Hugo R. Rosen, Joseph P. Madden, Paul Martin – 30 December 2003 – In the current era of critical‐organ shortage, one of the most controversial questions facing transplantation teams is whether hepatic retransplantation, which has historically been associated with increased resource utilization and diminished survival, should be offered to a patient whose first allograft is failing. Retransplantation effectively denies access to orthotopic liver transplantation (OLT) to another candidate and further depletes an already‐limited organ supply.

Françoise Lunel, Pascale Cresta, Damien Vitour, Christopher Payan, Bruno Dumont, Lionel Frangeul, Dorothée Reboul, Christine Brault, Jean‐Charles Piette, Jean‐Marie Huraux – 30 December 2003 – Several studies have shown a relationship between pretreatment hepatitis C virus (HCV) viral load and the response to interferon (IFN) therapy, creating a need for quantitative HCV‐RNA assays.

David E. Jones, Oliver F. James, Bernard Portmann, Alastair D. Burt, Roger Williams, Mark Hudson – 30 December 2003 – Two patients undergoing liver transplantation for classical end‐stage primary biliary cirrhosis (PBC) are described, who went on to develop de novo autoimmune hepatitis (AIH) in the transplanted liver. The presentation, in both instances, was with malaise and lethargy. Markedly elevated serum transaminases were found, together with a raised serum IgG and/or globulin fraction and histological features on liver biopsy typical of AIH.

Götz Kallien, Kerstin Lange, Eduard F. Stange, Jürgen Scheibner – 30 December 2003 – 3‐Hydroxy‐3‐methylglutaryl coenzyme A (HMG‐CoA) reductase inhibitors have been reported to suppress biliary cholesterol secretion and saturation. It remains unproven whether this is mediated by inhibition of cholesterol synthesis. Therefore, the effect of a long‐term administration of pravastatin on cholesterogenesis and on biliary lipid secretion was investigated in seven healthy volunteers. Placebo or 40 mg of pravastatin were taken daily at bedtime for 5 weeks using a double‐blind crossover design.

Ilana Harman‐Boehm, Leonid Zingman, Nir Hilzenrat – 30 December 2003

Jürgen Scheibner, Michael Fuchs, Erwin Hörmann, Eduard F. Stange – 30 December 2003 – Hepatic bile acid synthesis is regulated by recirculating bile acids, possibly by modulating the availability of newly synthesized and preformed cholesterol. Because data in the hamster on this mechanism are lacking, we fitted these animals with an extracorporeal bile duct and administered tritiated water intraperitoneally to label newly formed cholesterol.

Jonathan A. Dranoff, Mitchell McClure, Angela D. Burgstahler, Lee A. Denson, Aleta R. Crawford, James M. Crawford, Saul J. Karpen, Michael H. Nathanson – 30 December 2003 – The Na+‐taurocholate cotransport polypeptide (ntcp) is the primary transporter for the uptake of bile acids in the liver. The second messenger adenosine 3′:5′‐cyclic monophosphate (cAMP) rapidly increases ntcp protein concentration in the plasma membrane, yet the mechanism is unknown.

Janet Stephens, Mary Cosyns, Michelle Jones, Anthony Hayward – 30 December 2003 – Patients with acquired immune deficiency syndrome (AIDS) and boys with mutations of the CD154 gene (causing congenital X‐linked immunodeficiency with hyper‐IgM [XHIM]) are susceptible to chronic infections of the biliary tract with Cryptosporidium parvum (CP) that may lead to biliary sclerosis and ultimately to cholangiocarcinoma.

Tomohide Tatsumi, Tetsuo Takehara, Tatsuya Kanto, Noriyoshi Kuzushita, Akihiko Ito, Akinori Kasahara, Yutaka Sasaki, Masatsugu Hori, Norio Hayashi – 30 December 2003 – Human hepatocellular carcinoma (HCC) frequently recurs after primary therapy, resulting in poor prognosis. To try to find a way to prevent this, we examined the combined effectiveness of B7‐1 (CD80)‐gene transfer and interleukin‐12 (IL‐12) on the induction of protective antitumor immunity against poorly immunogenic BNL1ME A.7R.1 (BNL) mouse HCC cells. We introduced mouse B7‐1 gene into BNL1ME A.7R.1 cells.

Mitsuo Nagao, Yoshiyuki Nakajima, Michiyoshi Hisanaga, Nobuhiko Kayagaki, Hiromichi Kanehiro, Yukio Aomatsu, Saiho Ko, Hideo Yagita, Takatsugu Yamada, Ko Okumura, Hiroshige Nakano – 30 December 2003 – Escape from the immune surveillance may play an important role in tumor outgrowth and metastasis. Alteration of the Fas receptor (Fas)/ligand (FasL) system including soluble forms is regarded as one of the mechanisms preventing the immune system from rejecting the tumor cells. However, less attention has been paid to the role of Fas/FasL interaction in vivo.