Spectrum of liver disease and duck hepatitis B virus infection in a large series of chinese ducks with hepatocellular carcinoma

Agnes Duflot, Raj Mehrotra, Shun‐Zhang Yu, Luc Barraud, Christian Trepo, Lucyna Cova – 1 June 1995 – The striking difference in the geographical distribution of liver cancer in ducks raised the question of whether duck hepatitis B virus (DHBV), like mammalian hepadnaviruses, could be an oncogenic agent. Hepatocellular carcinomas (HCCs) have been found only in domestic ducks in Qidong, China, where hepatitis B virus infection and aflatoxin B1 (AFB1) are both risk factors and where a high frequency of human HCCs has been reported.

Hypocalcemia decreases the early and late responses to epidermal growth factor in rat hepatocytes

Marc Bilodeau, Sébastien J. Provencher, Stéphane Néron, Pierre Haddad, Sylvie Vallières, Marielle Gascon‐Barré – 1 June 1995 – Extreme variations in extracellular Ca2+ concentrations ([Ca2+]e) modify the signaling generated by many hormones and growth factors. However, the influence of physiological changes in [Ca2+]e on the response to hepatic mitogens remains largely unknown.

Implications of host pancreatic hormones in the restart of grafted liver

Tetsuya Kiuchi, Ernst R. Kuse, Karl J. Oldhafer, Burckhardt Ringe, Shogo Okamoto, Albrecht Bornscheuer, George Brabant, Yoshio Yamaoka, Rudolf Pichlmayr – 1 June 1995 – Regulatory roles of insulin and glucagon in hepatic metabolism and function are well described. However, little is known about implications of host pancreatic hormones in primary function of grafted liver. This study aimed to investigate it in relation to hepatic mitochondrial function.

Histidinemia in mice: A metabolic defect treated using a novel approach to hepatocellular transplantation

Clare Selden, Denis Calnan, Neil Morgan, Hervey Wilcox, Edward Carr, Humphrey J. F. Hodgson – 1 May 1995 – Histidinemia in mice and in humans is an autosomal recessive disorder of histidine metabolism that leads to high‐histidine levels in both plasma and urine and is caused by a lack of hepatic histidine‐α‐deaminase (histidase). We have used a novel approach to hepatocellular transplantation to effect a complete phenotypic cure of histidinemia in a mouse model.

Regression of bile duct damage and bile duct proliferation in the non‐rearterialized transplanted rat liver is associated with spontaneous graft rearterialization

Delai Zhao, Arthur Zimmermann, Larisa V. Kuznetsova, Anthony M. WheatleyD – 1 May 1995 – The aim of this study was to investigate the long‐term consequences of non‐rearterialization of the graft in rat liver transplantation. Liver transplantation with (AOLT) and without graft rearterialization (NOLT) was performed in anesthetized male Lewis rats. Quantitative morphometry and semiquantitative histopathology of the liver were performed at various times after operation. Volume fractions of tissue components were determined.

Bacterial and fungal infections after liver transplantation: An analysis of 284 patients

Jim J. Wade, Nancy Rolando, Karen Hayllar, John Philpott‐Howard, Mark W. Casewell, Roger Williams – 1 May 1995 – A prospective study of bacterial and fungal infections after liver transplantation in 284 adults was undertaken. One hundred seventy‐five (62%) became infected; bacterial or fungal infections occurred in 159 (56%) and 36 (13%) patients, respectively. Gram‐positive cocci, in particular Staphylococcus aureus and Enterococcus faecium, were the commonest bacterial pathogens, and bacteremia and wound infection were the most frequent bacterial infections.

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