Interaction between hepatitis B surface proteins and monomeric human serum albumin

Bernd Krone, Angela Lenz, Klaus‐Hinrich Heermann, Maria Seifer, Lu Xuangyong, Wolfram H. Gerlich – 1 June 1990 – HBsAg is known to bind to human serum albumin polymerized by glutaraldehyde, human serum albumin has been found in preparations of HBsAg by several investigators. However, it is not yet known whether natural human serum albumin binds to hepatitis B virus under physiological conditions. We studied the binding between natural or recombinant HBsAg and monomeric human serum albumin by immunological, biochemical and biophysical methods.

Hormonal responses to large paracentesis: Are discordant results due to technologic differences?

Joan Rodes – 1 June 1990 – The use of paracentesis has recently been reproposed as a safe and effective alternative to diuretics for management of ascites. We have investigated the clinical and biochemical effects of large‐volume paracentesis in 19 cirrhotics with tense ascites, and the relative changes in the hormones involved in sodium and water renal handling. Plasma renin activity (PRA), aldosterone (PA), and arginine vasopressin (AVP) levels and conventional liver and renal function tests were measured before and 1, 2 and 7 days after the paracentesis.

Chronic hepatitis caused by the hepatitis a virus

Yun‐Fan Liaw – 1 June 1990 – The case of a young man with hepatitis A and a chronic course is presented. The patient recived a short course of steroid therapy for recurrence of symptoms following acute hepatitis A. Thereafter liver enzymes have remained marginally elevated for 4 years and annual liver biopsies have shown evidence of chronicity. HAV IgM Ab persisted for 1034 days with subsequent development of HAV IgG Ab. The possiblity of other viruses in the aetiology and the role of steroids in the development of chronicity are discussed.

Pathogenesis of hepatocellular carcinoma in hereditary hemochromatosis: Occurrence in noncirrhotic patients

Michael D. Kew – 1 June 1990 – Previous reports have emphasized the association of primary hepatocellular carcinoma in patients with idiopathic hemochromatosis with cirrhosis. In contrast, patients with idiopathic hemochromatosis without cirrhosis have no increased risk of hepatocellular carcinoma. Phlebotomy therapy, by preventing the accumulation of parenchymal iron and subsequent cirrhosis, is believed to prevent hepatocellular carcinoma in the precirrhotic stage of the disease.

Risk factors for the development of hepatic cysts in autosomal dominant polycystic kidney disease

Patricia A. Gabow, Ann M. Johnson, William D. Kaehny, Michael L. Manco‐Johnson, Irene T. Duley, Gregory T. Everson – 1 June 1990 – Hepatic cysts are a major manifestation of autosomal dominant polycystic kidney disease. This study examined 239 autosomal dominant polycystic kidney disease patients and 189 unaffected family members to define the factors that influence the presence and severity of hepatic cysts. Autosomal dominant polycystic kidney disease patients with hepatic cysts were older than autosomal dominant polycystic kidney disease patients without such cysts (44.6 ± 1.1 yr vs.

Prevention of ursodeoxycholate hepatotoxicity in the rabbit by conjugation with N‐methyl amino acids

Adrian Schmassmann, Alan F. Hofmann, M. Antonietta Angellotti, Huong‐Thu Ton‐Nu, Claudio D. Schteingart, Carlo Clerici, Steven S. Rossi, Marcus A. Rothschild, Bertram I. Cohen, Richard J. Stenger, Erwin H. Mosbach – 1 June 1990 – The effect of dietary administration of four different amino acid (N‐acyl) conjugates of ursodeoxycholic acid on biliary bile acid composition, liver tests and hepatic morphology by light microscopy was examined in the rabbit.

Depressed liver regeneration after partial hepatectomy of germ‐free, athymic and lipopolysaccharide‐resistant mice

Robert P. Cornell, Barbara L. Liljequist, Kenneth F. Bartizal – 1 June 1990 – A hypothesis has been proposed by this laboratory that endogenous gut‐derived lipopolysaccharide is responsible for systemic endotoxemia in animals with acute liver injury particularly after partial (67%) hepatectomy. Systemic lipopolysaccharide and possibly fibrin aggregates or tissue debris then elicit release of cytokines from phagocytizing macrophages and/or monocytes that may be essential for normal liver regeneration.

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