Toshiki Kanemaki, Hiroaki Kitade, Masaki Kaibori, Kazushige Sakitani, Yoshifumi Hiramatsu, Yasuo Kamiyama, Seiji Ito, Tadayoshi Okumura – 30 December 2003 – Recent evidence indicates that inflammatory cytokines are involved in changes of blood glucose concentrations and hepatic glucose metabolism in infectious diseases, including sepsis. However, little is known regarding how cytokines interact with glucoregulatory hormones such as insulin. The objective of the present study is to investigate if and how cytokines influence insulin‐stimulated glycogen metabolism in the liver.

Debra Sudan, Ranjan Sudan, Dan Schafer, Alan Langnas – 30 December 2003

Carlos Valls, Juan Figueras, S. Bhattacjarya, A. P. Dhillon, B. R. Davidson – 30 December 2003

Stefano Ginanni Corradini, Cristina Ripani, Paola Della Guardia, Luca Giovannelli, Walter Elisei, Alfredo Cantafora, Massimo Codacci Pisanelli, Giovanni Domenico Tebala, Gennaro Nuzzo, Alessandro Corsi, Adolfo Francesco Attili, Livio Capocaccia, Vincenzo Ziparo – 30 December 2003 – In this study, we first developed and validated a new in vitro isolated, intra‐arterially perfused, gallbladder model and then applied the method to investigate the absorption of biliary lipids by the gallbladder wall and the effect of this process on the composition of human bile.

Terence Wong, Kayhan T. Nouri‐Aria, John Devlin, Bernard Portmann, Roger Williams – 30 December 2003 – Tolerance develops in a proportion of long‐term liver transplant recipients but currently cannot be identified before an attempt at withdrawal from immunosuppression therapy. In the present study, we have examined the immunophenotypic characteristics of the cellular infiltrate in portal tracts and lobules as observed in liver biopsy specimens in relation to the outcome of subsequent withdrawal from immunosuppression therapy.

Robert F. Rotundo, Robert A. Rebres, Paula J. Mckeown‐Longo, Frank A. Blumenstock, Thomas M. Saba – 30 December 2003 – It has been postulated that the in vivo removal of many plasma glycoproteins after desialylation is mediated by their interaction with a specific endocytic receptor on hepatocytes called the asialoglycoprotein receptor (ASGP‐R), which is known to have a high affinity for specific carbohydrate residues, such as galactose. However, this mechanism has never been proven in vivo, nor has a naturally occurring ligand for the ASGP‐R been identified.

Fernando Holzinger, Claudio D. Schteingart, Huong‐Thu Ton‐Nu, Carolina Cerrè, Joseph H. Steinbach, Hong‐Zen Yeh, Alan F. Hofmann – 30 December 2003 – Hepatocyte transport of six fluorescent bile acids containing nitrobenzoxadiazolyl (NBD) or a fluorescein derivative on the side chain was compared with that of natural bile acids using the single‐pass perfused rat liver.

Alexander J. Smith, J. Marleen de Vree, Roelof Ottenhoff, Ronald P. Elferink, Alfred H. Schinkel, Piet Borst – 30 December 2003 – Mice homozygous for a disruption in the Mdr2 gene (Mdr2 (−/−) mice) lack the Mdr2 P‐glycoprotein (P‐gp) in the canalicular membrane of the hepatocyte and are unable to excrete phosphatidylcholine into the bile. These mice develop a nonsuppurative cholestatic liver disease, presumably caused by the high concentrations of free cytotoxic bile acids in bile.

Stuart C. Gordon, Nasser Bayati, Ann L. Silverman – 30 December 2003 – Several reports suggest that posttransfusion hepatitis C causes more aggressive histological activity than disease that is acquired via other routes. We sought to determine whether mode of transmission affects disease outcome. We studied the demographics, presenting laboratory data, and clinical course of 627 consecutively evaluated nonalcoholic patients with chronic hepatitis C.

Alexander L. Gerbes, Veit Gülberg, Tobias Waggershauser, Josef Holl, Maximilian Reiser – 30 December 2003 – Renal effects of the transjugular intrahepatic portosystemic shunt (TIPS) were compared in 6 patients without ascites (group 1), 11 patients with ascites responding to diuretic treatment (group 2), and 6 patients with refractory ascites (group 3). Seven days after insertion of TIPS, 24‐hour urinary sodium excretion had increased in patients with ascites: 113 ± 16 mmol to 170 ± 30 mmol (P = .012) in group 2, and 22 ± 8 mmol to 77 ± 27 mmol (P = .050) in group 3.