Exploring the bidirectional interactions between human cytomegalovirus and hepatitis C virus replication after liver transplantation

Gaia Nebbia, Frank M. Mattes, Evangelos Cholongitas, Ana Garcia‐Diaz, Dimitrios N. Samonakis, Andrew K. Burroughs, Vincent C. Emery – 27 December 2006 – Recurrence of Hepatitis C (HCV) post‐liver transplantation (LT) is universal and its course is more aggressive than in immunocompetent individuals. Human cytomegalovirus (CMV) infection is a common post‐LT infection and has immunomodulatory effects that could adversely affect the outcome of HCV. To date, the effect of HCV replication on the dynamics of CMV have not been investigated.

Effect of side and size of graft on surgical outcomes of adult‐to‐adult live donor liver transplantation

See Ching Chan, Sheung Tat Fan, Chung Mau Lo, Chi Leung Liu – 27 December 2006 – By virtue of size, the right liver graft has become the workhorse of adult‐to‐adult live donor liver transplantation (ALDLT). Although favorable results of left liver ALDLT have also been reported, a head‐to‐head comparison of these 2 graft types both containing the middle hepatic vein had not been made. In this study, we compared the outcomes of 29 right liver and 16 left liver ALDLTs of comparable graft weight to recipient estimated standard liver volume ratio (GW/ESLV, 36.9% and 36.4%, respectively).

Risk factors for new‐onset diabetes mellitus following liver transplantation and impact of hepatitis c infection : An observational multicenter study

Faouzi Saliba, Mohamed Lakehal, Georges‐Philippe Pageaux, Bruno Roche, Claire Vanlemmens, Christophe Duvoux, Jérôme Dumortier, Ephrem Salamé, Yvon Calmus, Didier Maugendre, Diapason Study Group – 27 December 2006 – New‐onset diabetes mellitus (NODM) remains a common complication of liver transplantation (LT). We studied incidence and risk factors in 211 French patients who had undergone a primary LT between 6 and 24 months previously. This is a cross‐sectional and retrospective multicenter study. Data were collected on consecutive patients at a single routine post‐LT consultation.

Thyroid hormone preconditioning: Protection against ischemia‐reperfusion liver injury in the rat

Virginia Fernández, Iván Castillo, Gladys Tapia, Pamela Romanque, Sebastián Uribe‐Echevarría, Mario Uribe, Denise Cartier‐Ugarte, Gonzalo Santander, María T. Vial, Luis A. Videla – 22 December 2006 – Recently, we reported that oxidative stress due to 3,3′,5‐triiodothyronine (T3)‐induced calorigenesis up‐regulates the hepatic expression of mediators promoting cell protection.

Immune role of hepatic TLR‐4 revealed by orthotopic mouse liver transplantation

Beena John, Ingo Klein, I. Nicholas Crispe – 22 December 2006 – Activated CD8+ T cells migrate to the liver at the end of an immune response and go through apoptosis there, but this mechanism is impaired in mice lacking Toll‐like receptor‐4. This allowed us to test the importance of liver trapping in an ongoing immune response. In the absence of Toll‐like receptor‐4, reduced liver accumulation was associated with an increase in the circulating CD8+ T cell pool, more long‐lived memory T cells and increased CD8+ T cell memory responses.

Anti‐gp210 and anti‐centromere antibodies are different risk factors for the progression of primary biliary cirrhosis

Minoru Nakamura, Hisayoshi Kondo, Tsuyoshi Mori, Atsumasa Komori, Mutsumi Matsuyama, Masahiro Ito, Yasushi Takii, Makiko Koyabu, Terufumi Yokoyama, Kiyoshi Migita, Manabu Daikoku, Seigo Abiru, Hiroshi Yatsuhashi, Eiichi Takezaki, Naohiko Masaki, Kazuhiro Sugi, Koichi Honda, Hiroshi Adachi, Hidehiro Nishi, Yukio Watanabe, Yoko Nakamura, Masaaki Shimada, Tatsuji Komatsu, Akira Saito, Takeo Saoshiro, Hideharu Harada, Takeshi Sodeyama, Shigeki Hayashi, Akihide Masumoto, Takehiro Sando, Tetsuo Yamamoto, Hironori Sakai, Masakazu Kobayashi, Toyokichi Muro, Michiaki Koga, Zakera Shums, Gary L.

Hepatitis B virus promotes hepatocarcinogenesis in transgenic mice

Yanyan Zheng, Wen‐ling Chen, Stan G. Louie, T. S. Benedict Yen, Jing‐hsiung James Ou – 22 December 2006 – HBV is a major risk factor for hepatocellular carcinoma (HCC). However, whether HBV can directly cause HCC or only indirectly via the induction of chronic liver inflammation has been controversial. By using transgenic mice carrying the entire HBV genome as a model, we now demonstrate that HBV by itself is an inefficient carcinogen. However, it can efficiently promote hepatocarcinogenesis initiated by the carcinogen diethylnitrosamine (DEN).

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