p53 Mutations in nonmalignant human liver: Fingerprints of aflatoxins?

Mehmet Ozturk – 1 February 1995 – Fifty‐eight percent of hepatocellular carcinomas (HCCs) from Qidong, China, contain an AGG to AGT mutation at codon 249 of the p53 tumor suppressor gene, a mutation that is rarely seen in HCCs from Western countries. The population of Qidong is exposed to high levels of aflatoxin B1 (AFB1), a fungal toxin that has been shown to induce the same mutation in cultured human HCC cells.

A double‐blind, randomized, placebo‐controlled trial of prostaglandin E1 in liver transplantation

Keith S. Henley, Michael R. Lucey, Daniel P. Normolle, Robert M. Merion, Ian D. McLaren, Bruce A. Crider, Donald S. Mackie, Victoria L. Shieck, Timothy T. Nostrant, Kimberly A. Brown, Darrell A. Campbell, John M. Ham, Henry D. Appelman, Jeremiah G. Turcotte – 1 February 1995 – A double‐blind placebo‐controlled trial of intravenous prostaglandin PGE1 (40 μg/h) was conducted in adult orthotopic liver transplant recipients. Infusion was started intraoperatively and continued for up to 21 days. Patients were followed up for 180 days postoperatively.

Endothelin stimulates platelet‐activating factor synthesis by cultured rat Kupffer cells

Shamimunisa B. Mustafa, Chandrashekhar R. Gandhi, Stephen A. K. Harvey, Merle S. Olson – 1 February 1995 – Endothelins are potent peptide mediators that elicit glycogenolytic and vasoconstrictor actions in the liver. Endothelins were found to stimulate the synthesis and release of the lipid mediator platelet‐activating factor in cultured rat Kupffer cells. Endothelin‐mediated synthesis of platelet‐activating factor required extracellular calcium in that the calcium chelator, EGTA and nifedipine, a calcium ion channel blocker, inhibited platelet‐activating factor synthesis.

Ability of prolonged interferon treatment to suppress relapse after cessation of therapy in patients with chronic hepatitis C: A multicenter randomized controlled trial

Akinori Kasahara, Norio Hayashi, Naoki Hiramatsu, Masahide Oshita, Hideki Hagiwara, Kazuhiro Katayama, Michio Kato, Manabu Masuzawa, Harumasa Yoshihara, Yutaka Kishida, Yoji Shimizu, Atsuo Inoue, Hideyuki Fusamoto, Takenobu Kamada – 1 February 1995 – The aim of this study was to determine whether 12 months course of interferon alfa (IFN‐α) therapy could improve the beneficial effect of IFN in chronic hepatitis C. Eighty‐eight patients were treated with natural IFN‐α for either 28 weeks (45 cases) or 52 weeks (43 cases).

Quantitative analysis of transforming growth factor β1 messenger RNA in the liver of patients with chronic hepatitis C: Absence of correlation between high levels and severity of disease

Dominique Roulot, Hervé Durand, Thierry Coste, Jacques Rautureau, A. Donny Strosberg, Richard Benarous, Stefano Marullo – 1 February 1995 – Transforming growth factor β1 (TGFβ1) is a cytokine involved in liver fibrogenesis. Previous semiquantitative studies of patients with chronic viral hepatitis showed that liver TGFβ1 messenger RNA (mRNA) was increased, compared with normal controls and with patients with chronic hepatitis C virus (HCV) infection who responded favorably to interferon alfa (IFNα) treatment.

Interferon and ursodeoxycholic acid combined therapy in the treatmet of chronic viral C hepatitis: Results from a controlled randomized trial in 80 patients

Eveline Boucher, Hervé Jouanolle, Patrice Andre, Annick Ruffault, Dominique Guyader, Romain Moirand, Bruno Turlin, Christian Jacquelinet, Pierre Brissot, Yves Deugnier – 1 February 1995 – Because 70% to 75% of patients with chronic hepatitis C either do not respond to or relapse after interferon (IFN) therapy, and because ursodeoxycholic acid (UDCA) has been shown to reduce aminotransferase levels in patients with chronic hepatitis, we undertook a prospective controlled randomized trial of IFN (group I) versus IFN plus UDCA (group II) in 80 patients with chronic hepatitis C.

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