Search results for "Plate"

showing 10 items of 1689 documents

Soluble Platelet Release Factors as Biomarkers for Cardiovascular Disease

2021

Platelets are the main players in thrombotic diseases, where activated platelets not only mediate thrombus formation but also are involved in multiple interactions with vascular cells, inflammatory components, and the coagulation system. Although in vitro reactivity of platelets provides information on the function of circulating platelets, it is not a full reflection of the in vivo activation state, which may be relevant for thrombotic risk assessment in various disease conditions. Therefore, studying release markers of activated platelets in plasma is of interest. While this type of study has been done for decades, there are several new discoveries that highlight the need for a critical a…

0301 basic medicineACUTE MYOCARDIAL-INFARCTIONVON-WILLEBRAND-FACTORDEEP VENOUS THROMBOSISvenous thromboembolismCD40 LIGANDContext (language use)ReviewDiseaseCardiovascular Medicinearterial thrombosis030204 cardiovascular system & hematologyBioinformatics03 medical and health sciences0302 clinical medicineVon Willebrand factorPERIPHERAL ARTERY-DISEASENONVALVULAR ATRIAL-FIBRILLATIONmedicineDiseases of the circulatory (Cardiovascular) systematrial fibrillationPlateletACUTE ISCHEMIC-STROKEMyocardial infarctionPlatelet activationThrombusthrombosisbiologybusiness.industryACUTE CORONARY SYNDROMESbiomarkersmedicine.diseaseThrombosisC-REACTIVE PROTEIN3. Good healthP-SELECTIN LEVELS030104 developmental biologyRC666-701plateletsbiology.proteinCardiology and Cardiovascular MedicinebusinessFrontiers in Cardiovascular Medicine
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Evaluation of treatment response to enzyme replacement therapy with Velaglucerase alfa in patients with Gaucher disease using whole-body magnetic res…

2015

Abstract Objective This was a retrospective data analysis to evaluate the treatment response to enzyme replacement therapy (ERT) with Velaglucerase alfa using whole-body magnetic resonance imaging (MRI). Materials and methods A baseline and follow-up MRI were performed on 18 Gaucher Type 1 patients at an interval of 11.6 months. The MRI score systems determined the Bone-Marrow-Burden (BMB) score, the Dusseldorf-Gaucher score (DGS), and the Vertebra-Disc-Ratio (VDR). The Severity Score Index Type 1 (GD-DS3) was also assessed. Results The baseline MRI medians were: BMB, 7.00; DGS, 3.00; and VDR: 1.70; while, the follow-up MRI medians were: BMB, 7.00; DGS, 3.00; and VDR: 1.73. The baseline GD-…

0301 basic medicineAdultMalemedicine.medical_specialtyWhole body imagingSeverity of Illness Index03 medical and health sciences0302 clinical medicineBone MarrowStatistical significanceSeverity of illnessmedicineHumansEnzyme Replacement TherapyWhole Body ImagingStage (cooking)Molecular BiologyAgedRetrospective StudiesGaucher Diseasemedicine.diagnostic_testbusiness.industryVelaglucerase alfaPlatelet CountMagnetic resonance imagingRetrospective cohort studyCell BiologyHematologyEnzyme replacement therapyMiddle AgedMagnetic Resonance ImagingRecombinant ProteinsSurgery030104 developmental biologyTreatment OutcomeMolecular MedicineGlucosylceramidaseFemaleRadiologybusiness030215 immunologymedicine.drugFollow-Up StudiesBlood cells, moleculesdiseases
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A novel microglial subset plays a key role in myelinogenesis in developing brain.

2017

Microglia are resident macrophages of the central nervous system that contribute to homeostasis and neuroinflammation. Although known to play an important role in brain development, their exact function has not been fully described. Here, we show that in contrast to healthy adult and inflammation-activated cells, neonatal microglia show a unique myelinogenic and neurogenic phenotype. A CD11c(+) microglial subset that predominates in primary myelinating areas of the developing brain expresses genes for neuronal and glial survival, migration, and differentiation. These cells are the major source of insulin-like growth factor 1, and its selective depletion from CD11c(+) microglia leads to impa…

0301 basic medicineAgingmedicine.medical_treatmentNews & ViewsInsulin-Like Growth Factor IMyelin SheathCell AggregationNeural PlateMicrogliaACTIVATED MICROGLIAGeneral NeuroscienceExperimental autoimmune encephalomyelitisNeurogenesisIGF1BrainGene Expression Regulation DevelopmentalADULT BRAINUp-RegulationALZHEIMERS-DISEASEmedicine.anatomical_structureEXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITISMyelinogenesisGROWTHFemaleMicrogliaCNSEncephalomyelitis Autoimmune ExperimentalNeurogenesisCentral nervous systemCD11cBiologyGeneral Biochemistry Genetics and Molecular BiologyDEPENDENT MANNER03 medical and health sciencesmedicinePOSTNATAL-DEVELOPMENTAnimalsMolecular BiologyNeuroinflammationGeneral Immunology and MicrobiologyCD11cGrowth factorGene Expression ProfilingCENTRAL-NERVOUS-SYSTEMmedicine.diseaseGALECTIN-1CD11c AntigenMice Inbred C57BL030104 developmental biologynervous systemAnimals NewbornImmunologymyelinogenesisNeuroscienceBiomarkersThe EMBO journal
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Platelet Pathogen Reduction Technologies Alter the MicroRNA Profile of Platelet-Derived Microparticles

2020

Despite improvements in donor screening and increasing efforts to avoid contamination and the spread of pathogens in clinical platelet concentrates (PCs), the risks of transfusion-transmitted infections remain important. Relying on an ultraviolet photo activation system, pathogen reduction technologies (PRTs), such as Intercept and Mirasol, utilize amotosalen, and riboflavin (vitamin B2), respectively, to mediate inactivation of pathogen nucleic acids. Although they are expected to increase the safety and prolong the shelf life of clinical PCs, these PRTs might affect the quality and function of platelets, as recently reported. Upon activation, platelets release microparticles (MPs), which …

0301 basic medicineAmotosalenmedicine.medical_specialtySmall RNAlcsh:Diseases of the circulatory (Cardiovascular) systemmirasolCardiovascular Medicine030204 cardiovascular system & hematology03 medical and health sciences0302 clinical medicineclinical platelet concentrateInternal medicinemicroRNAmedicinePlateletHematologiPathogenOriginal ResearchRegulation of gene expressionHematologymicroRNApathogen reductionChemistryclinical platelet concentrate; pathogen reduction; mirasol; intercept; extracellular vesicles; small RNA-sequencing; microRNAHematology3. Good healthCell biologysmall RNA-sequencing030104 developmental biologylcsh:RC666-701extracellular vesiclesCardiology and Cardiovascular MedicineFunction (biology)interceptFrontiers in Cardiovascular Medicine
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Proteases, Protease-Activated Receptors, and Atherosclerosis

2018

Coagulation activation by the TF (tissue factor) pathway plays pivotal roles in triggering platelets and precipitating acute coronary syndromes. Although dual antiplatelet therapy is effective in secondary cardiovascular prevention, combining platelet antagonism with low-dose aspirin and the oral coagulation FXa antagonist rivaroxaban has a synergistic clinical benefit over monotherapy in preventing the composite outcome of cardiovascular death, stroke, or myocardial infarction.1 It is, therefore, of considerable interest to understand the roles of coagulation proteases and their cell signaling effects in the development of atherosclerosis and vascular inflammation. Acute thrombosis in anim…

0301 basic medicineApolipoprotein EProteasesReceptors Proteinase-Activated030204 cardiovascular system & hematologyArticleMice03 medical and health sciencesTissue factor0302 clinical medicineThrombinEndopeptidasesAnimalsReceptor PAR-2MedicinePlateletbusiness.industryArteriosclerosisAtherosclerosismedicine.diseaseThrombosis030104 developmental biologyCoagulationCancer researchCardiology and Cardiovascular MedicinebusinessPeptide Hydrolasesmedicine.drugArteriosclerosis, Thrombosis, and Vascular Biology
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The Involvement of Toll-like Receptor-2 in Arterial Thrombus Formation.

2018

There is emerging evidence for the participation of toll-like receptor-2 (TLR2) expressed on platelets and endothelial cells in the setting of arterial thrombosis. In isolated human platelets, TLR2/1 activation was demonstrated to induce platelet activation, secretion, aggregation, adhesion to collagen coatings and the formation of platelet-leukocyte conjugates, whereas murine platelets were less sensitive to TLR2/1 stimulation. Also, endothelial cells can be activated by stimulation with TLR2 agonists, resulting in increased expression of adhesion molecules, synthesis of inflammatory mediators and Weibel-Palade body exocytosis. Endothelial TLR2 signalling promotes atherosclerotic lesion de…

0301 basic medicineBlood Platelets030204 cardiovascular system & hematology03 medical and health sciences0302 clinical medicineVon Willebrand factormedicineAnimalsHumansPlateletPlatelet activationInflammationToll-like receptorbiologyCell adhesion moleculeChemistryEndothelial CellsCarotid Artery ThrombosisThrombosisHematologyArteriesmedicine.diseasePlatelet ActivationThrombosisPlaque AtheroscleroticToll-Like Receptor 2TLR2030104 developmental biologyCancer researchbiology.proteinHamostaseologie
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CD36-fibrin interaction propagates FXI-dependent thrombin generation of human platelets.

2019

Thrombin converts fibrinogen to fibrin and activates blood and vascular cells in thrombo-inflammatory diseases. Platelets are amplifiers of thrombin formation when activated by leukocyte- and vascular cell-derived thrombin. CD36 on platelets acts as sensitizer for molecules with damage-associated molecular patterns, thereby increasing platelet reactivity. Here, we investigated the role of CD36 in thrombin-generation on human platelets, including selected patients with advanced chronic kidney disease (CKD). Platelets deficient in CD36 or blocked by anti-CD36 antibody FA6.152 showed impaired thrombin generation triggered by thrombin in calibrated automated thrombography. Using platelets with …

0301 basic medicineBlood PlateletsCD36 AntigensCD36InflammationFibrinogenBiochemistryFibrin03 medical and health sciences0302 clinical medicineThrombinBlocking antibodyGeneticsmedicineHumansPlateletRenal Insufficiency ChronicMolecular BiologyFactor XIFibrinbiologyChemistryCell adhesion moleculeThrombinPlatelet ActivationBlood Coagulation FactorsCell biology030104 developmental biologybiology.proteinmedicine.symptom030217 neurology & neurosurgerycirculatory and respiratory physiologyBiotechnologymedicine.drugFASEB journal : official publication of the Federation of American Societies for Experimental BiologyREFERENCES
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Abacavir induces platelet-endothelium interactions by interfering with purinergic signalling: A step from inflammation to thrombosis.

2017

The controversy connecting Abacavir (ABC) with cardiovascular disease has been fuelled by the lack of a credible mechanism of action. ABC shares structural similarities with endogenous purines, signalling molecules capable of triggering prothrombotic/proinflammatory programmes. Platelets are leading actors in the process of thrombosis. Our study addresses the effects of ABC on interactions between platelets and other vascular cells, while exploring the adhesion molecules implicated and the potential interference with the purinergic signalling pathway. The effects of ABC on platelet aggregation and platelet-endothelium interactions were evaluated, respectively, with an aggregometer and a flo…

0301 basic medicineBlood PlateletsEndotheliumPlatelet AggregationAnti-HIV AgentsInflammationPharmacologyBiologyProinflammatory cytokine03 medical and health sciences0302 clinical medicinePlatelet Adhesivenessplatelet-endothelium interactionsVirologymedicineHumansPlatelet030212 general & internal medicinePlatelet activationPharmacologyInflammationCell adhesion moleculePurinergic receptorDeoxyguanine NucleotidesThrombosisPurinergic signallingIntercellular Adhesion Molecule-1Platelet ActivationAbacavirNRTIsDideoxynucleosidesCell biologycardiovascular diseasesP-Selectin030104 developmental biologymedicine.anatomical_structureCardiovascular DiseasesPurinesEndothelium Vascularmedicine.symptomSignal TransductionAntiviral research
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Impaired Platelet Function in Sept8-Deficient Mice In Vitro.

2020

AbstractSeptins (Septs) are a widely expressed protein family of 13 mammalian members, recognized as a unique component of the cytoskeleton. In human platelets, we previously described that SEPT4 and SEPT8 are localized surrounding α-granules and move to the platelet surface after activation, indicating a possible role in platelet physiology. In this study, we investigated the impact of Sept8 on platelet function in vitro using Sept8-deficient mouse platelets. Deletion of Sept8 in mouse platelets caused a pronounced defect in activation of the fibrinogen receptor integrin αIIbβ3, α-granule exocytosis, and aggregation, especially in response to the glycoprotein VI agonist convulxin. In contr…

0301 basic medicineBlood PlateletsGenotypePlatelet AggregationFibrinogen receptorIntegrinPlatelet Glycoprotein GPIIb-IIIa Complex030204 cardiovascular system & hematologyFibrinogenCytoplasmic GranulesExocytosisExocytosis03 medical and health sciences0302 clinical medicineLysosomeCrotalid VenomsmedicineAnimalsPlateletLectins C-TypeLactadherinMice KnockoutbiologyChemistryThrombinFibrinogenConvulxinHematologyPlatelet ActivationCell biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structurePhenotypebiology.proteinFemaleLysosomesSeptinsmedicine.drugThrombosis and haemostasis
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Temporal quantitative phosphoproteomics of ADP stimulation reveals novel central nodes in platelet activation and inhibition

2017

Adenosine diphosphate (ADP) enhances platelet activation by virtually any other stimulant to complete aggregation. It binds specifically to the G-protein-coupled membrane receptors P2Y1 and P2Y12, stimulating intracellular signaling cascades, leading to integrin aIIbb3 activation, a process antagonized by endothelial prostacyclin. P2Y12 inhibitors are among the most successful antiplatelet drugs, however, show remarkable variability in efficacy. We reasoned whether a more detailed molecular understanding of ADP-induced protein phosphorylation could identify (1) critical hubs in platelet signaling toward aggregation and (2) novel molecular targets for antiplatelet treatment strategies. We ap…

0301 basic medicineBlood PlateletsPHOSPHATASEImmunologyBlotting WesternUBIQUITINATIONBINDING PROTEIN STXBP5Biochemistry03 medical and health scienceschemistry.chemical_compoundGTP-binding protein regulatorsP2Y12HumansProtein phosphorylationPlatelet activationIloprostPHOSPHORYLATIONCOMBINATIONChemistryPhosphoproteomicsPATHWAYSCell BiologyHematologyPlatelet ActivationSIGNALING REVEALSCell biologyAdenosine DiphosphateAdenosine diphosphate030104 developmental biologyCLOPIDOGRELPhosphorylationPROTEOMICSSECRETIONSignal transductionPlatelet Aggregation InhibitorsSignal TransductionBlood
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