Early serum HBsAg drop: A strong predictor of sustained virological response to pegylated interferon alfa‐2a in HBeAg‐negative patients

Rami Moucari, Vincent Mackiewicz, Olivier Lada, Marie‐Pierre Ripault, Corinne Castelnau, Michelle Martinot‐Peignoux, Agnes Dauvergne, Tarik Asselah, Nathalie Boyer, Pierre Bedossa, Dominique Valla, Michel Vidaud, Marie‐Hélène Nicolas‐Chanoine, Patrick Marcellin – 27 March 2009 – Pegylated interferon alfa‐2a (PEG‐IFN) may induce sustained virological response (SVR) in 20% of hepatitis B e antigen (HBeAg)‐negative chronic hepatitis B (CHB) patients. In addition, loss of hepatitis B surface antigen (HBsAg) is achieved with a 10% yearly rate after treatment cessation in sustained responders.

Abrogation of hepatic ATP‐citrate lyase protects against fatty liver and ameliorates hyperglycemia in leptin receptor‐deficient mice

Qiong Wang, Lei Jiang, Jue Wang, Shoufeng Li, Yue Yu, Jia You, Rong Zeng, Xiang Gao, Liangyou Rui, Wenjun Li, Yong Liu – 27 March 2009 – Hepatic steatosis is a hallmark of nonalcoholic fatty liver disease (NAFLD) and a key component of obesity‐associated metabolic dysfunctions featuring dyslipidemia, insulin resistance, and loss of glycemic control. It has yet to be completely understood how much dysregulated de novo lipogenesis contributes to the pathogenic development of hepatic steatosis and insulin resistance.

Differential expression of lumican and fatty acid binding protein‐1: New insights into the histologic spectrum of nonalcoholic fatty liver disease

Michael Charlton, Kimberly Viker, Anuradha Krishnan, Schuyler Sanderson, Bart Veldt, A. J. Kaalsbeek, Michael Kendrick, Geoffrey Thompson, Florencia Que, James Swain, Michael Sarr – 27 March 2009 – The basis of hepatocellular injury and progressive fibrosis in a subset of patients with nonalcoholic fatty liver disease (NAFLD) is poorly understood. We sought to identify hepatic proteins that are differentially abundant across the histologic spectrum of NAFLD.

CD133+ liver cancer stem cells from methionine adenosyl transferase 1A–deficient mice demonstrate resistance to transforming growth factor (TGF)‐β–induced apoptosis

Wei Ding, Marialena Mouzaki, Hanning You, Joshua C. Laird, Jose Mato, Shelly C. Lu, C. Bart Rountree – 27 March 2009 – Methionine adenosyltransferase (MAT) is an essential enzyme required for S‐adenosylmethionine biosynthesis. Hepatic MAT activity falls during chronic liver injury, and mice lacking Mat1a develop spontaneous hepatocellular carcinoma by 18 months. We have previously demonstrated that CD133+CD45− oval cells isolated from 16‐month‐old Mat1a−/− mice represent a liver cancer stem cell population.

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