P Lampertico, E Del Ninno, A Manzin, M F Donato, M G Rumi, G Lunghi, A Morabito, M Clementi, M Colombo – 30 December 2003 – Short‐term interferon treatment of serum hepatitis B e antigen (HBeAg)‐negative carriers with serum hepatitis B virus (HBV) DNA and histological features of chronic hepatitis B has been largely unsuccessful. In a pilot study of long‐term treatment, 42 such patients were randomly assigned to 6 million units of interferon alfa 2b (IFN‐α2b) three times per week for 24 consecutive months (n = 21, 4 with cirrhosis) or to no therapy (n = 21, 3 with cirrhosis).

M Tacke, S Schmolke, V Schlueter, S Sauleda, J I Esteban, E Tanaka, K Kiyosawa, H J Alter, U Schmitt, G Hess, B Ofenloch‐Haehnle, A M Engel – 30 December 2003 – The second envelope protein (E2) of the hepatitis G virus (HGV) was expressed in Chinese hamster ovary (CHO) cells and showed a molecular weight of approximately 60 to 70 kd, with 15 to 25 kd of the size contributed by N‐linked glycosylation. An enzyme‐linked immunosorbent assay (ELISA) using HGV‐E2 was developed to test for antibodies to this protein (anti‐E2) in human sera.

F C Bekkering, J T Brouwer, S W Schalm, A Elewaut – 30 December 2003

D R Gretch – 30 December 2003 – Diagnostic tests for hepatitis C can be divided into the following two general categories: 1) serological assays that detect antibody to hepatitis C virus (anti‐HCV); and 2) molecular assays that detect, quantify, and/or characterize HCV RNA genomes within an infected patient. Serological assays have been subdivided into screening tests for anti‐HCV, such as the enzyme immunoassay (EIA), and supplemental tests such as the recombinant immunoblot assay (RIBA).

R S Koff – 30 December 2003 – The natural history of untreated chronic hepatitis C is controversial, and direct knowledge of the long‐term clinical and economic outcomes of current α interferon treatment regimens remains limited. Decision analytic models using available information on outcome probabilities and associated health care costs in the United States have been developed but are available only in abstract form.

K. Ramakrishnan Bhaskar, Bradley S. Turner, Shelley A. Grubman, Douglas M. Jefferson, J.Thomas LaMont – 30 December 2003 – Hepatic dysfunction in cystic fibrosis (CF) has been attributed to accumulation of viscous mucoid secretions in intrahepatic bile ducts. The purpose of our study was to compare glycoconjugate secretion by intrahepatic biliary epithelial (IBE) cells derived from normal livers and livers of CF patients with the delta F508 mutation of the cystic fibrosis transmembrane conductance regulator (CFTR).

Don C. Rockey, John J. Chung, Charlotte M. McKee, Paul W. Noble – 30 December 2003 – Hepatic injury and chronic wounding are characterized by increased synthesis of extracellular matrix proteins including hyaluronan (HA). Recently, it has been recognized that low‐molecular‐weight fragments of HA, but not native HA (e.g., high‐molecular‐weight HA), induce inflammatory gene expression, and activate the transcriptional regulator, nuclear factor κB (NF‐κB).

Zhi‐Qi Zhang‐Gouillon, Qi‐X. Yuan, Bing Hu, Norman Marceau, Barbara A. French, Karl Gaal, Yasuki Nagao, Y.‐J. Yvonne Wan, Samuel W. French – 30 December 2003 – Drug‐primed mice, created by a 5‐month feeding of diethyl‐1,4‐dihydro‐2,4,6‐trimethyl‐3,5‐pyridinedicarboxylate (DDC), followed by a 1‐month withdrawal, were refed ethanol or isocaloric dextrose (control) diets intragastrically for 7 days. The formation of Mallory bodies (MBs) was monitored by immunofluorescence and immunoperoxidase microscopy using antibodies to cytokeratin and ubiquitin, and also by electron microscopy.

Esther Granot – 30 December 2003 – Hyperlipidemia is frequently observed in patients who undergo renal, cardiac, bone marrow, or liver transplantation, and its contribution to the long‐term morbidity and survival of patients with organ transplants may be substantial. In the few studies that have focused on the pediatric age group, findings have been inconsistent. The lipoprotein profile of 10 children after liver transplantation was characterized and compared with those in normal population controls and 10 healthy siblings.

Maurizio Sampietro, Alberto Piperno, Loredana Lupica, Cristina Arosio, Anna Vergani, Noemi Corbetta, Ida Malosio, Michela Mattioli, Anna Ludovica Fracanzani, Maria Domenica Cappellini, Gemino Fiorelli, Silvia Fargion – 30 December 2003 – Sporadic porphyria cutanea tarda (PCT) is caused by a reduced activity of uroporphyrinogen decarboxylase (URO‐D) in the liver. Mild to moderate iron overload is common in PCT, as iron is one of the factors which trigger the clinical manifestations of the disease through the inactivation of URO‐D.