K Hiroishi, H Kita, M Kojima, H Okamoto, T Moriyama, T Kaneko, T Ishikawa, S Ohnishi, T Aikawa, N Tanaka, Y Yazaki, K Mitamura, M Imawari – 30 December 2003 – A cytotoxic T lymphocyte (CTL) response to the hepatitis C virus (HCV) nucleoprotein residues 88‐96 that are the minimal and optimal epitope for human leukocyte antigen (HLA) B44‐restricted CTLs was assessed in 27 HLA B44‐positive patients with chronic HCV infection. Serum HCV RNA concentration and the amino acid sequence of the residues 81‐100 were also determined.

S Mihm, A Fayyazi, H Hartmann, G Ramadori – 30 December 2003 – Hepatitis C virus (HCV) causes acute and often chronic hepatitis. On the basis of variations in nucleotide sequence, at least six genotypes and several subtypes have been identified. Histopathologically, chronic HCV infection is characterized by relatively mild hepatic inflammatory activity and a low degree of fibrosis, but hepatic lesions might be accompanied by bile duct damage, intraportal lymphoid aggregates, steatosis, or a combination of these manifestations. The histopathological lesions thus appear quite heterogeneous.

D Herion, J H Hoofnagle – 30 December 2003

K E Fladmark, B T Gjertsen, A Molven, G Mellgren, O K Vintermyr, S O Døskeland – 30 December 2003 – The hepatocytes in the mature normal liver are tightly coupled through gap junctions, except during compensatory hyperplasia (regeneration) after partial hepatectomy when the gap junctions become down‐regulated. The significance of this down‐regulation has been a long‐standing enigma. The present study of hepatocytes in primary culture and in the regenerating liver aimed at defining the relationship, if any, between hepatocyte gap junctional communication and proliferation.

Y Morita, Y Hayashi, Y Wang, T Kanamaru, S Suzuki, K Kawasaki, K Ohta, M Yamamoto, Y Saitoh, H Itoh, W F Doe – 30 December 2003 – It is well known that a urokinase‐type plasminogen activator receptor (uPAR) is a key protein in the plasminogen activation system, which plays a proteolytically important role in the invasion and metastasis of various cancer cells. To assess the expression of uPAR in hepatocellular carcinoma (HCC), we analyzed the expression of uPAR messenger RNA (mRNA) and the protein in 31 pair‐samples of solitary HCC and nontumorous liver tissues from the same patients.

R M Rai, S Loffreda, C L Karp, S Yang, H Lin, A M Diehl – 30 December 2003 – Tumor necrosis factor α (TNF), initiates a cytokine cascade that promotes hepatocyte proliferation after 70% partial hepatectomy (PH) but the mechanisms regulating TNF production after PH are unknown. We previously reported that gadolinium chloride (GdCl), an agent that depletes the liver of phagocytically active Kupffer cells, enhances hepatic expression of TNF messenger RNA (mRNA) and promotes liver regeneration after subsequent PH.

B Lee, H Kang, K Pyun, I Choi – 30 December 2003 – Nitric oxide (NO) synthesis is upregulated during chronic hepatic inflammation. The present study characterized the mechanisms involved in the induction of NO production and inducible NO synthase (iNOS) messenger RNA (mRNA) expression in murine embryonic liver cell line, BNL CL.2 cells. No production by BNL CL.2 cells was induced by interferon‐r (IFN‐r) plus lipopolysaccharide (LPS). However, other inflammatory cytokines such as interleukin (IL)‐β, tumor necrosis factor α (TNF‐α), and IL‐6 had no additional effects on it.

J R Jonsson, P G Hogan, R Thomas, C Steadman, A D Clouston, G A Balderson, S V Lynch, R W Strong, E E Powell – 30 December 2003 – The aim of this study was to prospectively investigate the peak levels and kinetics of donor leucocyte chimerism in human recipients following liver transplantation. The peak levels of chimerism were observed within the first 48 hours following transplantation and ranged from 0.15% to 20% of total peripheral blood mononuclear cells.

M G Pessoa, N A Terrault, L D Ferrell, J P Kim, J Kolberg, J Detmer, M L Collins, A J Yun, M Viele, J R Lake, J P Roberts, N L Ascher, T L Wright – 30 December 2003 – To examine the prevalence of hepatitis G virus (HGV) in end‐stage liver disease of unknown cause and the role of HGV infection in posttransplantation hepatitis, we studied 46 patients undergoing liver transplantation (mean age, 50 years; M: F, 18:28) with cryptogenic cirrhosis. HGV RNA was detected by polymerase chain reaction (PCR) and was quantified by a branched DNA (bDNA) assay.

M J Krowka – 30 December 2003