Detection by ligase chain reaction of precore mutant of hepatitis B virus

S. Minamitani, S. Nishiguchi, T. Kuroki, S. Otani, T. Monna – 30 December 2003 – The clinical diagnosis of infection with the most common precore mutant of hepatitis B virus (HBV), that with a point mutation from guanine to adenine at nucleotide 83 in the precore region, is important because the disease may progress rapidly despite interferon therapy. A practical method to detect this mutant is needed. With the ligase chain reaction (LCR), target DNA sequences can be amplified and single base mutations can be detected.

Liver transplantation in Asian patients with chronic hepatitis B

B. M. Ho, S. K. So, C. O. Esquivel, E. B. Keeffe – 30 December 2003 – It has been suggested that Asian patients have reduced survival after liver transplantation because of greater recurrence of hepatitis B virus (HBV). We analyzed the outcome of Asian and non‐Asian patients receiving transplants for chronic hepatitis B between May 1988 and March 1994. Baseline Child‐Pugh score and United Network for Organ Sharing (UNOS) status, HBV recurrence, and survival were compared between the two groups. All but one patient received variable doses of hepatitis B immune globulin.

Prenatal alcohol exposure affects galactosyltransferase activity and glycoconjugates in the Golgi apparatus of fetal rat hepatocytes

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.

Kupffer cells generate superoxide anions and modulate reperfusion injury in rat livers after cold preservation

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.

Membrane potential of hepatic mitochondria after acute cocaine administration in rats—The role of mitochondrial reduced glutathione

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.

Treatment of chronic hepatitis C with interferon alfa‐n3: A multicenter, randomized, open‐label trial

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.

Ursodeoxycholic acid therapy in pediatric patients with progressive familial intrahepatic cholestasis

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.

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