Search results for "Helium"

showing 10 items of 1689 documents

Plasmodium falciparumMalaria: Reduction of Endothelial Cell Apoptosis In Vitro

2005

ABSTRACTOrgan failure inPlasmodium falciparummalaria is associated with neutrophil activation and endothelial damage. This study investigates whether neutrophil-induced endothelial damage involves apoptosis and whether it can be prevented by neutralization of neutrophil secretory products. Endothelial cells from human umbilical veins were coincubated with neutrophils from healthy donors and with sera from eight patients withP. falciparummalaria, three patients withP. vivaxmalaria, and three healthy controls. Endothelial apoptosis was demonstrated by terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) and annexin V staining. The rate of apoptosis of cells was …

Umbilical VeinsProgrammed cell deathEndotheliumNeutrophilsPlasmodium falciparumImmunologyApoptosisBiologyMicrobiologyAntioxidantsAnnexinparasitic diseasesmedicineAnimalsHumansProtease InhibitorsMalaria FalciparumCells CulturedTUNEL assayImmune SeraEndothelial CellsPlasmodium falciparummedicine.diseaseAscorbic acidbiology.organism_classificationEndothelial stem cellInfectious Diseasesmedicine.anatomical_structureImmunologyParasitologyEndothelium VascularFungal and Parasitic InfectionsMalariaInfection and Immunity
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Activation of protein kinase C alpha and/or epsilon enhances transcription of the human endothelial nitric oxide synthase gene.

1998

In primary human umbilical vein endothelial cells (HUVECs), incubation with phorbol-12-myristate-13-acetate (PMA) enhanced basal and bradykinin-stimulated nitric oxide production. In the HUVEC-derived cell line EA.hy 926, PMA and phorbol-12,13-dibutyrate stimulated endothelial nitric oxide synthase (NOS III) mRNA expression in a concentration- and time-dependent manner. Maximal mRNA expression (3.3-fold increase) was observed after 18 hr. NOS III protein and activity were increased to a similar extent. The specific protein kinase C (PKC) inhibitors bisindolylmaleimide I (1 microM), Gö 6976 [12-(2 cyanoethyl)-6,7,12, 13-tetrahydro-13-methyl-5-oxo-5H-indolo[2,3-a]pyrrolo-[3, 4-c]carbazole] (1…

Umbilical VeinsProtein Kinase C-alphaTime FactorsEndotheliumTranscription GeneticDown-RegulationProtein Kinase C-epsilonBiologyBradykininTransfectionNitric oxidechemistry.chemical_compoundEnzyme StabilitymedicineHumansRNA MessengerEnzyme InhibitorsProtein kinase APromoter Regions GeneticCyclic GMPProtein kinase CCells CulturedProtein Kinase CPharmacologyKinaseMethane sulfonateBiological TransportMolecular biologyUp-RegulationEnzyme ActivationIsoenzymesmedicine.anatomical_structureChelerythrinechemistryGene Expression RegulationCell cultureMolecular MedicineTetradecanoylphorbol AcetateEndothelium VascularNitric Oxide SynthaseMolecular pharmacology
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Indomethacin enhances endothelial NO release — evidence for a role of PGI2 in the autocrine control of calcium-dependent autacoid production

1998

Objective: We studied whether NO or prostacyclin (PGI2), which are continuously released by endothelial cells, have autocrine/paracrine effects on the calcium-dependent autacoid production by modulating the intracellular Ca2+ concentration ([Ca2+]i). Methods: Histamine(His)-induced [Ca2+]i increases (Fura 2-method) and NO-dependent cGMP increase were measured in human umbilical vein endothelial cells (HUVECs) before and after cyclooxygenase inhibition or application of cAMP- and cGMP-elevating drugs. Results: 0.3 μM His increased endothelial [Ca2+]i from 77±2 nM to 418±59 nM. The His-induced [Ca2+]i increases were significantly attenuated following treatment with PGI2 (by 23%) and forskolin…

Umbilical Veinsmedicine.medical_specialtyEndotheliumPhysiologyIndomethacinProstacyclinNitric OxideFeedbackchemistry.chemical_compoundPhysiology (medical)Internal medicineCyclic AMPmedicineHumansCyclooxygenase InhibitorsAutocrine signallingCyclic GMPCells CulturedForskolinbiologyColforsinEpoprostenolEndothelial stem cellAutocrine CommunicationEndocrinologymedicine.anatomical_structurechemistrycardiovascular systembiology.proteinCalciumEndothelium VascularCyclooxygenaseCardiology and Cardiovascular MedicineAutacoidHistamineHistaminemedicine.drugCardiovascular Research
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Phytoestrogens increase the capacity of serum to stimulate prostacyclin release in human endothelial cells

2003

Both the estrogen receptor (ER) alpha and beta isoforms are expressed in the endothelium. The ER beta has been assigned a crucial role in normal vascular wall function. Prostacyclin has been ascribed a beneficial effect on vessel wall physiology. Isoflavones bind with higher affinity to ER beta. We investigated the hypothesis that their administration to postmenopausal women can promote endothelial prostacyclin production.Twenty-five healthy postmenopausal women with mild climacteric symptoms received capsules containing 55 mg/day isoflavones derived from soy and red clover for 6 months. Cultured human umbilical vein endothelial cells (HUVECs) were exposed for 24 h to serum collected before…

Umbilical Veinsmedicine.medical_specialtyTime FactorsEndotheliumAdministration OralAlpha (ethology)Estrogen receptorPhytoestrogensProstacyclinDrug Administration ScheduleUmbilical veinchemistry.chemical_compoundInternal medicinemedicineHumansEstrogens Non-SteroidalEstrogen receptor betaPlant Extractsbusiness.industryObstetrics and GynecologyGeneral MedicineMiddle AgedIsoflavonesBlood Physiological PhenomenaEpoprostenolIsoflavonesPostmenopauseEndocrinologymedicine.anatomical_structurechemistryFemaleTrifoliumPhytoestrogensEndothelium VascularPlant PreparationsSoybeansbusinessPlatelet Aggregation Inhibitorsmedicine.drugActa Obstetricia et Gynecologica Scandinavica
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Isolation and molecular characterization of brain microvascular endothelial cells from human brain tumors.

2002

Brain tumor formation and growth is accompanied by the proliferation and infiltration of blood capillaries. The phenotypes of endothelial cells that make up capillaries are known to differ not only in the tissues in which endothelial cells are located but also as a result of the microenvironment to which they are exposed. For this reason, primary cultures of brain endothelial cells were isolated from human brain tumors removed by surgery and compared with cells from normal tissue. The primary confluent monolayers that grew out of isolated capillary fragments consisted of closely associated, elongated, fusiform-shaped cells. But brain tumor-derived endothelial cells in culture exhibited sign…

Vascular Cell Adhesion Molecule-1Cell SeparationBiologyBlood–brain barrierAntigenvon Willebrand FactormedicineTumor Cells CulturedHumansCell adhesionCell SizeFluorescent DyesTight junctionBrain NeoplasmsBrainMembrane ProteinsCell BiologyGeneral MedicineHuman brainCarbocyaninesmedicine.diseaseIntercellular Adhesion Molecule-1PhosphoproteinsCell biologyMicroscopy Electronmedicine.anatomical_structureCell cultureBlood-Brain BarrierZonula Occludens-1 ProteinEndothelium VascularStem cellPlant LectinsE-SelectinInfiltration (medical)Developmental BiologyIn vitro cellulardevelopmental biology. Animal
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Increased expression of ICAM-1, E-selectin, and VCAM-1 by cultured human endothelial cells upon exposure to haptens.

1992

Contact allergens induce several accessory signals which promote the activation of antigen-specific T cells. One of these signals is the increased expression of adhesion molecules on antigen-presenting cells and endothelial cells. Epicutaneous application of non-toxic doses of 2,4-dinitrofluorobenzene (DNFB) onto the skin of non-sensitized individuals elicited progressive staining for ICAM-1 on dermal microvascular endothelial cells. To elucidate the question of whether contact allergens can act directly on endothelial cells to elevate their expression of surface structures that bind leukocytes, confluent monolayers of human umbilical vein endothelial cells were incubated with the contact a…

Vascular Cell Adhesion Molecule-1StimulationDermatologyImmunofluorescenceBiochemistryUmbilical veinchemistry.chemical_compoundE-selectinmedicineHumansNorthern blotRNA MessengerVCAM-1Molecular BiologyCells CulturedICAM-1medicine.diagnostic_testbiologyCell adhesion moleculeHLA-DR AntigensIntercellular Adhesion Molecule-1Cell biologychemistrybiology.proteinEndothelium VascularE-SelectinCell Adhesion MoleculesHaptensExperimental dermatology
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Anticancer therapy-induced vascular toxicity: VEGF inhibition and beyond

2017

Cardiotoxicity induced by chemotherapeutic agents and radiotherapy is a growing problem. In recent years, an increasing number of new drugs with targeted action have been designed. These molecules, such as monoclonal antibodies and tyrosine kinase inhibitors, can cause different type of toxicities compared to traditional chemotherapy. However, they can also cause cardiac complications such as heart failure, arterial hypertension, QT interval prolongation and arrhythmias. Currently, a field of intense research is the vascular toxicity induced by new biologic drugs, particularly those which inhibit vascular endothelial growth factor (VEGF) and its receptor (VEGF-R) and other tyrosine kinases.…

Vascular Endothelial Growth Factor APathologymedicine.medical_specialtyHeart Diseasesmedicine.medical_treatmentVascular toxicity VEGF cardiotoxicity new target therapy chemotherapy radiotherapy cardio-oncologyAntineoplastic Agents030204 cardiovascular system & hematologyQT intervalCardiooncology03 medical and health scienceschemistry.chemical_compoundCardio-oncology; Cardiotoxicity; Chemotherapy; New target therapy; Radiotherapy; Vascular toxicity; VEGF; Medicine (all); Cardiology and Cardiovascular Medicine0302 clinical medicineVascularReceptorsmedicineAnimalsHumansChemotherapyEndotheliumNew target therapyChemotherapyCardiotoxicityRadiotherapybusiness.industryVascular Endothelial Growth FactorMedicine (all)Cardiooncology; Vascular toxicity; New target therapyCardio-oncology; Cardiotoxicity; Chemotherapy; New target therapy; Radiotherapy; Vascular toxicity; VEGF; Animals; Antineoplastic Agents; Cardiotoxicity; Endothelium Vascular; Heart Diseases; Humans; Reactive Oxygen Species; Receptors Vascular Endothelial Growth Factor; Vascular Endothelial Growth Factor Amedicine.diseaseVEGFCardiotoxicityVascular endothelial growth factorRadiation therapyCardio-oncologyVascular endothelial growth factor AReceptors Vascular Endothelial Growth Factorchemistry030220 oncology & carcinogenesisHeart failureCancer researchEndothelium VascularVascular toxicityReactive Oxygen SpeciesCardiology and Cardiovascular MedicinebusinessTyrosine kinaseInternational Journal of Cardiology
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The impact of the receptor binding profiles of the vascular endothelial growth factors on their angiogenic features

2013

Abstract Background Vascular endothelial growth factors (VEGFs) are potential therapeutic agents for treatment of ischemic diseases. Their angiogenic effects are mainly mediated through VEGF receptor 2 (VEGFR2). Methods Receptor binding, signaling, and biological efficacy of several VEGFR2 ligands were compared to determine their characteristics regarding angiogenic activity and vascular permeability. Results Tested VEGFR2 ligands induced receptor tyrosine phosphorylation with different efficacy depending on their binding affinities. However, the tyrosine phosphorylation pattern and the activation of the major downstream signaling pathways were comparable. The maximal angiogenic effect stim…

Vascular Endothelial Growth Factor ASwineAngiogenesisBlotting WesternBiophysicsNeovascularization PhysiologicVascular permeabilityBiologyBiochemistryCapillary Permeabilitychemistry.chemical_compoundCell MovementHuman Umbilical Vein Endothelial CellsNeuropilinAnimalsHumansImmunoprecipitationPhosphorylationReceptorMolecular BiologyAortaCells CulturedCell Proliferationta1182Tyrosine phosphorylationrespiratory systemLigand (biochemistry)Vascular Endothelial Growth Factor Receptor-2Cell biologyVascular endothelial growth factorEndothelial stem cellchemistryBiochemistrycardiovascular systemEndothelium VascularPlasmidsSignal Transductioncirculatory and respiratory physiologyBiochimica et Biophysica Acta (BBA) - General Subjects
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Oxidative stress in vascular disease: causes, defense mechanisms and potential therapies

2007

Endothelial cells control vascular homeostasis by generating paracrine factors that regulate vascular tone, inhibit platelet function, prevent adhesion of leukocytes, and limit proliferation of vascular smooth muscle. The dominant factor responsible for many of those effects is endothelium-derived nitric oxide (NO). Endothelial dysfunction characterized by enhanced inactivation or reduced synthesis of NO, alone or in combination, is seen in conjunction with risk factors for cardiovascular disease. Endothelial dysfunction can promote vasospasm, thrombosis, vascular inflammation, and proliferation of the intima. Vascular oxidative stress and increased production of reactive oxygen species con…

Vascular smooth muscleEndotheliumArteriosclerosisPharmacologyNitric Oxidemedicine.disease_causeAntioxidantsReceptor Angiotensin Type 1Superoxide dismutaseRisk FactorsmedicineHumansEndothelial dysfunctionchemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologybusiness.industryAnticholesteremic AgentsGeneral Medicinemedicine.diseaseOxidative Stressmedicine.anatomical_structureMitochondrial respiratory chainchemistryImmunologybiology.proteinEndothelium VascularHydroxymethylglutaryl-CoA Reductase InhibitorsReactive Oxygen SpeciesCardiology and Cardiovascular MedicinebusinessOxidative stressNature Clinical Practice Cardiovascular Medicine
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Staphylococcus aureus alpha toxin mediates polymorphonuclear leukocyte-induced vasocontraction and endothelial dysfunction.

2002

The effect of Staphylococcus aureus alpha toxin (alpha-toxin) on selectin-mediated neutrophil adhesion was investigated in polymorphonuclear leukocyte- (PMN) induced vasocontraction and endothelial dysfunction. Adherence of human PMNs to rat aortic endothelium increased significantly following stimulation of the endothelium with alpha-toxin (0.1, 0.5, and 1 microg/mL). This effect could be significantly attenuated by monoclonal antibodies directed against P-selectin or fucoidin, a carbohydrate known to block selectins. Unstimulated human PMNs (10(6)cells/mL) were added to organ chambers containing rat aortic rings stimulated with alpha-toxin (0.5 microg/mL). PMNs elicited a significant vaso…

Vascular smooth muscleEndotheliumNeutrophilsBacterial ToxinsPharmacologyBiologyIn Vitro TechniquesCritical Care and Intensive Care MedicineMicrocirculationHemolysin ProteinsFibrinolytic AgentsmedicineCell AdhesionAnimalsHumansEndothelial dysfunctionStaphylococcus aureus alpha toxinAortaThrombinAzepinesTriazolesmedicine.diseaseRatsmedicine.anatomical_structureVasoconstrictionImmunologyEmergency MedicineEndothelium Vascularmedicine.symptomVasoconstrictionSelectinBlood vesselShock (Augusta, Ga.)
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