Philip Hilgard, Thomas Schreiter, Richard J. Stockert, Guido Gerken, Ulrich Treichel – 26 April 2004 – Hemolysis in patients with advanced alcoholic liver disease is a common clinical problem and indicates an unfavorable prognosis. In many cases, the etiology of the hemolysis remains unknown. We observed three patients with alcoholic liver disease, suffering from severe hemolytic anemia, requiring multiple blood transfusions. Steroid therapy was ineffective and two of the patients died.

Svetlana Radaeva, Rui Sun, Hong‐na Pan, Feng Hong, Bin Gao – 26 April 2004 – The central role of T cell activation in hepatocellular injury has been well documented. In this article, we provide evidence suggesting that T cells may also play a protective role in liver disease by releasing interleukin‐22 (IL‐22), a recently identified T cell‐derived cytokine whose biological significance is unclear.

Tri H. Le, Stephen H. Caldwell, Jan A. Redick, Bonnie L. Sheppard, Christine A. Davis, Kristen O. Arseneau, Julia C. Iezzoni, Elizabeth E. Hespenheide, Abdullah Al‐Osaimi, Theresa C. Peterson – 26 April 2004 – Megamitochondria with crystalline inclusions (MMC) have been previously described in nonalcoholic fatty liver; however, their distribution within hepatic zones is unknown. We sought to determine this distribution from the core liver biopsy specimens of 31 patients: 8 males and 23 females, age range 21 to 72 years.

Karla J. Helbig, Andrew Ruszkiewicz, Ljiljana Semendric, Hugh A.J. Harley, Shaun R. McColl, Michael R. Beard – 26 April 2004 – The factors that regulate lymphocyte traffic in chronic hepatitis C (CHC) are not completely defined. Interferon (IFN)‐inducible T cell α chemoattractant (I‐TAC) is a relatively new member of the CXCR3 chemokine ligand family that selectively recruits activated T cells to sites of inflammation. To determine if I‐TAC plays a role in CHC, we investigated I‐TAC expression in hepatitis C virus (HCV)‐infected liver biopsy material.

Jesus A. Villanueva, Charles H. Halsted – 26 April 2004 – Alcoholic liver disease is associated with abnormal hepatic methionine metabolism, including increased levels of homocysteine and S‐adenosylhomocysteine (SAH) and reduced levels of S‐adenosylmethionine (SAM) and glutathione (GSH).

Chien‐Jen Chen, Li‐Yu Wang, Yin‐Chu Chien – 26 April 2004

Adrian Reuben – 26 April 2004

Baochun Zhang, Shubing Liu, Michele D. Perpetua, William H. Walker, Brian G. Harbrecht – 26 April 2004 – The cyclic AMP response element (CRE) has been implicated in the regulation of the expression of many genes and cellular processes important in hepatocyte function. CRE sites exist in the promoter regions of several genes expressed during inflammation. Numerous studies on the role of CRE in hepatocyte gene expression have been performed in resting hepatocytes, but the role of CRE during inflammation is unknown.

Makoto Ochi, Hideki Ohdan, Hiroshi Mitsuta, Takashi Onoe, Daisuke Tokita, Hidetaka Hara, Kohei Ishiyama, Wendy Zhou, Yuka Tanaka, Toshimasa Asahara – 26 April 2004 – Although it is known that activation of natural killer (NK) cells causes liver injury, the mechanisms underlying NK cell‐induced killing of self‐hepatocytes are not clear. We demonstrated that liver NK cells have cytotoxicity against normal syngeneic hepatocytes in mice. Polyinosinic‐polycytidylic acid (poly I:C) treatment enhanced hepatocyte toxicity of liver NK cells but not that of spleen NK cells.

Nektarios Dikopoulos, Ursula Wegenka, Andrea Kröger, Hansjörg Hauser, Reinhold Schirmbeck, Jörg Reimann – 26 April 2004 – Large number of T cells traffic through the liver. In order to examine the effects of such traffic on the phenotype of hepatocytes, we vaccinated mice using DNA vaccines encoding antigens with MHC class I‐binding epitopes. Small numbers of activated CD8+ T blasts (105–106/liver) changed the surface phenotype and cytokine expression profile of hepatocytes (HCs).