression levels of human ghrelin mRNA and GHSR mRNA were quantified using a competitive RT-PCR method. To detect the gsp mutations, amplified Gs alpha subunit cDNA fragments were sequenced directly using RT-PCR method. There was no significant difference in the expression of ghrelin mRNA between mutation-positive and -negative adenomas. The expression of GHSR mRNA was significantly lower in gsp mutation-positive than -negative adenomas. There was a significant negative correlation between the levels of ghrelin mRNA and GHSR mRNA expression in mutation-negative adenomas; no such correlation was found in mutation-positive adenomas.\n\nQuestion:\nIs ghrelin mRNA and GH secretagogue receptor mRNA in human GH-producing pituitary adenomas affected by mutations in the alpha subunit of G protein?", "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:\nGhrelin and its receptor, growth hormone secretagogue (GHS) receptor (GHSR), are expressed in the normal pituitary gland and various types of pituitary adenoma. Somatic mutations in the subunit of Gs alpha protein (gsp), which led to a constitutive activation of adenylyl cyclase, are reported in GH-producing pituitary adenomas. We analysed the relationship between ghrelin mRNA and GHSR mRNA expression levels in gsp mutation-positive and -negative GH-producing pituitary adenomas. Pituitary adenoma tissue was obtained at surgery from 20 patients with acromegaly. The expression levels of human ghrelin mRNA and GHSR mRNA were quantified using a competitive RT-PCR method. To detect the gsp mutations, amplified Gs alpha subunit cDNA fragments were sequenced directly using RT-PCR method. There was no significant difference in the expression of ghrelin mRNA between mutation-positive and -negative adenomas. The expression of GHSR mRNA was significantly lower in gsp mutation-positive than -negative adenomas. There was a significant negative correlation between the levels of ghrelin mRNA and GHSR mRNA expression in mutation-negative adenomas; no such correlation was found in mutation-positive adenomas.\n\nQuestion:\nIs ghrelin mRNA and GH secretagogue receptor mRNA in human GH-producing pituitary adenomas affected by mutations in the alpha subunit of G protein?", "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:\nGhrelin and its receptor, growth hormone secretagogue (GHS) receptor (GHSR), are expressed in the normal pituitary gland and various types of pituitary adenoma. Somatic mutations in the subunit of Gs alpha protein (gsp), which led to a constitutive activation of adenylyl cyclase, are reported in GH-producing pituitary adenomas. We analysed the relationship between ghrelin mRNA and GHSR mRNA expression levels in gsp mutation-positive and -negative GH-producing pituitary adenomas. Pituitary adenoma tissue was obtained at surgery from 20 patients with acromegaly. The expression levels of human ghrelin mRNA and GHSR mRNA were quantified using a competitive RT-PCR method. To detect the gsp mutations, amplified Gs alpha subunit cDNA fragments were sequenced directly using RT-PCR method. There was no significant difference in the expression of ghrelin mRNA between mutation-positive and -negative adenomas. The expression of GHSR mRNA was significantly lower in gsp mutation-positive than -negative adenomas. There was a significant negative correlation between the levels of ghrelin mRNA and GHSR mRNA expression in mutation-negative adenomas; no such correlation was found in mutation-positive adenomas.\n\nQuestion:\nIs ghrelin mRNA and GH secretagogue receptor mRNA in human GH-producing pituitary adenomas affected by mutations in the alpha subunit of G protein?", "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 umbilical and uterine artery Doppler in predicting outcome of pregnancies suspected of fetal growth restriction (FGR). A prospective study included 353 singleton pregnancies complicated by an FGR fetus. University Hospital setting. Pregnancies suspected of FGR diagnosed by ultrasound fetal biometry during a 5-year period. Perinatal outcome in relation to uterine and umbilical artery Doppler. The women underwent Doppler examination of the umbilical and uterine arteries. Results from the uterine, but not the umbilical artery, were blind to the woman and managing obstetrician. The Doppler results were related to perinatal outcomes including small for gestational age newborns, caesarean delivery, premature delivery (<37 weeks of gestation) and admission of the newborn to a neonatal intensive care unit. Abnormal uterine artery Doppler velocimetry was seen in 120 (33.4%) pregnancies and abnormal umbilical artery Doppler in 102 (28.4%). There was a statistically significant correlation between abnormal Doppler of both the umbilical and uterine arteries and adverse outcome of pregnancy. The two vessels were comparable in predicting adverse outcome. Women with normal umbilical artery Doppler (251) were analysed separately. Abnormal uterine artery Doppler, seen in 61 (24.3%) of those women, showed a statistically significant correlation for adverse outcome of pregnancy.\n\nQuestion:\nAre uterine and umbilical artery Doppler comparable in predicting perinatal outcome of growth-restricted fetuses?", "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 umbilical and uterine artery Doppler in predicting outcome of pregnancies suspected of fetal growth restriction (FGR). A prospective study included 353 singleton pregnancies complicated by an FGR fetus. University Hospital setting. Pregnancies suspected of FGR diagnosed by ultrasound fetal biometry during a 5-year period. Perinatal outcome in relation to uterine and umbilical artery Doppler. The women underwent Doppler examination of the umbilical and uterine arteries. Results from the uterine, but not the umbilical artery, were blind to the woman and managing obstetrician. The Doppler results were related to perinatal outcomes including small for gestational age newborns, caesarean delivery, premature delivery (<37 weeks of gestation) and admission of the newborn to a neonatal intensive care unit. Abnormal uterine artery Doppler velocimetry was seen in 120 (33.4%) pregnancies and abnormal umbilical artery Doppler in 102 (28.4%). There was a statistically significant correlation between abnormal Doppler of both the umbilical and uterine arteries and adverse outcome of pregnancy. The two vessels were comparable in predicting adverse outcome. Women with normal umbilical artery Doppler (251) were analysed separately. Abnormal uterine artery Doppler, seen in 61 (24.3%) of those women, showed a statistically significant correlation for adverse outcome of pregnancy.\n\nQuestion:\nAre uterine and umbilical artery Doppler comparable in predicting perinatal outcome of growth-restricted fetuses?", "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 umbilical and uterine artery Doppler in predicting outcome of pregnancies suspected of fetal growth restriction (FGR). A prospective study included 353 singleton pregnancies complicated by an FGR fetus. University Hospital setting. Pregnancies suspected of FGR diagnosed by ultrasound fetal biometry during a 5-year period. Perinatal outcome in relation to uterine and umbilical artery Doppler. The women underwent Doppler examination of the umbilical and uterine arteries. Results from the uterine, but not the umbilical artery, were blind to the woman and managing obstetrician. The Doppler results were related to perinatal outcomes including small for gestational age newborns, caesarean delivery, premature delivery (<37 weeks of gestation) and admission of the newborn to a neonatal intensive care unit. Abnormal uterine artery Doppler velocimetry was seen in 120 (33.4%) pregnancies and abnormal umbilical artery Doppler in 102 (28.4%). There was a statistically significant correlation between abnormal Doppler of both the umbilical and uterine arteries and adverse outcome of pregnancy. The two vessels were comparable in predicting adverse outcome. Women with normal umbilical artery Doppler (251) were analysed separately. Abnormal uterine artery Doppler, seen in 61 (24.3%) of those women, showed a statistically significant correlation for adverse outcome of pregnancy.\n\nQuestion:\nAre uterine and umbilical artery Doppler comparable in predicting perinatal outcome of growth-restricted fetuses?", "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:\nHepatocellular carcinoma (HCC) is associated with inflammation, and roughly 30 % of the global population shows serological evidence of current or past infection with hepatitis B or hepatitis C virus. Resident hepatic macrophages, known as Kupffer cells (KCs), are considered as the specific tumor-associated macrophages (TAMs) of HCC, and can produce various cytokines-most importantly interleukin (IL)-6-to promote tumorigenesis of HCC. However, the roles of KCs and IL-6 in carcinogenesis in the liver are still unclear. We analyzed leukocyte-related peripheral blood data of 192 patients and constructed a mouse model in which the bone marrow was cleared out by irradiation and reconstructed using bone marrow donated from IL-6-deficient mice to further elucidate the hepatic pathological changes in response to toxic challenge and oncogenic gene mutation. Peripheral monocyte counts and serum IL-6 levels were significantly higher in patients with HCC than in those without HCC. In addition, there was a significant difference in the levels of IL-6 among individuals with different histopathological grades. In mice with selective IL-6 ablation in monocytes/KCs, we observed decreased toxic liver injury, inflammatory infiltration, and systemic inflammation. In Mdr2-deficient mice, which spontaneously developed HCC, the loss of IL-6 in monocytes/KCs resulted in inhibition of IL-6/signal transducer and activator of transcription 3 signaling, decreased serum IL-6 levels, and delayed tumorigenesis.\n\nQuestion:\nDoes deletion of interleukin-6 in monocytes/macrophages suppress the initiation of 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:\nHepatocellular carcinoma (HCC) is associated with inflammation, and roughly 30 % of the global population shows serological evidence of current or past infection with hepatitis B or hepatitis C virus. Resident hepatic macrophages, known as Kupffer cells (KCs), are considered as the specific tumor-associated macrophages (TAMs) of HCC, and can produce various cytokines-most importantly interleukin (IL)-6-to promote tumorigenesis of HCC. However, the roles of KCs and IL-6 in carcinogenesis in the liver are still unclear. We analyzed leukocyte-related peripheral blood data of 192 patients and constructed a mouse model in which the bone marrow was cleared out by irradiation and reconstructed using bone marrow donated from IL-6-deficient mice to further elucidate the hepatic pathological changes in response to toxic challenge and oncogenic gene mutation. Peripheral monocyte counts and serum IL-6 levels were significantly higher in patients with HCC than in those without HCC. In addition, there was a significant difference in the levels of IL-6 among individuals with different histopathological grades. In mice with selective IL-6 ablation in monocytes/KCs, we observed decreased toxic liver injury, inflammatory infiltration, and systemic inflammation. In Mdr2-deficient mice, which spontaneously developed HCC, the loss of IL-6 in monocytes/KCs resulted in inhibition of IL-6/signal transducer and activator of transcription 3 signaling, decreased serum IL-6 levels, and delayed tumorigenesis.\n\nQuestion:\nDoes deletion of interleukin-6 in monocytes/macrophages suppress the initiation of 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:\nHepatocellular carcinoma (HCC) is associated with inflammation, and roughly 30 % of the global population shows serological evidence of current or past infection with hepatitis B or hepatitis C virus. Resident hepatic macrophages, known as Kupffer cells (KCs), are considered as the specific tumor-associated macrophages (TAMs) of HCC, and can produce various cytokines-most importantly interleukin (IL)-6-to promote tumorigenesis of HCC. However, the roles of KCs and IL-6 in carcinogenesis in the liver are still unclear. We analyzed leukocyte-related peripheral blood data of 192 patients and constructed a mouse model in which the bone marrow was cleared out by irradiation and reconstructed using bone marrow donated from IL-6-deficient mice to further elucidate the hepatic pathological changes in response to toxic challenge and oncogenic gene mutation. Peripheral monocyte counts and serum IL-6 levels were significantly higher in patients with HCC than in those without HCC. In addition, there was a significant difference in the levels of IL-6 among individuals with different histopathological grades. In mice with selective IL-6 ablation in monocytes/KCs, we observed decreased toxic liver injury, inflammatory infiltration, and systemic inflammation. In Mdr2-deficient mice, which spontaneously developed HCC, the loss of IL-6 in monocytes/KCs resulted in inhibition of IL-6/signal transducer and activator of transcription 3 signaling, decreased serum IL-6 levels, and delayed tumorigenesis.\n\nQuestion:\nDoes deletion of interleukin-6 in monocytes/macrophages suppress the initiation of 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:\nTo characterize photopsias or light shows in patients self-reporting retinitis pigmentosa and determine associations between their location and patient-reported visual function. One hundred and twenty-seven self-reported patients with retinitis pigmentosa with varying levels of vision completed an anonymous survey on an Internet web site. One hundred and eighteen (93%) of the respondents reported photopsias. The majority (60%) who experience photopsias have them daily, 48% already had them before being diagnosed with retinitis pigmentosa, and 69% report interference with vision. The proportions noting photopsias mostly peripherally versus centrally were 53% of those reading normal or small print versus 35% requiring magnification (odds ratio, 2.3; 95% confidence interval, 1.0-5.5; P = 0.05); 61% of current drivers versus 41% who stopped or never drove (odds ratio, 2.6; 95% confidence interval, 1.0-6.7; P = 0.04); and 54% of individuals who easily navigate or have only minor difficulty in unfamiliar areas versus 29% of those with great difficulty or needing assistance with mobility (odds ratio, 3.0; 95% confidence interval, 1.2-6.7; P = 0.02).\n\nQuestion:\nIs a survey of photopsias in self-reported retinitis pigmentosa : location of photopsias related to disease severity?", "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 photopsias or light shows in patients self-reporting retinitis pigmentosa and determine associations between their location and patient-reported visual function. One hundred and twenty-seven self-reported patients with retinitis pigmentosa with varying levels of vision completed an anonymous survey on an Internet web site. One hundred and eighteen (93%) of the respondents reported photopsias. The majority (60%) who experience photopsias have them daily, 48% already had them before being diagnosed with retinitis pigmentosa, and 69% report interference with vision. The proportions noting photopsias mostly peripherally versus centrally were 53% of those reading normal or small print versus 35% requiring magnification (odds ratio, 2.3; 95% confidence interval, 1.0-5.5; P = 0.05); 61% of current drivers versus 41% who stopped or never drove (odds ratio, 2.6; 95% confidence interval, 1.0-6.7; P = 0.04); and 54% of individuals who easily navigate or have only minor difficulty in unfamiliar areas versus 29% of those with great difficulty or needing assistance with mobility (odds ratio, 3.0; 95% confidence interval, 1.2-6.7; P = 0.02).\n\nQuestion:\nIs a survey of photopsias in self-reported retinitis pigmentosa : location of photopsias related to disease severity?", "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 photopsias or light shows in patients self-reporting retinitis pigmentosa and determine associations between their location and patient-reported visual function. One hundred and twenty-seven self-reported patients with retinitis pigmentosa with varying levels of vision completed an anonymous survey on an Internet web site. One hundred and eighteen (93%) of the respondents reported photopsias. The majority (60%) who experience photopsias have them daily, 48% already had them before being diagnosed with retinitis pigmentosa, and 69% report interference with vision. The proportions noting photopsias mostly peripherally versus centrally were 53% of those reading normal or small print versus 35% requiring magnification (odds ratio, 2.3; 95% confidence interval, 1.0-5.5; P = 0.05); 61% of current drivers versus 41% who stopped or never drove (odds ratio, 2.6; 95% confidence interval, 1.0-6.7; P = 0.04); and 54% of individuals who easily navigate or have only minor difficulty in unfamiliar areas versus 29% of those with great difficulty or needing assistance with mobility (odds ratio, 3.0; 95% confidence interval, 1.2-6.7; P = 0.02).\n\nQuestion:\nIs a survey of photopsias in self-reported retinitis pigmentosa : location of photopsias related to disease severity?", "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:\nStaphylococcus lugdunensis is an emerging cause of endocarditis. To cause endovascular infections, S. lugdunensis requires mechanisms to overcome shear stress. We investigated whether platelets and von Willebrand factor (VWF) mediate bacterial adhesion to the vessel wall and the cardiac valves under flow. S. lugdunensis binding to VWF, collagen, and endothelial cells was studied in a parallel flow chamber in the absence and presence of platelets. In vivo adhesion of S. lugdunensis was evaluated in a mouse microvasculature perfusion model and a new mouse model of endocarditis. Contrary to other coagulase-negative staphylococci, S. lugdunensis bound to VWF under flow, thus enabling its adhesion to endothelial cells and to the subendothelial matrix. In inflamed vessels of the mesenteric circulation, VWF recruited S. lugdunensis to the vessel wall. In a novel endocarditis mouse model, local inflammation and the resulting release of VWF enabled S. lugdunensis to bind and colonize the heart valves.\n\nQuestion:\nDoes shear-Resistant Binding to von Willebrand Factor allow Staphylococcus lugdunensis to Adhere to the Cardiac Valves and Initiate Endocarditis?", "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:\nStaphylococcus lugdunensis is an emerging cause of endocarditis. To cause endovascular infections, S. lugdunensis requires mechanisms to overcome shear stress. We investigated whether platelets and von Willebrand factor (VWF) mediate bacterial adhesion to the vessel wall and the cardiac valves under flow. S. lugdunensis binding to VWF, collagen, and endothelial cells was studied in a parallel flow chamber in the absence and presence of platelets. In vivo adhesion of S. lugdunensis was evaluated in a mouse microvasculature perfusion model and a new mouse model of endocarditis. Contrary to other coagulase-negative staphylococci, S. lugdunensis bound to VWF under flow, thus enabling its adhesion to endothelial cells and to the subendothelial matrix. In inflamed vessels of the mesenteric circulation, VWF recruited S. lugdunensis to the vessel wall. In a novel endocarditis mouse model, local inflammation and the resulting release of VWF enabled S. lugdunensis to bind and colonize the heart valves.\n\nQuestion:\nDoes shear-Resistant Binding to von Willebrand Factor allow Staphylococcus lugdunensis to Adhere to the Cardiac Valves and Initiate Endocarditis?", "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:\nStaphylococcus lugdunensis is an emerging cause of endocarditis. To cause endovascular infections, S. lugdunensis requires mechanisms to overcome shear stress. We investigated whether platelets and von Willebrand factor (VWF) mediate bacterial adhesion to the vessel wall and the cardiac valves under flow. S. lugdunensis binding to VWF, collagen, and endothelial cells was studied in a parallel flow chamber in the absence and presence of platelets. In vivo adhesion of S. lugdunensis was evaluated in a mouse microvasculature perfusion model and a new mouse model of endocarditis. Contrary to other coagulase-negative staphylococci, S. lugdunensis bound to VWF under flow, thus enabling its adhesion to endothelial cells and to the subendothelial matrix. In inflamed vessels of the mesenteric circulation, VWF recruited S. lugdunensis to the vessel wall. In a novel endocarditis mouse model, local inflammation and the resulting release of VWF enabled S. lugdunensis to bind and colonize the heart valves.\n\nQuestion:\nDoes shear-Resistant Binding to von Willebrand Factor allow Staphylococcus lugdunensis to Adhere to the Cardiac Valves and Initiate Endocarditis?", "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 reduce infarct size in animal models of stroke and have been hypothesized to improve clinical outcomes after ischemic stroke. We examined the relationship between statin use before and during stroke hospitalization and poststroke survival. We analyzed records from 12 689 patients admitted with ischemic stroke to any of 17 hospitals in a large integrated healthcare delivery system between January 2000 and December 2007. We used multivariable survival analysis and grouped-treatment analysis, an instrumental variable method that uses treatment differences between facilities to avoid individual patient-level confounding. Statin use before ischemic stroke hospitalization was associated with improved survival (hazard ratio, 0.85; 95% CI, 0.79-0.93; P<0.001), and use before and during hospitalization was associated with better rates of survival (hazard ratio, 0.59; 95% CI, 0.53-0.65; P<0.001). Patients taking a statin before their stroke who underwent statin withdrawal in the hospital had a substantially greater risk of death (hazard ratio, 2.5; 95% CI, 2.1-2.9; P<0.001). The benefit was greater for high-dose (>60 mg/day) statin use (hazard ratio, 0.43; 95% CI, 0.34-0.53; P<0.001) than for lower dose (<60 mg/day) statin use (hazard ratio, 0.60; 95% CI, 0.54-0.67; P<0.001; test for trend P<0.001), and earlier treatment in-hospital further improved survival. Grouped-treatment analysis showed that the association between statin use and survival cannot be explained by patient-level confounding.\n\nQuestion:\nIs statin use during ischemic stroke hospitalization strongly associated with improved poststroke survival?", "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 reduce infarct size in animal models of stroke and have been hypothesized to improve clinical outcomes after ischemic stroke. We examined the relationship between statin use before and during stroke hospitalization and poststroke survival. We analyzed records from 12 689 patients admitted with ischemic stroke to any of 17 hospitals in a large integrated healthcare delivery system between January 2000 and December 2007. We used multivariable survival analysis and grouped-treatment analysis, an instrumental variable method that uses treatment differences between facilities to avoid individual patient-level confounding. Statin use before ischemic stroke hospitalization was associated with improved survival (hazard ratio, 0.85; 95% CI, 0.79-0.93; P<0.001), and use before and during hospitalization was associated with better rates of survival (hazard ratio, 0.59; 95% CI, 0.53-0.65; P<0.001). Patients taking a statin before their stroke who underwent statin withdrawal in the hospital had a substantially greater risk of death (hazard ratio, 2.5; 95% CI, 2.1-2.9; P<0.001). The benefit was greater for high-dose (>60 mg/day) statin use (hazard ratio, 0.43; 95% CI, 0.34-0.53; P<0.001) than for lower dose (<60 mg/day) statin use (hazard ratio, 0.60; 95% CI, 0.54-0.67; P<0.001; test for trend P<0.001), and earlier treatment in-hospital further improved survival. Grouped-treatment analysis showed that the association between statin use and survival cannot be explained by patient-level confounding.\n\nQuestion:\nIs statin use during ischemic stroke hospitalization strongly associated with improved poststroke survival?", "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 reduce infarct size in animal models of stroke and have been hypothesized to improve clinical outcomes after ischemic stroke. We examined the relationship between statin use before and during stroke hospitalization and poststroke survival. We analyzed records from 12 689 patients admitted with ischemic stroke to any of 17 hospitals in a large integrated healthcare delivery system between January 2000 and December 2007. We used multivariable survival analysis and grouped-treatment analysis, an instrumental variable method that uses treatment differences between facilities to avoid individual patient-level confounding. Statin use before ischemic stroke hospitalization was associated with improved survival (hazard ratio, 0.85; 95% CI, 0.79-0.93; P<0.001), and use before and during hospitalization was associated with better rates of survival (hazard ratio, 0.59; 95% CI, 0.53-0.65; P<0.001). Patients taking a statin before their stroke who underwent statin withdrawal in the hospital had a substantially greater risk of death (hazard ratio, 2.5; 95% CI, 2.1-2.9; P<0.001). The benefit was greater for high-dose (>60 mg/day) statin use (hazard ratio, 0.43; 95% CI, 0.34-0.53; P<0.001) than for lower dose (<60 mg/day) statin use (hazard ratio, 0.60; 95% CI, 0.54-0.67; P<0.001; test for trend P<0.001), and earlier treatment in-hospital further improved survival. Grouped-treatment analysis showed that the association between statin use and survival cannot be explained by patient-level confounding.\n\nQuestion:\nIs statin use during ischemic stroke hospitalization strongly associated with improved poststroke survival?", "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:\nWhile the evidence is conclusive regarding the positive effects of endurance training, there is still some controversy regarding the effects of resistance training on muscular capillarity. Thus, the purpose was to assess whether resistance strength training influences resting skeletal muscle microcirculation in vivo. Thirty-nine middle-aged subjects (15 female, 24 male; mean age, 54+/-9 years) were trained twice a week on an isokinetic system (altogether 16 sessions lasting 50 min, intensity 75% of maximum isokinetic and isometric force of knee flexors and extensors). To evaluate success of training, cross-sectional area (CSA) of the quadriceps femoris muscle and its isokinetic and isometric force were quantified. Muscular capillarization was measured in biopsies of the vastus lateralis muscle. In vivo, muscular energy and lipid metabolites were quantified by magnetic resonance spectroscopy and parameters of muscular microcirculation, such as local blood volume, blood flow and velocity, by contrast-enhanced ultrasound analyzing replenishment kinetics. The significant (P<0.001) increase in CSA (60+/-16 before vs. 64+/-15 cm(2) after training) and in absolute muscle strength (isometric, 146+/-44 vs. 174+/-50 Nm; isokinetic, 151+/-53 vs. 174+/-62 Nm) demonstrated successful training. Neither capillary density ex vivo (351+/-75 vs. 326+/-62) nor ultrasonographic parameters of resting muscle perfusion were significantly different (blood flow, 1.2+/-1.2 vs. 1.1+/-1.1 ml/min/100g; blood flow velocity, 0.49+/-0.44 vs. 0.52+/-0.74 mms(-1)). Also, the intensities of high-energy phosphates phosphocreatine and beta-adenosintriphosphate were not different after training within the skeletal muscle at rest (beta-ATP/phosphocreatine, 0.29+/-0.06 vs. 0.28+/-0.04).\n\nQuestion:\nDoes concentric resistance training increase muscle strength without affecting microcirculation?", "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:\nWhile the evidence is conclusive regarding the positive effects of endurance training, there is still some controversy regarding the effects of resistance training on muscular capillarity. Thus, the purpose was to assess whether resistance strength training influences resting skeletal muscle microcirculation in vivo. Thirty-nine middle-aged subjects (15 female, 24 male; mean age, 54+/-9 years) were trained twice a week on an isokinetic system (altogether 16 sessions lasting 50 min, intensity 75% of maximum isokinetic and isometric force of knee flexors and extensors). To evaluate success of training, cross-sectional area (CSA) of the quadriceps femoris muscle and its isokinetic and isometric force were quantified. Muscular capillarization was measured in biopsies of the vastus lateralis muscle. In vivo, muscular energy and lipid metabolites were quantified by magnetic resonance spectroscopy and parameters of muscular microcirculation, such as local blood volume, blood flow and velocity, by contrast-enhanced ultrasound analyzing replenishment kinetics. The significant (P<0.001) increase in CSA (60+/-16 before vs. 64+/-15 cm(2) after training) and in absolute muscle strength (isometric, 146+/-44 vs. 174+/-50 Nm; isokinetic, 151+/-53 vs. 174+/-62 Nm) demonstrated successful training. Neither capillary density ex vivo (351+/-75 vs. 326+/-62) nor ultrasonographic parameters of resting muscle perfusion were significantly different (blood flow, 1.2+/-1.2 vs. 1.1+/-1.1 ml/min/100g; blood flow velocity, 0.49+/-0.44 vs. 0.52+/-0.74 mms(-1)). Also, the intensities of high-energy phosphates phosphocreatine and beta-adenosintriphosphate were not different after training within the skeletal muscle at rest (beta-ATP/phosphocreatine, 0.29+/-0.06 vs. 0.28+/-0.04).\n\nQuestion:\nDoes concentric resistance training increase muscle strength without affecting microcirculation?", "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:\nWhile the evidence is conclusive regarding the positive effects of endurance training, there is still some controversy regarding the effects of resistance training on muscular capillarity. Thus, the purpose was to assess whether resistance strength training influences resting skeletal muscle microcirculation in vivo. Thirty-nine middle-aged subjects (15 female, 24 male; mean age, 54+/-9 years) were trained twice a week on an isokinetic system (altogether 16 sessions lasting 50 min, intensity 75% of maximum isokinetic and isometric force of knee flexors and extensors). To evaluate success of training, cross-sectional area (CSA) of the quadriceps femoris muscle and its isokinetic and isometric force were quantified. Muscular capillarization was measured in biopsies of the vastus lateralis muscle. In vivo, muscular energy and lipid metabolites were quantified by magnetic resonance spectroscopy and parameters of muscular microcirculation, such as local blood volume, blood flow and velocity, by contrast-enhanced ultrasound analyzing replenishment kinetics. The significant (P<0.001) increase in CSA (60+/-16 before vs. 64+/-15 cm(2) after training) and in absolute muscle strength (isometric, 146+/-44 vs. 174+/-50 Nm; isokinetic, 151+/-53 vs. 174+/-62 Nm) demonstrated successful training. Neither capillary density ex vivo (351+/-75 vs. 326+/-62) nor ultrasonographic parameters of resting muscle perfusion were significantly different (blood flow, 1.2+/-1.2 vs. 1.1+/-1.1 ml/min/100g; blood flow velocity, 0.49+/-0.44 vs. 0.52+/-0.74 mms(-1)). Also, the intensities of high-energy phosphates phosphocreatine and beta-adenosintriphosphate were not different after training within the skeletal muscle at rest (beta-ATP/phosphocreatine, 0.29+/-0.06 vs. 0.28+/-0.04).\n\nQuestion:\nDoes concentric resistance training increase muscle strength without affecting microcirculation?", "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 of electroacupuncture stimulation on behavioral changes and neuronal nitric oxide synthase expression in the rat spinal cord after nerve injury. Under pentobarbital anesthesia, male Sprague-Dawley rats were subjected to neuropathic surgery by tightly ligating and cutting the left tibial and sural nerves. Behavioral responses to mechanical stimulation were tested for 2 weeks post-operatively. At the end of behavioral testing, electroacupuncture stimulation was applied to ST36 (Choksamni) and SP9 (Eumleungcheon) acupoints. Immunocytochemical staining was performed to investigate changes in the expression of neuronal nitric oxide synthase-immunoreactive neurons in the L4-5 spinal cord. Mechanical allodynia was observed by nerve injury. The mechanical allodynia was decreased after electroacupuncture stimulation. Neuronal nitric oxide synthase expression was also decreased in L4-5 spinal cord by electroacupuncture treatment.\n\nQuestion:\nDoes acute electroacupuncture inhibit nitric oxide synthase expression in the spinal cord of neuropathic 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 of electroacupuncture stimulation on behavioral changes and neuronal nitric oxide synthase expression in the rat spinal cord after nerve injury. Under pentobarbital anesthesia, male Sprague-Dawley rats were subjected to neuropathic surgery by tightly ligating and cutting the left tibial and sural nerves. Behavioral responses to mechanical stimulation were tested for 2 weeks post-operatively. At the end of behavioral testing, electroacupuncture stimulation was applied to ST36 (Choksamni) and SP9 (Eumleungcheon) acupoints. Immunocytochemical staining was performed to investigate changes in the expression of neuronal nitric oxide synthase-immunoreactive neurons in the L4-5 spinal cord. Mechanical allodynia was observed by nerve injury. The mechanical allodynia was decreased after electroacupuncture stimulation. Neuronal nitric oxide synthase expression was also decreased in L4-5 spinal cord by electroacupuncture treatment.\n\nQuestion:\nDoes acute electroacupuncture inhibit nitric oxide synthase expression in the spinal cord of neuropathic 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 of electroacupuncture stimulation on behavioral changes and neuronal nitric oxide synthase expression in the rat spinal cord after nerve injury. Under pentobarbital anesthesia, male Sprague-Dawley rats were subjected to neuropathic surgery by tightly ligating and cutting the left tibial and sural nerves. Behavioral responses to mechanical stimulation were tested for 2 weeks post-operatively. At the end of behavioral testing, electroacupuncture stimulation was applied to ST36 (Choksamni) and SP9 (Eumleungcheon) acupoints. Immunocytochemical staining was performed to investigate changes in the expression of neuronal nitric oxide synthase-immunoreactive neurons in the L4-5 spinal cord. Mechanical allodynia was observed by nerve injury. The mechanical allodynia was decreased after electroacupuncture stimulation. Neuronal nitric oxide synthase expression was also decreased in L4-5 spinal cord by electroacupuncture treatment.\n\nQuestion:\nDoes acute electroacupuncture inhibit nitric oxide synthase expression in the spinal cord of neuropathic 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:\nWe evaluated changes in liver function parameters and risk factors for the deterioration of liver function 12 months after percutaneous radiofrequency ablation (RFA) therapy in patients with hepatocellular carcinoma (HCC). The subjects in this retrospective study comprised 102 patients with HCC who had undergone RFA therapy and exhibited no recurrence of HCC 12 months thereafter. Serial changes in serum total bilirubin and albumin, prothrombin time, and Child-Pugh score were evaluated before RFA and 3, 6, 9, and 12 months thereafter. Deterioration of liver function was defined when the Child-Pugh score increased by at least 2 at 12 months after RFA therapy. We determined the factors related to aggravation of liver function after RFA therapy. Liver function had deteriorated 12 months after RFA in 29 patients (28.4%). Serum albumin levels decreased significantly from before (3.7±0.1 g/dL, mean±SD) to 12 months after RFA therapy (3.3±0.1 g/dL, P=0.002). The Child-Pugh score increased significantly during the same time period (from 6.1±0.2 to 7.2±0.3, P<0.001). Pre-RFA thrombocytopenia (≤100,000/mm(3)) was revealed as a significant risk factor for the deterioration of liver function after RFA. However, no patients had episodes of bleeding as a complication of RFA.\n\nQuestion:\nDoes thrombocytopenia represent a risk for deterioration of liver function after radiofrequency ablation in patients with 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:\nWe evaluated changes in liver function parameters and risk factors for the deterioration of liver function 12 months after percutaneous radiofrequency ablation (RFA) therapy in patients with hepatocellular carcinoma (HCC). The subjects in this retrospective study comprised 102 patients with HCC who had undergone RFA therapy and exhibited no recurrence of HCC 12 months thereafter. Serial changes in serum total bilirubin and albumin, prothrombin time, and Child-Pugh score were evaluated before RFA and 3, 6, 9, and 12 months thereafter. Deterioration of liver function was defined when the Child-Pugh score increased by at least 2 at 12 months after RFA therapy. We determined the factors related to aggravation of liver function after RFA therapy. Liver function had deteriorated 12 months after RFA in 29 patients (28.4%). Serum albumin levels decreased significantly from before (3.7±0.1 g/dL, mean±SD) to 12 months after RFA therapy (3.3±0.1 g/dL, P=0.002). The Child-Pugh score increased significantly during the same time period (from 6.1±0.2 to 7.2±0.3, P<0.001). Pre-RFA thrombocytopenia (≤100,000/mm(3)) was revealed as a significant risk factor for the deterioration of liver function after RFA. However, no patients had episodes of bleeding as a complication of RFA.\n\nQuestion:\nDoes thrombocytopenia represent a risk for deterioration of liver function after radiofrequency ablation in patients with 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:\nWe evaluated changes in liver function parameters and risk factors for the deterioration of liver function 12 months after percutaneous radiofrequency ablation (RFA) therapy in patients with hepatocellular carcinoma (HCC). The subjects in this retrospective study comprised 102 patients with HCC who had undergone RFA therapy and exhibited no recurrence of HCC 12 months thereafter. Serial changes in serum total bilirubin and albumin, prothrombin time, and Child-Pugh score were evaluated before RFA and 3, 6, 9, and 12 months thereafter. Deterioration of liver function was defined when the Child-Pugh score increased by at least 2 at 12 months after RFA therapy. We determined the factors related to aggravation of liver function after RFA therapy. Liver function had deteriorated 12 months after RFA in 29 patients (28.4%). Serum albumin levels decreased significantly from before (3.7±0.1 g/dL, mean±SD) to 12 months after RFA therapy (3.3±0.1 g/dL, P=0.002). The Child-Pugh score increased significantly during the same time period (from 6.1±0.2 to 7.2±0.3, P<0.001). Pre-RFA thrombocytopenia (≤100,000/mm(3)) was revealed as a significant risk factor for the deterioration of liver function after RFA. However, no patients had episodes of bleeding as a complication of RFA.\n\nQuestion:\nDoes thrombocytopenia represent a risk for deterioration of liver function after radiofrequency ablation in patients with 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:\nAge-related macular degeneration (AMD) is the most common cause of irreversible visual impairment in the developed world. The two forms of advanced AMD, geographic atrophy and neovascular AMD, represent different pathological processes in the macula that lead to loss of central vision. Soft drusen, characterized by deposits in the macula without visual loss, are considered to be a precursor of advanced AMD. Recently, it has been proposed that a common missense variant, Y402H, in the Complement Factor H (CFH) gene increases the risk for advanced AMD. However, its impact on soft drusen, GA, or neovascular AMD--or the relationship between them--is unclear. We genotyped 581 Icelandic patients with advanced AMD (278 neovascular AMD, 203 GA, and 100 with mixed neovascular AMD/GA), and 435 with early AMD (of whom 220 had soft drusen). A second cohort of 431 US patients from Utah, 322 with advanced AMD (244 neovascular AMD and 78 GA) and 109 early-AMD cases with soft drusen, were analyzed. We confirmed that the CFH Y402H variant shows significant association to advanced AMD, with odds ratio of 2.39 in Icelandic patients (p = 5.9 x 10(-12)) and odds ratio of 2.14 in US patients from Utah (p = 2.0 x 10(-9)) with advanced AMD. Furthermore, we show that the Y402H variant confers similar risk of soft drusen and both forms of advanced AMD (GA or neovascular AMD).\n\nQuestion:\nDoes cFH Y402H confer similar risk of soft drusen and both forms of advanced AMD?", "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:\nAge-related macular degeneration (AMD) is the most common cause of irreversible visual impairment in the developed world. The two forms of advanced AMD, geographic atrophy and neovascular AMD, represent different pathological processes in the macula that lead to loss of central vision. Soft drusen, characterized by deposits in the macula without visual loss, are considered to be a precursor of advanced AMD. Recently, it has been proposed that a common missense variant, Y402H, in the Complement Factor H (CFH) gene increases the risk for advanced AMD. However, its impact on soft drusen, GA, or neovascular AMD--or the relationship between them--is unclear. We genotyped 581 Icelandic patients with advanced AMD (278 neovascular AMD, 203 GA, and 100 with mixed neovascular AMD/GA), and 435 with early AMD (of whom 220 had soft drusen). A second cohort of 431 US patients from Utah, 322 with advanced AMD (244 neovascular AMD and 78 GA) and 109 early-AMD cases with soft drusen, were analyzed. We confirmed that the CFH Y402H variant shows significant association to advanced AMD, with odds ratio of 2.39 in Icelandic patients (p = 5.9 x 10(-12)) and odds ratio of 2.14 in US patients from Utah (p = 2.0 x 10(-9)) with advanced AMD. Furthermore, we show that the Y402H variant confers similar risk of soft drusen and both forms of advanced AMD (GA or neovascular AMD).\n\nQuestion:\nDoes cFH Y402H confer similar risk of soft drusen and both forms of advanced AMD?", "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:\nAge-related macular degeneration (AMD) is the most common cause of irreversible visual impairment in the developed world. The two forms of advanced AMD, geographic atrophy and neovascular AMD, represent different pathological processes in the macula that lead to loss of central vision. Soft drusen, characterized by deposits in the macula without visual loss, are considered to be a precursor of advanced AMD. Recently, it has been proposed that a common missense variant, Y402H, in the Complement Factor H (CFH) gene increases the risk for advanced AMD. However, its impact on soft drusen, GA, or neovascular AMD--or the relationship between them--is unclear. We genotyped 581 Icelandic patients with advanced AMD (278 neovascular AMD, 203 GA, and 100 with mixed neovascular AMD/GA), and 435 with early AMD (of whom 220 had soft drusen). A second cohort of 431 US patients from Utah, 322 with advanced AMD (244 neovascular AMD and 78 GA) and 109 early-AMD cases with soft drusen, were analyzed. We confirmed that the CFH Y402H variant shows significant association to advanced AMD, with odds ratio of 2.39 in Icelandic patients (p = 5.9 x 10(-12)) and odds ratio of 2.14 in US patients from Utah (p = 2.0 x 10(-9)) with advanced AMD. Furthermore, we show that the Y402H variant confers similar risk of soft drusen and both forms of advanced AMD (GA or neovascular AMD).\n\nQuestion:\nDoes cFH Y402H confer similar risk of soft drusen and both forms of advanced AMD?", "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 compared the educational value of a multimedia module about aortic valve replacement as a preparation for the operating room with a print medium of identical content. One hundred twenty-six students were randomly assigned in a prospective study to either use the multimedia course (n = 69) or a print version (n = 57). A 20-item multiple-choice test was performed before and after learning with the respective medium. Both groups participated in an operation during which they were evaluated with 28 standardized tasks and questions. Individual motivation, computer literacy, and didactic quality of both media were assessed with psychometric tests. There were no significant differences in the multiple-choice pretest (multimedia, 30.6% +/- 12.4% versus print, 27.9% +/- 11.4%) and posttest responses (multimedia, 76.7% +/- 13.3% versus print, 76.9% +/- 11.1). Mean percentage of correct answers during the operation was 82.9% +/- 10% in the online group and 64.7% +/- 12% in the print group (p < 0.0001). The multimedia group needed significantly (p < 0.001) less study time (105 +/- 24 minutes) when compared with the text group (122 +/- 30 minutes). There were no statistically significant differences in motivation, computer literacy, and didactic quality of either medium.\n\nQuestion:\nDoes multimedia-driven teaching significantly improve students ' performance when compared with a print medium?", "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 compared the educational value of a multimedia module about aortic valve replacement as a preparation for the operating room with a print medium of identical content. One hundred twenty-six students were randomly assigned in a prospective study to either use the multimedia course (n = 69) or a print version (n = 57). A 20-item multiple-choice test was performed before and after learning with the respective medium. Both groups participated in an operation during which they were evaluated with 28 standardized tasks and questions. Individual motivation, computer literacy, and didactic quality of both media were assessed with psychometric tests. There were no significant differences in the multiple-choice pretest (multimedia, 30.6% +/- 12.4% versus print, 27.9% +/- 11.4%) and posttest responses (multimedia, 76.7% +/- 13.3% versus print, 76.9% +/- 11.1). Mean percentage of correct answers during the operation was 82.9% +/- 10% in the online group and 64.7% +/- 12% in the print group (p < 0.0001). The multimedia group needed significantly (p < 0.001) less study time (105 +/- 24 minutes) when compared with the text group (122 +/- 30 minutes). There were no statistically significant differences in motivation, computer literacy, and didactic quality of either medium.\n\nQuestion:\nDoes multimedia-driven teaching significantly improve students ' performance when compared with a print medium?", "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 compared the educational value of a multimedia module about aortic valve replacement as a preparation for the operating room with a print medium of identical content. One hundred twenty-six students were randomly assigned in a prospective study to either use the multimedia course (n = 69) or a print version (n = 57). A 20-item multiple-choice test was performed before and after learning with the respective medium. Both groups participated in an operation during which they were evaluated with 28 standardized tasks and questions. Individual motivation, computer literacy, and didactic quality of both media were assessed with psychometric tests. There were no significant differences in the multiple-choice pretest (multimedia, 30.6% +/- 12.4% versus print, 27.9% +/- 11.4%) and posttest responses (multimedia, 76.7% +/- 13.3% versus print, 76.9% +/- 11.1). Mean percentage of correct answers during the operation was 82.9% +/- 10% in the online group and 64.7% +/- 12% in the print group (p < 0.0001). The multimedia group needed significantly (p < 0.001) less study time (105 +/- 24 minutes) when compared with the text group (122 +/- 30 minutes). There were no statistically significant differences in motivation, computer literacy, and didactic quality of either medium.\n\nQuestion:\nDoes multimedia-driven teaching significantly improve students ' performance when compared with a print medium?", "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 examined subjective age and its cross-domain correlates in Chinese oldest-old. We conducted a secondary data analysis using cross-sectional data drawn from the 2006 Sample Survey on the Aged Population in Urban/Rural China, which consisted of a sample of 860 community-dwelling Chinese older adults aged 85 years and above. A small percentage (8%) of the oldest-old participants reported that they did not feel old. Binary logistic regression analyses revealed that urban living, better physical and self-reported cognitive functioning and mental health were all related to not feeling old, whereas chronological age was found to have no association with subjective age when controlling for indicators of physical and self-reported cognitive functioning.\n\nQuestion:\nDoes the cross-domain correlate of subjective age in Chinese oldest-old?", "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 examined subjective age and its cross-domain correlates in Chinese oldest-old. We conducted a secondary data analysis using cross-sectional data drawn from the 2006 Sample Survey on the Aged Population in Urban/Rural China, which consisted of a sample of 860 community-dwelling Chinese older adults aged 85 years and above. A small percentage (8%) of the oldest-old participants reported that they did not feel old. Binary logistic regression analyses revealed that urban living, better physical and self-reported cognitive functioning and mental health were all related to not feeling old, whereas chronological age was found to have no association with subjective age when controlling for indicators of physical and self-reported cognitive functioning.\n\nQuestion:\nDoes the cross-domain correlate of subjective age in Chinese oldest-old?", "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 examined subjective age and its cross-domain correlates in Chinese oldest-old. We conducted a secondary data analysis using cross-sectional data drawn from the 2006 Sample Survey on the Aged Population in Urban/Rural China, which consisted of a sample of 860 community-dwelling Chinese older adults aged 85 years and above. A small percentage (8%) of the oldest-old participants reported that they did not feel old. Binary logistic regression analyses revealed that urban living, better physical and self-reported cognitive functioning and mental health were all related to not feeling old, whereas chronological age was found to have no association with subjective age when controlling for indicators of physical and self-reported cognitive functioning.\n\nQuestion:\nDoes the cross-domain correlate of subjective age in Chinese oldest-old?", "role": "user" } ]