Oral bile acid treatment and the patient with zellweger syndrome

Kenneth D. R. Setchell, Patrizia Bragetti, Linda Zimmer‐Nechemias, Cynthia Daugherty, Maria Antonietta Pelli, Renato Vaccaro, Giorgio Gentili, Eleonora Distrutti, Giuliano Dozzini, Antonio Morelli, Carlo Clerici – 1 February 1992 – The cerebrohepatorenal syndrome of Zellweger is a congenital syndrome of multiple manifestations, including hepatomegaly and liver dysfunction. Treatment is generally of a supportive nature, aimed at improving nutrition and growth, controlling the central nervous system symptoms and limiting progression of liver disease.

Changes in transcripts of basement components during rat liver development: Increase in laminin messenger RNAs in the neonatal period

Shimon Reif, Donald Sykes, Thomas Rossi, Milton M. Weiser – 1 February 1992 – The expression of laminin and type IV collagen messenger RNA in rat liver was investigated in relation to liver development. Levels of messenger RNA for laminin chains A, B1 and B2, and α1 and α2 chains of type IV collagen were studied by Northern‐blot and dot‐blot analysis. Although the expression of messenger RNAs for laminin B1 and B2 chains was higher in 19‐day gestational fetal liver when compared with the adult, the highest level was detected in 15‐day newborns.

Temporal relationship of peripheral vasodilatation, plasma volume expansion and the hyperdynamic circulatory state in portal‐hypertensive rats

Luis A. Colombato, Agustin Albillos, Roberto J. Groszmann – 1 February 1992 – Peripheral vasodilatation and plasma volume expansion are required to generate the hyperdynamic circulatory state observed in portal hypertension.

Seroprevalence of hepatitis C virus nucleocapsid antibodies in patients with cryptogenic chronic liver disease

Jonathan Brown, Spyros Dourakis, Peter Karayiannis, Robert Goldin, Joe Chiba, Hiroyoshi Ohba, Tatsuo Miyamura, Howard C. Thomas – 1 February 1992 – The serological responses to two different hepatitis C virus antigens were studied by enzyme‐linked immunosorbent assay in a variety of chronic liver diseases and in healthy blood donors.

Treatment of refractory ascites: Is dialytic ultrafiltration better than paracentesis?

Salvatore Badalamenti, Francesco Salerno – 1 February 1992 – We compared the clinical efficacy and safety of large‐volume paracentesis and dialytic ultrafiltration in the treatment of refractory ascites in cirrhotic patients. A group of cirrhotic subjects (age 49–80 years) were randomly allocated to either continuous paracentesis (1–1.5 l/hour) or dialytic ultrafiltration until disappearance of ascites. Each patient was maintained on bed rest, fluid restriction (1 l/day) and a low (25 mmol/day) sodium diet for 14 days.

The effect of liver denervation on hepatic hemodynamics during hypovolemic shock in swine

J. Michael Henderson, Gregory J. Mackay, Alan B. Lumsden, Hussein M. Atta, Richard Brouillard, Michael H. Kutner – 1 January 1992 – This study tested the hypothesis that the denervated liver is more susceptible to hypovolemic shock than the normal liver. Fourteen swine, seven nondenervated and seven after liver denervation, were studied during hypovolemic shock to 50% of baseline blood pressure. Hepatic artery and portal vein flows were measured using transonic flow probes, and cardiac output and central venous pressure were measured using Swan‐Ganz catheters.

Hepatocyte growth factor/hepatopoietin A is expressed in fat‐storing cells from rat liver but not myofibroblast‐like cells derived from fat‐storing cells

Peter Schirmacher, Albert Geerts, Antonello Pietrangelo, Hans P. Dienes, Charles E. Rogler – 1 January 1992 – Hepatocyte growth factor/hepatopoietin A is a complete mitogen for parenchymal liver cells, and its expression is increased as an early response to acute liver injury. To identify the liver cell population responsible for hepatocyte growth factor gene expression, we investigated tissue sections and isolated and purified cell fractions from normal rat liver by in situ and Northern blot hybridization.

Does the precore mutant of hbv cause fulminant hepatitis?

Howard C. Thomas – 1 January 1992 – Background. A nosocomial outbreak of fulminant hepatitis B occurred in five patients in Haifa, Israel. Previous investigations identified the suspected source as a carrier of hepatitis B surface antigen who was positive for antibodies to hepatitis B e antigen and had chronic liver disease. We examined the strain of hepatitis B virus (HBV) that caused this epidemic, in order to identify specific mutations in the precore or core region.

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