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Biomedical subjects

W M Watkins

Publications and source records attributed to W M Watkins.

At least 127 records · Page 7Linked to original sources
PubMed1982

The stability of adrenaline ophthalmic solutions on sterilization and storage.

The stability of adrenaline ophthalmic solutions, at pH 5.8 and 7.4, to sterilization and storage conditions has been studied. Solutions sterilized by filtration or heating at 98 degrees C for 30 min showed no detectable degradation at either pH value, whilst sterilization at higher temperatures resulted in losses of up to 30%. Total degradation increased with increasing sterilization temperature at both pH values.

Drug Stability↗
PubMed1981

A human dispermic chimaera first suspected from analyses of the blood group gene-specified glycosyltransferases.

The red cells of a normal male blood donor, K.S., were first grouped as B but he was found to lack anti-A in his serum. Closer investigation revealed that his red cells had very weak A activity, demonstrable only by absorption and elution of anti-A. He is a non-secretor of ABH and a secretor of Lea. Blood group A-, B and H-gene specified glycosyltransferases were detected in his serum. In contrast to the finding of a B antigen of normal strength on his red cells, the B transferase in his serum was only about 30% of the normal level and, despite the very weak A activity of K.S's red cells, the A transferase level was about 50% of that found in the serum of group A individuals with normal strength of A antigen. Moreover, the A transferase on the basis of its pH optimum, Km values for donor and acceptor substrates, activation by divalent cations, isoelectric focusing profile and capacity to convert O to A-active cells, was characterized as the product of an A1 gene. A family study showed that K.S's wife is group A2 and that they have two sons, one group A2 and the other group B. The group B son is assumed to have inherited a B gene from the propositus but the level of B transferase in the son's serum is three times as high as that in his father's serum. The wife of the propositus and his group A2 son have normal A2 transferases in keeping with their A2 red cell status. The A2 son therefore appears to have inherited an A2 gene from his mother but neither the A1 nor the B gene shown to be carried by his father. The distribution of transferase activities in K.S's red cells differs from that in his serum. A level of B transferase within the normal range was found in his red cell membranes but a very low level of A transferase was detected. The discrepancies between the serum transferases and ABO red cell group, together with the pattern of inheritance within the family, led to a suspicion of chimaerism. This was confirmed by the finding of fibroblasts with the female 46XX karyotype in cultures of the propositus' skin. These results suggest that K.S. is a dispermic chimaera with two different cell lines of the genotypes BO and A1O or A1A1. The group A2 son is assumed to have inherited an O gene from his father. It seems probable that K.S.'s bone marrow and reproductive organs are comprised predominantly of the XY cell line which carried the blood group BO genotype whereas his skin and other tissues which contribute the A1 transferase to his plasma, are partly made up of the XX cell line which carries the blood group A1O or A1A1 genotype.

ABO Blood-Group System↗
PubMed1981

The genetic and enzymic regulation of the synthesis of the A and B determinants in the ABO blood group system.

Possible genetic models for the inheritance of the ABO blood groups are discussed in terms of the glycosyltransferase enzymes which complete the synthesis of the A and B determinants. Recent immunologic evidence in support of the allelic status of the ABO genes is reviewed. Results are presented of experiments which demonstrate that the B gene associated alpha-3-D-galactosyltransferase can be used to synthesis blood group A determinants.

ABO Blood-Group System↗
PubMed1980

An H-deficient blood with normal H transferase levels.

An H-deficient blood is described which, unlike other H-deficient, Bombay and para-Bombay bloods, has normal H transferase levels. In previous examples of Bombay and para-Bombay phenotypes the absence of H transferase has explained the lack of H substrate and therefore the weak A and B antigens which are characteristic of these phenotypes. This explanation obviously does not hold in the case described here and it is proposed that the biochemical block must be further back, either in the enzymes synthesising the oligosaccharide chains or in those making the GDP-fucose substrate for the H and the Le gene-specified fucosyltransferases. Inhibition of the synthesis of Leb substance, as well as H substance, although the saliva of the propositus contains the Le gene-specified transferase, supports this proposition.

ABO Blood-Group System↗
PubMed1980

Leukemia-induced alterations of serum glycosyltransferase enzymes.

Studies on blood group A and H glycosyltransferase enzymes in 54 patients with acute myeloid leukemia were carried out on serum derived from blood samples taken prior to treatment, and in 16 cases, further tests were performed during clinical remission and at the time of relapse. The enzyme assay procedures, using low-molecular-weight compounds as sugar acceptors and radioactive nucleotide sugars as the donor substrates, have been described by Chester et al. (Eur. J. Biochem., 69:583, 1976). Abnormally low values of H enzyme (expressed as percentage of radioactive sugar incorporated into product; (that is, 1 to 3%) were observed in practically all presentation sera, but the values reverted to normal levels (3 to 15%) at the time of clinical remission and then became low once more with the development of drug resistance and clinical relapse. A enzyme levels measured in presentation sera which had demonstrated abnormal H enzyme were mostly within the normal range. In 2 of 5 A1 patients; sera and in all of three A2 patients increases in enzyme levels were observed in remission as compared with presentation serum samples. The depression of biosynthetic enzymes in acute leukemic sera could not be accounted for on the basis of competitive inhibitors or catabolic enzymes. It is proposed that changes of serum glycosyltransferase enzymes reflect alterations in a leukemic cell population and that knowledge of these changes may be of value in prognosis in acute leukemia.

Blood Proteins↗