30 December 2003

Luke F. Hourigan, Graeme A. Macdonald, David Purdie, Vicki H. Whitehall, Claudia Shorthouse, Andrew Clouston, Elizabeth E. Powell – 30 December 2003 – Steatosis is a frequent histological finding in chronic hepatitis C infection; however, the pathophysiology of steatosis and its role in disease progression have not been established. We studied 148 consecutive patients with untreated chronic hepatitis C to assess the effect of body mass index, diabetes mellitus, alcohol consumption, hepatic iron content, and viral load on steatosis and hepatic fibrosis.

Charles D. Howell, Jian Li, Weiran Chen – 30 December 2003 – Intercellular adhesion molecule‐1(ICAM‐1) is expressed abnormally on the bile duct epithelium during the course of primary biliary cirrhosis (PBC), but the importance of ICAM‐1 and its lymphocyte function‐associated antigen‐1 (LFA‐1) receptor during the course of nonsuppurative destructive cholangitis (NSDC) has not been defined. To address this question, we defined the relationship between ICAM‐1 on the intrahepatic bile duct epithelium and the evolution of NSDC lesions in a mouse graft‐versus‐host disease (GVHD) model.

Matthias J. Bahr, Karen J. Vincent, Michael J. P. Arthur, Andrew V. Fowler, David E. Smart, Matthew C. Wright, Ian M. Clark, R. Christopher Benyon, John P. Iredale, Derek A. Mann – 30 December 2003 – In the injured liver hepatic stellate cells (HSCs) undergo a dramatic phenotypic transformation known as “activation” in which they become myofibroblast‐like and express high levels of the tissue inhibitor of metalloproteinase 1 (TIMP‐1). HSC activation is accompanied by transactivation of the TIMP‐1 promoter.

Ming‐Whei Yu, Shi‐Yi Yang, Yueh‐Hsia Chiu, Yi‐Ching Chiang, Yun‐Fan Liaw, Chien‐Jen Chen – 30 December 2003 – This study evaluated whether the codon 72 p53 polymorphism was related to hepatocellular carcinoma (HCC). Genotypes of p53were determined in 80 incident cases of HCC and 328 controls nested in a cohort study of 4,841 male chronic hepatitis B carriers. No overall increase in HCC risk with thePro variant allele of thep53 polymorphism was apparent.

Leda Bassit, Gabriela Ribeiro‐Dos‐Santos, Luiz C. Da Silva, Kioko Takei, Paula Villaça, Elias David‐Neto, Dalton Chamone, Amadeo Sáez‐Alquézar – 30 December 2003

Liam Fanning, Elizabeth Kenny, Margaret Sheehan, Bridin Cannon, Michael Whelton, Joe O'Connell, J. Kevin Collins, Fergus Shanahan – 30 December 2003 – Monitoring the progression of hepatitis C virus (HCV) includes clinical, biochemical, and histological parameters. Quantitation of viral load by reverse‐transcription polymerase chain reaction (RT‐PCR) may offer a more reliable marker of disease status. Conflicting reports on viral titers may reflect heterogeneity of patient population, mode of infection, and viral type/subtype.

Ikuo Wada, Hiroaki Kanada, Kimie Nomura, Yo Kato, Rikuo Machinami, Tomoyuki Kitagawa – 30 December 2003 – The mannose‐6‐phosphate/insulin‐like growth factor 2 receptor (M6P/IGF2R) suppresses cell growth through binding to the insulin‐like growth factor 2 (IGF2) and latent complex of the transforming growth factor‐β (TGF‐β). Recently, it was reported in the United States that loss of heterozygosity (LOH) and mutations in exons 27, 28, and 31 of the M6P/IGF2R gene are frequent in hepatocellular carcinomas (HCCs) and adenomas.

Akio Sato – 30 December 2003

Yurdana Castelruiz, Esther Larrea, Patricia Boya, María‐Pilar Civeira, Jesús Prieto – 30 December 2003 – Viral infections stimulate the transcription of interferon type I, which includes IFN‐alfa (IFN‐α) (13 subtypes) and IFN‐β (a single substance). Hepatitis C virus (HCV) infection is remarkable by its ability to evade host antiviral defenses; however, there is little information as to whether endogenous IFN is activated or not in this disease.