grant

Complement and thrombosis in HIT

Organization DUKE UNIVERSITYLocation DURHAM, UNITED STATESPosted 1 Jan 2025Deadline 30 Nov 2028
NIHUS FederalResearch GrantFY20265-HT5-Hydroxytryptamine5HT7S Gamma GlobulinAdhesionsAllergyAntibodiesAnticoagulant AgentsAnticoagulant DrugsAnticoagulantsAntigen-Antibody ComplexAntiheparin FactorAssayBindingBioassayBiologicalBiological AssayBiological MarkersBiologyBlood Coagulation Factor IIIBlood DiseasesBlood NeutrophilBlood Platelet Factor IVBlood PlateletsBlood Polymorphonuclear NeutrophilBlood leukocyteBlood monocyteBlood platelet factor 4CD142 AntigensCR3CR3 ReceptorCell BodyCell Communication and SignalingCell SignalingCell surfaceCellsCellular MatrixCellular injuryChemokine (C-X-C motif) Ligand 4Classical Complement PathwayClottingCoagulationCoagulation Factor IIICoagulation ProcessCoagulinCold Agglutinin DiseaseCold Hemagglutinin DiseaseComplementComplement 3 ReceptorComplement ActivationComplement InactivatorsComplement InhibitorsComplement ProteinsComplement ReceptorComplexCytoskeletal ModelingCytoskeletal OrganizationCytoskeletal Organization ProcessCytoskeletal ReorganizationCytoskeletal SystemCytoskeletonDataDiagnosisDiagnostic testsDiseaseDisorderDissociationECPCAEndothelial CellsEndotheliumEnteramineFactor 4Factor IIIFundingGasser's SyndromeGeneticGlomerular Procoagulant ActivityGlycosaminoglycansHematologic DiseasesHematological DiseaseHematological DisorderHemolytic-Uremic SyndromeHeparinHeparin BindingHeparin Neutralizing ProteinHeparinic AcidHippophaineIGIVIV ImmunoglobulinsIVIGIgGImmuneImmune ComplexImmune globulin IVImmunesImmunoglobulin GInjuryInstitutionIntegrin alpha-M beta-2Integrin alphaMbeta2InterventionIntracellular Communication and SignalingIntravenous AntibodiesIntravenous IGIntravenous Immune GlobulinIntravenous ImmunoglobulinsLaboratoriesLeukocytesLeukocytes Reticuloendothelial SystemLifeMac 1Mac-1 Adhesive ReceptorMac-1 AntigenMac-1 ReceptorMacrophage-1 AntigenMarrow NeutrophilMarrow leukocyteMarrow monocyteMarrow plateletMediatingMembraneMo1 Antigen ReceptorMo1 Glycoprotein ReceptorModelingMolecular InteractionMolecular WeightMucopolysaccharidesNeutrophilic GranulocyteNeutrophilic LeukocyteNon-lyticNonlyticPF4 GenePathogenesisPathogenicityPathologyPathway interactionsPatient outcomePatient-Centered OutcomesPatient-Focused OutcomesPhagocytosisPhasePlatelet Factor 4PlateletsPolymorphonuclear CellPolymorphonuclear LeukocytesPolymorphonuclear NeutrophilsPositionPositioning AttributePropertyProthrombinaseReceptor ProteinRecombinant Platelet Factor 4RiskRisk AssessmentRistocetin CofactorRistocetin-Willebrand FactorRoleSCYB4SerotoninSignal TransductionSignal Transduction SystemsSignalingSmall Inducible Cytokine B4Small Inducible Cytokine Subfamily B, Member 4TestingTherapeuticThrombocytesThromboplastinThrombosisTimeTissue FactorTissue Factor ProcoagulantTissue ThromboplastinTreatment EfficacyUpregulationUrothromboplastinWhite Blood CellsWhite Cellactivation productbio-markersbiologicbiologic markerbiological signal transductionbiomarkerblood disorderblood thinnercell damagecell injurycellular damagecellular targetingcold antibody hemolytic anemiacomplement pathwaycomplement pathway regulationcomplementationcytokinedamage to cellsdiagnostic assayendothelial cell procoagulant activitygamma-Thromboglobulinheparin boundheparin-induced thrombocytopeniaimprovedimproved outcomeinhibitorinjuredinjuriesinjury to cellsinsightintervention efficacyintracellular skeletonmembrane structuremonocyteneutrophilparoxysmal nocturnal hemoglobinuriapathwaypatient oriented outcomesplatelet factor IVpreventpreventingreceptorrelease factorresponsesocial roletargeted drug therapytargeted drug treatmentstargeted therapeutictargeted therapeutic agentstargeted therapytargeted treatmenttherapeutic efficacytherapy efficacythrombopoiesis inhibitorthromboticthrombotic diseasethrombotic disordervon Willebrand Factorvon Willebrand Proteinwhite blood cellwhite blood corpuscleαMβ2
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ABSTRACT
Heparin-induced thrombocytopenia (HIT) is a thrombotic disorder caused by ultra-large immune complexes

(ULICs) composed of IgG antibodies (Abs) to platelet factor 4 (PF4) and heparin (H). Even with prompt

recognition, discontinuation of heparin, and institution of alternative anticoagulants, thrombotic risk remains high

and persists for…

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Complement and thrombosis in HIT — DUKE UNIVERSITY | UNITED STATES | Jan 2025 | Dev Procure