Search results for "Umbilical Veins"

showing 9 items of 59 documents

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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The “caput medusae” sign in portal hypertension

2018

Umbilical Veinsmedicine.medical_specialtyUrology030218 nuclear medicine & medical imagingDiagnosis DifferentialVaricose Veins03 medical and health sciences0302 clinical medicineX ray computedInternal medicineHypertension PortalmedicineHumansRadiology Nuclear Medicine and imagingPortal hypertensionRadiological and Ultrasound Technologymedicine.diagnostic_testPortal Veinbusiness.industryGastroenterologyMagnetic resonance imagingHepatologymedicine.diseaseMagnetic Resonance ImagingPortal hypertension030211 gastroenterology & hepatologyRadiologymedicine.symptomTomography X-Ray ComputedbusinessSettore MED/36 - Diagnostica Per Immagini E RadioterapiaCaput medusaeMRICT
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Glyceraldehyde-3-phosphate dehydrogenase regulates endothelin-1 expression by a novel, redox-sensitive mechanism involving mRNA stability

2008

17 pages.-- PMID: 18809573 [PubMed].-- Printed version published on Dec 2008.

Untranslated regionUmbilical VeinsRNA StabilityRNA StabilityGlyceraldehyde-3'-phosphate dehydrogenase (GAPDH)Plasma protein bindingstomatognathic systemHumansmRNA stabilityS-Glutathionylation3' Untranslated RegionsMolecular BiologyGlyceraldehyde 3-phosphate dehydrogenaseRegulation of gene expressionMessenger RNAEndothelin-1biologyThree prime untranslated regionGlyceraldehyde-3-Phosphate DehydrogenasesArticlesCell BiologyGlutathioneOxidative StressGene Expression RegulationBiochemistryEndothelin-1 (ET-1)biology.proteinOxidation-ReductionProtein Binding
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Oxidative stress induces myeloperoxidase expression in endocardial endothelial cells from patients with chronic heart failure.

2009

Increased oxidative stress has been implicated in the pathogenesis of a number of cardiovascular diseases. Recent findings suggest that myeloperoxidase (MPO) may play a key role in the initiation and maintenance of chronic heart failure (CHF) by contributing to the depletion of the intracellular reservoir of nitric oxide (NO). NO consumption through MPO activity may lead to protein chlorination or nitration, leading to tissue damage. Primary cultures of human endocardial endothelial cells (EEC) obtained at heart transplantation of patients with CHF and human umbilical vein endothelial cells (HUVEC) were subjected to oxidative stress by incubation with hydrogen peroxide at non lethal (60 mic…

medicine.medical_specialtyPathologyUmbilical VeinsEndothelium3-chlorotyrosine endocardium endothelial cells myeloperoxidase oxidative stressPhysiologyGene Expressionmedicine.disease_causeUmbilical veinNitric oxidechemistry.chemical_compoundPhysiology (medical)Internal medicinemedicineHumansRNA MessengerCells Cultured3-ChlorotyrosinePeroxidaseHeart FailurebiologyReverse Transcriptase Polymerase Chain ReactionSettore BIO/16 - Anatomia UmanaNitrotyrosineMyocardiumEndothelial CellsHydrogen PeroxideOxidantsImmunohistochemistryEndothelial stem cellOxidative Stressmedicine.anatomical_structureEndocrinologychemistryMyeloperoxidaseChronic Diseasebiology.proteinTyrosineCardiology and Cardiovascular MedicineOxidative stress
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Progestogens reduce thromboxane production by cultured human endothelial cells.

2011

Objectives Progestogens have been poorly studied concerning their roles in endothelial physiology. Prostanoids are vasoactive compounds, such as thromboxane A2, a potent vasoconstrictor, and prostacyclin, a vasodilator. We examined the effects of two progestogens used clinically, progesterone and medroxyprogesterone acetate, on thromboxane A2 production by cultured human umbilical vein endothelial cells (HUVEC) and investigated the role of progesterone receptors and the enzymes involved in production of thromboxane A2 and prostacyclin. Methods Cells were exposed to 1‐100 nmol/l of either progesterone or medroxyprogesterone acetate, and thromboxane A2 production was measured in culture mediu…

medicine.medical_specialtyUmbilical VeinsAntineoplastic Agents HormonalThromboxaneBlotting WesternGene ExpressionProstacyclinMedroxyprogesterone AcetatePolymerase Chain ReactionProstacyclin synthaseThromboxane receptorThromboxane ProductionThromboxane A2chemistry.chemical_compoundThromboxane A2Hormone AntagonistsCytochrome P-450 Enzyme SystemInternal medicineProgesterone receptorMedicineHumansCyclooxygenase InhibitorsRNA MessengerCells CulturedProgesteronebiologyDose-Response Relationship Drugbusiness.industryObstetrics and GynecologyEndothelial CellsGeneral MedicineIntramolecular OxidoreductasesThromboxane B2MifepristoneEndocrinologychemistrycardiovascular systembiology.proteinPyrazolesThromboxane-A synthaseThromboxane-A SynthaseProgestinsbusinessmedicine.drugClimacteric : the journal of the International Menopause Society
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Glucose-induced loss of glycosyl-phosphatidylinositol-anchored membrane regulators of complement activation (CD59, CD55) by in vitro cultured human u…

2000

Aims/hypothesis. This study examines whether increased glucose concentrations are responsible for a decreased expression of membrane regulators of complement activation molecules. The effect of high glucose in determining an increase in membrane attack complex deposition on endothelial cells was also investigated. Methods. Endothelial cells were isolated from umbilical cord tissue, cultured in the presence of increased concentrations of glucose, and the expression of CD46, CD55, and CD59 was detected by ELISA (enzyme-linked immunosorbent assay) and by flow cytometry. Glucose-treated endothelial cells were also incubated with antiendothelial cell antibodies and fresh complement to assess the…

medicine.medical_specialtyUmbilical VeinsEndotheliumGlycosylphosphatidylinositolsEndocrinology Diabetes and MetabolismCellCD59 AntigensCD59Complement Membrane Attack ComplexBiologyUmbilical veinMembrane Cofactor ProteinAntigens CDPregnancyInternal medicineInternal MedicinemedicineHumansComplement ActivationCells CulturedMembrane GlycoproteinsCD55 AntigensCD46Cell biologyComplement systemEndothelial stem cellEndocrinologymedicine.anatomical_structureGlucoseFemaleEndothelium VascularComplement membrane attack complexDiabetologia
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Gastrin induces the interaction between human mononuclear leukocytes and endothelial cells through the endothelial expression of P-selectin and VCAM-…

2009

Gastric mucosal inflammation is frequently associated with hypergastrinemia, and a correlation exists between the level of gastrin and degree of gastritis. We have previously observed that gastrin promotes leukocyte-endothelial interactions and contributes to Helicobacter -induced inflammation in the rat mesentery. In the present study, we aimed to evaluate a possible proinflammatory activity of gastrin in humans. The interaction between human leukocytes [U-937 cells, peripheral blood polymorphonuclear (PMN), and peripheral blood mononuclear (PBMC) cells] and human umbilical vein endothelial cells (HUVEC) was analyzed in static and dynamic conditions. The endothelial expression of adhesion …

medicine.medical_specialtyUmbilical VeinsEndotheliumP-selectinPhysiologyLeukocyte adhesion moleculeVascular Cell Adhesion Molecule-1Cell CommunicationBiologyCholecystokinin receptorPeripheral blood mononuclear cellchemistry.chemical_compoundInternal medicineGastrinsmedicineCell AdhesionHumansLeukocyte RollingVCAM-1Cells CulturedGastrinEndothelial CellsCell BiologyFlow CytometryReceptor Cholecystokinin BEndothelial stem cellP-Selectinmedicine.anatomical_structureEndocrinologychemistryMicroscopy FluorescenceLeukocytes MononuclearAmerican journal of physiology. Cell physiology
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Progestogens stimulate prostacyclin production by human endothelial cells.

2005

BACKGROUND: The effects of progestogens on endothelial physiology are poorly studied. Prostacyclin is a potent vasodilator synthesized by two isoforms of cyclooxygenase (COX) in endothelium. We examined the effects of two clinically used progestogens, progesterone and medroxyprogesterone acetate (MPA), on prostacyclin production by cultured human umbilical vein endothelial cells (HUVEC) and the possible role of progesterone receptors and both COX enzymes. METHODS: Cells were exposed to 1-100 nmol/l of either progesterone or MPA and prostacyclin production was measured in culture medium. RESULTS: Both progestogens significantly increased prostacyclin release in a time- and dose-dependent man…

medicine.medical_specialtyUmbilical VeinsEndotheliumProstacyclinMedroxyprogesterone AcetateUmbilical veinInternal medicineProgesterone receptormedicineMedroxyprogesterone acetateHumansCyclooxygenase InhibitorsReceptorCells CulturedNitrobenzenesProgesteroneSulfonamidesbiologyCyclooxygenase 2 InhibitorsDose-Response Relationship DrugEstradiolRehabilitationObstetrics and GynecologyEndothelial CellsMembrane ProteinsEpoprostenolEndothelial stem cellMifepristoneEndocrinologymedicine.anatomical_structureReproductive MedicineCyclooxygenase 2Prostaglandin-Endoperoxide Synthasescardiovascular systembiology.proteinCyclooxygenase 1PyrazolesCyclooxygenaseEndothelium VascularProgestinsReceptors Progesteronemedicine.drugHuman reproduction (Oxford, England)
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Estradiol Stimulates Vasodilatory and Metabolic Pathways in Cultured Human Endothelial Cells

2009

Vascular effects of estradiol are being investigated because there are controversies among clinical and experimental studies. DNA microarrays were used to investigate global gene expression patterns in cultured human umbilical vein endothelial cells (HUVEC) exposed to 1 nmol/L estradiol for 24 hours. When compared to control, 187 genes were identified as differentially expressed with 1.9-fold change threshold. Supervised principal component analysis and hierarchical cluster analysis revealed the differences between control and estradiol-treated samples. Physiological concentrations of estradiol are sufficient to elicit significant changes in HUVEC gene expression. Notch signaling, actin cyt…

medicine.medical_specialtyUmbilical Veinsmedicine.drug_classScienceEstrogen receptorBiologyAmidohydrolasesTransforming Growth Factor beta1chemistry.chemical_compoundInternal medicinemedicineCluster AnalysisEstrogen Receptor betaHumansEstrogen receptor betaCell Biology/Gene ExpressionCells CulturedOligonucleotide Array Sequence AnalysisRegulation of gene expressionPrincipal Component AnalysisMultidisciplinaryEstradiolPhysiology/EndocrinologyReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingQPhysiology/Cardiovascular Physiology and CirculationREstrogen Receptor alphaEndothelial CellsReproducibility of ResultsActin cytoskeletonVasodilationEndocrinologychemistryGene Expression RegulationEstrogenCyclooxygenase 1MedicineSignal transductionAsymmetric dimethylarginineEstrogen receptor alphahormones hormone substitutes and hormone antagonistsMetabolic Networks and PathwaysResearch ArticleSignal TransductionPLoS ONE
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