Differential display and integrin alpha 6 messenger RNA overexpression in hepatocellular carcinoma

Nasim Ara Begum, Masaki Mori, Takashi Matsumata, Kenji Takenaka, Keizo Sugimachi, Graham F. Barnard – 1 November 1995 – Our aim was to isolate potentially important differentially expressed gene products from paired human hepatocellular carcinoma (HCC) and normal liver samples using the differential messenger RNA (mRNA) display technique. Total RNA samples were reverse transcribed with anchoring oligonucleotide primers and then amplified by the polymerase chain reaction (PCR) with additional upstream random primers.

Role of defective monocyte interleukin‐10 release in tumor necrosis factor‐alpha overproduction in alcoholic cirrhosis

Olivier le Moine, Arnaud Marchant, Donat de Groote, Camille Azar, Michel Goldman, Jacques Devière – 1 November 1995 – Monocytes of patients with alcoholic cirrhosis produce higher amounts of tumor necrosis factor‐alpha (TNF‐α) after lipopolysaccharide (LPS) stimulation. The mechanisms of this overproduction remain undefined. IL‐10 (IL‐10) is an antiinflammatory cytokine known to downregulate TNF‐α secretion by monocytes. The present study analyzes IL‐10 production by monocytes and its control on TNF‐α secretion in alcoholic cirrhosis.

Efficacy and safety of interferon alfa therapy in chronic hepatitis C with autoantibodies to liver‐kidney microsomes

Luca Todros, Giorgio Saracco, Marilena Durazzo, Maria Lorena Abate, Giovanni Touscoz, Luca Scaglione, Giorgio Verme, Mario Rizzetto – 1 November 1995 – Interferon alfa (IFN) therapy is efficacious in chronic viral hepatitides. It may, however, cause adverse immunologic reactions in patients with concomitant autoimmune phenomena. A minority of patients with chronic type C hepatitis have antibodies against liver and kidney microsomes (anti‐LKM) in serum. We therefore carried out this study to find out whether IFN is safe and efficacious also in this subgroup.

An outbreak of hepatitis A among south african patients with hemophilia: Evidence implicating contaminated factor VIII concentrate as the source

Mary‐Anne Kedda, Michael C. Kew, Richard J. Cohn, Stephen P. Field, Rosemary Schwyzer, Ernest Song, F. Fernandes‐Costa – 1 November 1995 – We report an outbreak of hepatitis A in nine South African hemophiliacs treated exclusively with infusions of factor VIII concentrate. The solvent/detergent (S/D) method (which does not inactivate nonenveloped viruses) was used for virus eradication.

Quantitation of cytomegalovirus in the blood of liver transplant recipients

David Mutimer, Anna Matyi‐Toth, Elwyn Elias, Jean Shaw, Katharina O'Donnell, Helena Kilgariff, James Neuberger, Bridget Gunson, Paul McMaster, Per Stalhandske – 1 November 1995 – An assay for quantitation of cytomegalovirus (CMV) has been developed. The assay combines DNA amplification and enzyme‐linked immunosorbent assay (ELISA) detection. In this study, the assay has been used to examine sequential buffycoats from 32 consecutive liver transplant recipients.

Feedback‐inhibition of glucagon‐stimulated glycogenolysis in hepatocyte/kupffer cell cocultures by glucagon‐elicited prostaglandin production in kupffer cells

Ursula Hespeling, Kurt Jungermann, Gerhard P. Püschel – 1 November 1995 – Prostaglandins, released from Kupffer cells, have been shown to mediate the increase in hepatic glycogenolysis by various stimuli such as zymosan, endotoxin, immune complexes, and anaphylotoxin C3a involving prostaglandin (PG) receptors coupled to phospholipase C via a G0 protein. PGs also decreased glucagon‐stimulated glycogenolysis in hepatocytes by a different signal chain involving PGE2 receptors coupled to adenylate cyclase via a Gi protein (EP3 receptors).

Dynamic measurements of the acute and chronic effects of lysosomotropic agents on hepatocyte lysosomal pH using flow cytometry

Brent M. Myers, Pamela S. Tietz, James E. Tarara, Nicholas F. Larusso – 1 November 1995 – Previous investigators measuring the pH of lysosomes have used digitized video microscopy (DVM) in freshly isolated or cultured cells. Although useful, this technique is time consuming, requires the use of an image analysis system, and is limited by the fact that measurements can be made in only a relatively small number of cells.

Vitamin E therapy of acute CCl4‐induced hepatic injury in mice is associated with inhibition of nuclear factor kappa B binding

Shu‐Ling Liu, Silvia Degli Esposti, Tony Yao, Anna Mae Diehl, Mark A. Zern – 1 November 1995 – Oxidative stress, with reactive oxygen intermediate formation, may represent a common mechanism by which liver injury is induced by diverse etiologies. Oxidative stress enhances nuclear factor kappa B (NF‐κB) activity, and NF‐κB activity has been shown to enhance the expression of cytotoxic cytokines. Acute hepatic injury caused by reactive oxygen intermediate production was induced by an intraperitoneal injection of CCl4 in mice.

Impaired biliary excretion and whole body elimination of methylmercury in rats with a congenital defect in biliary glutathione excretion

Nazzareno Ballatori, Zenaida Gatmaitan, Anh T. Truong – 1 November 1995 – Biliary excretion of methylmercury, a major route of elimination of this toxic compound, was less than 2% of control in Eisai hyperbilirubinemic (EHBR) rats, a mutant Sprague‐Dawley strain with a defect in biliary excretion of a variety of organic anions, including glutathione S‐conjugates and reduced glutathione (GSH). Biliary GSH excretion in EHBR rats was also <2% of controls, confirming previous findings.

Primary sclerosing cholangitis and ulcerative colitis: Evidence for increased neoplastic potential

Ulrika Broomé, Robert Löfberg, Béla Veress, Ljusk Siw Eriksson – 1 November 1995 – Primary sclerosing cholangitis (PSC) is a biliary destructive disease mostly affecting patients with ulcerative colitis (UC). PSC has been suggested to be an independent risk factor for the development of colorectal malignancy in UC. Patients with PSC also have an increased risk of developing cholangiocarcinoma. This study aimed at assessing the cumulative risk of colorectal neoplasia in PSC and UC, and also to determine risk factors for the development of cholangiocarcinoma.

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