J H Albrecht, A H Meyer, M Y Hu – 30 December 2003 – WAF1/Cip1/Sdi1 (p21) is the prototype of a family of proteins that inhibit cyclin‐dependent kinases and regulate cell cycle progression in eukaryotic cells. In addition to normal cell cycle progression, p21 is involved in growth suppression mediated by p53 and transforming growth factor β (TGFβ), differentiation, and apoptosis. To gain insight into the possible involvement of p21 in liver cell growth, the expression and regulation of the p21 gene was evaluated in rodent models of liver regeneration and specimens of human liver diseases.

G V Gregorio, B Portmann, F Reid, P T Donaldson, D G Doherty, M McCartney, A P Mowat, D Vergani, G Mieli‐Vergani – 30 December 2003 – To determine the clinical, biochemical, and histological features, and outcome of childhood autoimmune hepatitis (AIH), we reviewed the medical records of 52 children with AIH, 32 (median age: 10 [2‐15] years) anti‐nuclear and/or smooth muscle antibody (ANA/SMA) positive, 20 (7 [0.8‐14] years) liver/kidney microsomal antibody (LKM‐1) positive, with median follow‐up of 5 years (range 0.3‐19).

E Jacquemin, D Hermans, A Myara, D Habes, D Debray, M Hadchouel, E M Sokal, O Bernard – 30 December 2003 – Progressive familial intrahepatic cholestasis (PFIC) is a lethal inherited childhood cholestasis of hepatocellular origin. Different subtypes of PFIC have been described according to serum gamma‐glutamyl transpeptidase (GGT) activity. There is currently no effective medical therapy available for children with PFIC. We report on 39 patients with PFIC who received ursodeoxycholic acid (UDCA) orally (20‐30 mg/kg b.w./day) for a period of 2 to 4 years.

D M Simon, S C Gordon, M M Kaplan, R S Koff, F Regenstein, G Everson, Y M Lee, F Weiner, A Silverman, T Plasse, D Fedorczyk, M Liao – 30 December 2003 – We studied the antiviral effectiveness and safety of interferon alfa‐n3, a natural alpha interferon which contains multiple interferon species, in the treatment of previously untreated patients with chronic hepatitis C. Seventy‐seven patients were randomized to receive either 1.0, 2.5, 5.0, or 10.0 million units (MU) of interferon alfa‐n3 three times a week for 24 weeks and were then followed for an additional 24 weeks.

A Masini, D Gallesi, F Giovannini, T Trenti, D Ceccarelli – 30 December 2003 – Cocaine hepatotoxicity may be mediated by oxidative damage, possibly involving mitochondrial injury. The effect of an acute dose of cocaine in rats on the mitochondrial level of reduced glutathione, nicotinamide adenine dinucleotide (NADH) and nicotinamide adenine dinucleotide phosphate (NADPH), important determinants in cellular defense against oxidative stress, was investigated.

H Shibuya, N Ohkohchi, K Seya, S Satomi – 30 December 2003 – This study was designed to determine the source of reactive oxygen species (ROS) and whether Kupffer cells modulate the injury of perfused rat liver after cold preservation. The livers of male Lewis rats pretreated with schizophyllan glucan (SPG) (10 mg/kg, SPG group) or gadolinium chloride (5 mg/kg; Gd group) and untreated rats (control group) were preserved in University of Wisconsin solution for 0, 12, and 24 hours at 4 degrees C and then perfused for 60 minutes with oxygenated Krebs‐Henseleit bicarbonate buffer.

J Renau‐Piqueras, R Guasch, I Azorín, J Seguí, C Guerri – 30 December 2003 – Prenatal exposure to alcohol affects the morphological, structural, and functional features of the Golgi apparatus (GA), thus altering the glycosylation process in fetal hepatocytes. To elucidate the cellular mechanisms underlying these alterations, we have studied the effect of alcohol exposure in utero on the activity of liver galactosyltransferase, an enzyme involved in the glycosylation process, and on the hepatic glycoprotein sugar composition.

J Bruix – 30 December 2003

30 December 2003

30 December 2003