Alan L. Buchman, Mark D. Dubin, Adib A. Moukarzel, Donald J. Jenden, Margareth Roch, Kathleen M. Rice, Jeff Gornbein, Marvin E. Ament – 1 November 1995 – Patients receiving long‐term total parenteral nutrition (TPN) develop hepatic steatosis as a complication. Our previous studies have shown this to be caused, at least in part, by choline deficiency. We studied four patients (1 man, 3 women) aged 50 ± 13 years who had low plasma‐free choline concentrations 4.8 ± 1.7 (normal, 11.4 ± 3.7 nmol/mL). The patients had received TPN for 9.7 ± 4.7 years.

Raymond S. Koff – 1 November 1995

E. Anthony Jones – 1 November 1995

Axel M. Gressner, Birgit Lahme, Arnfried Brenzel – 1 November 1995 – The activation of proliferation of rat liver hepatic stellate cells (HSC) in cooperation with hepatocytes (PC) was studied using a coculture system and cell‐conditioned media, respectively. The proliferation of HSC was followed by incorporation of [3H] thymidine and BrdU into DNA and by DNA content per culture.

1 November 1995

Albert D. Min, Henry C. Bodenheimer – 1 October 1995

Keith D. Lindor, E. Rolland Dickson, Roberta A. Jorgensen, Monte L. Anderson, Russell H. Wiesner, Gregory J. Gores, Stephen M. Lange, Steven S. Rossi, Alan F. Hofmann, William P. Baldus – 1 October 1995 – Ursodeoxycholic acid (UDCA) and methotrexate (MTX) have both been proposed as treatments for patients with primary biliary cirrhosis (PBC). It has been suggested that a combination of the two drugs may offer advantages over either used separately. In this pilot study, we sought to evaluate the safety and efficacy of this combination for patients with PBC.

George Marinos, Francesco Torre, Shilpa Chokshi, Munther Hussain, Berwin E. Clarke, David J. Rowlands, Adrian L. W. F. Eddleston, Nikolai V. Naoumov, Roger Williams – 1 October 1995 – The T helper (Th) cell response to hepatitis B core antigen (HBcAg) was analyzed in 76 chronic hepatitis B virus (HBV) carriers with varying degrees of hepatic inflammation and HBV replication. Fifty‐five patients had active viral replication, 28 with minimal histological changes and normal alanine transaminase (ALT) and 27 with active hepatic inflammation and elevated ALT.

1 October 1995

James F. Whiting, Richard M. Green, Adam B. Rosenbluth, John L. Gollan – 1 October 1995 – Tumor necrosis factor–alpha (TNF,α), a cytokine that is produced in a variety of inflammatory diseases associated with cholestasis, is believed to be the primary mediator of the systemic effects of endotoxin. Thus, we have investigated the role of TNFα in the pathogenesis of endotoxin‐induced cholestasis in intact animals, and in the uptake of taurocholate by cultured hepatocytes.