Lan D. A. D'Agata, Maureen M. Jonas – 1 January 1995 – This work details the histologic findings in 84 liver biopsy specimens from 28 patients with progressive familial intrahepatic cholestasis (PFIC), who met the clinical criteria of early onset of chronic unremitting cholestasis, exclusion of any known metabolic or anatomic etiology, and low serum γ‐glutamyl transpeptidase (GGTP) values. Hepato‐canalicular cholestasis and disruption of the liver cell plate arrangement were early, uniform findings, and giant cell transformation was found in 56% of initial biopsies.

Ehoud Shmueli, Christopher O. Record, K. George M. M. Alberti, Alexander S. Petrides – 1 January 1995

William D. Payne – 1 January 1995

Howard N. Sankary, Lawrence McChesney, Elizabeth Frye, Steven Cohn, Preston Foster, James Williams – 1 January 1995 – Nonanastomotic strictures after liver transplantations are a source of significant morbidity, often necessitating retransplantation. The purpose of this study was twofold: first to identify features associated with the development of this lesion; second, to make technical modifications that will decrease the incidence of this problem. In the first part of this study, 15 of 131 patients were diagnosed with nonanastomotic biliary stricture.

Angelo Luca, Juan Carlos Garí‐Pagán, Faust Feu, Juan Carlos Lopez‐Talavera, Mercedes Fernández, Concepció Bru, Jaime Bosch, Juan Rodés – 1 January 1995 – This study investigated the correlation between changes in hepatic and systemic hemodynamics and femoral blood flow (FBF), measured by dual‐beam pulsed wave Doppler, in 58 portal hypertensive patients receiving propranolol (0.15 mg/Kg intravenously; n = 44) or placebo (n = 14) under double‐blind conditions. Placebo administration had no effects.

Filip Braet, Ronald De Zanger, Marijke Baekeland, Evelyne Crabbé, Patrick Van Der Smissen, Eddie Wisse – 1 January 1995 – This article describes the cytoskeleton associated with fenestrae and sieve plates of rat liver sinusoidal endothelial cells. Fenestrae control the exchange between the blood and parenchymal cells. We present evidence indicating that several agents that change the fenestrae and sieve plates also cause changes in the cytoskeleton. Cultured liver endothelial cells (LECs) were slightly fixed and treated with cytoskeleton extraction buffer.

Hans Peter Dienes, Guido Gerken, Bernd Goergen, Klaus Heermann, Wolfram Gerlich, K. H. Meyer zum Büschenfelde – 1 January 1995 – A number of naturally occurring hepatitis B virus (HBV) mutants unable to synthesize the hepatitis B e antigen (HBeAg) have been identified in patients characterized by HBV DNA and anti‐HBe in their serum. Because the analysis of the HBV‐associated DNA and antigens in the liver tissue is still not complete, we investigated the precore sequence of HBV DNA and its encoded proteins in the liver tissue of 32 patients positive for HBV DNA and anti‐HBe in their serum.

Anna S. F. Lok, Ulus S. Akarca, Sheila Greene – 1 January 1995 – We previously reported two mutually exclusive mutations in the precore region of hepatitis B virus: M1 (T‐1856, proline‐serine substitution at codon 15) and M2 (A‐1896, stop codon at codon 28). This study was conducted to determine if the presence of precore mutants affect spontaneous or interferon (IFN)‐induced hepatitis B e antigen (HBeAg) clearance.

Gerd‐Achim Kullak‐Ublick, Gustav Paumgartner, Frieder Berr – 1 January 1995 – Comparative studies between different patient groups have suggested that cholecystectomy enhances bacterial dehydroxylation of the primary bile acid cholic acid (CA) to the secondary bile acid deoxycholic acid (DCA). DCA may exert a cocarcinogenic effect on the colonic mucosa. In a short‐term follow‐up study on nine female patients we found no alterations of the CA or DCA pools after cholecystectomy.

Carmen García‐Ruiz, Albert Morales, Anna Colell, Antonio Ballesta, Joan Rodés, Neil Kaplowitz, José C. Fernández‐Checa – 1 January 1995 – Mitochondrial glutathione plays an important role in maintaining a functionally competent organelle. Previous studies have shown that ethanol feeding selectively depletes the mitochondrial glutathione pool, more predominantly in mitochondria from perivenous hepatocytes.