Patrick Baqué, Valérie Pierrefite‐Carle, Adolfo Gavelli, Nicole Brossette, Daniel Benchimol, André Bourgeon, Pascal Staccini, Marie‐Christine Saint‐Paul, Bernard Rossi – 30 December 2003 – The cytosine deaminase (CD) gene converts the nontoxic prodrug, 5‐fluorocytosine (5‐FC), into 5‐fluorouracil (5‐FU). We previously showed that injection of CD‐bearing cancer cells followed by 5‐FC treatment can act as an autologous tumor vaccine in a syngenic liver metastasis model in rats.

Yuki Terui, Takafumi Saito, Hisayoshi Watanabe, Hitoshi Togashi, Sumio Kawata, Yoshihiro Kamada, Shigeru Sakuta – 30 December 2003

Maribel Jaime, Maria Jessús Pujol, Joan Serratosa, Cristina Pantoja, Núria Canela, Oriol Casanovas, Manuel Serrano, Neus Agell, Oriol Bachs – 30 December 2003 – Liver cells from p21Cip1−/− mice subjected to partial hepatectomy (PH) progress into DNA synthesis faster than those from wild‐type mice. These cells also show a premature induction of cyclin E/cyclin‐dependent kinase (CDK) 2 activity. We studied the mechanisms whereby cells lacking p21Cip1 showed a premature induction of this activity.

Farin Amersi, Xiu‐Da Shen, Dean Anselmo, Judy Melinek, Suhasani Iyer, Daniel J. Southard, Masamichi Katori, Hans‐Dieter Volk, Ronald W. Busuttil, Roland Buelow, Jerzy W. Kupiec‐Weglinski – 30 December 2003 – A direct role of carbon monoxide (CO), an effector‐signaling molecule during heme oxygenase‐1 (HO‐1) catalysis of heme, in the protection against hepatic ischemia/reperfusion (I/R) injury needs to be established. This study was designed to determine the effects and downstream mechanisms of CO on cold I/R injury in a clinically relevant isolated perfusion rat liver model.

Michelle Craig Barton, David N. Stivers – 30 December 2003

Yi‐Shin Huang, Herng‐Der Chern, Wei‐Juin Su, Jaw‐Ching Wu, Shinn‐Liang Lai, Shi‐Yi Yang, Full‐Young Chang, Shou‐Dong Lee – 30 December 2003 – Antituberculosis drug–induced hepatitis is one of the most prevalent drug‐induced liver injuries. Isoniazid is the major drug incriminated in this hepatotoxicity. Isoniazid is mainly metabolized to hepatotoxic intermediates by N‐acetyltransferase (NAT). However, the association of polymorphic NAT acetylator status and antituberculosis drug–induced hepatitis is debatable.

Veit Gülberg, Klaus Haag, Martin Rössle, Alexander L. Gerbes – 30 December 2003 – Hepatic arterial buffer response (HABR) is considered an important compensatory mechanism to maintain perfusion of the liver by hepatic arterial vasodilation on reduction of portal venous perfusion. HABR has been suggested to be impaired in patients with advanced cirrhosis. In patients with hepatopetal portal flow, placement of a transjugular intrahepatic portosystemic shunt (TIPS) reduces portal venous liver perfusion.

David Bernstein, Leah Kleinman, Chris M. Barker, Dennis A. Revicki, Jesse Green – 30 December 2003 – Interferon therapy may exacerbate health‐related quality of life (HRQL) deficits associated with hepatitis C virus (HCV) early in the course of therapy. Treatment with polyethylene glycol–modified interferon (peginterferon) alfa‐2a (40 kd) provides improved sustained response over interferon alfa‐2a, but its effect on HRQL is unknown.

Igor Dvorchik, Michael Subotin, A. Jake Demetris, John J. Fung, Thomas E. Starzl, Samuel Wieand, Kareem M. Abu‐Elmagd – 30 December 2003 – This report investigates the influence of liver transplantation and concomitant immunosuppression on the course of progression of inflammatory bowel disease (IBD) and discusses statistical methodology appropriate for such settings.

Shuji Matsumura, Judy Van De Water, Hiroto Kita, Ross L. Coppel, Takao Tsuji, Kazuhide Yamamoto, Aftab A. Ansari, M. Eric Gershwin – 30 December 2003 – Patients with PBC produce a directed, specific response to a single immunodominant autoepitope of PDC‐E2 within the inner lipoyl domain. In contrast, immunized animals react to multiple epitopes and rarely recognize the inner lipoyl domain. In other autoimmune diseases, apoptosis plays a critical role in antigen presentation; the caspases and granzyme B are the key proteases in the generation of autoepitopes.