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D E Macfarlane

Publications and source records attributed to D E Macfarlane.

66 records · Page 4Linked to original sources
PubMed1977

Screening tests for syphilis. A comparison of the Treponema pallidum haemagglutination assay with two automated serological tests.

Two Treponema pallidum haemagglutination assay (TPHA) tests (Wellcome and Fuzizoki) were compared with the automated reagin test and the automated Reiter protein complement-fixation test in a routine screening system. The Wellcome TPHA was shown to lack sensitivity, and it is recommended that it should be used at a lower screening dilution. The Fuzizoki TPHA recorded a significant number of false positive and false negative results, and was therefore inferior to the fluorescent treponemal antibody absorption (FTA-ABS) test as a definitive test for syphilis. It is suggested that the TPHA be used in conjunction with a reagin test to replace some of the more inadequate screening tests currently in use. The automated screening tests were shown to have a similar sensitivity to the TPHA as well as several other advantages; they are recommended for testing large numbers of specimens.

Autoanalysis↗
PubMed1976

Evaluation of automated large-scale screening tests for syphilis.

Two methods of performing serological screening tests for syphilis are compared. One consisted of the Venereal Diseases Reference Laboratory (VDRL) slide test, the cardiolipin Wassermann reaction (CWR), and the Reiter protein complement fixation test (RPCFT) performed manually; the other was a fully automated system using two Technicon AutoAnalyzers (AAII), one for the automated reagin test (ART) and the other for automated complement fixation tests. The absorbed fluorescent treponemal antibody test (FTA-ABS) was used as a final arbiter in all cases found to be seropositive by either method. A pooled antigen consisting of a mixture of cardiolipin and Reiter protein was used for the automated complement fixation test, thus increasing the scope and capacity of the system. The AutoAnalyzer was shown to be capable of performing 400 cardiolipin and Reiter complement fixation tests and 700 automated reagin tests in an 8-hour day. Modification of the complement fixation test method to take advantage of the highly sensitive colorimeter resulted in a significant increase in sensitivity and a corresponding saving in reagents. Of the 7843 sera tested, 258 gave a positive result in one or more of the screening tests. The automated test detected many more Reiter positive sera (127) than the manual test (83). Conversely, fewer CWR positive sera were detected by the automated test (60) than by the manual test (82). There was little difference between the number of positive sera detected by the ART (73) and the VDRL slide test (71). In 19 instances the automated tests detected positive sera which registered as completely negative in the manual tests, and four seropositive cases which the automated tests had failed to detect were detected by the manual tests, and four seropositive cases which the automated tests had failed to detect were detected by the manual tests. It was concluded that a combination of the ART and automated Reiter protein complement fixation test (ARPCFT) would be ideal for use in a large-scale screening programme for the detection of syphilis.

Autoanalysis↗
PubMed1975

The role of thrombin in ADP-induced platelet aggregation and release: a critical evaluation.

The role of thrombin in ADP-induced aggregation and release in vitro was critically examined. The addition of heparin or hirudin to citrated platelet rich plasma did not prevent aggregation or release. The addition of citrate to heparinized plasma restored secondary aggregation and release. Hirudin did not prevent irreversible aggregation. These results are incompatible with the hypothesis that thrombin is a primary and necessary mediator of platelet aggregation (Ardlie & Han, 1974; Han & Ardlie, 1974a, b, c). This hypothesis is based in part on the assumption that EDTA enhances the elution of clotting factors from platelets; we found no enhanced elution of factors II, V, X, VIII, IX or XI when platelets were washed in EDTA.

Adenosine Diphosphate↗
PubMed1975

Hereditary giant platelet syndrome. Absence of collagen-induced coagulant activity and deficiency of factor-XI binding to platelets.

The platelets from two related patients with the hereditary giant platelet syndrome were examined. They were larger than normal but otherwise ultrastructurally normal; they contained increased storage pools of adenine nucleotides and heparin-neutralizing activity and took up serotonin at an increased rate. They aggregated normally with ADP and collagen but failed to aggregate with bovine factor VIII and Ristocetin. Some change in shape occurred with ADP, and the reduction in adenylate energy change after addition of ADP to platelet-rich plasma was smaller than normal. Platelet coagulant activities including contact product forming activity, intrinsic factor-Xa forming activity and platelet factor 3 activity were normal or increased, but collagen-induced coagulant activity was absent whether tested in washed platelet suspensions or platelet-rich plasma. Platelet washing experiments showed decreased binding of factors V and VIII to hereditary giant platelets and no detectable factor XI in washed platelet suspensions. It is concluded that (1) the hereditary giant platelets studied lacked a binding mechanism for factors, V, VIII and XI; (2) the normal development of collagen-induced coagulant activity apparently depends upon the binding of factor XI to the platelet membrane; and (3) the defective prothrombin consumption observed in these patients may have resulted from the failure of their platelets to bind factor XI.

Adenine Nucleotides↗
PubMed1975

The effects of ATP on platelets: evidence against the central role of released ADP in primary aggregation.

The influence of freshly purified ATP on the effects of aggregating agents on human platelets was studied. ATP inhibited aggregation induced by ADP competitively (Ki = 20 muM) and immediately without need for prior incubation. ATP had no effect on primary aggregation induced by adrenaline, thrombin, vasopressin, or 5-hydroxytryptamine (5HT). ATP inhibited the shape change and the consumption of metabolic ATP induced by ADP but did not inhibit these effects when induced by thrombin, vasopressin, or 5HT. ATP counteracted the inhibition by ADP of PGE1-stimulated cyclic AMP production in platelets but did not reduce inhibition by adrenaline. It is concluded that adrenaline, thrombin, 5HT, and vasopressin each can induce primary aggregation of human platelets by a mechanism independent of extracellular ADP.

Adenine↗