Medical hurricane: Health care reform and hepatology
Michael Charlton – 29 October 2009
Hepatitis B e antigen as a predictor for hepatitis B e antigen–positive chronic hepatitis B patients with peginterferon alfa‐2a therapy
En‐Qiang Chen, Hong Tang – 29 October 2009
Deletion of interleukin‐12p40 suppresses autoimmune cholangitis in dominant negative transforming growth factor β receptor type II mice
Katsunori Yoshida, Guo‐Xiang Yang, Weici Zhang, Masanobu Tsuda, Koichi Tsuneyama, Yuki Moritoki, Aftab A. Ansari, Kazuichi Okazaki, Zhe‐Xiong Lian, Ross L. Coppel, Ian R. Mackay, M.
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.
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.
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.
Evolution of hepatitis C virus in liver allografts
Anthony J. Demetris – 29 October 2009 – Key Points
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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
Outcomes after liver transplantation: Chronic kidney disease
Ranjeeta Bahirwani, K. Rajender Reddy – 29 October 2009 – Key Points
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.