Non‐Hodgkin's lymphoma presenting as a primary tumor of the liver: Presentation, diagnosis and outcome in eight patients

Jean‐Yves Scoazec, Claude Degott, Nicole Brousse, Janine Barge, Georges Molas, François Potet, Jean‐Pierre Benhamou – 1 May 1991 – We report the diagnostic, prognostic and therapeutic features of non‐Hodgkin's lymphoma in eight patients in whom the disease was seen as a primary tumor of the liver.

Direct evidence for cytotoxicity associated with expression of hepatitis delta virus antigen

Susan M. Cole, Eric J. Gowans, Thomas B. Macnaughton, Pauline De La M. Hall, Christopher J. Burrell – 1 May 1991 – It has been postulated that hepatocyte injury resulting from infection with hepatitis D virus may be caused by a direct virus cytotoxicity in contrast to immune‐mediated injury associated with hepatitis B virus. We have transfected HeLa and HepG2 continuous cell lines with a recombinant plasmid containing the hepatitis D antigen gene under the inducible control of the human metallothionein promoter.

Bile salts stimulate glycoprotein release by guinea pig gallbladder in vitro

Daniel P. O'Leary, Francis E. Murray, Bradley S. Turner, J. Thomas Lamont – 1 May 1991 – Alterations in the composition of bile during cholesterol gallstone formation appear to be responsible for increased release of gallbladder mucin, a potent cholesterol nucleating agent. We investigated the effects of bile salts on release of radiolabeled glycoproteins by explants of guinea pig gallbladder in organ culture.

Hepatic fibrosis and cirrhosis after chronic administration of alcohol and “low‐dose” carbon tetrachloride vapor in the rat

Pauline de la M. Hall, John L. Plummer, Anthony H. Ilsley, Michael J. Cousins – 1 May 1991 – Rats were exposed to carbon tetrachloride vapor, 5 days/wk, 6 hr/day, for periods of 5 or 10 wk at a concentration that by itself caused only fatty change with minimal liver cell necrosis and no fibrosis. The same carbon tetrachloride exposure when given in association with chronic alcohol feeding resulted in extensive hepatic fibrosis at 5 wk and established micronodular cirrhosis at 10 wk.

Thyroxine‐binding globulin, hyperthyroxinemia and hepatocellular carcinoma

Jorge J. Gumucio, Michael C. Kew – 1 April 1991 – To determine serum thyroxine‐binding globulin (TBG) levels, we used radioimmunoassay, and compared the results obtained with other tests in 231 patients with chronic hepatitis B virus infection to evaluate its clinical implications. All of these patients were hepatitis B surface antigen (HBsAg)‐positive.

Susceptibility to autoimmune chronic active hepatitis: Human leukocyte antigens DR4 and A1‐B8‐DR3 are independent risk factors

Peter T. Donaldson, Derek G. Doherty, Karen M. Hayllar, Ian G. McFarlane, Philip J. Johnson, Roger Williams – 1 April 1991 – After nearly 18 years of research, the association between human leukocyte antigens A1‐B8‐DR3 and autoimmune chronic active hepatitis still provokes debate. The principal reasons for this are disease heterogeneity and racial variation in the distribution of human leukocyte antigens between populations.

Impaired pressor reactivity in cirrhosis: Evidence for a peripheral vascular defect

Alastair J. Macgilchrist, David Sumner, John L. Reid – 1 April 1991 – The blood pressure responses to intravenous infusions of norepinephrine and angiotensin II, sympathetic and nonsympathetic vasoconstricting agents, respectively, were measured in 20 patients with cirrhosis (10 Child‐Pugh grade A and 10 Child‐Pugh grades B or C) and in 20 healthy subjects. The log PD20 (dose of agonist required to raise blood pressure by 20 mm Hg) for norepinephrine was 4.78 ± 0.36 (mean ± S.D.) in patients with severe cirrhosis and 4.36 ± 0.37 in controls, p < 0.01.

Localization of tumor necrosis factor–stimulated DNA synthesis in the liver

Kenneth R. Feingold, Mary E. Barker, Albert L. Jones, Carl Grunfeld – 1 April 1991 – Tumor necrosis factor and other cytokines mediate the body's response to infection and inflammation. Long‐term administration of tumor necrosis factor causes liver hypertrophy, and our laboratory has shown that tumor necrosis factor acutely increases hepatic DNA synthesis. The purpose of this study was to determine which specific cell types in the liver undergo DNA synthesis in response to tumor necrosis factor.

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