0000000000430665

AUTHOR

Nigel Mackman

showing 2 related works from this author

Atherothrombosis and Thromboembolism: Position Paper from the Second Maastricht Consensus Conference on Thrombosis

2018

AbstractAtherothrombosis is a leading cause of cardiovascular mortality and long-term morbidity. Platelets and coagulation proteases, interacting with circulating cells and in different vascular beds, modify several complex pathologies including atherosclerosis. In the second Maastricht Consensus Conference on Thrombosis, this theme was addressed by diverse scientists from bench to bedside. All presentations were discussed with audience members and the results of these discussions were incorporated in the final document that presents a state-of-the-art reflection of expert opinions and consensus recommendations regarding the following five topics: 1. Risk factors, biomarkers and plaque inst…

0301 basic medicinemedicine.medical_specialtyanticoagulantsADJUST ANTIPLATELET THERAPYPERCUTANEOUS CORONARY INTERVENTION030204 cardiovascular system & hematologyarterial thrombosisArticleantiplatelet therapyACTIVATED PROTEIN-CRED-BLOOD-CELLS03 medical and health sciences0302 clinical medicineVITAMIN-K ANTAGONISTSInternal medicineatherothrombosisIschaemic strokeNONVALVULAR ATRIAL-FIBRILLATIONmedicinePlateletatrial fibrillationACUTE ISCHEMIC-STROKEcoagulationATOMIC-FORCE MICROSCOPYCardiovascular mortalityischaemic strokeAtomic force microscopybusiness.industryConsensus conferenceHematologymedicine.diseaseThrombosis030104 developmental biologymyocardial infarctionCoagulationplateletsDIRECT ORAL ANTICOAGULANTSCardiologyPosition paperSYMPTOMATIC VENOUS THROMBOEMBOLISMatherosclerosisbusiness
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Plasma Kallikrein Contributes to Coagulation in the Absence of Factor XI by Activating Factor IX

2019

Objectives: FXIa (factor XIa) induces clot formation, and human congenital FXI deficiency protects against venous thromboembolism and stroke. In contrast, the role of FXI in hemostasis is rather small, especially compared with FIX deficiency. Little is known about the cause of the difference in phenotypes associated with FIX deficiency and FXI deficiency. We speculated that activation of FIX via the intrinsic coagulation is not solely dependent on FXI(a; activated FXI) and aimed at identifying an FXI-independent FIX activation pathway. Approach and Results: We observed that ellagic acid and long-chain polyphosphates activated the coagulation system in FXI-deficient plasma, as could be demo…

Malemedicine.medical_specialtyplasma kallikreinPREKALLIKREIN030204 cardiovascular system & hematologyPATHWAYMice03 medical and health sciencesTissue factor0302 clinical medicineThrombinInternal medicinemedicineAnimalsHEMOSTASIScoagulationBLOOD-COAGULATIONBlood CoagulationFactor XIFactor IXfactor IXPURIFICATIONbusiness.industryMOLECULAR-WEIGHT KININOGENThrombinPrekallikreinKallikreinfactor XIfactor XI deficiencyMice Inbred C57BLDEFICIENCYDisease Models AnimalTHROMBOSISEndocrinologyCoagulationTISSUE FACTOR030220 oncology & carcinogenesisHemostasisFemaleREDUCED INCIDENCECardiology and Cardiovascular Medicinebusinessmedicine.drug
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