Cholesterol gallstone formation represents a failure of biliary cholesterol homeostasis in which the physical-chemical balance of cholesterol solubility in bile is disturbed.Lithogenic bile is mainly caused by persist...Cholesterol gallstone formation represents a failure of biliary cholesterol homeostasis in which the physical-chemical balance of cholesterol solubility in bile is disturbed.Lithogenic bile is mainly caused by persistent hepatic hypersecretion of biliary cholesterol and sustained cholesterol-supersaturated bile is an essential prerequisite for the precipitation of solid cholesterol monohydrate crystals and the formation of cholesterol gallstones.The metabolic determinants of the supply of hepatic cholesterol molecules that are recruited for biliary secretion are dependent upon the input-output balance of cholesterol and its catabolism in the liver.The sources of cholesterol for hepatic secretion into bile have been extensively investigated;however,to what extent each cholesterol source contributes to hepatic secretion is still unclear both under normal physiological conditions and in the lithogenic state.Although it has been long known that biliary lithogenicity is initiated by hepatic cholesterol hypersecretion,the genetic mechanisms that cause supersaturated bile have not been defined yet.Identification of the Lith genes that determine hepatic cholesterol hypersecretion should provide novel insights into the primary genetic and pathophysiological defects for gallstone formation.In this review article,we focus mainly on the pathogenesis of the formation of supersaturated bile and gallstones from the viewpoint of genetics and pathophysiology.A better understanding of the molecular genetics and pathophysiology of the formation of cholesterol-supersaturated bile will undoubtedly facilitate the development of novel,effective,and noninvasive therapies for patients with gallstones,which would reduce the morbidity,mortality,and costs of health care associated with gallstones,a very prevalent liver disease worldwide.展开更多
A novel PEO-based composite polymer electro-lyte by using organic-inorganic hybrid EO20PO70EO20-em- mesoporous silica (P123-em-SBA15) as the filler has been developed. The experiment results show that P123-em- SBA15 c...A novel PEO-based composite polymer electro-lyte by using organic-inorganic hybrid EO20PO70EO20-em- mesoporous silica (P123-em-SBA15) as the filler has been developed. The experiment results show that P123-em- SBA15 can enhance the lithium-ion transference number of the composite polymer electrolyte, which is induced by the special topology structure of P123 in P123-em-SBA15 hybrid. In addition, room temperature ionic conductivity of the composite polymer electrolyte can also be increased by about two orders of magnitude. The excellent lithium transport properties suggest that PEO-LiClO4-P123-em-SBA15 com-posite polymer electrolyte can be used as electrolyte materi-als for all solid-state rechargeable lithium polymer batteries.展开更多
基金This work was supported in part by research grants DK101793 and DK106249(to DQ-HW),both from the National Institutes of Health(US Public Health Service).
文摘Cholesterol gallstone formation represents a failure of biliary cholesterol homeostasis in which the physical-chemical balance of cholesterol solubility in bile is disturbed.Lithogenic bile is mainly caused by persistent hepatic hypersecretion of biliary cholesterol and sustained cholesterol-supersaturated bile is an essential prerequisite for the precipitation of solid cholesterol monohydrate crystals and the formation of cholesterol gallstones.The metabolic determinants of the supply of hepatic cholesterol molecules that are recruited for biliary secretion are dependent upon the input-output balance of cholesterol and its catabolism in the liver.The sources of cholesterol for hepatic secretion into bile have been extensively investigated;however,to what extent each cholesterol source contributes to hepatic secretion is still unclear both under normal physiological conditions and in the lithogenic state.Although it has been long known that biliary lithogenicity is initiated by hepatic cholesterol hypersecretion,the genetic mechanisms that cause supersaturated bile have not been defined yet.Identification of the Lith genes that determine hepatic cholesterol hypersecretion should provide novel insights into the primary genetic and pathophysiological defects for gallstone formation.In this review article,we focus mainly on the pathogenesis of the formation of supersaturated bile and gallstones from the viewpoint of genetics and pathophysiology.A better understanding of the molecular genetics and pathophysiology of the formation of cholesterol-supersaturated bile will undoubtedly facilitate the development of novel,effective,and noninvasive therapies for patients with gallstones,which would reduce the morbidity,mortality,and costs of health care associated with gallstones,a very prevalent liver disease worldwide.
文摘A novel PEO-based composite polymer electro-lyte by using organic-inorganic hybrid EO20PO70EO20-em- mesoporous silica (P123-em-SBA15) as the filler has been developed. The experiment results show that P123-em- SBA15 can enhance the lithium-ion transference number of the composite polymer electrolyte, which is induced by the special topology structure of P123 in P123-em-SBA15 hybrid. In addition, room temperature ionic conductivity of the composite polymer electrolyte can also be increased by about two orders of magnitude. The excellent lithium transport properties suggest that PEO-LiClO4-P123-em-SBA15 com-posite polymer electrolyte can be used as electrolyte materi-als for all solid-state rechargeable lithium polymer batteries.
