Robin Patel, Sharlene L. Allen, Janice M. Manahan, Alan J. Wright, Ruud A.F. Krom, Russell H. Wiesner, David H. Persing, Franklin R. Cockerill, Rodney L. Thompson – 30 December 2003 – At Mayo Medical Center (Rochester, MN), surveillance rectal (and other‐site) cultures have been routinely collected from liver transplant recipients as part of a selective bowel decontamination program. Beginning in 1995, vancomycin‐resistant enterococcus (VRE) colonization and infection were identified in Mayo Clinic liver and kidney transplant patients through our surveillance cultures.

Martín Prieto, María D. Gómez, Marina Berenguer, Juan Córdoba, José M. Rayón, Miguel Pastor, Antonio García‐Herola, David Nicolás, Domingo Carrasco, Juan F. Orbis, José Mir, Joaquín Berenguer – 30 December 2003 – Transmission of hepatitis B virus (HBV) infection from donors who are negative for hepatitis B surface antigen (HBsAg−) but positive for antibody to hepatitis B core antigen (anti‐HBc+) has been reported. However, previous studies were generally performed in geographic regions with a low prevalence of anti‐HBc positivity in the liver donor population.

R. Chien, L. Yang, P. Lin, Y. Liaw – 30 December 2003 – To evaluate the incidence, severity, and course of ketoconazole‐ associated hepatic injury, 211 patients with onychomycosis were randomized by a ratio of 2:1 to receive either ketoconazole (137 patients) or griseofulvin (74 patients). All of them were seronegative for hepatitis B surface antigen (HBsAg) and anti‐hepatitis C virus (HCV) and had no biochemical abnormality before therapy. The two groups were comparable in age, sex, and pretherapy liver biochemical tests.

J. J. Chen, S. Schenker, G. I. Henderson – 30 December 2003 – Lipid peroxidation has been implicated in ethanol‐induced liver injury and observed in fetal liver and brain after maternal ethanol consumption with mitochondria being the target organelles. This process generates a highly reactive and toxic product, 4‐hydroxynonenal (HNE). In the present study, HNE levels and metabolism were assessed in mitochondria of fetal and maternal liver after in vivo ethanol exposure.

E. L. Thomas, S. D. Taylor‐Robinson, M. L. Barnard, G. Frost, J. Sargentoni, B. R. Davidson, S. C. Cunnane, J. D. Bell – 30 December 2003 – We investigated adipose tissue fatty acid composition in 22 moderately to severely malnourished patients with cirrhosis and in 22 healthy volunteers by in vivo carbon‐13 magnetic resonance spectroscopy (MRS). Gas‐liquid chromatography (GLC) of adipose tissue samples was also performed in 11 of the patients and in 4 volunteers.

K. H. Böker, G. Dalley, M. J. Bahr, H. Maschek, H. L. Tillmann, C. Trautwein, K. Oldhaver, U. Bode, R. Pichlmayr, M. P. Manns – 30 December 2003 – We analyzed the long‐term clinical course of 71 patients with RNA‐positive hepatitis C virus (HCV) infection after liver transplantation. Patients with reinfection after transplantation for HCV‐related liver disease, or de novo infection at transplantation were followed for up to 12 years. Cumulative survival for patients with HCV infection at 2, 5, and 10 years after transplantation was 67%, 62%, and 62%, respectively.

J. G. C. Kingham – 30 December 2003

A P Bautista – 30 December 2003 – This study tested the hypothesis that prolonged consumption of alcohol directly or indirectly, through endotoxin influx in the circulation, stimulates the Kupffer cells to produce macrophage inflammatory protein‐2 (MIP2) and up‐regulates the expression of adhesion molecules, i.e., CD18 on PMNs and its counter‐receptor, intercellular adhesion molecule‐1 (ICAM‐1), on hepatic cells.

S Rose, A Pizanis, M Silomon – 30 December 2003 – The present study evaluated the effect of the benzothiazepine Ca2+ channel blocker diltiazem (DZ) on altered hepatocellular Ca2+ regulation and oxidant injury during hemorrhagic shock/resuscitation. In anesthetized, male Sprague‐Dawley rats, hemorrhagic shock was induced by rapid blood withdrawal and maintaining the mean arterial blood pressure at 40 mm Hg over 60 minutes. Rats were then resuscitated with 60% of shed blood and threefold the shed blood volume of Ringer's lactate.

S Tsai, Y Liaw, M Chen, C Huang, G C Kuo – 30 December 2003 – One striking clinical feature of hepatitis C virus (HCV) infection is that more than 50% of patients with acute hepatitis C will develop chronic infection. To investigate its possible mechanisms, we examined the activation of type 2‐like T‐helper (Th2‐like) cells relating to the development of chronicity.