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.

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.

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.

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.

K C Wilhelmsen – 30 December 2003

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.

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.

C Sempoux, Y Horsmans, A Geubel, J Fraikin, B E Van Beers, J Gigot, J Lerut, J Rahier – 30 December 2003 – Radiation‐induced liver disease is recorded as a form of veno‐occlusive disease. Its pathogenesis remains unclear even if the initial injury likely occurs in the endothelial cells of central veins. The aim of our study was to investigate liver morphological features in relation to α‐isoform of smooth muscle actin expression in hepatic stellate cells in six patients treated by localized radiotherapy on the biliopancreatic area.

M Hou, P A Cahill, S Zhang, E M Redmond, J V Sitzmann – 30 December 2003 – Portal hypertension (PHT) is characterized by splanchnic hyperemia due to a reduction in mesenteric vascular resistance. The reasons for the decreased resistance include an increased responsiveness to a vasodilator substance.

G K Lau, A S Lok, R H Liang, C L Lai, E K Chiu, Y L Lau, S K Lam – 30 December 2003 – Adoptive immunity transfer has been reported to be effective in clearing chronic hepatitis B virus (HBV) infection. Two hundred twenty‐six patients who received allogeneic bone marrow transplantation (BMT) between May 1990 and September 1995 were screened for hepatitis B markers. Twenty‐one patients were hepatitis B surface antigen (HBsAg) positive before BMT. The median follow‐up period was 20 months (range, 2‐59 months).