Anatoliy I. Masyuk, Nicholas F. LaRusso – 30 January 2006 – The review focuses on the potential physiological and pathophysiological roles of aquaporins (AQPs), a family of water channel proteins, in the hepatobiliary system. Among 13 aquaporins (AQP0‐AQP12) cloned in mammals, seven AQPs have been identified in the liver and biliary tree. Accumulating evidence suggests that AQPs are likely involved in canalicular and ductal bile secretion, gluconeogenesis and microbial infection and may have other novel roles that affect liver function. (Hepatology 2006;43:S75–S81.)

Jordan J. Feld, T. Jake Liang – 30 January 2006 – Hepatitis C follows a variable course with some patients developing progressive liver fibrosis, cirrhosis and hepatocellular carcinoma, while others have minimal or no significant liver disease after decades of infection. Studies have identified both host and viral factors associated with disease progression.

David A. Shafritz, Michael Oertel, Anuradha Menthena, Dirk Nierhoff, Mariana D. Dabeva – 30 January 2006 – Although it was proposed almost 60 years ago that the adult mammalian liver contains hepatic stem cells, this issue remains controversial. Part of the problem is that no specific marker gene unique to the adult hepatic stem cell has yet been identified, and regeneration of the liver after acute injury is achieved through proliferation of adult hepatocytes and does not require activation or proliferation of stem cells.

Omar Almusa, Michael P. Federle – 30 January 2006 – Diagnostic imaging and interventional radiology play key roles in the evaluation and management of patients who are being evaluated for potential liver transplantation (LTX) and of those who have received a transplanted liver. Technical advances in imaging equipment and technique allow more accurate assessment and often obviate unnecessary or nontherapeutic surgery or invasive techniques such as catheter angiography. Liver Transpl 12:184–193, 2006. © 2006 AASLD.

Aparajita Dey, Arthur I. Cederbaum – 30 January 2006 – Acute and chronic ethanol treatment has been shown to increase the production of reactive oxygen species, lower cellular antioxidant levels, and enhance oxidative stress in many tissues, especially the liver. Ethanol‐induced oxidative stress plays a major role in the mechanisms by which ethanol produces liver injury. Many pathways play a key role in how ethanol induces oxidative stress. This review summarizes some of the leading pathways and discusses the evidence for their contribution to alcohol‐induced liver injury.

Anna S.F. Lok – 26 January 2006

Jeong Won Jang, Jong Young Choi, Si Hyun Bae, Seung Kew Yoon, U Im Chang, Chang Wook Kim, Se Hyun Cho, Jun Yeol Han, Young Sok Lee – 26 January 2006 – Reactivation of hepatitis B virus (HBV) during chemotherapy is well documented. However, there are limited data on this complication in patients with hepatocellular carcinoma (HCC) undergoing transarterial chemotherapy.

Markus Napirei, Alexei G. Basnakian, Eugene O. Apostolov, Hans Georg Mannherz – 26 January 2006 – An overdose of acetaminophen (APAP) (N‐acetyl‐p‐aminophenol) leads to hepatocellular necrosis induced by its metabolite N‐acetyl‐p‐benzoquinone‐imine, which is generated during the metabolic phase of liver intoxication. It has been reported that DNA damage occurs during the toxic phase; however, the nucleases responsible for this effect are unknown.

Antonio Craxì, Anna Licata – 26 January 2006

Laurent Castera, Juliette Foucher, Julien Bertet, Patrice Couzigou, Victor de Ledinghen – 26 January 2006