Incidence and clinical consequences of surface and polymerase gene mutations in liver transplant recipients on hepatitis B immunoglobulin

Norah A. Terrault, Shuan Zhou, Robert W. McCory, Timothy L. Pruett, John R. Lake, John P. Roberts, Nancy L. Ascher, Teresa L. Wright – 30 December 2003 – Mutations in the “a” determinant of the surface gene have been associated with failure of hepatitis B immunoglobulin (HBIg) prophylaxis.

DNA ribonucleases that are active against intracellular hepatitis B viral RNA targets

Yasuhiro Asahina, Yoshinori Ito, Catherine H. Wu, George Y. Wu – 30 December 2003 – DNA ribonucleases directed against direct repeat 1 (DR1) and polyadenylation signal regions of hepatitis B virus (HBV) messages were prepared with phosphorothioate modifications and varying arm lengths. DNA ribonucleases modified throughout the entire molecule and in the target binding arms were completely protected from degradation after incubation with serum. DNA ribonuclease modified only at the 5′ and 3′ termini remained 92.9% intact after incubation.

Characterization of a sodium‐dependent transport system for butyrobetaine into rat liver plasma membrane vesicles

Simona Berardi, Bruno Stieger, Sandra Wächter, Brigitte O'Neill, Stephan Krähenbühl – 30 December 2003 – Butyrobetaine transport into the liver was studied using isolated rat hepatocyte plasma membrane vesicles. In the presence of a sodium chloride gradient, an overshoot could be observed, indicating active sodium‐dependent transport. A similar overshoot was recorded in the presence of lithium, but not of potassium, cesium, or choline chloride.

Peptidase activities of the multicatalytic protease in rat liver after voluntary and intragastric ethanol administration

Terrence M. Donohue, Rowen K. Zetterman, Zhi‐Qi Zhang‐Gouillon, Samuel W. French – 30 December 2003 – Ethanol consumption slows down the rate of hepatic protein catabolism. The present study was conducted to determine whether ethanol consumption, given by voluntary (pair) feeding or by intragastric administration, affected the peptidase activities of the proteasome in rat liver. Rats were pair‐fed liquid diets containing either ethanol or isocaloric maltose‐dextrin.

Selective inhibition of hepatic collagen accumulation in experimental liver fibrosis in rats by a new prolyl 4‐hydroxylase inhibitor

Martin Bickel, Karl‐Heinz Baringhaus, Martin Gerl, Volkmar Günzler, Jiri Kanta, Ludwig Schmidts, Michael Stapf, Georg Tschank, Klaus Weidmann, Ulrich Werner – 30 December 2003 – Fibrosis and cirrhosis of the liver are often the result of chronic liver damage by a variety of different agents. Pathological accumulation of collagen, disruption of the lobular structure, and impaired hepatocellular function frequently lead to systemic involvement and fatal complications.

Accurate separation of biliary lipid aggregates requires the correct intermixed micellar/intervesicular bile salt concentration

Joanne M. Donovan, Audrey A. Jackson – 30 December 2003 – The intermixed micellar/intervesicular bile salt (BS) concentration (IMC), composed of BS monomers and simple micelles, is in dynamic equilibrium with mixed micelles and vesicles. Accurate separation of biliary lipid aggregates is believed to depend on accurately measuring the IMC. Using centrifugal ultrafiltration, we measured the IMC of cholesterol‐supersaturated model biles that were physiologically composed.

Pancreastatin receptor is coupled to a guanosine triphosphate–binding protein of the Gg/11α family in rat liver membranes

José Santos‐Álvarez, Carmen González‐Yanes, Víctor Sánchez‐Margalet – 30 December 2003 – Pancreastatin (PST), a recently discovered regulatory peptide derived from chromogranin A, has been shown to have a glycogenolytic effect in the hepatocyte that is mediated by increasing intracellular calcium. Our previous studies on pancreastatin signaling suggested that PST receptor is coupled to some G proteins in the plasma membrane of the hepatocyte. The nature of this interaction was investigated using antisera against Gq/11α by different approaches.

Hepatic uroporphyrinogen decarboxylase activity in porphyria cutanea tarda patients: The influence of virus C infection

Maria Jose Moran, Antonio Fontanellas, Eric Brudieux, Isabelle Hombrados, Victor de Ledinghen, Patrice Couzigou, Hubert de Verneuil, Rafael Enriquez De Salamanca – 30 December 2003 – Porphyria cutanea tarda (PCT) is caused by a decreased activity of the hepatic enzyme uroporphyrinogen decarboxylase (URO‐D). This deficiency causes overproduction, hepatic deposition, and increased excretion of uroporphyrin. Iron overload and hepatic viral infections are considered aggravating factors of the disease.

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