Decreased NK cell frequency in chronic hepatitis C does not affect ex vivo cytolytic killing

Chihiro Morishima, Denise M. Paschal, Chia C. Wang, Christina S. Yoshihara, Brent L. Wood, Anthony E. T. Yeo, Scott S. Emerson, Margaret C. Shuhart, David R. Gretch – 22 February 2006 – Prior studies have suggested that natural killer (NK) cell function might be impaired in chronic hepatitis C virus (HCV) infection. Circulating NK cell frequency and cytolytic activity were examined freshly ex vivo in HCV‐infected and uninfected subjects. Surprisingly, the intrinsic cytolytic activity of peripheral blood NK‐enriched cells was similar between HCV‐infected and uninfected groups (P = .91).

Changes in liver and plasma acetylcholinesterase in rats with cirrhosis induced by bile duct ligation

M. Salud García‐Ayllón, M. Ximena Silveyra, Asunción Candela, Antonio Compañ, Joan Clària, Rodrigo Jover, Miguel Pérez‐Mateo, Vicente Felipo, Salvador Martínez, Joan Galcerán, Javier Sáez‐Valero – 22 February 2006 – Classical studies of cholinesterase activity during liver dysfunction have focused on butyrylcholinesterase (BuChE), whereas acetylcholinesterase (AChE) has not received much attention. In the current study, liver and plasma AChE levels were investigated in rats with cirrhosis induced after 3 weeks of bile duct ligation (BDL).

HDAC inhibitor treatment of hepatoma cells induces both TRAIL‐independent apoptosis and restoration of sensitivity to TRAIL

Anita Pathil, Sorin Armeanu, Sascha Venturelli, Paolo Mascagni, Thomas S. Weiss, Michael Gregor, Ulrich M. Lauer, Michael Bitzer – 22 February 2006 – Hepatocellular carcinoma (HCC) displays a striking resistance to chemotherapeutic drugs or innovative tumor cell apoptosis–inducing agents such as tumor necrosis factor–related apoptosis‐inducing ligand (TRAIL). Recently, we found 2 histone deacetylase inhibitors (HDAC‐I), valproic acid and ITF2357, exhibiting inherent therapeutic activity against HCC.

Major influence of liver function itself but not of immunosuppression determines glucose tolerance after living‐donor liver transplantation

Martin Stockmann, Thomas Konrad, Sabine Nolting, Diana Hünerbein, Klaus‐Dieter Wernecke, Helena Döbling, Thomas Steinmüller, Peter Neuhaus – 22 February 2006 – Controversial data exists concerning the impact of immunosuppressive therapy on the development of post‐transplantation diabetes mellitus (PTDM). Therefore, we investigated glucose metabolism in healthy donors and in recipients of living‐donor liver transplants (LD‐LTX, n=18) without pre‐existing diabetes mellitus before, on day 10, month 6, and month 12 after intervention.

Genotype–phenotype correlation in hepatocellular adenoma: New classification and relationship with HCC

Jessica Zucman‐Rossi, Emmanuelle Jeannot, Jeanne Tran Van Nhieu, Jean‐Yves Scoazec, Catherine Guettier, Sandra Rebouissou, Yannick Bacq, Emmanuelle Leteurtre, Valérie Paradis, Sophie Michalak, Dominique Wendum, Laurence Chiche, Monique Fabre, Lucille Mellottee, Christophe Laurent, Christian Partensky, Denis Castaing, Elie Serge Zafrani, Pierre Laurent‐Puig, Charles Balabaud, Paulette Bioulac‐Sage – 22 February 2006 – Hepatocellular adenomas are benign tumors that can be difficult to diagnose.

Donor graft adenoviral iNOS gene transfer ameliorates rat liver transplant preservation injury and improves survival

Takashi Kaizu, Atsushi Ikeda, Atsunori Nakao, Yoshihito Takahashi, Allan Tsung, Junichi Kohmoto, Hideyoshi Toyokawa, Lifang Shao, Brian T. Bucher, Koji Tomiyama, Michael A. Nalesnik, Noriko Murase, David A. Geller – 22 February 2006 – The exact role of inducible NOS (iNOS) in liver ischemia/reperfusion (I/R) injury is controversial. This study was designed to investigate whether donor liver pretreatment with adenovirus encoding iNOS (AdiNOS) ameliorates I/R injury associated with liver transplantation.

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