Ignazio Roberto Marino, Howard R. Doyle, Luca Aldrighetti, Cataldo Doria, John McMichael, Timothy Gayowski, John J. Fung, Andreas G. Tzakis, Thomas E. Starzl – 1 December 1995 – We correlated donor and recipient factors with graft outcome in 436 adult patients who underwent 462 liver transplants. Donor variables analyzed were age, gender, ABO blood group, cause of death, length of stay in the intensive care unit, use of pressors or pitressin, need for cardiopulmonary resuscitation, terminal serum transaminases, and ischemia time.

Andre L. Weigert, Pierre‐Yves Martin, Michel Niederberger, Elisa M. S. Higa, Ivan F. McMurtry, Pere Gines, Robert W. Schrier – 1 December 1995 – The present experiments were designed to test if induction of nitric oxide synthase (NOS) plays a role in the systemic vasodilation observed in hepatic cirrhosis. Because endotoxin levels are elevated in cirrhosis, and endotoxin stimulates inducible nitric oxide synthase (iNOS) expression in several cell lines, aortas of carbon tetrachloride‐induced cirrhotic rats with ascites were evaluated for iNOS expression.

Raymond S. Koff – 1 December 1995

Giacomo Laffi, Marco Foschi, Emanuela Masini, Antonella Simoni, Laura Mugnai, Giorgio la Villa, Giuseppe Barletta, Pier Francesco Mannaioni, Paolo Gentilini – 1 December 1995 – An increased release of nitric oxide (NO), a powerful vasodilating agent, has been proposed to play a role in the pathogenesis of vasodilation and hyperdynamic circulation associated with advanced cirrhosis.

Paul C. Adams, Ann E. Kertesz, Leslie S. Valberg – 1 December 1995 – Although hereditary hemochromatosis is an autosomal recessive disease, most homozygotes are concerned with the genetic implications for their children. The optimal age for testing children and the cost implications of screening their children have not been clearly established.

Patrick Arbuthnot, Marie‐Pierre Bralet, Helene Thomassin, Jean‐Louis Danan, Christian Bréchot, Nicolas Ferry – 1 December 1995 – To target gene expression to malignant hepatic cells, we have constructed recombinant retroviral vectors containing a reporter gene encoding nuclear β‐galactosidase (nls‐LacZ) under transcriptional control of regulatory sequences from the rat α‐fetoprotein (AFP) or human insulinlike growth factor II (IGFII) genes. The AFP and IGFII P3 promoters activate transcription during fetal development and are often reactivated in hepatocellular carcinoma (HCC).

Shigeki Kuriyama, Toshiya Nakatani, Kazuhiro Masui, Takemi Sakamoto, Kentarou Tominaga, Masahide Yoshikawa, Hiroshi Fukui, Kazuhiro Ikenaka, Tadasu Tsujii – 1 December 1995 – In the field of gene therapy using retroviral vectors, it appears impossible to introduce a foreign gene into all target cells. Therefore adjacent cell killing, the socalled bystander effect, caused by genetically modified cells provides therapeutic advantages for gene therapy against cancers.

Francisco Rodriguez‐Frias, Maria Buti, Rosendo Jardi, Montserrat Cotrina, Luis Viladomiu, Rafael Esteban, Jaime Guardia – 1 December 1995 – The precore‐core gene of hepatitis B virus (HBV) was directly sequenced from serum samples of 42 patients with chronic B hepatitis (19 hepatitis B e antigen [HBeAg]+ and 23 anti‐HBe+). Viral genotypes were determined by comparison with 11 reference sequences and by restriction analysis. Genotype A was identified in 16 cases, genotype D in 24 cases, and other genotypes in 2 cases.

David Sacerdoti, Massimo Bolognesi, Giancarlo Bombonato, Angelo Gatta – 1 December 1995 – Doppler sonographic portal vein parameters are used for the noninvasive evaluation of portal hypertension in cirrhosis. The patency of a paraumbilical vein is a rather frequent finding in cirrhosis, which may affect hepatic hemodynamics and function. We evaluated portal and hepatic arterial parameters in 184 cirrhotic patients with and without a patent paraumbilical vein and the relationships with paraumbilical blood flow. A patent paraumbilical vein was found in 33.7% of patients.

Alan N. Langnas, Rodney S. Markin, Mark S. Cattral, Stanley J. Naides – 1 December 1995 – We recently observed that more than one third of pediatric patients who presented with non‐A, non‐B fulminant liver failure (FLF) also developed aplastic anemia (AA) either before or shortly after liver transplantation. Factors involved in the suppression of bone marrow could be the same as those causing hepatic failure. We considered parvovirus B19 a candidate etiologic agent because of the known tropism of B19 for erythroid precursors.