Search results for "Platelet"

showing 10 items of 786 documents

Magnetic Resonance Imaging and Ultrasound Evaluation after Breast Autologous Fat Grafting Combined with Platelet-Rich Plasma

2014

Text miningmedicine.diagnostic_testbusiness.industryPlatelet-rich plasmaUltrasoundSettore MED/19 - Chirurgia PlasticaMedicineSurgeryMagnetic resonance imagingAutologous fat graftingMagnetic resonance imaging Breast Autologous Fat GraftingbusinessBiomedical engineering
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LAAE-14, a new in vitro inhibitor of intracellular calcium mobilization, modulates acute and chronic inflammation.

2003

Abstract A new lipidic acid-amido ether derivative (LAAE-14) able to reduce dose-dependently the calcium increases mediated either by calcium ionophore ionomycin, by the endoplasmic reticular Ca 2+ -ATPase inhibitor thapsigargin, or by the chemotactic tripeptide N -formyl- l -methionyl- l -leucyl- l -phenylalanine (fMLP), in human neutrophils as well as in murine peritoneal macrophages, but not ATP, has been evaluated as a potential anti-inflammatory drug. This compound attenuated leukocyte activation by means of its inhibitory effect on the respiratory burst elicited in both types of cells by 12- O -tetradecanoyl phorbol 13-acetate, by inhibition of the degranulation process induced by cyt…

ThapsigarginNeutrophilschemistry.chemical_elementCalciumPharmacologyCarrageenanBiochemistryLeukotriene B4Calcium in biologyDinoprostonechemistry.chemical_compoundMiceCell MovementAnimalsEdemaHumansCytochalasin BNitritesPharmacologyInflammationPlatelet-activating factorPancreatic ElastaseTumor Necrosis Factor-alphaZymosanArthritis ExperimentalRatsDisease Models AnimalchemistryBiochemistryIonomycinAcute DiseaseChronic DiseaseLuminescent MeasurementsPhorbolMacrophages PeritonealTumor necrosis factor alphaCalciumBiochemical pharmacology
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A bacterial metabolite, trimethylamine N-oxide, disrupts the hemostasis balance in human primary endothelial cells but no coagulopathy in mice

2019

: The gut microbial metabolite, trimethylamine N-oxide (TMAO), was previously reported to induce platelet hypersensitivity, which leads to thrombotic risk. However, the molecular mechanism underlying the effects of TMAO on endothelial cells (EC), which is the primary vessel wall contact with the lumen, remains unclear. Here, we investigated the impact of TMAO on procoagulant activity (PCA) in EC and mice, for a possible link between microbiota and coagulation. To test the PCA of TMAO in EC, we performed one-stage clotting assays and converted into PCA. Antitissue factor (TF) antibody was used to test the TF role in PCA. Quantitative PCR was performed to measure the TF, thrombomodulin, IL-6,…

ThrombomodulinMetaboliteTrimethylamine N-oxide030204 cardiovascular system & hematologyPharmacologyThrombomodulinMethylaminesMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAnimalsHumansPlateletProtein kinase ABlood CoagulationCells CulturedHemostasisMessenger RNANF-kappa BEndothelial CellsHematologyGeneral MedicineOxidantsReal-time polymerase chain reactionchemistryHemostasis030215 immunologyBlood Coagulation & Fibrinolysis
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A critical evaluation of caplacizumab for the treatment of acquired thrombotic thrombocytopenic purpura

2020

Introduction: Acquired thrombotic thrombocytopenic purpura (aTTP) is a thrombotic microangiopathy caused by inhibitory autoantibodies against ADAMTS13 protein. Until recently, the combination of plasma exchange (PEX) and immunosuppression has been the standard front-line treatment in this disorder. However, aTTP-related mortality, refractoriness, and relapse are still a matter of concern. Areas covered: The better understanding of the pathophysiological mechanisms of aTTP has allowed substantial improvements in the diagnosis and treatment of this disease. Recently, the novel anti-VWF nanobody caplacizumab has been approved for acute episodes of aTTP. Caplacizumab is capable to block the adh…

Thrombotic microangiopathyExacerbationvirusesmedicine.medical_treatmentADAMTS13 ProteinDiseaseBioinformaticsAutoantigens03 medical and health sciencesPlatelet Adhesiveness0302 clinical medicineFibrinolytic AgentsProtein DomainsCrotalid Venomsvon Willebrand FactormedicineHumansImmunologic FactorsMulticenter Studies as TopicLectins C-TypeMolecular Targeted TherapyDrug ApprovalClinical Trials as TopicAcquired Thrombotic Thrombocytopenic PurpuraPlasma ExchangePurpura Thrombotic Thrombocytopenicbusiness.industryStandard treatmentfungiImmunosuppressionDrugs InvestigationalHematologyAptamers NucleotideSingle-Domain Antibodiesbiochemical phenomena metabolism and nutritionmedicine.diseaseCombined Modality TherapyRecombinant ProteinsADAMTS13AcetylcysteineTreatment Outcome030220 oncology & carcinogenesisDrug Therapy CombinationCaplacizumabbusinessImmunosuppressive Agents030215 immunologyExpert Review of Hematology
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COVID-19 as a Potential Trigger for Immune Thrombotic Thrombocytopenic Purpura and Reason for an Unusual Treatment: A Case Report

2021

AbstractImmune thrombotic thrombocytopenic purpura (iTTP) is a rare autoimmune disorder characterized by severely reduced activity of the von Willebrand factor (VWF)-cleaving protease ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) due to autoantibodies. This leads to the development of pathogenic multimers of VWF, causing a thrombotic microangiopathy with decreased number of platelets, hemolysis, and life-threatening tissue ischemia of mostly brain, heart, and kidneys. Standard treatment of iTTP involves daily plasma exchange to remove ultra large multimers of VWF, inhibitors, substituting ADAMTS13, and the accompaniment of an immunosuppressive …

Thrombotic microangiopathybiologybusiness.industryThrombotic thrombocytopenic purpuraAutoantibodyHematology030204 cardiovascular system & hematologymedicine.diseaseADAMTS1303 medical and health sciences0302 clinical medicineVon Willebrand factorhemic and lymphatic diseases030220 oncology & carcinogenesisImmunologybiology.proteinmedicineRituximabPlateletCaplacizumabbusinessmedicine.drugHämostaseologie
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Cardiovascular effects of air pollution

2017

Air pollution is composed of particulate matter (PM) and gaseous pollutants, such as nitrogen dioxide and ozone. PM is classified according to size into coarse particles (PM 10), fine particles (PM 2.5) and ultrafine particles. We aim to provide an original review of the scientific evidence from epidemiological and experimental studies examining the cardiovascular effects of outdoor air pollution. Pooled epidemiological studies reported that a 10 μg/m 3 increase in long-term exposure to PM 2.5 was associated with an 11% increase in cardiovascular mortality. Increased cardiovascular mortality was also related to long-term and short-term exposure to nitrogen dioxide. Exposure to air pollution…

Time FactorsCardiovascular mortalityOzoneair pollutionAir pollution030204 cardiovascular system & hematology010501 environmental sciencesmedicine.disease_causeCardiovascular SystemRisk Assessment01 natural sciencesArticleToxicology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRisk FactorsEnvironmental healthUltrafine particleAnimalsHumansoxidative stressMedicineNitrogen dioxidePlatelet activationBlood CoagulationAir quality index0105 earth and related environmental sciencesparticulate matterPollutantAir Pollutantsbusiness.industryEnvironmental ExposureGeneral MedicineParticulatesPrognosisPlaque Atheroscleroticmyocardial infarctionchemistryCardiovascular DiseasesReactive Oxygen SpeciesCardiology and Cardiovascular MedicinebusinessArchives of Cardiovascular Diseases
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Blood Component Therapy and Coagulopathy in Trauma: A Systematic Review of the Literature from the Trauma Update Group

2016

Background Traumatic coagulopathy is thought to increase mortality and its treatment to reduce preventable deaths. However, there is still uncertainty in this field, and available literature results may have been overestimated. Methods We searched the MEDLINE database using the PubMed platform. We formulated four queries investigating the prognostic weight of traumatic coagulopathy defined according to conventional laboratory testing, and the effectiveness in reducing mortality of three different treatments aimed at contrasting coagulopathy (high fresh frozen plasma/packed red blood cells ratios, fibrinogen, and tranexamic acid administration). Randomized controlled trials were selected alo…

Tranexamic acidPhysiologyGlycobiologylcsh:MedicineCardiovascular MedicinePathology and Laboratory MedicineBiochemistryVascular Medicinelaw.inventionDatabase and Informatics MethodsFresh frozen plasma0302 clinical medicineRandomized controlled trialCoagulopathyAnimal CellslawAntifibrinolytic agentFibrinogen; Fresh frozen plasma; Tranexamic acid; Antifibrinolytic agent.Medicine and Health Sciences030212 general & internal medicineDatabase Searchinglcsh:ScienceMultidisciplinaryPlasma ExchangeHematologyBlood Coagulation DisordersClinical Laboratory SciencesAntifibrinolytic AgentsBody FluidsBloodtraumaTranexamic AcidCardiovascular DiseasesResearch DesignMeta-analysisObservational StudiesFresh frozen plasmaAnatomyCellular TypesResearch ArticlePlateletsmedicine.medical_specialtyDeath RatesHemorrhageBlood Component TransfusionResearch and Analysis MethodsExternal validity03 medical and health sciencesSigns and SymptomsPopulation MetricsDiagnostic MedicinemedicineCoagulopathyHumansBlood TransfusionMortalityIntensive care medicineBlood CoagulationAntifibrinolytic Agents; Blood Coagulation Disorders; Humans; Mortality; Plasma Exchange; Tranexamic Acid; Wounds and Injuries; Blood Component Transfusion; Biochemistry Genetics and Molecular Biology (all); Agricultural and Biological Sciences (all)DemographyGlycoproteinsBlood CellsAntifibrinolytic agentPopulation BiologyCoagulation DisordersTransfusion Medicinebusiness.industrylcsh:RBleedingAntifibrinolytic agent.Biology and Life SciencesFibrinogen030208 emergency & critical care medicineCell Biologymedicine.diseaseSurgeryPeople and PlacesWounds and Injurieslcsh:QObservational studyPacked red blood cellsbusinessPLOS ONE
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Urokinase activates macrophage PON2 gene transcription via the PI3K/ROS/MEK/SREBP-2 signalling cascade mediated by the PDGFR-β

2009

Aims We have recently shown that urokinase plasminogen activator (uPA) increases oxidative stress (OS), cholesterol biosynthesis, and paraoxonase 2 (PON2) expression in macrophages via binding to its receptor, the uPAR. Since PON2 is regulated by both OS and cholesterol content, we hypothesized that uPA elicits a cascade of signal transduction events shared by NADPH oxidase and cholesterol biosynthesis that culminates in PON2 gene expression. Here, we investigated the signalling pathway that leads to the expression of PON2 in macrophages in response to uPA. Methods and results The increase in macrophage PON2 mRNA levels in response to uPA was shown to depend on PON2 gene promoter activation…

Transcription GeneticPhysiologyReceptor Platelet-Derived Growth Factor betaPhosphatidylinositol 3-KinasesPhysiology (medical)Gene expressionHumansExtracellular Signal-Regulated MAP KinasesTranscription factorCells CulturedMitogen-Activated Protein Kinase KinasesRegulation of gene expressionNADPH oxidasebiologyAryldialkylphosphataseKinaseMacrophagesNADPH OxidasesUrokinase-Type Plasminogen ActivatorCell biologySterol regulatory element-binding proteinUrokinase receptorGene Expression RegulationBiochemistryTissue Plasminogen Activatorbiology.proteinSignal transductionReactive Oxygen SpeciesCardiology and Cardiovascular MedicineSignal TransductionSterol Regulatory Element Binding Protein 2Cardiovascular Research
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Cross-talk between Different Enhancer Elements during Mitogenic Induction of the Human Stromelysin-1 Gene

1996

Platelet-derived growth factor (PDGF) induces the expression of human stromelysin-1, a matrix metalloproteinase involved in tumor invasion and metastasis. Here it is shown that stromelysin-1 gene induction by PDGF depends on Ras and involves three previously identified promoter elements (the stromelysin-1 PDGF-responsive element (SPRE) site, the two head-to-head polyomavirus enhancer A-binding protein-3 (PEA3) sites, and the activator protein-1 (AP-1) binding site). During mitogenic induction, these responsive elements appear to be organized in two independent transcriptional units, SPRE-AP-1 and PEA3-AP-1, which result from specific element cross-talking. Interestingly, expression of a dom…

Transcription GeneticProto-Oncogene Proteins c-junMolecular Sequence DataProtein Serine-Threonine KinasesBiologyTransfectionBiochemistryStromelysin 1Proto-Oncogene Proteins p21(ras)MiceProto-Oncogene ProteinsAnimalsHumansBinding siteEnhancerMolecular BiologyTranscription factorGeneProtein Kinase CProtein kinase CPlatelet-Derived Growth FactorBase SequenceActivator (genetics)Metalloendopeptidases3T3 CellsCell BiologyMolecular biologyRecombinant ProteinsDNA-Binding ProteinsProto-Oncogene Proteins c-rafTranscription Factor AP-1Enhancer Elements GeneticEnzyme Inductionbiology.proteinMatrix Metalloproteinase 3MitogensPlatelet-derived growth factor receptorJournal of Biological Chemistry
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Response: platelet transcriptome and proteome—relation rather than correlation

2013

We have demonstrated by a detailed statistical analysis of proteome and transcriptome data of human platelets and human cell lines that protein and transcript abundance in platelets, if at all, are only weakly correlated.[1][1] This analysis appears to be in contradiction to previous claims made

TranscriptomeCorrelationImmunologyProteomeStatistical analysisPlateletCell BiologyHematologyHuman cellBiologyProteomicsBiochemistryCell biologyBlood
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