Activation of murine kupffer cell tumoricidal activity by liposomes containing lipophilic muramyl dipeptide

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.

Antibodies to translation products of the pre‐S1 and pre‐S2 regions of the envelope gene of hepatitis B virus in fulminant hepatitis B

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.

Simvastatin, a competitive inhibitor of HMG‐CoA reductase, lowers cholesterol saturation index of gallbladder bile

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).

Hepatitis B virus infection and renal transplantation

Gabriel Garcia, F. Blaine Hollinger – 1 September 1988 – Hepatitis B virus (HBV) infection may induce severe hepatitis and affect long‐term survival of kidney transplant recipients. Persistent viral infection has been shown to occur despite the absence of usual serologic markers. The liver and serum HBV deoxyribonucleic acid (DNA) status of 90 patients were studied prospectively; recently transplanted patients, both hepatitis B virus surface antigen (HBsAg)‐positive and negative, with and without liver disease, were investigated with HBV serology, serum HBV DNA, and liver histology.

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