Pathogen DNA also contributes to interferon regulatory factor 3 activation in hepatic cells: Implications for alcoholic liver diseases
Yue Wang, Yingjun Guo, Fang Wang, Shuhan Sun – 24 November 2010
Modeling hepatitis B virus X–induced hepatocellular carcinoma in mice with the sleeping beauty transposon system
Vincent W. Keng, Barbara R. Tschida, Jason B. Bell, David A. Largaespada – 24 November 2010 – The mechanisms associated with hepatitis B virus (HBV)–induced hepatocellular carcinoma (HCC) remain elusive, and there are currently no well‐established animal models for studying this disease. Using the Sleeping Beauty transposon as a delivery system, we introduced an oncogenic component of HBV, the hepatitis B virus X (HBx) gene, into the livers of fumarylacetoacetate hydrolase (Fah) mutant mice via hydrodynamic tail vein injections.
Hypovitaminosis D and ethnic differences in insulin resistance
Hong‐Fang Ji – 23 November 2010
Nonalcoholic fatty liver in a developing country is responsible for significant liver disease
Ajay Duseja, Balkrishan Sharma, Amit Kumar, Shweta Kapil, Ashim Das, Radha K. Dhiman, Yogesh K. Chawla – 23 November 2010
Adipose to the rescue: Peripheral fat fuels liver regeneration
Sundararajah Thevananther – 23 November 2010
Liver enzymes and cardiovascular outcomes: A new research agenda
Yusuf Yilmaz, Ramazan Kurt, Cem Kalayci – 23 November 2010
Drug‐induced autoimmune hepatitis caused by anti–tumor necrosis factor α agents
Cumali Efe, Tugrul Purnak, Ersan Ozaslan, Staffan Wahlin – 23 November 2010
Treatment response in patients with autoimmune hepatitis
Christoph Schramm, Christina Weiler‐Normann, Christiane Wiegard, Stefanie Hellweg, Susanne Müller, Ansgar W. Lohse – 23 November 2010
The balancing act of hepatocyte apoptosis
Nicholas A. Shackel – 23 November 2010 – The cell death receptor Fas plays a role in the establishment of fulminant hepatitis, a major cause of drug‐induced liver failure. Fas activation elicits extrinsic apoptotic and hepatoprotective signals; however, the mechanisms by which these signals are integrated during disease are unknown. Tissue inhibitor of metalloproteinases 3 (TIMP3) controls the critical sheddase a disintegrin and metalloproteinase 17 (ADAM17) and may dictate stress signaling.