What is the clinical evidence from this study?

Study design: Other. Population: Platelet aggregation. Intervention: Thrombin binding to GPIbalpha. Primary outcome: Platelet aggregation and fibrin clot retraction.

January 1, 2003Thrombosis and Haemostasis

Thrombin binding to GPIbα induces platelet aggregation and fibrin clot retraction supported by resting αIIbβ3 interaction with polymerized fibrin

Q: What does this research mean for the field?

Thrombin binding to GPIbα induces fibrin binding to resting αIIbβ3, leading to fibrin-dependent platelet aggregation and clot retraction. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

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Key result

Thrombin binding to GPIbα induces fibrin-dependent platelet aggregation and clot retraction via resting αIIbβ3.

Population

Platelets desensitized for PAR-1 and PAR-4 thrombin receptors

Comparison

Thrombin binding to GPIbα vs Inhibition with monoclonal antibody VM16d…

Design

Preclinical

Authors

CDChristophe Dubois BSBeat Steiner NKNelly Kieffer

Discussion

Member takes

Overview

Should not yet alter antithrombotic practice; hypothesis-generating for PAR-independent thrombin signaling via GPIbα in human thrombosis.

Structured PICO

Population

Platelets desensitized for PAR-1 and PAR-4 thrombin receptors

Intervention

Thrombin binding to GPIbα

Comparator

Inhibition with monoclonal antibody VM16d, Mocarhagin, αIIbβ3 antagonists (RGDS, lamifiban), or GPRP-amide

Outcome

Platelet aggregation and clot retraction mechanismssurrogate

Demonstrates a novel PAR-independent mechanism of thrombin-induced platelet aggregation mediated by GPIbα and resting αIIbβ3 interaction with polymerized fibrin.

Cite This Study

Dubois et al. (2003) studied Platelet aggregation. Thrombin binding to GPIbalpha was evaluated on Platelet aggregation and fibrin clot retraction. Thrombin binding to GPIbalpha induces fibrin binding to resting alphaIIbbeta3, leading to fibrin-dependent platelet aggregation and clot retraction.

synapsesocial.com/papers/6aa52544c616a76b5feeb4e3 https://doi.org/10.1055/s-0037-1613473

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January 1, 2003Thrombosis and Haemostasis

Thrombin binding to GPIbα induces platelet aggregation and fibrin clot retraction supported by resting αIIbβ3 interaction with polymerized fibrin

View Full Paper

Ask AI

Bookmark

Key result

Thrombin binding to GPIbα induces fibrin-dependent platelet aggregation and clot retraction via resting αIIbβ3.

Population

Platelets desensitized for PAR-1 and PAR-4 thrombin receptors

Comparison

Thrombin binding to GPIbα vs Inhibition with monoclonal antibody VM16d…

Design

Preclinical

Authors

CDChristophe Dubois BSBeat Steiner NKNelly Kieffer

Discussion

Member takes

Overview

Should not yet alter antithrombotic practice; hypothesis-generating for PAR-independent thrombin signaling via GPIbα in human thrombosis.

Structured PICO

Population

Platelets desensitized for PAR-1 and PAR-4 thrombin receptors

Intervention

Thrombin binding to GPIbα

Comparator

Inhibition with monoclonal antibody VM16d, Mocarhagin, αIIbβ3 antagonists (RGDS, lamifiban), or GPRP-amide

Outcome

Platelet aggregation and clot retraction mechanismssurrogate

Demonstrates a novel PAR-independent mechanism of thrombin-induced platelet aggregation mediated by GPIbα and resting αIIbβ3 interaction with polymerized fibrin.

Cite This Study

synapsesocial.com/papers/6aa52544c616a76b5feeb4e3 https://doi.org/10.1055/s-0037-1613473

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

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