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At least 271 records · Page 15Linked to original sources
PubMed1982

[Separation of red blood cells from G6PD-deficient patients in dextran density gradients].

Red blood cells of 30 patients with G6PD deficiency were separated and characterized by means of isopyknic dextran density gradient centrifugation. The simultaneous determination of G6PD activity and the percentage of NADPH deficiency cells in relation to the maturation parameters of density, reticulocyte share, GOT and PK activity made it possible to recognize differences in the maturation of red blood cells with G6PD deficiency in normal persons as well as within a group of patients. In each case the more or less diminished enzyme activity of the cell suspension was accompanied by a marked enzyme deficiency of the youngest fraction. It is possible that NADPH defect cells are being eliminated at first. In many cases a direct correlation between the percentage of "empty cells" and the in vitro stability tests with and without NADP+ addition could be identified. Decreased maximal speed, changed kinetic behaviour, and instability of these variants are stressed as being the decisive parameters for the life expectation of red blood cells in patients with G6PD deficiency.

Anemia, Hemolytic↗
PubMed1984

[Characteristics of the Gd- alleles discovered in a population check of pupils in the city of Kostroma].

The population study of distribution of G-6-PD alleles among normal Russian school-children of Kostroma town was carried out. In total, 952 children were examined, 429 girls and 523 boys (from 7 to 18 years old). The frequency of Gd- alleles is 0.36%. Two Gd- alleles discovered in this study belong to the III class. One of them was characterized according to the WHO programme. This allele designated "Kostroma" has not been described earlier.

Alleles↗
PubMed1984

Analysis of haemopoiesis: the use of cell markers and in vitro culture techniques in studies of clonal haemopathies in man.

The clonal haemopathies have in common the expansion of a neoplastic stem cell which has retained a variable capacity for differentiation to granulocytes, monocytes, erythrocytes, and platelets. Although normal stem cells are present in such patients, their differentiation is somehow suppressed. However, their presence may be demonstrated either by cell culture studies, employing G6PD as the marker in appropriately selected cases, or by their emergence in patients subjected to marrow ablative chemotherapy. Suppression of normal stem cell growth and development does not require a hyperproliferative marrow, and the current data do not support the notion that normal stem cells are simply reduced in frequency by a vast increase in the numbers of neoplastic progenitors. It is likely, therefore, that such suppression involves cellular signals, operating over short distances (perhaps through cell-to-cell contact), which interfere with normal progenitors. Thus, stem cell culture techniques, in combination with cell markers, have provided a direct and informative way to approach the issues of disease pathogenesis, the kinetics of stem cell differentiation, and the interaction of normal and neoplastic cells in patients with clonal haemopathies.

Cells, Cultured↗
PubMed1983

Encapsulation of exogenous agents in erythrocytes and the circulating survival of carrier erythrocytes.

Erythrocytes can be made to entrap enzymes, lipids, drugs, pesticides, and large macromolecules by a variety of encapsulation procedures. Methods of encapsulation include hypotonic dilution and dialysis, lipid fusion, electrical hemolysis, and chemical perturbation. The survival of carrier erythrocytes is dependent on the method of encapsulation as is the encapsulation efficiency. Research has led to utilization of carrier cells for drug and enzyme-replacement therapies, for incorporation of DNA and antibodies into living cells, and for enhancement of the oxygen-carrying capacity of hemoglobin. Many of the possible uses of erythrocytes as carriers are explored.

Animals↗
PubMed1981

New stable mutant (Gd(-) variants: G6PD Tashkent and G6PD Nucus. Molecular basis of hereditary enzyme deficiency.

This paper represents studies on the molecular basis of G6PD deficiency in erythrocytes of 4 hemizygote patients. In all cases G6PD deficiency was due to an abnormal kinetic and (or) physico-chemical characteristics of the mutant enzymes. Two of 4 variants were characterized as G6PD EL Fayoum like (unstable, class 2). The other two are new variants: G6PD Tashkent (low Ki by NADPH, class 3) and G6PD Nukus (Km for G6P 127 microM, class 2). For the new mutant Gd(-) stable variants the amount of G6PD in total red cell population found immunologically was similar to the normal level. Stimulation of the pentose phosphate pathway (PPP) of G6PD Nucus erythrocytes insignificantly increased the rate of glucose consumption while in the case of G6PD Tashkent methylene blue raised the rate of PPP to half of the maximal rate of stimulated normal red cells.

Erythrocytes↗
PubMed1981

The influence of G-6-PD activity on the response of erythrocyte glutathione reductase to riboflavin deficiency.

Erythrocyte NAD(P)H2 glutathione oxidoreductase (EC 1.6.4.2.) activation coefficients (EGR AC) and D-glucose-6-phosphate: NADP 1-oxidoreductase, EC 1.1.1.49 (G-6-PD) activities were measured in 155 West African women to determine whether heterozygous G-6-PD deficiency produces false negative results in the EGR test for riboflavin deficiency. A positive correlation was found between EGR AC and G-6-PD activity demonstrating that heterozygous G-6-PD deficiency does result in abnormally depressed EGR AC values when G-6-PD activity is significantly reduced. However, heterozygous deficient genotypes with normal G-6-PD activity showed undepressed EGR AC values. These results indicate that, in its present form, the EGR test is not a suitable index of riboflavin status in subjects whose G-6-PD activity is less than 9 IU/g Hb when measured by the WHO-37 degrees assay.

Adult↗