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Biomedical subjects

W M Watkins

Publications and source records attributed to W M Watkins.

At least 145 records · Page 8Linked to original sources
PubMed1978

Inherited 'mosaicism' within the ABO blood group system.

A family with examples of the rare condition known as 'inherited mosaicism affecting the ABO blood groups' has been studied. In this family there were five examples of Bmos:O mosaicism. Blood group gene-specified transferase estimations were studied in this condition for the first time. In 'affected' members, levels of B gene-specified transferase were low, and amounted to only 7--10% of the activity of a normal control. It is proposed that Bmos is correctly classified as a new form of weak B.

ABO Blood-Group System↗
PubMed1976

Further observations on the Birmingham chimaera.

The appropriate ABH-gene specified glycosyltransferases in the plasma of the Birmingham chimaera were estimated. These observatiions and the demonstration of A1Leb blood group specific glycosphingolipid in the plasma indicate that the minority population of red blood cells probably represents the true blood groups of the patient.

ABO Blood-Group System↗
PubMed1976

Generic inequivalence between two brands of chloramphenicol capsule.

Generic inequivalence between two brands of chloramphenicol capsules has been investigated. Both brands complied with official standards for drug content and capsule disintegration time, and exhibited similar anti-bacterial activity when tested in vitro. A slow dissolution rate was observed with one brand which could be related to a formulation defect which might explain reported therapeutic inefficacy.

Capsules↗
PubMed1976

Immunochemical observations on the human blood group P system.

Haemagglutination inhibition experiments were carried out with anti-P1, anti-Pk and anti-P sera in an attempt to increase understanding of the chemical, genetical and serological relationships within the P system. The test-substances comprised a glycoprotein with human blood group P1 and Pk activity isolated from sheep hydatid cyst fluid, fragments isolated from the partial acid hydrolysis products of the P1Pk active glycoprotein, glycolipids, monosaccharides and di- and oligo-saccharides of known structure. The trisaccharide alphaGal(1 leads to 4)betaGal(1 leads to 4)GlcNAc isolated from the glycoprotein hydrolysis products, and earlier established as the P1 determinant (Cory et al., 1974), was the only low molecular weight compound that gave strong inhibition with human, rabbit and goat anti-P1 sera. A disaccharide alphaGal(1 leads to 4)Gal, also isolated from the glycoprotein hydrolysis products, failed to react with anti-P1 reagents but inhibited human anti-Pk sera as strongly as the trisaccharide. The glycolipid alphaGal(1 leads to 4)betaGal(1 leads to 4)Glc-Cer (Ceramide trihexoside) and other oligosaccharides containing alphaGal(1 leads to 4)Gal at the non-reducing terminal were also strong inhibitors of anti-Pk sera. Oligosaccharides with terminal alpha-galactosyl residues joined in other positional linkages gave definite, although less strong, inhibition. The inhibition results suggest a close structural relationship between the P1 and Pk determinants and indicate that the specificity of anti-Pk sera is less closely delineated than that of anti-P1. Human anti-P sera differed markedly from anti-P1 and anti-Pk and were not inhibited by any of the compounds containing alpha-galactosyl residues. The glycolipid betaGalNAc(1 leads to 3)alphaGal(1 leads to 4)betaGal(1 leads to 4)Glc-Cer (globoside) strongly inhibited the anti-P sera. The inhibition of anti-Pk and anti-P sera by ceramide trihexoside and globoside, respectively, confirms the observations of Naiki & Marcus (1974) and supports their conclusions that Pk is the precursor of P. The genetic relationship of the P1 antigen to P and Pk is not clear but biosynthetic pathways are discussed that might explain the absence of P1, Pk and P antigens in individuals of the p phenotype.

Blood Group Antigens↗