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P Gaffney

Publications and source records attributed to P Gaffney.

45 records · Page 3Linked to original sources
PubMed1981

Non-enzymatic glucosylation of fibrinogen.

Glucose, when incubated with fibrinogen, binds covalently to that protein. The reaction is non-enzymatic in type and is directly dependant on the time of incubation, temperature and pH. Glucosylation of fibrinogen is not altered by preincubation with aspirin. No preferential glucosylation of fibrinogen, fibrinogen chains or plasmin digestion products XYDE could be demonstrated, suggesting that glucose binding occur at several different sites. No abnormality of thrombin clotting or stability of glucosylated fibrinogen could be detected. These findings are discussed in relation to the previously described abnormalities of fibrinogen metabolism in diabetes mellitus.

Albumins↗
PubMed1980

Some observations on the release of extrinsic and intrinsic plasminogen activators during exercise in man.

Exercise was found to cause the release of 'extrinsic' plasminogen activators into the bloodstream. The 'intrinsic' plasma plasminogen activators were not significantly altered although factor VIII clotting activity and, to a lesser extent, its related antigen were both raised. A small amount of systemic fibrin(-ogen)olysis was indicated by the generation of fragment X and a slight reduction in the amount of intact A alpha-fibrinogen chain present. Plasminogen and antiplasmins were not significantly affected by exercise. We conclude that exercise-induced fibrinolysis is brought about solely by the release of plasminogen activators(s) from the vessel wall but that this enhanced level of fibrinolysis is insufficient to produce a marked degree of systemic fibrin(ogen) breakdown.

Adult↗
PubMed1978

Evaluation of the normal-lymphocyte-transfer test.

The normal-lymphocyte-transfer test has been advocated as a method of assessing the immuno-competence of lymphocytes from patients with breast and large-bowel cancer. Evidence is presented in this paper that the methodology is subject to many uncontrollable errors, that the reaction is the result of multiple factors, and that the size of the reaction is related to the age of the patient and not to the extent of the malignancy.

Adult↗
PubMedDate not supplied

Acute inhibitory effect of alcohol on sodium-lithium countertransport.

To assess a possible acute effect of environmental factors on sodium-lithium countertransport (SLC), we determined the activity of this transport system in 14 healthy volunteers, who are nonhabitual drinkers, before and 1 hour after intake of alcohol (0.8g/kg) with "Coke" as the vehicle. Alcohol significantly increased the "leak pathway" component of lithium efflux from a baseline value of 0.21 +/- 0.02 to 0.24 +/- 0.02 mmol/Lcell.h(p < 0.003); and reduced the Vmax of the transporter (0.38 +/- 0.05 to 0.31 +/- 0.04mmol/Lcell.h;p < 0.0005) without significantly changing its affinity for external sodium. The reduction in Vmax was dependent on the initial activity of the transporter (r2 = 0.5). A plot of reduction in Vmax against the product of initial Vmax value and blood alcohol level in each subject revealed a stronger relationship (r2 = 0.86), suggesting that the observed change in Vmax was also dependent on blood alcohol level. Coke alone did not change any of the parameters. We conclude that alcohol acutely inhibits SLC as well as alters erythrocyte membrane in a manner that increases passive lithium efflux.

Adult↗
PubMedDate not supplied

A study of the temporal effect of alcohol on human erythrocyte sodium-lithium countertransport in relation to membrane cholesterol and phospholipids.

The effect of a single dose of alcohol (0.8 g/kg), given with "diet coke," on erythrocyte sodium-lithium countertransport (SLC) in relation to membrane cholesterol and phospholipids was assessed over 24 h in 10 healthy volunteers. Baseline passive lithium efflux (0.168 +/- 0.008 mmol l-1 Cell H-1) was increased 1 h (0.202 +/- 0.014 mmol l-1 cell h-1; p < 0.030), and 4 h (0.200 +/- 0.014 mmol l-1 cell h-1; p < 0.020), but similar to that at 24 h postalcohol (0.173 +/- 0.011 mmol l-1 cell h-1). These changes were not associated with any change in intracellular lithium. Control SLC VMAX of 0.387 +/- 0.054 mmol l-1 cell h-1 fell at 1 h (0.328 +/- 0.050 mmol l-1 cell h-1; p = 0.0012) and 4 h (0.312 +/- 0.048 mmol l-1 cell h-1; p < 0.0005). Its value 24 h postalcohol (0.371 +/- 0.047 mmol l-1 cell h-1) was comparable to that at baseline. There was no significant change in the affinity of the transporter for external sodium throughout the experimental period, suggesting that the reduction in VMAX 1 and 4 h after alcohol ingestion resulted from a noncompetitive inhibition. Intracellular sodium 4 h after alcohol was lower than at baseline, but returned to the control value within 24 h. In a control group (n = 5), pretreatment with "diet coke" alone did not alter any of the measured parameters. It is concluded that alcohol pretreatment increases passive lithium efflux and decreases SLC Vmax. Both effects are evident up to at least 4 h postdosing, but recover within 24 h in the absence of further alcohol intake.

Adult↗