L N Bull, V E Carlton, N L Stricker, S Baharloo, J A DeYoung, N B Freimer, M S Magid, E Kahn, J Markowitz, F J DiCarlo, L McLoughlin, J T Boyle, B B Dahms, P R Faught, J F Fitzgerald, D A Piccoli, C L Witzleben, N C O'Connell, K D Setchell, R M Agostini, S A Kocoshis, J Reyes, A S Knisely – 30 December 2003 – Byler disease (ByD) is an autosomal recessive disorder in which cholestasis of onset in infancy leads to hepatic fibrosis and death.

J E Cardier, E Barberá‐Guillem – 30 December 2003 – In previous work, two anatomically distinct‐liver sinusoid endothelial cells (LEC): LEC‐1 and LEC‐2, have been described. We also reported that extramedullary hepatic hematopoiesis occurs only in close contact with LEC‐1, suggesting that these cells may provide the microenvironment necessary for the maintenance and growth of hematopoietic cells. In the present work, we studied the capacity of LEC‐1 and LEC‐2 to maintain in vitro hematopoiesis. LEC‐1 and LEC‐2 were isolated and cloned from livers of adult mice.

K C Wilhelmsen – 30 December 2003

G A Macdonald, K A Frey, B W Agranoff, S Minoshima, R A Koeppe, D E Kuhl, B L Shulkin, M R Lucey – 30 December 2003 – Increased activation of the central benzodiazepine receptor (BZR) appears to play an important role in hepatic encephalopathy (HE). However, there is controversy regarding whether the density or affinity of BZRs is altered.

T Daemen, M Velinova, J Regts, M de Jager, R Kalicharan, J Donga, J J L van der Want, G L Scherphof – 30 December 2003 – Liposomes with diameters of 200 to 400 nm containing phosphatidylserine (PS) or phosphatidylglycerol (PG) were injected intravenously into rats. Two hours after injection, 75% of the injected dose of PS liposomes was found in the liver and only 10% found in the spleen, while 35% of the PG liposomes was found in the liver and as much as 40% was found in the spleen.

S J Cotler, D R Gretch, M P Bronner, H Tateyama, M J Emond, C dela Rosa, J D Perkins, R L Carithers – 30 December 2003 – Although hepatitis G virus infection (HGV) is usually asymptomatic, it has been associated with mild hepatic injury. Whether hepatitis G co‐infection alters the natural history of other viral hepatitis infections remains to be determined. In the present study, we investigated whether hepatitis G impacts on the time to recurrent hepatitis or on the time to progression to fibrosis in hepatitis C‐infected patients who undergo liver transplantation.

S Mihm, A Fayyazi, G Ramadori – 30 December 2003 – Hepatitis C virus (HCV) causes acute and often also chronic liver disease. Hepatocellular injury might result from both a host response directed to inhibit viral spread and from processes initiated by the virus itself. To study mechanisms involved in hepatocellular injury, liver tissue from chronically HCV‐infected patients was analyzed for the expression of the inducible isoform of nitric oxide synthase (iNOS) and for interferon γ (IFN‐γ) by a quantitative, competitive reverse‐transcription‐polymerase chain reaction (RT‐PCR) technique.

T Pollicino, A R Zanetti, I Cacciola, M A Petit, A Smedile, S Campo, L Sagliocca, M Pasquali, E Tanzi, G Longo, G Raimondo – 30 December 2003 – Controversial data were recently published concerning the association of hepatitis B virus (HBV) variants with fulminant hepatitis (FH). In this study, we first analyzed the complete nucleotide sequences of HBV genomes isolated from serum samples from a surgeon and his mother, who was accidentally infected by the son; both died of FH.

R G Cameron, M G Neuman, L M Blendis – 30 December 2003 – Stellate cells have only recently received attention in patients with primary biliary cirrhosis (PBC). We used electron microscopy and morphometry to perform a qualitative and quantitative examination of lipid‐storing activity of stellate cells in liver biopsies of 26 patients with noncirrhotic and cirrhotic PBC. Parallel with this study, a comparative analysis of the morphology of stellate cells in 51 patients with livers of normal histology was performed.

A Colell, C Garcia‐Ruiz, A Morales, A Ballesta, M Ookhtens, J Rodes, N Kaplowitz, J C Fernandez‐Checa – 30 December 2003 – Ethanol intake depletes the mitochondrial pool of reduced glutathione (GSH) by impairing the transport of GSH from cytosol into mitochondria. S‐Adenosyl‐L‐methionine (SAM) supplementation of ethanol‐fed rats restores the mitochondrial pool of GSH. The purpose of the current study was to determine the effect of ethanol feeding on the kinetic parameters of mitochondrial GSH transport, the fluidity of mitochondria, and the effect of SAM on these changes.