Long‐term exclusive zinc monotherapy in symptomatic Wilson disease: Experience in 17 patients

Francisca H. H. Linn, Roderick H. J. Houwen, Jan van Hattum, Stefan van der Kleij, Karel J. van Erpecum – 29 October 2009 – Exclusive monotherapy with zinc in symptomatic Wilson disease is controversial. Seventeen symptomatic patients with Wilson disease were treated with zinc only. The mean age at diagnosis and start of treatment was 18 years (range 13–26) with approximately half presenting as adolescents. Presentation was exclusively hepatic, exclusively neurologic, and combined in seven, five, and five patients, respectively. The median follow‐up was 14 years (range 2–30).

Pan‐caspase inhibitor VX‐166 reduces fibrosis in an animal model of nonalcoholic steatohepatitis

Rafal P. Witek, W. Carl Stone, F. Gamze Karaca, Wing‐Kin Syn, Thiago A. Pereira, Kolade M. Agboola, Alessia Omenetti, Youngmi Jung, Vanessa Teaberry, Steve S. Choi, Cynthia D. Guy, John Pollard, Peter Charlton, Anna Mae Diehl – 29 October 2009 – Nonalcoholic fatty liver disease (NAFLD) is a potentially progressive liver disease that culminates in cirrhosis. Cirrhosis occurs more often in individuals with nonalcoholic steatohepatitis (NASH) than in those with steatosis (nonalcoholic fatty liver [NAFL]).

Impact of pegylated interferon and ribavirin on morbidity and mortality in patients with chronic hepatitis C and normal aminotransferases in France

Sylvie Deuffic‐Burban, Gérard Babany, Isabelle Lonjon‐Domanec, Pierre Deltenre, Valérie Canva‐Delcambre, Sébastien Dharancy, Alexandre Louvet, Françoise Roudot‐Thoraval, Philippe Mathurin – 29 October 2009 – Clinicians continue to raise questions concerning the necessity of treating chronic hepatitis C virus (HCV)‐infected patients with normal alanine aminotransferase (N‐ALT), in light of their slower progression to cirrhosis than patients with elevated alanine aminotraferase (E‐ALT).

Pharmacological inhibition of integrin αvβ3 aggravates experimental liver fibrosis and suppresses hepatic angiogenesis

Eleonora Patsenker, Yury Popov, Felix Stickel, Vreni Schneider, Monika Ledermann, Hans Sägesser, Gerald Niedobitek, Simon L. Goodman, Detlef Schuppan – 29 October 2009 – The vitronectin receptor integrin αvβ3 promotes angiogenesis by mediating migration and proliferation of endothelial cells, but also drives fibrogenic activation of hepatic stellate cells (HSCs) in vitro. Expecting antifibrotic synergism, we studied the effect of αvβ3 inhibition in two in vivo models of liver fibrogenesis.

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Michael W. Fried, Peter Button, Teerha Piratvisuth, George K. K. Lau, Patrick Marcellin, Wan‐Cheng Chou, Graham Cooksley, Kang‐Xian Luo, Seung Woon Paik, Yun‐Fan Liaw, Matei Popescu – 29 October 2009

New school in liver development: Lessons from zebrafish

Jaime Chu, Kirsten C. Sadler – 29 October 2009 – There is significant overlap in the genes and pathways that control liver development and those that regulate liver regeneration, hepatic progenitor cell expansion, response to injury, and cancer. Additionally, defects in liver development may underlie some congenital and perinatal liver diseases. Thus, studying hepatogenesis is important for understanding not only how the liver forms, but also how it functions.

CD4 T cells promote tissue inflammation via CD40 signaling without de novo activation in a murine model of liver ischemia/reperfusion injury

Xiuda Shen, Yue Wang, Feng Gao, Feng Ren, Ronald W. Busuttil, Jerzy W. Kupiec‐Weglinski, Yuan Zhai – 29 October 2009 – Although the role of CD4 T cells in tissue inflammation and organ injury resulting from ischemia and reperfusion injury (IRI) has been well documented, it remains unclear how CD4 T cells are activated and function in the absence of a specific antigen (Ag). We used a murine liver warm IRI model to determine first whether de novo Ag‐specific CD4 T cell activation was required and then what its functional mechanism was.

Experimental models for hepatitis C viral infection

Andre Boonstra, Luc J. W. van der Laan, Thomas Vanwolleghem, Harry L. A. Janssen – 29 October 2009 – Hepatitis C virus (HCV) infection is a leading cause of chronic liver disease. The majority of infected individuals develop a persistent infection, which is associated with a high risk of liver cirrhosis and hepatocellular carcinoma. Since its discovery 20 years ago, progress in our understanding of this virus has been suboptimal due to the lack of good model systems.

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