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. Author manuscript; available in PMC: 2011 Apr 1.
Published in final edited form as: Thromb Res. 2010 Feb 16;125S1:S35–S37. doi: 10.1016/j.thromres.2010.01.033

Figure 1. Contributions from cells, plasma, and blood flow (Virchow's Triad) regulate fibrin formation and therefore, fibrin network structure and stability.

Figure 1

Laser scanning confocal micrographs show recalcified, platelet-poor plasma (hemophilia A, normal, and 200% fibrinogen from left to right, respectively) spiked with AlexaFluor-488-labeled fibrinogen (10 μg/120 μL sample) and clotted by TF-bearing monocytes. Abnormally-coarse networks of thick fibers are associated with an increased risk of bleeding, whereas overly-dense networks of thin fibers are associated with an increased risk of thrombosis. Characterizing the specific mechanisms by which cells, plasma and blood flow regulate fibrin structure and stability is critical for understanding hemostasis and identifying effective targets for hemostatic and antithrombotic therapies.