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G W Bird

Publications and source records attributed to G W Bird.

At least 91 records · Page 5Linked to original sources

Further characterization of some heterophile agglutinins reacting with alkali-labile carbohydrate chains of human erythrocyte glycoproteins.

The nature of the receptor sites for several agglutinins is characterized by hemagglutination inhibition assays. The inhibitory activity of human erythrocytes glycoproteins, from which sialic acid, sialic acid and galactose or alkali-labile oligosaccharides have been removed, is compared to the inhibitory effect of compounds with known structure. It is shown that the lectin from Arachis hypogea and anti-T bind to alkali-labile galactosyl-residues. Agglutinins from Bauhinia purpurea and variegata (non- or N-specific), Maclura aurantiaca, Iberis amara, sempervirens, umbellata hybrida and umbellata nana (M- or nonspecific), Moluccella laevis (A- plus N-specific), Helix pomatia, Helix aspersa, Helix lucorum and Caucasotachea atrolabiata interact with alkali-labile N-acetylgalactosamine. The results obtained with the anti-A agglutinins from various snails suggest that human erythrocyte glycoproteins contain, besides the alkali-labile tetrasaccharide, a peptide-linked sialyl-N-acetyl-galactosaminyl-residue. The investigations do not allow a precise definition of the receptor sites for the lectins having M- or N-specificity.

Agglutinins↗

Effect of Bacteroides fragilis on the human erythrocyte membrane: pathogenesis of Tk polyagglutination.

Incubation of normal human erythrocytes with the supernatant of centrifuged culture of some strains of Bacteroides fragilis results in the exposure of Tk polyagglutination determinants on the erythrocyte membrane. These determinants are present on non papain-labile structures and are probably exposed by an enzyme mechanism. Other strains of B. fragilis were found to produce neuraminidase, haemolysins, and protease. It is suggested that early recognition of Tk determinants may be an aid to the diagnosis of B. fragilis infection.

Arachis↗

Anaemic crisis in sickle cell disease.

Sixteen episodes of acute anaemia necessitating urgent blood transfusion have been investigated in 13 children with sickle cell anaemia. In five out of seven episodes there was evidence of increased haemolysis while in 10 out of 16 episodes a profound fall in reticulocyte count indicated marrow erythroid cell failure. Cold agglutinins active at room temperature were detected in 13 episodes, and anti-I specificity was demonstrated in 11. Warmed blood of homologous ABO and Rhesus groups was administered without complication despite difficulty with cross-matching. The exacerbation of anaemia was not due to folate lack, glucose-6-phosphate dehydrogenase deficiency or splenic sequestration, and an infectious agent appeared responsible. The degree of anaemia in homozygous sickle cell disease is usually constant during asymptomatic periods. An episode of sudden profound anaemia (anaemic crisis) may, however, result from marrow hypoplasia, an exacerbation of haemolysis, splenic sequestration, or folate deficiency.

Acute Disease↗

Bomb outrage.

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Blood Banks↗