R. Thomas Holzbach – 1 July 1988 – Biliary sludge is a collection of mucus, calcium bilirubinate, and cholesterol crystals that is usually recognized by characteristic echoes on ultrasonography. Its pathogenesis, clinical significance, and ultimate prognosis remain uncertain. We therefore studied the origin of biliary sludge ultrasonic echoes, using an ex vivo liver‐gallbladder preparation, and determined the outcome of a group of patients identified to have gallbladder sludge by ultrasonography.

M. Sawkat Anwer, Larry R. Engelking, Kathleen Nolan, Dianne Sullivan, Peter Zimniak, Roger Lester – 1 July 1988 – Effects of bile acids on cystolic Ca++ activity and cell viability of isolated rat hepatocytes were studied to test the hypothesis that bile acids may produce hepatotoxicity by increasing cystolic Ca++ activity. Changes in cystolic Ca++ activity were calculated from time‐dependent changes in fluorescence of quin‐2 loaded hepatocytes. Release of lactate dehydrogenase and changes in propodium iodide fluorescence were used to assess cell viability.

Rolf Gebhardt, Hans‐Jörg Burger, Hans Heini, Karl‐Ludwig Schreiber, Dieter Mecke – 1 July 1988 – Glutamine synthetase shows a striking heterogeneous distribution in normal rat liver as consistently revealed by immunohistochemistry using a specific antiserum against the rat liver enzyme or a cross‐reacting antiserum. The effects of zonal liver injury induced by allylformate or CC14 on this distribution and on the activity of glutamine synthetase as well as of enzymes with different acinar distribution were investigated.

M. Buti, R. Esteban, R. Jardi, H. Allende, J. Guardia, M. Roggendorf – 1 July 1988

The Rome Group for Epidemiology and Prevention of Cholelithiasis (GREPCO) – 1 July 1988 – A population of male civil servants in Rome, Italy, was investigated to determine the prevalence of symptomatic and asymptomatic gallstone disease. Field activities started in December, 1982 and were concluded in July, 1984. Diagnosis was made using real‐time ultrasonography. Participation in the study was 71.5%.

Jerome B. Zeldis, Francis A. Farraye, Howard N. Steinberg – 1 July 1988 – Exposure of human bone marrow mononuclear cells to hepatitis B virus results in the suppression of the in vitro growth of several hematopoietic progenitor cells. We studied the degree of inhibition of erythroid progenitor cells that results as a function of the time of exposure of mononuclear cells to hepatitis B virus and the ratio of virus to mononuclear cells, the multiplicity of infection.

Hey‐Chi Hsu, Ming‐Yang Lai, Ih‐Jen Su, Ding‐Shinn Chen, Mei‐Hwei Chang, Pei‐Ming Yang, Chieng‐Yen Wu, Hong‐Chung Hsieh – 1 July 1988 – To elucidate the biologic significance of hepatocyte HBsAg, its expression patterns were correlated with virus replication and liver pathology in 578 liver biopsies taken from chronic HBsAg carriers aged 1 to 80 years. Five major patterns of hepatocyte HBsAg were identified: homogeneous [intense and discrete, (Pattern A), faint and discrete, (Pattern B) and faint and grouped (Pattern C)]; globular or spotty (Pattern D), and marginal (Pattern E).

Charles L. Mendenhall – 1 July 1988

Eduard F. Stange, Jürgen Scheibner, Christine Lutz, Hans Ditschuneit – 1 July 1988 – The regulation of bile acid synthesis was studied (i) in intact or colectomized rats receiving cholate or taurocholate as a dietary supplement and (ii) in experiments using chow‐fed animals with a graded intravenous or intraduodenal taurocholate infusion. After the 2‐week diet period a bile fistula was established and rates of taurocholate, tauromuricholate and taurochenodeoxy‐cholate secretion were quantitated by high‐performance liquid chromatography.

Sophie Roy, Gilles Pomier‐Layrargues, Roger F. Butterworth, P.‐Michel Huet – 1 July 1988 – It has been suggested, from studies of a rabbit model of fulminant hepatic failure, that hepatic encephalopathy might be related to an increase in brain γ‐aminobutyric acid uptake through a more permeable blood‐brain barrier, leading to an overactivity of brain γ‐aminobutyric acid‐mediated inhibitory neurotrans‐mission.