Curtis K. Argo, Paola Loria, Stephen H. Caldwell, Amedeo Lonardo – 9 May 2008 – A growing number of chronic liver disease patients, especially those with metabolic syndrome–associated nonalcoholic fatty liver disease or hepatitis C virus–associated dysmetabolic syndrome, will take statins to prevent cardiovascular disease. As a result, clinicians will weigh complex issues raised by the interaction of statins with liver metabolism in these disorders.

Tarik Asselah, Ivan Bièche, Ingrid Laurendeau, Michelle Martinot‐Peignoux, Valerie Paradis, Dominique Vidaud, Dominique‐Charles Valla, Pierre Bedossa, Patrick Marcellin, Michel Vidaud – 9 May 2008 – Gene expression technologies allow the analysis of gene networks whose expression is associated with specific pathological conditions compared with normal tissue. We hypothesized that histologically normal tissue obtained in different ways (percutaneous or surgical liver biopsies), usually used as normal controls in gene expression studies, could have different gene expression patterns.

Hilde Herrema, Terry G. J. Derks, Theo H. van Dijk, Vincent W. Bloks, Albert Gerding, Rick Havinga, Uwe J. F. Tietge, Michael Müller, G. Peter A. Smit, Folkert Kuipers, Dirk‐Jan Reijngoud – 5 May 2008 – Medium‐chain acyl–coenzyme A (CoA) dehydrogenase (MCAD) catalyzes crucial steps in mitochondrial fatty acid oxidation, a process that is of key relevance for maintenance of energy homeostasis, especially during high metabolic demand.

Daniel A. Langer, Amitava Das, David Semela, Ningling Kang‐Decker, Helen Hendrickson, Steven F. Bronk, Zvonimir S. Katusic, Gregory J. Gores, Vijay H. Shah – 5 May 2008 – Hepatic stellate cells (HSCs) contribute to portal hypertension through multiple mechanisms that include collagen deposition, vasoconstriction, and regulation of sinusoidal structure.

Felix Flohr, Jan Harder, Jochen Seufert, Hubert E. Blum, Hans C. Spangenberg – 5 May 2008

Eirini I. Rigopoulou, George N. Dalekos – 5 May 2008

Kanji Wakabayashi, Zhe‐Xiong Lian, Patrick S.C. Leung, Yuki Moritoki, Koichi Tsuneyama, Mark J. Kurth, Kit S. Lam, Katsunori Yoshida, Guo‐Xiang Yang, Toshifumi Hibi, Aftab A. Ansari, William M. Ridgway, Ross L. Coppel, Ian R. Mackay, M. Eric Gershwin – 2 May 2008 – There have been important advances in defining effector mechanisms for several human autoimmune diseases. However, for most human autoimmune diseases, the induction stage is less well defined and there are very few clues on etiology.

Ying‐Hong Shi, Wen‐Xing Ding, Jian Zhou, Jun‐Yi He, Yang Xu, Andrea A. Gambotto, Hannah Rabinowich, Jia Fan, Xiao‐Ming Yin – 2 May 2008 – Hepatocellular carcinoma (HCC) is one of the most common malignant tumors worldwide. Despite significantly improved diagnosis and treatment in recent years, the long‐term therapeutic effect is compromised by the frequent recurrence and metastasis, of which the molecular mechanisms are not fully understood.

Qiang You, Linling Cheng, Ross M. Kedl, Cynthia Ju – 2 May 2008 – The liver is known to favor the induction of immunological tolerance rather than immunity. Although Kupffer cells (KC) have been indicated to play a role in liver tolerance to allografts and soluble antigens, the mechanisms involved remain unclear. We hypothesized that KCs could promote immune tolerance by acting as incompetent antigen‐presenting cells (APC), as well as actively suppressing T cell activation induced by other potent APCs.

Guido Beldi, Yan Wu, Yara Banz, Michael Nowak, Lindsay Miller, Keiichi Enjyoji, Arvand Haschemi, Gennady G. Yegutkin, Daniel Candinas, Mark Exley, Simon C. Robson – 2 May 2008 – Concanavalin A (Con A)–induced injury is an established natural killer T (NKT) cell–mediated model of inflammation that has been used in studies of immune liver disease. Extracellular nucleotides, such as adenosine triphosphate, are released by Con A–stimulated cells and bind to specific purinergic type 2 receptors to modulate immune activation responses.