Julio Vorobioff, Guadalupe Garcia‐Tsao, Roberto Groszmann, Guillermo Aceves, Eduardo Picabea, Roberto Villavicencio, Jorge Hernandez‐Ortiz – 1 January 1989 – Ketanserin, a 5‐hydroxytryptamine‐2 receptor blocker, has been shown to decrease portal pressure in recent acute hemodynamic studies that have been performed both in experimental animals and portal hypertensive patients. The present study was designed to investigate the effects of chronic oral administration of ketanserin in portal hypertensive patients with cirrhosis.

Giorgio Hassan, Stefania Stefanini, Anna Maria Bargagli, Francesco Autuori – 1 January 1989 – The incorporation of 3H‐proline in cells of liver biopsy specimens from patients with chronic active liver diseases has been studied by light and electron microscopic autoradiography. The labeled proline is incorporated by hepatocytes of the external rows of the residual liver lobule, by the cells of the proliferating bile ductule and very actively by the plasma cells localized at the boundary between the inflammatory infiltrate and the liver lobule.

Richard B. Jennett, Michael F. Sorrell, Abbas Saffari‐fard, James L. Ockner, Dean J. Tuma – 1 January 1989 – Hepatic ethanol oxidation generates the reactive intermediate acetaldehyde, which binds to proteins. Previous work, using bovine brain tubulin as a model protein, has shown that acetaldehyde preferentially formed stable adducts on the α‐chain of the heterodimeric molecule. This binding resulted in functional impairment of the tubulin/microtubule system as evidenced by a decreased ability of adducted tubulin to form microtubules.

Morikazu Onji, Andrew M. L. Lever, Izumu Saito, Howard C. Thomas – 1 January 1989 – The interferon responsiveness of two cell lines transfected with the hepatitis B virus genome was investigated. A cosmid vector containing multiple copies of the hepatitis B virus genome was transfected into FL5‐1 cells; it reduced their sensitivity to interferons as measured by inhibition of the cytopathic effect of Sindbis virus challenge. Similar vectors transfected into HeLa cells reduced their sensitivity to interferon as measured by production of β2‐microglobulin.

Emilio Barberá‐Guillem, Ricardo Ayala, Fernando Vidal‐Vanaclocha – 1 January 1989 – We have measured the location of embryonic and adult hemopoietic foci in the liver tissue of postnatal and adult phenylhydrazine‐treated mice. Differentiation of acinar domains in liver tissue was made possible by carrying out succinate dehydrogenase histochemical reactions on liver cryostat sections.

Shou‐Dong Lee, Kwang‐Juei Lo, Yang‐Te Tsai, Jaw‐Ching Wu, Tzee‐Chung Wu – 1 January 1989 – A total of 128 HBsAg carrier infants born to HBeAg‐positive HBsAg carrier mothers were tested for serum HBsAg, HBeAg, hepatitis B virus DNA and anti‐HBc. Ninety‐three of them had received hepatitis B vaccination. Anti‐HBc had been found to be negative in sera of 12 infants who were HBsAg, HBeAg and hepatitis B virus DNA positive during the follow‐up period of 3 to 5 years.

J. Michael Henderson – 1 January 1989 – Operative ligation of portosystemic shunts is effective in controlling chronic portosystemic encephalopathy (CPSE) but is associated with significant mortality. Review of the records of five paients with CPSE treated with radiologic occlusion procedures showed that these are suitable alternatives to surgery. Three patients had alcoholic cirrhosis, one had hepatic fibrosis from schistosomiasis, and one had post‐necrotic cirrhosis. All had CPSE with progressive, severe cerebral impairment refractory to clinical treatment.

H. Juergen Nord – 1 January 1989

Carolyn N. d'Arville, Mysan Le, Thomas M. Kloppel, Francis R. Simon – 1 January 1989 – Reduced hepatic uptake and clearance of macromolecules in liver cirrhosis is due to two major factors: increased diffusional barriers, resulting primarily from the deposition of excessive connective tissue in the space of Disse, and hepatocellular dysfunction, manifested by receptor and/or postreceptor defects.

Martin Lombard, Adrian Bomford, Miriam Hynes, Nikolai V. Naoumov, Stephanie Roberts, John Crowe, Roger Williams – 1 January 1989 – The liver is the main site of iron accumulation and pathologic sequelae in hereditary hemochromatosis. Whether this is a result solely of inappropriately increased absorption of iron by the gastrointestinal tract or a more generalized regulatory failure of iron balance is unknown.