Search results for "Dot"

showing 10 items of 5147 documents

Dietary salt promotes ischemic brain injury and is associated with parenchymal migrasome formation

2018

Sodium chloride promotes vascular fibrosis, arterial hypertension, pro-inflammatory immune cell polarization and endothelial dysfunction, all of which might influence outcomes following stroke. But despite enormous translational relevance, the functional importance of sodium chloride in the pathophysiology of acute ischemic stroke is still unclear. In the current study, we show that high-salt diet leads to significantly worse functional outcomes, increased infarct volumes, and a loss of astrocytes and cortical neurons in acute ischemic stroke. While analyzing the underlying pathologic processes, we identified the migrasome as a novel, sodium chloride-driven pathomechanism in acute ischemic …

0301 basic medicineMalePathologyMacroglial CellsSodium ChlorideVascular MedicineBrain IschemiaMice0302 clinical medicineCytosolAnimal CellsMedicine and Health SciencesMedicineEndothelial dysfunctionStrokeNeuronsCerebral CortexCerebral IschemiaMultidisciplinaryQRPathophysiologyStrokeChemistryNeurologyPhysical SciencesImmunohistochemistryMedicineCellular Structures and OrganellesCellular TypesIntracellularResearch Articlemedicine.medical_specialtyScienceCerebrovascular DiseasesGlial Cells03 medical and health sciencesImmune systemIn vivoParenchymaAnimalscardiovascular diseasesVesiclesSodium Chloride DietaryMicroglial CellsNutritionIschemic StrokeOrganellesbusiness.industryChemical CompoundsBiology and Life SciencesCell Biologymedicine.diseaseDiet030104 developmental biologyCellular NeuroscienceAstrocytesBrain InjuriesSaltsbusiness030217 neurology & neurosurgeryNeurosciencePLoS ONE
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Endocannabinoid 2-arachidonoylglycerol is elevated in the coronary circulation during acute coronary syndrome

2019

Objectives The endocannabinoid system modulates coronary circulatory function and atherogenesis. The two major endocannabinoids (eCB), 2-arachidonoylglycerol (2-AG) and N-arachidonoylethanolamide (AEA), are increased in venous blood from patients with coronary artery disease (CAD). However, given their short half-life and their autocrine/paracrine mechanism of action, eCB levels in venous blood samples might not reflect arterial or coronary eCB concentrations. The aim of this cross-sectional study was to identify the local concentration profile of eCB and to detect whether and how this concentration profile changes in CAD and NSTEMI versus patients without CAD. Methods and results 83 patien…

0301 basic medicineMalePhysiologyMyocardial InfarctionCoronary Artery Disease030204 cardiovascular system & hematologyCoronary AngiographyVascular MedicineBiochemistryCoronary artery disease0302 clinical medicineMedicine and Health SciencesMedicineCoronary Heart DiseaseMyocardial infarctionNon-ST Elevated Myocardial InfarctionCoronary ArteriesAortaAged 80 and overMultidisciplinaryArachidonic AcidQREukaryotaNeurochemistryVenous bloodArteriesPlantsMiddle AgedLegumesLipidsCoronary VesselsBody Fluidsmedicine.anatomical_structureBloodCirculatory systemCardiologyMedicineArterial bloodEngineering and TechnologyFemaleAnatomyNeurochemicalsResearch ArticleBiotechnologyAcute coronary syndromemedicine.medical_specialtyCathetersScienceCardiologyBioengineeringArachidonic AcidsGlyceridesDiagnosis Differential03 medical and health sciencesCoronary circulationInternal medicineCoronary CirculationHumansAcute Coronary SyndromeAgedbusiness.industryMacrophagesOrganismsPeasBiology and Life Sciencesmedicine.diseaseCoronary arteries030104 developmental biologyCross-Sectional StudiesCardiovascular AnatomyBlood VesselsMedical Devices and EquipmentEndothelium VascularbusinessEndocannabinoidsNeurosciencePLoS ONE
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Functional role of endothelial CXCL16/CXCR6-platelet-leucocyte axis in angiotensin II-associated metabolic disorders.

2018

Aims Angiotensin-II (Ang-II) is the main effector peptide of the renin-angiotensin system (RAS) and promotes leucocyte adhesion to the stimulated endothelium. Because RAS activation and Ang-II signalling are implicated in metabolic syndrome (MS) and abdominal aortic aneurysm (AAA), we investigated the effect of Ang-II on CXCL16 arterial expression, the underlying mechanisms, and the functional role of the CXCL16/CXCR6 axis in these cardiometabolic disorders. Methods and results Results from in vitro chamber assays revealed that CXCL16 neutralization significantly inhibited mononuclear leucocyte adhesion to arterial but not to venous endothelial cells. Flow cytometry and immunofluorescence s…

0301 basic medicineMaleRHOAPhysiologyMice Knockout ApoE030204 cardiovascular system & hematology0302 clinical medicineLeukocytesReceptorCells CulturedMetabolic SyndromebiologyChemistryAngiotensin IIMiddle AgedAortic AneurysmVascular endothelial growth factor ALosartanmedicine.anatomical_structurecardiovascular systemFemaleCardiology and Cardiovascular Medicinemedicine.drugSignal TransductionAdultBlood Plateletsmedicine.medical_specialtyEndothelium03 medical and health sciencesPhysiology (medical)Internal medicinemedicineCell AdhesionAnimalsHumansPlatelet activationReceptors CXCR6Angiotensin II receptor type 1Endothelial CellsChemokine CXCL16Platelet ActivationAngiotensin IICoculture TechniquesMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinologyCase-Control Studiesbiology.proteinAngiotensin II Type 1 Receptor BlockersCardiovascular research
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Hepatitis E virus-induced primary cutaneous CD30(+) T cell lymphoproliferative disorder.

2017

International audience; BACKGROUND & AIM:Several types of unexplained extra-hepatic manifestations, including haematological disorders, have been reported in the context of hepatitis E virus (HEV) infection. However, the underlying mechanism(s) of these manifestations are unknown. We provide evidence that HEV has an extra-hepatic endothelial tropism that can engage cutaneous T cells towards clonality.METHODS:A patient with a CD30(+) cutaneous T cell lymphoproliferative disorder (T-LPD) and biopsy-proven chronic HEV infection received three rounds of oral ribavirin treatment, administered either without or with interferon, and eventually achieved a sustained virologic response (SVR). Patholo…

0301 basic medicineMaleSkin NeoplasmsLymphomaLymphomatoid papulosisT cellLymphoproliferative disordersKi-1 Antigen[SDV.CAN]Life Sciences [q-bio]/CancerExtra-hepatic manifestationNHL[ SDV.CAN ] Life Sciences [q-bio]/Cancer03 medical and health sciencesInterleukin 210302 clinical medicineEndothelial cellInterferonHepatitis E virusMedicineHumansCD30-positive cutaneous T cell lymphoproliferative disorderTropismHepatologybusiness.industryvirus diseasesMiddle Agedmedicine.diseaseVirologyHepatitis ELymphoma T-Cell CutaneousViral Tropism030104 developmental biologymedicine.anatomical_structureHEVImmunologyTissue tropism030211 gastroenterology & hepatologybusinessMemory T cellCD8medicine.drugJournal of hepatology
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Ticagrelor, but not clopidogrel, reduces arterial thrombosis via endothelial tissue factor suppression

2017

The P2Y12 antagonist ticagrelor reduces mortality in patients with acute coronary syndrome (ACS), compared with clopidogrel, and the mechanisms underlying this effect are not clearly understood. Arterial thrombosis is the key event in ACS; however, direct vascular effects of either ticagrelor or clopidogrel with focus on arterial thrombosis and its key trigger tissue factor have not been previously investigated.Methods and results: Human aortic endothelial cells were treated with ticagrelor or clopidogrel active metabolite (CAM) and stimulated with tumour necrosis factor-alpha (TNF-α); effects on procoagulant tissue factor (TF) expression and activity, its counter-player TF pathway inhibito…

0301 basic medicineMaleTicagrelorAdenosineTime FactorsPhysiology030204 cardiovascular system & hematology2737 Physiology (medical)0302 clinical medicineP2Y12AntithromboticCells CulturedClopidogrelReceptors Purinergic P2Y123. Good healthClopidogrelmedicine.anatomical_structureCoagulation10209 Clinic for CardiologyCardiologyCardiology and Cardiovascular MedicineTicagrelormedicine.drugBlood PlateletsAcute coronary syndromemedicine.medical_specialtyProteasome Endopeptidase ComplexTiclopidineEndotheliumDown-Regulation610 Medicine & health2705 Cardiology and Cardiovascular MedicineThromboplastinEquilibrative Nucleoside Transporter 103 medical and health sciencesTissue factorFibrinolytic AgentsPhysiology (medical)Internal medicinemedicineAnimalsHumanscardiovascular diseasesBlood Coagulationbusiness.industryTumor Necrosis Factor-alphaEndothelial CellsThrombosis1314 Physiologymedicine.diseaseMice Inbred C57BLDisease Models Animal030104 developmental biologyProteolysisPurinergic P2Y Receptor AntagonistsbusinessCarotid Artery InjuriesPlatelet Aggregation Inhibitors
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VEGF-B gene therapy inhibits doxorubicin-induced cardiotoxicity by endothelial protection

2016

Congestive heart failure is one of the leading causes of disability in long-term survivors of cancer. The anthracycline antibiotic doxorubicin (DOX) is used to treat a variety of cancers, but its utility is limited by its cumulative cardiotoxicity. As advances in cancer treatment have decreased cancer mortality, DOX-induced cardiomyopathy has become an increasing problem. However, the current means to alleviate the cardiotoxicity of DOX are limited. We considered that vascular endothelial growth factor-B (VEGF-B), which promotes coronary arteriogenesis, physiological cardiac hypertrophy, and ischemia resistance, could be an interesting candidate for prevention of DOX-induced cardiotoxicity …

0301 basic medicineMaleVEGFBVascular Endothelial Growth Factor BAnthracyclineAdipose Tissue WhiteCardiomyopathyheart failureApoptosisheart030204 cardiovascular system & hematologyPharmacologyta3111Mitochondria Heart03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorNeoplasmsmedicinepolycyclic compoundscancerAnimalsDoxorubicinTube formationCardiotoxicityMultidisciplinaryAntibiotics Antineoplasticbusiness.industryta1184MyocardiumEndothelial CellsGenetic TherapyBiological Sciencesmedicine.diseaseCardiotoxicity3. Good healthVascular endothelial growth factorMice Inbred C57BL030104 developmental biologychemistryLiverDoxorubicinHeart failureendothelial cellArteriogenesisbusinessmedicine.drugDNA Damage
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Biomarkers for vascular ageing in aorta tissues and blood samples.

2019

Abstract Objectives Functional and quantitative alterations and senescence of circulating and expanded endothelial progenitor cells (EPC), as well as systemic and tissue modifications of angiogenetic and inflammatory molecules, were evaluated for predicting age-related vessel wall remodeling, correlating them to intima media thickness (IMT) in the common carotid artery (CCA), a biomarker of early cardiovascular disease and aortic root dilation. Populations and methods A homogenous Caucasian population was included in the study, constituted by 160 healthy subjects (80 old subjects, mean age 72 ± 6.4, range 66–83 years; and 80 younger blood donors, mean age 26.2 ± 3.4, range 21–33 years), and…

0301 basic medicineMaleVascular Endothelial Growth Factor AAgingPhysiologySystemic inflammationBiochemistryCarotid Intima-Media Thickness0302 clinical medicineEndocrinologySA-β-Gal activityp21 and p16 genesMedicineTP53Receptor Notch1AortaEndothelial Progenitor CellsAged 80 and overeducation.field_of_studyChemotaxisInflammatory cytokinesmedicine.anatomical_structurecardiovascular systemBiomarker (medicine)Femalemedicine.symptomTP53 p21 and p16 genesSenescenceAdultEndotheliumInflammatory cytokineNotch and TLR4Carotid Artery CommonPopulationProinflammatory cytokine03 medical and health sciencesYoung AdultTP53 p21 and p16 genemedicine.arteryGeneticsHumansEPC cell populationeducationMolecular BiologyEPC cell populationsAgedAortabusiness.industryEndothelium age-related impairmentCell BiologyChemokine CXCL12Toll-Like Receptor 4EPC cell populations; Endothelium age-related impairment; Inflammatory cytokines; Notch and TLR4; SA-β-Gal activity; TP53 p21 and p16 genesSettore MED/23030104 developmental biologyIntima-media thicknessbusiness030217 neurology & neurosurgeryBiomarkersExperimental gerontology
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Uric acid treatment after stroke modulates the Krüppel-like factor 2-VEGF-A axis to protect brain endothelial cell functions: Impact of hypertension

2019

Uric acid (UA) is a promising protective treatment in ischaemic stroke, but the precise molecular targets underlying its in vivo beneficial actions remain unclear. High concentrations of UA inhibit angiogenesis of cultured endothelial cells via Krüppel-like factor 2 (KLF)-induced downregulation of vascular endothelial growth factor (VEGF), a pro-angiogenic mediator that is able to increase blood–brain barrier (BBB) permeability in acute stroke. Here, we investigated whether UA treatment after ischaemic stroke protects brain endothelial cell functions and modulates the KLF2-VEGF-A axis. Transient intraluminal middle cerebral artery (MCA) occlusion/reperfusion was induced in adult male sponta…

0301 basic medicineMaleVascular Endothelial Growth Factor AVascular endothelial growth factor-AAngiogenesisBiochemistryRats Inbred WKYAntioxidantschemistry.chemical_compound0302 clinical medicineRats Inbred SHRIschaemic strokeEvans BlueBlood-brain barrierBrainKrüppel-like factor 2Vascular endothelial growth factorEndothelial stem cellStrokeVascular endothelial growth factor Amedicine.anatomical_structureNeuroprotective AgentsTreatment OutcomeBlood-Brain Barrier030220 oncology & carcinogenesisHypertensioncardiovascular systemmedicine.symptommedicine.medical_specialtyKruppel-Like Transcription FactorsBrain damageBlood–brain barrierNeuroprotectionCell Line03 medical and health sciencesDouble-Blind MethodInternal medicinemedicineAnimalsHumanscardiovascular diseasesPharmacologybusiness.industryRatsUric Acid030104 developmental biologyEndocrinologychemistryEndothelium VascularAngiogenesisbusinessBiomarkers
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Stenosis coexists with compromised α1-adrenergic contractions in the ascending aorta of a mouse model of Williams-Beuren syndrome

2020

Williams-Beuren syndrome (WBS) is a rare disorder caused by a heterozygous deletion of 26-28 contiguous genes that affects the brain and cardiovascular system. Here, we investigated whether WBS affects aortic structure and function in the complete deletion (CD) mouse model harbouring the most common deletion found in WBS patients. Thoracic aortas from 3-4 months-old male CD mice and wild-type littermates were mounted in wire myographs or were processed for histomorphometrical analysis. Nitric oxide synthase (NOS) isoforms and oxidative stress levels were assessed. Ascending aortas from young adult CD mice showed moderate (50%) luminal stenosis, whereas endothelial function and oxidative str…

0301 basic medicineMaleWilliams SyndromeThromboxaneAdrenergiclcsh:MedicineAorta ThoracicNitric Oxide Synthase Type I030204 cardiovascular system & hematologymedicine.disease_causeAortic diseasesPhenylephrine0302 clinical medicineEthidiumMalalties hereditàrieslcsh:ScienceStenosisMultidisciplinarybiologyAnimal models in researchNitric oxide synthaseAortic Stenosis SupravalvularCardiovascular diseasesmedicine.drugGenetic diseasesmedicine.medical_specialtyNitric OxideArticle03 medical and health sciencesInternal medicinemedicine.arteryReceptors Adrenergic alpha-1Ascending aortamedicineAnimalsEstenosiPhenylephrinebusiness.industryMalalties cardiovascularslcsh:Rmedicine.diseaseValvular diseaseMice Mutant StrainsBlockadeElastinStenosisDisease Models AnimalOxidative Stress030104 developmental biologyEndocrinologybiology.proteinlcsh:QEndothelium VascularModels animals en la investigacióbusinessOxidative stressScientific Reports
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Exposure to perfluoroalkyl substances and thyroid function in pregnant women and children: A systematic review of epidemiologic studies

2017

Introduction: Thyroid hormones (THs) are especially important for brain maturation and development during the fetal period and childhood. Several epidemiological studies have assessed the possible association between exposure to perfluoroalkyl substances (PFAS) and thyroid outcomes during the early stages of life. We aimed to review this evidence. Methods: We conducted a systematic review in compliance with the PRISMA Statement (search conducted in PubMed and Embase, as well as in the citations of the selected articles). We chose studies if they dealt with thyroid-stimulating hormone (TSH), triiodothyronine (T3), thyroxin (T4), or thyroid dysfunctions, and perfluorohexane sulfonate (PFHxS),…

0301 basic medicineMalemedicine.medical_specialtyAdolescentPrenatal and infant exposureThyroid GlandPhysiology010501 environmental sciences01 natural sciencesPerfluorononanoic acidToxicology03 medical and health scienceschemistry.chemical_compoundEnvironmental Science(all)PregnancyEpidemiologymedicineHumansPerfluorononanoic acid (PFNA)Childlcsh:Environmental sciences0105 earth and related environmental sciencesGeneral Environmental Sciencelcsh:GE1-350ThyroidFluorocarbonsTriiodothyroninebusiness.industryThyroidEnvironmental ExposurePerfluorohexane sulfonate (PFHxS)3. Good healthPerfluorooctane030104 developmental biologymedicine.anatomical_structurechemistryAlkanesulfonic AcidsEnvironmental PollutantsFemalePerfluorooctane sulfonate (PFOS)Thyroid functionCaprylatesPerfluorooctanoic acid (PFOA)businessHormoneCohort studyEnvironment International
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