0000000000164446

AUTHOR

Dermot Kenny

showing 2 related works from this author

Persistent endotheliopathy in the pathogenesis of long COVID syndrome

2021

Background Persistent symptoms including breathlessness, fatigue, and decreased exercise tolerance have been reported in patients after acute SARS-CoV-2 infection. The biological mechanisms underlying this “long COVID” syndrome remain unknown. However, autopsy studies have highlighted the key roles played by pulmonary endotheliopathy and microvascular immunothrombosis in acute COVID-19. Objectives To assess whether endothelial cell activation may be sustained in convalescent COVID-19 patients and contribute to long COVID pathogenesis. Patients and Methods Fifty patients were reviewed at a median of 68 days following SARS-CoV-2 infection. In addition to clinical workup, acute phase markers, …

medicine.medical_specialtyLong COVIDCoronavirus disease 2019 (COVID-19)business.industryBrief ReportSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2)Acute-phase proteinAutopsyHematologyconvalescent COVID‐19GastroenterologyEndothelial stem cellPathogenesisThrombinInternal medicinemedicineBrief ReportsbusinessEndothelial cell (EC) activationmedicine.drugDECREASED EXERCISE TOLERANCEJournal of Thrombosis and Haemostasis
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Conformation-specific blockade of the integrin GPIIb/IIIa: a novel antiplatelet strategy that selectively targets activated platelets.

2006

Platelet activation causes conformational changes of integrin GPIIb/IIIa (α IIb β 3 ), resulting in the exposure of its ligand-binding pocket. This provides the unique possibility to design agents that specifically block activated platelets only. We used phage display of single-chain antibody (scFv) libraries in combination with several rounds of depletion/selection to obtain human scFvs that bind specifically to the activated conformation of GPIIb/IIIa. Functional evaluation of these scFv clones revealed that fibrinogen binding to human platelets and platelet aggregation can be effectively inhibited by activation-specific scFvs. In contrast to clinically used GPIIb/IIIa blockers, which ar…

Blood PlateletsCarotid Artery DiseasesBleeding TimePhysiologyAmino Acid MotifsMolecular ConformationEptifibatidePlatelet Glycoprotein GPIIb-IIIa ComplexFerric CompoundsAntibodiesMiceChloridesFibrinolytic AgentsmedicineAbciximabAnimalsHumansPlateletPlatelet activationChemistryFibrinogen bindingFibrinogenThrombosisTirofibanPlatelet ActivationMolecular biologyComplementarity Determining RegionsMice Inbred C57BLTirofibanImmunologyEptifibatidePlatelet aggregation inhibitorTyrosineCardiology and Cardiovascular MedicineGlycoprotein IIb/IIIaPeptidesPlatelet Aggregation Inhibitorsmedicine.drugCirculation research
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