Plasma Factor VIII Levels as a Biomarker for Venous Thromboembolism

Fibrin Sealants: Challenges and Solutions

“…Hemostasis (i) enables rapid closure of blood vessels while (ii) maintaining blood flow in the circulation and finally (iii) removal of the clot after vessel repair. , Hemostasis was previously categorized as primary (platelet activation) and secondary (coagulation), but it is a simultaneous interplay between platelet responses, coagulation proteins, and components of the vessel wall. ,− Nowadays, a cell-based model is frequently cited, consisting of three different and overlapping phases (initiation phase, amplification phase, and propagation phase; Figure ). ,− After injury of a vessel wall, platelet adhesion and aggregation occur at the damaged site through interactions of platelet receptors with extracellular ligands and soluble proteins (primary hemostasis). − Simultaneously, exposure of subendothelial tissue factors (TFs) at the injury site results in the activation of coagulation factors leading to activation, adhesion, and aggregation of both preexisting and circulating platelets (secondary hemostasis). ,, Repetitive loops in the coagulation system and platelet activation produce large amounts of fibrin that stabilize previously formed platelet thrombi . One of the major players in hemostasis is factor XIII, which catalyzes the formation of covalent cross-links between soluble fibrinogen, to form a fibrinogen network, and plasmin, which acts as an opposing player to factor XIII to degrade the fibrinogen network. , …”