<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>6(2)</volume><submitter>Brouns SLN</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Low plasma levels of protein C or protein S are associated with venous thromboembolism rather than myocardial infarction. The high coagulant activity in patients with thrombophilia with a (familial) defect in protein C or S is explained by defective protein C activation, involving thrombomodulin and protein S. This causes increased plasmatic thrombin generation.&lt;h4>Objective&lt;/h4>Assess the role of platelets in the thrombus- and fibrin-forming potential in patients with familial protein C or protein S deficiency under high-shear flow conditions.&lt;h4>Patients/methods&lt;/h4>Whole blood from 23 patients and 15 control subjects was perfused over six glycoprotein VI-dependent microspot surfaces. By real-time multicolor microscopic imaging, kinetics of platelet thrombus and fibrin</pubmed_abstract><journal>Research and practice in thrombosis and haemostasis</journal><pagination>e12678</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8900581</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Protein C or Protein S deficiency associates with paradoxically impaired platelet-dependent thrombus and fibrin formation under flow.</pubmed_title><pmcid>PMC8900581</pmcid><pubmed_authors>van Oerle R</pubmed_authors><pubmed_authors>Perrella G</pubmed_authors><pubmed_authors>Kuijpers MJE</pubmed_authors><pubmed_authors>Spiezia L</pubmed_authors><pubmed_authors>van Geffen JP</pubmed_authors><pubmed_authors>Simioni P</pubmed_authors><pubmed_authors>Tullemans BME</pubmed_authors><pubmed_authors>Brouns SLN</pubmed_authors><pubmed_authors>Campello E</pubmed_authors><pubmed_authors>Spronk HMH</pubmed_authors><pubmed_authors>Bulato C</pubmed_authors><pubmed_authors>van der Meijden PEJ</pubmed_authors><pubmed_authors>Heemskerk JWM</pubmed_authors></additional><is_claimable>false</is_claimable><name>Protein C or Protein S deficiency associates with paradoxically impaired platelet-dependent thrombus and fibrin formation under flow.</name><description>&lt;h4>Background&lt;/h4>Low plasma levels of protein C or protein S are associated with venous thromboembolism rather than myocardial infarction. The high coagulant activity in patients with thrombophilia with a (familial) defect in protein C or S is explained by defective protein C activation, involving thrombomodulin and protein S. This causes increased plasmatic thrombin generation.&lt;h4>Objective&lt;/h4>Assess the role of platelets in the thrombus- and fibrin-forming potential in patients with familial protein C or protein S deficiency under high-shear flow conditions.&lt;h4>Patients/methods&lt;/h4>Whole blood from 23 patients and 15 control subjects was perfused over six glycoprotein VI-dependent microspot surfaces. By real-time multicolor microscopic imaging, kinetics of platelet thrombus and fibrin</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Feb</publication><modification>2025-04-04T14:50:38.458Z</modification><creation>2025-04-04T14:50:38.458Z</creation></dates><accession>S-EPMC8900581</accession><cross_references><pubmed>35284776</pubmed><doi>10.1002/rth2.12678</doi></cross_references></HashMap>