By N.U. Bang
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Extra resources for Thrombosis and Bleeding Disorders. Theory and Methods
I f activated factor X I is dissociated from the factor X I I ^ - X I com plex, it would be inactivated by this inhibitor and new factor X I molecules would have the opportunity to complex with the already acti vated factor X I I . This would lead to a contin uous formation and deterioration of activated factor X I , ending in a complete consumption of factor X I during clotting. This is apparently not the case since factor X I is present in serum, indicating only a limited activation and con sumption.
According to Thies (1957) the gray substance of human brain is more active than the white substance. Brain extract throm boplastins are crude preparations. They can be further purified, and in the case of rabbit brain "brain thromboplastin (rabbit)" is obtained (Hecht et al. 1958). According to Hecht et al. (1958), this material is a complex lipid con sisting of sterol, glutamic acid, serine, ethanolamine, and probably sphingosine. This material rapidly activates prothrombin to thrombin via the extrinsic pathway.
1958). In contrast, Hecht (1966b) and Hecht and Oosterbaan van L i t (1967) could not separate brain thromboplastin into dis tinct protein and lipid moieties. They found the 15 amino acids described by Irsigler (1964) and Deutsch et al. (1964) also in the lipid portion and therefore concluded that the amino acids in these preparations were con taminants rather than a constituent of a specific phospholipoprotein. Phospholipids It was pointed out that neither the lipid por tion of lung thromboplastin nor the alcohol boiled brain thromboplastin function in the ex trinsic prothrombin activation pathway.