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Biomedical subjects

L M Snyder

Publications and source records attributed to L M Snyder.

At least 73 records · Page 4Linked to original sources
PubMed1977

L-Dopa peroxidase activity of human erythrocyte catalase.

The human red cell hemolysate was found to have 3-(3',4'-dihydroxphenyl)-L-alanine (L-dopa) peroxidase activity. During the purification of glutathione peroxidase and catalase by ammonium sulfate precipitation, ion exchange chromatography. Sephadex gel filtration, and preparative polyacrylamide disc electrophoresis, the L-dopa peroxidase activity was found to be associated with catalase. Both sodium azide, 8 mM, and 3-amino-1,2,4-triazole, 50 mM, besides inhibiting catalase, inhibited the L-dopa peroxidase activity in each fraction. Ethylenediamine tetraacetic acid (EDTA), 4 mM, had no effect on catalase or L-dopa peroxidase activity, indicating that the oxidation of L-dopa is not a nonenzymatic process mediated by metal ions. Although the electrophoretic mobility of catalase, L-dopa peroxidase, and glutathione peroxidase are similar, a homogeneous preparation of glutathione peroxidase was free of L-dopa peroxidase activity. L-Dopa peroxidase in human red cells was co-purified with catalase.

Azides↗
PubMed1977

Effect of propranolol on normal human erythrocytes.

The present study was undertaken to standardize the effect of propranolol on normal human red cells and thus establish certain parameters enabling us to evaluate propranolol's effect on pathological cells. Normal human erythrocytes lost 40 MEq. of potassium, decreased the intracellular pH by 0.06 units, and shifted the oxyhemoglobin dissociation curve 6.0 mm. Hg to the right in the presence of propranolol. The series of events and magnitude of the response induced by propranolol was time dependent and sensitive to temperature, pH, drug concentration, and erythrocyte concentration. Calcium was an absolute requirement for maximal propranolol action with simultaneous incorporation of trace amounts of radioactive calcium into the cell. Chelation of calcium with EDTA or EGTA inhibited the response to propranolol.

Calcium↗
PubMed1976

Effect of androgens on maturation and metabolism of erythroid tissue.

Specific changes taking place in the erythroid tissue following depletion or replacement of androgens were studied in rats. The reduction of testosterone levels in blood of orchiectomized animals did occur in conjunction with a decline of erythrocyte glucose-6-phosphate (G6P) and lactate levels. No evidence of anemia was observed. The subcutaneous administration of testosterone propionate (16.0 mg/kg) to orchiectomized rats restored, within 12 hours, blood testosterone levels as well as erythrocyte G6P levels and lactate production. The in vitro incorporation of glucose-1-14C into rat erythrocytes incubated with testosterone was comparable to that of control cells. A radioautographic study of rat erythroid marrow pulsed with glucose-1-14C showed a lower labeling when testosterone propionate was administered. The authors conclude that testosterone does directly affect glucose metabolism of erythroid cells, via the pentose shunt pathway. The possible role of the androgen-dependent enhancement of erythroid glycolysis is discussed in relation to the function of testosterone receptocytes present in marrow cells and a 17beta-hydroxysteroid dehydrogenase present in erythrocytes.

Animals↗
PubMed1975

32P distribution into 2,3-bisphosphoglyceric acid from human erythrocytes following molybdate-catalyzed hydrolysis.

Normal human washed erythrocytes were incubated in autologous plasma with 32P for varying periods of time. 2,3-Bisphosphoglyceric acid the major organic phosphate ester of red cells, was first isolated and purified by anion-exchange chromatography; subsequently, the C-2Pi was selectively hydrolyzed by a molybdate-catalyzed reaction. The C-2-bound Pi of 2,3-P2-glyceric acid was found to have a significantly higher specific activity than C-3 Pi. Intramolecular equilibration was not reached until the 180-min incubation. No evidence of overhydrolysis or internal randomization by the molybdate reaction was noted which was confirmed following hydrolysis of double-label 2,3-P2-glyceric acid 32P C-2, 33P C-3.

Chromatography↗
PubMed1975

Ultrastructural evidence for destruction in the halo nevus.

Nine halo nevi in various stages of regression were examined by electron microscopy for fine structural evidence of an immunological mechanism of tumor cell destruction and halo formation. Early regressing lesions (Stage I) showed nevus cells associated with infiltrating lymphocytes, monocytes, and plasma cells, but without nevus cell destruction. In later lesions (Stages II and III), vacuolar cytolysis was commonly observed in nevus cells. In Stage III lesions, portions of nevus cells are found within macrophages. The electron microscopic findings of lymphocyte, monocyte, and plasma cell infiltration of the tumor followed by vacuolar cytolysis support the concept of an immune reaction in regressing halo nevi.

Humans↗
PubMed1974

Hemostatic defect due to acquired circulating inhibitors against lipid procoagulant and factor VIII.

An 85 year old woman was studied because of severe bleeding. Acquired inhibitors to factor VIII and to phospholipid procoagulants were demonstrated. Platelet factor 3 (Pf3) assay was prolonged with both kaolin and Russell's Viper Venom (Stypven-R). It was normal with patient's washed platelets and normal plasma, but abnormal when normal platelets were incubated with patient's plasma. The inhibitor also blocked the coagulant action of Bell and Alton thromboplastin, inosithin, phosphatidyl ethanolamine and phosphatidyl choline, but not that of tissue thromboplastin or cardiolipin. All other platelet functions were normal. The inhibitors were purified by Al (OH3) absorption, heating at 56degrees, precipitation by 50% ammonium sulfate, followed by dialysis and DEAE-cellulose chromatography. A partial separation of the two inhibitors was achieved. Cyclophosphamide treatment resulted in cessation of bleeding and dissappearance of the inhibitors. This seems to be the first instance of an acquired circulating inhibitor specifically directed against phospholipid procoagulants in a patient who also had an inhibitor to Factor VIII.

Aged↗