Malcolm Mackinnon, Cindy Clayton, John Plummer, Michael Ahern, Patricia Cmielewski, Anthony Ilsley, Pauline Hall – 1 April 1995 – The role of iron deposition in initiating hepatic fibrosis in iron overload disorders is not clearly established, and it is becoming increasingly recognized that iron may be interacting with other potential liver‐damaging agents. The authors therefore examined the interplay of iron and alcohol in rats administered subtoxic doses of carbon tetrachloride (CCl4) vapor at 20 ppm in customized chambers.

Yolanta T. Kruszynska, Mohammad A. Ghatei, Stephen R. Bloom, Neil McIntyre – 1 April 1995 – A blunted initial insulin secretory response may contribute to oral glucose intolerance in cirrhosis. Oral glucose is a better stimulant to insulin secretion than intravenous (IV) glucose in part because of release of gut peptides, notably glucose‐dependent insulinotropic peptide (GIP) and glucagon‐like peptide 1 [7‐36 amide] (GLP‐1 [7‐36 amide]).

Olle Reichard, Hans Glaumann, Aril Frydén, Gunnar Norkrans, Robert Schvarcz, Anders Sönnerborg, Zhi‐Bing Yun, Ola Weiland – 1 April 1995 – Fourteen patients with chronic hepatitis C who had a sustained response to a 60‐week interferon alfa‐2b treatment course were followed, biochemically and virologically, 2 years after treatment cessation. Biopsies were repeated in 12 of 14 for histological and virological evaluation at 2‐year follow‐up.

Marshall J. Orloff, Richard H. Bell, Mark S. Orloff, A. Gerson Greenburg, William G. M. Hardison, J. Michael Henderson, Norman D. Grace – 1 April 1995

Brijesh C. Sharma, Rakesh Aggarwal, Subhash R. Naik – 1 April 1995

Scott L. Friedman – 1 April 1995 – Background/Aims: Liver fibrosis and cirrhosis represent common pathological findings in humans with iron overload. This study was undertaken to assess whether in vivo targeting of iron to liver parenchymal or nonparenchymal cells would differently affect collagen gene activity. Methods: Rats were treated with an iron diet or intramuscular injections of iron dextran, and in situhybridization analyses on liver samples were performed. Results: These iron treatments determined parenchymal or reticuloendothelial cell iron overload, respectively.

Donna L. Waters, Stuart F. A. Dorney, Margie A. Gruca, Hugh C. O. Martin, Robert Howman‐Giles, Alex E. Kan, Merl de Silva, Kevin J. Gaskin – 1 April 1995 – Focal and multilobular biliary cirrhosis are considered pathognomonic of cystic fibrosis (CF) and almost invariably have been reported in patients with steatorrhea. In contrast, patients with pancreatic sufficiency and normal absorption are considered less likely to develop liver or biliary tract problems.

Tania Roskams, Han Moshage, Rita de Vos, David Guido, Paul Yap, Valeer Desmet – 1 April 1995 – Because increasing evidence implicates heparan sulfate proteoglycans (HSPGs) as essential cofactors in receptor‐growth factor interactions, in cell‐cell recognition systems, and in cell‐matrix adhesion processes and yet little is known about their cellular distribution pattern and cellular sources in liver tissue, we used monoclonal antibodies specific for the core proteins of syndecan1, 2, 3, 4, glypican, and perlecan to investigate their immunohistochemical expression in normal adult human liver

Lorenzo Polimeno, Alessandro Azzarone, Qui Hua Zeng, Carmine Panella, Vladimir Subbotin, Brian Carr, Boumediene Bouzahzah, Antonio Francavilla, Thomas E. Starzl – 1 April 1995 – The proliferative response of the rat liver was measured after temporary or permanent total biliary obstruction (BDO) and in different regions after selective ligation of the lobar ducts draining the right 60% of the hepatic mass. The results were compared with those after 70% partial hepatectomy (PH).

Renee C. Lin, Barbara A. Miller, Timothy J. Kelly – 1 April 1995 – Previous studies have shown that plasma levels of high‐density lipoprotein (HDL) cholesterol and the two major protein components of HDLs, i.e., apolipoproteins AI and AII, were elevated in male alcoholic patients without serious liver injury. By contrast, alcohol effect on apolipoprotein E remains unclear. Apolipoprotein E is a major component of very low—density lipoprotein (VLDL) and a minor component of human high‐density lipoprotein.