M Casado, M Velasco, L Bosca, P Martin‐Sanz – 30 December 2003 – Treatment of rats at 21 days' gestation with lipopolysaccharide (LPS) induced type II NO synthase (iNOS) expression in maternal liver but completely failed to elicit this response in the corresponding fetal tissue. The impaired response of fetal liver cannot be attributed to alterations in the sensitivity of this organ to LPS or to proinflammatory cytokines involved in iNOS expression (tumor necrosis factor α [TNF‐α], interferon gamma [IFN‐γ]), because cultured fetal and adult hepatocytes similarly responded to these factors.

M Sakamoto, T Ueno, H Sugawara, T Torimura, R Tsuji, K Sujaku, M Sata, K Tanikawa – 30 December 2003 – Interleukin‐1β (IL‐1β) is closely involved in liver disorders. IL‐1β produces nitric oxide (NO) in vascular smooth muscle cells and relaxes vascular smooth muscle via cyclic guanosine 3′,5′‐monophosphate (cGMP). In this study, we evaluated the relaxing effect of IL‐1β on cultured Ito cells. Ito cells were isolated from the livers of male Wistar rats and cultured for 24 hours.

K Viitala, Y Israel, J E Blake, O Niemela – 30 December 2003 – Chronic ethanol ingestion has been suggested to trigger the formation of antibodies that recognize acetaldehyde‐protein condensates. In this study, assays for immunoglobulin (Ig) A, IgG, and IgM antibodies to acetaldehyde‐derived adducts were performed on sera of 140 alcohol consumers, 19 patients with nonalcoholic liver disease (NALD), 35 healthy nondrinking controls, and 10 nondrinking patients with IgA or IgG myeloma. Anti‐acetaldehyde (Ach)‐adduct antibodies of each Ig isotype were found from the alcohol abusers.

A C Anand, B H Ferraz‐Neto, P Nightingale, D F Mirza, A C White, P McMaster, J M Neuberger – 30 December 2003 – We have used a formal transplant protocol to select patients with alcoholic liver disease (ALD) for transplantation. We retrospectively analyzed all the patients with ALD who were referred specifically for transplantation to our Liver Unit between 1987 and 1994. Patients were selected for liver transplantation if they had end‐stage liver disease and had remained abstinent from the time they were medically advised to stop alcohol intake.

30 December 2003

T Armbrust, B Nordmann, M Kreißig, G Ramadori – 30 December 2003 – The subcomponent of complement C1, C1q, mediates complement activation via the classical pathway, and therefore may play an important role in the inflammatory processes in which complement activation is involved. The aim of our study was to investigate C1q synthesis by macrophages of normal and of acutely damaged livers. The localization of C1q in liver tissue was studied by immunohistochemistry.

J A Gonzalez‐Correa, J P De La Cruz, E Martin‐Aurioles, M A Lopez‐Egea, P Ortiz, F Sanchez de la Cuesta – 30 December 2003 – We used an animal model of extrahepatic biliary obstruction of 7 days' duration to study the production of thiobarbituric acid reactive substances (TBARS), total glutathione (TG), reduced glutathione (GSH), and oxidized glutathione (GSSG), and the enzymatic activities of GSH‐ peroxidase, GSSG‐reductase, and GSH‐transferase.

G A MacDonald, J K Greenson, E A DelBuono, W M Grady, R M Merion, T S Frank, M R Lucey, H D Appelman – 30 December 2003 – Cytomegalovirus (CMV) is a significant cause of morbidity in immunosuppressed patients. It is characterized in the liver by parenchymal microabscesses, usually containing CMV‐infected cells. However, not all hepatic microabscesses are due to CMV infection. In 1992, we described “mini” microabscess (MMA) syndrome, a distinct clinical syndrome that occurs in transplanted livers.

M H Lehmann – 30 December 2003

M Guido, M Rugge, G Leandro, I M Fiel, S N Thung – 30 December 2003 – Patients with chronic viral hepatitis are at high risk of developing cirrhosis, but the outcome of the disease in a given patient is unpredictable. Hepatic stellate cells have been demonstrated to be the most important cell type involved in hepatic fibrogenesis, regardless of the cause of the liver injury. The α isotype of actin (a phenotypic marker of smooth muscle cells) may be expressed by hepatic stellate cells, reflecting their “activation” to myofibroblast‐like cells.