L Grande, A Rimola, E Cugat, L Alvarez, J C Garcia‐Valdecasas, P Taurá, J Beltran, J Fuster, A M Lacy, F J González, J Tabet, A Cifuentes, R Rull, C Ramos, J Visa, J Rodés – 1 June 1996 – Although venovenous bypass (VVBP) has been suggested to protect the kidneys during liver transplantation and its systematic use has therefore been recommended, this beneficial effect of VVBP has not been clearly demonstrated.

H Takikawa, Y Sugiyama, J C Fernandez‐Checa, J Kuhlenkamp, M Ookhtens, N Kaplowitz – 1 June 1996 – We previously identified that Y′ bile acid binders (3α‐ hydroxysteroid dehydrogenases) interact with bile acids in intact rat hepatocytes using [3β‐3H, C24‐14C]bile acids and that indomethacin, a competitive inhibitor of 3α‐hydroxysteroid dehydrogenase, inhibits 3H‐loss from the C3‐position of bile acids as well as inhibits hepatic bile acid removal and excretion.

C R Leveille‐Webster, J Rogers, I M Arias – 1 June 1996 – The hepatic asialoglycoprotein receptor is responsible for rapid clearance of desiaylated glycoproteins from the circulation by receptor‐ mediated endocytosis. Previous in vitro studies in hepatocyte preparations from rats subjected to partial hepatectomy (PH) of 70% to stimulate hepatic regeneration showed decreased asialoglycoprotein (ASGP) receptor binding. We used an ASGP receptor‐targeted hepatic magnetic resonance imaging (MRI) agent, BMS 180550, to demonstrate similar changes in receptor biology in vivo.

M Moriyama, I Makiyama, M Shiota, K Uesugi, Y Kannan, M Ohta, K Kimura, T Sugano – 1 June 1996 – Ureagenesis from ammonia, alanine, and glutamine in the liver after partial hepatectomy (PH) was determined by using the liver‐perfusion system. The maximum rate of ureagenesis from ammonium chloride (10 mmol/L) in hepatectomized (HX) rats at 24 hours after surgery was obtained in the presence of ornithine, lactate, and pyruvate, and it was almost identical to that in sham‐operated (SO) rats.

T Niki, P J De Bleser, G Xu, K Van der Berg, E Wisse, A Geerts – 1 June 1996 – Fat‐storing cells are the major producers of extracellular matrix in the liver. A good immunocytochemical marker is, however, still lacking for this cell type. Desmin, frequently used by most investigators, fails to stain many pericentral fat‐storing cells in normal rat liver. The aim of the present study is to evaluate glial fibrillary acidic protein (GFAP) as an alternative marker of fat‐storing cells.

P J De Bleser, C D Scott, T Niki, G Xu, E Wisse, A Geerts – 1 June 1996 – The liver is reported to be the main source of soluble insulin‐like growth factor‐II/mannose 6‐phosphate (IGF‐II/M6P) receptor in adults. In view of the role of this receptor in the activation of transforming growth factor β (TGF‐β) during hepatic fibrogenesis, we have investigated the correlation between serum levels and tissue expression of the receptor during acute CCl4 intoxication of the rat.

C Colombo, P M Battezzati, M Podda, N Bettinardi, A Giunta – 1 June 1996 – Liver disease is increasingly recognized as a major cause of morbidity in cystic fibrosis (CF). Preliminary data suggest that ursodeoxycholic acid (UDCA) may be beneficial for treatment of this manifestation. We performed a double‐blind, multicenter trial in these patients to establish efficacy and safety of UDCA in terms of the improvement of clinical and nutritional indicators besides standard liver function tests.

G Nardone, M Romano, A Calabrò, P V Pedone, I de Sio, M Persico, G Budillon, C B Bruni, A Riccio, R Zarrilli – 1 June 1996 – Increased prevalence of hepatitis C virus (HCV) infection has been found in patients with hepatocellular carcinoma (HCC). The expression of insulinlike growth factor II (IGF‐II) has been linked to hepatocarcinogenesis in the experimental animal and in humans.

J Heathcote – 1 May 1996

G S Baroni, L D'Ambrosio, P Curto, A Casini, R Mancini, A M Jezequel, A Benedetti – 1 May 1996 – Interferon gamma (IFN‐γ) inhibits in vitro the activation of hepatic stellate cells (HSC), the primary extracellular matrix‐producing cells in liver fibrosis. This study was undertaken to determine in vivo the effect of IFN‐γ in the rat model of liver fibrosis induced by dimethylnitrosamine (DMN), where HSC activation represents an early response to cell injury. Rats were killed after 1 or 3 weeks of treatment with DMN, IFN‐γ, DMN + IFN‐γ, or saline.