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Jaime Pereira

Researcher at Pontifical Catholic University of Chile

Publications -  114
Citations -  3206

Jaime Pereira is an academic researcher from Pontifical Catholic University of Chile. The author has contributed to research in topics: Platelet & Platelet activation. The author has an hindex of 29, co-authored 114 publications receiving 2954 citations. Previous affiliations of Jaime Pereira include The Catholic University of America & University of Chile.

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Human platelets synthesize and express functional tissue factor

TL;DR: Human platelets not only assemble the clotting reactions on their membrane, but also supply their own TF for thrombin generation in a timely and spatially circumscribed process, which simplify, unify, and provide a more coherent formulation of the current cell-based model of hemostasis.
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Inflammation, not hyperhomocysteinemia, is related to oxidative stress and hemostatic and endothelial dysfunction in uremia.

TL;DR: Systemic inflammation, which is closely associated with augmented oxidative stress, endothelial cell dysfunction and hemostatic activation, emerges as a major cardiovascular risk factor in CRF.
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Acute thrombocytopenia after treatment with tirofiban or eptifibatide is associated with antibodies specific for ligand-occupied GPIIb/IIIa.

TL;DR: The findings indicate that acute thrombocytopenia after the administration of tirofiban or eptifibatide can be caused by drug-dependent antibodies that are “naturally occurring” or are induced by prior exposure to drug.
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High prevalence of bleeders of unknown cause among patients with inherited mucocutaneous bleeding. A prospective study of 280 patients and 299 controls

TL;DR: The results support the proposal that low plasma VWF levels, but also platelet function defects, should be considered risk factors rather than unequivocal causes of hemorrhages.
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Circulating platelet-derived microparticles in systemic lupus erythematosus. Association with increased thrombin generation and procoagulant state.

TL;DR: The increased number of circulating platelet-derived microparticles and their association with high ETP and activation of the coagulation system suggest that thesemicroparticles play an important role in the pathogenesis of the prothrombotic state in SLE patients.