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Biomedical subjects

C D Forbes

Publications and source records attributed to C D Forbes.

At least 307 records · Page 17Linked to original sources

Tranexamic acid in control of haemorrhage after dental extraction in haemophilia and Christmas disease.

In a double-blind trial tranexamic acid (AMCA, Cyclokapron), 1 g three times a day for five days, significantly reduced blood loss and transfusion requirements after dental extraction in patients with haemophilia and Christmas disease. No side effects were seen in either group of patients. Screening tests showed no toxic action of tranexamic acid on the liver, kidney, or heart.

Adolescent↗

Serum enzyme changes after intramuscular bleeding in patients with haemophilia and Christmas disease.

Serum creatine kinase, lactate dehydrogenase, aspartate and alanine transaminases, and aldolase were determined in 41 hospital inpatients with haemophilia or Christmas disease and no significant differences from the normal ranges were found.(3) Levels of these enzymes in a further 10 such patients who had sustained muscle haematomata were determined: in all of these there was a consistent rise in the level of creatine kinase, the peak occurring between 36 and 96 hours. In bleeding disorders a rise in serum creatine kinase levels may be useful as a diagnostic test for intramuscular haemorrhage.

Adolescent↗

Aggregation of human platelets by commercial preparations of bovine and porcine antihaemophilic globulin.

Infusion of commercial preparations of porcine and bovine antihaemophilic globulin into three haemophilic patients produced transient thrombocytopenia. This platelet-aggregating activity has been shown to be present in a wide range of animal plasmas and is related to the fibrinogen fraction. The mechanism of platelet aggregation by animal fibrinogen is discussed and some inhibitors of the reaction are described.

Adenosine↗

Action of a pyrimido-pyrimidine compound on platelet behaviour in vitro.

A pyrimido-pyrimidine compound (RA433) was found in vitro to be a significantly more potent inhibitor of platelet behaviour than the previously available pyrimido-pyrimidine compound RA8-dipyridamole. In a turbidimetric system RA433 inhibits platelet aggregation induced by adenosine diphosphate, collagen, and noradrenaline; further, in a glass-bead-column technique it is a powerful inhiitor of platelet adhesiveness.

Adenine Nucleotides↗

Effect of gaboon viper (Bitis gabonica) venom on blood coagulation, platelets, and the fibrinolytic enzyme system.

The action of the venom of the gaboon viper (Bitis gabonica) on blood coagulation, platelets, and the fibrinolytic enzyme system was studied. The results confirm that the venom of Bitis gabonica has a marked anticoagulant action in vitro. The venom appears to impair clot formation by a direct proteolytic action on fibrinogen, releasing soluble breakdown products.

Adenine Nucleotides↗

Studies on a complex mechanism for the activation of plasminogen by kaolin and by chloroform: the participation of Hageman factor and additional cofactors.

As demonstrated by others, fibrinolytic activity was generated in diluted, acidified normal plasma exposed to kaolin, a process requiring Hageman factor (Factor XII). Generation was impaired by adsorbing plasma with glass or similar agents under conditions which did not deplete its content of Hageman factor or plasminogen. The defect could be repaired by addition of a noneuglobulin fraction of plasma or an agent or agents eluted from diatomaceous earth which had been exposed to normal plasma. The restorative agent, tentatively called Hageman factor-cofactor, was partially purified by chromatography and had an apparent molecular weight of approximately 165,000. It could be distinguished from plasma thromboplastin antecedent (Factor XI) and plasma kallikrein, other substrates of Hageman factor, and from the streptokinase-activated pro-activator of plasminogen. Evidence is presented that an additional component may be needed for the generation of fibrinolytic activity in mixtures containing Hageman factor, HF-cofactor, and plasminogen.The long-recognized generation of plasmin activity in chloroform-treated euglobulin fractions of plasma was found to be dependent upon the presence of Hageman factor. Whether chloroform activation of plasminogen requires Hageman factor-cofactor was not determined, but glass-adsorbed plasma, containing Hageman factor and plasminogen, did not generate appreciable fibrinolytic or caseinolytic activity. These studies emphasize the complex nature of the mechanisms which lead to the generation of plasmin in human plasma.

Blood Coagulation Factors↗