Feng Zhou, Maureen N. Ajuebor, Paul L. Beck, Tai Le, Cory M. Hogaboam, Mark G. Swain – 15 July 2005 – The CD154–CD40 interaction is a critical costimulatory pathway modulating the cellular immune response. Moreover, fulminant hepatitis of various etiologies is characterized by a hepatic influx of CD154‐expressing T cells and an upregulation of CD40 expression on Kupffer cells and hepatocytes, implicating this pathway in the pathogenesis of fulminant hepatitis.

15 July 2005

Claudio E. Lagoa, Yoram Vodovotz, Donna B. Stolz, Franck Lhuillier, Carol McCloskey, David Gallo, Runkuan Yang, Elena Ustinova, Mitchell P. Fink, Timothy R. Billiar, Wendy M. Mars – 15 July 2005 – Hemorrhagic shock (HS) followed by resuscitation (HS‐R) is characterized by profound physiological changes. Even if the patient survives the initial blood loss, these poorly understood changes can lead to morbidity. One of the tissues most often affected is liver. We sought to recognize specific hepatic changes induced by this stressor to identify targets for therapeutic intervention.

Alexander Monto, Lorna M. Dove, Alan Bostrom, Sanjay Kakar, Phyllis C. Tien, Teresa L. Wright – 15 July 2005 – Liver disease in patients coinfected with HIV and hepatitis C virus (HCV) has received increasing attention in recent years. Steatosis is accepted as an important contributor to liver disease in patients with HCV, but despite coinfected patients having several reasons to have steatosis, the prevalence and significance of such changes has received scant attention.

Boris Görg, Matthias Wettstein, Sabine Metzger, Freimut Schliess, Dieter Häussinger – 15 July 2005

David D. McPherson – 15 July 2005

Xiaodong Wang, Yongke Lu, Arthur I. Cederbaum – 15 July 2005 – Cytochrome P450 2E1 (CYP2E1) may be a central pathway in generating oxidative stress, reactive oxygen species, and causing hepatotoxic injury by alcohol and various hepatotoxins. This study evaluated the ability of CYP2E1 to potentiate or synergize the hepatotoxicity of Fas in vivo. C57BL/6 mice were injected intraperitoneally with pyrazole (Pyr) to induce CYP2E1. Then, 16‐hour fasted mice were administered agonistic Jo2 anti‐Fas antibody ip. Other mice were treated with Pyr or Jo2 alone.

Leticia Muñoz, Agustín Albillos, Mónica Nieto, Eduardo Reyes, Lourdes Lledó, Jorge Monserrat, Eva Sanz, Antonio de la Hera, Melchor Alvarez‐Mon – 15 July 2005 – A systemic inflammatory state with increased circulating tumor necrosis factor alpha (TNF‐α) has been related to the bacterial infection susceptibility and hemodynamic derangement of patients with cirrhosis.

Christophe Hézode, Françoise Roudot‐Thoraval, Son Nguyen, Pascale Grenard, Boris Julien, Elie‐Serge Zafrani, Jean‐Michel Pawlotsky, Daniel Dhumeaux, Sophie Lotersztajn, Ariane Mallat – 15 July 2005

Tung‐Yu Tsui, Chi‐Keung Lau, Jian Ma, Xiaobing Wu, Yan‐Qing Wang, Stefan Farkas, Ruian Xu, Hans J. Schlitt, Sheung‐Tat Fan – 15 July 2005 – Liver fibrosis is the consequence of activation of hepatic stellate cells mediated by persistent or recurrent liver injury, where oxidative stress or inflammatory response resulting from immune cells and cytokines are involved. Targeting of hepatic stellate cells could be an important strategy for the therapy of liver fibrosis.