hepatocellular injury
- 网络肝细胞损伤;肝细胞性损伤
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Investigation on Double Direction Regulating and Controlling of Tissue Transglutaminase in Hepatocellular Injury and Proliferation
组织转谷氨酰胺酶在肝细胞损伤和增生中的双向调控机制的研究
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Conclusions Heavy alcohol intake is a risk factor of As , and its mechanisms is related to the lipid metabolic disturbance caused by chronic hepatocellular injury .
结论酗酒是汉人As的危险因子,其机制与慢性肝细胞损伤致脂质代谢紊乱有关。
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Mechanism of acetaminophen - induced hepatocellular injury
扑热息痛引起肝细胞损害的机制
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Protective effect of taurine and branched chain amino acid on lipid peroxidation in cultured hepatocellular injury in rats
牛磺酸和支链氨基酸对大鼠肝细胞氧化损伤的保护作用
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It suggests the protection , which is associated with anti-lipid peroxidation , of GPS on CCl_4 induced hepatocellular injury in vitro .
提示GPS能减轻CCL4能减轻CCl4对离体培养的大鼠肝细胞损伤,保护肝细胞DNA合成,其作用机理与抗脂质过氧化有关。
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Objective To study whether the melatonin ( MT ) can attenuate hepatocellular injury caused by ischemia-reperfusion ( I / R ) injury in rat liver .
目的利用大鼠肝脏热缺血再灌注(I/R)损伤模型,研究褪黑素(MT)对再灌注损伤肝脏的保护作用。
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Conclusion Taurine and branched chain amino acid can protect the hepatocytes injured by CCl 4 . The possible mechanism is the prevention of lipid peroxidation in cultured hepatocellular injury .
结论牛磺酸和支链氨基酸对CCl4所致的肝细胞损伤具有保护功能,其保护作用可能是通过抗脂质过氧化作用实现的。
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The HBV replication cycle is not directly cytotoxic to hepatocytes . It is now thought that host immune responses to viral antigens displayed on infected hepatocytes are the principal determinants of hepatocellular injury .
HBV的复制并不会直接对肝细胞造成损害,现在认为在感染的肝细胞中,宿主的免疫系统对病毒抗原的反应是肝损害的决定因素,机理不完全清楚。
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Than in healthy controls . The results indicate that NK activity , CD8 + T-cell subset and CD4 / CD8 ratio in patients with acute hepatitis C were relationship with the hepatocellular injury in patients with acute hepatitis C.
CD8~+T细胞亚群百分比的增加,可能与急性丙型肝炎患者的肝细胞损伤及发病机制有关。
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The substances resulted from inflammation , like reactive oxygen species and NO , cause hepatocellular injury and gene mutation . Consequently , tumor cells are formed . IFN - γ is a multifunctional cytokine , which plays an important part in the immune response of anti-infection and anti-tumor .
炎症反应过程中产生的活性氧、NO等能够损伤肝细胞引起细胞发生基因突变形成肿瘤细胞IFN-γ是一种多功能细胞因子,在机体的抗感染、抗肿瘤免疫反应中发挥重要作用。
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To study the relationship between hepatocellular injury in hepatitis B patient and hepatocyte stimulator substance , HSS )、 interleukin-8 ( IL-8 ), enzyme linked immunohistochemical assay ( ELISA ) was performed in 177 patients with hepatitis B to determine the serum levels of IL-8 and HSS .
为研究乙肝患者的肝细胞损害与白细胞介素8(IL-8)及肝细胞刺激物质(HSS)的关系,本文应用ELISA法检测177例乙肝患者血清的IL-8和HSS含量。
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Hepatocellular injury during hepatitis B virus ( HBV ) infection is postulated ^ to result from an human leucocyte antigen ( HLA ) restricted T-cell host immune response against HBV antigens . However , it is not known if HBV itself can induce HLA expression on infected hepatocytes .
乙型肝炎病毒(HBV)所致的肝细胞坏死,被认为是与人类白细胞抗原(HLA)有关的MHC限制的T细胞为主的免疫应答的结果。
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Conclusion : CD 54 was strongly expressed in HCC , but this could not evoke effective anti tumor immune response and / or induce hepatocellular immune injury . This may be related to the lower expression rate of HLA ABC .
结论:CD54在HCC组织中高度表达并不能引起有效抗肿瘤免疫应答和肝细胞免疫损伤,这可能与HLA-ABC表达率较低有关。
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CONCLUSION The hepatocellular immune injury and effective anti-tumor immune response might be induced by sufficient expression of CD54 , CD80 , CD86 and HLA-ABC concurrently , and absence or poor expression of CD80 and CD86 might be the main reason for immune escape of hepatocarcinoma .
结论CD54,CD80,CD86和HLA-ABC在LC和HCA3中的同时足量表达有可能引起肝细胞损伤和有效抗肿瘤免疫应答,而CD80,CD86表达的缺失或不足可能是HCC产生免疫逃避的主要原因。