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脂肪变性肝细胞
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  “脂肪变性肝细胞”译为未确定词的双语例句
     Effects of TNF alpha on expression of SREBP-1c mRNA and triglyceride contents in cultured steatosis hepatocytes
     TNF-α对脂肪变性肝细胞SREBP-1c的表达及甘油三酯含量的影响
短句来源
     Objective To explore the effects of TNF alpha on the expression of sterol-regulatory element binding protein-1c, SREBP-1c mRNA and the content of triglyceride (TG) in the models of cultured steatosis hepatocytes.
     目的探讨TNF-α对油酸诱导的脂肪变性肝细胞模型固醇调节元件结合蛋白1c(sterol-regulatoryelementbindingprotein-1c,SREBP-1c)mRNA的表达及甘油三酯(triglyceride,TG)含量的影响。
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     It were indicated that lipid droplets in liver cells induced by VPA could partly prevented with coadministration of VitE+CoQ10,and the lipid droplets also was confirmed by electron microscopic examination.
     VitE+CoQ10干预后脂肪变性肝细胞数目显著减少(P<0.01)。
短句来源
     In addition,it was showed that the lipid droplets in liver cells induced by VPA could prevented by coadministration of L-carnitine.
     L-肉碱干预后脂肪变性肝细胞数均有非常显著减少(P<0.01),表明L-肉碱能有效的阻止肝细胞脂肪变性。
短句来源
     The difference was significant(P<0.01). These indicated that lipid droplets in liver cells induced by VPA could effectively prevented with coadministration of L-carnitine.
     L-肉碱干预后脂肪变性肝细胞数均有非常显著减少(P<0.01),表明L-肉碱能有效的阻止肝细胞脂肪变性。
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  相似匹配句对
     2. Decreasing fatty degeneration of liver cell;
     2、减轻肝细胞脂肪变性
短句来源
     2. Alleviate the fat denaturatiDn of the liver cells.
     2、减轻肝细胞脂肪变性
短句来源
     Liver Cell Adenoma
     肝细胞腺瘤
短句来源
     MRI Diagnosis of Hepatocellular Carcinoma
     肝细胞癌的MRI诊断
短句来源
     7.obviousl fat degeneration of liver;
     ⑦肝脏显著脂肪变性;
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An ABC immunohistochemical study was made in the experimental liver injuries of rat caused by butter yellow (DAB), CCl4 intoxification and liquid nitrogen-caused frostbite to investigate the abnormal cytokeratin (CK ) expression in hepatocytes. (1) It was demonstrated, in the liver injuries caused by the frostbite and DAB, that the hepatocyte necrosis without fat degeneration could not directly cause the change in CK expression; (2) It was showed that, in the DAB-injured livers, the abnormal CK expression in...

An ABC immunohistochemical study was made in the experimental liver injuries of rat caused by butter yellow (DAB), CCl4 intoxification and liquid nitrogen-caused frostbite to investigate the abnormal cytokeratin (CK ) expression in hepatocytes. (1) It was demonstrated, in the liver injuries caused by the frostbite and DAB, that the hepatocyte necrosis without fat degeneration could not directly cause the change in CK expression; (2) It was showed that, in the DAB-injured livers, the abnormal CK expression in hepatocytes was not caused by fibrosis, and it was related mainly with oval cell proliferation, which confirming the induction role of the oval cells on the change of the CK expression in the neighbouring hepatocytes. Laminin (LN) was suggested to be one of the mducers in this process produced by the oval cells; (3) The CK- and LN-immiinohistochemical localization on the CCl4-caused hepatitis and cirrhotic livers demonstrated that the abnormal CK expression was in accord with the abnormal LN deposition both in the time phase and in their location. It was suggested that the destruction of the hepatic lobular structure could influence the CK expression in hepatocytes through the abnormal LN deposition, and LN, maybe with other basement membrane molecules, might be a inducer also in this process; (4) A new model of liver injury was prepared in rat by the local freezing with liquid nitrogen. Until the 7th day after the injury, there appeared some CK19-positive hepatocytes around the necrosis caused by the frostbite. The abnormal CK expression decreased and stopped as soon as the heputocytes connected together to form a contact limiting plate-like structure enclosing the necrosis and the lobuiar structure was repaired. This is a strong support to our hypothesis that the expression of "bile duct type"CKs in hepatocytes be one of the adaptive reactions in the repair process of the lobular structure. The significance of the abnormal CK expression was discussed.

作者应用ABC免疫组织化学技术显示,奶油黄(DAB)、液氮致局部冻伤及CCl_4所致的3种肝损伤中也有细胞角蛋白(CK)异常表达肝细胞.①在肝局部冻伤及DAB性肝损伤模型中,表明不伴脂肪变性的肝细胞坏死不能直接引起肝细胞CK表达的改变;②在DAB性肝损伤中,肯定了卵园细胞对肝细胞CK表达改变的诱导作用,提出层粘连蛋白(LN)是卵园细胞产生的诱导物之一;③在CCl_4性肝炎及肝硬变中进行了CK和LN免疫细胞化学定位,表明肝细胞CK异常表达和LN异常沉积无论在位相上还是在时相上都密切相关,提出肝小叶结构破坏可能通过LN异常沉积而影响肝细胞的CK表达,LN等基底膜物质也是这一过程的诱导物;④在我们设计的一种局部肝冻伤模型上证实,肝细胞CK异常表达是肝小叶结构修复过程中肝细胞的适应性反应.

An immunohistochemical and immunoelectron microscopical study was made in the experimental liver injuries caused by butter yellow(DAB),CCl_4 intoxification and liquid nitrogen caused frostbite to investigate the abnormal cytokeratin(CK)expression in hepatocytes.The result was as follows:(1)In the liver injuries caused by the frostbite and DAB intoxification,the hepatocyte necrosis without fat degeneration could not directly cause the change in CK expression;(2) In the DAB-injuried livers,the proliferating oval...

An immunohistochemical and immunoelectron microscopical study was made in the experimental liver injuries caused by butter yellow(DAB),CCl_4 intoxification and liquid nitrogen caused frostbite to investigate the abnormal cytokeratin(CK)expression in hepatocytes.The result was as follows:(1)In the liver injuries caused by the frostbite and DAB intoxification,the hepatocyte necrosis without fat degeneration could not directly cause the change in CK expression;(2) In the DAB-injuried livers,the proliferating oval cells,which were closely related with the CK19-positive hepatocytes, might play an inductive role in the CK expression, and laminin(LN)was demonstrated to be one of the inducers in this process;(3)In CCl_4-caused hepatitis and cirrhotic livers,itwas demonstrated that the abnormal CK expression was in accord with the abnormal LN deposition both in the time phase and in their distribution patterns,which suggested that the destruction of the lobular structure might influence the CK expression in hepatocytes through the LN deposition;(4)The electron and immunoelectron microscopical observations showed that the remarkable changes in the intermediate filament cytoskeleton of the hepatocytes in the CCl_4-injuried livers were accompanied with the appearance of the antigenic determinants of CK19;(5)A new model of liver injury was prepared in rat by the local freezing with liquid nitrogen,in which the CK19-positive hepatocytes appeared when the intactness of the limiting membrane of the hepatic lobule being destructed together with the fibrotic tissue proliferation, and disappeared when the lobular structure was repaired.This is a strong support to our hypothesis that the abnormal expression in hepatocytes was one of the local regenerative reactions in the repair process of the lobular structure.The significance of the abnormal CK expression was discussed.

本研究应用ABC免疫组化技术显示,奶油黄、液氮致局部冻伤及CCl_4所致的三种肝损伤中也有细胞角蛋白(CK)异常表达肝细胞。(1)在局部肝冻伤及奶油黄性肝损伤中表明不伴脂肪变性的肝细胞坏死不能直接引起肝细胞CK表达的改变;(2)在奶油黄性肝损伤中显示了卵圆细胞对肝细胞CK异常表达的诱导作用,表明层粘连蛋白(LN)可能是这种作用的媒介;(3)在CCl_4致慢性肝损伤中表明肝细胞CK异常表达和LN异常沉积无论在位相上还是在时相上都一致,提出肝小叶结构破坏可能也是通过LN异常沉积而影响肝细胞的CK表达;(4)应用电镜及免疫电镜技术表明CCl_4性肝损伤中肝细胞中间丝细胞骨架结构的改变伴随着CK19阳性抗原决定簇的出现;(5)设计了一种局部肝冻伤模型,利用这种模型表明,CK19阳性肝细胞在肝小叶结构完整性遭到破坏且伴纤维组织增生时出现,随小叶结构的恢复而消失。这是对关于肝细胞CK异常表达是肝小叶结构修复过程中局部肝细胞的修复性反应这一假说的有力支持。讨论了这种改变的意义。

Aging changes of male rat liver (25, 28 and 31 m) were observed by Electron microscopy. The results were as follows- From 25 m on, the riucli of some liver cells possessed more peripheral heterochromatin and less RER, and the form and the density of the mitochondria became diverse. Among those whose matrix became dark, their cristae were distinct or even vanished. In liver cells with fat degeneration, the mitochondria varied both in form and size, possessed vesicular cristae and dense matrix, but endoplasmic...

Aging changes of male rat liver (25, 28 and 31 m) were observed by Electron microscopy. The results were as follows- From 25 m on, the riucli of some liver cells possessed more peripheral heterochromatin and less RER, and the form and the density of the mitochondria became diverse. Among those whose matrix became dark, their cristae were distinct or even vanished. In liver cells with fat degeneration, the mitochondria varied both in form and size, possessed vesicular cristae and dense matrix, but endoplasmic reticulium disappeared. The microvilli both in the bile canaliculi and the Disse's space decreased in number, but collagenous fibrils increased in number in the Disse's space. From 31m on the microvilli in the Disse's space vanished and the endothelium became indistinct. A structure like basement membrane appeared both out of the hepatocyte and the endothelium.

对雄性18月、25月、28月及31月龄大鼠肝脏超微结构的加龄变化进行了透射电镜的观察.发现从25月龄开始肝细胞核有的出现异染色质增多、边集,粗面内质网逐渐减少.线粒体基质深浅不一,凡基质变深者其嵴亦由板状变为泡状,最深者嵴消失.在有脂肪变性的肝细胞,其线粒体大小悬殊,形态多样,基质增深,嵴多变为泡样;内质网消失.胆小管内与窦周隙中的微绒毛减少,而窦周隙中的胶原原纤维则增多.31月龄大鼠除上述现象外,窦周隙中不但微绒毛消失,而且内皮细胞结构不清,在其外与肝细胞膜的窦周隙面均出现不规则的基膜样结构.

 
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