Domenico Alvaro, Antonio Benedetti, Alessandro Gigliozzi, Adriano Bini, Paola Della Guardia, Tiziana la Rosa, Anne Marie Jezequel, Livio Capocaccia – 1 April 1995 – We investigated whether bile salts (BS) with different hydrophobic‐hydrophilic properties interact with ethanol on bile secretion, enzyme (aspartate transaminase [AST], lactate dehydrogenase [LDH]) release in the perfusate, liver ultrastructure, and vesicular exocytosis in the isolated perfused rat liver.

Bernard D. Clifford, Daniel Donahue, Lynda Smith, Edward Cable, Brigit Luttig, Michael Manns, Herbert L. Bonkovsky – 1 March 1995 – The advent of specific antiviral therapy for chronic hepatitis C has increased the importance of establishing the correct etiology of chronic hepatitis in patients, especially because interferon alfa (IFN‐α) has been reported to exacerbate autoimmune hepatitis (AIH), whereas corticosteroids increase viral replication in chronic hepatitis C.

Marie Anne Loriot, Patrick Marcellin, Nathalie Talbodec, Véronique Guigonis, Michèle Gigou, Nathalie Boyer, Annie Bezeaud, Serge Erlinger, Jean Pierre Benhamou – 1 March 1995 – The objective of this study was to evaluate the role of hepatitis B virus (HBV) precore mutations in patients with anti‐HBe—positive chronic hepatitis B with or without previous known HBe antigen (HBeAg) viremic phase, and to assess the potential implication of precore mutants in HBeAg—negative reactivation after loss of HBeAg.

Luigi Roffi, Guido Colloredo Mels, Guido Antonelli, Giorgio Bellati, Fabio Panizzuti, Alberto Piperno, Massimo Pozzi, Davide Ravizza, Giovanni Angeli, Ferdinando Dianzani, Giuseppe Mancia – 1 March 1995 – Recombinant interferon alfa (r‐IFNα2) has been shown to normalize the aminotransferase levels in approximately 50% of patients with chronic hepatitis C virus (HCV). Few patients experience a relapse during the treatment, in spite of a complete initial response (breakthrough). We studied 191 HCV Ab‐positive patients with histologically proven chronic hepatitis.

Pierre Bedossa, Eric Peltier, Benoit Terris, Dominique Franco, Thierry Poynard – 1 March 1995 – Transforming growth factor‐Beta 1 (TGF‐β1) is an important mediator of control of liver cell proliferation and replication. The aim of the current study was to compare TGF‐β1 gene expression, protein synthesis, and cell membrane receptors in normal liver, cirrhotic nodules, and neoplastic human livers. Five surgical resections for metastasis in an otherwise normal liver and 25 resections for hepatocellular carcinoma with cirrhosis were included in this study.

Sonsoles Hortelano, Beatrice Dewez, Ana M. Genaro, María J. M. Díaz‐Guerra, Lisardo Boscá – 1 March 1995 – The induction of hepatic nitric oxide synthase (NOS) and the biosynthesis of nitric oxide (NO) were studied in liver after partial hepatectomy (PH). NOS activity in the liver remnant was observed 4 to 6 hours after PH, and no differences were evidenced between the proximal and distal surgical areas.

Raymond S. Koff – 1 March 1995

Prodromos Hytiroglou, Neil D. Theise, Myron Schwartz, Eytan Mor, Charles Miller, Swan N. Thung – 1 March 1995 – Macroregenerative nodules (MRNs), probably representing a pathway for human hepatocarcinogenesis, are generally classified into type I MRNs (or ordinary adenomatous hyperplasia) and type II MRNs (or atypical adenomatous hyperplasia), on the basis of imprecise definitions of cytological and architectural atypia.

Tetsuo Takehara, Norio Hayashi, Yasuhide Miyamoto, Masato Yamamoto, Eiji Mita, Hideyuki Fusamoto, Takenobu Kamada – 1 March 1995 – The lack of a small animal model of hepatitis C virus (HCV) infection has impeded elucidation of the pathogenesis of HCV. The aim of this study was to develop an HCV‐expressing animal model by means of cationic liposome‐mediated in vivo gene transfer.

Shao‐Nan Huang, Francis V. Chisari – 1 March 1995 – Hepatocyte turnover rates were studied in two lineages of transgenic mice that overproduce the hepatitis B virus (HBV) large envelope protein and retain filamentous hepatitis B surface antigen (HBsAg) particles in the endoplasmic reticulum, resulting in the formation of ground glass hepatocytes. The high producer lineage (50‐4) develops a necroinflammatory liver disease that progresses to hepatocellular carcinoma (HCC), whereas the low producer lineage (107‐5) displays no histopathologic changes other than ground glass hepatocytes.