Search results for " Type III"

showing 10 items of 171 documents

Nitric oxide production and endothelium-dependent vasorelaxation ameliorated by N1-methylnicotinamide in human blood vessels.

2012

N 1 -methylnicotinamide (MNA + ) has until recently been thought to be a biologically inactive product of nicotinamide metabolism in the pyridine nucleotides pathway. However, the latest observations imply that MNA + may exert antithrombotic and anti-inflammatory effects through direct action on the endothelium. We examined both in vivo and in vitro whether the compound might induce vasorelaxation in human blood vessels through the improvement of nitric oxide (NO) bioavailability and a reduction of oxidative stress mediated by endothelial NO synthase (eNOS) function. MNA + treatment (100 mg/m 2 orally) in healthy normocholesterolemic and hypercholesterolemic subjects increased the l-argini…

AdultNiacinamidemedicine.medical_specialtyEndotheliumBrachial ArteryNitric Oxide Synthase Type IIIHypercholesterolemiachemistry.chemical_elementCalciumIn Vitro Techniquesmedicine.disease_causeNitric OxideNitric oxidechemistry.chemical_compoundN^{1}-methylnicotinamideDouble-Blind MethodEnosnitric oxideInternal medicineInternal MedicinemedicineHumansflow-mediated dilationCalcimycinCells Culturedendothelial nitric oxide synthaseoxidized low-density lipoproteinbiologyDose-Response Relationship DrugChemistrySuperoxidebiology.organism_classificationendothelial cellsAcetylcholineOxygenVasodilationOxidative Stressmedicine.anatomical_structureEndocrinologysuperoxideEndothelium VascularAcetylcholineOxidative stressmedicine.drugLipoproteinHypertension (Dallas, Tex. : 1979)
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Hereditary angioedema caused by missense mutations in the factor XII gene: clinical features, trigger factors, and therapy.

2009

Background Hereditary angioedema caused by mutations in the factor XII gene is a recently described disease entity that occurs mainly in women. It differs from hereditary angioedema caused by C1 inhibitor deficiency. Objective To assess the clinical symptoms, factors triggering acute attacks, and treatments of this disease. Methods Thirty-five female patients with hereditary angioedema and the factor XII mutations p.Thr309Lys and p.Thr309Arg who came from 13 unrelated families were studied. The observation period was 8.4 years on average (range, 2-26 years). Results Patients had on average 12.7 ± 7.9 angioedema attacks per year. Recurrent facial swellings occurred in all patients; skin swel…

Adultmedicine.medical_specialtyAbdominal painAdolescentmedicine.medical_treatmentImmunologyMutation MissenseSeverity of Illness IndexC1-inhibitorYoung AdultRisk FactorsSurveys and QuestionnairesImmunology and AllergyMedicineHumansHereditary Angioedema Type IIIAge of OnsetChildProgesteroneDanazolPregnancyAngioedemabiologybusiness.industryDanazolAngioedemas HereditaryHormone replacement therapy (menopause)Middle Agedmedicine.diseaseDermatologySurgeryPedigreeTranexamic AcidHereditary angioedemaFactor XIIbiology.proteinFemalemedicine.symptombusinessmedicine.drugThe Journal of allergy and clinical immunology
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Expression and distribution of key enzymes of the cyclic GMP signaling in the human clitoris: relation to phosphodiesterase type 5 (PDE5)

2011

The clitoris contributes to the normal female sexual response cycle. A significance of cyclic guanosine monophosphate (GMP) has been assumed in the control of clitoral vascular smooth muscle. As only a few investigations on the physiology of the vascular and non-vascular clitoral tissue have been carried out, knowledge on the mechanisms controlling this particular female genital organ is still vague. It has been suggested that human clitoral corpus cavernosum smooth muscle is regulated by nitric oxide (NO)/cyclic GMP and related key enzymes, such as NO synthases (NOSs) and the phosphodiesterase type 5 (PDE5). The present study evaluated in the human clitoris, by means of immunohistochemistr…

Adultmedicine.medical_specialtyVascular smooth muscleStromal cellAdolescentNitric Oxide Synthase Type IIIUrologyClitorisBiologyEndothelial NOSSecond Messenger SystemsClitorisNitric oxideYoung Adultchemistry.chemical_compoundInternal medicineCyclic GMP-Dependent Protein KinasesmedicineHumansVimentinProtein kinase ACyclic GMPCyclic guanosine monophosphateCyclic Nucleotide Phosphodiesterases Type 5Cyclic Nucleotide Phosphodiesterases Type 2Immunohistochemistrymedicine.anatomical_structureEndocrinologychemistrycGMP-specific phosphodiesterase type 5FemaleInternational Journal of Impotence Research
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No association between Glu298Asp endothelial nitric oxide synthase polymorphism and Italian sporadic Alzheimer's disease.

2003

A great amount of evidence suggests that neuroinflammation may be a major pathogenetic mechanism in the pathophysiology of sporadic Alzheimer's Disease (sAD). Recently, polymorphisms in the endothelial nitric oxide synthase (NOS3) gene have been associated to late onset Alzheimer's Disease in a British population. However, other groups failed to replicate this finding in Asiatic and Caucasian populations. We conducted a case-control study including a clinically well-defined group of 149 sAD patients and 149 age and sex matched controls to test the association between NOS3 Glu298Asp polymorphism and sAD in an ethnically homogenous Italian population. All subjects were genotyped at NOS3 and a…

Apolipoprotein EMalemedicine.medical_specialtySettore MED/09 - Medicina InternaApolipoprotein BNitric Oxide Synthase Type IIIPopulationDipeptidePolymorphism (computer science)Alzheimer DiseaseInternal medicinemedicineHumansAlleleeducationAgedAged 80 and overeducation.field_of_studyChi-Square DistributionPolymorphism GeneticbiologyGeneral NeuroscienceCase-control studyDipeptidesMiddle Agedmedicine.diseaseGenotype frequencyEndocrinologyItalyCase-Control StudiesImmunologybiology.proteinSettore MED/26 - NeurologiaFemaleAlzheimer's diseaseNitric Oxide SynthaseCase-Control StudieHumanNeuroscience letters
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Two Italian kindreds carrying the Arg136--Ser mutation of the Apo E gene: development of premature and severe atherosclerosis in the presence of epsi…

2003

Abstract Background and Aims: Type III hyperlipoproteinemia, or dysbetalipoproteinemia, is commonly associated with apolipoprotein E2 homozygosity (Cy Background and Aims: 12, Cy Background and Aims: 58). Apo E2-Christchurch (Arg136→Ser), a rare mutation of the Apo E gene, located in the receptor-binding domain of the protein, has been found to be associated in the vast majority of cases of dysbetalipoproteinemia. Methods and Results: This is the first report of two Italian kindreds carrying the Arg136→Ser mutation. One family is a four-generation kindred from Genoa (Liguria, Italy) with a high rate of mortality due to coronary artery disease: the proband was a 51-year-old woman with previo…

Apolipoprotein EProbandMaleSettore MED/09 - Medicina InternaGenotypeApolipoprotein E2ArteriosclerosisEndocrinology Diabetes and MetabolismMedicine (miscellaneous)Sequence HomologyBiologyArteriosclerosiPolymerase Chain ReactionCoronary artery diseaseApolipoproteins EGenotypeHyperlipoproteinemia Type IIImedicineHaplotypeHumansAlleleGenotypingAllelesGeneticsAlleleNutrition and DieteticsBase SequenceHaplotypeLipidMiddle Agedmedicine.diseaseLipidsPedigreeSettore MED/03 - Genetica MedicaHaplotypesMutationFemaleCardiology and Cardiovascular MedicineApolipoprotein E2HumanNutrition, metabolism, and cardiovascular diseases : NMCD
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Structure-activity relationship of staurosporine analogs in regulating expression of endothelial nitric-oxide synthase gene.

2000

In human umbilical vein endothelial cells and in human umbilical vein endothelial cell-derived EA.hy 926 cells, staurosporine (Stsp) and its glycosidic indolocarbazole analogs 7-hydroxystaurosporine (UCN-01) and 4'-N-benzoyl staurosporine (CGP 41251) enhanced nitric-oxide synthase (NOS) III mRNA expression (analyzed by RNase protection assay), protein expression (determined by Western blot), and activity [measured by rat fetal lung fibroblast (RFL-6) reporter cell assay] in a concentration- and time-dependent manner. In contrast, the bisindolylmaleimide analogs GF 109203X, Ro 31-8220 and Go 6983 had no effect on NOS III expression, and Go 6976, a methyl- and cyanoalkyl-substituted nonglycos…

BisindolylmaleimideNitric Oxide Synthase Type IIIBiologyEndothelial NOSNitric OxideGene Expression Regulation Enzymologicchemistry.chemical_compoundStructure-Activity RelationshipAlkaloidsmedicineCyclic GMP-Dependent Protein KinasesStaurosporineAnimalsHumansDrug InteractionsRNA MessengerEnzyme InhibitorsProtein kinase APromoter Regions GeneticProtein Kinase InhibitorsProtein kinase CCells CulturedProtein Kinase CPharmacologyKinaseTumor Necrosis Factor-alphaNitric Oxide Synthase Type IIIProtein-Tyrosine KinasesStaurosporineMolecular biologyCyclic AMP-Dependent Protein KinasesRatschemistryMolecular MedicineEndothelium VascularNitric Oxide SynthaseTyrosine kinaseProtein Kinasesmedicine.drugMolecular pharmacology
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Role of NO-synthases and cyclooxygenases in the hyperreactivity of male rabbit carotid artery to testosterone under experimental diabetes.

2009

Abstract Cardiovascular disease is the major cause of morbidity and mortality in diabetic patients, which in turn is also associated with low levels of serum testosterone. The working hypothesis was that diabetes might modify the mechanisms involved in the vascular actions of testosterone in isolated rabbit carotid arteries. Testosterone (10 −8 –3 × 10 −4  M) induced a concentration-dependent relaxation of precontracted carotid arteries, which was higher in diabetic than in control rabbits. In control rabbits neither endothelium removal nor the nitric oxide synthase (NOS) inhibitor N G -nitro- l -arginine ( l -NOArg, 10 −5  M) modified the relaxant action of testosterone, and the cyclooxyge…

Blood GlucoseCarotid Artery DiseasesMalemedicine.medical_specialtyArginineEndotheliumCharybdotoxinNitric Oxide Synthase Type IIIThromboxaneBlotting WesternIndomethacinNitric Oxide Synthase Type IIVasodilationProstacyclinNitric OxideNitroarginineDiabetes Mellitus ExperimentalImmunoenzyme TechniquesThromboxane A2Internal medicinemedicinePotassium Channel BlockersAnimalsCyclooxygenase InhibitorsTestosteronePharmacologybiologyDose-Response Relationship Drugbusiness.industryTestosterone (patch)EpoprostenolNitric oxide synthaseVasodilationEndocrinologymedicine.anatomical_structureCarotid ArteriesApaminCyclooxygenase 2cardiovascular systembiology.proteinPotassiumCalciumCyclooxygenaseEndothelium VascularRabbitsbusinessDiabetic Angiopathiesmedicine.drugPharmacological research
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Chronic peroxisome proliferator-activated receptorβ/δ agonist GW0742 prevents hypertension, vascular inflammatory and oxidative status, and endotheli…

2015

Endothelial dysfunction plays a key role in obesity-induced risk of cardiovascular disease. The aim of the present study was to analyze the effect of chronic peroxisome proliferator-activated receptor (PPAR)β/δ agonist GW0742 treatment on endothelial function in obese mice fed a high-fat diet (HFD).Five-week-old male mice were allocated to one of the following groups: control, control-treated (GW0742, 3 mg/kg per day, by oral gavage), HFD, HFD + GW0742, HFD + GSK0660 (1 mg/kg/day, intraperitoneal) or HFD-GW0742-GSK0660 and followed for 11 or 13 weeks. GW0742 administration to mice fed HFD prevented the gain of body weight, heart and kidney hypertrophy, and fat accumulation. The increase in …

Blood GlucoseMaleAgonistmedicine.medical_specialtyNitric Oxide Synthase Type IIIEndotheliumPhysiologymedicine.drug_classCaveolin 1Peroxisome proliferator-activated receptorThiophenesDiet High-FatGW0742MiceInsulin resistanceInternal medicineInternal MedicinemedicineAnimalsObesityPPAR deltaSulfonesEndothelial dysfunctionReceptorPPAR-betaAortachemistry.chemical_classificationInterleukin-6Tumor Necrosis Factor-alphabusiness.industryGlucose Tolerance TestPeroxisomemedicine.diseaseToll-Like Receptor 4VasodilationThiazolesEndocrinologymedicine.anatomical_structureAdipose TissuechemistryHypertensionAdiponectinEndothelium VascularInsulin ResistanceReactive Oxygen SpeciesCardiology and Cardiovascular MedicinebusinessJournal of Hypertension
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Mechanisms involved in the relaxant action of testosterone in the renal artery from male normoglycemic and diabetic rabbits.

2009

Kidney disease is a frequent complication in diabetes, and significant differences have been reported between male and female patients. Our working hypothesis was that diabetes might modify the vascular actions of testosterone in isolated rabbit renal arteries and the mechanisms involved in these actions. Testosterone (10(-8) to 10(-4)M) induced relaxation of precontracted arteries, without significant differences between control and diabetic rabbits. Both in control and diabetic rabbits endothelium removal inhibited testosterone relaxant action. In arteries with endothelium, incubation with indomethacin (10(-5)M), N(G)-nitro-l-arginine (10(-5)M) or tetraethylammonium (10(-5)M) did not modi…

Blood GlucoseMalemedicine.medical_specialtyEndotheliumNitric Oxide Synthase Type IIIThromboxaneBlotting WesternIndomethacinNitric Oxide Synthase Type IIProstacyclinVasodilationNitroarginineMuscle Smooth VascularDiabetes Mellitus ExperimentalImmunoenzyme TechniquesThromboxane A2Renal ArteryEnosInternal medicinemedicine.arteryDiabetes mellitusmedicinePotassium Channel BlockersAnimalsCyclooxygenase InhibitorsProstaglandins ITestosteroneRenal arteryPharmacologybiologyDose-Response Relationship Drugbusiness.industryTetraethylammoniumTestosterone (patch)medicine.diseasebiology.organism_classificationVasodilationEndocrinologymedicine.anatomical_structureCyclooxygenase 2Cyclooxygenase 1PotassiumCalciumEndothelium VascularRabbitsbusinessmedicine.drugSignal TransductionPharmacological research
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Vascular Dysfunction in Streptozotocin-Induced Experimental Diabetes Strictly Depends on Insulin Deficiency

2010

<i>Objective:</i> In previous studies we and others have shown that streptozotocin (STZ)-induced diabetes in rats is associated with vascular oxidative stress and dysfunction. In the present study, we sought to determine whether vascular dysfunction and oxidative stress strictly depend on insulin deficiency. <i>Methods:</i> The effects of insulin (2.5 U/day s.c., 2 weeks) therapy on vascular disorders in STZ-induced (60 mg/kg i.v., 8 weeks) diabetes mellitus (type I) were studied in Wistar rats. The contribution of NADPH oxidase to overall oxidative stress was investigated by in vivo (30 mg/kg/day s.c., 4 days) and in vitro treatment with apocynin. <i>Results:&…

Blood GlucoseMalemedicine.medical_specialtyNitric Oxide Synthase Type IIIEndotheliumPhysiologymedicine.medical_treatmentmedicine.disease_causeStreptozocinDiabetes Mellitus Experimentalchemistry.chemical_compoundInternal medicineDiabetes mellitusmedicineAnimalsInsulinRats WistarEndothelial dysfunctionNADPH oxidasebiologybusiness.industryMyocardiumInsulinAcetophenonesNADPH OxidasesStreptozotocinmedicine.diseaseRatsOxidative StressNG-Nitroarginine Methyl EsterEndocrinologymedicine.anatomical_structurechemistryApocyninbiology.proteinEndothelium VascularCardiology and Cardiovascular MedicinebusinessDiabetic AngiopathiesOxidative stressmedicine.drugJournal of Vascular Research
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