Modulation of hepatitis B virus replication and hepatocyte differentiation by MicroRNA‐1

Xiaoyong Zhang, Ejuan Zhang, Zhiyong Ma, Rongjuan Pei, Min Jiang, Joerg F. Schlaak, Michael Roggendorf, Mengji Lu – 14 February 2011 – MicroRNAs (miRNAs) are highly conserved small noncoding RNAs participating in regulation of various cellular processes. Viruses have been shown to utilize cellular miRNAs to increase their replication in host cells. Until now, the role of miRNAs in hepatitis B virus (HBV) replication has remained largely unknown. In this study, a number of miRNA mimics were transfected into hepatoma cell lines with HBV replication.

Interaction between Toll‐like receptors and natural killer cells in the destruction of bile ducts in primary biliary cirrhosis

Shinji Shimoda, Kenichi Harada, Hiroaki Niiro, Ken Shirabe, Akinobu Taketomi, Yoshihiko Maehara, Koichi Tsuneyama, Yasuni Nakanuma, Patrick Leung, Aftab A. Ansari, M. Eric Gershwin, Koichi Akashi – 14 February 2011 – Primary biliary cirrhosis (PBC) is characterized by chronic nonsuppurative destructive cholangitis (CNSDC) associated with destruction of small bile ducts.

Randomized trial of lamivudine versus entecavir in entecavir‐treated patients with undetectable hepatitis B virus DNA: Outcome at 2 Years

James Fung, Ching‐Lung Lai, John Yuen, Charles Cheng, Ringo Wu, Danny Ka‐Ho Wong, Wai‐Kay Seto, Ivan Fan‐Ngai Hung, Man‐Fung Yuen – 14 February 2011 – We aimed to determine the 2‐year outcomes of entecavir followed by lamivudine in patients with undetectable viral load (<12 IU/mL) and normal alanine aminotransferase (ALT) after initial entecavir treatment for at least 6 months. Patients were randomly assigned 1:1 to continue with entecavir or switch to lamivudine. Liver biochemistry and hepatitis B virus (HBV) DNA were determined at weeks 0, 4, 12, 24, 48, 72, and 96.

Lithocholic acid disrupts phospholipid and sphingolipid homeostasis leading to cholestasis in mice

Tsutomu Matsubara, Naoki Tanaka, Andrew D. Patterson, Joo‐Youn Cho, Kristopher W. Krausz, Frank J. Gonzalez – 14 February 2011 – Lithocholic acid (LCA) is an endogenous compound associated with hepatic toxicity during cholestasis. LCA exposure in mice resulted in decreased serum lysophosphatidylcholine (LPC) and sphingomyelin levels due to elevated lysophosphatidylcholine acyltransferase (LPCAT) and sphingomyelin phosphodiesterase (SMPD) expression.

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Tahany Awad, Kristian Thorlund, Goran Hauser, Davor Stimac, Mahasen Mabrouk, Christian Gluud – 14 February 2011

Inhibition of placental growth factor activity reduces the severity of fibrosis, inflammation, and portal hypertension in cirrhotic mice

Christophe Van Steenkiste, Jordi Ribera, Anja Geerts, Montse Pauta, Sònia Tugues, Christophe Casteleyn, Louis Libbrecht, Kim Olievier, Ben Schroyen, Hendrik Reynaert, Leo A. van Grunsven, Bram Blomme, Stephanie Coulon, Femke Heindryckx, Martine De Vos, Jean Marie Stassen, Stefan Vinckier, Jose Altamirano, Ramón Bataller, Peter Carmeliet, Hans Van Vlierberghe, Isabelle Colle, Manuel Morales‐Ruiz – 14 February 2011 – Placental growth factor (PlGF) is associated selectively with pathological angiogenesis, and PlGF blockade does not affect the healthy vasculature.

Hepatocyte‐targeted expression by integrase‐defective lentiviral vectors induces antigen‐specific tolerance in mice with low genotoxic risk

Janka Mátrai, Alessio Cantore, Cynthia C. Bartholomae, Andrea Annoni, Wei Wang, Abel Acosta‐Sanchez, Ermira Samara‐Kuko, Liesbeth De Waele, Ling Ma, Pietro Genovese, Martina Damo, Anne Arens, Kevin Goudy, Timothy C. Nichols, Christof von Kalle, Marinee K. L. Chuah, Maria Grazia Roncarolo, Manfred Schmidt, Thierry VandenDriessche, Luigi Naldini – 11 February 2011 – Lentiviral vectors are attractive tools for liver‐directed gene therapy because of their capacity for stable gene expression and the lack of preexisting immunity in most human subjects.

Drug‐induced cholestasis

Manmeet S. Padda, Mayra Sanchez, Abbasi J. Akhtar, James L. Boyer – 11 February 2011 – Recent progress in understanding the molecular mechanisms of bile formation and cholestasis have led to new insights into the pathogenesis of drug‐induced cholestasis. This review summarizes their variable clinical presentations, examines the role of transport proteins in hepatic drug clearance and toxicity, and addresses the increasing importance of genetic determinants, as well as practical aspects of diagnosis and management. (HEPATOLOGY 2011;)

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