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Biomedical subjects

M E KAPLAN

Publications and source records attributed to M E KAPLAN.

7 recordsLinked to original sources
PubMed1963

The effect of rheumatoid factors and of antigobulins of immune hemolysis in vivo.

Studies were undertaken in man and in the rat comparing the effects of rheumatoid factors and immune antiglobulins on red cells sensitized with incomplete antibodies. The interaction of immune antiglobulins with sensitized red cells produced (a) agglutination in vitro and (b) an accelerated sequestration of the sensitized cells in vivo. In contrast, rheumatoid macroglobulins, although capable of agglutinating Rh-sensitized red cells in vitro, did not modify their destruction in vivo. The failure of rheumatoid factors to function as antiglobulins in vivo appears to reflect their non-reactivity with sensitized cells in whole serum. It is suggested: (a) that the native (7S) gamma globulins of plasma competitively inhibit rheumatoid factors from reacting with fixed antibody in the blood stream; (b) that if these macroglobulins do indeed have pathogenetic activity, this may be limited to body fluids of low protein content.

Animals↗
PubMed1961

Inhibition of red cell sequestration by cortisone.

The effect of cortisone on the sequestration of (a) antibody-coated red cells and (b) incubated red cells was studied in rats. Cortisone administration inhibited the hepatic sequestration of red cells altered by non-immune as well as by immune injury. There was a latent period of 2 days between the institution of cortisone therapy and its first manifest effect on hepatic sequestration. The splenic sequestration of altered red cells was not inhibited by cortisone, and there was no inhibition of the sequestration of hemoglobin by either liver or spleen. It is suggested that steroids may inhibit hepatic sequestration through hemodynamic effects.

Animals↗
PubMed1950

Localization of antigen in tissue cells; cellular distribution of pneumococcal polysaccharides types II and III in the mouse.

The cytological distribution of the pneumococcal polysaccharides, types II and III, was followed in the tissues of the mouse. The most constant and striking concentrations of these polysaccharides were found in the cells of the reticulo-endothelial system, the ordinary capillary endothelium, and fibroblasts throughout the body. In addition, polysaccharide was detected in monocytes and lymphocytes, hepatic cells, cardiac and smooth muscle cells, uterine epithelium, and in steroid-forming cells in the adrenal cortex, testis, and ovary. Studies of the persistence of polysaccharide, type III, in the tissues were carried out after an injection of 4.0 mg. The polysaccharide remained for at least 75 days in the macrophages of lymphoid organs, the Kupffer cells of the liver, the interstitial macrophages in the myocardium, the lung septal cells, the capillary endothelium, and the renal glomerulus. After a single injection of 8 mg., it persisted for at least 6 months in the macrophages of the spleen, liver, and heart and in the endothelium of peritubular capillaries in the kidney. The smallest dose of polysaccharide which produced detectable amounts in any cells 24 hours after injection was 0.03 mg. The distribution of polysaccharide is compared with that of acid vital dyes and suspensoids, and the significance of its fixation in relation to its antigenicity and possible toxicity in mice is discussed.

Animals↗