Hageman factor activation and tight junction disruption in mice challenged with attenuated endotoxin

Summary Endotoxin treated with chromium chloride is less toxic to mice than the parent molecule, but can disrupt intestinal permeability barriers and has an enhanced ability to activate Hageman factor.We wish to thank Drs M.W. Brightman and T.S. Reese from the Department of Neurocytology, National Institutes of Health for the use of their Balzers freeze-fracture instrument.     

Requirement of a 5-lipoxygenase-activating protein for leukotriene synthesis

Leukotrienes, the biologically active metabolites of arachidonic acid, have been implicated in a variety of inflammatory responses, including asthma, arthritis and psoriasis. Recently a compound, MK-886, has been described that blocks the synthesis of leukotrienes in intact activated leukocytes, but has little or no effect on enzymes involved in leukotriene synthesis, including 5-lipoxygenase, in cell-free systems. A membrane protein with a high affinity for MK-886 and possibly representing the cellular target for MK-886 has been isolated from rat and human leukocytes. Here, we report the isolation of a complementary DNA clone encoding the MK-886-binding protein. We also demonstrate that the expression of both the MK-886-binding protein and 5-lipoxygenase is necessary for leukotriene synthesis in intact cells. Because the MK-886-binding protein seems to play a part in activating this enzyme in cells, it is termed the five-lipoxygenase activating protein (FLAP).     

Guaiacol-O-methyltransferase: A mammalian enzyme capable of forming di-O-methyl catecholamine derivatives

Résumé On a extrait et characterisé une enzyme capable de transférer aux catécholamines 4-O-méthyles le group méthyle provenant de l'S-adénosylméthionine et produire des substances diméthoxyques. Cette enzyme est active dans différents tissus de Mammifères.

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This work was supported by Public Health Service grants Nos. MH-08618 and MH-07961 and a Research Scientist's Award No. MH-14020, to A.J.F.     

Glia maturation factor influences recovery from injury in neonatal rat brains

Summary Newborn rats were injured with a puncture wound in one cerebral hemisphere. Experimental animals were treated with three i.p. injections of Glia Maturation Factor (GMF) at daily intervals starting from the time of injury, whereas control littermates were treated with equivalent amounts of bovine serum albumin. At 25 days old the size of the cerebral cortex at the plane of injury was measured on representative brain sections. In control rats the injured side was 18% smaller than the normal side whereas in GMF-treated animals the difference was only 1%. The results suggest a possible regulatory role of GMF in promoting tissue recovery from brain damage.Acknowledgments. This work was supported by the following research grants to Dr Lim: Veterans Administration Merit Review Award and Clinical Investigatorship Award, National Science Foundation grant No.BNS-8308341 and National Cancer Institute grant No. CA-31796. We thank Marjorie Strabala for preparing the histological sections and Dr Peter A. Lachenbruch and John Tsuang for statistical analysis.