a(HM:Thrombus)
Pretreating anticoagulated whole blood with tricarbonyldichlororuthenium(II) dimer, a CO donor, significantly reduced collagen exposure (Fig. 5A) and thrombus formation (Fig. 5B) induced by FeCl3. PubMed:19276082
Pretreating anticoagulated whole blood with tricarbonyldichlororuthenium(II) dimer, a CO donor, significantly reduced collagen exposure (Fig. 5A) and thrombus formation (Fig. 5B) induced by FeCl3. PubMed:19276082
One mechanism that may contribute to enhanced platelet thrombus formation is inhibition of the metalloprotease ADAMTS13 by free hemoglobin [20]. PubMed:29929138
Platelet thrombus formation in the ex vivo model occurred in the presence of hirudin (Fig. 1B); however, it was critically dependent on collagen activation of platelets as thrombus formation failed to develop using platelets deficient in the major collagen receptor GPVI/FcR -chain (FcR / mice) (data not shown). PubMed:19276082
Platelet thrombus formation in the ex vivo model occurred in the presence of hirudin (Fig. 1B); however, it was critically dependent on collagen activation of platelets as thrombus formation failed to develop using platelets deficient in the major collagen receptor GPVI/FcR -chain (FcR / mice) (data not shown). PubMed:19276082
Pretreating anticoagulated whole blood with tricarbonyldichlororuthenium(II) dimer, a CO donor, significantly reduced collagen exposure (Fig. 5A) and thrombus formation (Fig. 5B) induced by FeCl3. PubMed:19276082
Pretreating anticoagulated whole blood with tricarbonyldichlororuthenium(II) dimer, a CO donor, significantly reduced collagen exposure (Fig. 5A) and thrombus formation (Fig. 5B) induced by FeCl3. PubMed:19276082
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.