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Biomedical subjects

M Mackie

Publications and source records attributed to M Mackie.

28 records · Page 2Linked to original sources
PubMed1982

Familial antithrombin III deficiency.

Antithrombin III is the major physiological inhibitor of the coagulation mechanism and a deficiency of this protein results in a marked predisposition to venous thromboembolic disease. Three Scottish families with a deficiency of this protein are described and other reported families are reviewed. The properties, functions and methods of assay of antithrombin III are outlined; the molecular abnormalities, inheritance, clinical and laboratory characteristics of antithrombin III deficiency are described, and the use of antithrombotic drugs and human antithrombin III concentrates in this deficiency is discussed.

Adolescent↗
PubMed1981

Comparative studies on human activators of plasminogen.

Agents activating human plasminogen have been prepared from a variety of human sources, namely plasma, blood vessel endothelium and tissue. Their physical and functional properties have been found to differ from that of the urinary activator, urokinase. Antiserum to urokinase, while it quenched the activity of urokinase itself, had no effect on the activity of the plasma, endothelial or tissue activators.

Antifibrinolytic Agents↗
PubMed1978

Familial thrombosis: inherited deficiency of antithrombin III.

Several members of a family living on the west coast of Scotland and on one of the islands off the coast had serious thrombotic disease. The plasma antithrombin III (ATIII) concentrations were measured by both functional and immunological assay in all available members of the family. Concentrations were 25% to 66% of normal in 12 people, including all seven with thrombotic disease. The inheritance pattern was characteristic of an autosomal dominant disorder. Thrombotic disease generally affected the leg, mesenteric, and axillary veins, although one man who had died before the study began had had severe arterial atheroma. In women the first thrombotic symptoms usually occurred during pregnancy. None of these patients have developed thrombotic symptoms until they were at least 18, so four younger members of the family who have ATIII deficiency but no thrombotic disease may eventually develop symptoms.

Adolescent↗