Biomedical subjects
P Gilman
Publications and source records attributed to P Gilman.
Catabolic properties of aglycofibrinogen synthesized by tunicamycin-treated human hepatoma (HepG2) cells and rabbit hepatocytes.
Human hepatoma cell (HepG2) or rabbit hepatocyte monolayers were incubated with [35S]methionine in presence or absence of tunicamycin, a potent inhibitor of asparagine-linked glycosylation. The 35S-labeled nonglycosylated and control fibrinogens purified from the media were used to evaluate the influence of the oligosaccharide on the catabolic properties of this glycoprotein. Plasmin, pronase, cathepsin D or cathepsin B each degraded the nonglycosylated and control fibrinogens similarly, as evidenced by the release of trichloroacetic acid-soluble radioactivity and by SDS-polyacrylamide gel electrophoresis and autoradiography of plasmic digests. Nonglycosylated and control fibrin clots also showed no differences in susceptibility to plasmic digestion. The two forms of fibrinogen demonstrated the same plasma half-life in rabbits. These data indicate that the oligosaccharide does not influence the proteolytic stability or the in vivo plasma survival of fibrinogen, and suggest that other biochemical determinants may influence the catabolic properties of this molecule.
Inhibition of cell division and growth by a redox series of cyanine dyes.
A series of cyanine dyes used in photography, with reduction potentials from -1.35 to -0.20 volts, were tested for their ability to inhibit mitosis and cell growth in fertilized sea urchin eggs. Low concentrations of dyes with reduction potentials more negative than -1.0 volt generally inhibited mitosis and growth, whereas those with more positive reduction potentials did not. The active dyes penetrated the cell, entered all subcellular compartments, were bound to numerous macromolecules, and inhibited synthesis of macromolecules. Thus mitosis and growth may be retarded with substances that can alter electrochemical activity in cells.
Left ventricular performance in children with homozygous sickle cell anaemia.
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Oxygen consumption of the normal and failing heart during left heart bypass.
In order to determine whether myocardial oxygen consumption (MOC) is decreased during left heart bypass (LHB), two groups of 6 dogs each were subjected to 2 hours of heparinless LHB. Group 2 differed from Group 1 in that cardiogenic shock was induced by temporary coronary artery occlusion prior to LHB. In Group 1 animals (normal dogs), MOC decreased significantly during the surgical preparation but did not change appreciably during subsequent LHB. Upon completion of LHB, MOC increased slightly in all animals. This increase in MOC was insignificant, however, when adjusted to changes in mean aortic blood pressure (MAP). A highly positive linear correlation between MOC and MAP was noted regardless of whether the animals were on or off bypass. In Group 2 animals, MOC was markedly decreased after the iduction of cardiogenic shock but gradually increased during the 2 hours of LHB. Upon completion of bypass, MOC of the damaged heart increased to a remarkable degree, but not to initial control levels. However, the linear correlation between MOC and MAP, noted before the induction of cardiogenic shock, disappeared after shock and was not restored after 2 hours of apparently successful bypass. We have concluded that MOC is decreased surgical stress and is further decreased by temporary coronary artery occlusion. MOC is not, however, reduced by nearly total or total LHB in normal hearts. MOC is markedly decreased by cardiac damage but gradually increases in damaged hearts by the use of LHB.
Total body washout and ex vivo liver perfusion in acute hepatic failure. A comparative study.
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Pulsatile pressure-regulated coronary perfusion during ventricular fibrillation.
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