Osamu Isokawa, Takeshi Suda, Yutaka Aoyagi, Hirokazu Kawai, Takashi Yokota, Toru Takahashi, Kazuhiro Tsukada, Takeaki Shimizu, Shigeki Mori, Yoichi Abe, Yasafumi Suzuki, Minoru Nomoto, Yusaku Mita, Masahiko Yanagi, Hirotaka Igarashi, Hitoshi Asakura – 30 December 2003 – Hepatocellular carcinoma (HCC) mainly arises from the liver with chronic inflammation. Because telomere reduction reflects replicative history in somatic cells, we analyzed the possibility that liver tissues surrounding HCC consist of the cells carrying substantial reduction of telomere.

30 December 2003

Jörg Heller, Philippe Sogni, Khalid A. Tazi, Carine Chagneau, Odile Poirel, Richard Moreau, Didier Lebrec – 30 December 2003 – Hyporeactivity to vasoconstrictors in aortae from portal vein‐stenosed rats is associated with an increased activity of endothelial NO synthase (NOS3). In contrast, during sepsis, which is common in cirrhosis, vascular hyporeactivity is associated with an induction of inducible NOS2.

Richard J. Stockert, David C. Spray, Yang Gao, Sylvia O. Suadicani, Catherine R. Ripley, Phyllis M. Novikoff, Allan W. Wolkoff, Elliot L. Hertzberg – 30 December 2003 – The Trf1 cell line, selected from the human hepatoma cell line HuH‐7, manifests altered trafficking of various plasma membrane proteins. In particular, there is a striking loss of State 2 asialoglycoprotein receptors. This cell line is shown here to also manifest defects in function and assembly of gap junctions comprising connexin43 (Cx43). No alteration of Cx43 expression or phosphorylation was apparent.

Wladimiro Jiménez, Josefa Ros, Manuel Morales‐Ruiz, Miguel Navasa, Manuel Solé, Jordi Colmenero, Pau Sort, Francisca Rivera, Vicente Arroyo, Juan Rodés – 30 December 2003 – The present study assessed whether peritoneal macrophages isolated from cirrhotic patients produce nitric oxide (NO) and express NO synthase type II (NOS II) mRNA and protein. Patients with cirrhosis and ascites without peritonitis or with unresolved or resolved spontaneous bacterial peritonitis (SBP) were studied. Following paracentesis, ascites NO + NO content (NOx) was measured.

K. Rajender Reddy, Jay H. Hoofnagle, Myron J. Tong, William M. Lee, Paul Pockros, E. Jenny Heathcote, Donald Albert, Tenshang Joh – 30 December 2003 – The likelihood of a sustained response to a course of interferon in patients with chronic hepatitis C correlates with several clinical and viral factors, including age, viral genotype and initial levels of hepatitis C virus (HCV) RNA in serum. The role of race and ethnicity has not been assessed.

Yves Benhamou, Marie Bochet, Vincent Di Martino, Frederic Charlotte, Felipe Azria, Anne Coutellier, Michel Vidaud, François Bricaire, Pierre Opolon, Christine Katlama, Thierry Poynard, for the MULTIVIRC Group – 30 December 2003 – The natural history of hepatitis C virus (HCV) infection in human immunodeficiency virus (HIV)‐infected patients has never been studied according to the concept of liver fibrosis progression. The aim of this work was to assess the fibrosis progression rate in HIV‐HCV coinfected patients and in patients infected by HCV only.

Satoru Ozaki, Kenichi Harada, Takahiro Sanzen, Kishichiro Watanabe, Wilson Tsui, Yasuni Nakanuma – 30 December 2003 – Human telomerase, an enzyme associated with cellular immortality and tumorigenesis, is expressed by most malignant tumor cells. Human telomerase consists of human telomerase RNA (hTR) and telomerase protein components. One of the latter has been cloned and was termed telomerase‐associated protein 1 (TP1).

R. Christopher Benyon, Christopher J. Hovell, Marianna Da Gaça, Emma H. Jones, John P. Iredale, Michael J. P. Arthur – 30 December 2003 – Activated hepatic stellate cells (HSCs) are a potential source of gelatinase A, which accumulates in fibrotic livers. Progelatinase A activation requires its binding to a complex of membrane‐type matrix metalloproteinase (MT‐MMP) and tissue inhibitor of metalloproteinases (TIMP)‐2. These studies examine gelatinase A, MT1‐MMP, and TIMP‐2 synthesis by HSCs during activationin vitroand the potential role of gelatinase A in promoting HSC proliferation.

Alastair J. Strain – 30 December 2003 – Bone marrow stem cells develop into hematopoietic and mesenchymal lineages but have not been known to participate in production of hepatocytes, biliary cells, or oval cells during liver regeneration. Cross‐sex or cross‐stain bone marrow and whole liver transplantation were used to trace the origin of the repopulating liver cells. Transplanted rats were treated with 2‐acetylaminofluorene, to block hepatocyte proliferation, and then hepatic injury, to induce oval cell proliferation.