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Biomedical subjects

E Bogin

Publications and source records attributed to E Bogin.

At least 73 records · Page 4Linked to original sources
PubMed1981

Effect of parathyroid hormone on rat heart cells.

Myocardiopathy is common in uremia, but its cause in unknown. Excessive entry of calcium in heart cells by catecholamines has been shown to cause necrosis of myocardium. The high blood levels of parathyroid hormone (PTH) in uremia may also enhance entry of calcium into heart cells and exert deleterious effects on the heart. We examined the effect of PTH on rat heart cells grown in culture. Both amino-terminal (1-34) PTH and intact (1-84) PTH, but not the carboxy-terminal (53-84) PTH produced immediate and sustained significant rise in beats per minute and the cells died earlier than control. The effect was reversed if PTH was removed from medium, and was abolished by inactivation of the hormone. There was a dose-response relationship between both moieties of PTH and the rise in heart beats, but the effect of 1-84 PTH was significantly greater than that of 1-34 moiety. PTH stimulated cyclic AMP production within 1 min, and cyclic AMP remained significantly elevated thereafter. The effect of PTH required calcium, was mimicked by calcium ionophore, was prevented by verapamil and was not abolished by alpha- or beta-adrenergic blockers. PTH action was additive to phenylephrine and synergistic with isoproterenol. Sera from uremic parathyroidectomized rats did not effect heart beats, but sera from uremic rats with intact parathyroid glands or from uremic-parathyroidectomized rats treated with PTH had effects similar to PTH. Data indicate that (a) heart cell is a target organ for PTH and may have receptors for the hormone; (b) PTH increases beating rate of heart cells and causes early death of cells; (c) PTH effect appears to be due to calcium entry into heart cells; (d) the locus of action through which PTH induces calcium entry is different from that for catecholamines; and (e) uremic serum has no effect unless it contains PTH. Data suggest that myocardial damage may occur in uremia due to prolonged exposure to very high blood levels of PTH, and assign new dimensions to PTH toxicity in uremia.

Animals↗
PubMed1981

Effect of parathyroid hormone on erythropoiesis.

Inhibitors of erythropoiesis have been found in the blood of uremic patients but their nature has not been identified. These patients have excess blood levels of parathyroid hormone (PTH) and it is possible that PTH inhibits erythropoiesis. The present study was undertaken to examine the effect of intact PTH molecules and some of its fragments on human peripheral blood and mouse bone marrow burst-forming units-erythroid (BFU-E), on mouse bone marrow erythroid colony-forming unit (CFU-E), and granulocyte macrophage progenitors (CFU-GM), and evaluate the interaction between PTH and erythropoietin (Ep) on human BFU-E. Intact PTH (1-84 bPTH) in concentrations (7.5-30 U/ml;) comparable to those found in blood of uremic patients produced marked and significant (P less than 0.01) inhibition of BFU-E and mouse marrow GFU-GM, but not of mouse marrow CFU-E. Inactivation of 1-84 bPTH abolished its action on erythropoiesis. Increasing the concentration of Ep in the media from 0.67 to 1.9 U/ml overcame the inhibitory effect of 1-84 bPTH on BFU-E. The N-terminal fragment of PTH (1-34 bPTH) and 53-84 hPTH had no effect on BFU-E. The results demonstrate that (a) either the intact PTH molecule or a C-terminal fragment(s) bigger than 53-84 moiety exerts the inhibitory effect on erythropoiesis, and (b) adequate amounts of Ep can overcome this action of PTH. The data provide one possible pathway for the participation of excess PTH in the genesis of the anemia of uremia.

Animals↗
PubMed1980

A method for the determination of free neuraminic acid split from red blood cell receptors by attached Newcastle disease virus during simultaneous elution and hemolysis.

Determination of free neuraminic acid in chicken red blood cell (RBC) hemolysate becomes possible after deproteinization of the hemolysate by ethanol-chloroform followed by removal of the solvents by evaporation. This procedure permits the determination of in situ neuraminidase activity of virions preadsorbed on RBC receptors when the virus elution and hemolysis proceed simultaneously.

Animals↗
PubMed1977

Enzootic calcinosis in sheep and C-cells hyperplasia of the thyroid.

In nine sheep belonging to the same flock, C-cells hyperplasia of the thyroid, associated with calcinosis of the soft tissues is reported. The C-cells hyperplasia was probably due to excessive feeding with poultry waste, rich in calcium. The soft tissue mineralisation was a result of hypersecretion of calcitonin, a blood calcium-lowering hormone of the C-cells.

Animals↗
PubMed1977

Distribution of lactate dehydrogenase isoenzymes in normal and inflamed bovine udders and milk.

The patterns of distribution of lactate dehydrogenase (LDH) isoenzymes were determined in normal and inflamed bovine udder tissues, in normal and mastitic milk-leucocytes and serum. LDH1 was the most common isoenzyme found in all the types of tissues examined, normal tissues contained the lowest proportions of LDH5 whereas the inflamed tissues and leucocytes from mastitic milk showed a higher proportion of LDH4 and LDH5. It seems that the origin of the elevated LDH in mastitic milk is the leucocytes and the parenchyma cells of the udder. The significance of the shift in the molecular forms of LDH isoenzymes is discussed in relation to possible alternations in energy metabolism in the inflamed bovine mammary gland.

Animals↗
PubMed1977

Biochemical changes in fowl serum during infection with strains of Newcastle disease virus of differing virulence. Changes in serum proteins, uric acid, lipids and electrolytes.

Chickens aged five to six weeks were inoculated with three strains of Newcastle disease virus of differing pathogenicity. The serum level of the metabolites: total protein, albumin, globulin, uric acid, total lipids, cholesterol and electrolytes: calcium, magnesium, sodium and potassium were determined. The changes in serum levels of metabolites were as follows: velogenic infection was accompanied by decrease in total protein and albumin, reduction of lipids and cholesterol and increase in uric acid. No significant changes were found in the values of these metabolites in the serum of chickens infected with mesogenic strain. Lentogenic strain caused elevation of uric acid and cholesterol. All three strains caused decrease of the level of potassium in serum.

Animals↗