Localization of ammonia‐metabolizing enzymes in human liver: Ontogenesis of heterogeneity

Antoon F. M. Moorman, Jacqueline L. M. Vermeulen, Robert Charles, Wouter H. Lamers – 1 March 1989 – Immunohistochemical analysis of human liver (8 to 94 years) shows a compartmentation of ammonia‐metabolizing enzymes across the acinus. The highest concentration of carbamoylphosphate synthetase (ammonia) is found in the parenchymal cells around the terminal portal venules. Glutamine synthetase is found in a small pericentral compartment two to three cells thick.

Human embryotoxicity of pyrrolizidine‐containing drugs

Ryan J. Huxtable – 1 March 1989 – Hepatic veno‐occlusive disease is the most frequent cause of hepatic vein obstruction in children. Only the small and medium veins are involved. The initial vascular lesion is endothelial edema, followed by phlebosclerosis and occlusion of the small vessels, leading to secondary necrosis of liver cells, progressive fibrosis, and ultimately cirrhosis. The disease was first recognized in Jamaica in 1954, and subsequently reported from other parts of the world.

The etiology of acute hepatitis superimposed upon previously unrecognized asymptomatic HBsAg carriers

Chia‐Ming Chu, Yun‐Fan Liaw, Chia C. Pao, Miau‐Ju Huang – 1 March 1989 – To study the etiology of acute hepatitis superimposed upon previously unrecognized asymptomatic HBsAg carriers, paired sera were collected in acute and convalescence phases for measurement of HBeAg, anti‐HBe, hepatitis B virus DNA and anti‐delta from 76 adult patients with acute hepatitis who were HBsAg positive but IgM anti‐HBc negative or positive only at low titer. None of them were IgM anti‐hepatitis A virus positive on admission.

Propranolol does not alter cerebral blood flow and functions in cirrhotic patients without previous hepatic encephalopathy

Paul Calès, Max Pierre‐Nicolas, Antonio Guell, Jean‐Louis Mauroux, Anne Franco‐Sempe, Jean‐Pierre Vinel, Gilles Geraud, Jean‐Pierre Pascal – 1 March 1989 – Since it has been suggested that propranolol could lead to hepatic encephalopathy, we undertook a study to assess the effects of propranolol on cerebral blood flow and cerebral functions. Sixteen patients with alcoholic cirrhosis and large esophageal varices and without major hepatic dysfunction (Child‐Pugh score <14) or previous hepatic encephalopathy were randomized to receive either propranolol or placebo.

Stimulation of DNA synthesis in hepatocytes by kupffer cells after partial hepatectomy

Fujio Katsumoto, Kohji Miyazaki, Fumio Nakayama – 1 March 1989 – The role of Kupffer cells during reparative regeneration of rat liver was investigated with an in vitro experimental model. Conditioned media from primary cultures of Kupffer cells isolated from intact and regenerating liver were added to primary cultures of hepatocytes, and [3H]thymidine incorporation into DNA was studied. Kupffer cell‐conditioned media from intact liver and regenerating remnant liver significantly stimulated DNA synthesis in hepatocytes as compared with control media (p<0.05).

Isolation, culture and main characteristics of mouse fat‐storing cells: Interaction with viruses

Wan Chen, Jean‐Louis Gendrault, Anne‐Marie Steffan, Eric Jeandidier, André Kirn – 1 March 1989 – Fat‐storing cells were isolated from 15‐day‐old mouse sinusoidal cell cultures (Kupffer or endothelial cells), where they had multiplied abundantly; they were then purified by a negative selection method based on the fact that they do not possess Fc receptors, as do both other types of cells.

Does hypophosphatemia play a role in acute liver failure?

James P. Knochel – 1 March 1989 – This is the first record of hypophosphataemia in acute liver failure induced by paracetamol; it occurred in most of the patients and was severe (<0.3 mmol/l) in more than one third. At this level hypophosphataemia produces impaired oxygen transport and tissue hypoxia, abnormal leucocyte function, depressed platelet numbers and function, generalised muscle weakness, and disorder of the central nervous system; these are frequent complications of acute liver failure.

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