Search results for "Enos"

showing 10 items of 1576 documents

Pre- and postjunctional effects of diadenosine polyphosphates in the guinea-pig vas deferens.

1995

Abstract The pre- and postjunctional activities of a number of diadenosine polyphosphates were examined in the guinea-pig isolated vas deferens at the level of the membrane-potential, using a modified sucrose-gap technique. P1,P3-Di(adenosine 5′)triphosphate (Ap3A), P1,P4-di(adenosine 5′)tetraphosphate (Ap4A) and P1,P5-di(adenosine 5′)pentaphosphate (Ap5 A) all caused concentration-dependent depolarization of the smooth muscle membrane. The potency order was: Ap5A > Ap4A. Ap3A. P1, P2-Di(adenosine 5′)pyrophosphate (Ap2A) did not evoke depolarization even at the highest concentration tested (1 mM). All the dinucleotides caused a reduction in the amplitude of evoked excitatory junction…

Malemedicine.medical_specialtyGuinea PigsPharmaceutical ScienceIn Vitro TechniquesMembrane PotentialsVas DeferensAdenine nucleotideInternal medicinemedicineAnimalsPharmacologyDose-Response Relationship DrugChemistryPurinergic receptorAntagonistVas deferensReceptors PurinergicDepolarizationAdenosine receptorAdenosinemedicine.anatomical_structureEndocrinologyExcitatory postsynaptic potentialDinucleoside Phosphatesmedicine.drugThe Journal of pharmacy and pharmacology
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Endovascular Treatment of Spontaneous Internal Carotid Artery Dissection with Proximal Embolic Protection Device

2019

Background The aim of this study was to report the feasibility and outcomes with the endovascular treatment of spontaneous internal carotid artery dissections (ICADs) using a proximal embolic protection device (EPD). Methods This is a retrospective analysis of patients treated for spontaneous symptomatic ICAD using a proximal EPD from January 2017 to December 2018. Indication for treatment was the presence of neurologic symptoms. Early outcomes measured included technical success, perioperative mortality, and major cardiovascular or cerebrovascular complications. Late outcomes were recurrent neurologic symptoms, patency, and reinterventions. Results A total of 4 male patients with ICAD were…

Malemedicine.medical_specialtyICADAmaurosis FugaxCarotid Artery Internal Dissection030204 cardiovascular system & hematologySettore MED/22 - Chirurgia VascolareEmbolic Protection Devices030218 nuclear medicine & medical imaging03 medical and health sciences0302 clinical medicineproximal embolic protection deviceRestenosisinternal carotid artery dissectionmedicine.arteryAphasiamedicineHumansCarotid StenosisStrokeRetrospective StudiesInternal carotid artery dissectioncarotid artery stentingbusiness.industryEndovascular ProceduresGeneral MedicineAmaurosis fugaxPerioperativeMiddle Agedmedicine.diseaseSurgeryStenosisTreatment OutcomeIschemic Attack TransientendovascularStentsSurgeryInternal carotid arterymedicine.symptomCardiology and Cardiovascular MedicinebusinessCarotid Artery Internal
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Myocardial hypertrophy is associated with inflammation and activation of endocannabinoid system in patients with aortic valve stenosis.

2013

article i nfo Article history: Received 1 February 2013 Accepted 22 March 2013 Aims: Endocannabinoids and their receptors have been associated with cardiac adaptation to injury, inflam- mation and fibrosis. Experimental studies suggested a role for inflammatory reaction and active remodeling in myocardial hypertrophy, but they have not been shown in human hypertrophy. We investigated the asso- ciation of the endocannabinoid system with myocardial hypertrophy in patients with aortic stenosis. Main methods: Myocardial biopsies were collected from patients with aortic stenosis (AS) and atrial myxoma as controls during surgery. Histological and molecular analysis of endocannabinoids and their r…

Malemedicine.medical_specialtyInflammationCardiomegalyGeneral Biochemistry Genetics and Molecular BiologyMuscle hypertrophyFibrosisInternal medicinemedicineHumansGeneral Pharmacology Toxicology and PharmaceuticsAgedPressure overloadInflammationbiologybusiness.industryTenascin CGeneral MedicineAortic Valve Stenosismedicine.diseaseEndocannabinoid systemCTGFEndocrinologyAortic valve stenosisbiology.proteinlipids (amino acids peptides and proteins)Femalemedicine.symptombusinessEndocannabinoidsLife sciences
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Association between periodontal disease and prostate cancer: a systematic review and meta-analysis

2021

Background Periodontal disease is a chronic infectious disease caused by bacterial infection which may lead to various systematic diseases. Recently, increasing studies have explored the correlation of periodontal disease with the risk of prostate cancer. However, the findings were inconsistent. Hence, this study aims to investigate the association between periodontal disease and the risk of prostate cancer by a meta-analysis. Material and Methods PubMed, EMBASE, and Cochrane were searched for publications up to July 17, 2020. Cohort and case-control studies evaluating the risk of prostate cancer in patients with periodontal disease were included. A fixed or random-effect model was used to …

Malemedicine.medical_specialtyMEDLINEReviewCohort Studieszoledronic acid03 medical and health sciencesProstate cancer0302 clinical medicinePeriodontal diseaseRisk FactorsInternal medicineHumansMedicinePeriodontologyIn patientbisphosphonatesGeneral DentistryPeriodontal DiseasesUNESCO:CIENCIAS MÉDICASbusiness.industryProstatic Neoplasmsdenosumab030206 dentistrymedicine.diseaseConfidence intervalosteonecrosis of the jawOtorhinolaryngologyCase-Control StudiesMeta-analysisRelative riskCohortincidenceSurgerybusinessantiangiogenic drugMedicina Oral Patología Oral y Cirugia Bucal
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Impact of C-reactive protein and fibrinogen on cardiovascular prognosis in patients with stable angina pectoris: the AtheroGene study.

2006

Aims C-reactive protein and fibrinogen have been extensively studied and shown to be predictive for a first cardiovascular event in healthy individuals. We evaluated the potential clinical use of C-reactive protein and fibrinogen in patients already suffering from coronary artery disease (CAD). Methods and results In a substudy of the prospective Athero Gene registry, we assessed in 1806 patients with documented CAD and stable angina pectoris, the risk of cardiovascular death and non-fatal myocardial infarction ( n =183) over a median follow-up of 3.5 (maximum 7.7) years according to baseline levels of C-reactive protein and fibrinogen. C-reactive protein and fibrinogen were associated with…

Malemedicine.medical_specialtyMyocardial InfarctionFibrinogenDisease-Free SurvivalAngina PectorisCoronary artery diseaseRisk FactorsInternal medicinemedicineHumansIn patientMyocardial infarctionRisk factorbiologybusiness.industryC-reactive proteinConfoundingCoronary StenosisFibrinogenMiddle Agedmedicine.diseasePrognosisC-Reactive ProteinCardiovascular DiseasesCirculatory systembiology.proteinCardiologyFemaleCardiology and Cardiovascular MedicinebusinessBiomarkersmedicine.drugEuropean heart journal
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Cannabinoid type 1 receptor blockade promotes mitochondrial biogenesis through endothelial nitric oxide synthase expression in white adipocytes

2008

OBJECTIVE—Cannabinoid type 1 (CB1) receptor blockade decreases body weight and adiposity in obese subjects; however, the underlying mechanism is not yet fully understood. Nitric oxide (NO) produced by endothelial NO synthase (eNOS) induces mitochondrial biogenesis and function in adipocytes. This study was undertaken to test whether CB1 receptor blockade increases the espression of eNOS and mitochondrial biogenesis in white adipocytes. RESEARCH DESIGN AND METHODS—We examined the effects on eNOS and mitochondrial biogenesis of selective pharmacological blockade of CB1 receptors by SR141716 (rimonabant) in mouse primary white adipocytes. We also examined eNOS expression and mitochondrial biog…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIEndocrinology Diabetes and MetabolismAdipocytes WhiteImmunoblottingCitrate (si)-SynthaseWhite adipose tissueAMP-Activated Protein KinasesProtein Serine-Threonine KinasesMitochondrionDNA MitochondrialMicechemistry.chemical_compoundAdenosine TriphosphatePiperidinesReceptor Cannabinoid CB1AMP-activated protein kinaseMultienzyme ComplexesEnosAdipocyteInternal medicineInternal MedicinemedicineAnimalsPhosphorylationRNA Small InterferingReceptorCells CulturedDose-Response Relationship DrugbiologyReverse Transcriptase Polymerase Chain ReactionFlow Cytometrybiology.organism_classificationMitochondriaMice Inbred C57BLNitric oxide synthaseMetabolismEndocrinologychemistryMitochondrial biogenesisbiology.proteinSettore BIO/14 - FarmacologiaPyrazolesRimonabant
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Regulation of Oxygen Distribution in Tissues by Endothelial Nitric Oxide

2009

Nitric oxide (NO) decreases cellular oxygen (O 2 ) consumption by competitively inhibiting cytochrome c oxidase. Here, we show that endogenously released endothelial NO, either basal or stimulated, can modulate O 2 consumption both throughout the thickness of conductance vessels and in the microcirculation. Furthermore, we have shown that such modulation regulates O 2 distribution to the surrounding tissues. We have demonstrated these effects by measuring O 2 consumption in blood vessels in a hypoxic chamber and O 2 distribution in the microcirculation using the fluorescent oxygen-probe Ru(phen) 3 2+ . Removal of NO by physical or pharmacological means, or in eNOS −/− mice, abolishes this …

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIEndotheliumPhysiologychemistry.chemical_elementOxygen consumptionBiologyNitric OxideOxygenMicrocirculationNitric oxideElectron Transport Complex IVRats Sprague-DawleyMicechemistry.chemical_compoundOxygen Consumption:CIENCIAS MÉDICAS ::Medicina interna [UNESCO]EnosInternal medicinemedicineAnimalsHumansCytochrome c oxidaseEndotheliumHypoxiaUNESCO::CIENCIAS MÉDICAS ::Medicina internaMice KnockoutNitric Oxide Synthase Type IIINitric oxide:CIENCIAS MÉDICAS [UNESCO]biology.organism_classificationRatsOxygenEndocrinologymedicine.anatomical_structurechemistryUNESCO::CIENCIAS MÉDICASCirculatory systemBiophysicsbiology.proteinNitric oxide ; Endothelium ; Oxygen consumptionEndothelium VascularCardiology and Cardiovascular MedicineSignal TransductionCirculation Research
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Mechanisms underlying recoupling of eNOS by HMG-CoA reductase inhibition in a rat model of streptozotocin-induced diabetes mellitus

2007

Abstract Objective HMG-CoA reductase inhibitors have been shown to upregulate GTP cyclohydrolase I (GTPCH-I), the key enzyme for tetrahydrobiopterin de novo synthesis and to normalize tetrahydrobiopterin levels in hyperglycemic endothelial cells. We sought to determine whether in vivo treatment with the HMG-CoA reductase inhibitor atorvastatin is able to upregulate the GTPCH-I, to recouple eNOS and to normalize endothelial dysfunction in an experimental model of diabetes mellitus. Methods and results In male Wistar rats, diabetes was induced by streptozotocin (STZ, 60mg/kg). In STZ rats, atorvastatin feeding (20mg/kg/d, 7 weeks), normalized vascular dysfunction as analyzed by isometric tens…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIGTP cyclohydrolase INitric Oxide Synthase Type IIReductaseArticleDiabetes Mellitus ExperimentalCytochrome P-450 Enzyme SystemEnosInternal medicineAtorvastatinmedicineAnimalsNADH NADPH OxidoreductasesPyrrolesRats WistarEndothelial dysfunctionGTP CyclohydrolaseNADPH oxidasebiologyStem CellsBody WeightMicrofilament ProteinsTetrahydrobiopterinPhosphoproteinsmedicine.diseasebiology.organism_classificationBiopterinRatsEnzyme ActivationIntramolecular OxidoreductasesVasodilationNitric oxide synthaseDisease Models AnimalOxidative StressTetrahydrofolate DehydrogenaseDiabetes Mellitus Type 1EndocrinologyHeptanoic AcidsHMG-CoA reductaseNADPH Oxidase 1biology.proteinEndothelium VascularHydroxymethylglutaryl-CoA Reductase InhibitorsCardiology and Cardiovascular MedicineCell Adhesion MoleculesDiabetic Angiopathiesmedicine.drugAtherosclerosis
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Myocardial and lymphocytic expression of eNOS and nNOS before and after heart transplantation: Relationship to clinical status

2013

Abstract Aims The present study investigates the expression and clinical relevance of the constitutive NO synthases in heart and peripheral blood mononuclear cells (PBMCs) obtained from heart failure patients. Main methods mRNA and protein levels (qRT-PCR and immunoblot) of eNOS and nNOS were determined in: i) Left ventricle (LV, n = 4) and PBMCs (n = 10) from healthy donors; ii) LV, right ventricle (RV) and PBMCs of heart failure (HF) patients (n = 32); and iii) biopsies and PBMCs of the HF patients after cardiac transplant (n = 15). Key findings Expression of constitutive NOS isoforms in heart exhibits wide variability in HF patients, but this variability was not related to aetiology, dis…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIHeart Ventriclesmedicine.medical_treatmentCardiac indexNitric Oxide Synthase Type IPeripheral blood mononuclear cellGeneral Biochemistry Genetics and Molecular BiologyPredictive Value of TestsEnosInternal medicinemedicineHumansClinical significanceGeneral Pharmacology Toxicology and PharmaceuticsHeart FailureHeart transplantationbiologybusiness.industryGeneral MedicineMiddle Agedmedicine.diseasebiology.organism_classificationPulmonary hypertensionmedicine.anatomical_structureVentricleHeart failureLeukocytes MononuclearCardiologyHeart TransplantationFemalebusinessLife Sciences
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Chronic Therapy With Isosorbide-5-Mononitrate Causes Endothelial Dysfunction, Oxidative Stress and a Marked Increase in Vascular Endothelin-1 Express…

2011

Aims Isosorbide-5-mononitrate (ISMN) is one of the most frequently used compounds in the treatment of coronary artery disease predominantly in the USA. However, ISMN was reported to induce endothelial dysfunction, which was corrected by vitamin C pointing to a crucial role of reactive oxygen species (ROS) in causing this phenomenon. We sought to elucidate the mechanism how ISMN causes endothelial dysfunction and oxidative stress in vascular tissue. Methods and results Male Wistar rats ( n = 69 in total) were treated with ISMN (75 mg/kg/day) or placebo for 7 days. Endothelin (ET) expression was determined by immunohistochemistry in aortic sections. Isosorbide-5-mononitrate infusion caused si…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIIsosorbide DinitratePharmacologymedicine.disease_causeBiochemistryMicechemistry.chemical_compoundSuperoxidesEnosInternal medicinePhysiology (medical)medicineAnimalsNitric Oxide DonorsEnzyme InhibitorsRats WistarEndothelial dysfunctionCyclic GMPAortaMice KnockoutNADPH oxidaseEndothelin-1biologybusiness.industryNADPH Oxidasesmedicine.diseasebiology.organism_classificationEndothelin 1BosentanRatsNitric oxide synthaseEndothelial stem cellOxidative StressNG-Nitroarginine Methyl EsterEndocrinologychemistryApocyninbiology.proteinEndothelium VascularCardiology and Cardiovascular MedicineEndothelin receptorbusinessOxidative stressSignal Transductionmedicine.drugFree Radical Biology and Medicine
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