Moritaka Goto, Yoshiyuki Takei, Sunao Kawano, Kouichi Nagano, Shingo Tsuji, Eiji Masuda, Yoshiya Nishimura, Shigetoshi Okumura, Toru Kashiwagi, Hideyuki Fusamoto, Takenobu Kamada – 1 March 1994 – Hepatic microcirculatory perturbation is observed after ischemia/reperfusion. Endothelin‐1, a potent vasoconstrictive peptide, is known to modulate local circulation. This study was designed to examine whether endothelin‐1 participates in the mechanism of microcirculatory disturbance and damage of the liver after ischemia/reperfusion.

Mark Feitelson, Laura Lega, Juanhui Guo, Massimo Resti, Maria E. Rossi, Chiara Azzari, Baruch S. Blumberg, Alberto Vierucci – 1 March 1994 – The pathogenesis of posttransfusion hepatitis was determined in 14 children with β‐thalassemia. All had blood samples obtained in 1980 or 1981, were vaccinated against hepatitis B virus in 1983 and had another serum sample collected in 1989. Seven children had detectable antibodies against hepatitis C virus before vaccination, and all were positive in 1989.

Anna Linda Zignego, Marco Foschi, Giacomo Laffi, Monica Monti, Grazia Careccia, Roberto Giulio Romanelli, Enrichetta de Majo, Roberto Mazzanti, Giampiero Buzzelli, Giorgio la Villa, Paolo Gentilini – 1 March 1994 – We evaluated hepatitis B virus DNA and hepatitis C virus RNA in sera from 110 HBsAg and IgM HBc antibody–negative heavy drinkers (50 cirrhosis, 13 chronic active hepatitis, 25 fatty liver with or without mild to moderate fibrosis, alcoholic hepatitis or both and 22 healthy alcoholic subjects) with polymerase chain reaction.

Wan‐Long Chuang, Masao Omata, Toshiki Ehata, Osamu Yokosuka, Kazuhiko Hosoda, Fumio Imazeki, Masao Ohto – 1 March 1994 – The precore mutant hepatitis B virus often emerges from a mixed infection with combined wild‐type and precore mutant viruses. Nevertheless, the precore mutant does not seem to be an evolutionarily favored strain.

Deborah E. Sullivan, Michael A. Gerber – 1 March 1994 – Persistent infection by hepatitis C virus is a major risk factor for the development of hepatocellular carcinoma, but the mechanism of hepatocarcinogenesis is unknown. To study the association of hepatitis C virus with hepatocellular carcinoma, we sequenced part of the 5′ untranslated region of hepatitis C virus from the tumor tissue and the surrounding nontumorous liver of three patients with hepatocellular carcinoma. No sequence differences between tumor‐derived and liver‐derived hepatitis C virus isolates were detected.

Raymond S. Koff – 1 March 1994

William F. Balistreri – 1 March 1994 – “When medicine has really succeeded brilliantly in technology, as in immunization or endocrine‐replacement therapy, so that the therapeutic measures can be directed straight at the underlying disease mechanism and are decisively effective, the cost is likely to be very low indeed. It is when our technologies have to be applied halfway along against the progress of disease, or must be brought in after the fact to shore up the loss of destroyed tissue, that health care becomes enormously expensive.

Daniel P. O'Leary – 1 March 1994 – The more hydrophobic bile salts cause rapid release of preformed gallbladder mucin and other glycoproteins by gallbladder explants in vitro, whereas the less hydrophobic bile salts elicit a lesser response. This study was designed to determine (a) whether this short‐term effect was matched by a sustained increase in glycoprotein secretion over 24 hr and (b) whether it occurred when bile salts were presented in model biles rather than aqueous solution.

Jacquelyn J. Maher, Christina Tzagarakis – 1 March 1994 – Laminin is a heterotrimeric glycoprotein found in the perisinusoidal space of adult rat liver. The principal cellular source of laminin in liver is the lipocyte, with its three subunits measuring 324, 200 and 200 kD. The large subunit of lipocyte‐derived laminin is distinct from the A subunit of murine laminin (440 kD); its size suggests that it represents a peptide, called M, recently cloned from human placenta.

Rein M. J. Hoedemakers, Gerrit L. Scherphof, Toos Daemen – 1 March 1994 – We examined the effects of several hemopoietic growth factors on proliferation of rat liver macrophages in vitro. The proliferative response of liver macrophages to hemopoietic growth factors was assayed on the basis of [methyl‐3H]thymidine uptake. Macrophage colony‐stimulating factor and recombinant murine granulocyte‐macrophage colony‐stimulating factor stimulated [methyl‐3H]thymidine incorporation in a concentration‐dependent manner.