Promotion of liver regeneration/repair by farnesoid X receptor in both liver and intestine in mice

Lisheng Zhang, Yan‐Dong Wang, Wei‐Dong Chen, Xichun Wang, Guiyu Lou, Nian Liu, Min Lin, Barry M. Forman, Wendong Huang – 18 June 2012 – Farnesoid X receptor (FXR) is a member of the nuclear receptor superfamily and is the primary bile acid receptor. We previously showed that FXR was required for the promotion of liver regeneration/repair after physical resection or liver injury. However, the mechanism by which FXR promotes liver regeneration/repair is still unclear.

Oncogenic activation of glypican‐3 by c‐Myc in human hepatocellular carcinoma

Li Li, Ronghua Jin, Xiaoli Zhang, Fudong Lv, Lifeng Liu, Daojie Liu, Kai Liu, Ning Li, Dexi Chen – 18 June 2012 – Glypican‐3 (GPC3) is a heparan sulfate proteoglycan that has an important role in cell growth and differentiation, and its function in tumorigenesis is tissue‐dependent. In hepatocellular carcinoma (HCC), the overexpression of GPC3 has been demonstrated to be a reliable diagnostic indicator. However, the mechanisms that regulate the expression and function of GPC3 remain unclear.

Histopathological algorithm and scoring system for evaluation of liver lesions in morbidly obese patients

Pierre Bedossa, Christine Poitou, Nicolas Veyrie, Jean‐Luc Bouillot, Arnaud Basdevant, Valerie Paradis, Joan Tordjman, Karine Clement – 18 June 2012 – Nonalcoholic fatty liver disease (NAFLD) is highly prevalent and being overweight is a significant risk factor. The aim was to build an algorithm along with a scoring system for histopathologic classification of liver lesions that covers the entire spectrum of lesions in morbidly obese patients. A cohort of 679 obese patients undergoing liver biopsy at the time of bariatric surgery was studied.

IL‐29 is the dominant type III interferon produced by hepatocytes during acute hepatitis C virus infection

Heiyoung Park, Elisavet Serti, Onyinyechi Eke, Brian Muchmore, Ludmila Prokunina‐Olsson, Stefania Capone, Antonella Folgori, Barbara Rehermann – 18 June 2012 – Early, vigorous intrahepatic induction of interferon (IFN)‐stimulated gene (ISG) induction is a feature of hepatitis C virus (HCV) infection, even though HCV inhibits the induction of type I IFNs in vitro.

Analysis of the role of hepatic PPARγ expression during mouse liver regeneration

Vered Gazit, Jiansheng Huang, Alexander Weymann, David A. Rudnick – 18 June 2012 – Mice subjected to partial hepatectomy (PH) develop hypoglycemia, followed by increased systemic lipolysis and hepatic fat accumulation, prior to onset of hepatocellular proliferation. Strategies that disrupt these metabolic events inhibit regeneration. These observations suggest that alterations in metabolism in response to hepatic insufficiency promote liver regeneration. Hepatic expression of the peroxisome proliferator‐activated receptor gamma (PPARγ) influences fat accumulation in the liver.

Case report of successful peginterferon, ribavirin, and daclatasvir therapy for recurrent cholestatic hepatitis C after liver retransplantation

Robert J. Fontana, Eric A. Hughes, Henry Appelman, Robert Hindes, Dessislava Dimitrova, Marc Bifano – 18 June 2012 – A recurrent hepatitis C virus (HCV) infection after liver transplantation (LT) can lead to accelerated allograft injury and fibrosis. The aim of this article is to report the first ever use of daclatasvir (DCV; also known as BMS‐790052), a potent orally administered nonstructural 5A replication complex inhibitor, in combination with peginterferon α (PEG‐IFNα) and ribavirin in an LT recipient.

Hepatic enrichment and activation of myeloid dendritic cells during chronic hepatitis C virus infection

Victoria M. Velazquez, Huiming Hon, Chris Ibegbu, Stuart J. Knechtle, Allan D. Kirk, Arash Grakoui – 18 June 2012 – Chronic hepatitis C virus (HCV) infection is a serious disease that can result in numerous long‐term complications leading to liver failure or death. Approximately 80% of people fail to clear their infection, largely as the result of weak, narrowly targeting or waning antiviral T‐cell responses.

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