Prepore formation is hypothesized to be an obligate step in the insertion of Cry1Ab toxin into insect brush border membrane vesicles. We examined the architecture of the putative prepore when isolated using the publis...Prepore formation is hypothesized to be an obligate step in the insertion of Cry1Ab toxin into insect brush border membrane vesicles. We examined the architecture of the putative prepore when isolated using the published protocols [1] [2]. Our results demonstrate that the putative prepore form of Cry1Ab is a combination of receptor proteins attached to the toxin, when purified. The results also suggest that this prepore form as prepared by the methods published is different from other membrane-extracted oligomeric forms of Cry toxins and prepore of other toxins in general. While most other known prepores are composed of multimers of a single protein, the Cry1Ab prepore, as generated, is a protein-receptor complex oligomer and monomers of Cry toxins.展开更多
目的探讨急性脑梗死患者颈动脉粥样硬化斑块的稳定性与血管内皮功能的相关性。方法应用颈动脉彩色多普勒超声技术检查研究对象颈动脉粥样硬化斑块的大小、数目及性质。选取血管性假血友病因子(Von Willebrand factor,vWF)与可溶性血管...目的探讨急性脑梗死患者颈动脉粥样硬化斑块的稳定性与血管内皮功能的相关性。方法应用颈动脉彩色多普勒超声技术检查研究对象颈动脉粥样硬化斑块的大小、数目及性质。选取血管性假血友病因子(Von Willebrand factor,vWF)与可溶性血管内皮细胞蛋白C受体(Soluble endothelial protein C receptor,sEPCR)作为急性脑梗死患者血管内皮功能的评价指标。采用ELISA方法检测其血浆中vWF与sEPCR含量。根据颈动脉彩超的结果,将急性脑梗死患者分为不稳定性斑块脑梗死组、稳定性斑块脑梗死组,并选取健康对照组,组间比较采用独立样本t检验,并行简单相关分析。结果不稳定性斑块脑梗死组血浆中vWF与sEPCR含量显著高于稳定性斑块脑梗死组(P<0.001),急性脑梗死患者颈动脉粥样硬化斑块的稳定性与vWF及sEPCR呈负相关(P<0.001)。结论急性脑梗死患者血管内皮功能损伤越严重,则颈动脉粥样硬化斑块可能越不稳定。展开更多
The liver is unique in regenerative potential, which could recover the lost mass and function after injury from ischemia and resection. The underlying molecular mechanisms of liver regeneration have been extensively s...The liver is unique in regenerative potential, which could recover the lost mass and function after injury from ischemia and resection. The underlying molecular mechanisms of liver regeneration have been extensively studied in the past using the partial hepatectomy(PH) model in rodents, where 2/3 PH is carried out by removing two lobes. The whole process of liver regeneration is complicated, orchestrated event involving a network of connected interactions, which still remain fully elusive. Bile acids(BAs) are ligands of farnesoid X receptor(FXR), a nuclear receptor of ligand-activated transcription factor. FXR has been shown to be highly involved in liver regeneration. BAs and FXR not only interact with each other but also regulate various downstream targets independently during liver regeneration. Moreover, recent findings suggest that tissue-specific FXR also contributes to liver regeneration significantly. These novel findings suggest that FXR has much broader role than regulating BA, cholesterol, lipid and glucose metabolism. Therefore, these researches highlight FXR as an important pharmaceutical target for potentialuse of FXR ligands to regulate liver regeneration in clinic. This review focuses on the roles of BAs and FXR in liver regeneration and the current underlying molecular mechanisms which contribute to liver regeneration.展开更多
Background Deep venous thrombosis （DVT） can result in pulmonary embolism, a fatal complication that is due to the dislodgement and movement of a blood clot （thrombus） from a limb into the lungs. Genetic risk facto...Background Deep venous thrombosis （DVT） can result in pulmonary embolism, a fatal complication that is due to the dislodgement and movement of a blood clot （thrombus） from a limb into the lungs. Genetic risk factors related to DVT development include mutations in coagulation proteins, especially the endothelial protein C receptor （EPCR）, a component of the anticoagulation protein C （PC） pathway. The objective of the present study was to analyze the relationship between the 6936A/G polymorphism in the EPCR gene and the occurrence of DVT. Methods This study involved 65 patients with DVT and 71 age- and gender-matched healthy controls. Peripheral blood samples were collected from all subjects. Plasma levels of soluble EPCR （sEPCR） were measured by enzyme-linked immunosorbent assay. Genomic DNA was extracted and EPCR gene product was amplified by a standard PCR reaction. Gene product bands were sequenced to identify EPCR gene polymorphisms. Results In the control group, the level of sEPCR in subjects with 6936AG genotype was significantly higher than that in subjects with 6936AA genotype （（0.97_＋0.32） pg/ml vs. （0.61_＋0.24） pg/ml, P 〈0.01）. Similarly in the DVT group, the level of sEPCR in subjects with the 6936AG were greater than that in subjects with the 6936AA genotype （（0.87_-K）.21） pg/ml vs. （0.50-＋0.18） pg/ml, P 〈0.01）. The sEPCR level in DVT patients was significantly higher than that in healthy controls （（0.68_--K）.32） pg/ml vs. （0.54_--K）.22） pg/ml, P 〈0.05）. The 6936AG genotype frequency in DVT patients was significantly higher than that in healthy controls （P 〈0.05）. In contrast, the 6936AA genotype frequency in DVT patients was lower than that in healthy controls （P 〈0.05）. Subjects carrying 6936AG had an increased risk of thrombosis （OR=2.75, 95% CI： 1.04-7.30, P 〈0.05）. Conclusions EPCR gene 6936A/G polymorphism is associated with increased plasma levels of sEPCR. Subjects carrvinq 6936AG likely have an increa展开更多
文摘Prepore formation is hypothesized to be an obligate step in the insertion of Cry1Ab toxin into insect brush border membrane vesicles. We examined the architecture of the putative prepore when isolated using the published protocols [1] [2]. Our results demonstrate that the putative prepore form of Cry1Ab is a combination of receptor proteins attached to the toxin, when purified. The results also suggest that this prepore form as prepared by the methods published is different from other membrane-extracted oligomeric forms of Cry toxins and prepore of other toxins in general. While most other known prepores are composed of multimers of a single protein, the Cry1Ab prepore, as generated, is a protein-receptor complex oligomer and monomers of Cry toxins.
文摘目的探讨急性脑梗死患者颈动脉粥样硬化斑块的稳定性与血管内皮功能的相关性。方法应用颈动脉彩色多普勒超声技术检查研究对象颈动脉粥样硬化斑块的大小、数目及性质。选取血管性假血友病因子(Von Willebrand factor,vWF)与可溶性血管内皮细胞蛋白C受体(Soluble endothelial protein C receptor,sEPCR)作为急性脑梗死患者血管内皮功能的评价指标。采用ELISA方法检测其血浆中vWF与sEPCR含量。根据颈动脉彩超的结果,将急性脑梗死患者分为不稳定性斑块脑梗死组、稳定性斑块脑梗死组,并选取健康对照组,组间比较采用独立样本t检验,并行简单相关分析。结果不稳定性斑块脑梗死组血浆中vWF与sEPCR含量显著高于稳定性斑块脑梗死组(P<0.001),急性脑梗死患者颈动脉粥样硬化斑块的稳定性与vWF及sEPCR呈负相关(P<0.001)。结论急性脑梗死患者血管内皮功能损伤越严重,则颈动脉粥样硬化斑块可能越不稳定。
基金supported by the National Institutes of Health Fund (Nos.DK081343,DK090036 and GM104037 to Grace L.Guo)the National Natural Science Foundation of China (No.81302059)+2 种基金the Natural Science Foundation of Heilongjiang Province of China (No.LC2013C35)the Foundation of Educational Committee of Heilongjiang Province of China (No.12541300)supported by the Scientific Research Foundation for the Returned Overseas Chinese Scholars,State Education Ministry and Science Foundation for The Excellent Youth Scholars of the Fourth Hospital of Harbin Medical University in China
文摘The liver is unique in regenerative potential, which could recover the lost mass and function after injury from ischemia and resection. The underlying molecular mechanisms of liver regeneration have been extensively studied in the past using the partial hepatectomy(PH) model in rodents, where 2/3 PH is carried out by removing two lobes. The whole process of liver regeneration is complicated, orchestrated event involving a network of connected interactions, which still remain fully elusive. Bile acids(BAs) are ligands of farnesoid X receptor(FXR), a nuclear receptor of ligand-activated transcription factor. FXR has been shown to be highly involved in liver regeneration. BAs and FXR not only interact with each other but also regulate various downstream targets independently during liver regeneration. Moreover, recent findings suggest that tissue-specific FXR also contributes to liver regeneration significantly. These novel findings suggest that FXR has much broader role than regulating BA, cholesterol, lipid and glucose metabolism. Therefore, these researches highlight FXR as an important pharmaceutical target for potentialuse of FXR ligands to regulate liver regeneration in clinic. This review focuses on the roles of BAs and FXR in liver regeneration and the current underlying molecular mechanisms which contribute to liver regeneration.
文摘Background Deep venous thrombosis （DVT） can result in pulmonary embolism, a fatal complication that is due to the dislodgement and movement of a blood clot （thrombus） from a limb into the lungs. Genetic risk factors related to DVT development include mutations in coagulation proteins, especially the endothelial protein C receptor （EPCR）, a component of the anticoagulation protein C （PC） pathway. The objective of the present study was to analyze the relationship between the 6936A/G polymorphism in the EPCR gene and the occurrence of DVT. Methods This study involved 65 patients with DVT and 71 age- and gender-matched healthy controls. Peripheral blood samples were collected from all subjects. Plasma levels of soluble EPCR （sEPCR） were measured by enzyme-linked immunosorbent assay. Genomic DNA was extracted and EPCR gene product was amplified by a standard PCR reaction. Gene product bands were sequenced to identify EPCR gene polymorphisms. Results In the control group, the level of sEPCR in subjects with 6936AG genotype was significantly higher than that in subjects with 6936AA genotype （（0.97_＋0.32） pg/ml vs. （0.61_＋0.24） pg/ml, P 〈0.01）. Similarly in the DVT group, the level of sEPCR in subjects with the 6936AG were greater than that in subjects with the 6936AA genotype （（0.87_-K）.21） pg/ml vs. （0.50-＋0.18） pg/ml, P 〈0.01）. The sEPCR level in DVT patients was significantly higher than that in healthy controls （（0.68_--K）.32） pg/ml vs. （0.54_--K）.22） pg/ml, P 〈0.05）. The 6936AG genotype frequency in DVT patients was significantly higher than that in healthy controls （P 〈0.05）. In contrast, the 6936AA genotype frequency in DVT patients was lower than that in healthy controls （P 〈0.05）. Subjects carrying 6936AG had an increased risk of thrombosis （OR=2.75, 95% CI： 1.04-7.30, P 〈0.05）. Conclusions EPCR gene 6936A/G polymorphism is associated with increased plasma levels of sEPCR. Subjects carrvinq 6936AG likely have an increa
