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.

Xiang‐Dong Wang, Chun Liu, Jayong Chung, Felix Stickel, Helmut K. Seitz, Robert M. Russell – 30 December 2003 – Chronic ethanol intake may interfere with retinoid signal transduction by inhibiting retinoic acid synthesis and by enhancing activator protein‐1 (AP‐1) (c‐Jun and c‐Fos) expression, thereby contributing to malignant transformation. To determine the effect of ethanol on hepatic retinoid levels, retinoic acid receptors (RARs) and AP‐1 (c‐Jun and c‐Fos) gene expression, chronic ethanol (36% of total calorie intake) pair‐feeding was conducted on rats for a 1‐month period.

Dipok Kumar Dhar, Akira Yamanoi, Haruyuki Ohmori, Yuichi Nakashima, Akitaka Yamamoto, N. El‐Assal Osama, Hirofumi Kubota, Hitoshi Kohno, Naofumi Nagasue – 30 December 2003 – ET receptor blocker (TAK‐044) and NO donor (FK409) were used to improve the hepatic microcirculation following ischemia‐reperfusion injury. In the first experiment (60 minutes of ischemia), 15 dogs were divided into three groups: group A (control), saline; group B, TAK 5 mg/kg; and group C, FK 0.4 mg/kg.

Juan‐José Lasarte, Marta García‐Granero, Ascensión López, Noelia Casares, Nicolás García, María‐Pilar Civeira, Francisco Borrás‐Cuesta, Jesús Prieto – 30 December 2003 – To investigate the involvement of T‐cell response against hepatitis C virus (HCV) antigens in viral clearance after interferon therapy, we measured interleukin‐2 (IL‐2) production by peripheral mononuclear cells in response to HCV core in patients with chronic hepatitis C.

Ginny L. Bumgardner, Jiashun Li, Marie Heininger, Charles G. Orosz – 30 December 2003 – Adhesion molecules appear to play important roles in vascularized organ allograft rejection, because antibodies directed against them are effective in prolonging survival of vascularized organ allografts in rodents. However, the efficacy of these agents for cellular allografts is unknown. The current studies were undertaken to determine the role of intercellular adhesion molecule‐1 (ICAM‐1) and vascular cell adhesion molecule‐1 (VCAM‐1) on host immune responses to purified hepatocytes.

Philippe Roingeard, Camille Sureau – 30 December 2003 – The intracellular accumulation of empty hepatitis B virus (HBV) particles of filamentous shape leads to a direct cytopathic effect in so‐called ground‐glass hepatocytes. The aim of this study was to investigate how these filaments can be structurally formed at the cellular level. By electron microscopy, we reexamined the HBV‐producer HepG2T‐14 cells, which have been described as producing a substantial amount of empty HBV filaments compared with the other forms of HBV particles.

Kunio Okuda, Masayoshi Kage, Santosh M. Shrestha – 30 December 2003 – Budd‐Chiari syndrome (BCS) was initially defined as a symptomatic occlusion of the hepatic veins, but subsequent reports on various obliterative changes that occur in the hepatic portion of the inferior vena cava (IVC) and hepatic vein orifices have resulted in a broadened and ambiguous definition. Membranous obstruction of the inferior vena cava has been regarded by many as a congenital vascular malformation, but its relation to the classical BCS has remained obscure.

Gennaro D'Amico, Flavia Politi, Alberto Morabito, Adele D'Antoni, Daniela Guerrera, Gandolfo Giannuoli, Mario Traina, Giovanni Vizzini, Linda Pasta, Luigi Pagliaro – 30 December 2003 – β‐Blockers and sclerotherapy prevent long‐term upper digestive rebleeding in cirrhosis but they seem ineffective for early rebleeding. We compared octreotide with a placebo for the prevention of early rebleeding in cirrhotic patients.