Images

Folder for images

Whole blood clot
Whole blood clot SEM
Cover art
Distribution of fibrin fibers above a cell surface using Laser Scanning Confocal Microscopy and Transmission Electron Microscopy
Tissue factor-initiated coagulation
Scanning electron micrograph of a whole blood clot
Fibrin fibers over cell surface
TF initiated Coagulation
Tissue factor-initiated coagulation
Transmission electron micrograph of a whole blood clot
Normal & hemophilic plasma clots
Hemophilic clot
Confocal micrograph of hemophilic clot
Normal clot
Confocal micrograph of normal clot
Rouloux
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TEM A
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TEM B
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Whole blood clot B
Virchow's triad
Flow
Flow
Static
Static
Flow influences fibrin structure
Elevated fibrinogen and thrombosis
Carotid
Elevated fibrinogen increases fibrin(ogen) incorporation into thrombi following FeCl3 injury. Representative sections through thrombi following FeCl3 injury to the carotid artery
Saphenous
Elevated fibrinogen increases fibrin(ogen) incorporation into thrombi following FeCl3 injury. Representative sections through thrombi following FeCl3 injury to the saphenous vein
Normal
Confocal micrograph of normal clot
Hemo
Confocal micrograph of hemophilic clot
Virchow triad
Contributions from cells, plasma, and blood flow (Virchow's Triad) regulate fibrin formation and therefore, fibrin network structure and stability
Virchow's triad revisited
Arterial thrombosis
Interplay between abnormalities in blood components, the vasculature, and blood flow contribute to the development of arterial thrombosis. Arterial thrombosis involves the formation of platelet-rich “white clots” that form after rupture of atherosclerotic plaques and exposure of procoagulant material such as lipid-rich macrophages (foam cells), collagen, tissue factor, and/or endothelial breach, in a high shear environment. TM = thrombomodulin; II = prothrombin; IIa = thrombin; Fgn = fibrinogen; TF = tissue factor.
Venous thrombosis
Interplay among abnormalities in blood components, the vasculature, and blood flow contribute to the development of venous thrombosis. Venous thrombosis involves the formation of fibrin-rich “red clots” that result from exposure of procoagulant activity on intact endothelium plus plasma hypercoagulability, in reduced or static blood flow. Venous thrombi are thought to initiate behind valve pockets, in which reduced or static flow decreases wall shear stress that normally regulates endothelial cell phenotype. TM = thrombomodulin; EPCR = endothelial protein C receptor; II = prothrombin; IIa = thrombin; TF = tissue factor; Fgn = fibrinogen; RBC = red blood cells.
Microparticles
Circulating microparticles are derived from a variety of cell types including leukocytes, platelets, megakaryocytes, red blood cells, endothelial cells, and tumors. Microparticles (MP) carry cell-specific markers and functional properties of their parent cell.
Venn diagram
Arterial Thrombosis
Venous Thrombosis
Microparticles
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FXIII mediates RBC retention in thrombi
Factor XIII(a) (FXIII[a]) mediates red blood cell (RBC) retention in thrombi. During venous thrombosis (VT), platelets mediate thrombus contraction. FXIII activity increases RBC retention in retracted thrombi (left arrow). If FXIII activity is deficient or activation is delayed, fewer RBCs are retained, resulting in a smaller thrombus (right arrow).
Venous thrombi contain regions of high RBC and fibrin content
Venous thrombi contain regions of high red blood cell (RBC) and fibrin content. Left) Gross image of a segment of human venous thrombus (pulmonary embolus) collected at autopsy at UNC Hospitals. Note the presence of darker (RBC rich) regions. Image courtesy of Vincent J. Moylan, Jr, MS, PA(ASCP), UNC at Chapel Hill, School of Medicine. Right) Transmission electron micrograph of a pulmonary embolus showing the ‘brick-and-mortar’ organization of RBCs and fibrin within the thrombus.
FXIIIa cross-linking during fibrin formation
FXIIIa cross-linking during fibrin formation. Fibrinogen is a hexamer composed of 2 Aα- (purple), 2 Bβ- (blue), and 2 γ-chains (green). During coagulation, thrombin cleaves N-terminal fibrinopeptides from the Aα- and Bβ-chains, producing fibrin monomers which polymerize into protofibrils and subsequently, fibers. FXIIIa increases clot stability by introducing ε-N-(γ-glutamyl)-lysyl cross-links between residues in the γ- and α-chains of fibrin monomers within individual fibers. FXIIIa first introduces cross-links between γ-chains (forming γ-γ dimers) and subsequently between γ- and α-chains (forming high-molecular-weight species [γ-multimers, α-polymers, and αγ-hybrids]).
Contributions of FXIIIa to clot stability
Contributions of FXIIIa to clot biochemical and mechanical stability. FXIIIa cross-linking of plasma proteins (i.e., α2-antiplasmin [α2-AP]) increases the resistance of the clot to fibrinolysis. Cross-linking of the fibrin α- (purple) and γ-chains (green) stiffens fibrin fibers and increases the mechanical stability of the clot. Increased mechanical stability renders the clot more resistant to shear forces. α-chain cross-linking enables RBC retention during clot contraction.
Fibrinogen synthesis and expression
Fibrinogen synthesis and expression. Fibrinogen synthesis is regulated by both transcriptional and translational mechanisms. After individual fibrinogen chains are translated, fibrinogen assembly occurs stepwise. Single chains assemble first into Aα-γ and Bβ-γ precursors, then into Aα/Bβ/γ half-molecules, and finally into hexameric complexes (Aα/Bβ/γ)2. Once fibrinogen is released into blood, it circulates until thrombin cleaves fibrinopeptides from the Aα and Bβ chains (FpA and FpB, respectively) to form fibrin monomers. These monomers then polymerize in a half-staggered arrangement to form fibrin protofibrils and ultimately the fibrin network at a site of tissue injury.
Modifiers of fibrin(ogen) and association with disease
Modifiers of fibrin(ogen) and association with disease. Clot formation, structure, and stability are influenced by conditions present during fibrin generation. Abnormal clot formation is observed in several diseases.
Normal and Hemophilic Clots
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Networks formed under flow and stasis
Elevated Fibrinogen and Thrombosis