Linling Cheng, Qiang You, Hao Yin, Michael Holt, Christopher Franklin, Cynthia Ju – 28 December 2008 – Drug‐induced liver injury (DILI) is a challenging problem in drug development and clinical practice. Patient susceptibility to DILI is multifactorial, making these reactions difficult to predict and prevent. Clinical observations have suggested that concurrent bacterial and viral infections represent an important risk factor in determining patient susceptibility to developing adverse drug reactions, although the underlying mechanism is not clear.

Hong Tang, Liang Da, Yi Mao, Ying Li, Dong Li, Zhenhua Xu, Feng Li, Yifei Wang, Pierre Tiollais, Tsaiping Li, Mujun Zhao – 28 December 2008 – Human beclin 1 is the first identified mammalian gene to induce autophagy. It is commonly expressed at reduced levels in breast tumors; however, it is overexpressed in hepatitis B virus (HBV)‐infected cancerous liver tissues. To expose the possible mechanism and biological significance of this up‐regulation of beclin 1, we investigated the regulation of beclin 1 expression by HBV x protein (HBx) in hepatic or hepatoma cell lines.

Sanae Haga, Michitaka Ozaki, Hiroshi Inoue, Yasuo Okamoto, Wataru Ogawa, Kiyoshi Takeda, Shizuo Akira, Satoru Todo – 28 December 2008 – Liver regeneration comprises a series of complicated processes. The current study was designed to investigate the roles of phosphoinositide‐dependent protein kinase 1 (PDK1)‐associated pathways in liver regeneration after partial hepatectomy (PH) using liver‐specific Pdk1‐knockout (L‐Pdk1KO) and Pdk1/STAT3 double KO (L‐DKO) mice. There was no liver regeneration, and 70% PH was lethal in L‐Pdk1KO mice.

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.

Cristina Bosetti, Fabio Levi, Paolo Boffetta, Franca Lucchini, Eva Negri, Carlo La Vecchia – 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.

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

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.

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.

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.