Hailing Liu, Chau R. Lo, Mark J. Czaja – 30 December 2003 – Hepatocyte resistance to tumor necrosis factor α (TNF)‐induced apoptosis is dependent on activation of the transcription factor nuclear factor κB (NF‐κB). To determine the mechanism by which NF‐κB protects against TNF toxicity, the effect of NF‐κB inactivation on the proapoptotic c‐Jun NH2‐terminal kinase (JNK) signaling pathway was examined in the rat hepatocyte cell line RALA255‐10G.

Hitoshi Yoshiji, Shigeki Kuriyama, Junichi Yoshii, Yasuhide Ikenaka, Ryuichi Noguchi, Daniel J. Hicklin, James Huber, Toshiya Nakatani, Hirohisa Tsujinoue, Koji Yanase, Hiroo Imazu, Hiroshi Fukui – 30 December 2003 – The growth of any solid tumor depends on angiogenesis. Among the known angiogenic factors, basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF), are potent and representative factors involved in tumor development. It has been reported that bFGF and VEGF showed a synergistic effect in both in vitro and in vivo angiogenesis.

Yoshihiko Oka, Robert A. Waterland, J. Keith Killian, Catherine M. Nolan, Hong‐Seok Jang, Keiji Tohara, Seigo Sakaguchi, Tsuneyoshi Yao, Akinori Iwashita, Yutaka Yata, Terumi Takahara, Shin‐ichiro Sato, Kazuyuki Suzuki, Tomoyuki Masuda, Randy L. Jirtle – 30 December 2003 – Mannose 6‐phosphate/insulin‐like growth factor II receptor (M6P/IGF2R) tumor suppressor– gene mutation is an early event in human hepatocellular carcinoma (HCC) formation in the United States, but its role in hepatocarcinogenesis in Japan is unclear.

Cornelia Stumptner, Andrea Fuchsbichler, Hans Heid, Kurt Zatloukal, Helmut Denk – 30 December 2003 – Mallory bodies (MBs) consist of abnormal keratins, ubiquitin, heat shock proteins, and the protein p62. p62 is encoded by an immediate‐early response gene that rapidly responds to a variety of extracellular signals involved in cell proliferation, differentiation, and particularly oxidative stress.

Gianfranco Alpini, Leonardo Baiocchi, Shannon Glaser, Yoshiyuki Ueno, Marco Marzioni, Heather Francis, Jo Lynne Phinizy, Mario Angelico, Gene LeSage – 30 December 2003 – Accumulating bile acids (BA) trigger cholangiocyte proliferation in chronic cholestasis.

Kui Li, Tarl Prow, Stanley M. Lemon, Michael R. Beard – 30 December 2003 – Data suggesting that the hepatitis C virus (HCV) core protein influences normal cellular processes remain controversial. To determine the effects of core on cellular gene expression in hepatocytes, we developed a human hepatoma (Huh7)‐derived cell line with tightly regulated core expression under the control of a tetracycline‐regulated promoter. Cells expressing core did not have impaired proliferative abilities.

William M. Pandak, Phillip B. Hylemon, Shunlin Ren, Dalila Marques, Gregorio Gil, Kaye Redford, Darrell Mallonee, Z. Rano Vlahcevic – 30 December 2003 – Conversion of cholesterol into 7α‐hydroxylated bile acids is a principal pathway of cholesterol disposal. Cholesterol 7α‐hydroxylase (CYP7A1) is the initial and rate‐determining enzyme in the “classic” pathway of bile acid synthesis. An “alternative” pathway of bile acid synthesis is initiated by sterol 27‐hydroxylase (CYP27) with subsequent 7α‐hydroxylation of 27‐hydroxycholesterol by oxysterol 7α‐hydroxylase (CYP7B1).

Karan M. Emerick, Peter F. Whitington – 30 December 2003 – Alagille syndrome (AGS) causes intractable pruritus and disfiguring xanthomas because of retained bile acids and cholesterol. This study was performed to determine whether partial external biliary diversion (PEBD) is effective for relief of pruritus and xanthomas in AGS patients who fail conventional medical therapy. Between the years 1985 and 2001, 9 AGS patients underwent PEBD. Complete follow‐up data were available for all patients. The average age at PEBD was 4.8 (range 1.4‐10) years.

Harmeet Malhi, Pallavi annamaneni, Sanjeev Slehria, Brigid Joseph, Kuldeep K. Bhargava, Christopher J. Palestro, Phyllis M. Novikoff, Sanjeev Gupta – 30 December 2003 – To determine whether disruption of the hepatic sinusoidal endothelium will facilitate engraftment of transplanted cells, we treated Fischer 344 (F344) rats lacking dipeptidyl peptidase IV (DPPIV) activity with cyclophosphamide (CP). Electron microscopy showed endothelial injury within 6 hours following CP, and, after 24 and 48 hours, the endothelium was disrupted in most hepatic sinusoids.

Pascal Lebray, Yves Benhamou, Stanislas Pol, Robert P. Myers, Thierry Poynard, Vincent Di Martino – 30 December 2003