William C. Duane, Donald B. Hunninghake, Martin L. Freeman, Pete A. Pooler, Linda A. Schlasner, Roger L. Gebhard – 1 September 1988 – We tested the possibility that simvastatin, a competitive inhibitor of HMG‐CoA reductase related to mevinolin, might alter cholesterol saturation of gallbladder bile. Ten patients with Type IIa or IIb hypercholesterolemia underwent bile sampling before, and again after, treatment with 20 or 40 mg per day simvastatin for 7 to 13 weeks. Mean cholesterol saturation index of gallbladder bile fell from 1.01 to 0.77 during simvastatin treatment (p < 0.01).

Hanna Shalev‐Zimels, Zvi Weizman, Chaim Lotan, Dov Gavish, Zvi Ackerman, Abraham Morag – 1 September 1988 – To assess extent of hepatic involvement in measles, we evaluated prospectively 144 patients (ages 0.2 to 43 years) during an outbreak. Liver function parameters (AST, ALT, serum γ‐glutamyl transpeptidase and bilirubin) were determined on presentation and at 2 and 4 weeks.

Iku Ise, Fumio Tsuda, Shinobu Aihara, Atsuhiko Machida, Emiko Takai, Hideaki Miyamoto, Yoshihiro Akahane, Yuzo Miyakawa, Makoto Mayumi – 1 September 1988 – Sera from 11 patients with fulminant hepatitis B were tested for antibodies to translation products of the pre‐S1 and pre‐S2 regions of hepatitis B virus of IgM, IgA and IgG classes, as well as of IgA1, IgA2 and SIgA, with solid‐phase enzyme immunoassays using native viral polypeptides.

Nigel C. Phillips, John Rioux, Ming‐Sound Tsao – 1 September 1988 – The ability of liposomes containing a lipophilic muramyl dipeptide, N‐acetylmuramyl‐L‐alanyl‐D‐isoglutamine‐glycerol dipalmitate, to induce Kupffer cell tumoricidal activity has been investigated. Liposomal N‐acetylmuramyl‐L‐alanyl‐D‐isoglutamine‐glycerol dipalmitate was 16‐fold more potent than liposomal N‐acetylmuramyl‐L‐alanyl‐D‐isoglutamine and 2,400‐fold more potent than N‐acetylmuramyl‐L‐alanyl‐D‐isoglutamine in inducing Kupffer cell tumoricidal activity in vitro. A single i.v.

Achilles A. Demetriou, Andrew Reisner, Jay Sanchez, Stanley M. Levenson, Albert D. Moscioni, J. Roy Chowdhury – 1 September 1988 – We previously reported a method of intraperitoneal transplantation of liver cells attached to collagen‐coated microcarriers, which resulted in prolonged survival and function of the transplanted cells. In the present study, we evaluated the efficacy of liver cell transplantation in providing metabolic support during acute liver insufficiency induced by 90% partial hepatectomy in rats.

1 September 1988

Susan A. Cummings, Alberto J. Kaumann, Roberto J. Groszmann – 1 September 1988 – Ketanserin, a serotonin antagonist, is effective in lowering portal pressure in a rat model of portal hypertension. As ketanserin has α1‐adrenoceptor‐blocking properties in addition to its serotonin‐blocking effects, we sought to define further the mechanism of ketanserin's portal pressure‐lowering effect.

Debra L. Laskin, Fredika M. Robertson, Anne M. Pilaro, Jeffrey D. Laskin – 1 September 1988 – Phenobarbital is a potent inducer of hepatic cytochrome P‐450 and is a tumor promoter in the two‐stage model of liver carcinogenesis. In the present studies, we show that phenobarbital also induces an accumulation of activated macrophages in the livers of treated rats. These macrophages are larger and more stellate than resident Kupffer cells and are highly vacuolated.

Peter Skov Olsen, Steen Boesby, Preben Kirkegaard, Kim Therkelsen, Thomas Almdal, Steen Seier Poulsen, Ebba Nexø – 1 September 1988 – The role of epidermal growth factor on liver regeneration after partial hepatectomy in rats was investigated. After a 70% hepatectomy in rats, the concentration of epidermal growth factor in portal venous blood was unchanged compared with unoperated controls. However, small amounts of epidermal growth factor could be identified in portal venous blood after intestinal instillation of epidermal growth factor.

Bruce A. Runyon, John C. Hoefs, Timothy R. Morgan – 1 September 1988 – A prospective study identified 45 patients with malignancy‐related ascites among 448 ascites patients (10% of the total). Patients were categorized into five subgroups based on the pathophysiology of ascites formation. Each subgroup had a distinctive ascitic fluid analysis.