F Braet, R De Zanger, D Jans, I Spector, E Wisse – 1 September 1996 – This report describes the effect of the actin‐disrupting marine toxin latrunculin A on the cytoskeleton and fenestrae of liver endothelial cells (LECs). Fluorescence microscopy and whole mount‐transmission electron microscopic preparations of isolated, purified, and cultured LECs showed that latrunculin A, which sequesters actin monomers and depolymerizes actin filaments, caused profound changes in microfilament organization in LECs.

O A Rayyes, A Wallmark, C Florén – 1 September 1996 – The aim of this study was to elucidate the possible causes of elevated low‐density lipoprotein (LDL)‐cholesterol levels in transplanted patients treated with the immunosuppressant drug, cyclosporine. HepG2 cells, from a well‐differentiated cell‐line of hepatoma cells, were cultured and used as a model for in vitro hepatocytic LDL uptake. Different concentrations of cyclosporine, which were within the range of concentrations found in humans treated with cyclosporine, were added to tissue culture medium together with 125I‐LDL.

I Aguilar‐Delfin, F López‐Barrera, R Hernández‐Munoz – 1 September 1996 – It has been proposed that lipid peroxidation (LP) might be a modulator of cell division, influencing initiation and cessation of mitosis in regenerating liver. However, the understanding of the participating role of this event in the onset of liver proliferation has been hampered by the fact that both higher or lower LP have been reported after two‐thirds partial hepatectomy (PH).

J C Quero, I J Hartmann, J Meulstee, W C Hop, S W Schalm – 1 September 1996 – Neuropsychological tests used for the assessment of subclinical hepatic encephalopathy (SHE) may overdiagnose SHE because scores are usually not corrected for age. The aim of this study was to estimate the prevalence of SHE using two easy administrable psychometric tests (Number Connection Test part A [NCT‐A], Symbol Digit Test [SDT]) with age‐related normal values. In addition, spectral electroencephalogram (EEG) was used, which is the in‐house electrophysiological method for quantifying encephalopathy.

J Madon, H E Blum – 1 September 1996 – A highly efficient receptor‐mediated delivery system for DNA and oligodeoxynucleotides (ODNs) to avian liver cells has been established, using complexes of nonmodified human adenovirus particles and a protein conjugate consisting of N‐acetyl‐glucosamine‐modified bovine serum albumin, streptavidin, and Poly‐L‐lysine. The newly developed method of protein‐conjugate preparation and purification yielded highly stable complexes with high DNA delivery efficiency for constructs expressing the lacZ gene, hepatitis B virus (HBV) DNA, and ODNs.

1 September 1996

A Hui, M Sakamoto, Y Kanai, Y Ino, M Gotoh, J Yokota, S Hirohashi – 1 September 1996 – We analyzed the p16INK4 status of 6 hepatocellular carcinoma (HCC) cell lines and 32 primary HCC tumors, including 9 early‐stage tumors, to determine whether p16INK4 tumor‐suppressor gene inactivation participates in hepatocarcinogenesis.

C Trautwein, H Schrem, H L Tillmann, S Kubicka, D Walker, K H Böker, H J Maschek, R Pichlmayr, M P Manns – 1 September 1996 – Mutational changes in the pre‐S region of hepatitis B virus (HBV) were analyzed in 20 patients who experienced HBV reinfection after orthotopic liver transplantation (OLT). HBV DNA was extracted from patient sera before and after OLT. The pre‐S sequence was amplified via polymerase chain reaction, subcloned, sequenced, and analyzed.

Lawrence S Friedman – 1 September 1996

D E Johnston, C Kroening – 1 September 1996 – The contribution of hepatocytes to liver prostaglandin synthesis is controversial, partly because hepatocytes of varying purity have been studied. In this study, prostaglandin synthesis was examined in conventional and ricin‐purified rat hepatocytes that were incubated with gaseous carbon tetrachloride as a model stimulus for lipid peroxidation and prostaglandin synthesis. Hepatocytes that were incubated for 2 hours with 1 ml, of liquid CCl4/5 L gas volume showed no evidence of cell death or injury.