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At least 775 records · Page 43Linked to original sources
PubMed1976

Mitigation of graft-versus-host disease in mice by treatment of donors with bacterial endotoxin.

Treatment of DBA/2 (H-2d) mice with bacterial endotoxin prior to transplantation of their spleen and lymph node cells into immunosuppressed AKR (H-2k) mice prevented acute mortality from graft-versus-host (GVH) disease. AKR mice that received immunocompetent cells from untreated DBA/2 mice had a median survival time (MST) of 13 days. In contrast, AKR mice that received immunocompetent cells from endotoxin-treated DBA/2 donors had an MST of 54 days. Endotoxin treatment of AKR recipients was not essential for preventing mortality from acute GVH disease. Chimerism was proved by demonstrating that the lymphoid cells of long-term surviving AKR mice had the characteristics of DBA/2 lymphoid cells as measured by their response in mixed leukocyte culture (MLC) tests. Spleen cells from endotoxin-treated DBA/2 mice were able to stimulate, and to be stimulated by, AKR spleen cells in MLC assays. Furthermore, spleen cells from endotoxin-treated DBA/2 mice did not suppress the responses of DBA/2 or AKR spleen cells in 'three-party' MLC tests.

Animals↗
PubMed1983

Protonic inhibition of the mitochondrial oligomycin-sensitive adenosine 5'-triphosphatase in ischemic and autolyzing cardiac muscle. Possible mechanism for the mitigation of ATP hydrolysis under nonenergizing conditions.

Ischemic myocardium was produced by occluding the left circumflex coronary artery in anesthetized dogs for 10 or 20 min. Autolyzed myocardium was produced by incubating transmural samples of canine left ventricle at 37 degrees C for 5, 10, 15, 20, 40, or 60 min. Tissue pH was recorded continuously in each model using a microcombination pH electrode impaled into the midmyocardium. Mitochondria isolated from both ischemic and autolyzed tissue exhibited marked parallel depressions of oligomycin-sensitive ATPase activity, Km ATP, and Vmax. All of these parameters dropped more markedly during the zero flow autolytic process than during the low flow ischemia characteristic of the canine left circumflex occlusion model. The changes in the ATPase kinetic parameters paralleled closely the drop in tissue pH in each model. These ATPase kinetic changes were then reproduced in vitro both quantitatively and qualitatively by incubating isolated control mitochondria at the same pH values under nonenergizing conditions. It thus became evident that we had, in effect, utilized the oligomycin-sensitive ATPase as an in situ indicator of cell acidosis. Reperfusion of 15-min ischemic myocardium was accompanied by a complete reversal of the acidosis and of the ATPase activity inhibition. The ATPase inhibition demonstrable in vitro in isolated mitochondria occurred when the pH was lowered, but only when there was a concomitant dissipation of the transmembrane electrochemical gradient. The ATPase inhibition was then reversed completely during a subsequent state 4 incubation by a carbonyl cyanide p-trifluoromethoxyphenylhydrazone-sensitive process.

Adenosine Triphosphatases↗
PubMed1984

Mg2+ mitigates Ca2+-dependent cell killing by ionophore A23187.

The Ca2+, Mg2+ ionophore A23187 kills cultured cells in a manner which is dependent upon millimolar concentrations of Ca2+ (Schanne et al., 1979). The killing is thought to be caused by an increase in the cellular Ca2+ content following exposure of cells to the ionophore. We have found that the Ca2+-dependent killing of Balb/c 3T3 cells by ionophore A23187 is reversed by raising, and potentiated by lowering, the extracellular Mg2+ concentration. Ionophore treatment (5 micrograms/ml) causes a decrease in Ca2+ content within minutes, possibly by raising the intracellular concentration of free Ca2+ and thus stimulating its efflux. The response of Ca2+ content to ionophore concentration is biphasic, with low doses causing a decrease and high doses an increase. The sparing effect of Mg2+ on Ca2+-dependent killing of cells by the ionophore suggests that the ionophore kills cells by increasing the cytoplasmic concentration of free Ca2+, thereby creating a competition between Ca2+ and Mg2+ for certain Mg2+-requiring reactions needed for cell survival.

Animals↗
PubMed1980

Congenital cystic adenomatoid malformation in bilateral renal agenesis. Its mitigation of Potter's syndrome.

Potter's syndrome develops secondary to a deficiency of amniotic fluid, such as occurs in renal agenesis. Congenital cystic adenomatoid malformation (CCAM), on the other hand, is frequently accompanied by polyhydramnios. We describe a newborn with both renal agenesis and CCAM who had only mild features of Potter's syndrome. The pathogenesis of polyhydramnios in CCAM is discussed with regard to the ultrastructural findings of numerous type 2 pneumocytes lining the cysts. The association between CCAM and bilateral renal anomalies is emphasized.

Abnormalities, Multiple↗