Liver injuries are repaired by fibrosis and regeneration.The cause of fibrosis and diminished regeneration,especially in liver cirrhosis,is still unknown.Epithelialmesenchymal transition(EMT) has been found to be asso...Liver injuries are repaired by fibrosis and regeneration.The cause of fibrosis and diminished regeneration,especially in liver cirrhosis,is still unknown.Epithelialmesenchymal transition(EMT) has been found to be associated with liver fibrosis.The possibility that EMT could contribute to hepatic fibrogenesis reinforced the concept that activated hepatic stellate cells are not the only key players in the hepatic fibrogenic process and that other cell types,either hepatic or bone marrow-derived cells could contribute to this process.Following an initial enthusiasm for the discovery of this novel pathway in fibrogenesis,more recent research has started to cast serious doubts upon the real relevance of this phenomenon in human fibrogenetic disorders.The debate on the authenticity of EMT or on its contribution to the fibrogenic process has become very animated.The overall result is a general confusion on the meaning and on the definition of several key aspects.The aim of this article is to describe how EMT participates to hepatic fibrosis and discuss the evidence of supporting this possibility in order to reach reasonable and useful conclusions.展开更多
Chronic liver diseases with different aetiologies rely on the chronic activation of liver injuries which result in a fibrogenesis progression to the end stage of cirrhosis and liver failure.Based on the underlying cel...Chronic liver diseases with different aetiologies rely on the chronic activation of liver injuries which result in a fibrogenesis progression to the end stage of cirrhosis and liver failure.Based on the underlying cellular and molecular mechanisms of a liver fibrosis,there has been proposed several kinds of approaches for the treatment of liver fibrosis.Recently,liver gene therapy has been developed as an alternative way to liver transplantation,which is the only effective therapy for chronic liver diseases.The activation of hepatic stellate cells,a subsequent release of inflammatory cytokines and an accumulation of extracellular matrix during the liver fibrogenesis are the major obstacles to the treatment of liver fibrosis.Several targeted strategies have been developed,such as antisense oligodeoxynucleotides,RNA interference and decoy oligodeoxynucleotides to overcome this barriers.With this report an overview will be provided of targeted strategies for the treatment of liver cirrhosis,and particularly,of the targeted gene therapy using short RNA and DNA segments.展开更多
Aging behavior of Mg-3.6Y-0.5Zr and Mg-2.TNd-0.5Zr alloys was investigated by microhardness measurement and transmission electron microscopy.In the case of Mg-Y-Zr alloy,the presence ofβ″phase,a major strength- ener...Aging behavior of Mg-3.6Y-0.5Zr and Mg-2.TNd-0.5Zr alloys was investigated by microhardness measurement and transmission electron microscopy.In the case of Mg-Y-Zr alloy,the presence ofβ″phase,a major strength- ener,having base centered orthorhombic structure with its lattice constants of a-（β″）=0.64 nm,b-（β″）=2.22 nm, and c-（β″）=0.52 nm was identified.In the case of Mg-Nd-Zr alloy aged at 250℃,the presence ofβ″andβ′phases was identified.The crystal structure ofβ″phase was found to be DO-（19） and its orientation relationships with Mg matrix were [0001]-（β″）//[0001]-（Mg） and [01（？）0]-（β″）//[01（？）0]-（Mg）.Theβ′phase had face centered cubic structure and its orientation relationships with Mg matrix were [011]-（β′）//[0001]-（Mg） and [（？）1（？）]β′//[（？）110]）-（Mg）. The Mg-2.TNd-0.5Zr alloy showed higher hardness compared with Mg-3.6Y-0.5Zr alloy.展开更多
基金Supported by The National Research Foundation of Korea Grant funded by the Korean Government,No.2012R1A1A401015639
文摘Liver injuries are repaired by fibrosis and regeneration.The cause of fibrosis and diminished regeneration,especially in liver cirrhosis,is still unknown.Epithelialmesenchymal transition(EMT) has been found to be associated with liver fibrosis.The possibility that EMT could contribute to hepatic fibrogenesis reinforced the concept that activated hepatic stellate cells are not the only key players in the hepatic fibrogenic process and that other cell types,either hepatic or bone marrow-derived cells could contribute to this process.Following an initial enthusiasm for the discovery of this novel pathway in fibrogenesis,more recent research has started to cast serious doubts upon the real relevance of this phenomenon in human fibrogenetic disorders.The debate on the authenticity of EMT or on its contribution to the fibrogenic process has become very animated.The overall result is a general confusion on the meaning and on the definition of several key aspects.The aim of this article is to describe how EMT participates to hepatic fibrosis and discuss the evidence of supporting this possibility in order to reach reasonable and useful conclusions.
基金Supported by National Research Foundation of Korea Grant funded by the Korean Government,No.2012R1A1A401015639
文摘Chronic liver diseases with different aetiologies rely on the chronic activation of liver injuries which result in a fibrogenesis progression to the end stage of cirrhosis and liver failure.Based on the underlying cellular and molecular mechanisms of a liver fibrosis,there has been proposed several kinds of approaches for the treatment of liver fibrosis.Recently,liver gene therapy has been developed as an alternative way to liver transplantation,which is the only effective therapy for chronic liver diseases.The activation of hepatic stellate cells,a subsequent release of inflammatory cytokines and an accumulation of extracellular matrix during the liver fibrogenesis are the major obstacles to the treatment of liver fibrosis.Several targeted strategies have been developed,such as antisense oligodeoxynucleotides,RNA interference and decoy oligodeoxynucleotides to overcome this barriers.With this report an overview will be provided of targeted strategies for the treatment of liver cirrhosis,and particularly,of the targeted gene therapy using short RNA and DNA segments.
文摘Aging behavior of Mg-3.6Y-0.5Zr and Mg-2.TNd-0.5Zr alloys was investigated by microhardness measurement and transmission electron microscopy.In the case of Mg-Y-Zr alloy,the presence ofβ″phase,a major strength- ener,having base centered orthorhombic structure with its lattice constants of a-（β″）=0.64 nm,b-（β″）=2.22 nm, and c-（β″）=0.52 nm was identified.In the case of Mg-Nd-Zr alloy aged at 250℃,the presence ofβ″andβ′phases was identified.The crystal structure ofβ″phase was found to be DO-（19） and its orientation relationships with Mg matrix were [0001]-（β″）//[0001]-（Mg） and [01（？）0]-（β″）//[01（？）0]-（Mg）.Theβ′phase had face centered cubic structure and its orientation relationships with Mg matrix were [011]-（β′）//[0001]-（Mg） and [（？）1（？）]β′//[（？）110]）-（Mg）. The Mg-2.TNd-0.5Zr alloy showed higher hardness compared with Mg-3.6Y-0.5Zr alloy.
