F von Weizsäcker, S Wieland, H E Blum – 1 August 1996 – The hepatitis B virus (HBV) nucleocapsid consists of 240 viral core proteins that are arranged in a highly symmetrical structure, HBV replication can only take place inside intact nucleocapsids. In the present study, we investigated whether genetically engineered core mutants can inhibit viral replication by interfering with the formation of intact nucleocapsids. Using the duck hepatitis B virus (DHBV) model, a series of core protein mutants was generated.

C N van der Veere, M Sinaasappel, A F McDonagh, P Rosenthal, P Labrune, M Odiévre, J Fevery, J Otte, P McClean, G Bürk, V Masakowski, W Sperl, A P Mowat, G M Vergani, K Heller, J P Wilson, R Shepherd, P L Jansen – 1 August 1996 – This study represents a multicenter survey on the management of patients with Crigler‐Najjar syndrome (CNS) type 1. The aim of the survey was to find guiding principles for physicians in the care of these patients. Fifty‐seven patients were included. At the time of inclusion, 21 patients had received a liver transplant (37%).

M Masuhara, M Yasunaga, K Tanigawa, F Tamura, S Yamashita, I Sakaida, K Okita – 1 August 1996 – Hepatocyte growth factor (HGF) and transforming growth factor α (TGF‐α) stimulate liver regeneration, whereas transforming growth factor β 1 (TGF‐β 1) inhibits it in rats. However their significance in human liver diseases, especially in severe acute liver injury, remains unclear. We studied HGF, TGF‐α, and TGF‐β 1 messenger RNA (mRNA) expression in the livers of patients with live diseases using a competitive reverse transcriptase polymerase chain reaction.

K Kogure, Y Zhang, M Kanzaki, W Omata, T Mine, I Kojima – 1 August 1996 – When 1 μg 125I‐follistatin was administered into a rat intravenously, radioactivity levels in serum decreased rapidly. Analysis with a biexponential equation showed that the initial half‐ life and the terminal half‐life were 4.0 and 130.8 minutes, respectively. After 2 hours of infusion, approximately 9% of the follistatin infused remained in the liver, which was much more than that in kidney, spleen, pancreas, intestine, or lung.

U Eckhardt, J A Horz, E Petzinger, W Stüber, M Reers, G Dickneite, H Daniel, M Wagener, B Hagenbuch, B Stieger, P J Meier – 1 August 1996 – The peptidomimetic thrombin inhibitor CRC 220, 4‐methoxy‐2,3,6‐trimethylphenylsulfonyl‐L‐aspartyl‐D‐4‐amidinop henylalanyl‐ piperidide, is taken up into isolated rat hepatocytes through active, carrier‐mediated transport. This uptake is inhibited by bile acids. Functional expression in Xenopus laevis oocytes was performed to identify the transport system responsible for the hepatocellular CRC 220 uptake. Injection of poly(A)+RNA in X.

D T Wong – 1 August 1996

I K Schumacher, T Okamoto, B Kim, N R Chowdhury, J R Chowdhury, I J Fox – 1 August 1996 – Transplantation of hepatocytes has been shown to provide metabolic support during liver failure in experimental models. The potential clinical application of hepatocyte transplantation, however, is limited by the need for readily available, well‐characterized cells, and a worldwide shortage of donor organs.

R Oren, I Dotan, M Papa, Y Marravi, H Aeed, J Barg, L Zeidel, R Bruck, Z Halpern – 1 August 1996 – The coexistence of hyperkinetic circulation, hypermetabolism, and hyperactivity of the sympathetic nervous system is encountered in both cirrhosis and hyperthyroidism. Several drugs, such as propylthiouracil and propranolol, that are beneficial for treating some patients with chronic liver diseases are also prescribed for the treatment of thyrotoxicosis.

Z Ma, S S Lee – 1 August 1996 – In cirrhosis, cardiac contractile function has been extensively documented to be abnormal. At baseline, cardiac output is increased, and this is one of the characteristics of hyperdynamic circulation. However, when cirrhotic patients are challenged by pharmacological or physiological stress, ventricular hyporesponsiveness is revealed. Similar patterns have been noted in cirrhotic animal models.

M G Pessoa, T L Wright – 1 August 1996