Alan R. Giles

TL;DR: Pathologic fibrinolysis as a cause of bleeding is much better understood as a result of the application of new and improved assays for components of the fibrinelytic system.

TL;DR: In vitro observations support the possibility that increased HNE cleavage of F.IX in vivo may contribute to the disregulation of hemostasis that occurs in conditions such as disseminated intravascular coagulation (DIC).

TL;DR: There was a rapid loss of high-molecular-weight multimers of the circulating vWF, with full recovery within 1 hour, and there was increased morphological evidence of metabolic organelle activity associated with replacement of WP bodies, presumably due to de novo synthesis of the basic protomer and its packaging in high-satellite-weight multimeric form in the storage organelles.

TL;DR: Data suggest that the extrinsic, factor VII-dependent factor X activation provides only a minor pathway of thrombin generation in vivo, and factor VIIa may prove useful in the treatment of haemophilia A patients with acquired inhibitors to factor VIII.

TL;DR: Missense mutations in the region of the gene that encodes the GpIb binding domain represent recurring new mutations representing the disease causing mutations in a large number of type IIB vWd families.