Bile salt–induced pro‐oxidant liver damage promotes transplanted cell proliferation for correcting Wilson disease in the Long‐Evans Cinnamon rat model

Brigid Joseph, Sorabh Kapoor, Michael L. Schilsky, Sanjeev Gupta – 27 April 2009 – Insights into disease‐specific mechanisms for liver repopulation are needed for cell therapy. To understand the efficacy of pro‐oxidant hepatic perturbations in Wilson disease, we studied Long‐Evans Cinnamon (LEC) rats with copper toxicosis under several conditions. Hepatocytes from healthy Long‐Evans Agouti (LEA) rats were transplanted intrasplenically into the liver.

Locating the stem cell niche and tracing hepatocyte lineages in human liver

Tariq G. Fellous, Shahriar Islam, Paul J. Tadrous, George Elia, Hemant M. Kocher, Satyajit Bhattacharya, Lisa Mears, Douglas M. Turnbull, Robert W. Taylor, Laura C. Greaves, Patrick F. Chinnery, Geoffery Taylor, Stuart A.C. McDonald, Nicholas A. Wright, Malcolm R. Alison – 27 April 2009 – We have used immunohistochemical and histochemical techniques to identify patches of hepatocytes deficient in the enzyme cytochrome c oxidase, a component of the electron transport chain and encoded by mitochondrial DNA (mtDNA).

Follow‐up of Chinese liver transplant recipients in Hong Kong

Sheung Tat Fan, Haibo Wang, Banny K. Lam – 27 April 2009 – The outcome of liver transplantation in China remains speculative. From 1998 to 2007, 177 adult Hong Kong patients underwent liver transplantation in China and were subsequently followed up at Queen Mary Hospital, Hong Kong. One hundred six (59.9%) patients had hepatocellular carcinoma (HCC). The grafts were probably derived from uncontrolled non–heart‐beating donors. The 1‐month mortality rate was 4.0%. The 1‐, 3‐, and 5‐year overall survival rates were 73.9%, 59.0%, and 53.9%, respectively.

Hepatitis B virus DNA levels and outcomes in chronic hepatitis B

Chien‐Jen Chen, Hwai‐I Yang, Uchenna H. Iloeje, The REVEAL‐HBV Study Group – 27 April 2009 – Serum hepatitis B virus (HBV) DNA levels can fluctuate markedly during the course of chronic HBV infection. Both case‐control and cohort studies have shown a significant, dose‐response association between serum HBV DNA levels measured at the time of initial evaluation and the subsequent risk of cirrhosis. A similar direct relationship has been shown for the risk of hepatocellular carcinoma (HCC) in cross‐sectional, case‐control, and cohort studies.

Recommendations for identification and public health management of persons with chronic hepatitis B virus infection

Cindy M. Weinbaum, Eric E. Mast, John W. Ward – 27 April 2009 – Early identification of persons with chronic HBV infection enables infected persons to receive necessary care to prevent or delay onset of liver disease, and enables the identification and vaccination of susceptible household contacts and sex partners, interrupting ongoing transmission.

Liver biopsy findings in chronic hepatitis B

Haresh Mani, David E. Kleiner – 27 April 2009 – Liver biopsy plays a central role in treatment algorithms in patients with hepatitis B and remains the gold standard for evaluating hepatic pathology. The pathology of hepatitis B is diverse and reflects the natural history of infection. An acute hepatitic pattern with lobular disarray is seen in acute infection, during acute flares of disease, and with acute hepatitis D superinfection. In chronic hepatitis B, inflammation is less pronounced in the immune‐tolerant phase and is prominent during immune‐mediated viral clearance.

Side effects of long‐term oral antiviral therapy for hepatitis B

Robert J. Fontana – 27 April 2009 – The aim of this review is to summarize the safety profile of the five approved oral nucleoside analogs used to treat chronic hepatitis B virus (HBV) infection, focusing on both the class adverse effects and those that have been reported with individual agents, as well as their safety in pregnancy. All nucleoside analogs have a “Black Box” warning because of their potential for inhibition of human DNA polymerase gamma involved in mitochondrial DNA replication.

Exogenous thioredoxin prevents ethanol‐induced oxidative damage and apoptosis in mouse liver

Jessica I. Cohen, Sanjoy Roychowdhury, Patricia M. DiBello, Donald W. Jacobsen, Laura E. Nagy – 27 April 2009 – Ethanol‐induced liver injury is characterized by increased formation of reactive oxygen species (ROS) and inflammatory cytokines, resulting in the development of hepatic steatosis, injury, and cell death by necrosis and apoptosis. Thioredoxin (Trx), a potent antioxidant and antiinflammatory molecule with antiapoptotic properties, protects animals from a number of inflammatory diseases.

Subscribe to