Gianfranco Alpini, John O. Phillips, Benjamin Vroman, Nicholas F. Larusso – 1 August 1994

Yukio Kato, Ke‐Xin Liu, Toshikazu Nakamura, Yuichi Sugiyama – 1 August 1994 – Because hepatocyte growth factor is known to have affinity for heparin, we studied the binding isotherm and found that hepatocyte growth factor has a high‐affinity binding site for 35S‐heparin with an equilibrium dissociation constant of approximately 0.6 nmol/L. We then analyzed the pharmacokinetic behavior of the heparin–hepatocyte growth factor complex in rats.

Rebecca F. Harrison, Mervyn H. Davies, James M. Neuberger, Stefan G. Hubscher – 1 August 1994 – Fibroobliterative lesions and fibrous cholangitis are characteristic histological lesions of primary sclerosing cholangitis. To determine whether such lesions can be found in the liver allograft, and whether they represent recurrent disease, we reviewed all consecutive histological material taken at greater than 6 mo after transplantation in a 3‐yr period from a series of 207 liver transplantations (22 with primary sclerosing cholangitis, 185 controls without primary sclerosing cholangitis).

Michéle Chevallier, Sylviane Guerret, Philippe Chossegros, Françoise Gerard, Jean‐Alexis Grimaud – 1 August 1994 – The evaluation of hepatic fibrosis on histological sections is of great interest for the staging and follow‐up of chronic liver disease. Because no reliable scoring system is yet available, we have designed a semiquantitative scoring system in which the four main sites of fibrotic deposit — centrilobular vein, portal tract and perisinusoidal space, together with width and number of septa when present — are analyzed.

Yilmaz Cakaloglu, J. Michael Tredger, John Devlin, Roger Williams – 1 August 1994 – We have investigated the importance of cytochrome P‐450IIIA enzyme activity in influencing dosage of the immunosuppressive drugs FK 506 and cyclosporine after liver transplantation. Cytochrome P‐450IIIA enzyme activity in vivo was measured 1 yr postoperatively in 37 stable orthotopic liver graft recipients (21 receiving FK 506 and 16 given cyclosporine) by the erythromycin breath test and the production of monoethylglycinexylidide from lignocaine.

Masahiro Uehara, Noriyuki Sato – 1 August 1994 – To evaluate whether neutrophil bactericidal function, the ability to produce oxygen‐derived free radicals, is altered in patients with chronic liver disease, we measured chemiluminescence amplified by a luciferin analog (Cypridina luciferin analog‐dependent chemiluminescence) and luminol (luminol‐dependent chemiluminescence) in response to N‐formyl‐Met‐Lue‐Phe by neutrophils from patients with chronic liver diseases due to C and/or B type hepatitis: chronic active hepatitis, cirrhosis and hepatocellular carcinoma.

Tomasz I. Michalak, Bo Lin – 1 August 1994 – Hepadnaviral antigens exposed on hepatocytes serve as targets and as possible modulators of immunopathogenic reactions causing liver damage. To identify molecular species of viral proteins at the liver cell surface and the relationship between their expression and the persistence and severity of virus‐induced liver injury, we examined woodchuck hepatitis virus core and envelope polypeptides in host hepatocyte plasma membranes from acute and chronic hepatitis.

Reynaldo Gacad, Kristine Kaminsky‐Russ, Kevin D. Mullen, Peter Widler, Hans U. Fisch, Arthur Zimmermann, Thomas E. Schläepfer, Jürg Reichen, Peter‐Schoch – 1 August 1994

Markus Lindauer, Konstantin Beier, Alfred Völkl, H. Dariush Fahimi – 1 August 1994 – The hepatic zonation of peroxisomes and four of their matrical enzyme proteins (catalase, acyl coenzyme A oxidase, multifunctional protein, thiolase) has been investigated in normal male rats and after treatment with three divergent hypolipidemic drugs by means of automatic image analysis and quantitative immunoelectron microscopy. The induction of peroxisomal enzymes was confirmed by Western blotting and enzyme activity determinations in liver homogenates and in highly purified peroxisome fractions.

David E. Johnston, Rahul Jasuja – 1 August 1994 – We had found several methods of hepatocyte isolation to be inadequate for removing Kupffer and endo thelial cells and so developed a method of selectively killing these nonparenchymal cells in hepatocyte cultures using the known selective uptake and toxicity of the protein synthesis inhibitor ricin and its A chain by nonparenchymal cells. Kupffer cells were quantitated with the Ku‐1 monoclonal antibody.