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Biomedical subjects

A Zipursky

Publications and source records attributed to A Zipursky.

At least 91 records · Page 5Linked to original sources
PubMed1976

Leukemic reticuloendotheliosis. A failure of monocyte production.

In five cases of leukemic reticuloendotheliosis studied, profound monocytopenia was demonstrable. In 48 normal subjects, monocyte counts ranged from 215 to 921 per cubic millimeter, whereas in the five patients with leukemic reticuloendotheliosis, the counts ranged from 0 to 17 per cubic millimeter. The properties of the "hairy" cell are consistent with those of an incompletely developed monocyte. The susceptibility to infection, characteristics of these patients, may result from a lack of normal monocytes in blood and tissues.

Adult↗
PubMed1976

Leukocyte density and volume in normal subjects and in patients with acute lymphoblastic leukemia.

A method is described for the separation of blood and bone marrow leukocytes on the basis of buoyant density, using a discontinuous Ficoll-Hypaque density gradient. The median cell densities of monocytes and lymphocytes were found to be 1.067-1.077 and 1.073-1.077 g/ml, respectively. The cells of the myeloid series were shown to increase in density with maturation; the myeloblasts had the lowest density (1.064-1.065 g/ml) and the neutrophils the highest (greater than 1.080 g/ml). Cell volumes have been determined on isolated cell populations. The findings were: monocytes, 534 +/- 47 cu mu; lymphocytes, 247 +/- 18 cu mu; and neutrophils, 468 +/- 24 cu mu. Fourteen patients with acute lymphoblastic leukemia were studied. In four patients, the lymphoblasts were of low density (less than 1.068 g/ml), whereas the remaining patients had high density (greater than 1.068 g/ml) lymphoblasts. These four patients had large numbers of lymphoblasts in the peripheral blood and a poor prognosis. Lymphoblast volumes were not different in these two groups and were unrelated to prognosis.

Cell Separation↗
PubMed1976

The hematology of bacterial infections in premature infants.

A series of premature infants was studied for the presence of bacterial infection. On the basis of clinical evidence and bacteriological studies, they were divided into three groups in which sepsis was considered to be proven, possible, or unlikely. Band neutrophil counts were elevated most frequently in the "sepsis-proven" group and the elevation occurred usually within 24 hours of onset of signs of disease. Qualitative changes in neutrophils (Döhle bodies, toxic granulation, and vacuolization) were more frequent in the sepsis-proven group and, together with the band count, provided valuable techniques for the diagnosis of bacterial infections. Thrombocytopenia occurred frequently in the sepsis-proven group and seemed to result from increased utilization or destruction of platelets rather than failure of production. In such cases, evidence of intravascular coagulation was minimal and it was concluded that thrombocytopenia had resulted from a direct effect of the bacteria or its products on platelets and/or endothelium.

Bacterial Infections↗
PubMed1975

Massive transplacental hemorrhage: clinical manifestations in the newborn.

Thirteen newborn infants had transplacental hemorrhage in excess of 30 ml. Fetal blood in the maternal circulation was demonstrated in all cases by the acid elution technique. Anemia was noted in five babies either at birth or within the first 24 hours of life. One baby was stillborn, the death possibly being related to fetal hemorrhage. The other seven babies were clinically normal in spite of massive transplacental hemorrhage. The hemoglobin values and reticulocyte counts were normal at birth and the first 5 days of life. The data on this group of babies suggest that the clinical manifestations of transplacental hemorrhage are related not only to the size of the hemorrhage but also to the time at which the hemorrhage occurs.

Anemia, Hypochromic↗
PubMed1974

Sulfhydryl groups of the erythrocyte membrane and their relation to glycolysis and drug-induced hemolytic anemia.

Hemolytic anemia caused by oxidative drugs is thought to result from the oxidation of intracellular and membrane sulfhydryl groups of the erythrocyte. This process is more likely to occur in those erythrocytes in which the intracellular mechanism for reduction of disulfides is abnormal (e.g., glucose-6-phosphate dehydrogenase deficiency). If a membrane sulfhydryl group is critical in the pathogenesis of druginduced hemolytic anemia, it follows that this specific group must be dependent on intracellular reductive mechanisms for maintenance of the reduced state. This report describes a sulfhydryl group(s), involved in membrane structure, which is (are) dependent on intracellular metabolism for maintenance of the reduced state. It is postulated that this metabolically dependent membrane sulfhydryl group may play a role in the pathogenesis of drug-induced hemolytic anemia. Membrane sulfhydryl groups were studied by observing the effect of sulfhydryl blocking agents, e.g., N-ethyl-maleimide (NEM), on the recovery of erythrocyte ghosts after osmotic lysis. It was shown that NEM interfered with ghost recovery by reacting with membrane sulfhydryl groups. The concentration of NEM (as determined by [(14)C] NEM binding) necessary to cause this effect was lower than that necessary to produce changes in osmotic fragility or cation permeability, or to cause Heinz body formation. In the absence of glucose, these sulfhydryl groups became disulfides, but could be returned to the reduced state by restoring glycolysis or by adding dithiothreitol. Phenylhydrazine hemolytic anemia was induced in pigs, and membrane changes of the type described above occurred early in the pathogenesis of the disease.

Anemia, Hemolytic↗
PubMed1968

The nonerythropoietic component of early bilirubin.

The early labeled bilirubin consists of two primary components. The more rapidly synthesized of the two is independent of erythropoiesis (nonerythropoietic), whereas the second fraction is related to red cell production (erythyropoietic). The present studies concern the origin of the nonerythropoietic component. The nonerythropoietic, early labeled bilirubin was studied in bile fistula rats with (delta ALA)-4-(14)C delta aminolevulinic acid and glycine-2-(14)C as precursors. That nephrectomy did not reduce the size of this component despite the large and rapidly turning over pool of renal heme suggests that this pool may be of minor importance in its production. Intoxication with lead to a level that reduced hepatic heme synthesis was associated with a decrease in early bilirubin formation. The synthesis of this bilirubin was assessed in animals with phenobarbital-induced heme protein and cycloheximide-suppressed protein synthesis. Rats pretreated with phenobarbital at a dose level of 60 mg/kg with induction of cytochrome P-450 synthesis showed a minor increase in early labeling when glycine-2-(14)C but not when delta ALA-4-(14)C was used as precursor. Rats given cycloheximide at a dose level that markedly reduced hepatic protein and cytochrome P-450 synthesis but allowed heme synthesis to continue at 60% of its pretreatment level synthesized normal or increased amounts of early bilirubin from delta ALA-4-(14)C. Allylisopropylacetamide intoxication caused little change in early bilirubin formation, whereas aminotriazole given at a time after maximal hepatic heme labeling produced a small but significant increase in the appearance of labeled bilirubin. These findings indicate that early bilirubin production is little influenced by increased hepatic porphyrin synthesis or by changes in the rapidly turning over heme protein P-450. A minimal increase attends catalase inactivation by aminotriazole. Normal or increased synthesis takes place in the presence of suppression of protein synthesis. This finding suggests that the nonerythropoietic early bilirubin may itself consist of two subcomponents. The first of these may arise from free tissue heme or its precursors, and the second may derive from the turnover of the heme proteins. The first subcomponent may serve as a regulatory mechanism for the removal of heme synthesized in excess of its protein acceptor. A composite scheme is proposed for the origin of the total early bilirubin from heme compartments in tissue and marrow.

Amides↗