Nancy Leung, Cheng‐Yuan Peng, Hie‐Won Hann, Jose Sollano, Judy Lao‐Tan, Chao‐Wei Hsu, Laurentius Lesmana, Man‐Fung Yuen, Lennox Jeffers, Morris Sherman, Albert Min, Kimberly Mencarini, Ulysses Diva, Anne Cross, Richard Wilber, Juan Lopez‐Talavera – 28 December 2008 – This study was undertaken to compare the early antiviral activity and viral kinetic profiles of entecavir (ETV) versus adefovir (ADV) in hepatitis B e antigen positive nucleoside‐naïve adults with chronic hepatitis B (CHB).

Calogero Cammà, Salvatore Petta, Vito Di Marco, Fabrizio Bronte, Stefania Ciminnisi, Giusalba Licata, Sergio Peralta, Fabio Simone, Giulio Marchesini, Antonio Craxì – 28 December 2008 – Indirect methods to predict the presence of esophageal varices (EV) in patients with cirrhosis are not sensitive enough to be used as a surrogate for endoscopy. We tested the effectiveness of liver stiffness measurement (LSM) by transient elastography and the presence of insulin resistance (IR), a marker associated with fibrosis progression, in the noninvasive prediction of portal hypertension.

Jesús M. Banales, Tatyana V. Masyuk, Sergio A. Gradilone, Anatoliy I. Masyuk, Juan F. Medina, Nicholas F. LaRusso – 28 December 2008 – PCK rats, an animal model of autosomal recessive polycystic kidney disease (ARPKD), develop cholangiocyte‐derived liver cysts associated with increased intracellular adenosine 3′,5′‐cyclic adenosine monophosphate (cAMP), the inhibition of which suppresses cyst growth.

Haixin Yuan, Hong Zhang, Xunwei Wu, Zhe Zhang, Dan Du, Wenchao Zhou, Shuhua Zhou, Cord Brakebusch, Zhengjun Chen – 28 December 2008 – Cdc42, a member of the Rho guanosine triphosphatase (GTPase) family, plays important roles in the regulation of the cytoskeleton, cell proliferation, cell polarity, and cellular transport, but little is known about its specific function in mammalian liver. We investigated the function of Cdc42 in regulating liver regeneration. Using a mouse model with liver‐specific knockout of Cdc42 (Cdc42LK), we studied liver regeneration after partial hepatectomy.

Raj Vuppalanchi, Naga Chalasani – 28 December 2008 – Nonalcoholic fatty liver disease (NAFLD) is among the most common causes of chronic liver disease in the western world. It is now recognized that these patients have myriad of important co‐morbidities (e.g., diabetes, hypothyroidism and metabolic syndrome). The workup of patients with suspected NAFLD should consist of excluding competing etiologies and systemic evaluation of metabolic comorbidities. NAFLD is histologically categorized into steatosis and steatohepatitis, two states with fairly dichotomous natural history.

Rajat Singh, Yongjun Wang, Youqing Xiang, Kathryn E. Tanaka, William A. Gaarde, Mark J. Czaja – 28 December 2008 – Activation of c‐Jun N‐terminal kinase (JNK) has been implicated as a mechanism in the development of steatohepatitis. This finding, together with the reported role of JNK signaling in the development of obesity and insulin resistance, two components of the metabolic syndrome and predisposing factors for fatty liver disease, suggests that JNK may be a central mediator of the metabolic syndrome and an important therapeutic target in steatohepatitis.

Raoul Poupon, Olivier Chazouilleres, Christophe Corpechot – 28 December 2008

Allen D. Brinker, Ronald T. Wassel, Jenna Lyndly, Jose Serrano, Mark Avigan, William M. Lee, Leonard B. Seeff – 28 December 2008 – Telithromycin is the first of a new class of ketolide antibiotics with increased activity against penicillin‐resistant and erythromycin‐resistant pneumococci. This agent received approval by the United States Food and Drug Administration (FDA) in 2004 for treatment of upper and lower respiratory infections. Following market introduction, spontaneous reports of telithromycin‐associated hepatotoxicity, including frank liver failure, were received.

Cristina Bosetti, Fabio Levi, Paolo Boffetta, Franca Lucchini, Eva Negri, Carlo La Vecchia – 28 December 2008

Harel Dahari, Emi Shudo, Ruy M. Ribeiro, Alan S. Perelson – 28 December 2008 – Typically, hepatitis B virus (HBV) decays in patients under therapy in a biphasic manner. However, more complex decay profiles of HBV DNA (e.g., flat partial response, triphasic, and stepwise), for which we have no clear understanding, have also been observed in some treated patients.