Interferon‐lambda genotype and low serum low‐density lipoprotein cholesterol levels in patients with chronic hepatitis C infection

Josephine H. Li, Xiang Qian Lao, Hans L. Tillmann, Jennifer Rowell, Keyur Patel, Alexander Thompson, Sunil Suchindran, Andrew J. Muir, John R. Guyton, Stephen D. Gardner, John G. McHutchison, Jeanette J. McCarthy – 23 May 2010 – Recently, genetic polymorphisms occurring in the interferon (IFN)‐lambda gene region were associated with response to IFN‐based treatment of hepatitis C infection. Both infection with the hepatitis C virus and IFN therapy are associated with decreased serum cholesterol and high cholesterol has been associated with increased likelihood to respond to IFN.

Hypertrophic cardiomyopathy and dysregulation of cardiac energetics in a mouse model of biliary fibrosis

Moreshwar S. Desai, Zainuer Shabier, Michael Taylor, Fong Lam, Sundararajah Thevananther, Astrid Kosters, Saul J. Karpen – 23 May 2010 – Cardiac dysfunction is a major cause of morbidity and mortality in patients with end‐stage liver disease; yet the mechanisms remain largely unknown. We hypothesized that the complex interrelated impairments in cardiac structure and function secondary to progression of liver diseases involve alterations in signaling pathways engaged in cardiac energy metabolism and hypertrophy, augmented by direct effects of high circulating levels of bile acids.

Combinatorial effects of interleukin 10 and interleukin 4 determine the progression of hepatic inflammation following murine enteric parasitic infection

Diana B. Douglas, Daniel P. Beiting, John P. Loftus, Judith A. Appleton, Susan K. Bliss – 23 May 2010 – Mice lacking the immunoregulatory cytokine interleukin 10 (IL‐10) develop necrotizing hepatitis after infection with Trichinella spiralis, and inflammation is dependent on the migration of intestinally activated CD4+ T cells into the liver. Hepatic production of IL‐4 is elevated in these mice, and we hypothesized that it plays a role in the development of hepatic pathology.

Durability of peginterferon alfa‐2b treatment at 5 years in patients with hepatitis B e antigen–positive chronic hepatitis B

Vincent Wai‐Sun Wong, Grace Lai‐Hung Wong, Kenneth Kar‐Lung Yan, Angel Mei‐Ling Chim, Hoi‐Yun Chan, Chi‐Hang Tse, Paul Cheung‐Lung Choi, Anthony Wing‐Hung Chan, Joseph Jao‐Yiu Sung, Henry Lik‐Yuen Chan – 23 May 2010 – Approximately 30%‐40% of patients with hepatitis B e antigen (HBeAg)‐positive chronic hepatitis B treated with peginterferon and/or lamivudine achieve HBeAg seroconversion 6 months after the end of treatment. The durability and long‐term effect of treatment are unknown.

S‐adenosylmethionine regulates dual‐specificity mitogen‐activated protein kinase phosphatase expression in mouse and human hepatocytes

Maria Lauda Tomasi, Komal Ramani, Fernando Lopitz‐Otsoa, Manuel S. Rodríguez, Tony W. H. Li, Kwangsuk Ko, Heping Yang, Fawzia Bardag‐Gorce, Ainhoa Iglesias‐Ara, Francesco Feo, Maria Rosa Pascale, José M. Mato, Shelly C. Lu – 23 May 2010 – Increased mitogen‐activated protein kinase (MAPK) activity correlates with a more malignant hepatocellular carcinoma (HCC) phenotype. There is a reciprocal regulation between p44/42 MAPK (extracellular signal‐regulated kinase [ERK]1/2) and the dual‐specificity MAPK phosphatase MKP‐1/DUSP1.

Novel mechanism of fetal hepatocyte injury in congenital alloimmune hepatitis involves the terminal complement cascade

Xiaomin Pan, Susan Kelly, Hector Melin‐Aldana, Padmini Malladi, Peter F. Whitington – 23 May 2010 – Evidence suggests that most neonatal hemochromatosis (NH) is the phenotypic expression of gestational alloimmune fetal liver injury. Gestational alloimmune diseases are induced by the placental passage of specific reactive immunoglobulin G and often involve the activation of fetal complement by the classical pathway leading to the formation of membrane attack complex (MAC) as the effector of cell injury.

Subscribe to