BACKGROUND： Liver inflammation or hepatitis is a result of pluripotent interactions of cell death molecules, cytokines, chemokines and the resident immune cells collectively called as microenvironment. The interplay ...BACKGROUND： Liver inflammation or hepatitis is a result of pluripotent interactions of cell death molecules, cytokines, chemokines and the resident immune cells collectively called as microenvironment. The interplay of these inflammatory mediators and switching of immune responses during hepatotoxic, viral, drug-induced and immune cell-mediated hepatitis decide the fate of liver pathology. The present review aimed to describe the mechanisms of liver injury, its relevance to human liver pathology and insights for the future therapeutic interventions.DATA SOURCES： The data of mouse hepatic models and rele- vant human liver diseases presented in this review are system- atically collected from PubMed, ScienceDirect and the Web of Science databases published in English. RESULTS： The hepatotoxic liver injury in mice induced by the metabolites of CC14, acetaminophen or alcohol represent ne- crotic cell death with activation of cytochrome pathway, for- mation of reactive oxygen species （ROS） and mitochondrial damage. The Fas or TNF-a induced apoptotic liver injury was dependent on activation of caspases, release of cytochrome c and apoptosome formation. The ConA-hepatitis demonstrat- ed the involvement of TRAIL-dependent necrotic/necroptotic cell death with activation of RIPK1/3. The a-GalCer-induced liver injury was mediated by TNF-a. The LPS-induced hepatitis involved TNF-a, Fas/FasL, and perforin/granzyme cell death pathways. The MHV3 or Poly（I：C） induced liver injury was mediated by natural killer cells and TNF-a signaling. The necrotic ischemia-reperfusion liver injury was mediated by hypoxia, ROS, and pro-inflammatory cytokines; however, necroptotic cell death was found in partial hepatectomy. The crucial role of immune ceils and cell death mediators in viral hepatitis （HBV, HCV）, drug-induced liver injury, non-alcohol- ic fatty liver disease and alcoholic liver disease in human were discussed. CONCLUSIONS： The mouse animal models of hepatitis provide a parallel approach for the study of human liver pathology. Blocking or stimulating the pathways associated with liver cell death could unveil the novel therapeutic strategies in the management of liver diseases.展开更多
A system consisting of two atoms interacting with a two-mode vacuum is considered, where each atom is resonant with the two cavity modes through two different competing transitions. The effect of mode--mode competitio...A system consisting of two atoms interacting with a two-mode vacuum is considered, where each atom is resonant with the two cavity modes through two different competing transitions. The effect of mode--mode competition on the atom--atom entanglement is investigated. We find that the entanglement between the two atoms can be induced by the mode--mode competition. For the initial atomic state ｜／varPsi（0）／rangle, whether the atoms are initially separated or entangled, a large or even maximal entanglement between them can be obtained periodically by introducing the mode--mode competition. For the initial atomic state ｜／varPhi（0）／rangle, the strong mode--mode competition can prevent the two atoms entangled initially from suffering entanglement sudden death; besides, it makes them in a more stable and longer-lived entanglement than in the non-competition case.展开更多
Extending the double Jaynes Cummings model to a more complicated case where the mode-mode competition is considered, we investigate the entanglement character of two isolated atoms by means of concurrence, and discuss...Extending the double Jaynes Cummings model to a more complicated case where the mode-mode competition is considered, we investigate the entanglement character of two isolated atoms by means of concurrence, and discuss the dependence of atom atom entanglement on the different initial state and the relative coupling strength between the atom and the corresponding cavity field. The results show that the amplitude and the period of the atom atom entanglement evolution can be controlled by the choice of initial state and relative coupling strength, respectively. We find that the phenomenon of entanglement sudden death （ESD） is sensitive to the initial conditions. The length of the time interval for zero entanglement depends not only on the initial degree of entanglement between two atoms but also on the relative coupling strength of atom field interaction. The ESD effect can be weakened by enhancing the mode-mode competition between the three- and single-photon processes.展开更多
基金supported by a grant from Higher Education Commission(HEC)at University of Agriculture,Faisalabad,Pakistan(No.20-4613/NRPU/R&D/HEC/14/45)
文摘BACKGROUND： Liver inflammation or hepatitis is a result of pluripotent interactions of cell death molecules, cytokines, chemokines and the resident immune cells collectively called as microenvironment. The interplay of these inflammatory mediators and switching of immune responses during hepatotoxic, viral, drug-induced and immune cell-mediated hepatitis decide the fate of liver pathology. The present review aimed to describe the mechanisms of liver injury, its relevance to human liver pathology and insights for the future therapeutic interventions.DATA SOURCES： The data of mouse hepatic models and rele- vant human liver diseases presented in this review are system- atically collected from PubMed, ScienceDirect and the Web of Science databases published in English. RESULTS： The hepatotoxic liver injury in mice induced by the metabolites of CC14, acetaminophen or alcohol represent ne- crotic cell death with activation of cytochrome pathway, for- mation of reactive oxygen species （ROS） and mitochondrial damage. The Fas or TNF-a induced apoptotic liver injury was dependent on activation of caspases, release of cytochrome c and apoptosome formation. The ConA-hepatitis demonstrat- ed the involvement of TRAIL-dependent necrotic/necroptotic cell death with activation of RIPK1/3. The a-GalCer-induced liver injury was mediated by TNF-a. The LPS-induced hepatitis involved TNF-a, Fas/FasL, and perforin/granzyme cell death pathways. The MHV3 or Poly（I：C） induced liver injury was mediated by natural killer cells and TNF-a signaling. The necrotic ischemia-reperfusion liver injury was mediated by hypoxia, ROS, and pro-inflammatory cytokines; however, necroptotic cell death was found in partial hepatectomy. The crucial role of immune ceils and cell death mediators in viral hepatitis （HBV, HCV）, drug-induced liver injury, non-alcohol- ic fatty liver disease and alcoholic liver disease in human were discussed. CONCLUSIONS： The mouse animal models of hepatitis provide a parallel approach for the study of human liver pathology. Blocking or stimulating the pathways associated with liver cell death could unveil the novel therapeutic strategies in the management of liver diseases.
基金supported by the National Natural Science Foundation of China (Grant No. 10374025)the Foundation of Education Bureau of Hunan Province, China (Grant Nos. 06A038 and 06C080)the Zhanjiang Projects for Development of Science and Technology, China (Grant No. 2008C10019)
文摘A system consisting of two atoms interacting with a two-mode vacuum is considered, where each atom is resonant with the two cavity modes through two different competing transitions. The effect of mode--mode competition on the atom--atom entanglement is investigated. We find that the entanglement between the two atoms can be induced by the mode--mode competition. For the initial atomic state ｜／varPsi（0）／rangle, whether the atoms are initially separated or entangled, a large or even maximal entanglement between them can be obtained periodically by introducing the mode--mode competition. For the initial atomic state ｜／varPhi（0）／rangle, the strong mode--mode competition can prevent the two atoms entangled initially from suffering entanglement sudden death; besides, it makes them in a more stable and longer-lived entanglement than in the non-competition case.
基金Project supported by the National Natural Science Foundation of China (Grant No 10374025)the Foundation of Education Department of Hunan Province of China (Grant Nos 06A038 and 06C080)the Science and Technology Project of Zhanjiang City (Grant No 2008C10019)
文摘Extending the double Jaynes Cummings model to a more complicated case where the mode-mode competition is considered, we investigate the entanglement character of two isolated atoms by means of concurrence, and discuss the dependence of atom atom entanglement on the different initial state and the relative coupling strength between the atom and the corresponding cavity field. The results show that the amplitude and the period of the atom atom entanglement evolution can be controlled by the choice of initial state and relative coupling strength, respectively. We find that the phenomenon of entanglement sudden death （ESD） is sensitive to the initial conditions. The length of the time interval for zero entanglement depends not only on the initial degree of entanglement between two atoms but also on the relative coupling strength of atom field interaction. The ESD effect can be weakened by enhancing the mode-mode competition between the three- and single-photon processes.
