简介：Livercelltransplantationpresentsclinicalbenefitinpatientswithinbornerrorsofmetabolismasanalternative,oratleastasabridge,toorthotopiclivertransplantation.Thesuccessofsuchatherapeuticapproachremainslimitedbythequalityofthetransplantedcells.Cryopreservationremainsthebestoptionforlong-termstorageofhepatocytes,providingapermanentandsufficientcellsupply.However,isolatedadulthepatocytesarepoorlyresistanttosuchaprocess,withasignificantalterationboth...

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简介：ThispaperisconcernedwithastochasticHBVinfectionmodelwithlogisticgrowth.First,byconstructingsuitablestochasticLyapunovfunctions,weestablishsufficientconditionsfortheexistenceofergodicstationarydistributionofthesolutiontotheHBVinfectionmodel.Thenweobtainsufficientconditionsforextinctionofthedisease.Thestationarydistributionshowsthatthediseasecanbecomepersistentinvivo.

简介：客观：在试验性的出血性的吃惊老鼠在心肌层和hepatocyte线粒体的功能上调查海水沉浸的效果。方法:24只男Wistar老鼠被划分成三个组(8在各个组织的n=)：控制组，HSL组(土地上的出血性的吃惊组)和HSS组(在海水的出血性的吃惊组)。血液动力学的参数，H~+-ATPase(adenosinetriphosphatase)的活动，succinatedehydrogenase(同步数字系列)和Ca~(2+)-Mg~(2+)-ATPase，在心肌层和hepatocytemitochondria的钙内容被测量，越过内部mitochondrialmembrane的质子translocation的变化被分析。结果：hernodynamic索引和H~+-ATPase的活动，同步数字系列，在HSS组的Ca~(2+)-Mg~(2+)-ATPase是比在控制组和HSLgroup的那些显著地低的(P<0.05)。在HSS组，在心肌层andhepatocyte的织物和线粒体的钙层次与控制组和HSL组相比显著地被提高(P<0.05)。在在三个组之中的质子translocation的Therewas不重要的差别。结论：Thisinvestigation证明那海水沉浸能加重出血性的吃惊老鼠的条件。

简介：AbstractNon-alcoholic fatty liver disease (NAFLD) is emerging as the most common chronic liver disease worldwide. It refers to a range of liver conditions affecting people who drink little or no alcohol. NAFLD comprises non-alcoholic fatty liver and non-alcoholic steatohepatitis (NASH), the more aggressive form of NAFLD. NASH is featured by steatosis, lobular inflammation, hepatocyte injury, and various degrees of fibrosis. Although much progress has been made over the past decades, the pathogenic mechanism of NAFLD remains to be fully elucidated. Hepatocyte nuclear factor 4α (HNF4α) is a nuclear hormone receptor that is highly expressed in hepatocytes. Hepatic HNF4α expression is markedly reduced in NAFLD patients and mouse models of NASH. HNF4α has been shown to regulate bile acid, lipid, glucose, and drug metabolism. In this review, we summarize the recent advances in the understanding of the pathogenesis of NAFLD with a focus on the regulation of HNF4α and the role of hepatic HNF4α in NAFLD. Several lines of evidence have shown that hepatic HNF4α plays a key role in the initiation and progression of NAFLD. Recent data suggest that hepatic HNF4α may be a promising target for treatment of NAFLD.

简介：人的导致的pluripotent茎(iPS)房间类似于胚胎的茎(ES)房间，和罐头强烈地增殖并且区分进许多房间类型。然而，人的iPS房间的肝的区别还没被报导了。在这份报告，人的iPS房间被导致由一个逐步的协议区分进肝的房间。肝房间标记的表达式和人的iPS的肝相关的函数导出房间的房间被监视并且与区分的人的ES房间和主要人的hepatocytes的相比。在白天7点的约60%区分的人的iPS房间表示了肝的标记alphafetoprotein和白长袍的。在白天21点的区分的房间包括白朊Asecretion，肝糖合成，脲生产和可诱导的细胞色素P450活动展出了肝房间功能。肝的标记的表示和iPS的肝相关的功能导出房间的肝的房间比得上人的ES导出房间的肝的房间的。这些结果证明人的iPS房间，类似于人的ES房间，能高效地被导致区分房间进象hepatocyte一样。

简介：探索骨头的效果的目的有带hepatocyte生长因素的adenoviral向量的导出髓的间充质的干细胞(BMSC)transfected(HGF，Ad-HGF)在灼伤创伤愈合上。从男Wistar老鼠的方法BMSC用由密度坡度centrifugation中等、与包含20%胎儿的牛的浆液(FBS)的DMEM有教养的Percoll分开被分开并且净化。当时，BMSC是有在感染(MOI)的100复合的最佳的基因transduction效率的Ad-HGF的transfected。transfection和在暂停的HGF的表示的效率被流动cytometry检测，酶分别地连接了immunosorbent试金(ELISA)。32只雌老鼠受到90慥?灳瑩吗？

简介：AbstractBackground:Pulmonary microvascular endothelial cells (PMVECs) were not complex, and the endothelial barrier was destroyed in the pathogenesis progress of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Previous studies have demonstrated that hepatocyte growth factor (HGF), which was secreted by bone marrow mesenchymal stem cells, could decrease endothelial apoptosis. We investigated whether mTOR/STAT3 signaling acted in HGF protective effects against oxidative stress and mitochondria-dependent apoptosis in lipopolysaccharide (LPS)-induced endothelial barrier dysfunction and ALI mice.Methods:In our current study, we introduced LPS-induced PMEVCs with HGF treatment. To investigate the effects of mammalian target of rapamycin (mTOR)/signal transducer and activator of transcription 3 (STAT3) pathway in endothelial oxidative stress and mitochondria-dependent apoptosis, mTOR inhibitor rapamycin and STAT3 inhibitor S3I-201 were, respectively, used to inhibit mTOR/STAT3 signaling. Moreover, lentivirus vector-mediated mTORC1 (Raptor) and mTORC2 (Rictor) gene knockdown modifications were introduced to evaluate mTORC1 and mTORC1 pathways. Calcium measurement, reactive oxygen species (ROS) production, mitochondrial membrane potential and protein, cell proliferation, apoptosis, and endothelial junction protein were detected to evaluate HGF effects. Moreover, we used the ALI mouse model to observe the mitochondria pathological changes with an electron microscope in vivo.Results:Our study demonstrated that HGF protected the endothelium via the suppression of ROS production and intracellular calcium uptake, which lead to increased mitochondrial membrane potential (JC-1 and mitochondria tracker green detection) and specific proteins (complex I), raised anti-apoptosis Messenger Ribonucleic Acid level (B-cell lymphoma 2 and Bcl-xL), and increased endothelial junction proteins (VE-cadherin and occludin). Reversely, mTOR inhibitor rapamycin and STAT3 inhibitor S3I-201 could raise oxidative stress and mitochondria-dependent apoptosis even with HGF treatment in LPS-induced endothelial cells. Similarly, mTORC1 as well as mTORC2 have the same protective effects in mitochondria damage and apoptosis. In in vivo experiments of ALI mouse, HGF also increased mitochondria structural integrity via the mTOR/STAT3 pathway.Conclusion:In all, these reveal that mTOR/STAT3 signaling mediates the HGF suppression effects to oxidative level, mitochondria-dependent apoptosis, and endothelial junction protein in ARDS, contributing to the pulmonary endothelial survival and barrier integrity.

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