Antonio Colecchia, Davide Festi – 22 December 2006

Mladen I. Yovchev, Petar N. Grozdanov, Brigid Joseph, Sanjeev Gupta, Mariana D. Dabeva – 22 December 2006 – Hepatic progenitor/oval cells appear in injured livers when hepatocyte proliferation is impaired. These cells can differentiate into hepatocytes and cholangiocytes and could be useful for cell and gene therapy applications.

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).

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.

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.

Leonardo L. Schiavon, Roberto J. Carvalho Filho, Janaína L. Narciso, Juliana P. Sampaio, Valéria P. Lanzoni, Maria Lucia G. Ferraz, Antonio Eduardo B. Silva – 22 December 2006

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.

Stephen N. Wong, K. Rajender Reddy, Emmet B. Keeffe, Steven‐Huy Han, Paul J. Gaglio, Robert P. Perrillo, Tram T. Tran, Timothy L. Pruett, Anna S.F. Lok – 11 December 2006 – Patients with hepatocellular carcinoma (HCC) receive a higher MELD score and may undergo liver transplantation (OLT) earlier compared to patients with cirrhosis, potentially decreasing waiting list mortality. However, post‐OLT survival may be reduced by recurrence of HCC. We compared clinical outcomes between patients with HBV‐cirrhosis and no HCC and patients with HBV‐HCC.

Lorenzo D'Antiga, Monica Del Rizzo, Carlo Mengoli, Umberto Cillo, Graziella Guariso, Lucia Zancan – 11 December 2006 – Epstein‐Barr virus (EBV) infection is the main cause of post‐transplant lymphoproliferative disease (PTLD). Little is known on chronic carrier state and its relation with late PTLD. We aimed to study EBV infection in the long‐term after paediatric liver transplantation (OLT). We conducted a retrospective review of 34 children monitored for a median of 5.8 years (range 1.5‐17.7). 21 were IgG seronegative (group A) and 13 seropositive (group B) before OLT.

Inmaculada Fernández, Juan Carlos Meneu, Francisco Colina, Ignacio García, Raquel Muñoz, Gregorio Castellano, Antonio Fuertes, Manuel Abradelo, Carlos Lumbreras, Enrique Moreno, José Antonio Solís‐Herruzo – 28 November 2006 – Treatment of recurrent hepatitis C in liver transplant is controversial. The aim of our study was to evaluate the clinical and histological efficacy of pegylated interferon alpha 2b (PEG‐IFN) and ribavirin therapy of recurrent hepatitis C after liver transplantation (LT).